6th year SPECIAL SURGERY

HEAD & NECK

25) Congenital anomalies of the maxillofacial area. Rabbit mouth. Wolf's mouth. Principles
of treatment

https://www.youtube.com/watch?v=U9VlwGkql08

 Incidence of cleft lip and palate – 1:600

 Isolated cleft palate 1:1000, more common in oriental population
 Cleft palate (15%) > Cleft lip (40%)

Etiology: -

 Genetic - fam history of affected 1st degree relative increases risk 1:25
 Environmental: -
o maternal epilepsy + drugs
o teratogens - rubella virus, thalidomide

Syndromes associated with Cleft palate: - Pierre Robin syndrome

 Although most clefts of the lip and palate occur as an isolated deformity, Pierre Robin
syndrome is the most common sequence
 It includes: -
o Isolated cleft palate
o Micrognathia (small lower jaw) and retrognathia (jaw displaced backwards)
o Glossoptosis (Posteriorly displaced tongue)
o Early respiratory and feeding difficulties

Syndromes associated with Cleft lip + Palate: -

 Sticklers (ophthalmic + musculoskeletal abnormalities)

 Shprintzen’s (cardiac abnormalities)
 Down syndrome
 Treacher-Collin’s (absent cheek bones, micrognathia, hearing loss, malformed ears)

LAHSAL classification

 Describes the site, size, extent and type of cleft

Cleft Lip

 Developmental error in the formation of the upper lip will lead to formation of cleft
lip – disruption of muscles of upper lip and nasolabial region
 Facial muscles are divided into 3 rings of Delaire: - NOSELIP; around LIP;
LIPMENTUM
o Nasolabial Muscles – transverse nasalis, levator labii superioris alaeque nasi,
levator labii superioris
o Bilabial Orbicularis Oris – oblique head, horizontal head, lower lip
o Labiomental Muscles – depressor anguli oris, depressor labii inferioris,
mentalis
Classification: -

1. Unilateral - nasolabial and bilabial rings are disrupted on one side

2. Bilateral - muscular rings are disrupted on both sides
3. Incomplete - cleft lip has not extended up to nostril
4. Complete - extends to the floor of nose
5. Uncomplicated
6. Complicated - associated with either cleft alveolus and/or cleft palate

Clinical: -

 Disfigurement
 Inability to suckle
 Decreased speech
 Distortion of dental arch

Diagnosis: -

 Antenatal diagnosis by US after 18 weeks of gestation

Cleft palate

 Anatomy: - https://www.youtube.com/watch?v=TO97fCz59bo (Notes)

 Incidence – 1: 2000
 Failure of fusion of the 2 palatine processes: -
1. primary palate- alveolus and upper lip
2. secondary palate- hard and soft palate
  Soft palate - muscles are oriented transversely with no attachment to
hard palate. In cleft soft palate- muscles are oriented in
anteroposterior direction, inserting into post edge of hard palate
 Hard palate anatomy
 Cleft palate formed failure of fusion of 2 maxillary processes or fusion btw maxillary
and frontonasal process

Types: -

1. Soft palate only - asymptomatic

2. Intermaxillary - btw the 2 maxilla processes
3. Bipartate – intermaxillary + extends to one side of premaxilla
4. Tripartate - intermaxillary + extends to both sides of premaxilla

Classification: -

1. Incomplete - cleft of the hard palate remains attached to the nasal septum + vomer
2. Complete - vomer + nasal septum completely separated from palatine processes
o May be bifid uvula
o Whole length of soft palate
o Whole length of soft palate + post part of hard palate

Clinical: -

 Difficulty suckling & swallowing

 Speech & hearing
 Respiratory tract infections (wide pharynx- swallowingnasal regurgitation
pharyngitis, rhinitis, otitis media, deafness)
 Aspiration pneumonia
 Teeth malformations
 Pierre ribbon syndrome

Treatment: -

 Pre-Op tx: -
o Feeding: most feed + thrive well, use soft bottles, modified teats, enlarge hole
in teat, dropper, special spoon
o Airway: nasopharyngeal intubation, surgical adhesion of tongue to lower
lip(labrioglossopexy) in first few days after birth
 Operation: -
o Principle: -
 Cleft lip surgery: attaches + reconnects muscles around oral sphincter
 Cleft palate: bring together mucosa + muscles with minimal scarring
o Goal: - normal appearance of lip + nose with normal speech, dentition + facial
growth
 o Technique: -
 Millard criteria is used to undertake surgery for cleft lip: (rule of 10
must be fulfilled)
 Weight over 10 pounds
 Over 10 weeks old
 Over 10gm% haemoglobin
o Millard’s technique – 2 flaps (one from the clefted side
and one from the non-clefted side) and the orbicularis
muscle are reconnectedand then the vermillion is
adjusted to the contour of the lip
 Revision surgery done 2 years after the 1st surgery and done in cases
of lip deformity, misaligned vermillion, nose deformity, poor nose tip
projection, asymmetrical cupids bow etc.
o Delaire technique and sequence used for timing for primary cleft lip and
palate procedures: -
 Cleft lip alone: -
 Unilateral – 1 operation at 5-6 months
 Bilateral – 1 operation at 4-5 months
 Cleft palate only: -
 Soft palate only – 1 operation at 6 months
 Soft + hard palate – 2 operations
o Soft at 6 months
o Hard at 18 months
 Cleft lip and palate: -
 Unilateral – 2 operations
o Cleft lip + soft palate at 5-6 months
o Hard palate at 18 months
 Bilateral – 2 operations
o Cleft lip + soft palate at 4-5 months
o Hard palate at 18 months

Congenital Anomalies of Face

1. Coloboma of Face
o Is a cleft connecting eye and the mouth angle; can
be unilateral or bilateral

2. Macrostomia
o MACROSTOMIA = is a rare medical condition, defined as
an enlargement of the mouth at the oral commissure.
 o It is a rare genetic deformity of the skin, muscular and tissue surrounding the
mouth
o It can severely delay speech and language development
o Treatment – myoplasty or plastic surgery of the muscles

3. Microstomia
o It is a rare congenital reduction in the size of the mouth
that is severe enough to compromise nutrition and quality
of life
o Treatment – commisuroplasty (re-create the corners of
the mouth and make mouth wider)

26) Injuries in the maxillofacial region. Open and closed

 60% pts with severe facial trauma have multisystem trauma and airway compromise,
20-50%- brain injury, 1-4% cervical spine injuries, 0.5-3% blindness

Etiology: -

 Violence, snow + freezing weather

 Falls, sporting activities

Clinical features: -

 Pain, bruising, oedema

o Feature of all fractures – develops within 60-90mins – not immediately:
o Impairs airway – swelling of tongue, facial + pharyngeal tissues
 Visible lacerations, injuries to brain/cervical spine
 Immediate (inhalation of tooth fragments, accumulation of blood, loss of tongue
control)
 Delayed airway obstruction

Examination of patient: -

 Facial injury can distract whole body examinations

 Rapid onset of edema can compromise examination – edema of eyelids = difficulty to
examine pupils
 Tenderness = potential fracture
 Asymmetry
 Cranial nerves: paraesthesia suggests fracture proximally along course of nerve
o Facial palsy, low visual acuity, damage to floor of orbit – CN3,4,6 – diplopia
 X-ray/CT

Assessment: -
 Targeting care: Glasgow coma scale
 Predicting outcome: Abbreviated injury scale and injury severity scale
 Assessing critically injured patients: APACHE II

Initial Hospital Care: -

 Triage the causality

 ABCDE

Emergency Management: -

 Airway control: -chin lift, jaw thrust, oropharyngeal suction, manually move tongue,
cervical immobilization
 Intubation
 Haemorrhage control: -
o Maxillofacial: direct pressure, avoid blind clamping of wounds
o Nasal: direct pressure, ant and post pressure
o Pharyngeal- packing around ET tube

Diagnosis: -

 History
 Clinical examination: -ATLS approach,
o Inspection, palpation, visual examination
o physical examination- inspection of symmetry/foreign bodies, palpate face,
check for face stability
 Imaging and CT

Classification of traumas to the face: -

 Upper 1/3rd – above the eyebrows

 Middle 1/3rd – above the mouth (Le forte for maxillary fractures)
 Lower 1/3rd - Mandible

Fracture of Facial Skeleton

NEED TO DO FACIAL NERVE AND ARTERY + MUSCLES

Bones of the skull: -https://www.youtube.com/watch?v=uxmD2XMaBM8

1. Zygomatic Fracture

 Most common of middle 1/3 of face.

 Damage to infraorbital n = numbness of Cheek
 Signs+ symptoms: -
o Periorbital ecchymosis = caused by blood tracking along tissue plains into
periorbital tissues, causing discoloration in the upper and lower eyelids.
o Flattening of malar prominence
 oFlattening of zygomatic arch
oPain, tenderness, ecchymosis of maxillary or buccal surface
oDeformity
oTrismus = When your jaw muscles become so tight that you can't open your
mouth, you may have a condition known as trismus.
o Epistaxis = nosebleed
 Diagnosis: -
o radiography- occipitomental view
o CT- coronal and axial section

Treatment: -

 Indications: -
o Diplopia – double vision
o Restriction of mandibular movements
 Fracture reduced by Gillies Temporal Approach
o Incision in hairline, superficial to temporal fossa
o Channel made down to body of zygomatic bone
o Bristows or Roew’s elevator inserted beneath body of zygoma + force applied
in opposite direction to displacement of fracture

 

  
 o Detail surgery website here
 If unstable fracture = ORIF (plates and screws at frontozygomatic suture, infraorbital
rim, inferior buttress of zygoma)

2. Blowout Fracture of Orbit

 Direct trauma to globe of eye can push it back within the orbit – blunt objects
 Weakest part = floor of orbit
 Orbital contents can (necrosis of tissue) herniate into maxillary antrum = muscular
dysfunction
 Txt: - Bone graft to repair orbital floor

3. Naso Orbital Ethmoidal Complex Fracture

 Involves nasal bones, frontal process of maxilla, medial + infraorbital rims + maxillary
processes
 Disruption of medial canthal lig = traumatic tele canthus (eyes deviate), lacrimal
disruption and ductal tears

CF: -

 Flattened nasal bridge/ saddle shaped deformity

 Widened nasal bridge
 CSF rhinorrhoea = drainage of CSF through the nose
 Epistaxis
 Intranasal palpation- movement of medial canthus

3 types: -

1. Large fragment of medial orbit, medical canthal insertion is intact

2. Comminution of bones, fracture lines does not extend into medial canthal insertion
3. Same as ii but fracture lines extend

Treatment: -

 Debridement and closure of open wound, reduction and stabilization of bone

fracture
 Detached canthus- trans nasal wiring technique, canthopexy

4. Fractures of mandible (3rd most common)

 Assaults and falls- 3rd molar, socket of canine tooth

 Condylar neck = weakest – most common fracture location – mental nerve paresis

 “Guardsman fracture”: blow to chin can cause fracture of maxilla (indirect fracture)
 Masseter, medial and lateral pterygoid and temporalis draw fracture medial and
posterior – fracture of angle is unfavourable

S+S: -

 Head/neck- tenderness
 Malocclusion = teeth are not aligned properly
 trismus, sublingual hematoma
 Altered sensation V3, crepitus
 mandibular pain
 separation of teeth with intraoral bleeding
o Unilateral condyle fracture – decreased translational movement, functional
height of condyle, deviation of chin from fracture, open bite opposite to
fracture
o Bilateral fracture – anterior open bite

Dx: - X-ray mandible

Txt: -

 Closed Reduction (non-displaced fracture)

 Open Reduction: contraindications- rigid fixation using: compression plates, lag
screws OR semirigid fixation: miniplates, trans osseous wiring, external fixators

5. Condylar and Sub condylar

 Closed reduction in children, teens and if intracapsular fractures

 ORIF

6. Maxillary Fractures

Classification: - Le Forte

1. Le Forte I: Allows motion of maxilla while nasal bridge is stable

o S+S: - edema, malocclusion of teeth, motion of maxilla
2. Le Forte II: pyramidal fracture- maxilla, nasal bones, medial aspect of orbits
o S+S: - facial edema, nasal flattening, traumatic tele canthus, epistaxis,
rhinorrhoea
3. Le Forte III: fractures through maxilla, zygoma, nasal bones, ethmoid bones, base of
skull
o S+S: - Dish faced deformity, epistaxis, CSF rhinorrhoea, sever airway
obstruction
Dx: - coronal and axial CT

Txt: -

 Closed reduction with inter maxillary fixation (unilateral fractures)

 Open reduction (intra osseous wiring, using micro/ mini plates)

7. Internal Orbital Fractures

 In conjunction with other facial fractures or isolated (blow out fracture)

S+S: -

 sub conjunctival ecchymosis

 crepitations
 displaced palpebral fissure
 unequal pupillary levels
 diplopia = double vision
 Enophthalmos = posterior displacement of the eyeball within the orbit
Txt: -

 small defect – no surgery

 reconstruction (intrasinus approach to orbital floor or external approach to internal
orbital floor)

8. Pan-Facial Fracture

 Expose all fracture reconstruct AP projections reconstruct width of face

(frontozygomatic suture)  recreate NOE area restore height  restore
occlusion maxilla and mandible closer to teeth

Soft-Tissue Injuries: -

1. Facial Lacerations: -

 Have excellent blood supply + heal well

 Txt: - Sutured asap (absorbable sutures) + broad spec Ab given

2. Skin Loss: -

 Bite injuries – nose + ear

 Small tissue losses = can be sutured closed
 Large tissue losses = reconstruction with grafts

3. Facial Nerve Injury: -

 Lateral face wound can damage facial nerve

 Primary repair should be attempted – several nerve endings approximated using
operating microscope
 4. Parotid Duct: -

 Lacerations in same vicinity as those with facial nerve can transect parotid duct
 Txt: - cannula placed in parotid gl from within mouth  the proximal duct is then
passed over the cannula so approximation of the severed portion of the duct can
occur.
 Cannula left in position for several days to prevent post-anatomic stricture

5. Lacrimal Apparatus: -

 Tissues are grossly edematous

 Epiphora (overflow of tears) = complication

27) Inflammatory processes of the maxillofacial area. Tumors

Inflammatory diseases of the face and jaws

Classification: -

Non-odontogenic Odontogenic
 Furuncle/carbuncle  Abscess & phlegmons
 Erysipelas  Odontogenic osteomyelitis
 Sialadenitis  Lymphadenitis
 Other- actinomycosis  Periostitis

 Maxillofacial area – face and jaw

1. Cellulitis
 Def: - It is a bacterial infection of the skin and subcutaneous tissues caused by beta
haemolytic Strep B
 It is usually associated with broken skin or pre-existing ulceration
 Clinical features: -
o An expanding area of erythematous, edematous tissue that is painful
o Lymphangitis, lymphadenitis
o Associated with fever, malaise and leucocytosis
 Treatment – if an abscess forms, it must be drained
2. Abscess
 Def: - It is a localised collection of pus produced by pyogenic organisms or
sometimes injections of irritants
 It is a hard, red painful swelling which then softens and becomes fluctuant
 If it is NOT drained, it can discharge into cavity
 Clinical features: - bacterial infection, swinging fever, malaise, anorexia, sweating
 Treatment: -
o Because the lining of an abscess cavity tends to impede drug penetration
from the circulation to the site of infection, the cavity itself needs drainage
o Once an abscess has fully formed, it often doesn’t respond to antibiotics
 o Process of drainage: -
 Before incision, the skin over the abscess should be cleansed with
antiseptic solution
 The physician should cut into the lining of an abscess allowing the pus
to escape through a drainage tube or by leaving the cavity open
 Once the tube is in place, the physician closes the incision site with
simple stitches and applies sterile dressing
 Drainage is done for several days to help prevent the abscess from
reforming
 Once the drainage is complete, the tube is removed and the abscess is
allowed to heal
3. Furuncle (boil)
 Def: - a furuncle is an acute purulent inflammation of the pilar (hair) follicle and the
surrounding tissue
 A furuncle is a deep folliculitis, infection of the hair follicle – NFL
 It is NOT formed on hairless area
 On the face, it can be complicated by a pyelophlebitis spreading along the facial
veins  resulting in thrombosis of the cavernous sinus
 It is most commonly caused by the Staph. Aureus
 Treatment: -
o Locally – 70% alcohol, 2% salicylic acid in alcohol, 5-10% iodine
o The hair around the area should be shaved
o Do NOT squeeze the pimple, because this can destroy the protective barrier
o If antibiotics are used, they should be effective against MRSA
4. Toxic epidermal necrolysis (Steven Johnson Syndrome)
 Def: - It is an autoimmune reaction to stimuli such as drugs (anticonvulsants,
sulphonamides, allopurinol and NSAIDs), which results in structural defects in the
epidermal-dermal junction
 There is symmetrical macular eruption which begins on the face and spreads to the
extremities
 It evolves into blisters exposing the dermis
 Nikolsky’s sign – when lateral pressure is applied to the blister, it results in the
epidermis detaching from the basal layer

 Treatment: -
o Wound care, debridement of devitalised tissue
o Temporarily cover the skin until re-epithelisation is allowed to progress –
this decreases skin infection and dehydration (can cover with biological
dressing – allograft skin)
o Steroids should NOT be used due to high risk of sepsis
5. Odontogenic cysts
 An ODONTOGENIC CYST = is a fluid-filled sac that develops in the jaw bone over a
tooth that hasn't erupted yet.
 They arise from odontogenic epithelium left behind in the mandible as tooth buds
out
 Epithelial remnant can form a cyst with 2-3 diameter
 There is swelling in the bone  the bone can fracture when it is touched as it is very
thin
 Treatment: -curettage, resection, enucleation (removal of the cyst without cutting or
dissection)
Tumours of the face
Classification: -
 Epidermal
o Benign: -PSS
1. Papilloma
2. Senile keratosis
3. Seborrheic keratosis (basal cell papilloma)
o Malignant: -BSB
1. Bowen’s disease
2. Squamous cell carcinoma
3. Basal cell carcinoma
 Benign and malignant melanoma
1. Papilloma (skin tag)
 PAPILLOMA = is a benign, pedunculated tumour pigmented with melanin

 SEBORRHEIC KERATOSIS/AGE WART (basal

cell papilloma) = it is a yellow-ish brown
raised lesion that appears greasy. It is a
benign wart-like growth on the skin
o It affects people above 40 years old

2. Bowen’s disease
 Def: - It is a slow growing, red, scaly plaque/patch on the skin. It is a very early form
of skin cancer
 It can be mistaken for psoriatic plaque
 It affects the squamous cells of the epidermis,
which are in the outermost layer of the skin
 HPV DNA can be found in some lesions
 Causes: - UV radiation, HPV infection, ionising
radiation
 Treatment: -
o Excision, cryotherapy, curettage and autotherapy
o If it is left untreated, squamous cell carcinoma will ensue
3. Squamous cell carcinoma (epithelioma)
 It is the second most common skin cancer after basal cell carcinoma
 It is mainly caused by chronic sun exposure and generally affects elderly people on
skin exposed to sun
 Risk factors: - solar keratosis, Bowen’s disease, HPV infection
 Clinical features: -
o It can appear as a carcinomatous ulcer
with indurated, raised everted edges
and a central scab
o Raised scaly lump on sun-exposed sites
o It can develop slowly over the years
from a red scaly sun spot that slowly
thickens and enlarges to become an
intraepidermal carcinoma (Bowen’s disease), which can then progress to
become a fully SCC involving the deeper layers of the skin
 Treatment: -
o Excision and radiotherapy
o If the regional lymph nodes are involved, then must remove all of the lymph
nodes that provide lymphatic drainage for the cancerous area to prevent
lymphatic spread
4. Basal cell carcinoma (rodent ulcer)
 It is the most common skin cancer affecting white people
 90% cases affect the face – around the eyes, nasolabial field exposure to sun or
radiation
 It appears as a raised, rolled but NOT everted edges. It consists of pearly nodules
over which fine blood vessels can be seen (telangiectasia)
 It starts as a small nodule which grows slowly with central ulceration and scabbing
 It spreads slowly and can affect the skull (erosion) – thus the name rodent – erosion
of the nose, eye and face
 Treatment – excision and radiotherapy
5. Melanoma
 It develops from melanocytes in the basal layer of the epidermis
 Classification: -
o Intradermal (naevus)
o Junctional
o Compound
o Juvenile
o Malignant
 Melanoma begins as a flat, light brown to black spot, that looks like a mole.
o However, unlike moles, melanomas grow progressively larger, and as they
enlarge, they change in shape and colour so the spot becomes increasingly
irregular in shape or colour
 Signs of malignant melanoma: -
o Increase in size
o Increase in pigmentation
o Bleeding
o Irregular border
o Itching and pain
 Treatment: -
o Excision and immunotherapy with
high dose interferon a2b
o It is resistant to radiotherapy/chemotherapy
Tumours of the jaw
1. Ambeloblastoma
 It arises from ameloblasts which are responsible for forming the crown of teeth
 It is a painless tumour which causes swelling of the jaw
 It can become malignant if it extends into soft tissue

2. Malignant lymphoma
 It is a malignant tumour of B-lymphocytes associated with EBV infection
 It is a painless swelling of the jaw which distorts the jaw
  Treatment: - local excision.
o The lower jaw may need a bone graft to resected portion of the mandible

28) Congenital, traumatic, inflammatory diseases of the neck

Congenital diseases of the neck

1. Cystic hygroma (lymphangioma)
 Def: -It is a fluid-filled sac that results from blockage in the
lymphatic system
 It appears as a soft bulge under the skin and is most commonly
located in the neck or head region
 As the baby grows in the womb, the cyst can develop from pieces of
embryonic lymphatic tissue – derived from clusters of lymph
channels that failed to connect and become normal lymphatic
pathways
 It can be associated with nuchal lymphangioma, fetal hydrops, Down
syndrome or Turner’s syndrome
 Treatment: -
o If the fetus has a large hygroma, C-section delivery should be done and
monitor the airways
o Thin needle aspiration to reduce the volume
o Surgical removal – although there is a chance of
recurrence
Trauma to the neck
1. Upper cervical spine (skull-C2)
1) Hangman fracture
o Combined distraction and extension e.g., in
hanging, may result in fracture of the C2 pedicles
and disruption of the soft tissues between C2 and C3
o The risk of spinal cord injury and quadriplegia is high
o Treatment – surgical stabilisation
2) C1 burst fracture (Jefferson fracture)
o C1 (atlas) bears the weight of the head
o Axial load applied to the top of the head, such as
diving into a shallow swimming pool, can fracture C1 in a characteristic ‘burst’
pattern
o The fracture is unstable and injury to the spinal cord at this level results in
death
o Treatment – surgical, either to fuse the skull to the spine, or to immobilise
the cervical spine with a halo brace until healing occurs
3) C2 peg fracture
 o The atlas rotates around a peg of bone arising from C2. The peg called dens
o Hyperextension of the neck may result in fracture of the peg
o It is a common injury in elderly who fall from standing, hitting their chin on
the floor and forcing the neck into extension
o Treatment – collar for 8 weeks. However, if the fracture is displaced or non‐
healing, surgical screw fixation is done

2. Sub axial cervical spine (C3-C7)

1) Facet joint dislocation
o The FACET JOINTS are obliquely orientated joints towards the posterior part
of the vertebra. They allow movement between
adjacent vertebrae
o On a true normal lateral X-ray, the left and right
facet joints directly overlie each other
o Distraction and flexion (e.g., in rapid deceleration)
may result in dislocation of the facet joints
o Diagnosis: - lateral X‐ray shows that one vertebra is
subluxed anterior to the other and congruence
(same shape and size) of the facets is lost, producing
a double shadow
o Treatment – reduce and stabilise the dislocation
2) Clay shoveler’s fracture
o An avulsion of the tip of the C7 spinous process may occur due a sudden pull
of the trapezius muscle
o Treatment – the fracture is painful but stable and can be treated
conservatively
3) Body fracture (teardrop fracture)
 Hyperflexion combined with axial load may result in
fractures of the anterior aspect of the vertebral body –
this is also called teardrop fracture
 If the force is big enough, the posterior elements of the
spine may be distracted, making the spine unstable
 Treatment – surgical fixation combined with bone graft
and fusion of adjacent vertebrae

Inflammatory diseases of the neck

1. Ludwig’s angina ! at least remember the names
 Def: -It is an inflammatory edema of the
submandibular region and floor of the mouth, due to Streptococcal infection
 It is a type of severe cellulitis
 The infection includes both sides of the mylohyoid muscles causing edema and
inflammation so much that the tongue is displaced, resulting in dysphagia and
dyspnea
 Treatment – broad spectrum antibiotics and curved submental incision to drain
both of the submandibular triangles of the neck
 2. Cervical lymphadenitis (cat scratch disease)
 Acute
o The affected lymph nodes are enlarged and tender and there may be
pyrexia, anorexia and malaise
o Treatment – directed to the primary focus of infection e.g., tonsillitis or a
dental abscess
 Chronic
o It can be caused by tuberculosis or be secondary to a malignant disease e.g.,
squamous cell carcinoma
o Treatment – TB medication, chemotherapy, remove the lymph nodes
3. Tuberculosis adenitis
 In most cases the tuberculous bacilli gain access through the
tonsils
 80% cases are limited to the lymph nodes, but a primary focus
in the lungs must be examined
 Mainly affects young children and young adults
 Diagnosis – fine needle aspiration taken from the neck
 Treatment – chemotherapy if the abscess fails to resolve then
excision

29) Tumors of the neck. Tracheostomy. Types and indications

Primary tumours of the neck

1. Chemodectoma (carotid body tumour)
 Def: -It is a rare, benign tumour mainly affecting people who live in high altitudes
due to chronic hypoxia, leading to carotid body hyperplasia
 The tumour arises from the chemoreceptor cells on the medial side of the carotid
bulb and at this point the tumour is adhered to the carotid wall

 Clinical features: -
o Slowly, enlarging painless lump at the carotid bifurcation
o Pharyngeal mass pushes the tonsils medially. The mass is firm, rubbery and
pulsatile
o Bruit may be present
 BRUIT = also called vascular murmur, is the abnormal sound
generated by turbulent flow of blood in an artery due to either an
area of partial obstruction or a localized high rate of blood flow
through an unobstructed artery.
 Diagnosis: -
o Carotid angiogram, MRI
o Contraindications – biopsy and fine needle aspiration
 Treatment: -
o The tumour is NOT removable due to large mass close to the carotid
bifurcation and thus bypass must be considered to restore arterial continuity
in the carotid system
o Radiotherapy has NO effect
2. Vagal body tumours ! do Vagus nerve pathway
 Vagal paragangliomas arise from the paraganglionic
tissue of the Vagus nerve just below the base of the skull, near the jugular foramen
 Vagal paragangliomas are rare tumors that develop in the retro styloid
compartment of the parapharyngeal space.
 They arise from an island of paraganglion tissue derived from the neural crest that is
located on the Vagus nerve.
 Clinical features: - they are slow growing painless masses located in the
anterolateral neck region
 Diagnosis: - CT and MRI
 Treatment: - surgical excision
3. Peripheral nerve tumours (Schwannomas)
 SCHWANNOMAS are solitary encapsulated tumours attached to or surrounded by
nerve
 The Vagus nerve is the most common location
 Neurofibromas also arise from the Schwann cell
 Diagnosis: - CT and MRI to differentiate between other pharyngeal tumours
Tracheostomy
 Tracheostomy indications; Types & procedure – more important
 Def: - Tracheostomy is a procedure that relieves airway obstruction or protects the
airway by creating an entrance into the trachea through the skin of the neck
 Must tell the person they will NOT lose their voice permanently (THIS IS NOT A
DISNEY MOVIE AND YOU ARE NOT ARIEL)
 Tracheostomy tubes are of 2 types – plastic or silver
 Indications: -
o Emergency when the patient is in extremis and the larynx can NOT be
intubated (this is difficult, especially in obese patients)
o Acute upper airway obstruction e.g., inhaled foreign body, large
pharyngolaryngeal tumour
o Potential upper airway obstruction e.g., major surgery involving the oral
cavity, pharynx, larynx or neck
o Protection of the lower airway e.g., protection against aspiration of saliva in
unconscious patients as a consequence of head injuries or coma
o Patients requiring prolonged artificial respiration – best done within 10 days
of ventilation
Types of tracheostomies: - ! at least remember the names
1. Emergency tracheostomy
 Local anaesthesia can be used, or if the patient is unconscious, it is
NOT needed
 A vertical midline incision is made from the inferior aspect of the
thyroid cartilage to the suprasternal notch and continued down
between the infrahyoid muscles
 There may be heavy bleeding from the wound, especially if the neck is
congested as a result of the patient’s efforts to breathe around an
acute airway obstruction – NO steps are taken to control this
haemorrhage, although an assistant and suction are valuable
 The doctor should feel carefully for the cricoid cartilage using the
index finger of the free hand, while retracting the skin edges by applying pressure
using the thumb and middle finger
 If it is an extreme emergency situation, another vertical incision can be made straight
into the trachea at the level of the 2nd, 3rd and 4th ring.
 o The knife blade is rotate through 90 degrees, thus opening the trachea.
o At this point, the patient may cough violently as blood enters the airways –
must be careful to NOT lose the position of the scalpel in the trachea.
o Insert a tube into the trachea as soon as possible and suck out blood and
secretions
 Once the emergency is controlled, reposition the tracheostomy as soon as possible
 FIND PICTURES OR VIDEO FOR THIS PROCEDURE!!!
2. Elective tracheostomy
 The advantage of this procedure is that there is complete airway control at all times,
unhurried dissection and careful tube placement
 After general anaesthesia and endotracheal intubation, the patient is positioned with
a combination of head extension and placement of an appropriate sandbag under
the shoulders

 A transverse incision can be done in the elective situation and the tracheal isthmus
is divided carefully and oversewn
o Tension sutures are placed either side of the tracheal fenestration in children
o A Bjork flap is used in adults – a 4-5mm wide U-shaped incision is made
through the 2nd, 3rd and 4th tracheal rings resulting in a flap which is sutured to
the skin to secure the tracheostomy lumen
3. Percutaneous tracheostomy
 A transverse incision is made between the 1st and 2nd tracheal rings and blunt
dissection of the midline is done
 A 22-gauge needle is inserted between the 2nd and 3rd tracheal rings. When air is
aspirated into the syringe, the guidewire is introduced and protected, after which
dilators are placed
 All dilators are inserted in a sequential way from smallest to largest diameter
 The tracheostomy tube is then inserted along the dilator and guidewire
 Then the guidewire and dilator is removed and the cuff of the tracheostomy tube is
inflated and the breathing circuit is connected. The endotracheal tube can now be
removed

30) Goitres. Special forms of goitres

Anatomy: - THYROID GLAND.docx

Selfless medicosis - Goitres

 GOITRE = enlargement of the thyroid gland

Classification: -

 Goitres can be divided into 5 main types: -

1. Simple non-toxic
a. Diffuse hyperplastic
b. Pubertal
c. Colloid goitre
d. Multinodular (MNG)
2. Toxic
a. Graves’ disease (primary thyrotoxicosis)
b. Secondary thyrotoxicosis (MNG)
c. Diffuse toxic goitre
3. Neoplastic
a. Benign
b. Malignant
4. Thyroiditis
a. Hashimoto’s
b. DeQuervain
c. Riedel’s
5. Other
a. Acute bacterial
b. Thyroid cyst
c. Thyroid abscess
d. Amyloid goitre
Goitre grading: - 0-3
 Stage 0: -No visible goitre
 Stage 1a: - Goitre is detectable
 Stage 1b: - Visible/palpable goitre when neck is extended
 Stage 2: - Visible goitre with neck in normal position; palpitation not needed for dx
 Stage 3: - Very large goitre that can be easily seen

Special forms of goitres: -

1. Reidel’s Thyroiditis
 Rare form of thyroiditis in which chronic inflam (fibrosis) process involves one or
both lobes of thyroid
 Gland slightly enlarged with infiltration of adjacent tissues – fasciae, muscles, nerves,
bv, trachea + oesophagus
Pathology: -

 Decreased number + size of thyroid follicles – replaced by dense fibrous tissue

Etiology: -

 Late-stage Hashimoto’s or inflam origin

 Mistaken clinically for thyroid Ca, but histologically gl is replaced by fibrous tissue
with chronic inflam cells

Clinical: -

 Women, 50 yrs, asymptomatic

 Compressive symptoms due to increased goitre size - dysphagia, dyspnea, recurrent
laryngeal nerve
 Pts usually euthyroid with normal TSH + low/normal free T4

Diagnosis: -

 Radioactive iodine uptake – shows patchy uptake with hot + cold nodules
 Thyroid function test show hypothyroidism
 Thyroid Ab (autoantibody against thyroid) shown in serum (lower titres than in pts
with Hashimoto’s)

Treatment: -

 Thyroxin – tx of choice
 Wedge resection of gl if trachea compression
 Surgical resection reserved for goitres that: IF
o continue to increase despite T4 suppression
o cause obstructive symptoms
o have malignancy suspected
o cosmetically unacceptable
 Total thyroidectomy: require T4 therapy for life
2. De Quervain’s Thyroiditis (Granulomatous Thyroiditis)
 Rare, affecting young women often follows a viral infection of upper respiratory
tract that causes inflammatory response with infiltration of lymphocytes, neutrophils
and multinucleated giant cells

Causes: - viral infx- like mumps and flu

Clinical: -

 Thyroid – congested, swollen + mildly tender

 Gland slightly enlarged, firm + tender. Fever, malaise
 Gl is usually adherent to surrounding tissues but unlike Reidel’s it can be dissected
freely + very easily
4 stages: -

1. Thyroid becomes acutely congested, swollen + mildly tender (1-2 months)

2. Gl remains enlarged but becomes non tender. Pt is euthyroid
3. Pt turns to hypothyroid state
4. Remission or recovery may occur – all 4 stages ≈ 6 months

Diagnosis: -

 Febrile pt, WBC normal. High ESR

 Needle biopsy/fine needle aspiration – definitive dx

Treatment: -

 Corticosteroids – prednisolone 40mg daily for 7 days

 ***Surgical tx contraindicated***
 Self-limiting – rarely leads to hypothyroidism
3.Hashimoto’s
 Autoimmune disease – pt develops both humoral + cell mediated reaction to own
thyroid
 Anti-thyroid peroxidase Ab are present in serum
 May present with goitre – firm rubbery in consistency (due to fibrosis of gl) – 25%
present hypothyroidism

Clinical: -

 Insidious onset – may be asymptomatic

 Main complaint = large neck size + pain in region of thyroid
 Hypothyroidism can cause fluid retention  edema  compression of peripheral
vessels/nerves = low pitched voice, poor hearing, slurred speech due to large
tongue + compression of median nerve (carpal-tunnel syndrome)
 Infiltration of dermis = non-infiltrating edema (myxedema)
 Periorbital puffiness, lemon-yellow tint to skin, facial pallor due to vasoconstriction +
anaemia, malar flush, tiredness, weight gain, depression
 Diagnosis: -

 Increased thyroid Ab
 Biopsy confirmation
 Prolonged hypothyroidism – ECG = bradycardia, abnormal ST + T wave
 Hypothyroidism = ↓T4 + ↑TSH

Treatment: -

 Small goitre + euthyroid = no tx

 Hypothyroidism + goitre = full replacement dose of thyroxine
 Surgery indications: -
o Pressure & S+S, extremely enlarged goitre, cosmetic reason, difficult to
exclude malignant neoplasm
o Subtotal thyroidectomy
 Nodular disease = hormone therapy, surgical excision – lobectomy + excision of
isthmus

31) Thyrotoxicosis (Grave’s disease)

 Selfless medicosis & Thyrotoxicosis - Txt

 THYROTOXICOSIS = Extremely elevated levels of thyroid hormones in the
bloodstream
 Enlargement of gland with toxic symptoms

Etiology: - Hyperthyroidism

 Grave’s Disease
 Excessive intake of thyroid hormones in replacement therapy
 Toxic thyroid adenoma

Graves’s Disease

 Def: - autoimmune condition of the thyroid gland in which circulating TSH receptor
autoantibodies lead to overstimulation of the thyroid gland and excess thyroid
hormone production

Clinical: - signs of hyperthyroidism

 Sweating, weight loss, sleep disturbances

 Diffuse Goitre - Gland is smooth with uniform enlargement
 Ophthalmopathy - lid retraction, lid lag
 Pretibial myxoedema – swollen muscles in foot

Etiopathogenesis: -

 Auto Ab (detectable in serum) bind to + stimulate TSH receptor  these Ab have

prolonged stimulatory effect compared with TSH  hence “long-acting” thyroid
stimulators  Hyperactivity of acinar cells; Gland is very vascular with little colloid
 Lymphocyte infiltration = predominant feature

Pathophysiology: -

 TSH-receptor stimulating IgG immunoglobulin (TRAb; type II hypersensitivity

reaction) ↑ thyroid function and growth  hyperthyroidism and diffuse goitre
 TRAb also stimulate: -
o Orbital fibroblasts  fibroblast proliferation, hyaluronic acid synthesis, and
differentiation of fibroblasts to adipocytes ophthalmopathy with
exophthalmos
o Dermal fibroblasts = Deposition of glycosaminoglycans (GAGs) in connective
tissue pretibial myxoedema

Clinical: - Symptoms of hyperthyroidism

 Triad of Grave’s disease: -

1. Diffuse Goitre
 Smooth, uniformly enlarged goitre
 Bruit may be heard at the superior poles of the lobes (due to high
vascularity)
2. Ophthalmopathy
 Exophthalmos (Bulging eyes)
 Ocular motility disturbances
 Lid retraction (exhaustion of muscles) and conjunctival conditions
3. Dermopathy (pretibial myxoedema)
 Nonpitting edema and firm plaques on the anterior/ lateral aspects of
both legs

Diagnosis: -

 Serum increases in T3, T4 – decreased TSH

 Measure of thyroid antibodies
o ↑ TRAbs (specific)
o ↑ anti-TPO and anti-Tg (nonspecific)
 Thyroid scintigraphy (radiotracer administered into pt → shows diffuse uptake of
radioactive iodine)
o CI in pregnancy
 Thyroid US with colour doppler
o Indicated in preg women if TRAbs (TSH recep abs) low

Thyroid Storm: -

 Life-threatening complication of thyrotoxicosis

 Acute severe presentation: -
o Fever
o Tachycardia
o Delirium (confusion)
 Precipitated by infection in a pt with unrecognized/inadequately treated
thyrotoxicosis
 Txt: - supportive
o Fluid resuscitation
o Beta blockers
o Anti-antibody drugs

Treatment: -

 1st line  Antithyroid Drugs

o Carbimazole: 10mg every 8 hrs + sedation + bed rest in acute phase for 12
mnths
o If s+s continues 6 mnths more ➔ surgery
 B-blockers: in pts with severe hyperthyroidism. Propranolol = symptomatic
improvement of CVS s+s
  Surgery: - PATIENT MUST BE EU-THYROID to avoid thyroid storm after surgery
o Subtotal – leaving behind 8 g of thyroid tissue
 Adv: – no need to take thyroxine
 Dis: - high recurrence rate hence another surgery in 8-10 yrs
o Total
 Adv: - No chance of recurrence
 Dis: -external thyroxine will be needed to be prescribed for whole life;
damage surrounding anatomical structures
 Radioactive Iodine
o Radioactive Iodine completely destroys thyroid gland
o Can take up to 6 months
o Need thyroxine replacement
o Should not be done in those wanting to get pregnant or have more kids and
in children; a lot of side effects

32) Thyroid carcinoma

Thyroid carcinoma ; Tumors of thyroid gland ; Thyroidectomy

 Majority of thyroid cancers are well-differentiated carcinomas

 2 in 100,000
 Affects women 2x more than men in pre-existing goitres
 Following radiation of neck in childhood

Thyroid gland anatomy: -

 2 cells: -
o Follicular cells (AKA thyrocytes)  T3, T4  ↑ basic metabolic rate i.e.,
 produce more proteins
 burn more energy, ↑CO,
 stimulate bone resorption
 activates sympathetic nervous system (SNS)
o Parafollicular cells (AKA C cells) → calcitonin – lowers blood ca2+ levels
 Blood supply: -
o Superior thyroid artery (STA) arising from the external carotid artery (ECA)
o Inferior thyroid artery (ITA) branching from the thyrocervical trunk, branch of
subclavian a
 Venous drainage: - superior, middle, and inferior thyroid veins
o The superior + middle veins drain into the internal jugular vein
o Inferior empties into the brachiocephalic vein

 Parathyroid: -
o PTH = causes bone breaks down, to release Ca2+ into blood and increase its
concentration increase Ca2+
o Calcitonin = opposes the action of PTH decrease Ca2+

Classification: -

Differentiated Undifferentiated
1. Papillary 1. Medullary
2. Follicular 2. Anaplastic
3. Hurtle cell
 4. Papillofollicular

TNM Staging: -

 Regional LN are cervical and upper mediastinal nodes

Risk factors: -

 Papillary cancer: -
o Iodine abundance is linked to papillary cancer
o Low dose radiation can lead to thyroid nodules (COLD NODULES) and
papillary thyroid cancer
o kRAS + PTC oncogenes associated with thyroid cancer
o Genetic: -Papillary Carcinoma*: associated with RET/PTC rearrangement and
BRAF mutations
o Ionizing Radiation (particularly during childhood): mostly associated with
papillary carcinoma
 Follicular cancer: -
o Iodine def may lead to follicular cancer
o Genetic: -Follicular Carcinoma: associated with PAX8- PPAR-γ rearrangement
and RAS mutation
 Medullary Carcinoma: associated with MEN2 (RET gene) or Familial Medullary
Carcinoma
Differentiated: -
1. Papillary carcinoma

 Most common (80%); good prognosis; More common in females 3:1; peak incidence
in 30-50s
 Mainly affects young children and young adults but has good prognosis
 Derived from follicular cell
 Risk factors: - RET & BRAF mutations; radiation exposure as child
 Spread: - Lymphatic
 Secretes thyroglobulin; takes up radioiodine
 It is a slow growing, encapsulated cancer. it is dependent on TSH stimulation

o TSH levels in these patients is high and thus this is called a hormone-
dependant tumour
 Woolner classification for Papillary carcinoma: -
1. Occult primary – no invasion; no metastasis (<1.5mm)
2. Intra thyroid – confined to thyroid gland
3. Extra thyroid - invasion of adjacent structures

 Txt: - lobectomy; High risk pts get radioiodine tx

2. Follicular carcinoma
 Epidemiology: - 10% frequency; More common in females 3:1; peak in 40s – 60s
 Derived from follicular cells
 Risk factors: - RAS mutations; It is more common in areas where endemic goitres are
common
 Spread: - hematogenous
o Vascular invasion; locally invasive, invades through the thyroid capsule
 Secretes thyroglobulin; takes up radio-iodine
 Txt: - lobectomy
 Thyroglobulin immunostaining is positive
 Mainly affects young children and young adults
3. Hurtle cell carcinoma

 It is a variant of follicular carcinoma which contains abundant oxyphil cells and

spreads more commonly to regional lymph nodes than follicular carcinoma
Undifferentiated: -

1. Medullary carcinoma
 Epidemiology: - 5% frequency; more aggressive than follicular with early metastases
 It arises from parafollicular C cells (hyperplasia) and secretes calcitonin (calcitonin
acts as a tumour marker)
 Risk factors: - MEN 2A 7 2B association; RET mutation (proto-oncogene)
 Spread: - early metastasis
 Does NOT secrete thyroglobulin; does not take up radioiodine
 Txt: - Total thyroidectomy
 No TSH suppression
2. Anaplastic carcinoma
 It is an undifferentiated very aggressive, rare carcinoma
 Epi: = 3% frequency; poor prognosis; most deadly; More common in makes 2:1; peak
in 60-80s
 Spread: - infiltrative into local structures; widespread metastatic; early mortality
 There is rapid local spread with compression and invasion into the trachea
 Mainly affects elderly and has a very poor prognosis – 1 year survival
 Treatment – external radiotherapy (mortality w/I 6 months) no cure

Clinical features: -
 Early – rarely noticeable, sometimes firm, painless thyroid nodules may be noted
 Late – dysphagia, voice hoarseness due to vocal cord paresis and tracheal
obstruction
!
o Horner’s syndrome which causes a triad of: -
 decreased pupil size
 eyelid drooping and
 decreased sweating on the affected side of the face – due to
disruption of a nerve
o Berry’s sign – involvement of carotid sheath leads to absence of carotid pulse
– seen in anaplastic and follicular carcinoma
Diagnosis: -
 Lab tests
1. Thyroid function tests – basal TSH, T3 and T4
2. Tumour markers – thyroglobulin is measured as a follow up to thyroidectomy
in follicular or papillary thyroid carcinoma
3. Calcitonin – found in patients with medullary thyroid carcinoma
 Neck x-ray
 Radioiodine scans show cold nodules – papillary carcinoma
 Ultrasound-guided core needle biopsy/fin needle aspiration – to confirm diagnosis
Treatment: -
 Well-differentiated tumours are treated by a combination of surgery, thyroid
suppression by thyroxine and radioiodine
o Total thyroidectomy – for patient at high risk of recurrence
o Thyroid lobectomy – for uni-focal, papillary tumours less than 1cm in
diameter with absence of lymph node metastasis
o External radiotherapy – anaplastic
o Total thyroidectomy – medullary
o Subtotal lobectomy – follicular and papillary tumours
 THORAX
33) Chest injuries - closed and open. Pneumothorax. Haemothorax – HUGE TOPIC!!!

Anatomy: -

 Topographic thoracic lines: - mid clavicular, ant axillary, mid axillary, post axillary line

 Intercostal space: artery, vein, nerve on inferior margin of rib

 Thoracic inlet and outlet: 1st rib and 12th rib+ xiphisternal joint respectively
 Thoracic Organs: Trachea, bronchi, mediastinum, diaphragm
 Lungs – right= 3 lobes; left= 2 lobes

 Thoracic injuries account for 25% of all injuries

 Causes of chest injuries: - gunshot wound, sharp objects, shrapnel, car accident,
crush wound, stab wound

Classification of chest injuries: -

Open Closed
1) Non- penetrating 1) Soft tissue + muscle
2) Penetrating 2) Without rib fracture
a. Injury of parietal/ visceral 3) With 1-3 rib fracture
layers of pleura 4) Rib fracture >4cm
b. Without organ injury
c. With organ injury

 Pneumothorax: -
o Open
o Closed
o Tension
 Haemothorax: -
o Low – 50-300ml
o Medium – 300-600ml
 o High – fills up chest cavity
Pathophysiology of chest injuries: -

Blunt trauma !
 It occurs due to kinetic energy forces. There is NO open injury
 It can be subdivided into: -
1. Blast – pressure waves cause tissue disruption. It can tear blood vessels and
cause traumatic diaphragm rupture
2. Crush (compression) – the body is compressed between an object and a hard
surface. There is direct injury of the chest wall and internal structures
3. Deceleration – the body was in motion and struck a fixed object. There is
blunt trauma to the chest wall
 Age factors: -
o A paediatric thorax has more cartilage and absorbs more force
o A geriatric thorax has calcification and osteoporosis and suffers more
fractures
Penetrating trauma
 It can be subdivided into: -
1. Low energy e.g., knife wounds – only structures penetrated are disrupted
2. Medium energy e.g., bullet wound from hand gun – the primary tissue
damage is LESS than high energy trauma
3. High energy e.g., bullet wound from rifle/shotgun
Clinical features: -
 Pain – can be diffuse or concentrated
 Respiratory asphyxia, haemoptysis, flail chest, shock, cyanosis
 Jugular vein distention – enlarged veins of the neck in compression injuries
Assessing the casualty: -
 Assess mental status (AVPU) – alert, voice, pain, unresponsive
 ABCDE – airways, breathing, circulation, disability (mental and physical), exposure
Treatment: -
 During the first few minutes, must assess possibility of endotracheal intubation,
needle decompressions and pericardiocentesis
 Resuscitation and drainage of the haemothorax
 Control the bleeding – the vessels may need tying off
Deadly dozen for life injuries
 Immediately life-threatening injuries: -
1. Airway obstruction
2. Tension pneumothorax !
3. Pericardial tamponade
4. Open pneumothorax
5. Massive haemothorax
 6. Flail chest
 Potentially life-threatening injuries: -
1. Aortic injuries
2. Tracheobronchial injuries
3. Myocardial contusion
4. Rupture of diaphragm
5. Oesophageal injuries
6. Pulmonary contusion
Pericardial tamponade
 Def: -It is a type of pericardial effusion in which fluid, pus, blood, clots and gas
accumulate in the pericardium, resulting in compression of the heart
 Clinical features: - Beck’s triad
1. Low BP !
2. Enlarged JVP
3. Muffled heart sounds
 DDX: -tension pneumothorax (has distended JVP)
 Treatment: - pericardiocentesis
o It is done in the sub-xiphoid space between the 4th and 5th ribs at a !
45-degree angle
Flail chest
 It occurs when a segment of the rib cage breaks under extreme stress and becomes
detached.
o This free part then moves independently during inspiration, and moves
inwards instead of outwards
 Diagnosis: -paradoxical motion of chest wall, CT, x-ray
 Treatment: - oxygen, analgesia (epidural is best), physiotherapy.
o If physiotherapy does NOT work then do open reduction internal fixation
surgery with plates
Pneumothorax (collapsed lung)
 Normal lung physiology – with normal breathing, the diaphragm relaxes and moves
back up, which causes the intra-pleural pressure to go from -3 to -1mmHg (chest
normally has negative pressure).
 This causes the lungs NOT to stretch as much so they shrink and contract back, which
also contracts the alveoli inside. Air goes from the alveoli to the trachea and outside
the mouth
 In PNEUMOTHORAX, there is a hole through the intra-pleural place which causes the
intra-pleural pressure to drop to 0 because the atmospheric pressure outside the
chest is connected to the space inside the thorax – the lung is NO longer getting
pulled out and it collapses
 In pneumothorax, air leaks into the space between the lungs and chest wall !
(pleural space) and the air pushes on the outside of the lungs and makes it collapse
 Clinical features – NO breath sounds
 Treatment – puncture at 2nd intercostal space and put drainage at 5th intercostal
mid axillary line
1. Tension pneumothorax
 In TENSION PNEUMOTHORAX, air is trapped in the pleural space under positive !
pressure (pleural cavity pressure is GREATER than atmospheric pressure), so air
gets sucked into the chest cavity, resulting in displacement of mediastinal structures
and compromise of cardiac and pulmonary function
 Air is getting in but not able to get out
 Clinical features: -
o Patient panics
o Tachypnoea
o Dyspnea (shortness of breath)
o Distended JVP
o Decreased BP and
o Decreased preload
 Immediate treatment – rapid decompression by insertion of a large bore needle 3
inches deep into the 2nd intercostal mid-clavicular line of the affected side, followed
by insertion of a chest tube through the 5th intercostal space in the anterior axillary
line
2. Open pneumothorax (sucking chest wound)
 In open pneumothorax, the pleural cavity pressure is EQUAL than atmospheric
pressure, due to a large open defect in the chest.
 Air accumulates in the hemithorax (half of the chest) with each breath instead of the
lungs, and results in hypoventilation and hypoxia
 Treatment – close the defect with sterile occlusive plastic dressing taped on 3 sides
to act as a flutter type valve, insert a chest tube.
o If the lungs do NOT reinflate place a drain in low pressure suction (5cm
water)

Closed pneumothorax
 In closed pneumothorax, the pleural cavity pressure is LESS than atmospheric
pressure, due to air blebs that rupture due to high altitude or diving
  A bleb is caused by alveolar rupture
 About 75% of cases are in young men who tend to be tall & have a family history
 Air blebs are usually found at the apex of lungs or on the upper border of lobes
Massive haemothorax
 Def: - It is a collection of blood in the pleural cavity
 The blood comes from injury to heart or great vessels, lung contusion or injury to
parietal vessels
 Types: -
o Low – less than 50ml of blood in pleural space at angle between the
diaphragm and chest
o Middle – 300-600ml blood in pleural space up to the 5th rib
o Total – blood covers entire cavity
o Sub-total – blood is up to the sub-clavicle and collapses the lung
 Clinical features: -
o Decreased ventilation
o Haemorrhagic shock
o Flat neck veins
o NO breath sounds
o Dull percussion
 Diagnosis: - chest x-ray is standard, CT
 Treatment: -
o Blood transfusion – correct the hypovolemic shock
o Insert drain to aspirate the blood from the pleural cavity
o Thoracentesis – insert needle into 7th/8th intercostal space by mid-axillary
line to remove blood – any lower can puncture the liver or spleen

34) Acute and chronic mastitis. Abscesses

 Breast assessment ; Mastitis + Abscess

Surgical anatomy: -

 Base situated over 2nd – 6th rib in mid clavicular line

 Parenchyma contains 15-20 main lactiferous ducts
 Lymphatic drainage: - Important for metastasis
o 75% to axillary nodes
o 20% internal mammary
o 5% to lymphatics near the neck of the ribs (post intercostal
nodes)

Acute Mastitis (lactational)

 Def: - Bact infection of breast due to staph aureus

 Associated with breastfeeding, fissures develop in nipples providing route of entry
for microbes

Clinical: -

 Erythematous (cellulitis – whole breast is red – 1st stage)

 Breast with purulent nipple discharge
 May progress to abscess (when redness is limited to area of abscess – 2nd stage)
 Edema, usually unilateral
 Pain, swelling, tenderness of breast
 Later stage (systemic) = pyrexia, tachycardia + leucocytosis

Diagnosis: -

 Breast milk cultures or imaging (US) may be required if there is no response to initial
tx

Treatment: -

 Continued drainage + antibiotics

o Non-MRSA – dicloxacillin; cephalosporins; erythromycin
o MRSA – clindamycin; IV vancomycin
 Supportive care: - NSAIDs. Emptying of breast; warm compress
 Abscess: - aspiration + Ab
o If fails: - Incision + Drainage
 Lidocaine applied 30 mins before surgery
 1. Incise 2. Breakdown loculations with fingers/forceps 3. Spread 4.
Drain put in

Periductal Mastitis (Non-lactational)

 Inflammation of sub areolar ducts. Seen in smokers

Pathology: -

 Smokers = low vit A  so columnar cells undergo sq metaplasia as less vit A to

maintain the epithelium
 Columnar – sq. keratin is produced which blocks the ducts  inflamed  Periductal
Mastitis

Clinical: -

 Tender mass in sub areolar region

 Pain + nipple discharge
 Nipple retraction (granulation tissue develops due to inflam)
o Myofibroblasts are in granulation tissue, pulling nipple in

Diagnosis: - US shows thickened duct or abscess

 Treatment: -

 Ab (flucloxacillin) + stop smoking

 Recurrent peri areolar inflam = total duct excision
 Abscess= incision + drainage + needle aspiration

Chronic mastitis

 Follows continuous antibiotic tx

 Inadequate drainage of abscess cavity
 Too tight packaging of abscess cavity
 2 uncommon chronic inflammatory conditions of the breast: -
1. Lymphocytic Lobulitis: occurs in pts with autoimmune diseases particularly type 1
dm
o CF: Presents as firm irregular lump
o Dx: core biopsy
o Tx: no tx required
2. Granulomatous Mastitis: secondary to systemic conditions (sarcoidosis, TB, foreign
material (silicone))
o Non-caseating, non-necrotising granulomatous inflammation
o May grow Corynebacterium
o CF: - peripheral breast mass; skin ulcers, small abscess, peripheral infx
 Mimic breast cancer
o DX: - core needle biopsy, US; gram stain
o Tx: tx of any organisms cultured + exclusion of malignancy

Breast Abscess

 Def: - an encapsulated accumulation of pus within the breast tissue

 Is the main complication of mastitis

Clinical: -

 Breast pain, erythema, and edema

 Purulent discharge from the nipple of the affected breast
 Fever + Nausea
 Fluctuating mass on palpation

Treatment: -

 Incision and drainage

 Needle aspiration is possible for abscesses less than 5 cm in diameter

35) Benign neoplasms. Precancerous diseases of the mammary gland

Benign tumors of Breast

 All tumours have 2 basic components: -

 Benign tumours mainly form encapsulated or circumscribed masses that expand and
push aside the surrounding normal tissues without actually invading, infiltrating or
metastasising

Anatomy: -

 Modified sweat gland – derived from ectoderm

 Each breast consists of 15-20 lobules
 Breast extends from 2nd – 6th rib – sternum to mid axillary line
 Lies in the superficial fascia, superficial to the pectoral fascia
 Axillary tail of Spence – upper outer portion of the breast

Fibroadenoma

 Tumors of fibrous tissue + glands

 Most common benign neoplasm of the breast
 Prevalent in young women 15-25 yrs (premenopausal)
 Benign + encapsulated– shows similar hormonal activity as normal breast tissue
(basically just extra ducts)
 Gross appearance: easily movable, solitary round rubbery lesion – measure 2-4cm
in diameter
 Estrogen sensitive – grows during pregnancy
 Benign = no risk of malignancy

Clinical: -

 painless, smooth, nontender, well localised swelling

 No node enlargement

Treatment: -

 Laser ablation, microwave ablation, cryoablation

 Peri areolar incision, inframammary incision

Intraductal Papilloma

 Occurs in the lactiferous duct or sinus near the nipple

 Serous or serosanguineous nipple discharge (bloody)
 Pre-menopausal women – must be distinguished from papillary carcinoma

Gross: -
  Solitary, small lesion, commonly located in the major mammary duct close to the
nipple

Treatment: -

 Microdochectomy – excise duct

 Multiple masses = simple mastectomy

Phyllodes Tumour

 Fibroadenoma like with overgrowth of fibrous component

 Characterised “leaf like” projections – on biopsy

 Post-menopausal women. Can be malignant

Clinical: -

 Painless, slow growing solitary lump in breast

 Skin may be stretched, shiny, dilated veins shown over the lesion
 Recurrence is common
 Usually, unilateral
 Rapid growth

Diagnosis: -

 Mammography
 Fine needle aspiration cytology (FNAC)

36) Carcinoma of the mammary gland

Carcinoma of Breast; Treatment

 Breast cancer is the 2nd common malignancy in women (lung is 1st)

 Most breast cancers are adenocarcinomas
 Histopathologic classification differentiates between ductal and lobular carcinomas
 The 2 most common types of breast cancer are: -
o Invasive ductal carcinoma, which accounts for 70– 80% of all cases and
o the less aggressive invasive lobular carcinoma
 Both types typically develop from non-invasive carcinomas, i.e.,
o ductal carcinoma in situ (DCIS), and
o lobular carcinoma in situ (LCIS)

Risk factors: - mostly related to estrogen exposure

 Female, cancer usually arises in post-menopausal women - >40yrs

 Early menarche/ late menopause
 Obesity, Atypical hyperplasia (increased estrogen)
 1st degree relative; BRCA1 + BRCA2 gene
o Tumor suppressor gene BReast CAncer 1 & 2; 17q chromosome 13
 Higher in north America and north Europe
 Women who have never given birth are at higher risk
 Women with long term therapy with estrogen have lower risk
 Increased risk after exposure to radiation
 Contraceptives do not increase risk
 Incidence increases with age

Classification of malignant breast tumor: -

1. Non-invasive
o Ductal carcinoma in Situ
o Lobular carcinoma in Situ
2. Invasive
o Invasive ductal carcinoma (MC adenocarcinoma)
o Invasive lobular carcinoma (Multifocal + Bilateral)
3. Unilateral/Bilateral
4. Unifocal, Multifocal, Multicentric

Types: - Invasive & Non-invasive

1. Ductal carcinoma in situ

o Does not usually produce a mass, benign mostly with atypical hyperplasia of
duct
o Paget’s disease of nipple = DCIS that extends up to the ducts to involve the
skin of the nipple – presents as nipple ulceration + erythema
2. Invasive ductal carcinoma
o Mass detected by physical (>2cm) or mammography (>1cm)
o Disrupting of skin or retraction of nipple
o Types: -
 Tubular
  mucinous (older women – good prognosis)
 medullary
 inflammatory carcinoma
3. Lobular carcinoma in situ
o Does not produce mass or calcification - discovered incidentally on biopsy
o Multifocal or bilateral
o Tx: tamoxifen (to decrease carcinoma)
4. Invasive lobular carcinoma
o Grows in single file pattern-in single row or target like fashion around ducts
o No mass lesion; difficult to palpate
o No duct formation due to lack of E.cadherin
o Goes to muscle, BM – metastasis

Clinical: -

 Most frequently in upper outer quadrant

 Vomiting blood (hematemesis) – due to metastasis to lung;
Anaemia
 Hard lump, irregular edges with limited mobility, with indrawing
of the nipple, retracted skin
 As disease advance – skin involvement with frank ulceration +
fixation to the chest wall
 Rare symptom: - painful, nipple discharge
 Inflammatory carcinoma – skin is indurated, red, warm,
edematous - “peau d’orange”

Differential: -

 Benign tumor (fibroadenoma, dysplastic nodule, filoid tumor)

 Cyst, abscess

Spread: -

 Local spread: tumour increase in size + invades other portions of breast

 Lymphatic metastasis: primarily in axillary + internal mammary lymph nodes
o Tumours in post 1/3 of breast more likely to drain to the internal mammary
nodes
 By blood stream: through this route skeletal metastasis occurs
o Lumbar vertebrae, femur, thoracic vertebrae, rib + skull affected
o Bone most common metastasis
o Liver – jaundice; Ab pain, nausea
o Lungs, dyspnea, haemoptysis

Staging: - TNM (stage 2 most common)

 Clinical Stages: -
1. Limited to breast
2. Breast to axillary
3. Muscle involvement
4. Chest wall + supraclavicular nodes
 Axillary lymph nodes: -
o Primary level: sentinel lymph nodes – on lat side of breast
o Secondary: intra pectoral – in b/w pectoralis minor + teres major
o Tertiary: sub clavicular

Diagnosis: -

 Triple assessment: -
1. Clinical examination (including examination of axillary and supraclavicular LN),
2. Imaging
3. Biopsy
 Mammogram, breast US, MRI, Biopsy (core needle biopsy, fine needle aspiration,
surgical biopsy), CXR, FBC, LFT – recommended for early-stage breast cancer
 Tumour markers (CA 15-3, CA 27-29)
 Triple-negative breast cancer = Estrogen negative + progesterone-negative + HER2-
negative (more aggressive high-grade tumours)

Treatment: - do this properly from the video

 Tx usually invasive surgery mastectomy or breast conserving treatment with or

without reconstruction (using implants, natural tissue- free/ pedicle flap)
 Meds: anti-estrogenic agents = tamoxifen* (can cause uterine cancer), monoclonal
ab (Herceptin)
  MRM -Modified Radical Mastectomy
o Excised mass of whole breast, large portion of skin inc nipple, all of the fat +
lymph nodes of axilla
o Axillary veins + nerves to serratus ant + lat dorsi should be preserved
o Intercostal brachial nerves divided – sensation changes post op
o Wound drained using wide bore suction tube
 Systemic treatment of breast cancer: chemotherapy, hormonal therapy, targeted
therapy, bisphosphonates
 Provided as: -
o 1. Neoadjuvant therapy (pre-op)
o 2. Adjuvant therapy (post op)
o 3.Therapy for metastatic disease
 Sandwich therapy = surgery – chemo – surgery

Complication: -

 N = nerve injury (Thoracodorsal & Long thoracic nerve)

 I = infections
 S = seroma – accumulation of serous fluid under flaps – most common complication
of axillary surgery
 E= Edema
 Axillary LN dissection -lymphedema, impaired shoulder movements, cutaneous
sensory disturbances in axillary region, limb infx

Prognosis or predictive factors: -

 Based on TNM staging – metastasis most important factor

o Spread to axillary lymph nodes most useful prognostic factor
 Sentinel lymph node (Guarding or 1st lymph nodes) biopsy* used to assess axillary
lymph nodes
o Inject breast with radioactive substance – this drain to axillary lymph nodes–
then remove 1st line of lymph nodes for biopsy
o Saves from taking all lymph nodes

37) Lung cysts - congenital and acquired. Echinococcus of the lung

 Def: -A lung cyst is a round parenchymal area of low attenuation with a thin wall
between 1-4mm thick
 The thickness of the wall is what differentiates it from a pulmonary cavity
(pulmonary cavity thickness is more than 4mm thick and bulla has thickness less than
1mm)

Congenital cysts – Epithelial cyst

 Epithelial cysts are lined with respiratory epithelium cells
 It is often associated with cervical rib and cardiac anomalies
 It can be a large single cyst or multiple small cysts
 Clinical features: -
o Dyspnea
o Chest tightness
o Fever
o Cough and
o Haemoptysis
 Diagnosis – chest x-ray shows spherical shadowing containing air, fluid or both
 Treatment – excision of the cyst and antibiotics
Acquired cysts
1. Emphysematous cyst !
names
 It develops due to degenerative changes in the lung with
destruction of the normal alveolar framework and rupture of the alveolar walls
 Clinical features: -dyspnea, severe persistent cough
 Complications: - spontaneous pneumothorax, chronic bronchitis
 Treatment: - if the cyst is generalised excision is impractical so obliteration by
plication with multiple sutures is done

2. Pseudocyst
 It is NOT a cyst to start with but inflammatory conditions lead to cavity formation
which behave like cysts
 It is associated with staph/pneumonic infection, pulmonary TB or after lung abscess

Echinococcal cyst/hydatid cyst

 It is caused by the parasite Echinococcus granuloses (dog tapeworm)
 Dog is the definitive host, sheep, cattle and human are intermediate hosts
 The liver is affected most commonly (60-80% cases), and the lungs are affected in 10-
30% cases in the lower lobes
 The cysts are able to grow in the lungs due to negative pressure which results in 3
layers: -
1. Outer peri-cyst – derived from compress host organ tissues
2. Intermediate hyaline ectocyst – non-infective
3. Inner endocyst – contains viable parasite
 Clinical features: -
o Fever, cough, dark sputum, anorexia, weight loss
 Complications: -
o Rupture into pleural space
o Allergic shock
o Perforation into bronchioles
o Pleural effusion
  Diagnosis: -
o Chest x-ray
o Blood test shows eosinophilia
o Liver function tests – increased liver enzymes
o Cassoni skin test – specific for allergy to Echinococcus
 Treatment: -
o Surgery – to eradicate the parasite
 Lobectomy
 When a small part of the parenchyma is affected, sectorial resection is
done or inject NaCl into the cyst which causes it to dry up and then it
is aspirated
 PAIR – puncture, aspirate, inject NaCl, re-aspirate
o Chemotherapy – anthelminthic drugs for patients who can NOT tolerate
surgery

38) Tumors of the lung. Carcinoma

 Lung cancer – just watch the video honestly THERE ARE 2 PARTS BTW
 It is the most common cause of death from cancer
 It can be divided into 2 types: -
!
1. Primary lung cancer – starts in the lungs (Bronchogenic)
 Small cell carcinoma
 Non-small cell carcinoma
 Adenocarcinoma
 Squamous
 Large cell
2. Secondary lung cancer – metastasis
Causes: -
 Smoking (90% cases)– squamous metaplasia, dysplasia, carcinoma in situ
 Asbestos (especially in adenocarcinoma)
 Passive smoking
 Atmospheric pollution
 Radiation
 Diet low in vitamin A
 Chronic scarring (TB, asbestos)

Pathogenesis: -
 Activation of growth promoting oncogenes
o ONCOGENES are genes that direct cell growth. If altered/mutated, an
oncogene can promote or allow uncontrolled cancer growth
 Inactivation of tumour suppressor genes
Classification: -
 Lung cancers are divided into 2 main groups: -
1. Non-small cell lung cancer – 80% ! ASL
a. Adenocarcinoma (most common) peri
b. Squamous cell carcinoma central
c. Large cell carcinoma peri
2. Small cell lung cancer – 20% central

Non-small cell lung cancer (NSCLC)

1. Adenocarcinoma (most common)
 Account for 40% of all lung cancers
 They are associated with smoking, BUT are mainly seen in non-smokers
 More common in women
 They start in the mucous-secreting glandular cells, and tend to develop in the
smaller airways such as alveoli
 They are usually located at the outer edges of the lungs - peripheral
 They have a tendency to spread to the lymph nodes, brain and bones
 ADENOCARCINOMA IN SITU – it is a subtype which develops at multiple sites in the
lungs and spreads along pre-existing alveolar walls
 Patients have better prognosis than other types of lung cancer

2. Squamous cell carcinoma

 It is associated with smoking more than the other NSCLC
!
 They start in the squamous cells which line the inside of the airways in the lungs
 They are usually located in the central chest area or in the main bronchi
 Cause obstruction of the airways (dry cough)superinfection (purulent cough)
 The epithelial cells that line the airway become mutated and change from columnar,
cuboidal to squamous cell
 The tumour location is responsible for the symptoms of cough, trouble breathing,
chest pain (compression of nerves) and blood in sputum (due to rupture of bvs)
 If the tumour grows to a large size, x-ray/CT may show a cavity in the lung – classic
sign of squamous cell lung cancer
 It can metastasise to brain, spine and other bones, adrenal glands and liver

3. Large cell carcinoma

 They are less differentiated forms of squamous cell and adenocarcinomas
 They can be found anywhere in the lung, but is often found in the outer edges of the
lungs
 More common in men
Small cell lung cancer – 20%
 They are more aggressive than NSCLC and are strongly related to smoking
 They involve neuroendocrine cells which mutate and release hormone-like
substances (paraneoplastic syndrome)
o PARANEOPLASTIC SYNDROME = symptoms that come from elsewhere in
body
 They are highly malignant and rapidly-growing and usually metastised by the time it
is found
 They are almost always inoperable. Respond to chemotherapy, but the prognosis is
poor
 It can be divided into 2 stages: -
!
1. Limited stage – cancer is confined to one lung and lymph nodes may be
affected
2. Extensive stage – cancer has spread to other lung and has invaded lymph
nodes and other body parts
Clinical features: -
 Haemoptysis, dyspnea, wheezing, chest pain
 Pleural pain – indicates invasion of pleura
 Hoarse voice
 Persistent cough that does NOT go away
 Swelling in the face and neck
 Weight loss, fatigue, loss of appetite, difficulty swallowing

Lung cancer staging for NSCLC: -

 TNM staging system is used and is divided into 4 stages
o T – tumour size of the primary tumour and if it has grown into adjacent
structures
o N – node – are the regional lymph nodes affected and how
o M – metastasis – is there distant metastasis e.g., adrenal glands, bones,
brain, other lung or distant lymph nodes
1. Stage 0 – cancer is ‘in place’ and has NOT spread from where it first developed
2. Stage 1 – cancer is only in one lung and has NOT spread to any lymph nodes or
metastised. Less than 3cm size
3. Stage 2 – cancer is only in one lung and has NOT spread to any lymph nodes or
metastised to distant body parts. 3-7cm size
4. Stage 3 – cancer has spread within the chest but has NOT metastised to distant
body parts. More than 7cm
5. Stage 4 – tumour has metastised to distant parts of the body. It can be of any size
and may or may NOT have spread to lymph nodes
Diagnosis: -
 Genetic testing
  Lung biopsy
o Fine-needle aspiration biopsy of the lung
 CT scan is used to locate abnormal tissue or fluid in the lung and then
a small incision is made on the chest and biopsy needle is inserted and
sample is removed and checked under a microscope for cancer
o Endoscopic ultrasound-guided fine needle aspiration biopsy
 An endoscope with a probe and biopsy needle is inserted through the
mouth and oesophagus.
 The probe bounces sound waves off body tissues to make echoes that
form an image of the lymph nodes near the oesophagus.
 The picture helps the doctor decide where to place the biopsy needle
to remove tissue from the lymph nodes.
 The sample is removed and checked under a microscope for cancer
o Bronchoscopy
 Bronchoscope in inserted through the mouth, trachea and major
bronchi into the lungs to look for abnormal areas.
 Tissue sample may be taken to check under microscope
 Use antibodies to check for certain antigens (markers) in a sample of tissue. This is
used to differentiate different types of cancer
 Once diagnosis is made, stage the cancer using MRI, CT, PET scan, bone scan

Treatment: -
 Surgery
(i) Lobectomy (method of choice) – remove a whole lobe of the lung
(ii) Wedge resection – remove a tumour and some of the normal tissue around it
(iii) Pneumonectomy – remove one whole lung
(iv) Sleeve resection – remove part of the bronchus
o However, since small-cell cancer is usually found in both lungs, surgery alone
is NOT often used. Once the doctor removes all the cancer cells that are seen,
chemotherapy or radiation therapy is done to kill remainder cancer cells
 Radiation therapy: -
(i) External radiation therapy – machine outside the body sends radiation
towards the cancer
(ii) Internal radiation therapy – radioactive substance sealed in needle or
catheter is placed directly into or near the cancer
 Chemotherapy
 Targeted drug therapy – drugs are used to attack specific cancer cells. They are less
harmful to normal cells compared to chemotherapy or radiation therapy
 Laser therapy – laser beam is used to kill cancer cells

39) Lung abscesses. Lung gangrene. Bronchiectasis

Lung abscess
 Def: - it is a localised area of necrosis of the lung tissue and the formation of pus-
!
filled cavities due to microbial infection
 A lung abscess is a thick-walled cavity that contains purulent material
 They can be divided into 2 types: -
1. Primary lung abscess – caused by infection within the lung e.g., pneumonia
2. Secondary lung abscess – complication of other lung diseases or infection
from another part of the body
 They can be divided into acute (< 6 weeks) and chronic (> 6 weeks)
Causes: -
 S. aureus or K. pneumonia
 Aspiration (most common) e.g., food, gastric contents
 Alcoholism
o People who drink excessive alcohol experience bouts of vomiting and altered
levels of consciousness  this increases the chances of inhaling stomach
contents and bacteria into the lungs, which can cause an infection
 Septic embolism – infected blood clot travels via the blood from elsewhere e.g., in
thrombophlebitis
 Blocked mucous – mucous can form behind a tumour or foreign object in the wind
pipe and lead to an abscess. If bacteria get into the mucous, the blockage stops the
patient from coughing it out
Pathogenesis: - !
 Most abscesses eventually rupture into an airway, producing a lot of sputum
which gets coughed up. A ruptured abscess leaves a cavity in the lung that is filled
with fluid and air
 Sometimes the abscess ruptures into the space between the lungs and the chest
wall (pleural space), filling the space with pus. This condition is called EMPYEMA
Clinical features: -
 Cough with foul-smelling sputum, which is sometimes blood-stained (haemoptysis)
 Clubbing of the fingers and toes (less oxygenedema of toesclubbing)
 Pleuritic chest pain
 Chest examination usually reveals signs of consolidation; signs of cavitation are
rarely found
Diagnosis: -
 Sputum test – check for bacteria or viruses
 CBC – check for infection
 X-ray – shows a dense opacity with cavitation and/or a fluid level
! Note – sometimes a pre-existing emphysematous bulla becomes infected
and appears as a cavity containing an air-fluid level
 CT – allows better anatomical visualisation. Differentiates abscess from empyema or
bulla with an air-fluid level
 o Abscess appear rounded radiolucent lesion with a thick wall and ill-defined
border
Treatment: -
 Antibiotics
!
o Clindamycin 600mg IV every 8 hours in the drug of choice
o For very serious infections involving MRSA, vancomycin is drug of choice
 Surgery
o Drain empyema’s
o If the lung abscess does NOT resolve and medical treatment fails, surgical
drainage, lobectomy or pneumonectomy might be needed
Pulmonary gangrene (necrotising pneumonia and gangrene)
 Necrotizing pneumonia is a rare and severe complication of bacterial CAP
(Community Acquired Pneumonia)
 It is characterised by necrosis and liquefaction and cavitation of pulmonary tissue
 Pulmonary gangrene is the final stage of progressive devitalisation of pulmonary
parenchyma if the necrotising pneumonia progresses uncontrollably
Causes: -
 Staphylococcus aureus (most common) – especially in young immunocompetent
patients
 Klebsiella pneumoniae
 Pseudomonas aeruginosa pneumonia
Pathogenesis: -
 In necrotising pneumonia, there is a decrease in the blood supply to the lungs,
which leads to areas of cellular death.
 The lack of blood supply due to damaged blood vessels results in impaired delivery
of antibiotics to the infections, thus allowing further progression of infection
Clinical features: -
 Typical signs and symptoms of pneumonia
 With progression of the disease, signs of systemic chronic illness ensue such as night
sweats, weight loss and anaemia
Diagnosis – same diagnosis method as CAP and lung abscess: -
 CT – shows distinct areas of low attenuation with decreased parenchymal
enhancement (representing liquefaction) in all or parts of the affected area of
infection (consolidation)
 X-ray – shows bulging fissures due to the intense inflammatory exudation present
and shows extensive right upper lobe consolidation, with bulging of the horizontal
fissure
Treatment: -
 The main method of treatment is supportive with appropriate antibiotics.
!
However, if patients fail to improve, surgery may be a life-saving option
  Any patients admitted with severe CAP is treated with broad-spectrum antibiotics –
penicillin and azithromycin
Bronchiectasis
 Bronchiectasis
 Def: - chronic inflammation of the bronchi and bronchioles, leading to permanent
dilation and thinning of them
 Chronic suppurative airway infection with sputum production progressive scarring
and lung damage occurs
Causes: - !
 Congenital defect affecting airway ion transport or ciliary function e.g., cystic fibrosis
 Acquired secondary to damage to the airways by a destructive infection, inhaled
toxin or foreign body
o Children – pneumonia, inhaled foreign body
o Adult – suppurative pneumonia, pulmonary TB, bronchial tumours
Clinical features: -
 Chronic foul-smelling sputum production
 Haemoptysis
 Decreased breath sounds – indicates lobar collapse
 Poor general health – weight loss, anorexia, low-grade fever and failure to thrive in
children
 Coarse crackles can be heard over the infected areas
Diagnosis: -
 X-ray – may show dilated bronchi with thickened bronchial walls and sometimes
multiple cysts containing fluid
 CT (more sensitive than x-ray) – shows thickened, dilated bronchi and cysts at the
ends of the bronchioles
 Ciliary test function using saccharine tablets (if feel in throat more than 20 min)
 Sputum examination – may contain S. aureus, Pseudomonas aeruginosa etc.
 Sweat electrolytes – patients with CF have increased sodium and chloride in their
sweat

Treatment: -
 Physiotherapy
 Inhaled bronchodilators and corticosteroids – enhance airway flow
 Antibiotic therapy e.g., aminopenicillin or a macrolide
 Surgery
o Surgical removal of affected portions of lung
o Bronchial artery embolization – for haemoptysis

40) Spontaneous pneumothorax. Empyema and metastatic tumors of the pleura

1. Spontaneous pneumothorax (collapsed lung)
 PNEUMOTHORAX = presence of air outside the lung in the pleural space
 In pneumothorax, air leaks into the space between the lungs and chest wall (pleural
space) and the air pushes on the outside of the lungs and makes it collapse
 SPONTANEOUS PNEUMOTHORAX = spontaneously occurring presence of air in the
pleural space in patients without clinically apparent underlying lung disease
o It can be divided into 2 types: -
(i) Primary spontaneous pneumothorax
 Occurs due to leak from a small bleb, vesicle or bullae
(ii) Secondary spontaneous pneumothorax
 The pleura leaks due to an underlying lung disease e.g., TB,
necrotising tumour

 What causes blebs: -

o Etiology unknown
o A bleb is caused by alveolar rupture
o Blebs are thought to occur as a result of subpleural alveolar rupture, due to
overload of the elastic fibers.
o More common in taller men; found at apex
 Clinical features: - sharp pleuritic pain, dyspnea
 Treatment: - puncture at 2nd intercostal space and put drainage at 5th intercostal mid
axillary line and supplemental O2

Difference b/w spontaneous and tension pneumothorax: -

 Pneumothorax can be classified as “simple” or “tension.”
 A simple pneumothorax is non-expanding. In a tension pneumothorax, a “one way
valve” defect allows air into but not out of the pleural space.
2. Empyema (pyothorax)
 pyothorax - pathology explained well here ; Diagnosis & Txt explained well here
 Def: - It is a collection of pus in the pleural cavity
 Normally only 5-15 ml in pleural space
 Causes: -
o It is never a primary cause
o Secondary conditions that predispose to empyema: - TB (70%), lung abscess,
bronchiectasis, chest wall wound, Iatrogenic like needle biopsy chest surgery
etc;
 Pathology: -
o Initially serous fluid collects which eventually becomes purulent
o Presence of thick pus with a thick cortex of fibrin and coagulum over the lung
 Pathological types: - !
1. Exudative phase – there is protein rich effusion. If this becomes infected
empyema occurs. Antibiotics may be enough
2. Fibrinopurulent phase – over the next few days, the fluid thickens
3. Organising phase – lungs are trapped by a thick cortex. Surgery needed
 Clinical features: -
o Pain in chest, tenderness, difficulty breathing
o Dullness on percussion
o Decreased chest wall movement
 o NO breath sounds
 Diagnosis: -
o Chest x-ray & CT scan (only if >300ml can be seen) better used US which
can see about 50ml
o Blood test – CRP & ESR
o Thoracocentesis – confirmatory test!!
 Culture test of pleural fluid
 Golden criteria investigation of empyema by Thoracocentesis : -
o Pleural effusion (fluid more than 5-15ml)
o + Gram staining of pleural fluid – staph aureus
o pH <7.2
 Treatment: -
o Exudative phase – antibiotics may be enough (depending on causative
organism) e.g., -
 Amoxicillin 1gm TDS
 Tazobactam + piperacillin
o Supplemental o2
o Chest tube drainage (water seal drainage)
o Fibrinopurulent phase – antibiotics, intercostal tube drainage
o Decortication – thickened pleural sac is stripped off from the lung via
thoracotomy, antibiotics are important
3. Metastatic tumours of the pleura – Malignant pleural effusion
 The only primary malignancy of the pleura is malignant mesothelioma
!
 MALIGNANT PLEURAL EFFUSION = is an advanced malignancy disease, in which there
is metastatic involvement of the pleura from primary malignancy at the lungs,
breast or other body sites
 PLEURAL EFFUSION = build-up of fluid between the two layers of the pleura
 MALIGNANT PLEURAL EFFUSION = build-up of fluid and cancer cells that collects
between the chest wall and lungs

41) Mediastinitis

The mediastinum
 Mediastinum – the central component of the chest, in between the lung
 It is divided into 3 compartments: -
1. Anterior compartment – located between the sternum and anterior surface
of the surface of heart and great vessel
 Contains the thymus gland, internal mammary artery and vein, lymph
nodes and fat
2. Middle compartment – it is located great vessels and trachea
 Contains pericardium, heart, ascending and transverse aorta, superior
and inferior vena cava, brachiocephalic artery and vein, trachea and
main bronchi, lymph nodes and central portions of pulmonary artery
and vein
3. Posterior compartment – it includes the
paravertebral sulci and
paraesophageal area
 Contains descending aorta,
oesophagus, thoracic duct,
azygous and hemi-azygous veins
and lymph nodes

Mediastinitis

 Def: -It is a potentially life-threatening inflammation of the

mediastinum
! classification
Wright’s classification: -
 Type I: Mediastinitis presenting within 2 weeks of OP in the absence of Risk factors
 Type II: Mediastinitis presenting 2-6 weeks after OP in the absence of RF
 Type III
o III a: Mediastinitis Type I with 1 or more RF
 o III b: Mediastinitis Type II with one or more RF
 Type IV
o IV a: Mediastinitis I, II OR III after one failed therapeutic trial
o IV b: Mediastinitis I, II OR III with more than 1 failed therapeutic trial.
 Type V: Mediastinitis presenting for the first time more than 6 weeks after the OP

Basically: - 1&2 – NO risk facts; 3a &b – 1&2 +RFs; 4 -1,2&3 + therapy; 5- 1 st time

1. Acute mediastinitis
 Def: -It is a fulminant process that spreads rapidly along the continuous fascial planes !
connecting the cervical and mediastinal compartment
o FULMINANT = developed suddenly and severely
 Causes: -
o Oesophageal perforations e.g.,
 Boerhaave’s syndrome in which the patient vomits against a closed
glottis which causes pressure in the oesophagus to increase and
eventually burst at its weakest point at the lower 1/3 oesophagus
o Deep sternal wound infection
o LUDWIG’S ANGINA – bilateral infection of submandibular space which can
spread to mediastinum
 LUDWIG ANGINA = is a type of bacterial infection that occurs in the
floor of the mouth, under the tongue.
 It often develops after an infection of the roots of the teeth (such as
tooth abscess) or a mouth injury.
 Pathophysiology: -
o Infection can inflame the mediastinal structures and cause physiological
compromise by compression, bleeding, systemic sepsis or a combination
 Clinical features: -
o Fever, chest pain, tachycardia, dysphagia, respiratory distress
 Diagnosis: -
o Chest x-ray with air in the mediastinum, pleura or peritoneum
o Retropharyngeal abscess
o Ludwig’s angina - The infection includes both sides of the mylohyoid muscles
causing edema and inflammation so much that the tongue is displaced,
resulting in dysphagia and dyspnea
o Aspiration biopsy
 Treatment – treat the primary problem
o Oesophageal perforation – primary closure of the perforation site.
 First mucosal closure and then muscle closure, supported by a flap of
parietal pleura
o Oropharyngeal abscess – antibiotics (e.g., clindamycin) and drainage
2. Chronic mediastinitis
!
  Def: -It is sclerosing or fibrosing mediastinitis due to chronic mediastinal
inflammation
 The inflammation originates from the lymph nodes (most commonly from
granulomatous infection such as TB)
 Chronic low grade inflammation results in fibrosis and scarring
 It can cause compromise of the superior vena cava and azygous veins
 Clinical features: -
o Oesophageal involvement – dysphagia, haematemesis
o Tracheal bronchial involvement – cough, haemoptysis, dyspnea, wheezing
o Pulmonary vein obstruction – congestive heart failure
 Treatment: -
o There is NO definitive treatment
o Anti-TB drugs for active infection
o Surgery – to relieve airway/oesophageal obstruction or for vascular
reconstruction (e.g., inserting a vascular or airway stent)

42) Tumors and cysts of the mediastinum. Superior vena cava syndrome. Mediastinal
emphysema

Mediastinal tumours
 THYMIC HYPERPLASIA = it is enlargement of the thymus. It is very common after
chemotherapy
 Tumours of the mediastinum according to location: -
o Anterior – thymoma, germ cell tumour !
o Posterior – neurogenic tumours, mesenchymal tumours
o Superior – lymphoma
o Middle – lymphoma, mesenchymal tumours

Classification of mediastinal tumors: -

1. Superior
a. Retrosternal goitre – thyroid gland didn’t ! classification
move up
b. Thymoma
2. Anterior
a. Thymoma
b. Lipoma
c. Germ cell tumor - teratoma
3. Middle
a. Cystic lesions – pericardial, bronchogenic & lymphomas
4. Posterior- neurogenic tumors
a. Neurofibromas
b. Schwannomas
 c. Gangliomas

Types: -
1. Thymoma
o It is the most common mediastinal tumour. It is derived from the thymus
gland
o It is located in the anterior mediastinum
o Diagnosis and treatment – thymectomy
2. Germ cell tumour
o They are mostly found in the anterior mediastinum !
o They contain elements of all three cell types – mesoderm, endoderm
and ectoderm
o They are benign and cystic, although they can compress neighbouring
structures
o Treatment – chemotherapy
3. Thymic carcinoma
o It is a malignant tumour, that can spread to bone and liver
o Treatment – complete resection and radiation after resection
Mediastinal cysts
 They are most commonly located in the middle mediastinum
1. Pericardial cyst
o They are mostly asymptomatic and found by chance, most commonly in the
right costophrenic angle region
o The cyst has clear fluid and lined with single layer of mesothelial cells
2. Bronchogenic cyst !
o They are developmental anomalies that occur during embryogenesis due to
abnormal budding of the foregut or tracheobronchial tree
o The cyst contains protein-rich mucoid material, smooth muscle and cartilage
o Treatment – complete removal of the cyst wall via posterolateral
thoracotomy
3. Thymic cyst
o They are mostly asymptomatic and found by chance.
o They have NO consequences – simple cysts
Mediastinal emphysema
 Def: -It is the presence of free air or gas in the mediastinum
 It originates from the alveolar space or the conducting airways !
 Causes: -
o Increased pulmonary pressures
o Excessive coughing
o Blunt force trauma to the chest
o Lung cancer
 Clinical features: - retrosternal chest pain which is worse during inspiration,
dyspnea (shortness of breath), jaw pain
 Diagnosis: -
o Chest x-ray shows air in the mediastinum
o Hamman sign – precordial systolic crepitation and diminution of heart
sounds
 Treatment: -
o It spontaneously resolves. Nitrogen washout with 100% oxygen
o Surgery – it is done when the mediastinal emphysema causes
cardiorespiratory compromise
Superior vena cava syndrome
!
 superior vena cava syndrome - better watch the video -_-
 Compression of the superior vena cava impairs the venous backflow to the right
atrium, which results in venous congestion in the head, neck and upper extremities
 Causes: -
o Compression – malignant mediastinal tumours, bronchogenic carcinoma (on
upper apex of lung squamous and small cell carcinoma), thymic cancer, non-
Hodgkin’s lymphoma
o Mediastinal fibrosis, aortic aneurysm
o Pancost tumor (superior sulcus tumor)
 Clinical features: -
o Complete obstruction causes dyspnea, facial swelling, cyanosis, cough,
headache
o Venous distention of the neck and chest wall, facial edema, edema of upper
extremity, cyanosis
o (Since less blood returning to right atrium) Hypotension tachycardia
o Cough & shortness of breath
 Diagnosis: -
o Chest x-ray shows widened mediastinum and also shows a mass in the right
side of the chest
o Venography – invasive contrast venography is diagnostic
o Pemberton sign: -
 Ask patient to raise both arms above head
 Normal pts – nothing
 SVC syndrome +ve test facial swelling, neck swelling, cough,
dyspnea, respiratory distress & even cyanosis
 Treatment: -
o Oxygen and elevate the head
o Radiotherapy
o Thrombolytic drugs e.g., streptokinase, urokinase
o Surgical bypass or stenting
43) Congenital diseases of the esophagus. Diverticula. Stricture

Anatomy of oesophagus
 Hollow tube ̴ 25cm – extends to stomach
 4 segments: -
o Cervical = left of neck due to trachea thus easily accessible via neck
o Diaphragmatic (3-5cm)
o Thoracic = passes through post mediastinum – narrowing slightly behind
aortic arch + great vessels
o Abdominal ( ̴1 – few cm)
 oesophageal-gastric junction: squamous + gastric columnar ep
Esophageal atresia
 Def: - It is a congenital defect in which the continuity of the oesophagus is
interrupted
 It can be divided into 5 types: - ! classification
1. Type A (85%) – isolated esophageal atresia
 Presence of a ‘gap’ between the two oesophageal bling pouches with
no fistula present
2. Type B (10%) – atresia with proximal fistula
 Upper oesophageal pouch connects abnormally to the trachea. The
lower oesophageal pouch ends blindly
3. Type C (1%) – atresia with distal fistula
 Upper oesophageal pouch ends blindly. Lower oesophageal pouch
connects abnormally to the trachea
4. Type D (1%) – atresia with double fistula
 Both upper and lower oesophageal pouches make an abnormal
connection with the trachea in two separate, isolated places
5. Type E (4%) – Isolated fistula
 The oesophagus is fully intact and capable of its normal functions,
however, there is an abnormal connection between the oesophagus
and the trachea

 Clinically, new-borns have abundant saliva output from the mouth

 When suckling, cyanosis, dyspnea and suffocation can occur due to milk passing into
the trachea instead of the oesophagus
 The main concern is aspiration pneumonia, which can be lethal in new-borns if not
managed correctly
Diagnosis: -
 There are several methods of making a diagnosis, such as: - !
o A plastic tube is introduced into the upper blind portion and is
inflated with air. Bubbles can be heard over the sternum and this is called
Elephant’s sign
o MRI imaging
o Bipolar contrast investigation
 The proximal pouch has a mercury weighted dilator and the distal
portion is filled with contrast via gastrostomy
Treatment: -
 The most immediate and effective treatment in most cases is a surgical repair to
close the fistula(s) and reconnect the two ends of the oesophagus to each other
 Emergency transfer is needed for specialised care in an appropriate specialised unit a
hospital
 During transportation, continuous aspiration of the upper respiratory tract must !
be done
 Systemic antibiotics are given
 The surgery must be performed within 12 hours after admission to the specialised
care unit
 If treatment isn’t done within 24 hours, the prognosis is poor
Oesophageal diverticula
 Def: -It is an outpouching of the mucosa throughout the muscular layer of the
oesophagus
! classification

 It can be divided into 3 types: -

 1. Zenker (pharyngeal) = it is FALSE diverticulum, as the protrusion is above the
cricothyroid sphincter
2. Mid-oesophageal = it is true diverticulum, caused by traction from
mediastinal inflammatory lesions (e.g., TB) or motility disorders
3. Epiphrenic = it is FALSE diverticulum just above the diaphragm. It is usually
accompanied by a motility disorder e.g., achalasia

 A TRUE DIVERTICULUM involves all layers of the intestinal tract wall

 A FALSE DIVERTICULUM occurs when herniation of the mucosa and submucosa
occurs through a defect in the muscular wall
 Clinical features: -
o Pain during feeding – milk can NOT move to the upper part and causes
aspiration
o Zenker diverticulum fills with food and can be regurgitated when the patient
bends or lies down – can cause aspiration pneumonia
 Treatment: -surgical resection with a mystomy (a muscle is cut from the site of the
diverticulum to the cardia, to relieve the functional obstruction)
Oesophageal strictures

 Def: -It is a narrowing or tightening of the oesophagus, resulting in difficulty

swallowing
 Causes: -
o Proximal/mid oesophageal: - tumour, infectious oesophagitis, drug induced
(NSAIDs)
o Distal oesophageal: - GERD, adenocarcinoma, Crohn’s disease
 Clinical features: - heartburn, dysphagia, weight loss, chest pain
 Diagnosis: - barium swallow gives information on the location, length and diameter
of the stricture
 Treatment: - mechanical endoscopic dilation using Maloney dilator

44) Cardiospasm/ Achalasia

 Achalasia

Achalasia (Cardiospasm)

 Def: -It is a disorder in which the lower oesophageal sphincter fails to relax and
there is absent peristalsis
 Food has difficulty passing into the stomach and the oesophagus above the lower
oesophageal sphincter becomes distended
Cause and pathology: -

 Loss of ganglion cells in the myenteric (Auerbach) plexus

 The destruction of ganglion cells in the oesophageal wall is associated with
disintegration of the axoplasm and myelin sheaths within the Vagus nerve supplying
the oesophagus and degenerative changes in the dorsal motor nucleus of the Vagus
 Can be idiopathic or due to infection
 Degeneration results in hypertension of lower oesophageal sphincter. Failure of the
sphincter to relax on swallowing, oesophageal dilation, increased pressure and
retention of ingested material
 In earliest stages, oesophagus is of normal calibre and still exhibits contractible (but
not peristalsis).
 With time, the oesophagus dilates and contractions disappear, so the oesophagus
mainly empties by the hydrostatic pressure of its contents – this is always
incomplete, leaving residual food and fluid
 The ‘megaoesophagus’ becomes tortuous with persistent retention oesophagitis due
to formation of food residues – accounts of increased incidence of carcinoma
Clinical features: -

 Dysphagia (difficulty in swallowing) – patient complains of choking, coughing or an

abnormal sensation of food sticking to the back of the throat when swallowing
food AND liquids
 Pain – often mistaken for reflux
 Regurgitation
 Chest pain
 Weight loss
 Aspiration pneumonia – danger of aspiration of oesophageal contents into the lungs
when the person lies down
 Stasis of food may produce inflammation and ulceration proximal to the lower
oesophageal sphincter
Diagnosis: -

 Barium swallow x-ray – shows: -

o dilated intra-thoracic oesophagus with impaired emptying
o absence of gastric air bubble and
o a tapered narrowing of the lower oesophagus (bird beak picture)
  Oesophageal manometry – DIAGNOSTIC
o Intraluminal pressure sensors measure the contractility of the oesophagus
and its sphincters.
o Shows that lower oesophageal sphincter does NOT relax on swallowing,
there is NO peristalsis and increased pressure
 Endoscopy – only effective in advanced disease, but is useful to rule out pseudo
achalasia
Differential diagnosis: -

 Diffuse oesophageal spasm

 Pseudo achalasia
 Angina !
Treatment: - Better explained in video

 There is no way to prevent or reverse achalasia, thus treatment is aimed at

decreasing lower oesophageal sphincter pressure
 Nitrates or calcium channel blockers – relieve dysphagia by decreasing LES pressure
– taken 15-45 mins before eating – NOT SO EFFECTIVE
o LES = Lower Esophageal Sphincter
 Botulinum toxin injection – inhibits acetylcholine release from nerve endings, thus
decreasing LES pressure
o Not permanent, lasts for one year. Restricted to elderly pt.
 Pneumatic dilation – a cylindrical balloon is positioned across the LES and inflated to
3cm. However, one complication is oesophageal perforation can occur
 Heller myotomy (treatment of choice)– it is a surgical procedure in which muscles
of the cardia are cut, allowing food and liquids to pass to the stomach
o Major complication: - GERD
o Surgeons thus add a partial ant fundoplication (wrapping the fundus of
stomach around the LES to make it tighter). 90% success

Diffuse + Segmental Esophageal Spasms

  Def: -Uncoordinated contraction of oesophagus
 DES: characterized by substernal pain and dysphagia, different from achalasia
because its problem of the esophageal body
 Differs from classic achalasia: -
o primarily a disease of the esophageal body
o Produces less degree of dysphagia
o causes more chest pain
o Less effect on pt general condition
 Dx to differentiate both is done by esophagram + Esophageal manometry
 Impossible to differentiate achalasia from DES on basis of symptoms alone
Pathophysiology: -

 Unclear
 Basic motor abnormality is rapid wave progression down the oesophagus
 Hypertrophy of muscularis layer + degeneration of esophageal branch of vagus
nerve observed in this disease (but not constant)
Diagnosis: -

 Esophageal manometry: frequent occurrence of simultaneous wave forms + multi

peaked esophageal contractions (high amplitude + duration) over the entire length
of esophagus
o Criteria of 30% or more peristaltic waveforms out of 10 wet swallows has
been used to differentiate DES from vigorous achalasia
 Radiological = corkscrew oesophagus or pseudo diverticulosis in advanced disease
Treatment: -

 Heller’s myotomy + ant fundoplication

45) Tumors of the esophagus. Carcinoma

 Esophageal carcinoma ; Staging + Treatment

Benign tumors: -

 Rare
 E.g., True papilloma’s, adenomas, hyperplastic polyps
 Majority = non-epithelial in origin. Stromal / lipoma / granular cells
 Most small + asymptomatic. Must do biopsy to rule out malignancy

Malignant tumors: -

 Non-epithelial primary malignancies are also rare

 Secondary malignancy rarely involves the oesophagus

Carcinoma of the Oesophagus

  6th most common cancer – poor survival rate
 2 most common types: -
1. Squamous cell: affects upper 2/3 of oesophagus – more common
2. Adenocarcinoma: lower 1/3 of oesophagus

Risk factors: -

 GERD – for adenocarcinoma especially if progress to Barret’s esophagus

 Smoking – for squamous cell carcinoma

Spread: - 3 ways

 Directly through esophageal wall

 Lymphatics: lymph nodes from sup mediastinal to celiac axis
 Blood Stream: liver, lungs, brain, bones

Clinical: -

 Usually asymptomatic in early stages; Tumour is well established before dx

 Progressive dysphagia with weight loss (about 4 months)
 Advanced malignancy symptoms occur due to invasion: -
o Voice hoarseness – due to laryngeal nerve palsy
o Esophageal-pharyngeal fistula – coughing etc
o Ascites – due to metastasis to liver (metastasis in livercirrhosisportal HTN
fluid leakage from liverascites)

Diagnosis: -

 Endoscopy with biopsy = 1st line investigation – direct view of esophageal mucosa
 CT scan – to check for metastasis and extent to infiltration
 Bronchoscopy: many middle + upper 1/3 carcinomas are sufficiently advanced at
time of dx that trachea/bronchi: already involved
o Can reveal impingement / invasion of main airways

Treatment: - GIVEN BETTER IN VIDEO

 At time of dx many pts have incurable disease

o Aim of palliative tx = overcome debilitating or distressing s+s – dysphagia
predominant symptom thus aim is to restore swallowing
o When tumour reaches submucosal layer = has access to lymphatics
 Esophagectomy (resection):
VASCULAR
46) Ischemic diseases of the limbs. Acute arterial insufficiency. Treatment

Chronic lower limb ischemia – watch this one especially if no time 2 videos btw;
Chronic Txt

Acute ischemia

Ischemic diseases of the limbs

 Lower extremity occlusive diseases are classified into: -

1. Acute limb ischemia – 90% are either thrombotic or embolitic – sudden loss
of limb perfusion
2. Chronic limb ischemia – due to atherosclerotic changes of the lower
extremity that manifest from asymptomatic to limb-threatening gangrene
Aetiology: -

 Atherosclerosis
 Embolism
 Arteriopathies – Raynaud’s disease, Buerger’s disease
 Diabetes
 Scleroderma
 Physical agents e.g., trauma, tourniquet

Fontaine classification/ Rutherford’s classification: -

 Fontaine: -
o Stage 1 – Asymptomatic
! classification
o Stage 2a – Mid claudication
o Stage 2b – Moderate-severe claudication
o Stage 3 – Ischemic rest pain
o Stage 4 – Ulceration or gangrene
 Rutherford: -

Grade Category Clinical

0 0 Asymptomatic
1 Mild claudication
1 2 Moderate claudication
3 Severe claudication
2 4 Ischemic rest pain
3 5 Minor tissue loss
4 6 Ulceration or gangrene

CLAUDICATION is pain in your thigh, calf, or buttocks that happens when you walk

Classification of Limb Ischemia: -

 Fontaine classification
o Stage 1 – no clinical symptoms
 o Stage 2 – intermittent claudication (mild or severe)
 INTERMITTENT CLAUDICATION is muscle pain that happens when
you're active and stops when you rest.
o Stage 3 – ischemic rest pain
o Stage 4 – gangrene, ischemic ulcer
Clinical features: -

 5 P’s: - Pain, paraesthesia, paralysis, pulselessness, poikilothermic (perishing cold)

!
o POIKILOTHERMIC = the inability to regulate core body temperature
 Atrial bruits – auscultation of subclavian, carotid and femoral arteries
o Bruits are blowing vascular sounds resembling heart murmurs that are
perceived over partially occluded blood vessels.
 Altered sensation and decreased function/movements of the affected limb
 Cold periphery, numbness
 Atrophy of muscles
 Absent pulse of limb arteries
 Non-healing ulcers – due to low blood flow
Diagnosis: -

 Doppler ultrasound blood flow detection !

 Duplex scan – best diagnostic
o Shows how fast blood is flowing through a blood vessel and in which
direction it is flowing
 Ankle-brachial pressure index (ABPI) – Ankle pulse/Brachial pulse
o Resting ABPI 1 – normal
o Resting ABPI 0.9 – degree of arterial obstruction
o Resting ABPI 0.3 – imminent necrosis
 Arteriography – inject radiopaque solution into arterial tree via retrograde
percutaneous catheter
 Lipid profile
 Coagulation profile
Treatment: -Treat cause

 Anticoagulant
 Thrombolysis
o Narrow catheter is passed into the occluded vessel and left embedded into
the clot.
o Tissue plasminogen activator (TPA) is infused directly onto clot and regular
arteriogram is carried out.
o Lysis is achieved within 24 hours
 Surgery – embolectomy.
o The artery is clamped and opened transversely.
 o The thrombus is extracted by passing a Fogarty balloon embolectomy
catheter
 Surgical revascularisation/Bypass
 Endovascular stent insertion
Complications of arterial revascularisation: -

 Swelling of the leg may occur after revascularisation  this can cause increased
compartmental pressure leading to muscle necrosis in the untreated leg.
o Must do fasciotomy to relieve the intercompartmental pressure
 Thrombolytic therapy – streptokinase/urokinase
 If occlusion is NOT resolved, venous thrombosis occurs due to stagnation of blood,
which can result in gangrene
 Amputation
 Muscle necrosis
47) Burger's disease. Raynaud's disease

Thrombangiitis obliterans (Buerger’s disease) (Burger’s + cigarettes)

 Buerger's disease – short and concise!!!

 Def: - It is a progressive non-atherosclerotic inflammatory disorder that mainly
affects small and medium sized arteries, veins and nerves of the upper and lower
extremities
 It is most commonly seen in men between 20-40 years old who are heavy smokers
Causes: -

 Smoking!!!
 It has been postulated that the disease is an ‘autoimmune reaction’ in which the
body’s immune system attacks the body’s own tissues and this is triggered by some
constituent of tobacco
Pathogenesis: -

 Thrombosis and obliteration occur in small-medium sized arteries and veins

 Once the blockage occurscollateral vessels open and through these collaterals,
blood supply is maintained to the ischemic areas.
 If the patient continues to smoke the disease will progress into the collateral
vessels also and block them too leading to severe ischemia with rest pain,
ulceration and gangrene
 Chronic phase of the disease shows a decrease in hypercellularity and frequent
recanalization of vessel lumen
 The end stage lesion is an organised thrombus and blood vessel fibrosis
Clinical features: -

 The initial symptoms of Buerger’s disease include: -

 o CLAUDICATION (pain induced by insufficient blood flow during exercise) in
the hands or feet
 The pain may begin in the extremities and radiate to other parts of
the body
o Numbness and tingling in the limbs
o RAYNAUD’S PHENOMENON – a condition in which the distal extremities
(fingers, toes, hands and feet) turn white when exposed to cold
o Skin ulcerations and gangrene of the digits
o Painful, blue discolouration of fingertips
o Pain worse at night
o Blue fingertips
 Despite the severity of ischemia, Buerger’s disease does NOT involve other organs,
like most other forms of vasculitis.
o Even as the ulcers and gangrene develop, organs such as the lungs, kidneys
and brain remain unaffected!
o The reasons for this confinement is unknown
Classification of Buerger’s disease: - Hands, Legs, thighs and abdomen and everything

 Type 1 – Upper extremity

 Type 2 – Crural (leg/Foot)
! classification
 Type 3 – Femoral type (femoropopliteal)
 Type 4 – Aortoiliac
 Type 5 – Generalised type
Diagnosis: -

 The disease can be mimicked by many other diseases that cause decreased blood
flow to the extremities
 The disease may be confused with atherosclerosis,
endocarditis, clothing disorders of the blood etc.
 Angiograms of the upper and lower extremities can be
useful in making the diagnosis of Buerger’s disease
o It shows a ‘corkscrew’ appearance of the arteries
due to vascular damage
o The angiograms may also show occlusions or
stenosis in multiple areas of the arms and legs
Treatment: -

 Stop smoking! – this is the only treatment known to be effective

 Patients who continue to smoke are the ones who require amputations of the fingers
and toes!
Raynaud’s disease

 Raynaud's Phenomena – short & concise

!
  Def: -it is an idiopathic disorder characterised by colour changes in the skin that
occur spontaneously or are induced by exposure to cold or emotional stress
 Caused by vasoconstriction + spasm
 More common in women 5:1; Ages 16-40; cold weather
Stages: -

1. In a classic episode, the skin initially exhibits pallor due to arterial spasm and
ischemia – white stage !
2. It is then followed by cyanosis due to suffusion of blood in the capillaries and
venules – blue stage
3. It is then replaced by erythema + flushing – red stage
 It is normally painless by may be painful (throbbing pain)
 The colour changes are most common in the fingers, toes, ears and nose
Clinical features: -

 Usually, medial four digits and palm are involved. Thumb is spared
 Pallor – due to arterial spasms and ischemia (white stage)
 Throbbing pain – during revascularisation
Diagnosis: -

 Primary Raynaud’s disease is diagnosed by following the Allen Brown criteria: -

o At least two of the three colour changes occur during attacks due to cold and
stress
o Episodes occur periodically for at least two years
o The attacks occur in both hands
Diagnosis: -
 Physical examination
 ANA test – to test for autoimmune disorders
 Thermography
 Arteriography
Treatment: -

 Primary initial treatment consists of avoiding smoking, emotional upsets and cold
exposure
 Avoid vasoconstrictors – nicotine is a potent vasoconstrictor (stop smoking)
 Vasodilators – verapamil, nifedipine, diltiazem
 Some medications such as calcium blockers reduce peripheral vasospasms
 Sympathectomy – only done in severe cases by a neurosurgeon
o SYMPATHECTOMY = is an irreversible procedure during which at least one
sympathetic ganglion is removed.

48) Atherosclerotic and diabetic gangrene of the limbs

Gangrene

Gangrene (Greek: erosive ulcer)

 Def: -it is true necrosis but with the possibility of large-scale tissue involvement
 Macroscopic death of tissue
 Whole extremity or part extremity involvement generally means the gangrene is
extending from the skin right down to the bone
NB!!!

 If the liver, bowel or gall bladder is involved without infection, the term NECROSIS is
used
 If the liver, bowel or gall bladder is involved with infection, the term GANGRENE is
used
 Acute interruption of blood flow causes gangrene
 Chronic interruption of blood flow can result in either necrosis or gangrene
Diabetic foot and diabetic gangrene

Problems in a diabetic foot: -

 Ulceration
 Abscess and cellulitis of foot
o CELLULITIS = is a common bacterial skin infection that causes redness,
swelling, and pain in the infected area of the skin
 Strep and staph
 Osteomyelitis of different bones of the foot
 Diabetic gangrene
 Arthritis of the joints
Classification – according to Miggoto classification of the diabetic foot: -

 Grade 0 – foot symptoms like pain only

 Grade 1 – superficial ulcers
 Grade 2 – deep ulcers
! classification
 Grade 3 – ulcer with brown induration
 Grade 4 – forefoot gangrene
 Grade 5 – full foot gangrene
Pathogenesis: -

 High glucose levels in the tissues  good culture for bacteria thus infection is
common
 Diabetic microangiopathy causes blockage of micro-circulation leading to hypoxia
 Diabetic atherosclerosis decreases blood supply  and causes gangrene. Thrombosis
can be precipitated by infection causing infective gangrene
 Increased glycosylated haemoglobin in the blood causes defective oxygen
dissociation leading to more hypoxia
 Clinical features: -

 Pain in the foot

!remember achacha

 Ulceration
 Absence of sensation, absence of pulse in foot (posterior tibial and dorsalis pedis
arteries)
 Loss of joint movements
 Abscess formation
 Ketoacidosis, septicaemia or myocardial infarction may occur
Diagnosis: -

 Blood sugar, urine ketone bodies

 Doppler study of lower limb to assess arterial patency
 Glycosylated haemoglobin estimation
 Pus for culture
Treatment: -

 The foot can be saved only if there is good supply

 Diabetes is controlled by INSULIN ONLY
 Antibiotics
 Surgical debridement of wound and regular dressing. Keep feet dry and clean
 Drugs – vasodilators, dipyridamole, low dose aspirin
 Control diet and obesity
 Amputate the gangrene area

49) Varicose veins of the limbs

Varicose veins & Varicose veins dx + txt – honestly watch both you were asleep -_-

Veins

 Veins usually have valves to allow blood to flow in one direction. The exception is
iliac, vena cava, portal system and cranial sinuses, which have NO valves !
 There are 3 main types of veins: -
1. Deep veins
 CONDUIT VEINS = they take blood from the limbs to the
heart e.g., tibial, popliteal, femoral
 PUMPING VEINS = they venous sinuses in the calf muscles
which pump blood towards major veins. They can also be
called the peripheral heart
2. Superficial veins
 Great saphenous vein
 Short saphenous vein
3. Perforating veins
  They connect the superficial veins to the deep veins
 The direction of blood flow is from superficial to deep veins. Reversal
of blood. Reversal of blood flow returns in varicose veins
Varicose veins

 VARICOSE VEINS = are dilated, tortuous, elongated veins in the leg. Blood is able to
flow in reverse direction through the faulty valves
 Risk factors: - hereditary, female, occupation with prolonged standing, immobility,
tight clothing, high heels, pregnancy
Classification: -

 It can be divided into: -

(i) Long/great saphenous vein varicosity
(ii) Short/small saphenous vein varicosity
(iii) Varicose veins due to perforator incompetence
!
 Or it can be divided into: -
1. Thread veins – they are small varices around the ankle which look like
dilated, red/purple veins (up to 1mm diameter)
2. Reticular varices – they are slightly larger than thread veins, located in the
subcutaneous/subdermal region (1-3mm diameter)
3. Varicose veins – they are dilated, tortuous, elongated superficial veins in the
subcutaneous tissue (saphenous compartment) (more than 3mm diameter)
o Combination of any of the above

Clinical features: -

 Dragging pain, painful walk, postural discomfort

 Heaviness in the legs
 Night time cramps
 Edema of the feet
 Discolouration/ulceration in the feet
Diagnosis: -
!
 Brodie-Trendelenburg test
o Vein is emptied by elevating the limb and applying a tourniquet just below
the saphenous-femoral junction.
o The patient is asked to stand quickly.
o When the tourniquet is released, rapid filling from above shows saphenous-
femoral incompetence

 Venous Doppler – check venous flow, venous patency and venous reflux
 Duplex ultrasound scan – shows direct visualisation of veins
 Varicography – a contrast is injected into the variceal vein to give detailed
anatomical mapping of the varicose vein
Differential diagnosis: -

 Vasculitis
 Orthostatic edema
 Lymphedema
Treatment: -
!
 Pressure stockings
 Elevate the limb – relieves the edema
 Drugs – Diosmin 450mg
o Diosmin is a venoactive drug supporting circulatory health through various
actions on blood vessels; it supports lymphatic drainage and improves
microcirculation while increasing venous tone and elasticity.
 Sclerotherapy
o Injecting sclerosants into the vein can provide complete sclerosis of the vein
o The sclerosant will permanently damage the internal lining of the vein wall.
o This will then set off an inflammatory cascade which eventually leads to the
vein hardening over or becoming solid “dead” material.
Complications: -

 DVT
 Infection
 Haematoma formation, bruising, edema of the limb
50) Thrombophlebitis, phlebitis, phlebothrombosis. Postphlebitic syndrome

1. Deep vein thrombophlebitis

 Def: - it is an acute disease characterised with thrombus formation in a vein and

aseptic inflammation
Aetiology: -

1. Biochemical factors
o Excess thromboplastin formation during surgery, trauma, necrotic
demarcation or malignancy
o Increase of thromboplastin, prothrombin, fibrinogen due to the result of
emotion, stress or thrombotic disposition
2. Hydrodynamic factors
o Venous stasis can occur in cardiac diseases, operations, shock, bed rest and
abdominal compressions due to tumours
3. Disturbing venous wall factors
o Allergic, traumatic chemical and environmental factors are included
Risk factors for DVT: -

 Poor blood circulation due to heart failure or prolonged immobilisation

 Venous injury due to surgery or trauma
 Increased blood clotting due to an increase in platelet count or a decrease in
anticlotting factors
Thrombus formation – pathogenesis: - PUT A DIAGRAM FOR THIS!!!

 Thrombosis is usually initiated when alterations in the vascular endothelium cause

platelets to adhere to the subendothelial connective tissue
 Collagen binds to platelet receptors to activate enzymes that catalyse the release of
arachidonic acid
 After activation, platelets release mediators such as ADP, which allows fibrinogen to
attach and link to adjacent platelets
 Platelet-derived growth factor is also released which stimulates growth and
migration of fibroblasts and smooth muscle cells with the vessel wall
 The primary haemostatic plug is strengthened after several minutes by the activation
of coagulation pathway which causes the production of thrombin and the conversion
of plasma fibrinogen into fibrin
Clinical features: -

 Increased body temperature – Michael’s sign !

 Tachycardia – Maller’ sign
Diagnosis: -
!
 Homan’s test – basically pain in calf on dorsiflexion
o Patient is made to lie down in a prone position and the feet are dorsally
flexed.
o If DVT exists, pain occurs due to the calf muscles compression of the affected
being over the interosseal membrane

 Phlebography
 Duplex scanning – combines B mode imaging and Doppler sign analysis
Treatment: -

 Bed rest with the limb elevated – decreases peripheral venous pressure and provides
symptomatic relief from swelling and pain
 Facilitate bowel movements – administer fibre or stool softeners
 Systemic anticoagulation – it is needed to suppress clot formation and allow gradual
clot lysis. Heparin is used
 Thrombolytic therapy –streptokinase has been used effectively to treat DVT

2. Superficial thrombophlebitis

 Def: - It is superficial vein thrombosis with inflammation !

 It can occur with varicose veins
 It can occur in the upper or lower limb
Types: -

(i) Acute – due to IV cannulation, trauma, minor infections

(ii) Spontaneous – polycythaemia vera, Buerger’s disease
Clinical features: -

 Skin swelling, redness and pain and fever

 Cord-like thickening of the veins
 The process encircles the vein and adjacent connective tissue with the skin
 In some cases, a suppurative phlebitis may occur
o SUPPURATIVE (SEPTIC) THROMBOPHLEBITIS = describes thrombosis in a
vein that occurs in the setting of inflammation and infection.
o This condition is characterized by the presence of a thrombus that is
associated with inflammation and pus formation (suppuration) both in the
venous wall and surrounding the vessel.
Treatment: -

 Elevation
 Analgesics for the pain
 Drugs: - heparin, venotonics, anti-aggregants, anti-inflammatory
 Local anticoagulant ointment as a compress for 8 hours
3. Phlebitis

 Def: - It is inflammation of a vein

4. Deep vein thrombosis (phlebothrombosis)

 DVT

 Def: - embolism in deep vein

 3 factors that cause DVT are Virchow’s triad: -
1. Stasis !
2. Hypercoagulability
3. Vessel wall injury
Causes: -

 After operation (most common) – 20% patients after surgery develop DVT
 Trauma – to the leg, ankle, thigh or pelvis
 Immobility – bed ridden patients, or person travelling for long period of time
 Obesity, pregnancy
 Oral contraceptives – oestrogen
Clinical features: -

 Fever
 Severe pain and swelling in the calf and thigh
 Leg is tense, tender, warm, pale or bluish
 Core features: - Swelling, pain, redness
 Phlegmasia cerulea dolens – if veins blocked both collateral & deep
o Limb becomes blue (cyanotic)
o An uncommon but potentially life-threatening complication of acute DVT
characterized by marked swelling of the extremities with pain and cyanosis,
which in turn may lead to arterial ischemia
 Phlegmasia cerulea alba – arteries block
 o If arterial supply blocked toolimbs become white
 Positive Homan’s sign – passive forceful dorsiflexion of the foot with extended knee
causes tenderness in the calf

Diagnosis: -

 Venous doppler ultrasound

 Duplex scanning – shoes non-compressible vein which is wider than normal
 CT/MRI
 To check for risk factors: - CBC, ESR/CRP, antithrombin 3
Treatment: -

 Rest, elevation of limb, bandaging the entire limb

 Anticoagulants – heparin and warfarin
o Initially give heparin for 7 days followed by warfarin for 3-6 months
 Thrombolytics – streptokinase, urokinase

Management: -
 General: -
o Move after surgery ASAP – reduces chances of DVT
o Graduated stockings
o Elevated limb
 Medical: -
o Low molecular weight heparin (in kidney damage patients use
unfractionated heparin) – immediate action (act on APTT)
 o Fondaparinux - indirect inhibitor of factor 10a (similar to LMWH)
o Warfarin – long term action (act on INR)
o Start both heparin and warfarin together
 Thrombolysis
o Used in proximal veins (e.g., iliac vein)
o Directly inject tPA, streptokinase or urokinase at the clot
 Surgical thrombectomy
o Venous stenting

5. post-phlebitic syndrome

 Def: - It is the development of signs and symptoms of chronic venous insufficiency

AFTER DVT
 It is a long-term complication of DVT
Clinical features: -

 Pain, cramps, heaviness, itching, tingling

 Hyperpigmentation, skin induration, blanching
Treatment: - same as DVT

 Elevation
 Ultrasound-guided thrombolysis
 Compression stockings
 Anticoagulants – initially heparin and then warfarin

51) Lymphangitis, lymphadenitis, elephantiasis

 Lymphangitis

1. Lymphangitis

 Def: -It is an acute, non-suppurative infection (no pus) and spreading inflammation
of the lymphatic vessels of the skin and subcutaneous tissues due to Streptococci,
Staphylococci and Clostridium species
 Main: - strep pyogenes
 Erysipelas is a type of lymphadenitis
o ERYSIPELAS is a type of cellulitis (skin infection) generally caused by a group
of Strep A
Clinical features: -

 Streaky redness, which upon pressure blanches and then the redness reappears
when pressure is released – red streaks going upwards – diagnostic!!!
 Palpable tender regional lymph nodes
 Fever, tachycardia
 Lower limb lymphadenitis – groin lymph nodes are enlarged
 Upper limb lymphadenitis – edema on dorsum of hand
 Toxaemia and septicaemia can occur
Treatment: -

 Antibiotics e.g., penicillin (broad spectrum like ampicillin, 3rd gen cephalosporins like
ceftriaxone etc.)
 Elevation, bed rest, and warm compress
 NSAIDs – strong analgesics like opioids
 Glycerine magnesium sulphate dressing
2. Mesenterial lymphadenitis

 Def: -It is inflammation of the mesenteric lymph nodes, which are located in the
membrane that connects the intestine to the abdominal wall (mesentery)
 The membrane provides lubrication so that the organs can move within the
abdominal cavity
 It is common in children and young women
Types: -

 It can be divided into 2 types: -

1. Primary
 On imaging, it is seen as right-sided mesenteric lymphadenopathy
that does NOT have identifiable acute inflammatory process or has
only mild wall thickening of the terminal ileum (less than 5mm)
2. Secondary
 On imagining, it is seen to be associated with a specific, identifiable
inflammatory condition (e.g., Crohn’s disease), with clearly
detectable terminal ileal thickening
Causes: -

 Infection: - !
o Yersinia enterolitica infection (most common)
o Bacterial infection e.g., Salmonella, Staphylococcus, Streptococcus, TB
o Viral infection – gastroenteritis (stomach flu)
o Parasitic infection – Guardia lamblia
 Cancer: - lymphoma, breast cancer, pancreatic cancer, lung cancer
 Inflammatory conditions: - Crohn’s disease, pancreatitis, diverticulitis (inflammation
of large intestine)
Clinical features: -

 Abdominal pain in right lower quadrant (right iliac fossa)

 Slight fever, nausea, vomiting, diarrhoea, abdominal colicky
 Tender lymph nodes may be palpable in RIF
 History of ingestion of raw pork in places with endemic Yersinia
 Diagnosis: -

 CBC – leucocytosis
 Blood sample serology for diagnosis of etiologic agents e.g., Yersinia enterolitica
 Urine analysis – to exclude UTI
 Ultrasound of abdomen
 CT of abdomen – shows enlarged mesenteric lymph nodes, with or without
associated ilial wall thickening and a normal appendix
Differential diagnosis: -

 Acute appendicitis – in mesenterial lymphadenitis, the lymph nodes tend to be

bigger, more in number and more widely distributed than in appendicitis
 Meckel’s diverticulum
Treatment: -

 Broad spectrum antibiotics: -metronidazole, clindamycin, ampicillin, amoxicillin

 Treat pain and rehydrate the patient
 Surgery is done if appendicitis can NOT be excluded with certainty, just to be safe
and appendectomy is done
3. Elephantiasis

 Def: -Elephantiasis is enlargement and hardening of limbs or body parts due to

tissue swelling
Cause and pathogenesis: -
!
 The most common cause of lymphedema worldwide is the Wusheria bancrofti
(filariasis) parasitic infestation of lymph nodes, which causes elephantiasis
o When the mosquito Culex fatigans sucks blood from a person infected with
filaria the filariae grow into larvae in the abdomen of the mosquito
o When a human is bitten by the infected mosquito the larvae reach the lymph
nodes where they are liberated as embrions which leave the lymph nodes
and enter the circulation through the thoracic duct
Treatment: -

 Elevate the limb, exercise, weight loss

 Topical anti-fungal – 1% clotrimazole
 Surgery – Charles’ excisional surgery
o The lymphoedematous tissue is excised and the area is
covered with a skin graft

ABDOMEN
52) Characteristics of the anterior abdominal wall and general study of hernias. Congenital
defects of the anterior abdominal wall
 Structure of the abdominal wall
 The abdominal wall is divided into posterior, anterior and lateral walls
ANATOMY OF THE ANTERO-LATERAL ABDOMINAL WALL
 From thoracic cage to pelvis
 Boundaries: -
o Superiorly: - 7th -10th rib cartilage and xiphoid process
o Inferiorly: - Inguinal ligament and sup margins of antero-lateral aspects of
pelvic girdle

 12 layers: -
1) Skin

2) Camper fascia
 Superficial fatty layer of subcutaneous tissue
3) Scarpa fascia
! Each muscle has its own fascia
4) Superficial investing fascia
5) External oblique muscle

6) Intermediate investing fascia

7) Internal oblique muscle

8) Deep investing fascia

9) Transversus abdominis muscle

10) Transversalis fascia

11) Extraperitoneal fat
 12) Parietal peritoneum

Muscles of the abdominal wall: -

 4 muscles and their attachments, direction of fibers, innervation, actions: -
 Flat abdominal muscles: -
1. External oblique
2. Internal oblique
3. Transversus abdominis
 All 3 end in aponeurosis
o APONEUROSIS = Sheets of fibrous tissue that anchor muscles to bone, deep
fascia or other muscles
 Fuse in the middle Linea alba
o Runs from xiphoid process to pubic symphysis
1. External Oblique
 Largest
 Origin: -
o External surfaces of 5th – 12th ribs
 Insertion: -
o Linea alba
o Pubic tubercle
o Anterior half of iliac crest
 Posterior fibers are almost vertical and travel towards the iliac crest
 Anterior fibers fan out medially
 Inferior margin also forms the Inguinal ligament
o Connects the superior iliac spine to pubic tubercle

 Innervation: -
o Thoracoabdominal nerves (ant rami of T7-T11)
o Subcostal nerve (ant ramus of T12)
 Actions: -
o Flexes and rotates the trunk
o Compresses and supports organs w/I the abdominal cavity during expiration
2. Internal Oblique
 Fibers run perpendicularly to the external oblique run inferolateral
 Origin: -
o Thoracolumbar fascia (broad tissue attached to the spine)
o Anterior 2/3rd of the iliac crest
o Tissue deep to lateral 1/3rd of Inguinal ligament
 Insertion: -
o Inferior border of 10th – 12th ribs posteriorly
o Linea alba anteriorly
 Innervation: -
o Thoracoabdominal nerves (T7-T11 anterior rami)
o Subcostal nerve (T12)
o L1 anterior ramus
 Actions: -
o Compresses and supports abdominal viscera
o Flex and rotate trunk (bring shoulder to contralateral hip)
3. Transversus Abdominus
 Fibers run transversely
o Except the inferior fibers which run parallel to the internal oblique
 Origin: -
o Internal surface of 7th-12th costal cartilages
o Thoracolumbar fascia
o Iliac crest
o Connective tissue deep to lateral 1/3rd of inguinal ligament
 Insertion: -
o Linea alba
o Pubic crest

 Innervation: -
o Thoracoabdominal nerves (T7-T11)
o Subcostal nerve (T12)
o L1 anterior ramus
 Actions: -
o Compress abdominal contents
o Increase intra-abdominal pressure
 Helpful during forced expiration
o No role in trunk movement
Vertical muscles: -
1. Rectus abdominis muscle
 Set of vertically oriented paired muscles that lie right at the midline of the anterior
abdominal wall
 Origin: -
o Pubic symphysis
o Pubic crest
 Insertion: -
o Xiphoid process
o 5th – 7th costal cartilage
 Innervation: -
o Anterior rami of: -
 Thoracoabdominal (T7-T11)
 Subcostal (T12)
 Actions: -
o Powerful flexor of the trunk
o Stabilize tilt of pelvis
o Compress abdominal viscera
 Separated in the midline by Linea alba
 Enclosed by the rectus sheath
o Anterior layer of rectus sheath
anchors the rectus muscle
transversely by tendinous
intersections create 6 pack
2. Pyramidalis muscle
 Smaller triangular shaped muscle and lies anterior to rectus
abdominis
 Origin: -
o Anterior surface of pubis
 Insertion: -
o Linea alba
 Absent in up to 20% of people
 Action: - tense the Linea alba
Rectus sheath
 Strong incomplete covering of the rectus abdominis muscle and the pyramidalis
muscle
 Also contains: -
o Superior epigastric artery
o Inferior epigastric artery
 Function: -
o Protect structures w/I it
 Formed by the interweaving of aponeurosis of the flat abdominal muscles
 Divided into ant and post layer
 Not uniform throughout hence composition divided in 3 main areas: -

o Above the costal margin

 Only external layer aponeurosis
 No posterior layer therefore lies directly on thoracic wall
o Below costal margin to just below umbilicus
 Contains ant and post layer
 Int oblique aponeurosis splits into 2 layers
 Anterior lamina of the internal oblique merges with the aponeurosis
of the external oblique to form the anterior layer of the rectus sheath
 Posterior layer is formed by posterior lamina of the internal oblique
which merges with the aponeurosis of the transverse abdominis
 o Below arcuate line to pubic crest
 Begins approx. 1/3rd of the distance from the belly button to the pubic
crest
 Anterior layer of the rectus sheath is formed by the aponeurosis of all
3 muscles
 Post formed by the transversalis fascia

 ARCUATE LINE = demarcation b/w the posterior layer of the rectus sheath and the
transversalis fascia

Internal surface of the anterolateral abdominal wall: -

 Covered in parietal peritoneum
 Peritoneum below umbilicus divides into 5 diff folds: -
1. Median umbilical fold – median umbilical ligament
2. 2 medial umbilical folds – medial umbilical ligament
3. Lateral umbilical fold – cover inf epigastric arteries
Sensory innervation: -
 Thoracoabdominal nerves (t7-t11)
o Lateral cutaneous branches – exit at the midaxillary line
o Ant cutaneous branches – near the midline
 T7-T9 innervate skin above umbilicus
 T12at umbilicus
 T11below umbilicus
 Subcostal nerve (T12)
o Run in neurovascular plane after running below the ribs
o Sensory innervation to skin b/w umbilicus and iliac crest
 Iliohypogastric (L1)
o Internal oblique
o Transversus muscle
o Skin overlying upper inguinal and hypogastric regions
 Ilioinguinal (L1)
o Inferior portion of internal oblique and transverse abdominis
o Skin over lower inguinal region, mons pubis, ant scrotum or labia majora and
medial thigh

 Neurovascular plane – b/w int. oblique and transversus abdominis

o Where the nerves run
Arterial supply: -
 Superior epigastric artery !
o Branch of internal thoracic artery
o Sup portion of rectus abdominis
 Inferior epigastric artery
o Branch of external iliac artery
o Anastomose with sup epigastric artery
 Other arteries need to know later if time
Venous drainage: -
 Internal thoracic vein
 Sup and inf epigastric veins external iliac veinfemoral vein
Lymphatic drainage: -
 Above umbilicus: -
o Axillary lymph nodes
o Parasternal lymph nodes
 Below umbilicus: -
o Superficial inguinal lymph nodes

Hernias

!
 HERNIA = is an abnormal protrusion of a viscus or part of a viscus through an
opening (artificial or natural), with a sac covering it
 There are 3 components of a hernia – covering, sac and content
1. Sac: diverticulum of peritoneum consisting of mouth, neck, body + fundus –
neck usually well defined
2. Covering: derived from layers of abdominal wall through which sac passes
3. Contents: -
(i) omentum = omentocele
(ii) intestine = enterocele; more commonly small
bowel but may be large intestine or appendix
(iii) a portion of the circumference of the intestine =
Richter’s hernia
(iv) a portion of the bladder (or a diverticulum) may
constitute part of or be the sole content of a direct
inguinal, a sliding inguinal or a femoral hernia;
(v) ovary with or without the corresponding fallopian tube
(vi) a Meckel’s diverticulum = a Littre’s hernia LM
(vii) Fluid, as part of ascites or as a residuum thereof
 Inguinal hernia is the most common hernia (73% cases)
 Groin hernias are 25 times more common in men than women
 Femoral hernia is more common in women

NB: -
 INCARCERATED HERNIA !
o The term ‘incarceration’ is often used loosely as an alternative to obstruction
or strangulation but is correctly employed only when it is considered that the
lumen of that portion of the colon occupying a hernial sac is blocked with
faeces
 STRANGULATED HERNIA
o Blood supply impaired, rendering the contents ischaemic.
o Gangrene may occur as early as 5–6 hours after the onset of the first
symptoms.
 o Although inguinal hernia may be 10 times more common than femoral
hernia, a femoral hernia is more likely to strangulate because of the
narrowness of the neck and its rigid surrounds
Types: -
 They can be divided into 2 main types: - !
1. External hernia
 An abnormal lump which can be detected by clinical examination of
the abdomen or groin.
2. Internal hernia
 Occur when the intestine (the ‘viscus’) passes beneath a constricting
band or through a peritoneal window (the ‘defect’) within the
abdominal cavity or in the diaphragm
Classification: -
1. Clinical features classification: -
1. REDUCIBLE HERNIA – the hernia is reduced on its own or by the patient or
surgeon
2. IRREDUCIBLE HERNIA – the contents can NOT be returned to the abdomen
due to narrow neck, adhesions, overcrowding. It can result in strangulation
3. OBSTRUCTED HERNIA – it is an irreducible hernia with obstruction, but blood
supply to the bowel is NOT affected. It eventually results in strangulation
4. STRANGULATED HERNIA – it is an irreducible hernia with obstruction to blood
flow
5. INFLAMED HERNIA – due to inflammation of the contents of the sac e.g.,
appendicitis
2. Classification general: -
1. Congenital
2. Acquired
3. Classification according to content: -
1. omentum = omentocele
2. intestine = enterocele; more commonly small bowel but may be large
intestine or appendix
3. a portion of the circumference of the intestine = Richter’s hernia
4. a portion of the bladder (or a diverticulum) may constitute part of or be the
sole content of a direct inguinal, a sliding inguinal or a femoral hernia;
5. ovary with or without the corresponding fallopian tube
6. a Meckel’s diverticulum = a Littre’s hernia
7. Fluid, as part of ascites or as a residuum thereof
4. Classification according to location/site: -
1. Inguinal
2. Femoral
3. Obturator
 4. Diaphragmatic
5. Lumbar
6. Spigelian
7. Umbilical
8. Epigastric
9. Gluteal
10. Sciatic

Causes: -
 Straining
 Lifting heavy objects
 Chronic cough e.g., TB, chronic bronchitis, bronchial asthma, emphysema
 Chronic constipation
 Obesity, pregnancy
Clinical features: -
 Sudden pain, generalised abdominal pain (colicky in character), nausea + vomiting,
increase in hernia size, on examination hernia is tense, extremely tender +
irreducible, no expansion cough impulse
 Spontaneous cessation of pain must be viewed with caution – could be sign of
perforation
 If strangulated urgent surgery
Treatment: -
 Simple suture closure, mesh repair
1. Midline scar is opened – adhesions are lysed + the ileostomy taken down
2. Mobilised segment of bowel removed
3. End to end anastomoses to connect bowel with ileocecal stump
4. Large piece of mesh is locked down to the fascia to reinforce the ventral aspect
Treatment: -
 2 types: -
1. Herniorrhaphy
(i) Longitudinal incision over hernia
(ii) Herniated tissue is pushed back
(iii) Hernia sac is removed
(iv) Edges of healthy muscle are stitched
o Used when mesh placement is C/I: -
 Active infection or necrosis of
herniated tissue
 Mesh is cost prohibitive
2. Hernioplasty (Mesh/Tension-free hernia
repair)
(i) Flat sterile mesh patch is placed over
weakened muscle opening
 (ii) Mesh stitched into surrounding tissues
o Performed in most cases since has a lower recurrence rate

Congenital anomalies of the abdominal wall

 There are 4 congenital anomalies of the abdominal wall: -
1. Gastroschisis !GOUI
2. Omphalocele
3. Umbilical hernia
4. Inguinal hernia
1. Gastroschisis
 Def: -It is an anomaly in which a new born is born with his/her intestines sticking out
of the baby’s body, through a hole other than the belly button
 The hole is usually towards the right of the umbilical cord
 There is no membrane covering the exposed organs
2. Omphalocele
 Def: - It is an anomaly in which an infant’s intestine or other abdominal organs are
outside of the body because of a hole in the belly button
 The intestines are covered by a thin layer of tissue and can easily be seen
3. Umbilical hernia
 Def: - It is a hernia that occurs in the belly button area
 When the fetus is growing and developing during pregnancy, there is a small opening
in the abdominal muscles so that the umbilical cord can pass through, connecting
the mother to the fetus
 After birth, the opening in the abdominal muscles closes as the baby matures
 However, a loop of intestine can move into the opening between the abdominal
muscles and cause a hernia
4. Inguinal hernia
 Def: -It is a hernia that occurs in the groin area
 A male fetus grows and matures during pregnancy and the testicles develop in the
abdomen and then move down into the scrotum through the inguinal canal
 Shortly after the baby is born, the inguinal canal closes, preventing the testicles from
moving back into the abdomen
 However, if this area does not close off completely, a loop of intestines can move
into the inguinal canal through a weakened area of the lower abdominal wall
 Girls can also develop hernias in this area, because even though they do not have
testicles, they do have an inguinal canal
53) Inguinal hernias

Inguinal hernia
Inguinal canal anatomy
 The inguinal canal is approximately 4cm long and located above the medial half of
the inguinal ligament and extends from the deep inguinal ring to the superficial
inguinal ring
 Canal that extends from the anterior superior iliac spine and descends to the pubic
tubercle

 Allows spermatic cord in male and round ligament in females

 2 inguinal rings: -
o Superficial ring  w/I external oblique aponeurosis
o Deep ring
 4 boundaries: -
o Ant wall Aponeurosis of external oblique
o Post wall Transversalis fascia + Conjoint tendon
o Roof Transverse abdominis & Internal oblique muscle
o Flooringuinal ligament
NB: -
 Deep inguinal ring runs lateral to inf epigastric artery
 Conjoint tendon lies directly posterior to superficial ring
o Formed by the merging of the internal oblique and transverse abdominis
aponeurosis when they attach to the pubic tubercle
o Conjoint tendon important in strengthening the inguinal canal directly
posterior to the superficial inguinal ring
 Summary of boundaries of inguinal canal: -

Contents: -
 Female: - Round ligament of the uterus + Ilioinguinal nerve
o Embryological remnants as ovaries descended
o Enters deep ring and exits superficial ring and merges with fat of labia majora
 Male: - Spermatic chord + ilioinguinal nerve
o Spermatic chord: - 3 arteries + 3 nerves + 3 additional
1. Ductus deferens things
 Allows sperm produced in testes o3 arteries: -
to travel back up into the urethra
1. Artery to ductus deferens
2. Testicular artery
3. Cremasteric artery

o3 nerves: -
 2.
Artery of ductus deferens
3.
Testicular artery
4.
Cremasteric artery
5.
Pampiniform venous plexus
6.
Sympathetic nerve fibres
7.
Genital branch of genitofemoral nerve
 Cutaneous innervation from the skin of the scrotum
8. Lymphatic vessels
Covering of spermatic chord: -
 Spermatic chord has coverings which followed it descend from the abdomen
 Hence, 3 layers cover the spermatic chord, all of which are derived from structures in
the abdominal wall: -
1. External spermatic fascia = External oblique
2. Cremasteric fascia = Internal oblique
!
3. Internal spermatic fascia = Transversalis fascia
 The transverse abdominis doesn’t follow and only forms the roof as the testes
doesn’t pass through it
Inguinal hernia: -
 HERNIA = protrusion of a structure through the wall that surrounds it
 INGUINAL HERNIA = protrusion of part of the contents of the abdomen through the
inguinal region of the abdominal wall
 Hernias in inguinal region account for 75% of all hernias – more common in men
 Etiology: -
o Changes in intra-abdominal pressure
o Contents of abdomen
o Potential sites of weakness
 2 potential signs of weakness: - superficial and deep inguinal rings
 2 diff types: - direct and indirect
!!!!! The relation of each hernia to the inferior epigastric vessels is important
Direct Indirect
Acquired Congenital
Occurs at PATENT PROCESS VAGINALIS = failure
of the deep inguinal ring to sufficiently close
once the testes have migrated
Protrusion occurs at level of superficial ring Protrusion occurs at deep inguinal ring
where testes pushing against the conjoint
tendon w/I Hesselbach’s triangle
Occurs medial to inf epigastric artery Lateral to epigastric artery and veins
Takes with it a hernial sac created by Not limited by hernial sac
peritoneum and transversalis fascia
Can be reduced i.e., can be popped back in
Doesn’t enter scrotum Can enter into scrotum

Hesselbach’s Triangle: -
  Borders: -
 Inferior: - Inguinal ligament
 Laterally: -Inf epigastric vessels
 Medially: -lateral border of Rectus abdominis muscle

Inguinal hernia (groin hernia) -DO THIS PART AGAIN FROM STUDENT NOTES!!!
Types of inguinal hernia: -
 It can be divided into 2 types: -
1. Indirect hernia (more common) – comes out through internal ring along with
the cord
2. Direct hernia – occurs through posterior wall of the inguinal canal through
Hesselbach’s triangle. The hernia sac is medial to the inferior epigastric
gastric
1. Indirect inguinal hernia (more common)
 More common in younger people and more common in men
 More common in the right side in 1st decade of life and then incidence becomes
equal in 2nd decade of life
 The hernia sac is thin and the neck is narrow and lies lateral to the inferior
epigastric vessels
 The contents of the hernia are either small intestine, large intestine, omentum or a
combination of all of these
 It can be divided into 3 types: -
1. Buboncele – the hernia sac is confined to the inguinal canal !
2. Funicular – the sac extends along the
length of the inguinal canal and
through the superficial inguinal ring,
but does NOT extend to the scrotum or
labia majora
3. Complete (scrotal) – the hernia sac
passes through the inguinal canal and
superficial inguinal ring and extends into the scrotum or labium. The testes lie
within the lower part of the hernia
2. Direct inguinal hernia (35% cases)
 More common in elderly and uncommon in women and children
 It is always acquired, due to weakening of posterior wall of the inguinal canal
 The hernia is medial to the inferior epigastric artery
 It occurs through Hesselbach’s triangle – bounded by inferior epigastric artery
laterally, lateral border of rectus medially and inguinal ligament below
 It is divided into medial and lateral depending on which part of the Hesselbach’s
triangle is arises from
 It rarely descends into the scrotum and strangulation is NOT as common as indirect
hernia. However, it is still possible
Causes: -
 Straining
 Chronic cough e.g., TB, bronchial asthma, bronchitis
 Smoking, obesity, multiple pregnancies, ascites
 Strenuous activity
 Acquired deficit in abdominal wall
Clinical features: -
 Visible, palpable groin protrusion or bulge
 Palpation of the inguinal canal: With the patient standing, palpate from the scrotal
skin towards the superficial (external) inguinal ring. Ask the patient to cough or
strain and bear down (valsalva maneuver). Bulging can be felt with a fingertip.
 Increase of symptoms during physical activity (walking or standing, coughing,
sneezing, abdominal pressure)
 Systemic S+S in case of intestinal obstruction- colicky abdominal pain, vomiting,
abdominal distension, constipation
 Lump expansible on cough impulse*
 Dragging pain and swelling in the groin
 Inguinal discomfort, with or without a lump – due to stretching of the tissues of the
inguinal canal and occurs typically when intraabdominal pressure is increased
 A lump is usually obvious to the patient, is often precipitated by increasing
intraabdominal pressure, and may reduce completely with rest and lying down
 The patient initially is examined standing to demonstrate the lump and possible
cough impulse, and then lying down to allow the hernia to be reduced
Diagnosis: -
 Internal ring occlusion test !
(i) Internal ring is located half inch above the mid inguinal point.
(ii) After reducing the contents of the hernia in lying position, the internal ring is
occluded using the thumb.
(iii) The patient is then asked to cough.
o If a swelling appears medial to the thumb, then the hernia is direct hernia.
o If a swelling does NOT appear and appears when you release the thumb, then
the hernia is an indirect hernia
  Ring invagination test
o After reducing the hernia, the index finger is invaginated from the bottom of
the scrotum, and is gradually pushed up and rotated to enter the superficial
inguinal ring.
o The impulse on coughing is felt at the tip of the invaginated finger
 Zieman’s test
(i) Place your index finger on the deep inguinal ring and the middle finger on the
superficial inguinal ring and the ring finger on saphenous opening.
(ii) Ask the patient to cough.
o If the impulse is felt on the index finger, it is an indirect hernia
 Per rectal examination (MUST BE DONE)
 Inguinal hernia in women – increased labia major on palpation when compared to
contralateral side
Differential diagnosis: -
1. Femoral hernia
2. Undescended testes
3. Hydrocele
4. Groin abscess
Treatment (always surgery): - SO THIS FROM THE DOCUMENT!!!
 HERNIORRHAPHY = posterior wall of the inguinal canal is repaired
 HERNIOPLASTY = prosthetic mesh is used to cover and support the posterior wall of
the inguinal canal
 Bassini’s herniorrhaphy
o The conjoint tendon is sutured onto the inguinal ligament. A J-shaped incision
called a ‘Tanner slide’, is made in the anterior rectus sheath to allow the
conjoint tendon to ‘slide’ down towards the inguinal ligament without
tension
o Nylon darn repair – the weakened transversalis fascia is plicated from the
pubic tubercle to the deep ring. A second continuous nylon suture is inserted
as a loose darn from the inguinal ligament below to the anterior aspect of the
conjoint tendon and aponeurosis of the internal oblique above, extending
from the pubic tubercle medially to beyond the deep ring laterally

Treatment: -mostly for indirect types

 Herniotomy = excise the sac of the hernia; high chance of recurrence
o Oblique incision a bit lateral to superficial ring
o Remove superficial and deep fascia
o Incise the external oblique aponeurosis in the direction of the fibres till you
see the superficial inguinal ring
o Incise up the inguinal canal
o You see the spermatic chord
o Separate the spermatic chord from the hernia
 o Tie the neck of the hernia at the deep inguinal ring with sutures and excise
the hernia
 Herniorrhaphy = remove sac and strengthen posterior wall
1. Lytes method
 Narrow the deep inguinal rings borders
2. Modified Basini’s repair
 Suture the posterior conjoint tendon to the anterior inguinal ligament
3. Shouldice repair – Double breast transversalis fascia + Bassini’s
 Transversely cut the fascia transversalis (that makes the deep
inguinal ring)
 Overlap the 2 flaps on the fascia transversalis together and suture
them using double breasting method (so this is behind the conjoint
tendon)
 In addition, suture the conjoint tendon and the inguinal ligament like
in the modified Basini’s method
4. Maloney Darn repair
 Using darn (a type of nylon suture) – suture figure 8’s in the posterior
wall
5. Lichtenstein (mesh) repair – GOLD STANDARD!!!
 Suture a mesh into the conjoint tendon superiorly and inferiorly to
the inguinal ligament
For direct inguinal canal – strengthen the Hesselbach’s triangle using mesh
54) Femoral hernia
Femoral hernia

Sam webster notes: -

FEMORAL SHEATH ANATOMY

 Connective tissue/fascia
 Transversalis fascia and iliopsoas facia come together to form a funnel FEMORAL SHEATH
o Wider at top narrower at bottom
 Sheath passes deep to the inguinal ligament and into the upper thigh
 Sheath ends with blending with the adventitia (the CT of the blood vessels)
 Surround the blood vessels BUT NOT THE NERVE
 About 3-4 cm long
 Inside the femoral sheath is divided into 3 compartments: - (3 tubes w/I a tube)
o Lateral compartment – femoral artery + femoral branch of the genitofemoral nerve
o Middle compartment – femoral vein
o Medial compartment – Lymph node of Cloquet
 Femoral artery branch of the EXTERNAL ILIAC ARTERY and when it passes deep to the
inguinal ligament called the FEMORAL ARTERY
 EXTERNAL ILIAC VEIN also become FEMORAL VEIN when it crosses inguinal ligament
 FEMORAL NERVE IS LATERAL, the vein is medial
 Femoral nerve passes deep to the inguinal ligament but is OUTSIDE the femoral sheath

 Purpose of sheath: -
o Allows the blood vessels to slide up and down as we move the hip joint
FEMORAL CANAL

 The ‘empty’ medial compartment is called the FEMORAL CANAL

NB: - Space w/I the sheath is the canal

 Reason it exists: -
o If the blood flow from the lower limb increases the vein can dilate
o IF there is increased intra-abdominal pressureblood cannot flow upvein dilate
FEMORAL TRIANGLE

 Borders: -
o Inguinal ligament – superiorly
o Sartorius muscle – laterally
o Adductor longus – medially
 Femoral sheath is w/I the femoral triangle
NB: -

 Difference with the inguinal canal: -

o The inguinal canal is superior to the inguinal ligament
o It’s a muscular tube
o Connects the abdominal canal with the scrotum or labia majora

 The most superficial vein is the SAPHENOUS VEIN

 Hence the opening is called the SAPHENOUS OPENING or RING
o Its how it goes from superficial to the fascia lata to deep to the fascia lata
o Its where it drains into the FEMORAL VEIN
 The femoral canal also has a femoral ring – where we see an opening
 The femoral pulse when assessing blood flow to lower limb is also taken at the femoral
vessels
FEMORAL HERNIA

 Small bowel has a mesentery that allows it to move around while the large bowel doesn’t
make it fixed in place
 Femoral = thigh
 Femoral hernia would be medial to femoral vein
 Inferior to the inguinal ligament
  Femoral sheath surrounds the femoral vessels
 Medial to femoral vein – space called FEMORAL CANAL
o Allows femoral vein to expand

 Potential weak point

 Small bowel would run posteriorly to the inguinal ligament and appear inferior to the
inguinal ligament
 Lower limb covered by Ct cover – FASCIA LATA
 Hernia would be inferior and lateral to the pubic tubercle
 Hernia can compress femoral vein which can cause other effects in the lower body
Causes: -

 Anatomical weak point

 Small bowel has a mesentery and is able to move around
 Chronic raising of intra-abdominal pressure with: -
o Constipation
o Breathing difficulties
o Pregnancy
 Can cause femoral vein to dilatepush surrounding CT widens femoral canal
 More common on the RIGHT SIDE OF THE BODY
 More common in women than men since women have a larger pelvis
 Can be more dangerous since it’s a smaller space higher risk for strangulation
Treatment: -

 Surgical
 Medical emergency

Femoral canal anatomy

 Femoral canal occupies most medial compartment of femoral sheath
 The femoral canal is 1.25cm long extends from the femoral ring (above) to the
saphenous opening (below)
 It contains fat, lymphatics, lymph node of Cloquet
  Boundaries: -
o Anteriorly – inguinal ligament
o Posteriorly –Cooper ligament, pubic bone
o Medially – lacunar ligament
o Laterally – a thin septum separating it from the femoral vein
 Inside the femoral sheath is divided into 3 compartments: - (3 tubes w/I a tube)
o Lateral compartment – femoral artery & femoral branch of the genitofemoral
nerve
o Middle compartment – femoral vein
o Medial compartment – Lymph node of Cloquet

 F artery + vein enclosed by femoral sheath – an extension of transversalis fascia. F.

Nerve lies outside the femoral sheath
Femoral hernias
 The hernia sac descends downwards to the saphenous opening and then escapes out
into the loose areolar tissue to expand out like a retort
 Occurs medial to the femoral vein
 It is more prone to obstruction and strangulation – 40% are associated with
obstruction/strangulation, thus making them emergency cases
 More common in women, especially those that have given birth multiple times
 Rare before puberty
 It can be associated with inguinal hernia also
Pathology: -
 If hernia passes through saphenous hiatus – irreducible (incarcerated) – as it expands
+ no longer confined to inelastic wall of femoral canal
Classification: -
 Reducible
 Irreducible
 strangulated
Causes: -
 Wide femoral canal
 Multiple pregnancies
 increased intra-ab pressure
 previous groin injury for inguinal hernia repair
 increases with advancing age, chronic cough, constipation
Clinical features: -
 Rare before puberty
 F>M
 S+S less pronounced than inguinal hernias
 Swelling more apparent on standing + straining
 Swelling in the groin below and lateral to the pubic tubercle (inguinal hernia is
above and medial to the pubic tubercle)

 Dragging pain, swelling, impulse on coughing, reducibility

 Features of intestinal obstruction when there is obstruction and strangulation –
painful, tender, irreducible swelling without any impulse
 Gaur’s sign – distention of the superficial epigastric vein occurs due to pressure by
the hernia sac
Diagnosis: -
 Primarily a clinical dx; Groin US used when dx inconclusive
 Swelling in the groin below and lateral to the pubic tubercle (inguinal hernia is
above and medial to the pubic tubercle)
Differential diagnosis: -
 Inguinal hernia (Ring Occlusion Test)
 Saphena varix- saccular enlargement of the termination of the long saphenous vein.
o Swelling disappears completely when pt lies down while femoral hernia sac
usually is still palpable
 Enlarged Cloquet lymph node
 Femoral aneurysm
Treatment: -
!
 Need to operate ASAP as constant risk of strangulation
1) Low OP (Lockwood)
 Sac dissected out below inguinal lig via a groin crease incision.
2) High OP (McEvedy)
  Vertical incision over femoral canal upwards above inguinal lig sac
dissected out through lower part of incision
 Advs: - if resection of intestine is required there is sufficient room
 Dis: - if infx occurs, incisional hernia may develop
3) Lotheissen’s OP – Inguinal approach
 Inguinal canal opened like in inguinal herniorrhaphy.

55) Umbilical hernia, cysts and fistulas of the umbilicus

Umbilical hernia
 Def: -It is a herniation through a weak umbilical scar (cicatrix)
 It develops due to absence of umbilical fascia or incomplete closure of umbilical
defect
 The weakest part in the umbilical cicatrix is the upper part, where the hernia begins
 Can be divided into 2 types: -
1. Congenital – common in new-born boys and infants
2. Acquired – common in women and due to smoking, obesity, chronic cough
etc.
 Occurs in 20% new-borns
 Affects men more
 It is associated with Down syndrome
 Clinical features: -
o Swelling in the umbilical region within first few months of birth.
o The swelling size increases during crying and can be felt with finger during
crying
 Treatment: -
o Conservative
 95% cases resolve spontaneously within the few months of birth
 Can be made quicker by adhesive strapping across the abdomen
o Surgery – for hernia bigger than 2cm
 Primary closure of the defect – hernia sac is dissected
 Umbilectomy – only done in adults with large umbilical hernia
Paraumbilical hernia
 Def: -It is a protrusion of herniation through Linea alba, just above or below the
umbilicus
 The contents of the hernia are usually omentum, small intestine and large intestine
 It has a tendency for adhesion, irreducibility and obstruction
 Affects women more
 Causes: -
o Obesity, multiple pregnancies
o Flabby abdominal wall
 Clinical features: -
 o Swelling with smooth surface and distinct edges
o Dragging pain and impulse on coughing
o Intestinal colic can be seen in large hernias – due to subacute intestinal
obstruction
 Treatment – always surgery
o Dissection of hernia sac and placement of mesh in retro rectus plane and
under the umbilicus
o Mayo’s operation – herniotomy is done
o After surgery – use abdominal binder and lose weight
Umbilical cyst (urachal cyst)
 It arises from the remnant of the urachus and it seen as a swelling in the midline at !
the lower abdomen as an extraperitoneal mass
o URACHUS = is a fibrous remnant of the ALLANTOIS, a canal that drains the
urinary bladder of the fetus that joins and runs within the umbilical cord.
 The fibrous remnant lies in the SPACE OF RETZIUS, between the
transverse fascia anteriorly and the peritoneum posteriorly

 It can get infected, or rupture into the umbilicus or peritoneal cavity

Umbilical fistula
 Causes: - !
o After surgery
o TB
o Patent urachus
 Clinical features: -
o Faecal discharge or urinary discharge, mucoid discharge
o Pain, tenderness and excoriation in and around the umbilicus
 Diagnosis: -
o Fistulogram, CT fistulogram
o Ultrasound of abdomen
o Discharge study
 Treatment: -
o Fistulectomy and resection of bowel segment and anastomosis of the bowel
56) Postoperative and other internal and external SPIEGEL hernias, in the triangles of Petit
and Grynfeltt

Spiegel hernia
 Spiegel hernia – hernia though Spigelian fascia
o Bounded by the Linea semilunaris laterally and the lateral edge of the rectus
muscle medially

 It is a type of interparietal hernia that occurs at the level of the arcuate line through
Spigelian point
 The hernia sac lies either deep to the internal oblique or between the internal and
external oblique muscles
 It can occur above or below the umbilicus – 90% occur below the umbilicus
 Common in women over 50 years old
 Causes: -
o Obesity
o multiple pregnancies
o chronic cough
o old age
 Clinical features: -
o Soft, reducible mass lateral to the rectus muscle and below the umbilicus,
with impulse on coughing
 Diagnosis: - ultrasound of abdomen
 Treatment: - herniotomy surgery

Lumbar hernias
Osmosis notes: -
 Protrusion of organs through fascial defects in the posterolateral abdominal wall
 Risk factors: -
o Trauma or surgery
 Symptoms: -
o Palpable posterolateral mass that: -
 increases in size with coughing and strenuous activity
 Reducible & disappears when individual lies down
o Vague back pain
o Bowel obstruction
o Urinary obstruction
o Can develop into a pelvic mass
 Arise in 2 possible defects in the lumbar region: - G is first hence superior
o Superior lumbar triangle aka Grynfeltt triangle
 Borders: -
 Superiorly – 12th rib
 Laterally – internal oblique
 Medially -quadratus lumborum
 Floor – transversalis fascia & aponeurosis of transversus
abdominis muscle
 Roof – external oblique & latissimus dorsi muscle
o Inferior lumbar triangle aka Petit triangle
 Borders: -
 Lateral -external oblique
 Medially – lateral border of latissimus dorsi
 Inferior – Iliac crest
 Floor- lumbodorsal fascia
o LUMBODORSAL FASCIA = Aponeurosis of internal
oblique & transverse abdominis

 Diagnosis: -
o Hernia and edges of defect can be identified through palpation when
standing and lying down

 Def: -Lumbar hernias are rare posterior abdominal hernias through either the
superior or inferior triangle
  Contents of hernia: - stomach, small or large intestine, omentum, ovary, spleen,
kidney etc.
 Causes: -
o Congenital – 20% cases
o Spontaneous – 55% cases
o Trauma, fracture of iliac crest, hepatic abscess, pelvic bone infection
 Types: -
1. Petite’s hernia – occurs through lower lumbar triangle hernia
2. Grynfeltt hernia (more common) – occurs through upper
lumbar triangle hernia
 Differential diagnosis: - !
o Cold abscess
 Cold abscess = an abscess that lacks the intense
inflammation usually associated with infection.
 This may be associated with infections due to bacteria
like tuberculosis and fungi like blastomycosis that do not tend to
stimulate acute inflammation.
o Lumbar phantom hernia (muscular bulge as a result of local muscular
paralysis due to nerve supply interference to the affected muscle)
o Lipoma
 Treatment: - repair using fascial flaps

57) Diaphragmatic hernias - congenital and acquired and other internal hernias

 DIAPHRAGMATIC HERNIA = is hernia of the abdominal contents through the

diaphragm and into the chest
 Types: -
o It can be divided into 2 types: -
1. Congenital
a. Eventration – weakening one !
b. Hernia through foramen Bochdalek (most common)
c. Hernia through foramen Morgagni
d. Congenital oesophageal hernia (rare)
2. Acquired
a. Traumatic
b. Spaseal hiatus
Congenital diaphragmatic hernias
1) Eventration
 It is weakening of the diaphragm due to atrophy and loss of muscle of part or all of
one leaf of the diaphragm
 The diaphragm is thin, becomes attenuated and inactive and is higher than normal
and immobile
 Mainly affects children
 Clinical features: -
o Asymptomatic
o Wheezing
o exercise intolerance
o extreme respiratory distress
 Diagnosis: -
o Chest x-ray – shows the
abnormality
 DDX: - diaphragmatic hernia through
foramen Bochdalek
 Treatment: - plication of diaphragm through laparotomy
o DIAPHRAGMATIC PLICATION is a procedure used to surgically treat
diaphragmatic eventrations/paralysis.
o The procedure involves repositioning and/or reshaping the diaphragm to
expand lung capacity and ultimately, improve breathing difficulties caused by
these conditions.
2) Hernia through foramen Bochdalek (most common)
 It occurs due to failure of fusion of pleuroperitoneal canal, resulting in a direct
!
communication between the pleura and peritoneum on the left side of the
chest (95% cases occur in left-side of chest)

 The colon is the most common abdominal organ to be involved

 80% cases do NOT have a hernia sac
 It is posterolateral diaphragmatic hernia
 Clinical features: -
o respiratory embarrassment
o bowel sounds in left side of chest
o mediastinal shift towards right side
o scaphoid abdomen
 SCAPHOID ABDOMEN is the term given to an inward concavity of the
anterior abdominal wall.
 Diagnosis: -chest x-ray, barium enema
  Treatment: -laparotomy and dissection of the sac (if present) and closure of the
defect in the diaphragm using non-absorbable suture
3) Hernia through foramen Morgagni
 The defect lies between the sternal and costal attachments of the diaphragm and is
located in front and towards the right
 The colon is the most common abdominal organ to be involved
 It is parasternal diaphragmatic hernia
 Clinical features – usually does asymptomatic
Acquired diaphragmatic hernias
1) Traumatic diaphragmatic hernia
 Causes: - car accident, crush injury, penetrating injury, blunt injury
 The patient goes into shock
 Clinical features: - respiratory distress, guarding and rigidity in abdomen, shock
2) Hiatal hernia
 It is the most common diaphragmatic hernia
 It can be divided into 3 types: -

1. Sliding hernia (most common) – cardia migrates back and forth between the
posterior mediastinum and peritoneal cavity
2. Rolling hernia (paraesophageal hernia) – herniation of stomach fundus or
other abdominal contents (colon, spleen) through a hiatus
3. Combined
 Diagnosis – x-ray of abdomen, barium meal
 Treatment: -surgical excision of hernia sac and repair of the defect

58) Diseases of the stomach. Gastric or peptic ulcer: Modern surgical treatment

 Better to watch all the videos - Intro; Diagnosis ; Surgical TXT - Bilroth 1 & 2;
Complications of surgery ; Complications of Peptic Ulcer
 Anatomy Notes - STOMACH
 PEPTIC ULCER = Term used to describe a group of ulceration disorders that occur in
areas of upper GI that are exposed to acid-pepsin secretions
 Defects in gastric/duodenum mucosa that extend into the submucosa or deeper

Classification for Gastric ulcer – Daintree Johnson: -

Type Location Acid

 hypersecretion

I Lesser curvature No

II Body of stomach and duodenum Yes

III Prepyloric Yes

IV Higher on lesser curve, near gastroesophageal No

junction

V Anywhere (medication induced) No

Etiology: -

 H. Pylori (major cause)

 NSAIDs (inhibits Prostaglandins)
 Zollinger-Ellison Syn: gastrin secreting tumour or hyperplasia of islets cells in
pancreas causing overproduction of G acid

Pathology: -

 Muscle injury + inhibition of PG (prostaglandin = inhibits acid secretion) synthesis

 Most common forms of peptic ulcer: -
o duodenum (occur at any age 3x more common)
o gastric (older age group – affects men > women)

Clinical: -

 Upper epigastrium pain

o Gastric ulcer – worsens during eating (since more acid produced)
o Duodenal ulcer – pain becomes better after eating (food brings down the
acidity of chyme)
Diagnosis: -

 History of NSAIDs
 Gastroduodenoscopy.
o All gastric ulcers should be biopsied (change of malignancy – only for gastric
ulcer)
 Urease test for H Pylori

Treatment: -

 PPIs – 1st line

o H2 antagonists if don’t work
 For H pylori antibiotics - clarithromycin, amoxicillin, metronidazole, and tetracycline
 Surgery (PTO): indicated by bleeding, perforations, obstructing + non-healing

Complications: - PUBG

 Haemorrhage: most common complication – melena, hematemesis

 Perforation: peritonitis
 Penetration: ulcer penetrates to adjacent organs
 Pyloric stenosis/obstruction: healing peptic ulcer (pu) within pyloric location = over
production of fibrous tissue
 Malignancy: rare. Only occurs in gastric ulcer NOT duodenal
o Rough border = malignancy

Operations for Gastric + Duodenal ulcers: - well explained in video

 Bilroth I Gastrectomy: for gastric ulcer

 Bilroth II Gastrectomy: for duodenal ulcer

 Gastrojejunostomy: proximal loop of jejunum anastomosed to post wall of stomach –

Billlroth I & II
o Jejunal loop can be ulcerated due to direct exposure to gastric acid
 Truncal Vagotomy + Drainage
 o Principle: secretion of vagus nerve = highly involved in acid secretion –
denervation of antropyloroduodenal segment
o Because vagus nerve are conductors of motor impulses to stomach,
denervation results in gastric stasis when vagotomy is done alone
o So need drainage = Heineke-Mikulicz Pyloroplasty: involves a longitudinal
incision across pylorus that is then closed transversely
o Pyloroplasty = destroys pyloric sphincter so gastric content can flow without
stopping drainage – can cause dumping syndrome
 Highly Selective Vagotomy - Surgical GOLD STANDARD for duodenal ulcers
o Part of vagus that supplies parietal cell is denerved

59) Pyloric stenosis

 Gastric Outlet Obstruction

 Def: -Condition where there is an obstruction at the level of the pylorus which is the
outlet of the stomach

Etiology: - 2 most common causes

1. Secondary to peptic ulcer – due to fibrosis

2. Obstruction due to tumor - Gastric cancer, pancreatic cancer, cancer of Ampulla of
Vater

Clinical: -

 Pain – unremitting, absent in some

 Vomiting – lacking bile
o Effortless vomiting 1-2 hrs after eating; with smell since mixed with HCl
 o If vomiting occurs sooner like in 30 mins after eating -obstruction in
esophagus; vomit has no smell too since not mixed with HCL
 Weight loss
 Distended abdomen
 Metabolic effects: -
o Hypokalemic + Hypochloremic – due to vomiting HCL out
o Metabolic alkalosis – vomiting HCL
o Paradoxical aciduria – due to the kidney trying to conserve Na+ at the
expense of excreting K+ initially kidney then starts conserving K+ by
secreting H+ aciduria

Diagnosis: - In the order of: -

1. Upper GI endoscopy – use NG tube first to clear stomach so can view clearly
2. Barium swallow -definitive dx
o Better to do endoscopy first since Barium coats stomach for a while especially
since can’t escape due to obstruction
o Results show no barium after stomach; stomach may be distended till pelvis
sometimes
 X – ray – shows no air after pylorus

Treatment: -

 NG tube and aspirate stomach contents

 Rehydration with IV with Normal saline (NaCl) + KCL
 Definitive txt based on cause: -
o Stenosis – gastrojejunostomy
o Pyloroplasty – to widen pylorus

60) Perforated ulcer

 Perforated peptic ulcer

Epidemiology + Etiology: -

 M>F 20:1
 NSAIDs – responsible for most perforations
 Most perforations occur b/w meals on empty stomach
 FREE PERFORATION = when duodenal gastric contents spill freely into ab cavity
diffuse peritonitis
o 90% of perforated DU occur in ant. Duodenal bulb (ant wall is thin + free)
o 60% in lesser curvature
o 40% throughout

Pathology: -
 Perforation occurs when an anteriorly/laterally placed ulcer erodes through the full
thickness of the wall of duodenum into peritoneal cavity spilling acid peptic juice,
bile + pancreatic juice
 Ulcer at lesser curvature perforates into greater sac (omentum)
 Ulcer at post wall – perforates into lesser sac
 Pathology can be divided into 3 types: -
1. Acute perforation
(i) Stage 1 – stage of peritonism
 PU perforates, acid peptic juice, bile, pancreatic juice come
into general peritoneal cavity
 Pt in severe pain – Hippocratic face
(ii) Stage 2 - stage of reaction
 Peritoneum reacts to it by secreting peritoneal fluid copiously
– this gives for short time
 Lasts 3-6 hrs
(iii) Stage 3 - stage of peritonitis
 This stage then is diffuse bactperitonitis
 12hrs after perforation
2. Subacute perforation
 “Leaking peptic ulcer” – circumscribed area of peritoneal cavity
becomes contaminated by leakage
3. Chronic perforation
 Ulcer perforates but area is walled off by adhesion OR by viscera such
as liver, colon

Clinical: - Pain

 Duodenal Ulcer = decreases soon after meal; later, pain increases a few hours after
meal (Cause the food you eat won’t be acidic so neutralise a bit)
 Gastric Ulcer = pain is continuous + increases after meal (increased HCL secretion
during meal)
 Hippocratic Face = peritonitis pain
 Blumberg Sign rebound tenderness (Rigidity = cause underlying peritonitis causes
overlying muscles to keep contracted)
 Silent abdomen with NO bowel sounds

Diagnosis: -

 Increased WBC, increased serum amylase (increased leakage of pancreatic enzymes

from perforation + absorption by peritoneal lymphatics)
 Dx on physical examination
 Aspiration of peritoneal cavity= bile-stained fluid
 Gastroscopy = contraindicated* – causes shock from intestine pain
  Gastrogratin – soluble contrast. *Do NOT use barium*
 CXR = free gas under right cupula of diaphragm
 CT imaging more accurate

Treatment: -

 Surgery = suture of perforation – laparoscopic

 Omental patching = using a piece of omentum and suturing over the ulcer
 Roux-en-Y duodenojejunostomy
 Pancreaticoduodenectomy
 Bilroth II
 Abx – pre + post op
 Resuscitation

61) Bleeding ulcer

 Bleeding peptic ulcer

 Complication of peptic ulcer that is an acute or chronic lesion

Forrest classification for Bleeding Ulcers: -

Acute Ulcers: -

 Cause severe bleeding – difficult to dx – develop rapidly + heal w/o scar within a few
weeks
 May only be dx IF endoscopy done within 1-2 days of bleeding
o Small, discrete lesion with hyperemic margin + sometimes large vessel
exposed at base of ulcer
 Gastric lesions occur with low rate of acid
 Duodenal lesions occur with high rate of acid

Chronic Ulcers: -

 Increased tendency of haemorrhage IF pt is of blood O group

 Initial haemorrhage is not fatal – becomes fatal when recurrent haemorrhage occurs
OR sudden severe haemorrhage
 Bleeding may not stop so easily by natural hemostasis

Clinical: -

 Sense of ill-being with light-headedness, sweating, pallor when haemorrhage occurs

 Ab pain, black tarry stools (melena) + hematemesis
 In case of DU – melena is present
 In case of GU – hematemesis occurs 1st then melena
 Signs of anemia
 Signs of shock due to blood loss- Low BP, tachycardia, tachypnoea

Treatment: -

 Conservative tx: -
o PPI (proton pump inhibitor)
o Tranexamic Acid = Antifibrinolytic agent – reduces bleeding rate by
encouraging clot formation (also used in heavy menstrual bleeding in
females)
o IV infusion of blood. Nasogastric tube introduced
  Endoscopic cauterisation of vessels OR clipping of vessels
 Localised epinephrine injection (vasoconstrictor)
 Surgical: - for continuous bleeding or recurrent
o Common source of bleeding comes from gastroduodenal artery
o Open surgery localise ulcer trace which vessels are bleeding well
placed suture of bleeding vessel

62) Volvulus of the stomach. Gastroptosis, bezoars, foreign bodies and other diseases of
the stomach and duodenum

1) Gastric volvulus
 Def: - It is a twist in the axis of the stomach by more than 180 degrees
 The twist may be: -
o Organo-axial (more common) – common in elderly (horizontal)
o Mesenterico-axial – common in children (vertical)
o Combined

Causes: -
 Type 1
o Occurs in two-third cases
o Considered to be due to abnormal laxity of the gastrosplenic,
gastroduodenal, gastrophrenic, and gastrohepatic ligaments.
o It is more common in adults
 Type 2
o Occurs in one-third patients
o usually associated with congenital or acquired abnormalities that result in
abnormal mobility of the stomach
Pathology: -
 The stomach twists upwards between the esophagogastric junction and
pyloroduodenal junction !!!!!
 It is associated with rolling hiatus hernia or diaphragmatic eventration

Clinical features: -

 Borchardt’s triad: - !!!!

 1. Acute epigastric pain
2. Violent ineffective vomiting (retching) and
3. Can NOT pass nasogastric tube
Diagnosis: -
 Plain chest x-ray and abdomen in erect posture – shows retrocardiac gas filled
viscous with dilated bowel loop in the abdomen
 Barium meal x-ray
 CT scan abdomen
Treatment: -
 Anterior gastropexy surgery – untwist the volvulus and gastropexy by fixing the
anterior wall of the stomach to the anterior abdominal wall
 Treat the hiatus hernia
 Do gastrectomy is the stomach is gangrenous
2) Gastroptosis
 Def: - It is abnormal downward displacement of the stomach
 It is NOT a life-threatening condition
 The condition causes digestive symptoms and constipation
 More common in women
 It can be divided into 2 types: -
1. Congenital
2. Acquired
Causes: -
 Congenital anomalies of the ligaments of the stomach
 Lengthening the mesentery of an organ such as the large intestine
o MESENTERY = is a fold of membrane that attaches the intestine to the
abdominal wall and holds it in place
 Vitamin deficiency
 Sharp decrease in body weight
 Post-surgical intervention with the aim of removal of a stomach tumour
 Irrational nutrition – small protein diet
 Surgery to remove ascites
Stages of gastroptosis: - !!!!

1. Stage 1 – the small curvature of the stomach is located about 3cm above the line of
the gallbladder
2. Stage 2 – the small curvature of the stomach is at the level as the interostium line
3. Stage 3 – the bottom of the stomach is far below the gallbladder
Clinical features: -
 Minor abdominal pain that occurs after eating
 Nausea without vomiting, fatigue and decreased performance
 Characteristic rumbling sound
 Increased gas formation
 Enlarged abdomen
 Reluctance to eat — due to increase in symptoms after eating
 Faeces have a dense consistency – this is due to weakening of the tone of the
muscles of the intestine and stomach
Diagnosis: -
 EFGDS (esophagofibrogastroduodenaoscopy) — shows the expansion of the cavity of
the affected organ and decrease its peristalsis
 Reviewing the radiography of the peritoneum with the use of a contrast medium –
confirms diagnosis
 EGG — shows decrease in electrical activity of the stomach
 Peritoneal ultrasound — will help to identify the omission of other internal organs
Treatment: -
 Diet therapy and physiotherapy
 Exercise and therapeutic massage
 Surgery
 Drugs e.g., antispasmodics, anabolic steroids
3) Bezoars
 BEZOAR = a mass found trapped in the GI system that is unable to exit the stomach
(though it can occur in other areas)
 PSEUDOBEZOAR = is an indigestible object intentionally passed into the digestive
system
 A bezoar in the oesophagus is common in young children
Types of bezoars
 Depending on the content: -
 1. Food bolus – carry the archaic and positive meaning of bezoar and are
composed of loose aggregates of food items
2. Lactobezoar – food composed of inspissated milk. Mainly seen in premature
infants given formula food
3. Pharmacobezoar – mainly tablets or semisolid masses of drugs
4. Phytobezoar – composed of indigestible plant material e.g., cellulose and are
seen in patients with impaired digestion and decreased gastric motility
5. Trichobezoar (Rapunzel syndrome) – bezoar formed from hair. The hairball
can cause ulceration, GI bleeding, perforation and obstruction
 Depending on location: -
1. Tracheobezoar – bezoar in trachea
2. Fecalith – bezoar in large intestine
Treatment: -
 Open surgery or laparoscopic surgery

63) Cancer of the stomach. Complications. Operations at different localizations

Gastric cancer + classification; Gastric cancer spread + signs; Gastric cancer Dx + TXT

Etiology + Epidemiology: -

 Poor prognosis
 M>F
 Mortality increases with age
 Increased cancer = low socioeconomic status
 Incidence increased in Japan, China, Chile, Iceland
 No single etiologic factor known as a direct cause of gastric carcinogenesis

Risk factors: -

 Environment
 Diet: increased intake of preserved foods, pickled veg. nitrate + nitrites – active
carcinogens (the n-nitrosamines)
o Ascorbic acid (vit C) prevents this conversion of nitrites to nitrosamine
 H. pylori: cause epithelial cell proliferation + production of growth regulatory
peptides
 Adenomatous Polyp: composed of atypical gland + nuclear abnormalities: high
mitotic count; 10-20% of polyps >2cm become cancer; divided into: -
o 1. Tubular Adenoma (Adenomatous Polyp) or
o 2. Villous
 Previous gastric op
 Other pre-disposing factors: pernicious anemia, menetriers disease
 o MENETRIERS DISEASE is a rare disorder characterized by giant mucosal folds
in the proximal part of the stomach, diminished acid secretion, and a protein-
losing state with hypoalbuminemia.

Pathology: -

 Arise from gastric mucosa cells anywhere in stomach but with increased frequency at
antrum + pylorus
 Lesser curvature > greater curvature
 Recently dx have been noted at cardia + GE junction = importance: prognosis of
proximal gastric tumours is worse* than that of distal tumours

Classification: - 3 types

1) Histopathological classification by Lauren – **most useful**

1. Intestinal types (53%)

o Tumor resembles colonic carcinomas (i.e., glandular pattern)
o Arises in areas of intestinal metaplasia + dysplasia and forms polypoid
tumors /ulcers
o LESS aggressive
2. Diffuse (33%)
o Tumor composed of tiny clusters of small uniform cells
o In contrast are deeper, decreased inflam infiltration
o Poor differentiation + POOR prognosis
3. Mixed (14%)

2) Japanese Classification – for early cancers (Mucosa + submucosa)

3) Borrmann’s Classification – for late cancers (Muscularis and beyond)

Metastasis: -

1. Direct
o Muscularis, serosa
o Adjacent organs like pancreas, colon, liver
2. Lymphatic

o Lymphatic drainage follows the same as arterial supply all drain into celiac
lymphatics
o This brings some specific clinical signs
3. Blood - Haematogenous Spread via Portal Vein
o Mainly Lung & Bone
4. Transperitoneal
o Indicates incurability
o Can give rise to ascites

Clinical features due to metastasis: -

TNM Grading: -

Genetics: -

 APC-mutations (APC = Adenomatous Polyposis Coli; tumor suppressor gene) – low

freq in diffuse cancer
 E-cadherin (tumor suppressor gene) mutation – 50% in diffuse cancer
 P53 (T. suppressor gene) inactivation
 TGF (transforming growth factor) + VEGF (Vascular Endothelial GF) over-expressed
 Loss of heterozygosity in BCL2 gene (inhibitor of apoptosis)

Spread: -
 Spread within gastric wall into regional lymphatics  invasion to adjacent organs;
 Hematogenous spread via portal v or systemic circulation

Clinical: -very few specific symptoms early on

 Early satiety, bloating, N+V, anorexia, weight loss

 Ulcer-like pain = continuous pain suggests extension beyond stomach walls;
 Substernal/ precordial pain associated with tumor of cardia or GEJ
 Bleeding from tumour = iron def anaemia
 Obstruction = dysphagia
 Ascites, peritoneal disease
 Palpable metastatic lymph nodes
o TROISIER'S SIGN = is the finding of a palpable left supraclavicular lymph
node; this is called Virchow's node (stomach is on left)

 Non-metastatic effects: - (Trousseau’s sign) + DVT

o Thrombophlebitis (procoagulating factors produced by cancer cells 
repeated attacks of thrombosis which causes Trousseau’s Syndrome =
carpopedal spasm after taking blood pressure)
o DVT (same reason as above)

Diagnosis: -

 Endoscopy with biopsy – gold standard

 CT – to check for invasion
 Double-contrast barium meal – not done anymore
 Blood tests

DDX: -

 PUD
 Stenosis
 Gastritis

Treatment: -

 Incurable pt should not be subjected to radical surgery that cannot help them
 o Evidence of incurability = haematogenous metastasis + involvement of
peritoneum (N4 nodal disease)
 Operative tx by different locations: -
1. Subtotal Gastrectomy - proximal stomach preserved
 Distal + Intestinal Type Tumours
2. Total Gastrectomy
 Widespread Carcinoma, Proximal Carcinoma, Diffuse Type
 Upper midline incision  stomach, greater + lesser omentum with
hepatic artery nodes around stomach also removed
 lymphadenectomy + oesophagojejunostomy (join esophagus to
jejunum)

3. Palliative Surgery
 pts suffering from obstruction/bleeding = palliative resection
4. Lymphadenectomy
 16 groups of lymph nodes; 12-16 = distant metastasis
  early stomach cancer = subtotal resection with D2 dissection
5. Radio + Chemotherapy – poor response

64) Precancerous diseases of the stomach: polyposis, gastritis, neurinoma, fibroma,

fibroids. Other tumors

 PRECANCEROUS CONDITIONS OF THE STOMACH = are changes to the stomach cells

that make them more likely to develop cancer
1) Polyposis
 Def: -It is a growth in the lining of the stomach
 It can be divided into 3 types: -
1. Hyperplastic (most common)
2. Fundic gland polyps
3. Adenoma – most likely to become stomach cancer
 Causes: - aging, stomach acid levels too high or low
 Risk factors: - gastritis, GERD, ulcers, H. pylori
 Clinical features: - pain, nausea, vomiting, heartburn, loss of appetite, blood in vomit
or stool
 Treatment: - surgery – gastrostomy or partial gastrectomy
2) Gastritis
 Def: -It is inflammation of the stomach lining (gastric mucosa)
 It can be divided into 5 types: -!!!!
1. Type A
 It is an autoimmune disease with formation of anti-parietal cell
antibodies
 Since intrinsic factor is also produced by the parietal cells, there is
malabsorption of vitamin B12 which results in pernicious anaemia
 G cell hyperplasia occurs with increased serum gastrin levels
 There is formation of microadenoma of enterochromaffin like cells
(ECL), with predisposition to gastric carcinoma
  Does NOT affect the antrum (lower funnel shaped part of stomach)

2. Type B
 Occurs due to H. pylori infection
 Affects the antrum
 Patient is prone to peptic ulcer disease
3. Reflux gastritis
 Occurs due to enterogastric reflux is common after gastric surgeries
 Treatment: -prokinetic drugs e.g., metoclopramide
 Enhances gastrointestinal motility by increasing the frequency
or strength of contractions
4. Erosive gastritis
 Occurs due to agents that disturb the gastric mucosal barrier e.g.,
NSAIDs, alcohol
 Occurs due to inhibition of COX-1 receptor enzyme which results in
decreased prostaglandin production (prostaglandin is cytoprotective)
 COX-2 mediated NSAIDs will NOT cause erosive gastritis
5. Stress gastritis
3) Neurinoma (Schwannoma)
 It is a tumour of the neurilemma (peripheral nerve sheath)
 66% cases occur in the antrum
 Clinical features: -
o Large size neurinoma causes discomfort, nausea, vomiting, decrease muscle
tone and thus decreased GI emptying
o Recurrent bleeding, which can cause anaemia
 Diagnosis: - peristalsis persists at the region of filling defect while the spasm is
lacking
 Treatment: - partial gastrectomy
4) Fibroma e.g., neurofibroma, gastric fibroma
 Def: -It is a benign capsulated tumour arising from fibrous tissue
 They are firm, circumscribed nodules less than 4cm in size. They appear as
submucosal nodules
 Treatment: - excision
5) Fibroids
  Def: -They are benign, well-circumscribed, smooth muscle tumours
 Large fibroids can cause swelling and discomfort in the lower abdomen or cause
constipation or painful bowel movements
 Diagnosis: - ultrasound, MRI
 Treatment: - surgical removal (myomectomy – uterus saved, only fibroids removed)

65) Gallstone disease. Formation of bile stones. Clinical picture and complications

Cholelithiasis

Anatomy: -

 Located in RUQ b/w right & left fossa of liver

 Intraperitoneal organ; Location right 9th rib
 Temp storage (30-50ml) of bile
 Pear-shaped
o Fundus (least vascularized, thus susceptible to ischemia), body + neck +
infundibulum (Hartman’s pouch- widened pouch at neck)
 Bile secreted into GIT from GB via biliary tree (duct)
 Cystic duct connects GB to CBD – has valves of heister
 These ducts extend from liver + communicate with GB + pancreas + open into
duodenum
 CBD passes post to proximal duodenum + joins pancreatic duct forming
hepatopancreatic Ampulla of Vater (empties into duodenum, which is known as
duodenal papilla + is regulated by sphincter of Oddi)

 Innervations: -
 o Sympathetic fibres – celiac plexus
o Parasympathetic – Vagus
o Sensory from right phrenic nerve
 Blood supply: -
o Celiac Trunk  common hepatic a  proper hepatic a  cystic a

 Cystic a = behind CBD – lies in Calot’s triangle, where it’s divided into ant + post
branches + supplies GB – also supplies cystic duct via small branches
 Calot’s triangle = formed by under surface of liver, cystic duct, common hepatic duct

 Blood supply also comes to the GB from the liver

 Venous drainage: -
Venous drainage of the neck of the gallbladder is via the cystic veins drain
directly into the portal vein
o Venous drainage of the fundus + body of the gallbladder flows into the
hepatic sinusoids
 Lymphatics: -
o Lymph from the gallbladder drains into the cystic lymph nodes (situated at
the gallbladder neck) hepatic lymph nodesthe coeliac lymph nodes

Cholelithiasis

 Def: - stone in GB
 Epidemiology: - W>M; age>40
 Risk factors: - 5F’s
 o Fat
o Female
o Fertile
o Family hx

Types of stones: - Stone formation pathology explained better in video too

1. Cholesterol Stones – most common

o At least 55% cholesterol
o Most cholesterol stones = radiolucent, <10% radiopaque
o Formation involves 4 simultaneous conditions: -
 Supersaturation = bile supersaturated with cholesterol (hypersecretion
of ch)
 Hypomotility (stasis) = of GB promotes nucleation (formation of
crystals
 Nucleation = ch monohydrate crystals form + agglomerate to become
macroscopic - secretion of nucleating factors (e.g., mucus
glycoproteins)
 Accretion = hypersecretion of mucin in GB traps nucleated crystals –
aggregation into stones
2. Pigment stones
I. Brown stones
 <1cm, soft/musky can form either in GB OR in bile ducts
 Occur due to infection; most common E. coli
 Secondary to bact infx caused by stasis – thus stones consist of Ca
bilirubinate + bact cell bodies
 E. coli produce B-glucuronidase de-conjugates bilirubin
precipitates with Ca  stone
II. Black stones
 Associated with haemolytic disorders or cirrhosis (excess breakdown
of RBCsexcess unconjugated bilirubin)
 Are usually small, brittle
 Formed by supersaturation of Ca bilirubinate (Ca salt of unconjugated
bilirubin)
 Normally, conjugated bilirubin is de-conjugated in bile at a slower rate
however when there is excess conjugated bilirubin = increased
unconjugated bilirubin  precipitation of Ca  supersaturation

Clinical: -

 50% gallstones are asymptomatic

 Biliary Colic Pain - Especially postprandial
 o Vagal stimulation (e.g., cholecystokinin release following a fatty meal) 
gallbladder contraction attempts to force the stone into the cystic duct
o May radiate to the epigastrium, right shoulder, and back (referred pain)
 Constant, dull RUQ pain lasting < 6 hours
 Symptoms caused due to obstruction
 Jaundice – obstruction in gallbladder leads to release of conjugated bilirubin into
the bloodstream
o Difference from acute cholecystitis that has NO jaundice
 Basically, If stone – colicky pain, history of 6 months or previous such episode before;
and jaundice
 Murphy’s Sign – pain in RUQ exacerbated during inspiration when examiner palpates
o If positive suggests acute inflammation
o Deep palpitation in right hypochondrium patient in deep painstops
breathing (inspiratory arrest)  +ve
 Pain radiates to tip of right shoulder due to irritation of phrenic nerve (C3-C5)
 BOAS Sign – change in sensation below scapula in back
o Area below tip of scapula T10-T11
 If acute – N+V
 Courvoisier’s Sign = Palpable non-tender GB
o For chronic cholecystitis
o More sinister dx – results from distal CBD obstruction secondary to part
pancreatic malignancy

Diagnosis: -

 US – gold standard
 CBC – leucocytosis
 LFT’s
 MRCP
 HIDA scan

Complications: -

In the gallbladder In bile ducts In intestine

Biliary colic Biliary obstruction Intestinal obstruction
obstructive jaundice gallstone ileus
Acute/chronic cholecystitis Acute cholangitis
Empyema Acute pancreatitis
Mucocele – due to chronic Mirizzi synd (common
irritation of GB wall hepatic duct obstruction)
Perforation
 Treatment: - TREATMENT EXPLAINED BETTER IN VIDEO

 Resuscitation due to N+V – IV-line fluids

 Pain relief analgesics – opioids (Tramadol)
 Antibiotics – 2nd gen cephalosporins (covers G+ -E. coli and G- like strep)
 Monitor vitals
 After patient stabilised do cholecystectomy after 6 weeks = called INTERVAL
cholecystectomy (If done in same admission called EARLY – not preferred but done if
initial resuscitation not successful)
o Since initially due to acute inflammation hard to do operation
 Cholecystectomy procedure: - Laparoscopic OR Open
o Laparoscopic
 Pneumoperitoneum – pumping CO in abdomen to see structures
 Ports – umbilicus
 Percutaneous cholecystectomy – through skin put drain (used when patient not
stable)
 Laparoscopic standard

66) Cholecystitis

 CHOLECYSTITIS = Inflammation of the gallbladder

 W>M
 Increased incidence if history of gallstones

Risk factors: -

 Pregnancy/ hormone therapy

 Old age
 Obesity/rapid weight gain
 Diabetes

Classification of cholecystitis: - !!!!

 Acute calculous
 Acute Acalculous
 Chronic cholecystitis

Types – better explained classification: -

1. Calculous cholecystitis – inflammation as a complication of gallstones

(i) Acute = cystic duct obstruction/ GB inflammation of sudden onset;
associated with intense pain
(ii) Chronic = chronic inflammation & fibrosis
 Less pain intensity
 Mechanical irritation from gallstones
  Recurrent attacks of acute
2. Acalculous cholecystitis – inflammation due to GB stasis & ischemia
o No gallstones
o Usually critically Ill/immunocompromised pt

Acute Cholecystitis: -

 Def: - acute inflammation of the gall bladder; most common complication of

gallstones

Etiology: -

 Gallstones – mainly
 Stricture + kinking of cystic duct
 Torsion of gallbladder
 Pressure of overlying lymph node on duct
 Bacteria cultured in 50% of the cases but considered to be secondary

Choledocholithiasis

 CHOLEDOCHOLITHIASIS= bile stones in CBD

 Types of CBD stones: -
o Primary = recurrent = originate in CBD; soft, smooth, yellow colour
o Secondary = originate in gallbladder
 S+S: episodic jaundice, pain, sepsis
 Dx: PTC (percutaneous transhepatic cholangiogram), ERCP, US, lab tests

Pathophysiology/Pathology: - 4 main factors

1. Obstruction/Stasis
o Inflammation + distention of GB (with pus) blood flow + lymphatics is
compromisedmucosal ischemia + necrosis can become gangrenous +
complicated with infx acute emphysematous cholecystitis (gas in the
gallbladder)
2. Chemical Irritation
o Erosion of mucosa by stone  bile salts are v. toxic to cells
3. Bacterial Infx
4. Pancreatic Reflux - cause of biliary pancreatitis
o (Tx: IV fluids, abx, analgesia; if persistent high amylase = biliary
decompression)

Clinical: -

 RUQ pain that radiates to right scapula

o BOAS sign = hyperesthesia below the right scapula
 Occurs due irritation of phrenic n.
 o Prolonged <>6hrs) after a fatty meal

 Fever, N/V, local peritonitis

 +ve Murphy’s sign

 +ve Ortner’s sign (tenderness when hand taps edge of right costal arch)
 If stones move to CBD = obstructive “jaundice”
 Tender palpable mass = pathogenic of acute cholecystitis

Diagnosis: -

 Physical examination
 LFTs: -
o ↑ bilirubin & Alkaline phosphatase
o Mild ↑ of ALT & AST
 Blood = increased WBC
o > 12000-15000 = acute cholecystitis
o >20000 = gangrenous cholecystitis, perforation, cholangitis
 US – *thick wall + shrunken GB* + edema (double -wall sign)
 X-ray = identifies ≈ 10% of cases (porcelain GB = calcification of GB)
 HIDA scan
o Only specific test for acute cholecystitis
o IV inj of contrast – excreted by liver into biliary duct system
o In acute cholecystitis – GB not seen as GB outlet of CBD is obstructed

DDX: -

 Perforated or penetrating ulcer

 Acute pancreatitis
 Acute appendicitis
 Gallbladder colic
 Acute pyelonephritis
 Cholangitis

Treatment: -

 Pain relief; IV fluids, Abx

Surgical txt: -

1. Cholecystectomy – definitive txt

 o 2 approaches – laparoscopic (preferred) but Open in complicated cases
o Complications – bile duct injury, biliary leaks
2. Percutaneous cholecystectomy
o Drainage to decompress with a tube pierced percutaneously under
radiological guidance
o Reserved for pts CI to surgery and acalculous cholecystitis or other methods
not working
3. ERCP (Endoscopic retrograde Cholangiopancreatography)
o Used for diagnosis and txt
o Dormia basket can be used to pull stone

Chronic cholecystitis

 Empyma = pus in gallbladder

o Obstruction bile stasis bacteria pus
 Mucocele = collection of mucus in gall bladder BUT no infection
 Acute acalculous cholecystitis – patients in ICU or burn victims
 Acute Emphysematous cholecystitis – air in GB
o Due to perforationperitonitis
 Cholecystoses = chronic inflammatory disease of GB; deposits of cholesterol in
submucosa w/o direct stone formationpolyps from the wall
o Strawberry GB – yellow cholesterol in wall
 Alkaline phosphatase & Gamma glutamate transferase

67) Inflammatory diseases of the biliary tract. Cholangitis, cholangiolitis

Cholangitis

 In acute cholecystitis – no jaundice

 Main causative agents – E. coli or Klebsiella pseudomonas
 Abs – cephalosporins
 Txt: - stone removal with ERCP or if stricture stent placement with ERCP

1) Cholangitis
 Def: - It is inflammation of the bile ducts, usually caused by bacterial infection
 Causes: -
o Biliary tract obstruction (most common)
o Biliary tract stricture – due to infection, ERCP etc
o Bacterial infection e.g., E. coli, Klebsiella
o Parasite obstruction
o Cancer at head of pancreases can cause obstruction
Pathogenesis: -
 The biliary tree normally has NO bacteria due to protective mechanisms
 o The sphincter of Oddi is a mechanical barrier
o The biliary system normally has low pressure to allow bile to flow freely
though, the continuous flow of bile flushes bacteria, if present, into the
duodenum and does NOT allow bacterial infection to occur
 Bacterial contamination in the absence of obstruction alone does NOT result in
cholangitis.
o However, increased pressure due to obstruction in the bile duct widens the
spaces between the cells lining the duct and brings bacteria-contaminated
bile into contact with the bloodstream
 Increased biliary pressure decreases IgA production in the bile, which results in
bacteraemia and gives rise to systemic inflammatory response with fever,
tachycardia, increased respiratory rate and increased WBCs
 Biliary obstruction also impairs the immune system by impairing the function of
certain immune cells e.g., neutrophils and modifying the levels of immune hormones
e.g., cytokines
Clinical features: -
 Charcot’s triad – Pain in RUQ + jaundice + fever
o Remember in acute cholecystitis no jaundice!!!
 Tenderness and pain in upper right abdomen
 Clay-coloured stools, dark urine – signs of obstructive jaundice
 Reynaud’s Pentad: -
o Charcot’s triad + septic shock (due to infection spreading more) + mental
confusion (due to accumulation of bile products in brain)
Diagnosis: -
 US – diagnostic
 CBC – leucocytosis
 LFTS – ALP & GGT will be high + bilirubin
o Alkaline phosphatase
 ALP is an enzyme found throughout the body, but it is mostly found in
the liver, bones, kidneys, and digestive system.
 A high ALP level does not reflect liver damage or inflammation.
 A high ALP level occurs when there is a blockage of flow in the biliary
tract or a build-up of pressure in the liver--often caused by a gallstone
or scarring in the bile ducts.
o GGT = Gamma Glutamyl transferase
o ALP only high in bone disease
o ALP + GGT high in biliary obstruction
Treatment: -
 IV antibiotics – strong gram negative (E. coli and Klebsiella) – cephalosporins or
levofloxacin
 ERCP – to reliver stone or place stent
 Emergency endoscopic sphincterotomy
 o SPHINCTEROTOMY = also called a lateral internal sphincterotomy, is a type of
procedure that is used to cut the anal sphincter.
 Percutaneous transhepatic biliary drainage in high obstructions (PTBD)
o PERCUTANEOUS TRANSHEPATIC BILIARY DRAINAGE (PTCD) = is the
placement of a drain into bile ducts using needles inserted through the skin.
 Insert stent into CBD to keep it open
 Remove gallstones
 Laparotomy-drainage of CBD-T-tube insertion
o The T tube is a draining tube placed in the common bile duct after common
bile duct exploration.
o It provides external drainage of bile into a controlled route while the patient
heals and the original pathology is resolved

Sclerosing cholangitis
 Def: - It is a fibrous thickening of the CBD and biliary duct wall, associated with
multiple strictures and dilation in between the strictures
 It can be divided into 2 types: -
1. Primary sclerosing cholangitis – associated with ulcerative colitis, Crohn’s
disease. It eventually leads to biliary cirrhosis
2. Secondary sclerosing cholangitis – it is due to stones, trauma, chemotherapy,
transplantation etc.
 Clinical features: -
o intermittent jaundice
o weight loss
o fever
o pruritis
 PRURITIS = Itchy skin is an uncomfortable, irritating sensation that
makes you want to scratch.
o abnormal liver functions
 Diagnosis – ERCP shows beaded appearance of biliary tree
o Endoscopic retrograde cholangiopancreatography is a technique that
combines the use of endoscopy and fluoroscopy to diagnose and treat certain
problems of the biliary or pancreatic ductal systems.
o During ERCP, doctors use an endoscope and X-rays to view injectable dye as
it travels through pancreatic and bile ducts.
 Treatment: -
o T tube drainage
o Stenting
o large dose steroids
2) Cholangioloitis
 Def: - It is inflammation of the smallest bile ducts, which are called cholangioles (bile
capillaries) and the metaplastic ducts
  It can occur due to obstruction of the cholangioles
 Acute cholangiolitis is associated with bile duct obstruction and also any liver disease
related to prominent cholestasis that also involves the periportal zones

68) Mechanical jaundice – IF YOU HAVE TIME WATCH THE FING VIDEO!!

 Mechanical Jaundice - Courvoisier’s sign explained well here; Choledocholithiasis

 Def: -Conjugated hyperbilirubinemia due to obstruction in the biliary channels
 Def: -It is jaundice that develops due to biliary obstruction (partial or complete or
intermittent)
 It causes conjugated hyperbilirubinemia
o Some bilirubin is bound to a
certain protein (albumin) in the
blood. This type of bilirubin is
called UNCONJUGATED, OR
INDIRECT, BILIRUBIN.
o In the liver, bilirubin is changed
into a form that your body can
get rid of. This is called
CONJUGATED BILIRUBIN OR
DIRECT BILIRUBIN.
Causes: -
 Congenital – biliary atresia
 Inflammatory – ascending cholangitis, sclerosing cholangitis
 Obstructive – common bile duct stones, biliary stricture, parasitic infection
 Neoplastic – carcinoma of the head of the pancreas, cholangiocarcinoma, Klatskin
tumour
 Extrinsic compression of the common bile duct by lymph nodes or tumours
Pathophysiology: -
 It occurs due to intrahepatic or extrahepatic biliary outflow obstruction which
results in cholestasis which means conjugated hyperbilirubinemia released into
blood
 Bile acid secretion into the gut is impaired which results in defective absorption of
fat and fat-soluble vitamins
 Malabsorption of fat causes steatorrhea and deficiencies of: -
o Vitamin A – visual problems, thick skin
o Vitamin D – osteomalacia
o Vitamin E – peripheral neuropathy, cerebellar ataxia
o Vitamin K – bleeding tendencies (poor synthesis of prothrombin and
conversion of prothrombin to thrombin)
Effects of obstructive jaundice: -
 In the liver: -
o Enlarged green bile-stained liver shows dilated intrahepatic biliary radicles
o Once intraductal common bile duct (CBD) pressure increases  bile
decreases  bile secretion from the liver is decreases  which results in
formation of white bile in the CBD
 In the biliary tree: -
o Recurrent inflammation – cholangitis
 In the bowel: -
o Digestion is impaired due to absence of bile, which results in decreased fat
absorption and faeces are bulky and fatty
o Retention of bile salts and bile pigments in the blood and body fluids occurs

Clinical features: -
 Courvoisier’s sign – in a patient with obstructive jaundice, if the gallbladder is
palpable, it is NOT due to gallstones
o Gallbladder not palpable in stones WHY?
 Stones in gallbladderchronic inflammation of gall bladder
wallsfibrosis of gall bladder doesn’t increase in size
o Gallbladder palpable due to cancer WHY?
 Obstruction due to cancer bile collects in gallbladderexpands
palpable
 Charcot’s triad –RUQ pain+ fever+ jaundice– indicates cholangitis
 Severe jaundice
 Pruritis (itchiness)
 Pale, fatty stools – due to lack of bilirubin in intestinal tract and decreased fat
absorption
 Weight loss and loss of appetite
 Pain in right hypochondrium, palpable gallbladder
 Dark urine – due to excess conjugated bilirubin being excreted (normally
urobilinogen is excreted which is NOT dark yellow)
Diagnosis: -
 Liver function tests: -
o Bilirubin – raised
o AST & ALT (increased when hepatocytes are injured) – not increased
o ALP & GGT (increased when walls of biliary tree dilate) – ↑3-4 times
 Measure serum albumin – normal value is more than 3.5gm%
 Increased prothrombin time – normal value is 12-16 seconds
 Ultrasound of abdomen
 MRCP (magnetic resonance cholangiopancreatography) – has 99% specificity.
o Shows hepatobiliary and pancreatic systems, including the pancreas,
gallbladder, bile ducts, pancreas and pancreatic duct
 Tumour markers – CA199 for pancreatic cancer
Treatment: -
 Initial resuscitation with IV fluids, Vit k and clotting factors (obstruction causes liver
problems clotting factor shortage) + antibiotics
 Common bile duct stones – ERCP stone removal + lap cholecystectomy
 Carcinoma of pancreas – Whipple operation or ERCP stenting
o A WHIPPLE PROCEDURE = aka a pancreaticoduodenectomy is a complex
operation to remove the head of the pancreas, the first part of the small
intestine (duodenum), the gallbladder and the bile duct.

 Biliary stricture – stenting

 Klatskin tumour – radical resection or palliative stenting
o A KLATSKIN TUMOR (or hilar cholangiocarcinoma) = is a cholangiocarcinoma
(cancer of the biliary tree) occurring at the confluence of the right and left
hepatic bile ducts.
  Biliary atresia – liver transplant
 Vitamin K injections
 Pruritis – once the cause is treated and obstruction is relieved, the pruritis will
regress

69) Liver. Trauma to the liver and biliary system

 Liver Trauma

Anatomy of Liver: -

 In right hypochondriac + epigastric region

 Liver divided by falciform ligament (fold of mesentery) into large right lobe + smaller
left lobe
 Falciform lig extends superiorly becoming coronary lig which lies on superior border
of liver – helping to suspend liver into ab cavity from diaphragm
 In free border of falciform lig is the ligamentum teres (AKA round lig; obliterated
umbilical vein)
o This fibrous cord extends from liver to umbilicus
 Blood supply = hepatic artery (20%) + hepatic portal vein (80%)
 Portal-venous Anastomosis: -
1. Esophageal = left gastric vein  azygous vein
2. Rectal (haemorrhoids) = mid + inf rectal vein
3. Caput medusa = paraumbilical veins – superficial epigastric v
Injuries to the liver + bile ducts

Injury to GB

 Uncommon
 Penetrating injuries due to gunshot wound/stab
 Non-penetrating: contusion, avulsion, laceration, rupture, traumatic cholecystitis
 Tx: cholecystectomy

Extrahepatic bile ducts: -

 Causes: -
o Iatrogenic factors during cholecystectomies (esp laparoscopic as decreased
view), OR
o During gastrectomy when mobilisation of duodenum is required
 Diagnosis: -
o intra op bile leak + abnormal cholangiogram
o CT, US – increased LFTs
 Treatment: -
o Small injury = T. tube (draining tube placed in CBD)
o Major injury = Roux-en-Y hepaticojejunostomy procedure
 Jejunum is directly anastomosed the bile duct
 Gallbladder and other ducts are removed;
 Different procedure to roux en Y itself
o Those dx post op require transhepatic catheter for biliary decompression

Liver injury

 Liver Trauma
American Association for Surgery – Liver Trauma Classification: -

 Grade 1: -
o Hematoma: subscapular = <10%
o Laceration: capsular tear - <1cm
 Grade 2: -
o Hematoma: subscapular = <10-50%
o Laceration: capsular tear – 4-3cm
 Grade 3: -
o Hematoma: <50%
o Laceration: >3cm
 Grade 4: -
o Laceration: parenchymal disruption 25-75%
 Grade 5: -
o Laceration: parenchymal disruption >75%
 Grade 6: -
o Hepatic avulsion

Injury of liver can be classified into: - (Glisson’s Capsule classification)

1. Trans capsular Injury: - when rupture of liver has involved Glisson’s Capsule
(encapsulates ALL portions of liver, e.g., liver itself, hepatic a., portal vein, bile ducts)
o Blood + bile in peritoneal cavity
o CF: biliary leakage = biliary peritonitis
2. Subcapsular: - Glisson’s capsule intact – blood collected deep to capsule, found on
superior surface of organ
o Haematoma – can be infx abscess
3. Central Injury: - interruption of the parenchyma of liver

Complications: -

 Blunt trauma may be associated with hepatic parenchymal emboli which can move
to the right heart + lung causing death
 Infarction of liver tissue
 *Haemorrhage most imp cause of death in injury to liver*
 *Hepatorenal Syndrome: -
o Damaged liver cells  portal hypertension  splanchnic a. (due to NO
release) + systemic vasodilation  decreased arterial blood volume
activation of RAAS  renal vasoconstriction  renal cell necrosis

Diagnosis: -

 Plain AXR (fluid in peritoneum)

 CT
 Angiography (for hematobilin – blood in bile ducts)

Treatment: -

 Haemodynamically stable pts = conservative

 Protocol for Blunt trauma patients: - hypovolemia (due to bleeding)
1. Initial management
 ATLS (Advanced Trauma Life Support)
 First check ABCDE
(AirwaysBreathingCirculationDisabilityExposure)
 FAST scan (Focused Assessment with Sonography in Trauma)
 Spine scan
 Pelvic X-ray
 Chest X ray
 Send blood labs immediately to check for any bleeding disorders
2. Non-Operative Management
 If patient becomes hemodynamically stable with initial management
non-operative management
 Close observation – ICU
 CT scan with contrast
 If bile leak – ERCP
 Arterial embolization
3. Operative Management -If blood in peritoneum – take to OT
 PPP management
 I. Pressure – to stop bleed for clot formation
II. Pringles manoeuvre – to differentiate where the bleeding is
from: - The Hepatic artery & Portal vein OR Hepatic Vein &
Inferior Vena Cava
o Clamping hepatoduodenal lig; this limits blood flow
through hepatic artery + portal vein, thus controlling
bleeding from liver)

o If bleeding stops then from Hepatic artery+ Portal vein

if not from IVC + Hepatic vein
III. Packing
o Packs placed around liver to compress and stop
bleeding
 Definitive procedure – after stabilisation through laparotomy: -
o Selective vascular repair
o Non-anatomical liver resection – to remove necrotic areas
o Anatomical resection
o Total vascular exclusion (stopping blood supply to liver for 45 mins after
which opened)
o Liver transplant

70) Echinococcus of the liver

 Cyst of liver can be: -

o Parasitic (hydatid cysts – Echinococcus Granulosus) OR
o Non-parasitic (lymphatic, endothelial, blood, dermoid cysts)

Hydatid Disease (Cyst)

Hydatid disease of liver

 A parasitic disease of tapeworms of the Echinococcus type
 2 types of cysts can form: -
1. Unilocular Cyst (cyst with no septum)- caused by E. Granulosus – most
common
2. Alveolar Cyst (cyst with septa)- caused by E. multilocularis

Etiology + Epidemiology: -

 Zoonotic disease = occurs primarily in sheep-grazing areas of the world

 Dogs – definite host
 Humans – intermediate host – larvae live in humans
 Causative agent: tape worm = Echinococcus

Pathophysiology: -

 Dogs are definite hosts – adult tapeworm attached to villi of ileum. Eggs passed in
dogs’ stool
 Sheep = intermediate hosts; humans = accidental intermediate hosts
 In humans: -
o Cysts reach duodenum parasitic embryo releases an oncosphere with
hooks that penetrate mucosa gain access to the blood stream
Oncosphere reaches liver (most commonly)/lungLarval stage ensues aka
*hydatid cyst*
 3 wks after infx – visible hydatid cyst develops + grows in a spherical manner
 Hydatid Cyst – 3 layers: -
1. PERICYST = Fibrous capsule derived from host tissue; grey in colour
2. ECTOCYST = Outer gelatinous membrane; formed by parasitic cells –
appearance of white of hard-boiled egg
3. ENDOCYST = Inner germinal membrane; consist of nuclei – gives rise to brood
capsule with scolicies – secretes fluid + forms outer layer
 Brood Capsule = small intracystic cellular masses in which future worm heads
develop into scolices

 In definite hosts, scolicies develop into adult tapeworm

 In intermediate hosts, they differentiate into new hydatid cysts
 Hydatid cysts can undergo calcification indicating degeneration

Clinical: -

 Largely asymptomatic until complications occur

 75-80% of cysts located on right lobe of liver (better portal vein flow) + are singular
 Symptoms occur usually due to pressure to adjacent organs
o Ab pain, dyspepsia, N/V, jaundice (obstruction), fever, hepatomegaly
 Rupture = disseminated Echinococcus – fatal anaphylactic reaction

Diagnosis: -

 CT/MRI/US: hydatid cyst seen = well differentiated. Rosette appearance if daughter

cysts present
o Cysts with well defined septa and moving membranes
 ELISA
 Bloods: eosinophilic, increased LFTs
 Serologic tests: Casoni’s test: intradermal inj of 0.2ml of fresh sterile hydatid fluid –
produces wheal of 5cm in diameter within 1/2hr – (hypersensitivity test for skin)

Treatment: -
  Medical - Albendazole 10mg/kg – given for small cysts or pre-op to make cysts
smaller
 PAIR (Puncture; Aspirate; Inject with hypertonic saline; Re-aspirate after 25 mins)
 Surgical excision. Conservative for elderly pt with small asymptomatic cyst
 Chlorhexidine (antiseptic), alcohol, cetrimide (antiseptic) – instilled in cyst. This will
destroy scolices
o Cyst is aspirated, flushed with hypertonic saline
o Cyst then can be excised via re-aspiration
o Large/multiple cyst(s) = partial hepatectomy
 Epinephrine ready during op in case of anaphylactic shock

71) Liver abscesses

 Can be divided into pyogenic liver abscess (bacterial) or amoebic liver abscess
(entamoeba histolytica)

Pyogenic liver abscess Amoebic liver abscess

Number Often multiple Usually, single
Location Either lobe of liver Right lobe, near diaphragm
Presentation Subacute Acute
Jaundice Mild Moderate
Diagnosis Cluster sign on CT Amoebic serology
Treatment Drainage + Abx Metronidazole

Pyogenic Liver Abscess

Pyogenic Liver Abscess

Etiology: -

 Bacteria – E. coli most common

o Klebsiella, S. aureus, Enterococci, Bacteroides
 Routes of entry: -
1. Portal Vein = appendicitis or diverticulitis
2. Biliary Tree (most common) – cholangitis (partial obstruction by gallstone) OR
(ascending biliary tree infection)
3. Hepatic Artery – sepsis or generalized septicaemia
4. Direct extension of nearby infection – cholecystitis, lungs, stomach etc

Pathogenesis: -

 E. coli = most common cause

 Biliary obstruction bile stasis  potential for bacterial colonisation  infx
ascend to liver or ascending infx from GIT via portal vein
 Right lobe mostly involved due to preferential laminar blood flow to right side
 50% abscess are solitary

Clinical: -

 High grade fever (in comparison to mild fever of amoebic)

 NO hepatomegaly
 Fever & chills -signs of infection
 RUQ pain
 Mild jaundice (differentiate from HYATID that has severe jaundice)
 Liver is soft but tender (not enlarged usually)
 Malaise + N/V

Diagnosis: -

 US: round oval hypogenic area

 Blood culture -to detect bacteria
 Blood test: -
o hyperbilirubinemia; increased ALP + transaminase in case of partial
obstruction
o leucocytosis – due to infection
 CT: Cluster Sign - aggregation of multiple small lesions in an area to form solitary big
large abscess

DDX: -

 Amoebic abscess
 Hydatid cysts

Treatment: -

 Broad spectrum abx – to control ongoing bacteraemia

o Ampicillin + aminoglycosides (gentamicin)/metronidazole
o OR 3rd gen cephalosporin + metronidazole
 Percutaneous drainage of abscess under US

Amoebic Abscess

Amoebic Liver Abscess

 A complication of amoebic dysentery

 E. histolytica passes from colonic lesion via portal vein to liver
 Usually affects superior + posterior portions of right lobe**
 Epidemiology: - Poor social and living conditions
o Exists as trophozoite outside the body
o Spread = faecal-oral route
o Infective form = cyst
 Pathology: - 2 phases – ACUTE & CHRONIC

 Cyst swallowed (resistant to GI acid)  enters SIreaches LI where trophozoites

released + multiply invades colon wall necrosis flask shaped ulcer (bloody
diarrhea) portal veingoes to liver
 Abscess develops with a thick chocolate brown pus (which is liquefied necrotic liver
tissue)

Clinical: -

 Pain in Right Hypochondrium

 Weight loss – loss of appetite
 Anemia
 In acute- fever; chronic might or might not have fever (Mild fever compared to
pyogenic liver abscess)
 History of amoebic dysentery (2-3 weeks before) – bloody diarrhea in acute phase
due to ulcers
 Hepatomegaly (different from pyogenic where NO hepatomegaly)
 No jaundice here (differentiate from HYATID that has severe jaundice)

Complication: -

 Abscess can burst can cause peritonitis

 Can infect pleural cavity of lungs
 Can affect pericardium of heart

Diagnosis: -

 US, CT, Aspiration – microscopy

 Bloods – leucocytosis, anaemia
 ELISA – antibodies against E. histolytica

Treatment: -

 Metronidazole 750mg for 5-10 days

 Large abscess = US guided needle aspiration
o Route = 9/10th intercostal space b/w anterior + posterior axillary lines

72) Tumors of the liver, gallbladder and bile ducts

Liver tumours – most come from metastasis

Primary benign liver tumours - 2
1. Haemangioma
 It is the most common benign tumour of the liver
 85% are asymptomatic
 Affects women more 3:1
 It is usually a solitary tumour, but can be multicentric
 Clinical features: -
o Abdominal pain and vomiting – due to compression over gastrodudoenum
o Calcification – 10% cases
o Compressibility of tumour – diagnostic feature
o Acute thrombosis with sudden onset of pain and fever can mimic liver
abscess
 Diagnosis: -
o Ultrasound and CT of abdomen confirm diagnosis
o MRI – 100% sensitive
 Differential diagnosis: -
o Hepatoma (hepatocellular carcinoma)
o Hepatic adenoma
o Liver abscess
 Treatment: -
o First radiotherapy is done to decrease the size of the tumour followed by
hemi hepatectomy
o Do NOT do needle aspiration and biopsy
 Percutaneous biopsy of a hepatic haemangioma carries an increased
risk of haemorrhage.
2. Hepatic adenoma
 Affects women more 10:1 – considered to be due to use or oral contraceptives
 It is present as a solitary nodular lesion
 It can become malignant; thus, resection is important!
 Clinical features: -
o Upper abdominal pain (most common)
o Haemorrhage is common
 Diagnosis: -
o Ultrasound and CT of abdomen confirm diagnosis
o MRI – 100% sensitive
 Treatment
o Surgical resection
 RESECTION = is the surgical removal of part or all of a damaged organ
or structure, particularly the removal of a tumor.
Primary malignant liver tumours - 1
1. Hepatoma (hepatocellular carcinoma HCC)
 It is the most common type of primary liver cancer
 Affects men more 4:1
 More common in right lobe
 Spread of tumour: -
o Blood spread: - spreads to lungs, kidneys, adrenals, bones, meninges
 o Lymphatic spread: - spreads to hilar nodes, celiac nodes, pericardial nodes
and paracaval nodes
 Causes: -
o Alcoholic cirrhosis, smoking
o Hepatitis B and hepatitis C infection
o Hepatic adenoma – potentially malignant
o Haemochromatosis alpha1 antitrypsin deficiency
 Clinical features: - 40 % asymptomatic; found by mistake during US
o Weight loss – since cancer cells are eating all the nutrients since extra cells
o Painless mass in right hypochondriac region
o Jaundice – due to hepatic dysfunction or obstruction due to huge tumor size
(Intrahepatic jaundice)
o Anaemia – due to metastasis to bones (which makes RBCs)
o Hard, enlarged liver, smooth/irregular
o Cirrhotic liver may be nodular
o Ascites, splenomegaly and features of portal hypertension
o Hepatic thrill and bruit – put three fingers over the liver, percuss the middle
finger and get the impulse on the other two fingers
o GI bleeding can occur due to portal hypertension or portal vein invasion by
the tumour
 Diagnosis: -
o Ultrasound of abdomen (done 1st since non-invasive): -shows hyperechoic
mass; mosaic pattern with thin halo and lateral shadows
o Triphasic CT scan of abdomen: - shows size, location and extent, vascularity,
portal vein invasion and lymph node status
 Blood supply of tumor is hepatic artery
o Histopathology – to confirm whether benign or malignant
o Tumour markers – increased AFP
 Not highly specific for hepatocellular carcinoma
o Liver function test
o Celiac angiography/CT angiography – shows vascularity of the tumour.
Important for planning hepatic resection
 Child’s Pugh score – for liver cirrhosis
o Test albumin, bilirubin & prothrombin; ascites; hepatic encephalopathy
(metabolic functions affected)
o Used in carcinoma since cirrhosis accompanies cancer
 Staging: - TNM
o Metastasis checked first
 Differential diagnosis: -
o Liver abscess
o Hydatid cyst
o Secondaries in liver
 Treatment: -
 o SURGERY is gold standard; but only indicated when no metastasis
 Resection (removing only part of liver)– if mass small and local WITH
NO vascular invasion
 Liver transplant
 Indications – solitary lesions less than 6.5 cm or if nodular
should be less than 8 cm in total
 CI: - distant metastasis & vascular invasion
o Hemi hepatectomy – if the tumour is limited to one lobe (70% liver removal is
compatible with life)
o Total hepatectomy with orthotopic liver transplant – for cirrhotic patient
 ORTHOTOPIC TRANSPLANTATION = in which the native liver is
removed and replaced by the donor organ in the same anatomic
location as the original liver.
 Local ablation therapies: - reduce size of tumor; better prognosis
1. Percutaneous ethanol
 Ethanol causes local inflammation necrosis
2. Radiofrequency ablation
 US guided; radio waves
 Great outcomes for tumors less than 4 cm
 CI: - If close to major vessels and bile ducts
3. Trans arterial chemo
 Catheter passed through femoral vein till hepatic artery inject
chemotherapeutic agent into tumor and close the hepatic artery so
tumor gets no blood supply

Gallbladder tumours
Pathology – types of gallbladder cancer
 In 90% cases, it is adenocarcinoma
o 3 types of adenocarcinomas have been identified: - !!!
1. Nonpapillary adenocarcinoma (most common)
2. Papillary adenocarcinoma
3. Mucinous adenocarcinoma
o The tumour is most commonly nodular
 NODULAR FASCIITIS is a rare, noncancerous tumor. It can appear in
soft tissue anywhere on your body. Nodular fasciitis mimics malignant
(cancerous) tumors, which makes it a challenge to diagnose.
 Spread of tumour: -
o Direct spread to liver, bile duct, duodenum, colon and kidney
o Blood spread – spreads to liver, lungs and bones
o Lymphatic spread – spreads to lymph node of Lund, periportal nodes,
peripancreatic and peri duodenal nodes
Causes: -
 3% gallstones with cholecystitis will develop cancer of the gallbladder
 Gallstones – 90% gallbladder tumours are associated with gallstones
 Inflammatory bowel disease
 Hepatitis B, hepatitis C
Clinical features: -
 Pain in right hypochondrium
 Hard, non-tender mass in right upper abdomen
 Jaundice is common
 Weight loss
 Acute presentation of cholecystitis (acute bacterial inflammation of the gallbladder)
Diagnosis: -
 Ultrasound of abdomen and CT of abdomen
 Liver function tests
 Tumour markers – increased CA199 (80% cases)
Treatment: -
 Cholecystectomy with resection of liver segments 4 and 5 – extended
cholecystectomy with perihepatic lymph node removal.
o All peri choledochal lymph nodes should be removed
 It is a very aggressive tumour! Overall prognosis is poor due to early spread and
aggressive nature of the tumour

Bile duct tumour (cholangiocarcinoma)

 It is an aggressive adenocarcinoma which presents as obstructive jaundice
 It can be divided into 3 types: - !!!!
o Perihilar (most common) – 65% - (Klatskin tumour comes under this)
o Intrahepatic – 10%
o Distal – 25%
Causes/risk factors: -
 Primary sclerosing cholangitis
 Hepatolithiasis
 Hepatitis B, hepatitis C
Clinical features: -
 Painless obstructive jaundice – main feature
 Palpable liver, which is either smooth and soft (hydrohepatotic), or hard nodular
(secondaries)
 Weight loss
Diagnosis: -
 Ultrasound and CT of abdomen
 Liver function tests
 ERCP (endoscopic retrograde cholangio-pancreatography)
 Treatment: -
 Treatment is difficult because most of the lesions are high up in the hilar region,
infiltrating the liver, portal vein etc.
 If operable – portal region clearance with hemi hepatectomy is done
 If inoperable (more common) – stenting is done to relieve jaundice
 Chemotherapy

Cholangiocarcinoma

 Def: - carcinoma of bile ducts not gallbladder

Risk factors: -

 Cholangitis
 Choledochal cysts
 Stone
 Ascariasis (worms)

Clinical: -

 Weight loss (anorexia)

 Obstructive jaundice syndrome -
o Pain – mild/ on and off
o Clay coloured stool
 Palpable gall bladder – couversoirs law

Diagnosis: -

 LFT’s – ALP & GGT high

 Tumor marker – CA 19-9
 Triphasic CT scan – diagnostic
 MRCP
 ERCP – can relieve obstruction a bit by placing stent & can take biopsy

Classification: -

 Type 1 - Intrahepatic – blockage of bile duct w/I liver

 Type 2 – Bifurcation b/w right & left hepatic + common hepatic
 Upper extrahepatic – right & left hepatic + common hepatic duct
o Type 3A - Common hepatic + right hepatic
o Type 3B – Common hepatic + left hepatic
 Lower extrahepatic – Cystic + common bile duct

Treatment: -

 Local (Type 1 & 2) – lymphadenectomy + remove common bile ducts + gall bladder
 o Roux-en-Y hepaticojejunostomy – a segment of jejunum taken and directly
joined to the liver for the bile secretions while the duodenum remains
attached to the pancreas

 For Type 3- 4
o Possibility of metastasis into the liver
o Hepatectomy (Partial liver resection)
 If tumor at common bile duct – resect + Whipple’s procedure
o Head of pancreas + duodenum and bile duct removed
o Join right & left hepatic ducts + tail of pancreas + stomach to jejunum

73) Portal hypertension. Varicose veins of the esophagus

Portal hypertension

Portal hypertension
 The portal vein provides 75% of blood flow to the liver with all nutrients to maintain
its integrity and gives 50% oxygen supply to the liver
 PORTAL HYPERTENSION = is defined as sustained elevation of the portal venous
pressure more than 10mmHg (Normal portal venous pressure is 5-10mmHg)
 Portal hypertension it also defined as an increase in hepatic venous pressure
gradient (HVPG) above 5mmHg
o HVPG = is the difference between the wedged hepatic venous pressure and
free hepatic venous pressure
 HVPG above 10mmHg – portosystemic shunting develops
 HVPG above 20mmHg – bleeding oesophageal varices
 An increase in portal pressure stimulates portosystemic circulation. Sites of
portosystemic collateralisation include: -
o Lower end of oesophagus – between left gastric and short gastric veins with
azygous vein, resulting in oesophageal varices (most common)
 Esophageal veinazygous veinsuperior vena cavaright atrium of heart
o Umbilicus – between paraumbilical vein and anterior abdominal vein,
resulting in caput medusae
 Periumbilical veins of ant abdominal wall superficial epigastric
veinsGreat saphenous femoralexternal iliac veins met by blood
from inf epigastric veinIVCheart
o Lower end of rectum – between superior haemorrhoidal vein and inferior,
middle haemorrhoidal vein, resulting in piles
 Lower 2/3rd of rectum rectal veinsinternal pudendalinternal iliac;
joined by blood from middle rectal veins common iliac veinsIVC
o Bare area of liver
Causes: -
1. Increased portal resistance
o The increased resistance may be: -
 Prehepatic – portal/splenic vein thrombosis, trauma, congenital
hepatic fibrosis, sarcoidosis
 Hepatic (80% cases) – alcoholic cirrhosis, hepatitis, Wilson’s disease
 Post-hepatic – constrictive pericarditis, veno-occlusive disease
2. Altered portal blood flow
Clinical features: -
 Triad of portal hypertension: -
oesophageal varices splenomegaly ascites
 General – weakness, tiredness, weight loss, abdominal pain, jaundice, edema,
impotence, pallor, cyanosis, hypotension
 Features of variceal bleeding – anaemia, melaena, shock, hematemesis
 Features of liver cell failure – spider angioma, cyanosis, testicular atrophy
 Features of encephalopathy
Diagnosis: -
 HVPG hepatic venous pressure gradient (gold standard to diagnose)
 Ultrasound of abdomen – shows liver status, portal vein, ascites and splenomegaly
 Contrast CT – shows nodules, collaterals, portal vein status/thrombosis and
splenomegaly
 Blood-Hb% - anaemia due to bleeding, bone marrow suppression. Pancytopenia
shows leukopenia, thrombocytopenia
 Liver function tests – increased bilirubin
 Ascites tap- fluid is checked for cells, proteins.
o Serum ascitic fluid albumin more than 1.1. suggests high gradient and thus
portal hypertension
Treatment: -
 General – treat anaemia, inject vitamin K, give nutrition
 Treat oesophageal varices
 Treat ascites
 Decrease portal pressure
o Surgery – portosystemic shunt
o Drugs – propranolol
 Liver transplant
Varices
Types of varices: -
 They can be divided into 2 types: -
1. Oesophageal varices (80% cases) – in the lower third of the oesophagus and
usually 3 or more in number
2. Gastric varices (20% cases) – it is in the fundal or upper part of the stomach
Oesophageal varices
 Def: -They are enlarged blood vessels in the oesophagus
 They develop when normal blood flow to the liver is blocked. Thus, to go around the
blockage, blood flows into smaller blood vessels that aren’t supposed to carry large
volumes of blood
 They often occur due to obstructed blood flow through the portal vein, which carries
blood from the intestine, pancreas and spleen to the liver
Causes: -
 High portal vein pressure
 Cirrhosis
 Thrombosis
 Parasitic infection – damages liver and other organs
Clinical features: -
 They don’t usually cause symptoms unless they bleed
 Vomiting large amounts of blood
 Black tarry or bloody stools
 Loss of consciousness – severe cases
 Signs of liver disease – jaundice, ascites, easily bleeding
Diagnosis: -
 Hb%, liver function tests, blood urea and serum creatinine
 Endoscopy – to grade the varices
1. Minimal varices without luminal prolapse
2. Moderate varices with luminal prolapse and minimal obscuring of OG
junction
3. Large varices with luminal prolapse and moderate obscuring of OG junction
 4. Very large varices with luminal prolapse and complete obscuring of OG
junction
 Endoscopic sclerotherapy or variceal band ligation should be done while doing
initial endoscopy to confirm variceal bleed
Treatment: -
 Treatment before bleed: -
o Drugs to decrease portal pressure – propranolol (decreases portal pressure
by 20%)
o Endo therapy – endoscopic variceal banding/ligation
 Treatment after bleed: -
o Emergency management of variceal bleeding
o Trans jugular intrahepatic portosystemic shunt (TIPS) – diverts blood flow
away from the portal vein
o Drugs to decrease blood flow to portal vein – vasopressin

PORTAL HYPERTENSION: -

 Def: - Increase in pressure of the portal vein

Diagnostic criteria: -

 Hepatic vein pressure – FHVP (Free Hepatic Venous Pressure)

 Portal vein pressure – WHVP (Wedged Hepatic Venous pressure)
o WHVP usually higher than FHVP
 Normal WHVP - FHVP = 5-6 mmHg

Diagnosis: -

 Measured at Internal jugular vein

 Catheter inserted at IJVheartIVC

Grading: -

 10 mmHg- clinically significant

 >12mmHg – complications will develop

Causes: -

 Liver cirrhosis
o Compensation: -
 Fluid leaves Portal vein ascites develops
 Collateral pathways: -Portosystemic
 Oesophagus -oesophageal varices
 Umbilicus -caput medusae
 Rectum
 Splenomegaly – due to backflow of blood into spleen
  Pancytopenia (reduction of all blood cells) – due to
splenomegalyhypersplenismdestruction of blood cells

Diagnosis: -

 Portal Vein Pressure measurement

 Blood CP
 Endoscopy – to check for esophageal varices
 US – to check liver status

Management: -

 Prevention of variceal bleed -beta blocker (propranolol)(reduce pressure in vessels)

o Prophylactic banding of variceal
 Endoscopic banding of varices
 Acute variceal bleed – prevent shock (due to blood loss)
o IV fluids
o Vasopressor drugs e.g., Terlipressin (vasoactive drug used in the management
of low blood pressure) – obv is norepinephrine
 Reduce the bleeding from vessels
o Antibiotics – broad spectrum IV (due to development of peritonitis) -
ceftriaxone
o Endoscopy – to see where the bleeding is from IMP!!! (Banding or
sclerotherapy)
 Balloon tamponade – stop bleeding varices
o Esophageal transection

74) Pancreas - congenital and traumatic diseases

Embryology of pancreas: -
https://www.youtube.com/watch?v=ZGuCzh-a5U8
 Embryo at 4th -5th week
 Sagittal section: - head end and tail end
 Begins at mouth end and ends at caecal end
 Gut tube is broken into 3 main parts: -
o Foregut – stomach, duodenum and pancreas
o Midgut
o Hindgut
 Septum transversum – forms part of diaphragm and is border
for thorax region
o Loops around heart forming fibrous pericardium – hence
innervation by phrenic nerve
 Red long line at back known as dorsal aorta
 o Going to develop into abdominal aorta
o Celiac artery supplies this part of gut tube
o Sup mesenteric midgut
o Inf mesenteric hindgut
 Gut tube starts to widen backwards at junction of diaphragm
 Dorsal Mesentery behind become pancreas & spleen–
hence why pancreas becomes retroperitoneal
 Ventral outpouching diverticulum -liver, gallbladder and
ventral pancreas
 Dorsal diverticula – pancreas
o Gets bigger and longer
 Important demarcation point of foregut into midgut
o Since everything above supplied by celiac
artery and everything below sup mesenteric
artery touch of pancreas supplied by
superior mesenteric artery
 Stomach starts to pouch out at back
o As stomach swings around brings ventral
pancreas behind which makes it sit behind and
below the dorsal pancreas
o 2 parts of pancreas starts to merge
o Common bile duct also swings around dumps into major duodenal papillae
o Majority of dorsal pancreas duct joins ventral pancreas duct with the bile
duct all combine at major duodenal papillae
o Minor duodenal papillae – from accessory duct
higher up; more bicarbonate
o Hence first part of pancreas neutralizes acidic
secretions
 Since majority of these backwards – covered by
mesentery hence retroperitoneal
o Only tail portion of pancreas with spleen comes
inside hence intraperitoneal
 Derivatives: -
o Ventral portion gives most of uncinate process and a bit of head
o Rest comes from dorsal pancreas
 Why important?
 Blood supply: -
o Dorsal pancreas – supplied by splenic artery (branch of
celiac artery)
o Head and uncinate process – superior pancreatic artery
(branch from celiac artery gastroduodenal artery
<supplies lower part of stomach and duodenum>
little branch sup pancreatic artery)
 o Inf pancreatic duodenal branch of Superior
mesenteric artery (comes from below)
Congenital pancreas diseases
1. Annular pancreas
 It occurs due to failure of complete rotation of ventral bud of the pancreas, which
results in a ring of pancreatic tissue encircling the second part of the duodenum,
causing obstruction
 It contains a duct that joins the main pancreatic duct
 It can be divided into 2 types: -
o Neonatal type – produces symptoms of intestinal obstruction
o Adult type – has symptoms of duodenal ulcer and bilious vomiting
 Clinical features: -
o Upper abdomen distention
o Bilious vomiting
o Visible gastric peristalsis
 Diagnosis: -
o Plain x-ray of abdomen – shows double bubble appearance
o Barium meal – shows obstruction at the second part of the duodenum
 Treatment: -
o Duodenduodenostomy (treatment of choice) – anastomosis with the
purpose of bypassing the obstructed segment of the duodenum
o Do NOT resect the ring, since it will result in pancreatic fistula
2. Ectopic pancreas (accessory pancreatic tissue)
 It is an abnormality in which pancreatic tissue grows outside the normal anatomical
location of pancreas and without vascular or other anatomical connections to the
pancreas
 Sites - it can occur in: -
o stomach wall
o small intestine
o Meckel’s diverticulum
 MECKEL'S DIVERTICULUM is an outpouching or
bulge in the lower part of the small intestine.
The bulge is congenital (present at birth) and is a leftover of the
umbilical cord.
o in the hilum of the spleen or
o greater omentum

 30% contain Islet of Langerhans cells – endocrine tissue

o The islets of Langerhans contain four cell types that each secrete a different
peptide: alpha cells secrete glucagon, beta cells secrete insulin, delta cells
secrete somatostatin, and P (F) cells secrete pancreatic polypeptide.
 Complications: -
 o In the stomach – it can undergo cystic degeneration
o In the intestine – it can cause INTUSSUSCEPTION (one segment of the
intestine ‘telescopes’ into another, causing an intestinal obstruction) and can
cause GI bleeding
o In Meckel’s diverticulum – any of the complications mentioned above
3. Pancreatic divisum
 Def: -It is an abnormality in which a single pancreatic duct is NOT formed, but
instead there are two dorsal and ventral ducts
 Basically, separate ventral & dorsal ducts
 It occurs due to failure of fusion of the ventral and dorsal pancreatic ducts
 The ventral pancreatic bud forms uncinate process and inferior part of the head of
the pancreas
 The dorsal pancreatic bud forms the body and tail of the pancreas

4. Congenital cystic fibrosis

 Def: -It is an inherited autosomal recessive disease that is a generalised dysfunction
of exocrine glands, resulting in defective mucous secretion
 Viscid mucin is produced, which results in obstruction of the ducts
 Stasis of pancreatic secretions, alveolar rupture due to increased pressure occurs
later
 As a result of alveolar rupture pancreatic enzymes leak outside resulting in
pancreatitis
Clinical features: -
 Severe exocrine dysfunction – due to blockage of pancreatic ducts, which occurs
due to increased pancreatic enzymes that result in duct ectasia
 Chronic pulmonary disease – due to blockage of bronchi and bronchioles
 Severe malnutrition
 Steatorrhea (presence of excess fat in faeces)
 Salty sweat
 Pancreatitis
 Absence of vas deference in men
 Cirrhosis of liver due to bile plugging
Diagnosis: -
 DNA study
 Pulmonary function tests
 Sweat test for sodium and chloride – increased in cystic fibrosis
 Treatment: -
 Prognosis is poor
 Low fat and salt rich diet
 Respiratory physiotherapy
 Pancreatic enzyme supplements
Trauma of pancreas
 It is rare due to the anatomical location of the pancreas – RETROPERITONEUM
 Injury is usually associated with injuries to the liver, duodenum, spleen, portal
system, biliary system or kidneys
 Deep force in the epigastrium can cause crushing injuries to the body of the
pancreas against the vertebra
 Types of injuries: -
1. Parenchymal contusion or laceration without duct disruption
2. Parenchymal injury with duct disruption
3. Complete transection of the pancreas
4. Massive destruction of pancreatic head
 Grading of injuries: -
o Grade 1 – minor contusion/laceration without duct injury
o Grade 2 – major contusion/laceration without duct injury
o Grade 3 – distal transection or injury with duct involvement
o Grade 4 – proximal transection or injury with ampulla involvement
o Grade 5 – massive disruption of the pancreatic head
 Clinical features: -
o Pain in epigastrium
o Features of shock – pallor, tachycardia, sweating, hypotension, tachypnoea
o Increase in serum amylase level
 Diagnosis: -
o CT scan – confirms diagnosis
o ERCP to confirm disruption (endoscopic retrograde cholangio-
pancreatography)
 Treatment: -
o Conservative – fluid management, blood transfusion, antibiotics, pain relief
o Surgery – done if there is major ductal disruption, vascular injury or extensive
injury to head of pancreas

75) Acute pancreatitis, forms. Etiopathogenesis. Treatment

 Def: -It is a reversible, acute inflammation of the pancreas with increased pancreatic
enzyme levels in the blood and urine
 It is divided into 2 phases: -
1. Early – first 2 weeks
2. Late – after 2-3 weeks
Causes: -
 Gallstones (most common) – cause ductal obstruction
 Alcohol abuse (second most common)
 Cystic fibrosis
 Crohn’s disease
 Pancreatic tumour, pancreatic duct stricture, trauma to pancreas
 Drugs e.g., corticosteroids, tetracycline, oestrogens, diuretics
Pathogenesis: -
 It is ultimately caused by autodigestive injury of the gland itself
 Abnormal activation of the pancreatic enzymes trypsin, elastase and lipase results in
autodigestion of the pancreas.
 The enzymes can damage tissue and activate the complement system and the
inflammatory cascade producing cytokines and causing inflammation and edema
 The released toxins can cause necrosis thus acute renal failure
 Acute pancreatitis increases the risk of infection by compromising the gut barrier,
resulting in bacterial translocation from the gut lumen into the circulation
 The activated enzymes and cytokines that enter the peritoneal cavity cause a
chemical burn and third spacing of fluid which results in hypovolemic shock
o THIRD-SPACING = occurs when too much fluid moves from the intravascular
space (blood vessels) into the interstitial or “third” space—the non-functional
area between cells.
o This can cause potentially serious problems such as edema, reduced cardiac
output, and hypotension.
Clinical features: -
 Sudden onset (since acute) of severe, agonising upper abdominal pain which is
referred to the back
 Pain increases with food intake (since more enzymes produced when eating)
 Tenderness, rebound tenderness, guarding, rigidity and abdominal distention
 Features of shock and vomiting, high fever, tachypnoea and cyanosis
 Pulmonary insufficiency, ARDS and respiratory failure
o ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) = is a life-threatening
condition where the lungs cannot provide the body's vital organs with
enough oxygen
 DIC
o DISSEMINATED INTRAVASCULAR COAGULATION (DIC) = is a rare but serious
condition that causes abnormal blood clotting throughout the body's blood
vessels.
 Grey-Turner sign – discolouration of flanks
 Cullen’s sign – superficial edema and bruising in the subcutaneous fatty tissue
around the umbilicus
Diagnosis: -
 Characteristic abdominal pain
 Increased pancreatic enzymes – more than 3 times normal amount
 Left side of the diaphragm is elevated and left-sided pleural effusion occurs
 Plain x-ray – shows sentinel loop of dilated proximal small bowel, air-fluid level in
the duodenum, renal halo sign
o The HALO appears as ground-glass attenuation on imaging, due to
enhancement of the perirenal fat from the retroperitoneal collection of
pancreatic exudates

 Spiral CT (gold standard) – shows edema, altered fat and fascia planes, fluid
collections, necrosis, bowel distention and haemorrhage
o Spiral computed tomography (SCT) differs from conventional CT (CCT) in that
regions of the body can be rapidly imaged via continuous scanning.
o The most important advantages of helical CT over conventional CT are (1) the
shorter examination time, which decreases image degradation from motion
artifact
 Hypocalcaemia – since calcium is used for saponification
o Acute pancreatitis can result in fat necrosis, typically occurring in the
peripancreatic retroperitoneum, omentum and mesenteric root.
Saponification may be associated with fat necrosis both in the
retroperitoneum and in distant subcutaneous, periarticular, or marrow fat.
o Pancreatitis can be associated with tetany and hypocalcaemia. It is caused
primarily by precipitation of calcium soaps in the abdominal cavity,
 Liver function tests
Differential diagnosis: -
  Cholecystitis – acute pancreatitis has more severe pain in upper abdomen,
tenderness in right hypochondrium and epigastrium
Treatment: -
 Conservative (70% cases)
o Rehydration using ringer lactate solution
o Pain relief – do NOT give morphine since it causes spasm of sphincter of
Oddi
o Fresh frozen plasma and platelet concentrate in cases of severe
haemorrhagic episode or DIC
o Antibiotics – 3rd generation cephalosporins to decrease anticipated sepsis
o Calcium gluconate – to treat hypocalcaemia
o IV ranitidine – to prevent stress ulcers and erosive bleeding
o Anticholinergics – to decrease sphincter pressure
o Haemodialysis – in case of renal failure
 Surgical (30% cases)
o Done if patient condition is deteriorating or if there is pancreatic infected
necrosis
o Open surgery is done to remove intra and extra pancreatic necrotic materials,
pancreatic fluid and toxins

Acute pancreatitis: -

 Def: - Acute inflammation of pancreas with variable involvement of neighbouring

tissues
 Associated with raised pancreatic enzymes in blood and urine

Causes: - I GET SMASHED

 Idiopathic
 Gall bladder stones
 Ethanol (alcohol)
 Trauma
 Steroids
 Mumps (& other infections)
 Autoimmune
 Scorpion/ Spider bites
 Hyperlipidemia/Hypercalcemia
 ERCP
 Drugs

Clinical: -

 Acute onset
 Severe epigastric pain for 1 day with multiple episodes of vomiting
 N+V
 Tenderness in epigastric region
 Signs of infection: -
o Fever
o Hypotension
o Tachycardia
o Tachypnoea
 Serum amylase/lipase increase
 Pain radiating backwards
 Grey-Turner’s sign - bluish discolouration of flanks (due to blood oozing out when
enzymes saponify peritoneum)
 Cullens sign – bluish discoloration of umbilicus (due to saponification of peritoneum)

Diagnosis: -

 Serum amylase/lipase
o Remember lipase is more sensitive and specific; lipase even remains in blood
longer
o Amylase increases in other dxs like perforated duodenal ulcer
 Increases more than 4 times in pancreatitis (Normal is 60-110 U/L) -
can go more than 2000 U/L
 US – to check if gallstones present
 CT scan – diagnostic gold standard
 CBC/ CRP – to check patient condition
 LFTs for gallstones – AST increases
 Serum calcium – will decrease
o Free FFAs from saponification + Ca2+ salts released from pancreas combine
and form calcium salts settle in retroperitoneal area
 BUN – will increase (since kidneys get damaged too)
 Glucose – high (since insulin not being secreted from pancreas)
 MRI/MRCP
 ERCP – after 72 hrs since too much edema & ducts too fragile
 Endoscopic US
 Laparotomy – if confused if peritonitis or pancreatitis

Ranson’s criteria: - To check for severity GALL/ETOH

 To heck for severity since hard to predict

 Some tests done on admission while rest done after 48hrs
 On admission: -
o Blood Glucose
o Age more than 55yrs
o Leucocytosis
 o LFTs – LDH & AST
 After 48hrs: -
o Electrolytes – Calcium
o Third space fluid collection (Edema) & BUN
o Oxygen
o Hematocrit
 0-2 – no mortality
 >6 – 70-90% mortality

Complications: -

 Local
o Acute fluid collection
o Abscess
o Pseudocysts
o Pancreatic necrosis
 Systemic
o Pleural effusion pneumonia
o Pericardial effusion
o Hypovolemia - due to 3rd space

Management: - ALWAYS SUPPORTIVE

 Mild: -
o Admit patient
o IV fluids
o Monitor vitals
o Analgesics – opioids
o Antibiotics – not always (Gall stones no sense)
o Treat cause
o Usually, pts can be sent home after 3-4 days
 Severe: -severe hypocalcaemia & hyperglycaemia
o Admit to ICU
o Aspirate stomach using NG tube
o Oxygen
o IV fluids
o Wait till 72 hrs and stone removal with ERCP
 Surgery: -infective necrosis
o CT guided wide bore needle used to drain necrotic material
 Open surgery in pancreatitis is also high mortality that’s why pushed off as much as
possible
o Necrosectomy = removal of necrotic pancreatic tissue
 o Followed by 2 drains: - one to irrigate one to drain

76) Chronic pancreatitis. Cysts and fistulas of the pancreas

1. Chronic pancreatitis
 Def: - It is persistent, progressive, irreversible damage of the pancreas due to
chronic inflammation
 Affects men more
 It can be divided into 3 phases: - !!!!
1) Early – pancreatic edema, chronic inflammation, normal secretory function
2) Moderate – early fibrosis, only few acinar cells, exocrine dysfunction
3) Late – fibrosis, loss of secretory function, diabetes
Causes: -
 Alcohol (most common) – 80% cases
o Alcohol decreases pancreatic blood flow, releases free radicals, creates
pancreatic ischemia and activates pancreatic stellate cells which produce
abundant extracellular matrix and collagen
 Gallstones
 Malnutrition, diet
 Cystic fibrosis
 Congenital anomaly – pancreatic divisum, annular pancreas
 Trauma
Clinical features: -
 Severe, persistent pain in epigastric region
 Exocrine dysfunction – diarrhoea, weight loss, loss of appetite
 Malabsorption which results in steatorrhea
 Mild jaundice
 Triad of chronic pancreatitis (occurs in less than a third patients)
(i) Steatorrhea
(ii) Diabetes
(iii) Pancreatic calcification
 Mass per abdomen – just above the umbilicus, tender, nodular, hard, felt on
deep palpation and does NOT move with breathing
Diagnosis: -
 Ultrasound of abdomen – shows duct dilation, gallstones, liver status, common bile
duct
 CT scan – shows calcification, gallstones, duct stricture and dilation, fibrosis and
common bile duct status
 Plain x-ray – shows calcifications (65% cases)
 Oral glucose tolerance test – tests for diabetes
 ERCP – shows dilated duct and strictures
 Liver function tests
Treatment: -
 Treat pain, maldigestion and nutrition
 Pancreatic enzyme supplements, vitamins and minerals
 Oral hypoglycaemics or insulin – to treat diabetes
 Ascitic taps – to treat pancreatic ascites
 PPI – to control steatorrhea
 Treat complications e.g., pseudocysts of pancreas, pancreatic ascites, CBD stricture
due to edema or inflammation
 Surgery
(i) Pancreatic duct decompression (drainage) – decreases pain and retains
existing exocrine and endocrine functions
(ii) Pancreatic resection (total pancreatomy) – relieves pain and removes entire
diseased tissue. Can do Whipple surgery
 A pancreaticoduodenectomy, also known as a Whipple procedure, is a
major surgical operation most often performed to remove cancerous
tumours from the head of the pancreas.
 It is also used for the treatment of pancreatic or duodenal trauma, or
chronic pancreatitis.
2. Pancreatic cysts – pseudocyst of pancreas
 Def: - It is a localised collection of
pancreatic fluid, usually 3 weeks after
acute pancreatitis attack
 Acute pancreatitis results in formation
of pseudocyst in 50% cases, of which
20-40% cases resolve spontaneously
 Site of pseudocyst – less sac (between
colon and stomach), duodenum,
jejunum, colon, hilum of spleen
 Initially the wall of the cyst is thin but
later it becomes fibrosed and thickened
 It is lined by a fibrin layer, but has NO endothelium – thus it is called PSEUDOCYST
 It contains brownish fluid with sludge-like necrotic material and can become
infected to form an infected pseudocyst or pancreatic abscess
Clinical features: -
 Soft, smooth swelling in epigastric region, that does NOT move with breathing
 If it is infected, it will be a tender mass and the patient will be toxic with fever and
chills
 Baid sign – if Ryle’s tube is passed, it is felt abdominally, because the stomach is
stretched towards the abdominal wall
Diagnosis: -
 Ultrasound of abdomen – shows size and thickness of pseudocyst
 CT scan – better than ultrasound. Shows size, shape, number, wall thickness,
contents and extent of necrosis in pancreas and calcification
 Barium meal – shows widened vertebrogastric angle with displaced stomach
Treatment: -
 Conservative – observe it with follow-up ultrasound since 50% pseudocysts resolve
spontaneously within 3-4 weeks
 Surgery – endoscopic drainage of pseudocyst
3. Pancreatic fistula
 Def: - an abnormal communication between the pancreas and other organs due to
leakage of pancreatic secretions from damaged pancreatic ducts
Causes: -
 After Whipple operation for acute pancreatitis
 Splenectomy
 Trauma
 After external drainage for infected pseudocyst of pancreas
Clinical features: -!!!!

 Patient is in catabolic state (i.e., muscle wasting)

o When you're in a CATABOLIC STATE, you're breaking down or losing overall
mass, both fat and muscle.
 Skin excoriation
o Excoriation disorder (also referred to as chronic skin-picking or
dermatillomania) is a mental illness related to obsessive-compulsive
disorder.
o It is characterized by repeated picking at one's own skin which results in skin
lesions and causes significant disruption in one's life.
 Electrolyte imbalance and malnutrition
 Sepsis
Diagnosis: -
 CT scan – shows exact site of communication to pancreas
 Abdominal ultrasound – rules out pseudocyst
 ERCP – shows demonstrate leakage of the dye from the pancreatic duct into the
surrounding area or along the fistulous tract and proximal obstruction, if any
 Amylase level in pleural fluid, peritoneal fluid and in the discharge will be high
Treatment: -
 Conservative – in majority of cases after surgery, the fistula discharge stops within
1-3 weeks
o Zinc oxide cream – for skin excoriation
o Correct electrolyte imbalance
o Antibiotics
 Surgery
o Roux-enY anastomosis
o Resection of fistula with pancreas
Pseudocyst: -

 Normal cyst covered by epithelium, anything else pseudocyst

 PSEUDOCYST = organised necrotic tissue
 Acute pancreatitis edemacell deathgranulation tissue surrounds fluid filled
necrotic area pseudocyst

Clinical: -

 Usually after an episode of acute pancreatitis 3-4 wks before

 Soft movable mass in epigastric region
 Less appetite-epigastric fullness (due to compression of stomach)
 Might have gastric outlet obstruction features too
 If compress bile ducts -obstructive jaundice features

Diagnosis: -

 US
 CT scan
 Us guided aspiration – to differentiate b/w cyst and carcinoma
o Check for amylase and CEA (Carcinomic Embryonic Antigen) Tumor marker
o Is cystamylase will be high
 ERCP

Complication: -

 Rupture peritonitis
 Obstructive features

Management: -

 Resolves on its own usually if no complications

 If bigger than 6 cm and not resolves for 3 months and size increasing intervene: -
o Endoscopic drainage
o Endoscopic placement of stent b/w cysts and stomach
o Open drainage: -
 If closer to stomach -CYSTOGASTROSTOMY = sutures b/w cysts and
posterior wall of stomach
 If closer to duodenum – CYSTODUODENOSTOMY

77) Carcinoma of the pancreas. Operations at different localizations

Neoplasms of exocrine pancreas; Txt - Whipple

Pancreatic tumours
 They can be divided into 2 main types: -
1. Exocrine tumours
 2. Endocrine tumours
Exocrine pancreatic tumours
 Adenoma in ampulla
 Cystadenocarcinoma of pancreas
Pancreatic carcinoma
 Affects men more
 80% of pancreatic cancers are metastatic by the time they are diagnosed
 Location: -
o 70% cases occur in the head of the pancreas, including the periampullary
region
o 30% cases occur in the body and the tail of the pancreas
 70% of cases are adenocarcinoma of duct cell origin
o ADENOCARCINOMA = is a type of cancer. It develops in the glands that line
your organs.
Causes: -
 Alcohol and smoking
 High energy diet, rich in fat
 Chronic pancreatitis
 Diabetes – increases risk 10 times
 Cirrhosis, obesity
Periampullary carcinoma
 The tumour occurs at or near the ampulla of Vater and can be:
1. Adenocarcinoma from head of pancreas close to the ampulla – 50% cases
2. Tumour from ampulla of Vater – 30% cases
3. Distal bile duct carcinoma – 10% cases
4. Duodenal carcinoma adjacent to the ampulla – 10% cases
 Spread of tumour: -
o Local spread – spreads to adjacent structures like duodenum, portal vein,
retroperitoneum
o Distant spread – spreads to liver, lings, adrenals, brain, bone etc.
o Lymphatic spread – spreads to perihepatic nodes around the duodenum and
CBD (common bile duct), celiac and subplyroic nodes
 Clinical features: -
o Obstructive jaundice
o Weight loss and loss of appetite
o Pain in right hypochondrium, epigastrium or left hypochondrium, depending
on tumour location
o Back pain – due to retroperitoneal nerve involvement or pancreatic duct
obstruction
o Silvery stool – due to mixing of undigested fat with metabolised blood from
the ooze of periampullary growth
 o Ascites
o Palpable, nontender, soft, smooth gallbladder
o Enlarged liver, nontender, smooth, firm, due to dilated bile filled biliary
radicles

 Diagnosis: -
o Liver function tests: -
 increased serum bilirubin
 decreased serum albumin and
 increased PT time
o Ultrasound of abdomen – shows gallbladder, liver, CBD size, lymph node
status, portal vein and ascites
o Spiral CT scan – shows size of tumour, portal vein infiltration and
retroperitoneal lymph nodes
o Tumour markers – CA199
 Differential diagnosis: -
o Common Bile Duct (CBD) stone
o Lymph node compressing CBD
o Retroperitoneal mass/tumour/lymph nodes
 Treatment: -
o Criteria for resection: -
 tumour size less than 3cm
 periampullary tumours
 growth is NOT adherent to portal system
o Only 10-15% pancreatic carcinomas of the head are
operable
o Whipple operation
  done by removing the tumour with the head and neck of the
pancreas, C loop of duodenum, distal stomach, 10cm proximal
jejunum, lower end of CBD, gallbladder and perihepatic lymph nodes
o Total pancreatectomy with lymph node clearance (better)
o In inoperable cases, can do chemotherapy or Roux-en-Y
choleduchojjunostomy to palliate obstructive jaundice, duodenal obstruction
and pain
Neoplasms of exocrine pancreas: -

 Highest mortality cause of late presentation

 Localisation: -
o Head of pancreas – most common (70%)
o Body
o Tail
o Ampulla of Vater
o Periampullary cancer - If 2 cm around Ampulla of Vater

Types: -

 Cancer of head of pancreas

Clinical: -

 Palpable GB – Couversoirs law

o 2 masses felt: -
 Mass that moves with breathing – GB
 Mass that is not moving – carcinoma since retroperitoneal
 Obstructive Jaundice
 Weight loss anorexia
 Gastric outlet obstruction

Diagnosis: -

 LFTs- ALP & GGP will increase

 US
 CT scan – staging and metastasis
 MRI
 CA 19-9 – tumor marker

Treatment: -

 CI: -
o Distant metastasis -hematogenous & lymphatic
o Portal vein metastasis
 Before surgery give: - (In obstructive jaundice and neoplasms of pancreas pts)
o Vit K injections
 o Clotting factors
 Bile duct obstruction will affect liver tooreduce clotting factors
o Diuretics – mannitol to prevent hepatorenal shutdown
 To make sure kidney perfusion and urine output remains normal
 Due to acute tubular necrosis due to bile obstruction (Bilirubin can go
till 30 g/dl; normal is less than 2 g/dl) bilirubin gets stuck in tubes
 Diuretics will help this (bilirubin will be diluted and will less like to get
stuck)
o Glucose – since liver is not storing glucose
 Drain bile too if distended GB
 Whipple’s procedure: -
o Remove: - duodenum; pylorus of stomach; head of pancreas, Bile duct +
biliary tree (hepatic ducts spared) + GB
o Hepaticojejunostomy + pancreatojejunostomy + gastrojejunostomy
 Why remove GB?
o CCK enzyme is produced by head of pancreas
o CCK enzyme responsible for contraction of Gallbladder
o Hence if head of pancreas removed CCK stopped stasis of bile

78) Benign and malignant endocrine tumors of the pancreas

Endocrine tumours
 They are associated with MEN syndrome (type 1 Werner’s syndrome)
o Multiple endocrine neoplasia (MEN) syndromes are inherited disorders that
affect the endocrine system !!!!
 MEN1 syndrome usually causes tumors in the parathyroid gland,
pituitary gland, or islet cells of the pancreas. (PPP)
 MEN2 syndrome usually causes tumors in the thyroid gland,
parathyroid gland, or adrenal gland. (PAT)
 They are associated with parathyroid adenoma, pituitary adenoma and peptic
ulcers
 They are usually small, multiple and malignant (40-50%)
 Types of endocrine tumours: -
1. Insulinoma (most common) – 60% cases
2. Gastrinoma (second most common)
3. Glucagonoma
1. Insulinoma BI
 It is commonly benign (85% cases)
 It arises from beta cells of the pancreas, which secrete insulin in excess causing
profound hypoglycaemic features
 Affects men and women equally
 90% of insulinomas are less than 2cm in size and
 Clinical features: -
o Abdominal discomfort, trembling, sweating, hunger, dizziness, hallucinations
o Patient is overweight due to overeating
o Whipple’s triad: -
(i) Attack of hypoglycaemia in fasting state
(ii) Blood sugar below 45mg% during the attack and
(iii) Symptoms relieved by glucose
 Diagnosis: -
o Insulin radioimmunoassay – insulin level above 7µU/ml and insulin/glucose
ratio above 0.3 means insulinoma
o MRI to localise the tumour
 Treatment: -
o Distal pancreatectomy (removal of tail and body of pancreas and the spleen)
– enucleation of all tumours
o Control hypoglycaemia – beta blockers, verapamil, steroids, growth hormone
o Calcium channel blockers
2. Gastrinoma
 Def: -Gastrinoma are neuroendocrine tumors characterized by the secretion of
gastrin with resultant excessive gastric acid production causing severe peptic ulcer
disease and diarrhoea, a combination referred to as the Zollinger-Ellison syndrome
(ZES).
 It is almost always malignant and presents with secondaries in the liver, lymph
nodes, lungs or bones !
 It arises from non-beta cells (G cells) of the pancreas, which secrets high level of
gastrin
o G-cells are neuroendocrine cells responsible for
the synthesis and secretion of gastrin.
o They are primarily found in the pyloric antrum but can also
be found in the duodenum and the pancreas.
 It is the most common endocrine pancreatic tumour seen in MEN 1 syndrome
 Affects men more
 It is common in Gastrinoma triangle – Passaros triangle
 Diagnosis: -
o Gastrin assay – gastrin above 200pg/ml means gastrinoma
o MRI to localise the tumour
 Treatment – 60% cases are curable
o Distal pancreatectomy (removal of tail and body of pancreas and the spleen)
– enucleation of all tumours
o Gastrectomy may be needed
3. Glucagonoma
 Def: -A glucagonoma is a pancreatic alpha-cell tumor that secretes glucagon, causing
hyperglycaemia and a characteristic rash
 It is commonly malignant (80% cases) and 80% cases spread to the liver
 It arises from alpha cells of the pancreas
 Affects women more
 Clinical features: -
o Diabetes – 90% cases
o Necrolytic migratory erythema – 65% cases
 Necrolytic migratory erythema (NME) is a characteristic skin rash
most often associated with the glucagonoma, an alpha-cell tumor of
the pancreatic islets.

o Stomatitis
 STOMATITIS = a general term for an inflamed and sore mouth
o Diarrhoea and weight loss
o Anaemia and features of amino acid deficiency
 Diagnosis: -
o Increased serum glucagon level. Fasting glucagon level above 50pmol/l
means glucagonoma
o MRI to localise tumour
 Treatment: -
o Distal pancreatectomy (removal of tail and body of pancreas and the spleen)
– enucleation of all tumours
o Prednisolone – controls diarrhoea
 o Enteral/parenteral nutrition – to treat anaemia and amino acid deficiency
o IV amino acid infusion – to treat necrolytic dermatitis

79) Injuries to the spleen. Clinical manifestation, Mechanism of trauma Manifestation,

Types of splenic trauma. Treatment and prognosis

Splenectomy

 Spleen is the biggest lymphatic organ

 Spleen protected under ribcage – though it is most commonly affected organ in blunt
injury
 Mortality rate after blunt splenic injury ≈ 9%

Blood supply: -

 Arterial Supply: Splenic A. (biggest branch of coeliac trunk)

 Venous Drainage: Splenic V
o Splenic vein + Sup. Mesenteric vein portal vein

Etiology: -

 Blunt abdominal trauma (most common, due to traffic and sports accidents)
 Penetrating trauma (gunshot wounds, stab wounds)
 Non-traumatic (infection, medical procedures (colonoscopy)
 Haematological diseases e.g., sickle cell, Thalassemia; thrombocytopenic purpura
 Medications
 Pregnancy
 (explosives)
 <1% of cases of infectious mononucleosis can cause splenic rupture

Clinical: -

 LUQ pain
 Kehr’s Sign – pain referred up to the left shoulder due to subdiaphragmatic nerve
root irritation
 With free intra-peritoneal blood – diffuse Ab pain, peritoneal irritation + rebound
tenderness (Blumberg’s Sign)
 Shock (hypovolaemic) - increased HR, low BP, tachypnoea, anxiety, pallor – if
increased bleeding
 Ballance’s sign – signs of dullness to percussion in LUQ and shifting dullness to
percussion in RUQ (because in left flank, the blood is coagulated, but in the right it’s
still fluid)

Diagnosis: -

 Bloods – FBC + Hb levels

 CT in stable pt with contrast
 FAST (Focused Abdominal Sonographic Technique) = quickly i.d.s presence/absence
of peritoneal fluid
 Splenic angiography
 X-ray

Grading of Spleen Injury by American Association for the Surgery of Trauma (AAST): -

 Basically 5 grades – laceration and subcapsular hematoma

o 1cm
o 1-3 cm
o 3-10 cm
o >10cm
o Splenic tissue maceration
Treatment: -

 Initial = A, B, C – at this point pt falls into 2 categories based on vital signs: -

1. Hemodynamically stable or
2. Unstable - Low BP +/- increased HR (cause most often = bleeding)
 If bleeding from spleen = splenectomy
 Pre-operative preparations: -
o Coagulation profile (PT, PTT should be normal since immunity already
lowand if remove spleen can cause thrombotic episodes)
o DVT (Deep vein thrombosis)
o Vaccinations (of capsulated bacteria)– pneumococcal (Strep pneumonia),
meningococcal (N. meningitis), H. influenzae B
 Can cause widespread septicaemia & w/I 2 days can cause death since
spleen not there to control
 If emergency give immediately after operation
o Prophylactic antibiotics e.g., for malaria in endemic areas
 Splenectomy: - ligate 2 ligaments (Gastrosplenic ligament & Splenorenal ligament) +
splenic arteries

Complications: -
  Haemorrhage
 Damage to nearby organs (tail of pancreas, stomach, Lungs)
 Atelectasis – puncture of lung
 OPSI (Opportunistic Post Splenectomy infections) – H. influenza or post strep

80) Acute appendicitis - forms, clinical picture, treatment

Anatomy: -
 The appendix is a blind ended tube connected to the cecum and is located in the
right-left quadrant
 Blood supply – APPENDICEAL ARTERY  branch of the ileocecal artery  superior
mesenteric artery  abdominal artery
 Morphologically undeveloped end of the cecum

Positions: - Retro-caecal most common followed by sub-caecal

Acute appendicitis: -
 ACUTE APPENDICITIS = is sudden inflammation of the appendix due to bacterial
infection
 Organisms: -
o E. coli (85%)
o Enterococci (30%)
 Common in young men

Classification: -
 Prof Beshev: -
1. Simple
 2. Destructive
 Prof Stoykov: -
1. Appendiceal Colic
2. Simple superficial appendicitis
3. Destructive Appendicitis
a) Phlegmonous
b) Gangrenous
c) Perforated
4. Complicated appendicitis
a) Appendicular infiltrate
b) Appendicular abscess
c) Diffuse purulent peritonitis
Types: -
1. Acute non-obstructive appendicitis (catarrhal/mucosal appendicitis)
o It is caused by acute inflammation of the mucous membrane with secondary
infection without obstruction
o It may lead to resolution, fibrosis, recurrent appendicitis or eventual
obstructive appendicitis
2. Acute obstructive appendicitis
o Pus collects in the blocked lumen of the appendix, which is black,
gangrenous, edematous and rapidly progresses, resulting in perforation at
either the tip or base of the appendix.
o This results in peritonitis, formation of appendicular abscess or pelvic abscess
3. Recurrent appendicitis
o Repeated attacks of non-obstructive appendicitis lead to fibrosis and
adhesions, which recurrent appendicitis
4. Subacute appendicitis
o It is a milder form of acute appendicitis
5. Stump appendicitis
o It is a retained long stump of appendix after a laparoscopic appendectomy
Classification of acute appendicitis according to ultrasound findings: -
1. Catarrhal – the layer of the appendiceal wall is clear. Submucosal layer is NOT
hypertrophied
2. Phlegmonous – the layer of the appendiceal wall is indistinct. Submucosal layer is
hypertrophied
3. Gangrenous – the layer of the appendiceal wall is disrupted. Submucosal layer is
indistinct and partially lost
Types according to lab lesson: -
 Divided into 2 major ones: -
1. Perforating
2. Non perforating
Causes: -
 Numerous theories none of which 100% sure
 All coming in mind if suspicious for acute appendicitis
 Luminal obstruction of entrance of appendix
 Increased intra luminal pressure perfect environment for bacterial translocation
and overgrowth
 In some cases, lymphoid hyperplasia can be the cause of luminal obstruction
 Acute most common in 20-30yrs old patients in which there is most expressed
lymphoid hyperplasia
 In some patients fasciculitis something like stone located in appendix leading to
obstruction and acute inflammation
 Fibrosis, CT adhesions can lead to folding of appendix itself obstruction
inflammation
 Foreign bodies leading to obstruction
 Neoplastic processes leading to obstruction

Etiopathogenesis: -
 Luminal obstructionincreased intra luminal pressurebacteria overgrowth of
mixed flora E. coli and fragilisacute inflammation
 If patient not treated on timenecrosisperforationleakage of bowel content in
free abdominal cavity
Clinical features/diagnosis: -
 History: -
o Pain may start par umbilically before moving down to right lower quadrant
o Sudden abdominal pain in right flank of abdomen
o Nausea and vomiting not profuse not relieving patient
o Anorexia or loss of appetite
o Fever not well expressed not high fever usually if patient has fever is no
more than 38 degrees
o In day in which symptoms occur the patient has constipation
o Abdominal bloating and distention
o Pain expressed in right flank right ilia fossa
o Specific on pain: -
 Migratory pain = pain starts in region of abdomen which is distant to
right iliac fossa like in epigastrium and after a few hours migrate to
right lower quadrant
 Pain constant
 Worsening on movement and coughing
 Usually, patients with this disease lie still in bed and try not to move
 Anorexia
 Nausea and vomiting not relieving
 In rare cases with atypical position may have diarrhoea or
haematuria if pelvic location of appendix inflamed appendix
irritating urinary bladder or rectum of patient
 Physical examination: -
 o Focal tenderness with guarding at McBurney point
o Start palpation at most distant point from pain point
o Deep palpation to look for focal tenderness
o If there is such a thinghigh suspicious
o Some specific signs to look for: -
 Rovsings sign= means that you are supposed to
perform deep palpation of abdomen and try to
move gases in colon backwards direction starting
from left iliac fossa going on colon with hands in
order to reach right iliac fossa to distant cecum and
patient says more severe pain
 Dunphy’s sign = If patient asked to cough pain
cause during coughing increase intra-abdominal
pressure and feel more severe pain if inflammation
 Obturator sign = If perform internal rotation of right hippain
 Iliopsoas sign = more severe pain if ask patient to perform flexion of
hip
 If perform digit rectum examination or transvaginal pain during
examination
 Other signs: -
o Not local general
o Hypertension, tachycardia, distended abdomen with gargling sounds
o In phlegmonous or perforation: -
 Abscess formation surrounding inflamed appendix
 Mass in right iliac fossa in appendicitis with abscess formation
Diagnosis: -
 Lab findings: -
o TBC is leucocytosis higher level of leucocytes in peripheral blood
o Elevated level of C-reactive protein sign of acute inflammation in particular
with patient in right abdominal pain
o Urinalysis of patientif women and fertile age perform pregnancy test
 Imaging: -
o Abdominal USlook for inflammation, if greater than 6 mm with pain due to
transducersacute inflammation
o Perpendicular fluid or increased echogenicity of fat of mesentery of appendix
another sign
o In not informativeCT of
abdomen to look for
enlargement
 o Double wall thickness greater than 6mm and thickening of appendicular wall
and presence of calculi on investigation
o If not informativeperform MRI
o Stone giving echo shadowreason for luminal obstruction
Diagnosis: -score called Alvarado score
 Made by some symptoms and lab findings and all get some points and sum up points
and tell patient has appendicitis

Basically tenderness and leucocytosis is 2 each (8 in total) - MANTRELS

Differential diagnosis: -
 Acute mesenteric lymphadenitis typical for children react with some
inflammation of mesenteric lymph nodes
 Viral infectionsinflammation of respiratory tract develop abdominal pain could
imitate clinical manifestation
 Caecal diverticulitis or Meckel diverticulitis
 Crohn’s disease
 Renal colic pain
 Acute pelvic inflammatory pain in young girls
 Gynaecological like torsion of ovaries, ovulation, rupture of cysts and ectopic
pregnancy with rupture of ovarian tube
Treatment: -
 Preoperative preparation
 Treatment only operative
 Operate on emergency
 If clinical manifestations not well expressed
may wait for a few hours to observe
clinical manifestation and operate or no
 May administer antibiotics prior to surgery
 Treatment: -
o open appendectomy or
o laparoscopic one
81) Acute appendicitis in children, adults and pregnant women

Appendicitis

Acute appendicitis in children

 Rare
 Also, neonates really rare
 Usual affect 20-30 yrs
 In children complicated form of diseases like perforation
 In neonates hard to know as kids cannot speak and where there is pain, become
lethargic with distention and abdominal irritability
 In young childreninfarcts surround inflamed area for infection not to spread to
abdomen
 Diff diagnosis: -GIMML
o Intussusception (typical for 5-6 months old)
 INTUSSUSCEPTION = is a life-threatening illness and occurs when a
portion of the intestine folds like a telescope, with one segment
slipping inside another segment.
o Palpable abdominal mass with jelly stool mixed with blood
o Viral or bacterial gastroenteritis
o Anatomical variation like malrotation pain out of proportion than physical
status no signs of muscular defence or peritoneal irritation
o Teenage girlspregnancy
 Around 12-13 child bearing age be aware, include in ddx in young
teenage girls
o Mesenteric lymphadenitis due to previous respiratory tract disease
inflammation after infection
 o Torsion of great omentum irritating pain in acute appendicitis
o Specific disease affecting sex: - ovarian torsion or in boys’ right testes
Acute appendicitis in pregnancy
 Usually in 1st or 2nd trimester
 Hard for diagnosis: - abdominal discomfort and unspecify complaints hard to
diagnose
 Due to growing uterusdisplaced pain hence doesn’t look for McBurney point on
right flank of abdomen
 Rebound tenderness and guarding may NOT be evident
 There is a 15% risk of premature labour
 Fetal death is 5% but becomes 30% once the appendix perforates
 After 6 months, maternal mortality increases 10 times more and can lead to
premature labour
 Perforation is more common in third trimester
 Treatment – surgery
Acute appendicitis in elderly
 Gangrene and perforation are common
 With age, the abdominal wall becomes laxed, thus location is poor and so peritonitis
occurs early on
 In elderly patients, appendicitis may present with different clinical features than
younger patients.
o The general tendency is for the inflammatory components to be less
pronounced.
o Temperature is usually lower, and the leukocyte count is lower, and there is
less pain and tenderness

82) Mesenteric lymphadenitis

 Def: - It is inflammation of the mesenteric lymph nodes, which are located in the
membrane that connects the intestine to the abdominal wall (mesentery)
 The membrane provides lubrication so that the organs can move within the
abdominal cavity
 It is common in children and young women
Classification: -
 It can be divided into 2 types: -
1. Primary = No aetiology factors; Mild terminal ileum thickening <5mm
2. Secondary = Underlying cause; Significant terminal thickening >5mm
 Terminal Ileitis
 Inflammatory Bowel disease
 o Y – Yersinia enterolitica
o M – Tuberculosis
o C – Candida
o A - Actinomycosis
 Small bowel Ischemia
Causes: -
 Infection !
o Yersinia enterolitica infection (most common)
o Bacterial infection e.g., Salmonella, Staphylococcus, Streptococcus, TB
o Viral infection – gastroenteritis (stomach flu)
o Parasitic infection – Guardia lamblia
 Cancer – lymphoma, breast cancer, pancreatic cancer, lung cancer
 Inflammatory conditions – Crohn’s disease, pancreatitis, diverticulitis (inflammation
of large intestine)
Clinical features: -
 Abdominal pain in right lower quadrant (right iliac fossa)
 Slight fever, nausea, vomiting, diarrhoea, abdominal colicky
 Tender lymph nodes may be palpable in RIF (Right Iliac Fossa)
 History of ingestion of raw pork in places with endemic Yersinia
Diagnosis: -
 CBC – leucocytosis
 Blood sample serology for diagnosis of etiologic agents e.g., Yersinia enterolitica
 Urine analysis – to exclude UTI
 Ultrasound of abdomen
 CT of abdomen – shows enlarged mesenteric lymph nodes, with or without
associated iliac wall thickening and a normal appendix
Differential diagnosis: -
 Acute appendicitis – in mesenterial lymphadenitis, the lymph nodes tend to be
bigger, more in number and more widely distributed than in appendicitis
 Meckel’s diverticulum
 Ectopic pregnancy
Treatment: -
  Broad spectrum antibiotics – metronidazole, clindamycin, ampicillin, amoxicillin
 Treat pain and rehydrate the patient
 Surgery is done if appendicitis can NOT be excluded with certainty, just to be safe
and appendectomy is done
83) Mekel’s diverticulum. Diverticulitis. Haemorrhage. Perforation

Mekel’s diverticulum

 https://www.youtube.com/watch?v=pNAww-da8Vw
 DIVERTICULUM = outpouching of the gut wall
o Can be TRUE (involves ALL layers of intestinal wall) or FALSE (mucosa +
submucosa protruding through a mucosal defect)
 Most common CA of SI
 Def: - embryologic derivative of vitelline duct (connection b/w foregut + yolk sac)
 Normally, it is obliterated bw 8th to 9th week.
 Rule of 2’s: -
o 2% of population
o 2 yr old most common age +
o 2x more in boys
o 2 inches long
o 2ft proximally located to ileocecal valve
o 2 types of ectopic tissue - (gastric + pancreatic)
 25% of MD are connected to umbilicus via a fibrous strand, usually arises proximal to
ileocecal valve.
 Blood Supply: Via persistent vitelline vessels within a distinct mesentery
 !!! Cells found in vitelline duct are pluripotent, thus can differentiate into
heterotrophic tissue (this may cause development of adenocarcinoma)
o 2 most common types of tissue found: - !!!!
 Gastric Mucosa = 50%
 Pancreatic Mucosa = 5%
 Tumors are uncommon in MD, some include: -
o Benign = lipoma, leiomyoma, neurofibroma, angioma
o Malignant = leiomyosarcoma, adenocarcinoma, carcinoid

Etiopathogenesis: -

 Results from incomplete closure of omphalomesenteric duct (vitelline duct)

 Can present as: -!!!!
o Vitelline duct fistula – if both ends are open
o Mekel’s diverticulum – closure on umbilical side
o Umbilical sinus – If duct not closed on umbilical side
Clinical: -

 Asx unless complications arise

Complications: -

 Bleeding due to ulceration of ileal mucosa that occurs adjacent to acid-producing

gastric mucosa
o S+S: - (abdominal pain is rare, but pallor + lethargy may be seen)
 Intestinal obstruction = due to volvulus of intestine around fibrous band
 Intussusception – maybe ileocolic or ileoileal associated with urge to defecate, early
vomiting, currant jelly stool
 Littre’s hernia – presence of Meckel’s diverticulum in hernial sac as content. It occurs
as an inguinal or femoral hernia
 Diverticulitis = appears similar to appendicitis; failure to diagnose diverticulitis could
lead to perforation, peritonitis + death
 Umbilical Anomalies = if fibrous band found on laparotomy, should be removed (risk
of internal herniation and volvulus)
 Fistula = draining, cannulation and dye injection useful for diagnosis; elective surgical
exploration + laparotomy used for TX

Diagnosis: -

 Discovered incidentally
 Radioisotope Scanning 99mTc – taken up by mucus-secreting cells of gastric mucosa
of diverticulum
 Enteroclysis small bowel enema under fluoroscopy may show the Meckel’s
diverticulum. It is probably the most accurate investigation

Treatment: -

 Asymptomatic diverticulum can be left alone when found under laparotomy

 Surgery: - diverticulectomy + removal of any assoc bands
 Indications: -
o Done if age is less than 40 years
o Diverticula is longer than 2cm
o Presence of fibrous bands to the umbilicus or mesentery, since these are risk
factors for the development of complications
 Method – resection of short segment of ileum containing the Meckel’s diverticulum
and end-to-end anastomosis

Diverticulitis: -

 Def: - Inflam + infx assoc with a diverticulum

 Most commonly seen in sigmoid low fibre diet, because this leads to increased
pressure and thus diverticulum
o Most diverticula occur in the sigmoid colon because it has the smallest
diameter

o Additionally, areas where the blood vessels that supply the wall traverse the
muscular layer make these areas weaker making it more likely for diverticula
to form
 As diverticula form BV separates from the intestinal wall only by
mucosa  more likely to rupture  painless rectal bleeding

o Diets low in fibre

 Diverticulitis not associated with rectal bleeding – because blood vessels become
scarred during inflammation
  It is a complication and accounts for 10-20% of symptomatic features of Meckel’s
diverticulum
Clinical: -

 Patient has LLQ pain and tenderness

 It is difficult to distinguish from appendicitis, failure to diagnose quickly can result in
perforation, peritonitis and death

Treatment: -

 It responds well to antibiotics and does NOT require surgery

 Increased fibre content.
 Failure to respond, results in abscess formation

Complications: -

 Fever, increased WBCs, increased CRP.

o Treatment – analgesics, IV fluids and antibiotics
 If perforation occurs, it results in peritonitis with/without shock
o Treatment – Hartman procedure – resect the rectosigmoid with closure of the
anal stump and formation of end colostomy
 Haemorrhage – it is sudden and painless and causes rectal bleeding
o Treatment = colonic resection, after stopping the bleeding

84) Terminal ileitis. Small bowel tumors. Crohn's disease

Terminal ileitis
 Def: -It is inflammation of the terminal part of the ileum (small intestine)
 It is normally associated with Crohn’s disease or Yersinia infection
 Signs + TXT – same as Crohn’s
Inflammatory bowel diseases: -
 They can be divided into 2 diseases: -
1. Crohn’s disease
 2. Ulcerative colitis
Crohn’s disease (regional enteritis)
 Def: - It is a granulomatous, non-caseating (w/o necrosis), transmural (entire
thickness of wall) inflammatory condition that can affect the entire thickness of the
bowel wall
 It can affect any part of the GI tract from the mouth to the anus, but most commonly
affects the end of the small intestine (ileum) and the beginning of the colon
 In 60% cases, the terminal ileum (small intestine) is involved
 Affects women more and also affects Jewish people more
Causes: -
 Infection – Mycobacterium paratuberculosis !
 Defective mucosal barrier
 Immunologic – increased autoantibodies
 Genetic – family history, affected chromosome 16q12
 Smoking, diet and food allergy
Pathology: -
 Skip lesions – Multiple areas may be involved with some parts of normal bowel
 Mesentery is thickened
 Involves all layers of bowel wall
 Ulcers – fissuring of mucosa + submucosa
 Stricture formation due to fibrosis
Clinical features: -
 Triad: - !
1. Abdominal pain
2. Diarrheal urgency (porridge like)
3. Weight loss
 Acute presentation (5%): -
o It mimics acute appendicitis with severe diarrhoea.
o Often there will be localised of diffuse peritonitis
 Chronic: -
o 1st stage: -
 Mild diarrhoea, colicky pain, fever, anaemia
 Mass in right iliac fossa which is tender, firm, non-mobile along with
recurrent perianal abscess
nd
o 2 stage: -
 Acute or chronic intestinal obstruction due to cicatrisation with
narrowing
rd
o 3 stage: -
 Fistula formation – enterocolic, enteroenteric, enterovesical,
enterocutaneous etc.
Diagnosis: -
!
 Barium meal – shows cobblestone appearance of mucosa, cicatrisation of ileum
and rose-thorn appearance of small intestine wall
 Colonoscopy – shows normal rectum with colon showing ulcers and fistula in late
cases. It also shows cobblestone appearance of colon
 Serum markers – 90% patients with Crohn’s disease have positive ASCA (anti-
saccharomyces cerevisiae antibody) and negative pANCA (perineural antineutrophil
cytoplasmic antibody)
Differential diagnosis: -
 Ulcerative colitis (only colon and rectum are affected – (large intestine)) – 98%
patients with ulcerative colitis have negative ASCA and positive pANCA !
Treatment: -
 Medical: -
o Amino salicylates e.g., sulfasalazine (control inflammation)
o Steroids e.g., prednisone – induce disease remission in initial phase
o Immunomodulators e.g., Azathioprine – inhibits the cell-mediated immunity
o Avoids NSAIDs
 Surgery: -
o Indications: -
 Done if medicine does NOT work
 there is intestinal obstruction
 fistula formation
 perforation or perianal problems
1. Ileocecal resection – 6-12 inches removed
2. Total proctocolectomy with end ileostomy – remove all colon, rectum + anus
 Indication – pt with Crohn’s of entire colon + rectum
3. Total colectomy with ileorectal anastomosis – spares rectum + anus
4. Segmental colon resection – when inflammation limited to a specific
segment of colon
Intestinal tumours
 They are rare and account for 3% of all GI tumours – even though the small intestine
accounts for 80% of the total length of the GI tract and 90% of the mucosal surface
area of the GI tract
 Reasons why it is rare: -
o Rapid transit time – 30mins-2hrs – so the mucosa is exposed to little toxins
and metabolites
o High levels of luminal IgA provide immunity
o Alkaline mucous rich luminal content is protective
 Diagnosis: -
o CT of abdomen – to assess the small intestine, lymph nodes and surrounding
organs
o Small intestine enterolysis
 ENTEROLYSIS = surgical division or removal of intestinal adhesions.
o CT angiography – to identify vascular tumours
Risk factors: -
 Crohn’s Adenocarcinoma
 Celiac lymphoma
 Peutz-Jeghers syndrome (increased risk of polyps)Adenocarcinoma
 Radiation enteritis Lymphoma
Types of intestinal tumours: -

Benign Malignant
Adenoma Primary adenocarcinoma
GI stromal tumors Lymphoma
Lipoma Carcinoid
Peutz-Jeghers syndrome GIST
Haemangioma

Great summary: -https://www.youtube.com/watch?v=qdxH_tjCTx8

https://www.youtube.com/watch?v=B5zaJqweUgI
Benign small intestine tumours: -
1. Leiomyoma (aka stromal tumors)
o It is the most common benign small intestine tumour
!
o It arises from interstitial cell of Cajal
 Cajal cells – pacemaker for contraction of smooth muscle
o CF: - Grow intramurally thus cause obstruction, bleeding
o Most commonly found in stomach, jejunum, ileum and rarely in duodenum
o Txt: - Surgical resection
2. Adenomas (15% cases)
o Def: -Benign tumors of glandular origin
o 3 types: -
 True (pre-malignant)
  Villous
 Brunner gland
o Majority in ileum, jejunum + duodenum
o Sx: - bleeding + obstruction
o Txt: - endoscopic removal /surgical resection (pancreas preserving
duodenectomy if in duodenum)
3. Lipoma
o Def: - benign tumor of fatty tissue
o Most common in ileum
o Usually occurs as a single intramural submucosal lesion
o RF: - Men in 60s
o Sx: - Bleeding + obstruction
o Txt: - excision
o No malignant potential
4. Haemangioma
o HAEMANGIOMA = is a usually benign vascular tumor derived from blood
vessel cell types
o Def: - submucosal abnormal proliferative vessels
o Jejunum most common site
o CF: - small bowel bleed
o Dx: - angiography, Technetium 99 RBC scanning or capsule endoscopy
o Txt: -
 Endoscopic sclerotherapy
 Angiographic embolization
 Resection of small bowel
 Peutz-Jeghers syndrome
o Autosomal dominant syndrome of mucocutaneous pigmentation + GI polyps
o Sx: -
 Intestinal hematomas
 Polyps affecting whole of SI + colon causing haemorrhage +
intussusception, obstruction
 Pigmented lesion of face, lips, palms and soles
o Txt: - small resection for removal; cure not possible
o Dx: - Genetic testing, family history etc
Malignant small intestine tumours
1. Adenocarcinoma – 40% cases
o It is the most common malignant small intestine tumour
o Mainly affects the duodenum and jejunum
o Can spread to lymph nodes
o RF: - Crohn’s disease, adenoma, celiac diseases
o Sx: -
 Colicky abdominal pain
  N+V
 Weight loss
 Bleeding, obstruction
 Jaundice
o Dx: -
 Capsule endoscopy
 TNM
o Treatment: -surgical resection. But it has a poor prognosis
2. Non-Hodgkin’s lymphoma – 25% cases
o Non-Hodgkin's lymphoma is a type of cancer that begins in your lymphatic
system.
o The GI tract is the most common site of extra nodal NHL
!
o The spleen, liver, lymph nodes and blood peripheral smear appear normal
o It can be divided into 2 types: -
a) B cell type (most common) – 75% cases – common in ileum
b) T cell type – has poor prognosis
o Sx: -
 Acute – obstruction/perforation peritonitis
 Chronic- malaise, weight loss, diarrhoea, ab mass
o 25% cases develop perforation
o Treatment – surgical resection and chemotherapy
o Poor prognosis
3. Carcinoid tumour – 30% cases
o Arise from enterochromaffin cells (neuroendocrine cells that aid in HCL
production by secreting histamine) in the crypts of Lieberkühn
o Tumor secretes high levels of serotonin
o Sx: - N+V, diarrhoea, obstruction, bleeding
o Txt: - surgical resection
4. GIST (Gastrointestinal Stromal Tumor)
o Def: - Mesenchymal tumor of large + ulcerated jejunum; arise from intestinal
cells of Cajal
o Sx: - melena, pain, weight loss, obstruction
o Dx: - Histochemistry; tumor markers
o Txt: - Excision/ Resection

85) Diseases of the colon - congenital. Diverticulosis. Ulcerative haemorrhagic colitis.

Tuberculosis. Polyps. Polyposis.

Sam webster anatomy: - https://www.youtube.com/watch?v=lWw8iOkGe9g

Notes: - LARGE INTESTINE osmosis notes

Diverticulosis
 DIVERTICULA (many) = abnormal outpouching of colon wall = congenital OR
acquired
 DIVERTICULUM = one pouch
 DIVERTICULOSIS = it is a condition of diverticula
 DIVERTICULITIS = it is acute inflammation of a diverticulum
 Epidemiology: -
o more common in women
o increases with age
o Diet low in fibre
 Location varies with geographical location: -
o Westernized Nations = predominately left sided diverticulosis; 95% in sigmoid
o Asia + Africa = diverticulosis is rare and usually right-sided

a) Congenital Diverticula (TRUE): -

 Distinguished from acquired be being composed of ALL layers of bowel wall

 E.g., Meckel’s Diverticulum
 Asx, but some contain gastric mucosa = ulcers

b) Acquired Diverticula (FALSE): -

 Composed of mucosa + submucosa; not all layers of wall + are pulsing in nature
o Mucosa lining of colon herniates through muscularis propria + covered by
serosa
 Pathogenesis: -
o Occurs in area with relative weakness where blood vessels penetrate the wall
 o Tunnels formed from blood vessels weaken muscle + diverticula manifest due
to increased intracolonic pressure
 Etiology: -
o Decreased fibre diet – segmental contractions of colon are more vigorous +
prolonged = increased intraluminal pressure
o Herniation of mucosa through circular muscle
o F>M; 40-50yrs
o Mainly found in sigmoid (as is the narrowest). Emerge b/w taenia coli; may
contain fecolith
o Obesity, lack of physical activity
 Risk factors: -
o advanced age
o constipation
o connective tissue disorder – Marfan’s Syn;
o hereditary
o extreme weight loss
o heavy metal consumption
 Clinical features: -
o Asx in majority
o Fatigue, decreased breathing, light headedness = due to anaemia
o Painless bloody stools
o Perforation, obstruction, constant pain in LLQ – radiates to back, left flank,
groin;
o N/V
o In intestinal obstruction, bleeding, change in bowel habits
 Diagnosis: -
o Contrast CT – imaging of choice in acute diverticulitis
o X-ray – shows thickened wall, ileus, constipation, small bowel obstruction
o Colonoscopy – rule out malignancy
o Barium enema – used when pt has strictures or tortuous sigmoid OR
colonoscopy is difficult
 CI: - Barium enema (may leak out into ab) + colonoscopy (cause
perforations in bowel wall) contraindicated in acute diverticulitis
 DDX: -
o Carcinoma, polyps
o Crohn’s, Ulcerative Colitis, Ischemic Colitis
 Txt: -
o Conservative: -
 Medical = increase fibre (fybogal)
 Abx = 7-10 days, broad spectrum, ciprofloxacin + metronidazole
  Mesalazine, probiotics
 Bowel rest = NBM, NGT (nasogastric tube)
o Surgery: -
 Indications: - peritonitis, sepsis, perforation, fistula, recurrent
 surgery after acute inflammation heals
 resection + anastomosis
 Complication: -
o phlegmon/abscess (commonly in sigmoid)
o thigh abscess, perforation, fistula
o septic thrombophlebitis
o haemorrhage

Ulcerative colitis

 Def: - Relapsing + remitting inflam disorder of colonic mucosa (confined to mucosa

+ submucosa)
 Affect rectum (proctitis) + extend to involve part of colon (left-sided colitis) or entire
colon (pancolitis)
 Never spreads proximal to ileocecal valve

Etiology: -

 10-20/100,000
 more common in developed countries
 Pt <30yrs (younger pts)
 F>M
 Increased in Whites + Jews
 Primarily affects mucosa + submucosa
 Risk of toxic megacolon in T. colon

CF: -

 Diarrhoea (+/- blood + mucus)

 Crampy ab discomfort – colicky pain
 Bowel freq = relates to severity
 ↓Appetite
 2 types: -
o Fulminant (5%) – severe form
o Chronic (95%)

Dx: -

 Bloods: FBC, WBC, ESR, CRP, LFT

 Stool: to exclude campylobacter, c. difficile, salmonella
 Ab X-ray: colonic dilation, mucosal thickening
 Colonoscopy
 Barium enema: *contraindicated when having attack

Txt: -

 Conservative: -
o sulfasalazine + mesalamine (amino salicylates)
o azathioprine (immunomodulator)
 Surgery: -
o proctocolectomy + permanent ileostomy
o ileal pouch anal anastomosis

Polyps (Benign tumors)

 Def: - A polyp is a tumour/swelling that arises from the mucosal surface and projects
into the bowel lumen beyond the surface epithelium

Types: -

1. Juvenile Polyps: -infants + young

o Pedunculated found in rectum + distal colon
o Familial tendency.
o M>F
o Polyps are vascular + secrete mucus.
o Txt: - Removed = endoscopy
2. Adenomatous Polyps: - gland-like growths that develop on the mucous membrane
that lines the large intestine
o Pedunculated; Rectum + sigmoid
o Asx – but may produce anaemia from Crohn’s colitis, Ab pain, diarrhoea
3. Villous Papilloma: - lesions that spread around circumference of bowel + secrete
copious amounts of mucus
o CF: -
 Mucus discharge = spurious diarrhoea loss of K+ = metabolic
acidosis + lethargy
  Muscle weakness, mental confusion
o Risk of malignant change
o Txt: -
 Endoscopic removal with a snare or diathermy coagulation
 Larger masses = wide excision
4. Familial Polyps: inherited autosomal dominant condition in which lots of adenomas
develop throughout the colon + rectum early in 2nd decade of life
o CF: - Asx but may be bleeding, ab pain + diarrhoea
o Risk of developing carcinoma = 100% in 15 yrs
o Tx: panproctolectomy with ileal pouch – anal anastomoses

Tuberculosis of Large Bowel

 Def: - Ulcerative TB occurs secondary to TB and occurs due to inhaling TB bacilli

 Patho: - Multiple ulcers form in the terminal ileum and the overlaying serosa is
thickened and covered in tubercules
 Clinical features: - diarrhoea, weight loss
 Diagnosis: - barium meal swallow – shows NO filling of lower cecum and ascending
colon due to narrowing of the ulcerated segment
 Treatment: - IRPES
o Resection if there is perforation or obstruction
o TB antibiotics

86) Colon cancer. Characteristics depending on the location

https://www.youtube.com/watch?
v=zFprEB0BtK0&list=PLceyvI4SWtj4m14TsPD3psSisz8OgmGp1&index=68
 Adenocarcinoma of Colon + Rectum = 3rd most common cancer after lung + breast
in women and prostate + lung in men
 F>M; hereditary
 Sporadic + familial forms
 Sigmoid + rectum affected the most
 Diameter of R. colon = 5-6cm
 L. colon = 3-4cm – to stop stools – cancer more common here
 No exact differentiation of sigmoid from rectum

Risk factors: -

 Higher in black males

 Incidence increases with age
 Hx of neoplastic polyps = 90%
 IBD (UC, Crohn’s)
 Genetic (FAP) - Familial adenomatous polyposis (FAP) – 100% risk
 Diet = decreased fibre;
 Alcohol; smoking
 Family hx – 1st degree relatives with genetic predisposition

Polyps (Benign Tumors)

 Takes 8-10yrs for polyp to transform into cancer

 Clinical: -
o polyps are asymptomatic but can ulcerate + bleed
o cause tenesmus in rectum
o if large, can cause obstruction

Types: -

1. Hyperplastic Polyp
o Found in rectum + sigmoid
o 2-5mm
o Same colour as mucosa or slightly paler
o NOT neoplasms, cannot itself increase risk of neoplasms
2. Hamartoma
o Non-neoplastic growth; in colon
o Includes: -
 Juvenile (presents as rectal bleeding + prolapse of mass + ab pain)
 Peutz-Jeghers Polyps (autosomal dom- mutation of chromosome 19)
 characterized my multiple hamartomatous polyps, melanocytic
macules of lips, buccal mucosa + digits;
 PJS increases the risk of other cancers - lung, breast, thyroid,
etc);
3. Adenomatous Polyp - Adenomas classified into: -
(i) Polypoid
 lesion may be 1-5mm
 pedunculated OR sessile
 SESSILE = A sessile polyp is a flat, abnormal tissue growth on
the lining of the large intestine (colon)
 relatively smooth but broken by clefts into multiple nodules
(ii) Villous
 velvety soft texture
 larger than polypoid
 frequently sessile
(iii) Mixed - changes in b/w polypoid + villous

Associated inherited disorders: - READ MORE IF TIME ON 2 COLUMS

 Familial Adenomatous Polyposis (FAP): -

o Def: - 100s-1000s of colon/rectal polyps
o 2nd - 3rd decade of life
o Autosomal dominant; mutation of APC (chromosome 5)
 Hereditary Non-Polyposis Colorectal Cancer (HNPCC): -
o More common than FAP
o mutation of mismatch repair genes  microsatellite instability

Pathogenesis: -

 APC genes (T. suppressor gene)  mutation genetic damage  malignancy

 Colorectal Polyps = mass projects into colon lumen
o Sessile or Pedunculated – removal via colonoscopy
 Peutz-Jeghers Synd = AD Syndrome
o characterised hamartomatous polyps + hyperpigmentation of buccal
mucosa, lip + digits

Clinical: -

1. In right-sided + caecal = bleeding

2. In left sided + sigmoid = constipation; tenesmus
3. Rectum = bleeding, mucus, change in bowel habits
 Generally: - pain, mass, change in bowel habit, weight loss, vomiting
Diagnosis: -

 Digital Rectal Examination

 Proctosigmoidoscopy
 FBC (anaemia)
 Colonoscopy can visualize lesion <5mm
 Sigmoidoscopy + Biopsy
 Tumor markers: - CA 19-9, CA 50, CA 195

DDX: -

 Adenocarcinoma
 Lymphoma
 Kaposi’s sarcoma
 Crohn’s colitis
 Diverticulosis

Staging: -TNM + Dukes classification

Duke’s Classification: -

 A = tumour in mucosa + submucosa

 B = invasion of muscle wall
 C = invasion of regional lymph nodes
o C1= metastasis to regional LN
o C2= metastasis to LN at mesenteric vessels
 D = distant spread
Aster-Coller Classification: -

 A = tumour in mucosa + submucosa

 B1= lesion involves muscularis – does NOT penetrate
 B2 = lesion penetrates muscularis to peritoneum
 C1= metastatic tumor in Lymph Nodes but tumor itself is confined in bowel wall
 C2= metastatic tumor in LN + tumor itself penetrated through entire bowel
 D = distant spread

TNM staging: -

Spread: -

 Excellent blood and lymph supply; easy to spread

 local invasion, lymphogenic, hematogenic, implantation

Treatment: -

 Initial tx = radiotherapy (to decrease size –adjuvant therapy + neoadjuvant) but if

colon cancer, can do surgery first
o Adjuvant chemo with 5-FU (Fluro uracil) + radio for Colon Cancer (for 6 mo)
o Capecitabline – metastatic cancer chemotherapy
 Surgery = regional LN are always removed
o right or left hemicolectomies, intermediate colectomy, extended right/left
hemicolectomy, subtotal/total colectomy
  Abdomino-Perineal Resection AKA MILES OPERATION - For rectal cancer (distal 1/3)
o Involves removal of anus, rectum, part of sigmoid, LN’s followed by the
remaining part of sigmoid brought out permanently as an opening
(colostomy)
 Hartmann’s Procedure – AKA proctosigmoidectomy
o Involves resection of recto-sigmoid colon with closure of anorectal stump +
formation of an endcolostomy

Characteristics depending on localisation: -

 Carcinoma of left side of colon: - lumen is smaller, most tumours here. Rectal
bleeding + change in bowel habit, tenesmus. Pain = constant
 Carcinoma of right side of colon: - faecal content = liquid. Iron deficiency anaemia,
mass, dull, nagging pain in RLQ
 Carcinoma of T. colon: - may be mistaken for carcinoma of stomach, anaemia, colic
pain
 Carcinoma of sigmoid: -papillary growth. Tenesmus. Mass. Colic pain. Mucus + blood
in faeces

87) Trauma of the abdominal wall and abdominal organs -CONTINUE FROM HERE!!

Abdominal trauma
 It is a major surgical emergency
 25% trauma patients need surgical exploration of the abdomen
 Major vessel injury e.g., IVC or mesenteric vessels can be life threatening unless
treated early
 Method of injuries: -
o Blunt trauma – spleen is most common organ involved
o Penetrating injury e.g., stab or GSW
 o Abdominal wall injury
 The following cases can be implied by the following clinical features: -
o Internal injury: -
 Distention
 Tenderness
 rebound tenderness
 fullness and dullness in the flank
o Significant hemoperitoneum – tachypnoea, hypotension, shock
General clinical features: -
 Features of shock – pallor, tachycardia, hypotension, sweating, cold periphery
 Abdominal distention
 Pain, tenderness, rebound tenderness, guarding and rigidity and dullness in the flank
on percussion
 Respiratory distress, cyanosis
 Bruising over the skin of the abdominal wall
Diagnosis: -
 Ultrasound of abdomen
o FAST (focused abdominal sonar trauma) is done – rapid, non-invasive,
portable bedside method to investigate the pericardium, splenic, hepatic and
pelvic areas
 Diagnostic peritoneal lavage – done in blunt injury.
o One litre of normal saline/Ringer lactate is infused into the peritoneal cavity
and the patient is moved in different positions, after which the fluid content
is aspirated from the abdomen for assessment
 CT scan – assesses retroperitoneum and solid organ injuries
Injuries to abdominal organs
1. Duodenal injury
 Types of injuries – it can be haematoma or lacerations
 Lacerations can cause duodenal disruption and may extend into the ampulla, distal
CBD or pancreas
 CT scan is diagnostic
 Treatment: -
o Haematoma without extension – treated conservatively with nasogastric
aspiration, antibiotics and IV fluids
o Lacerations – treated with sutures and stenting
2. Pancreatic injury
 Types of injuries – it can be contusion or severe lacerations: -
(i) Parenchymal contusion or laceration without duct disruption
(ii) Parenchymal injury with duct disruption
(iii) Complete transection of the pancreas
(iv) Massive destruction of pancreatic head
 Clinical features: -
o Pain in epigastrium
o Features of shock – pallor, tachycardia, sweating, hypotension, tachypnoea
o Increase in serum amylase level
 Diagnosis: -
o CT scan – confirms diagnosis
 Treatment: -
o Conservative – fluid management, blood transfusion, antibiotics, pain relief
o Surgery – done if there is major ductal disruption, vascular injury or extensive
injury to head of pancreas
 Distal pancreatectomy
 Whipple operation or total pancreatectomy – last resort
3. Small intestine injury
 Types of injuries – it can be blunt injury or stab injury
 Clinical features: - !
o London’s sign – there is pattern bruising over the abdominal wall which
means small intestine injury and its site
o Monk’s localising zones in the abdomen – shows the location of the small
intestine injury
 Diagnosis: -
o Plain x-ray of abdomen – shows gas under abdomen with ground-glass
appearance
o Ultrasound of abdomen
 Treatment: -
o Laparotomy and closure of perforation if it is small
o Resection and anastomosis – done in case of extensive injury or multiple
injuries
4. Liver injury
 Types of injuries: -
(i) Subcapsular haematoma
(ii) Lacerations
(iii) Deeper injuries
(iv) Lacerations with disruption of hepatic lobes or segments
 Clinical features: -
o Features of shock due to severe bleeding – pallor, hypotension, tachycardia,
sweating
o Abdominal distention with dull flank, guarding, tenderness and rigidity
o Rupture of right lobe is more common than rupture of left lobe and results
in hemoperitoneum
o Bile leak from the injured site – can lead to biliary peritonitis
 Diagnosis: -
o Chest x-ray to look for rib fractures
 o Ultrasound of abdomen
o Diagnostic
 Treatment: -
o IV fluids, blood transfusion
o Factor VII – it is very effective and makes INR normal (but it is very expensive)
o Specific treatment: -
 Blood transfusions
 Small liver tears are sutured with vicarly
 Large tear – deep sutures, push, plug, pack (direct compression, plug
the deep track injuries using a silicone tube and pack the wound) !
 Liver resection – NOT usually done for injuries
 Pringle manoeuvre – compress
the porta near the foramen
Winslow for 30 min to control
bleeding
 The foramen of Winslow
is the only natural
communication between
the greater peritoneal
cavity and the lesser sac.
 Aka epiploic foramen or
the omental foramen
 The Pringle manoeuvre is a
procedure to stop the liver's blood
supply during a liver surgery. A
clamp is applied over the hepatic
vascular pedicle, the channel that
contains the hepatic duct, hepatic
artery and the portal vein.
Hepato-duodenal lig = hepatic duct + hep artery + portal vein
5. Spleen injury (ruptured spleen)
 Types of injury: -
1. Splenic subcapsular haematoma
2. Clean incised wound over the surface – can be
treated by splenorrhaphy
3. Lacerated wound
4. Splenic hilar injury – causes torrential
haemorrhage and may cause death. Emergency
splenectomy is done
5. Splenic injury associated with other injuries
e.g., left kidney, tail of pancreas, left lung,
diaphragm, left colon
 Clinical features: -
 o Pain, tenderness and abdominal rigidity in upper left quadrant
o Balance’s sign – left sided abdominal dullness that will NOT shift
o Kehr’s sign – pain in left shoulder 15 minutes after foot end elevation
o Features of shock – pallor, tachycardia, restlessness, hypotension
 Diagnosis: -
o Ultrasound of abdomen – test of choice!
o CT scan – shows splenic injury and type
 Treatment: -
o Initial treatment – central venous line for perfusion and monitoring,
antibiotics, blood transfusion, nasogastric tube aspiration
o Surgery
 Emergency splenectomy – done for rapid control of bleeding
 Partial splenectomy
 Splenorrhaphy – spleen is repaired and salvaged by suturing the
wound carefully
6. Renal injury
 It is usually treated conservatively
 Surgery is done if there is hilar injury, progressive bleeding or failure of the
conservative treatment

88) Multiple and combined injuries

Types of trauma injuries: -

1. MONOTRAUMA = involves only one anatomical compartment or organ e.g., just the !
liver or just the skin of the hand
2. MULTIPLE TRAUMA = involves 2 organs from different anatomical compartments
e.g., chest and abdominal wall
3. POLYTRAUMA = involves three different anatomical compartments e.g., head,
pelvis, lungs
4. SIMULTANEOUS/COEXISTING TRAUMA = involves more than one organ from the
same compartment e.g., heart and lungs
5. COMBINED TRAUMA = involves more than one mechanism of trauma e.g., a
mechanical and a chemical trauma OR it can involve trauma from burns and/or
radiation exposure with crush trauma
Polytrauma
 POLYTRAUMA involves multiple injuries, which are typically complex and at least
one of the injuries is life-threatening and requires immediate care
 It differs from general multiple injuries in a patient, as these are often not severe or
life threatening
 It often has long lasting effects on the patient and can result in physical, cognitive,
psychological or psychosocial impairments and disability
 It is mainly caused by critical accidents and is especially common in the military as a
result of combat
 Due to the severity of injuries, immediate emergency care is crucial, as mortality risk
is very high.
o Most deaths occur within the first hour after an injury.
o However, in some instances, there is nothing that can be done medically to
treat the condition
 The next crucial stage occurs between 1 – 4 hours after the accident and is often
referred to as the “golden hour” and it is often when most of the emergency
treatment occurs. !
o During this stage, the most common cause of death is from hypovolemic
shock.
o Once a patient passes through this stage and is stabilised, the individual’s
chance of survival increases greatly
 However, the patient is still at risk of developing complications or succumbing to
multiple organ failures. This can occur within the first few weeks of recovery
 Treatment: -
o Due to the nature of polytrauma and the risks involved throughout the
course of treatment, you must take a long-term approach to treatment and
care
1) Initial treatment involves emergency treatment and management and occurs
within the first few hours of the accident.
 This stage is used to treat and manage any of the immediate, life-
threatening conditions
2) The second stage of treatment is called acute care and involves care during
the first few weeks of recovery.
 During this time, the patient is hospitalized and other injuries are
treated.
 This period is also used to provide further treatment for the critical
injuries and ensure that the patient does NOT develop further
complications
3) The final stage of care extends beyond the initial few weeks, and may
continue throughout the duration of the patient’s life.
 Care during this stage focuses on long-term injuries and disabilities
such as traumatic brain injury or musculoskeletal injuries that need
extensive therapy and recovery time
Military polytrauma
 It is often due to blast trauma and can result in the following injuries: -
!
1) Auditory – tympanic membrane rupture, cochlear damage, hearing loss,
distorted hearing, tinnitus
2) Eye, orbit face – perforated globe, air embolism, fractures
3) Respiratory – blast lung, haemothorax, pneumothorax, pulmonary contusion
and haemorrhage, aspiration pneumonia, sepsis
 4) Digestive – bowel perforation, haemorrhage, ruptured liver or spleen, sepsis,
rectal bleeding
5) Circulatory – cardiac contusion, myocardial infarction from air embolism,
shock, peripheral vascular injury
6) CNS – concussion, closed or open brain injury, haemorrhage, edema, stroke,
small blood vessel rupture, spinal cord injury
7) Extremity – traumatic amputation, fractures, crush injuries, burns, cuts,
lacerations
8) Emotional – PTSD, survivors’ guilt, post-concussion syndrome, depression
 The most common injury in the military due to blast trauma is traumatic brain
injury e.g., epidural or subdural haematoma subarachnoid haemorrhage, brain
contusion etc.
Evaluations and treatment: -
 Glasgow coma scale is used in the 48hrs to evaluate the severity of traumatic brain
injury
 Skull and neck x-rays are used to check for bone fractures and spinal instability in
patients with mild to moderate injuries
 CT scan can be used to identify any skull bone fractures, check for haemorrhage,
hematomas, contusions, brain tissue swelling and tumours
Common injuries: -
 Skull fracture
o Depressed skull fracture – caused by pieces of broken skull pressing into the
brain tissue
o Penetrating skull fracture – caused by something piercing the skull e.g.,
bullet, knife
 Contusion – it is bruising of the brain tissue and can occur due to skull fracture or
when the brain shakes back and forth within the skull (countercoup)
 Diffuse axonal injury (shearing)
o Caused by countercoup and is characterised by damage to neurons and the !
subsequent loss of connections among them.
o Once this occurs, there is the potential for the breakdown of communication
among all neurons in the brain
 Haematoma
o It occurs due to damage of one of the major blood vessels in the head
o It can be divided into 3 types: -
1. Epidural Hematoma – bleeding occurs between the skull and the
dura
2. Subdural Hematoma – the blood is confined between the dura and
the arachnoid membrane
3. Intracerebral Hematoma – bleeding occurs within the brain itself
 ANOXIA = injury occurs as a result of complete lack of oxygen to the organ’s tissues.
While there may still be blood flow to the tissues, there is NO oxygen present
  HYPOXIA = it is similar to anoxia in that there is a lack of oxygen to the organ’s
tissues, however in hypoxia, there is minimal oxygen present

89) Intestinal obstruction - classification, pathophysiological mechanisms

https://www.youtube.com/watch?
v=PDpmtktLlpo&list=PLceyvI4SWtj4m14TsPD3psSisz8OgmGp1&index=70

 Def: - GI luminal contents prevented from passing distally due to mechanical

occlusion or paralysis of intestinal muscles

Classification: - !!!!

 Mechanical (Adynamic)
1. Obstruction
(i) Intraluminal (in lumen)– foreign bodies, gall stone, meconium
(ii) Extraluminal (outside wall) compressive – Adhesions, hernia, abscess
(iii) Intramural (in wall)- Tumors, Crohn’s, strictures
(iv) Pseudo obstruction (Due to NO2 – no mechanical cause)
2. Strangulation – Blood supply is impaired – necrosis after 6 hrs)
 Volvulus
 Intussusception
 Incarceration of hernia
3. Adhesive (common following post OP) – causes partial obstruction
 B/w Bowel loops
 B/w Large Intestine
 B/w small intestine
 Dynamic
1. Spastic
2. Paralytic – botulism toxin

Simple or Strangulated Obstruction: -

 Simple: mechanical blockage of flow of bowel contents w/o compromising viability

of intestinal wall
 Strangulated: usually involves a closed-loop obstruction in which the vascular supply
to a segment of intestine is compromised
o Therefore, can lead to infarction
o Assoc. with increased morbidity + mortality therefore important to
acknowledge signs: - Increased HR, fever, leucocytosis, constant non-
cramping Ab pain

Etiology: -
 Intraluminal – foreign bodies, gall stones, meconium
 Intramural – tumours, Crohn’s, strictures
 Extra-luminal – adhesions, hernia’s, carcinomas, abscess, sup mesenteric artery
syndrome
 75% of cases are due to intra-abdominal adhesions from previous abdominal
surgery

Pathophysiology: -

 Early on in the case of obstruction - increased intestinal motility + contractile

activity in an attempt to propel contents post-obstruction thus increase in peristalsis
= diarrhoea
 As obstruction progresses – (edema of wall) bowel dilates thus H2O + electrolytes
accumulate intraluminally + in bowel wall therefore loss of fluids – dehydration +
hypovolemia
o In case of proximal obstruction loss of fluid = hypovolemia, hypokalaemia,
metabolic alkalosis; Shock may occur
 As intraluminal pressure increases in bowel can lead to decrease in mucosal
blood flow therefore if bowel becomes twisted there is increased risk of ischaemia
bowel perforation peritonitis
 Rapid proliferation of bacteria: Normally, jejunum + proximal ileum are stable due to
peristalsis and interdigestive migrating myoelectrical complex but in bowel
obstruction = contaminated by E. coli + klebsiella  this can lead to sepsis

Clinical: -

 4 cardinal features: -
1. Colicky abdominal pain – usually 1st symptom
2. Distention
3. Absolute constipation (no feces of flatulence)
4. Vomiting – early in high obstruction, later in low obstruction
 Severe dehydration
 Hypokalaemia (body trying to preserve Na)
 Tachycardia, hypotension, hypovolemic shock

Diagnosis: -

 4 D’s: -
1. Distinguish mechanical obstruction from ileus
2. Determine etiology of obstruction
3. Discriminate partial from complete
4. Discriminate simple from strangulated
 Erect X-ray – to determine where gas is
 Contrast radiograph with gastrograffin – establish degree of obstruction
 o NB: - in dehydrated pt, can exacerbate dehydration. Is hyperosmolar – can
stimulate peristalsis
 CT – definitive dx to determine cause
 Lab test – electrolytes, urea (shows dehydration), FBC

DDX: -

 Ileus
 Appendicitis
 Gastroenteritis

Treatment: -

 Fluids + electrolytes replacement (Ringer Lactate solution) – need KCl

 Monitor vitals + urine output
 NGT (nasogastric tube decompression) to decrease vomiting + decrease distention +
decrease risk of aspiration
 Analgesia, antibiotics, antiemesis
 Operative tx: -Generally surgery is mandatory if small bowel obstruction
o Rectify underlying cause: -
 Henia is reduced + repair hernia orifice
 If secondary to adhesions – those are cut
 If tumour – bypass
 Placement of colostomy
 If Crohn’s – tx = conservatively OR chronic bowel resection
o Inspect affected bowel for non-viability
o Resection of non-viable bowel

90) Strangulation ileus. Volvulus of sigmoid colon

Selfless medicosis - volvulus

Strangulation Ileus

 When blood supply of the intestine is compromised

Pathophysiology: -

 Strangulation Ileus occurs due to adhesion or when loop of distended bowel twists
on mesenteric pedicle  arterial occlusion leads to bowel ischaemia + necrosis 
if untreated perforation, peritonitis, death
 Strangulation causes loss of blood + plasma into strangulated segment luminal
fluids + bloody peritoneal fluids are considered to be toxic peritoneum absorbs
toxic material causing systemic effects
 Obstruction of Large Bowel produces less fluid + electrolyte disturbances than small
bowel
 Colon Obstruction can act like closed-loop due to incompetent ileocecal valve
 Cecum is the most likely site for perforation

Etiology: -

 Predisposing factors = anatomical features (Mekel’s diverticulum, long cecum etc) +

previous surgery
 Provocative factors = rough food + low fluid intake
o Direct pressure on bowel = hernias, adhesions
o Interrupted mesenteric blood flow = volvulus. Intussusception
o Increased intraluminal pressure = closed loop obstruction

Classification = Melnikov Classification

 Extracorporeal Adhesion (peritoneum folds, tumor, enlarged organ, nodes)

 Intramural = tumor of intestines, stenosis, invaginations
 Organs = foreign body, stones

Diagnosis: -

 Barium enema – Bird beak sign

 Physical examination for mass
 Tenderness, guarding = peritonitis
 Ab auscultation (Mechanical Obstruction – series of increasing bowel sounds)

Clinical: -

 Signs of mechanical obstruction

 Ab tenderness
 Constant severe pain (strangulation + peritonitis)
 Crampy pain in proximal obstruction
 Fever, increased HR
 Leucocytosis
 Constipation, failure to pass flatus

Treatment: -

 NG tube to clear out stomach

 Fluids begin with IV NaCl solution + later KCl, blood + plasma (in case of shock)
 Abx (especially if strangulation is suspected)
 Surgery to relieve strangulation = operative reduction or excision depending on cause
+ placement of colostomy

DDX: -

 Ascites (has fluid wave, shifting dullness, fullness in flank)

Volvulus of sigmoid colon

 VOLVULUS = when a loop of intestine twists around itself + the mesentery that
supports it  therefore leads to partial/complete bowel obstruction

 Any portion of large bowel can twist where it is attached to mesentery

 Sigmoid is most common site – due to communication with a long mesentery with
narrow parietal attachment

Risk factors: -

 Chronic constipation
 Aging, + *high fibre diet*,
 Pregnancy
 More common in males

Clinical: -Very similar to distal colon cancer

 Sudden Ab pain
 Constipation
 Ab distention
 Rebound tenderness
 Increased HR

Diagnosis: -

 Radiographs – enable prompt dx

o Coffee bean or Omega sign (2nd pic)
o CT shows dilated sigmoid colon with Whirl Sign from twisting mesentery
 WHIRL SIGN = represents the superior mesenteric artery at the centre
surrounded by bowel loops
  Sigmoidoscopy – can be therapeutic initially as well

Treatment: -

 Fluid + electrolyte replacement

 Endoscopic Distortion = For obstruction not so massive decompression using rectal
tube (stent) via sigmoidoscope (not for patients who may have necrosis); If success
elective OP should follow as high rick of occurrence
 Sigmoidopexy = Fix sigmoid to lateral wall; high risk of occurrence though
 Surgery should immediately follow
o HARTMANN OP = sigmoid colectomy with closure of rectum + end colostomy

91) Obstructive ileus

Paralytic ileus
 Def: -It is a state in which the intestines fail to transmit peristalsis due to
neuromuscular mechanism i.e., Auerbach’s and Meissner’s plexus
Causes: -
 Post-operative – usually occurs 3-5 days after an operation
 Spinal fracture
 Retroperitoneal hemorrhage
 Peritonitis
 Trauma
 Endocrine (e.g., diabetes mellitus, hypothyroidism, porphyria, uremia)
 Vascular (e.g., mesenteric infarct)
 Inflammation of intra-abdominal organs (e.g., appendicitis, cholecystitis) and
peritonitis
 Medication (e.g., anticholinergics, opioids, antidepressants)
 Electrolyte imbalances (especially hypokalemia) contribute to paralytic ileus by
interfering with the normal ionic movements during smooth muscle contraction
Pathophysiology: -
 Activation of α and β-receptors due to intestinal stress → arrested peristalsis→
bowel wall distention → progresses as detailed above in mechanical bowel
obstruction
 Clinical features: -
 Similar to mechanical obstruction
 Abdomen distention
!
 Steady pain (not colicky like in mechanical obstruction)
 Patient may pass diarrhea
 Absence of bowel sounds
Differential diagnosis: -
 X-ray = Gas throughout intestine inc. colon
 X-ray with contrast = barium – helps distinguish ileum from mechanical obstruction
Treatment: -
 Correct metabolic + electrolyte abnormalities – NaCl stimulates peristalsis
 Electro stimulation with probes on ant ab wall
 Enema as last line
 Laparotomy to exclude hidden causes + allows more bowel decompression to be
done

92) Intussusception

Selfless medicosis - Intussusception video

 INTUSSUSCEPTION = “telescoping” of one portion of intestine into the other

 Most common cause of intestinal obstruction in early childhood (6-36 mnths)
 Ileocecal junction most common location due to developed lymphatic system,
narrow lumen, poor fixation

Etiology: -

 In paediatrics cases – idiopathic (6 months infant at risk due to change from milk –
food)
o Young children always susceptible to infection hyperplasia of Peyer’s
patches edematous increased risk of intussusception
o M>F
 In older children + adults = RARE
 Is associated with: Meckel’s diverticulum, polyps, intestinal neoplasm
 Can occur after ab surgery

Pathogenesis: -

 Believed to be due to imbalance in longitudinal forces along intestinal wall

 Imbalance can be caused by: -
o A mass acting as a lead point (polyp, tumor, lipomata, Meckel’s Diverticulum)
o A lead point could be an enlarged lymph node (Peyer’s Patch)
o By disorganized pattern of peristalsis
 Telescoping of lumen into lumen of intestine distal to it  drags mesentery along
obstruction and impaired lymphatic drainage  increase pressure  vascular
compromise  ischemia of interssusceptum  infarcts  bloody stool  trans
mural necrosis & perforation

Clinical: -

 Triad: -
o Colicky abdominal pain (due to some level of obstruction)
o Red currant jelly stool (mucus mixed with blood due to some perforation)
o Palpable ab mass (sausage shaped)
 Hypovolemic shock suggests ischemia or necrosis*

Diagnosis: -

 History
 Right iliac fossa empty
 X-ray shows a mass
 Ab.US = can show *Target Sign* or Doughnut Sign of intussuscepted layers of bowel

 Barium enema – shows a claw sign

o Contrast enema contraindicated in presence of free intra-ab air = peritonitis

DDX: -

 Appendicitis, gastroenteritis, pyloric stenosis

Treatment: -
  Non-operative: -
o Correct hypovolemia + electrolytes and then reduction
o Hydrostatic reduction by enema using contrast or air is diagnostic +
therapeutic
 Contraindicated if in S.I. – as enema won’t reach there OR in case of
peritonitis + hypovolemic shock
 Success in reduction ≈ 80%
o In case of recurrence – another hydrostatic reduction attempt should be done
– if fails, then surgery
o Fluids + abx (in case of sepsis)
 Operative: -
o Indications: -Unstable pt; peritonitis; ischemia/perforation; tumor or other
underlying pathology; failure to reduce with hydrostatic pressure
o Laparoscopy to confirm dx + tx – avoids large incision
o Transverse incision on right side of abdomen, intussusception reduced by
squeezing the mass retrograde from distally to proximally until completely
reduced
o Bowel resection if can’t surgically reduce

93) Arterial embolism and thrombosis of mesenteric vessels

SMA syndrome- medicosis perfectionalis; Zero to finals – more to point and notes
Mesenteric vessel ischemia
 ACUTE MESENTERIC ISCHEMIA is a group of disorders characterized by sudden stop
of blood supply to the intestines, due to embolism, or thrombosis
 It results in ischemia and necrosis
 The superior mesenteric artery is affected more commonly than the inferior
!
mesenteric artery
Causes: -
 Embolism – 50% cases
o Sources include mural infarct, atheroma from aorta or aneurysm,
endocarditis vegetations, left atrial myxoma
 MURAL THROMBI = are thrombi that attach to the wall of a blood
vessel and cardiac chamber
o Chronic cases are associated with atherosclerotic lesions of celiac, or SMA or
IMA
 Thrombosis
o It may block the origin of the superior mesenteric artery and can cause
ischemia of the full length of the small intestine – it may be life threatening
o It may be due to atherosclerosis, aortic aneurysm
 Non-occlusive
 o It can be due to hypotension or hypoperfusion
o It can also be due to vasospasm due to shock
Types: - !!!!

1. Acute – sloughing of intestinal mucosa occurs in 3 hours. Infarction of entire

thickness of bowel occurs in 6 hours
2. Chronic – it is a slow and gradual process
3. Extensive – involved large segment of the bowel (small or large intestine)
4. Localized
Pathology: - !!!!

 The bowel and mesentery become friable, edematous, discolored and collected
with fluid and blood
 Once gangrene occurs perforation can lead to peritonitis
 Acute mesenteric ischemia: -
o If blood flow to the bowel wall is completely blocked bowel infarction will
occur
o Intestinal bacteria can also enter the bloodstream and abdominal cavity
resulting in sepsis, haemodynamic collapse and multiorgan system failure
 Chronic mesenteric ischemia: -
o There is slow stenosis of 2 or more main arteries of the intestines, which
results in post-prandial mismatch between the splanchnic blood flow and
intestinal blood flow (cause of post-prandial pain)
o Collaterals form between the arteries to compensate for the blood flow
Clinical features: -!!!!

 Acute
o Abdominal pain that is out of proportion in relation to tenderness
o Nausea, vomiting
!
o Persistent vomiting, bloody diarrhea, followed by shock and toxicity
o Initially the abdomen is soft, but later tenderness develops, rebound
tenderness, distention, guarding and rigidity
o Bloody diarrhea – confirmed by rectal examination
 Chronic
o Post-prandial abdominal pain – most important (pain after eating)
o Abdominal angina – recurrent colicky pain
o Bloody diarrhea – confirmed by rectal examination
Diagnosis: -
 Plain x-ray in erect posture
 CT scan – rule out atherosclerosis
 Angiogram or CT angiogram – shows wall thickening, distended bowel loops, air-fluid
levels
 Blood tests – total count is increased with a decrease in hemoglobin
 Treatment: -
 Embolectomy (removal of blood clot)
 Mesenteric artery bypass
 Emergency laparotomy – the block is identified and removed and the vessel is
opened and thus the bowel is repercussed
 If patient has arrived after 24-48 hours, gangrene may have already occurred. In this
case resection and anastomosis is done !
 If the patient arrives within 6 hours it is possible to prevent gangrene and salvage
the bowel
 In acute condition, thrombolysis using streptokinase is done
 Chronic mesenteric arterial ischemia – surgical revascularization using
aortomesenteric bypass graft and mesenteric endarterectomy

94) Venous thrombosis of the mesenteric vessels

Anatomy – DO THIS AGAIN!!!!

 Superior mesenteric vein
o The superior mesenteric vein arises from the mesentery of the small
intestine and drains blood from the terminal ileum, cecum and vermiform
appendix.
o It terminates by uniting with the splenic vein forming the portal vein
o The portal vein then takes the nutrients absorbed from the intestine to the
liver, where the nutrients are processes and prepared to be distributed
throughout the body
o Main function of the SMV is to drain blood from the distal GI tract – small
intestine
 Inferior mesenteric vein
o The inferior mesenteric vein drains blood from the large intestine and
rectum
o It terminates by uniting with the splenic vein which then unites with the
SMV forms the portal vein
o Main function is to drain blood from the hindgut of the GI tract – colon and
rectum
Venous thrombosis of mesenteric vessels
 MESENTERIC VEIN THROMBOSIS = is a blood clot in one or more of the major veins
that drain blood from the intestines
 There are 3 veins that carry blood from the intestines: -
1. superior mesenteric veins
2. Inferior mesenteric vein
3. splenic vein
 These veins deliver nutrient-rich blood to the liver through the hepatic portal vein
 Superior mesenteric vein affected more commonly (95% cases) – thus affecting
ileum, jejunum or colon
Causes: -
 The exact cause is unknown but can be due to diseases that cause swelling of the
tissues surrounding the veins
o E.g., appendicitis, diverticulitis, inflammatory bowel disease, abdominal
surgery or trauma, pancreatitis, abdominal tumour
 Birth control pills
 Predisposition to clotting (clotting disorders) e.g., thrombophilia, anti-thrombin III
deficiency, sickle cell disease
 Smoking increases risk of blood clots
Pathology: -!!!!

 As blood flow stagnates increased venous pressure  leads to efflux of fluid into
tissues causing profound bowel wall edema which can cause submucosal
haemorrhage
 If venous return from the bowel wall is completely blocked bowel infarction will
occur
 Intestinal bacteria can also enter the bloodstream and abdominal cavity resulting in:
o Sepsis
o Haemodynamic collapse and
o Multiorgan system failure
Types: -
 It can be divided into 3 types: -
1. Acute – caused by new-onset symptomatic thrombosis of SMV or its !
branches, with no collateral veins formed
2. Subacute – ischemia occurs, but enough collaterals are formed to allow
blood flow recovery
3. Chronic MVT – dilated collateral vessels which can bleed due to high venous
pressures
Clinical features: -
 Abdominal pain, bloating, constipation, fever, vomiting, nausea
 Lower GI bleeding, bloody stools/diarrhoea
 Septic shock
Diagnosis: -
 CT scan, MRI, ultrasound
 Angiogram
Treatment: -
 Blood thinners e.g., heparin (main treatment)
!
 Thrombectomy
 In acute condition, thrombolysis using streptokinase is done
  If severe infection like peritonitis occurs intestines are removed surgically and
ileostomy or colostomy is inserted
 Chronic mesenteric vein thrombosis – treated with: -
o anticoagulation or propranolol
o esophageal variceal banding

95) Non-occlusive disorders of the mesenteric circulation

 Def: -It is acute mesenteric ischemia in the absence of obstruction of the mesenteric
vessels
 It is a common complication of patients with acute circulatory failure and thus !
accounts for most deaths in ICU
 It results in ischemia and necrosis
 The superior mesenteric artery is affected more commonly than the inferior
mesenteric artery
 Risk factors: -
o Age over 50
o History of acute myocardial infarction, congestive heart failure, aortic
insufficiency
Causes: -
 Mesenteric artery vasoconstriction (most common)
 Vasoconstricting drugs/pressor drugs e.g., norepinephrine, epinephrine,
vasopressin
 It can be due to systemic hypotension or hypoperfusion – due to chronic heart
failure or myocardial infarction
 Blunt abdominal trauma
 It can also be due to vasospasm due to shock or drugs e.g., amphetamines, cocaine
Pathophysiology: -
 Low blood flow states result in altered splanchnic blood flow which results in
poor mucosal perfusion, without an actual obstruction of the vessels
o 'SPLANCHNIC CIRCULATION' = describes the blood flow to the abdominal
gastrointestinal organs including the stomach, liver, spleen, pancreas, small
intestine, and large intestine.
Clinical features: -
 It is common in patients who are critically ill or in ICU
 It is associated with other comorbidities e.g., congestive heart failure, arteriovascular
disease
 Non-specific symptoms which can be fatal
 Clinical GI symptoms – abdominal pain, feeding intolerance, GI hemorrhage, diarrhea
 Biological features of tissue ischemia – elevated arterial lactate levels !
 Increased serum levels of lactate dehydrogenase and transaminases – feature of
cell lysis
 Diagnosis: -
 CT – shows bowel ischemia in watershed areas
 CT angiography – shows mesenteric arterial narrowing and decreased superior
mesenteric artery caliber
Treatment: -
 Vasodilators e.g., papaverine or prostaglandin E1 !
 Hemodynamic support and monitoring
 Anti-coagulants e.g heparin or warfarin
 Resect necrotic bowel loops

96) Peritonitis - etiopathogenesis, forms, treatment

Anatomy - DO THIS AGAIN!!!

 Peritoneal cavity – it is covered by a single layer of mesothelial cells on connective
tissue
 The PERITONEUM is a continuous, semi-permeable and transparent membrane
lining the abdominal cavity
 The peritoneum consists of 2 layers: -
1. Parietal peritoneum – covers the abdominal cavity, including the abdominal
wall, diaphragm and pelvis. It is innervated by somatic and visceral nerves
2. Visceral peritoneum – covers all intraperitoneal viscera. It is relatively
insensitive and only has afferent innervation from ANS
 The biliary tract and mesentery of the small bowel have greater innervation than the
small intestine, thus pain from the gallbladder and common ducts is more
accurately localized than from the small intestine
 Intraperitoneal organs – stomach, spleen, liver (visceral peritoneal)
 Retroperitoneal organs
o Primary – esophagus, rectum, kidneys (parietal peritoneum)
o Secondary – colon (ascending and descending part), aorta, ureters,
duodenum, pancreas (parietal peritoneum)
 MESENTERY = it is a double layer of visceral peritoneum, which connects the
intraperitoneal organs to the posterior abdominal wall and provides a pathway for
nerves, blood vessels and lymphatics
 OMENTUM = it is sheets of visceral peritoneum that extends from the stomach and
proximal part of the duodenum to the other abdominal organs
o Greater omentum – has 4 layers. The greater curvature is the proximal part
of the duodenum
o Lesser omentum – has 2 layers. The lesser curvature is proximal part of the
duodenum to the liver
Classification: -
 Anatomical location (what the professor wants)
 o Localized
o Diffuse – more than 2 zones
o Total
 Etiological: -
o Acute
 Spontaneous
 Infection
o Secondary
 Chemical sepsis
 Trauma
 Drug induced
o Chronic
 Foreign body
 Cancerous
 Peritoneal exudate: -
o Bile
o Blood
o Meconium
o Chyle
o Urine
 Pathological classification: -
o Fibrinous
o Serofibrinous
o Purulent
o Hemorrhagic
o Anaerobic/gangrene

Peritonitis
 Def: - Peritonitis is inflammation of the parietal and serosal layer of the peritoneum,
either due to bacterial infection or due to chemicals e.g., gastric or bile
 Normally the peritoneum has 100ml fluid, but this increases during peritonitis due to
transudate containing polymorphonuclear leucocytes
 The peritoneal cavity is normally sterile. However, in perforated duodenal or gastric
!
ulcers, the peritoneal cavity becomes infected, resulting in bacterial peritonitis
 Bacteria causing peritonitis: -
o Bacteria from GI tract – E. coli, Streptococci, Staphylococcus, Klebsiella
o Bacteria NOT from GI tract – Pneumococcus (from fallopian tubes),
Chlamydia, Mycobacterium
Causes/Mode of infection: -
 Perforation of GI tract – duodenal ulcer, gastric ulcer, enteric ulcer or colonic ulcer,
Meckel’s diverticulum perforation
 Surgery
 Penetrating blunt trauma
 Appendicitis, diverticulitis
 Via fallopian tubes
 Via blood spread – in septicaemia
Types: -
 It can be divided into 3 types: -
1. Primary (1% cases) – due to bacterial infection without an apparent
intrabdominal source of infection e.g., bacterial infection of ascitic fluid
2. Secondary (most common) – due to bowel perforation
3. Tertiary – seen in post-operative patients (after laparotomy) due to leak or
bowel necrosis
 It can be divided into 3 types: -
1. Localized – it may resolve by proper therapy. However, if it progresses, it
may form generalized peritonitis. It may form abscess like pelvic, subphrenic
etc.
2. Generalized – NOT treated surgically and has near 100% mortality rate
3. Total – inflammation of all abdominal cavity
Stages of peritonitis: -
1. Initial (reactive) stage – increased bowel sounds. Up to 24 hours
2. Toxic stage – 24-72 hours
3. Terminal stage – more than 72 hours. No pain due to necrosis
Primary peritonitis
 It is commonly due to pneumococci, streptococci, haemophilus
 There is NO documented source of infection. !
o Infection usually spreads from the lower genitals though the fallopian tubes,
or from upper respiratory tract infection
 It is common in young girls between 3-9 years old and is uncommon after 10 years
of age
 Causes/risk factors: -
o Malnourished child
o Child with nephritis
o Cirrhotic patients with ascites – 30% patients with ascites in cirrhosis will
develop spontaneous bacterial peritonitis. In 90% cases the peritonitis is due
to E. coli
o Chlamydia infection
 Treatment: -
o Mortality is high!
o Diagnostic tapping, tube peritoneal drainage
o Broad spectrum antibiotics – combination of aminoglycosides, cephalosporins
and metronidazole
o Local instillation of antibiotics into the peritoneal cavity – for quick and
effective results
Secondary peritonitis
 It is secondary to any bowel or visceral pathology e.g., appendicitis, perforation
 The cause is bacterial contamination of a known source e.g., perforation of GI tract
 E. coli is responsible in 70% cases
 Causes: -
o Duodenal perforation
o Burst appendicitis
Tertiary peritonitis
 It occurs after any abdominal surgeries, and is defined as persistent or recurrent
intra-abdominal infection after an adequate treatment for primary or secondary
peritonitis
 It usually occurs within 48 hours of surgery
 It is very common in immunosuppressed patients due to ineffective peritoneal host
defenses against microbes
 The infection occurs due to – E. faecalis, S. epidermidis etc.
 Treatment: -
o Mortality rate is more than 50%
o Aggressive antibiotic therapy, antifungal therapy
o Exploration of the abdomen and thorough wash
o Colostomy/ileostomy
o Platelet transfusions, FFP and packed cells
o Ventilator and ICU are often needed
 Complications – DIC, septicemia, hemorrhage
Chemical peritonitis
 It is peritoneal inflammation due to substances other than bacteria. Most severe and
common form is of perforated peptic ulcer
Chronic (sclerosing peritonitis)
!
 It is characterized by dense adhesions, especially between loops of small bowel
 Patients have subacute small bowel obstruction or acute-on-chronic small bowel
obstruction
 Treatment – surgical stripping of fibrous tissue from the underlying intestine – but
the surgery is long
 Intrabdominal fistulas can form
Pathogenesis: - !!!!

 Lots of fluid is secreted into the peritoneal cavity which is infected, containing
bacteria and toxins, which results in shock and toxaemia and its effects
 Fibrinogen forms fibrin which attempts to localise the infection and results in the
bowel becoming adhered to each other with fluid collecting between the loops
 The peritoneum becomes thick, edematous and loses its glistening appearance and
there may also be pus present
 The peritoneal cavity is normal sterile. However, in perforated duodenal or gastric
ulcers, the peritoneal cavity becomes infected, resulting in bacterial peritonitis
Clinical features: -
 Sudden onset of severe abdominal pain, initially localised then spreading
throughout abdomen !
 Tenderness – initially localised but then becomes diffused
 Blumberg’s sign – rebound tenderness at McBurney’s point in right iliac fossa (Mc
Burney’s point is a point of tenderness located one third of the way between an
imaginary line drawn between the umbilicus and the hip)
 Guarding and rigidity
 Abdominal distention with silent abdomen. Absent bowel sounds due to paralytic
ileus
 Fever may be absent – due to loss of pyogenic reaction.
 The total blood count may be very low in severe peritonitis
 Perforated peptic ulcer – acute epigastric pain, radiating to right lower quadrant
 Acute cholecystitis – has pain for several hours in right upper quadrant, which is then
referred to right scapula or shoulder
Diagnosis: -
 Chest x-ray in standing position with abdomen – shows ground glass appearance of
the abdomen with gas under the diaphragm suggesting perforation
 Ultrasound of abdomen – shows fluid in the abdominal cavity
 CT scan – confirms the cause or rules out conditions such as pancreatitis. Also shows
bowel ischemia, gangrene, perforation and amount of pus/fluid in the peritoneal
cavity
 MRI – shows abdominal abscess
 Serum amylase – 4 times higher than normal value
 Four quadrant abdominal tap – shows pus or infected fluid. In suspected
pancreatitis, the fluid should be analysed for amylase level, which will be high
 Diagnostic peritoneal lavage – result of more than 500WBCs/ml indicates peritonitis
Differential diagnosis: -
 Pancreatitis – back pain is common in pancreatitis. CT scan is used to differentiate
 Intestinal obstruction – there will be distention, vomiting and pain. Plain x-ray shows
dilated bowel loops and CT scan confirms diagnosis
Treatment: -
 Antibiotic therapy – 3rd generation cephalosporins
 IV fluids – improve tissue perfusion and corrects hypotension and improves urine
output
 Nasogastric tube aspiration – decompresses the bowel and decreases toxic fluid
 Insert Foley catheter asap – to assess urine volume, which indicates intravascular
volume replacement
 Blood transfusion, FFP, platelet transfusion
 Surgery– laparotomy
 o In bowel perforation – close the perforation
o In intestinal obstruction – resect the gangrene area and do anastomosis
o In appendicitis – do appendectomy
o Peritoneal lavage

97) Rare forms of peritonitis. Abdominal sepsis

Rare types of peritonitis - Tuberculosis peritonitis

 It is a chronic disease of the peritoneum !
 It is always secondary peritonitis – primary lesions are located in the lungs, peri
bronchial lymph nodes, bones and joints and spread to the peritoneum via blood or
lymph nodes
 It can also be caused by the direct transmission of the infection by the mesenteric
lymph nodes, the intestines and the female genitals
Types/pathology: -
 It can be divided into 3 types: - !
1. Serous type (wet types) – large amounts of clear exudate and tubercles
diffusely scattered on the peritoneum
2. Dry form (adhesive form) – massive adhesions between the intestinal folds
and the omentum
3. Purulent form – presence of caseous-purulent outbreaks of mesenteric
lymph nodes develop purulent peritonitis
Causes/Pathogenesis: -
 Intoxication – from bacterial toxins, from decay of cells and tissues
 Haemodynamic disorders – hypotension, hypovolemia
 Electrolyte imbalance – dehydration, hypokalaemia, hyponatremia, hypocalcaemia
 Hypercoagulability
Clinical features: -
 Initial phase (early phase): -
 From onset of disease to 6-12 hours for perforative peritonitis
 From onset of disease to 24-48 hours for non-perforative peritonitis
(inflammatory peritonitis) !
o Strong, persistent pain
o Peritoneal irritation
o Blumberg’s sign – tenderness and rebound tenderness all over the abdomen
o Fever, nausea, vomiting, thirsty, leucocytosis
 Late stage: -
 Period after 12-24 hours in perforative peritonitis
 Period after 24-48 hours in non-perforative peritonitis (inflammatory
peritonitis)
o Ballooned and painful abdomen
 o Severely impaired general conditions
o Hippocratica facies – sharpened traits, sunken eyes with dark circles, !
lethargic look
o Cold and cyanotic limbs
o Fever, nausea, vomiting, thirsty
o Superficial and rapid breathing
o Paralytic ileus
o In auscultation of the abdomen, the so-called Grave silence in the abdomen-
do not perceives peristalsis
 Terminal stage: -
 Period after 24 hours in perforative peritonitis and
 Period after 5th day in non-perforative peritonitis (inflammatory
peritonitis)
o Patient condition is extremely severe.
o There may be euphoria, non-alcoholic hiccups, hallucinations, vomiting of
black material, leucocytosis with suppuration
Diagnosis: -
 Done on the basis of anamnesis (remembering things from previous supposed
existence– presence of peptic ulcer disease, gynaecological disease, surgery etc.
 X-ray – shows free gas under the diaphragm
Abdominal sepsis
 It is a condition with high mortality and morbidity
 Some organisms of the GI tract are capable of causing intraabdominal sepsis e.g., E.
coli, Klebsiella, Enterobacter etc.
 After minimal intraabdominal contamination e.g., simple appendicitis or bowel
obstruction without perforation
 Antibiotics should be given for 24 hours
 Criteria for stopping antibiotic treatment includes: -
o Clinical response (afebrile condition for 28 hours). Normal WBC count
o No abdominal tenderness, pain or Blumberg’s sign
Causes of intraabdominal sepsis: -
 Appendicitis – affects younger people more
 Diverticulitis – affects older people more
 Cholecystitis, cholangitis
 Intra-abdominal abscess
Intrabdominal sepsis in elderly
 The cause is often different than that in younger people.
 This is due to physiological changes that occur with age that affect vital functions
such as wound healing, oxygen delivery to the tissues and eradication of infection
o With age, the skin loses elasticity and blood supply, making it more fragile
and more prone to injury and infection
 o The lungs lose their elasticity, resulting in less compliance and withdrawal.
 Hypoventilation of the bases of the lungs is impaired.
 A lifetime of inhalation of environmental pollutants also causes
parenchymal fibrosis, inhibits ciliary action and increased mucus
production.
 These factors lead to decreased oxygenation of the arterial blood and
a concomitant decrease in oxygen delivery to the peripheral tissues
o Atherosclerotic changes in the arterial system increased peripheral vascular
resistance in older patients. Because of this and other cardiovascular
diseases, older individuals are less able to withstand intra-abdominal sepsis
 Older people have different sites of infection, may have unclear symptoms and a
longer history, and may be more severely ill with a worse prognosis !
 Characteristics of intraabdominal sepsis in elderly: -
o Symptoms (nausea, vomiting and fever) are slower, wiped out and duration
of the symptoms is more than twice as long
o They are less likely to have high fever and are less likely to have leucocytosis
Causes of abdominal sepsis and the elderly situation: -
1. Acute appendicitis
 It may have atypical presentation in elderly patients, thus making it difficult to
diagnose. Delays in diagnosis are more common in the older population, and are
joined with a higher rate of perforation, generalized peritonitis and death
 Changes in the appendix with age include: -
o atrophy of the intraluminal lymphoid tissue and
o thinning of the appendix wall, which makes the appendix more susceptible
to inflammation
o Atherosclerosis decreases blood supply, lumen narrows, and muscles
become fibrous and fat-laden
 Small changes in intraluminal pressure can lead to rapid ischemia, gangrene and
perforation at a much faster rate in the elderly
 A perforated appendix in an elderly patient may occur as distal obstruction of the
small intestine or right colon, and may need to be distinguished from caecum
carcinoma during surgery
 Diagnosis – ultrasonography (80% sensitivity and 95% specificity)
2. Diverticulitis
 It is very common in elderly patients. 25% of patients in their 60’s and 40% of
patients in their 70’s has diverticula
o Diverticulosis occurs when small, bulging pouches (diverticula) develop in
your digestive tract. When one or more of these pouches become inflamed
or infected, the condition is called diverticulitis.
 Older patients are more likely to have diverticular perforations that lead to
generalized rather than localized peritonitis. These patients have a shorter and
faster progressing course of the disease
  Diagnosis – CT scan with water-soluble contrast enema
 Complications: -
o Wound infections, urinary retention, and urinary tract infections
o Anastomotic leak - requires switching to Hartmann procedure
 HARTMANN'S PROCEDURE is a type of colectomy that removes part
of the colon and sometimes rectum (proctosigmoidectomy).
 The remaining rectum is sealed, creating what is known as
Hartmann's pouch.
 The remaining colon is redirected to a colostomy. It can be reversed
later.
o Hemodynamic instability, malnutrition, severe anaemia, immunosuppression,
diffuse peritonitis, and questionable viability of the bowel wall are
contraindications to single-stage surgery. In these situations, a two-step
procedure should be used
Treatment: -
 Rapid diagnosis with appropriate imaging techniques
 Give broad spectrum antibiotics within the ‘golden hour’ time period. Antibiotics
can prevent local and haematogenous spread and decrease late complications
 Fluid resuscitation
 Surgery to control the source of infection e.g., appendectomy, cholecystectomy

98) Abdominal compartment syndrome

 Def: -It is organ dysfunction caused by increased intrabdominal pressure more than
12mmHg (intraabdominal hypertension)
 Normal intraabdominal pressure is 2-7mmHg
 The organ dysfunction is usually respiratory, cardiovascular and renal, but can
involve any organ
 ABDOMINAL PERFUSION PRESSURE = it is the pressure that maintains enough
abdominal blood flow
Causes: -
 Major abdominal trauma, post-operative haemorrhages after damage control
surgery with abdominal packing
 Retroperitoneal haemorrhage
 Ruptured aortic aneurysm
 Forcible reduction of massive hernia
Effects of abdominal compartment syndrome: -
 Cardiovascular system: -
o Tt is sudden, rapidly progressive, decreasing the venous return to the heart
(due to IVC compression) and
o Increasing the peripheral resistance
o With decreased cardiac output
 Respiratory system: -
o Intrapleural pressure is increased proportionately to the abdominal pressure.
o There is upward displacement of the diaphragm, hypoxia, hypercapnia,
acidosis, respiratory failure, ARDS etc.
 Renal system: -
o Decreased renal blood flow and GFR causes oliguria and renal failure
 GI system: -
o Mesenterial venous hypertension
o Bowel wall edema and ischemia
 CNS: -
o cerebral edema
o hypoxia and unconsciousness
Clinical features: -
 Tender, distended abdomen
 Decreased urine output – oliguria
 Airway obstruction
 Decreased venous return
 Cardiac arrest

Diagnosis: -
 Measure urinary bladder pressure – bladder pressure reflects intrabdominal
!
pressure
o The pressure is graded according to Burch grading: - MEMORIZE THIS!!
 Grade 1: 10-15cm water – IAP pressure is 12-15mmHg
 Grade 2: 15-25cm water – IAP pressure is 16-20mmHg
 Grade 3: 25-35cm water – IAP pressure is 21-25mmHg
(decompression needed beyond this stage)
 Grade 4: more than 35cm water – IAP pressure is more than 25mmHg
 Based on duration: -
1. Hyperacute: sec to mins → sneeze/cough/defecation
2. Acute: Hours → Trauma/ Haemorrhage (surgical)
3. Subacute: Days → (Medical)
4. Chronic: Years → Obesity, Pregnancy
Treatment: -
 Mortality is 40%
 Silastic sheet created chimneys sutured to fascia. Pressure free abdominal closure
should be the target
 Temporary methods of closure – towel clips, temporary mesh placement,
 Definitive method of closure – biological mesh closure, closure using skin graft or
flaps
99) Diseases of the rectum. Diagnostic features. Differential diagnosis

Anatomy: -
 Most distal segment of large intestine
 Temporary storage of faeces
 Sigmoid colon – rectum – anal canal
 About 15 cm long
 Absence of taenia coli, haustra + omental appendices
 2 major plexuses: -
o Sacral – follows curve of sacrum + coccyx
o Anorectal – formed by tone of puborectalis muscle
 Men: prostate + seminal vesicles lie ant to inf rectum
 Women: thin rectovaginal septum separates ant inf rectum from vagina
Peritoneal coverage: -
 Sup 1/3 of rectum – ant + lat sides covered by peritoneum
 Mid 1/3 – only covered by peritoneum
 Lower 1/3 – no peritoneum coverage
 In males – rectum + post bladder = rectovesical pouch
 In female – rectum to post vagina + cervix = rectouterine pouch – Douglas pouch
Arterial supply: -
 Sup rectal a – continuation of IMA
 Mid rectal a – branch of int iliac a
 Inf rectal a – branch of int pudendal a – branch of int iliac a
Venous drainage: -
 Sup rectal vein – drains into portal venous system – anastomoses in anal canal
(portocaval anastomosis)
 Internal iliac – mid + inf veins (internal pudendal – inf iliac) – empty into systemic
circulation
Nervous: -
 Rectum receives sensory + autonomic innervation
Anal canal
 Final segment of GI tract, extends from anorectal ring (formed by fusion of int + ext
end sphincter + puborectalis muscle)
 Anal verge about 4 cm
 Located within anal triangle of perineum.
 Passes in an inf.post direction
 Except during defaecation anal canal is collapsed by int + ext anal sphincters
 Anal valves form a circle aka pectinate line
o Divides anal canal into 2. Which differ in structure + neurovascular supply
o Neurovascular supply: -
 Arteries
  Above line: sup rectal a + anastomosing branch of middle
rectal a
 Below line: inf rectal a
 Nerves
 Above line: visceral innervation via inf. Hypogastric plexus
 Below line: somatic innervation via inf anal nerves (branch of
pudendal n)
Somatic pain is in the muscles, bones, or soft tissues.
Visceral pain comes from your internal organs and blood vessels.
 Epithelium
 Above line: columnar
 Below: strat. Sq
 Haemorrhoids
 Above line: internal haemorrhoid’s (not painful)
 Below line external haemorrhoid’s (painful)
Rectal diseases: -
 Colorectal ca,
 Haemorrhoids
 Anal fissure,
 Anorectal anomalies
 Faecal incompetence
 Rectal prolapse
 Anal fistula
 Anorectal abscess
 Anal ca
 Proctitis
 Anal prolapse
 Rectocele (bulging of front wall of rectum into vagina aka post vaginal prolapse
Common symptoms: -
 Ab pain
 pelvic pain
 anorectal pain
 lower GI bleeding
 constipation + obstructed defecation
 Diarrhoea
 Altered bowel habit
 Discharge pus/mucus
 Prolapse
 Weight loss
Diagnosis: -
 Endoscopy – anoscopy, proctoscopy, sigmoidoscopy, colonoscopy
 Plain X-ray, CT, MRI, PET
  Angiography
 Endorectal, endoanal US
 Stool studies
 Faecal occult blood testing
 Tumor markers; Digital rectal exam

100) Carcinoma of the rectum

 Any tumour within 15cm proximal to the anal margin is called a rectal tumour
 More than 95% are adenocarcinoma
o Adenocarcinoma is a type of cancer. It develops in the glands that line your
organs.
 Affects women more
 Spread of tumour: -
1. Local spread – initially it spreads locally circumferentially and then later it
spreads out to the muscular coat and perirectal tissue. Then it spreads to the
prostate, bladder, seminal vesicles in men and uterus and vagina in females
2. Lymphatic spread – colonic, pararectal, midrectal and obturator lymph nodes
3. Haematogenous spread – liver, lungs, adrenals and other areas
Causes: -
 Family history – 1st-degree relative increases risk 2 times
 Diet: -
o Red meat and saturated fatty acids – increase risk
o High fibre diet – decreases risk
 Alcohol and smoking
Classification – Duke’s staging: -
 A – confined to the bowel wall, mucosa and submucosa
 B – extends across the bowel wall to the muscularis propria with NO lymph node
involvement
 C – lymph nodes are involved
 D – distant spread to liver, lungs, bone, brain etc.
Clinical features: -
!
 Bleeding from the rectum (may mimic haemorrhoids)
 Spurious diarrhoea – occurs in early morning due to mucous accumulation in the
rectum overnight
o SPURIOUS DIARRHOEA = Chronic constipation where the bowel is blocked by
hard, impacted faeces, but some liquid manages to seep past the blockage.
 Bloody slime – mucous in the stool
 TENESMUS = painful incomplete defecation with bleeding
o Sense of incomplete evacuation and constipation
 Presenting as piles – due to proximal venous congestion by the tumour
 Anaemia, malnutrition, weight loss and loss of appetite
 Diagnosis: -
 90% rectal growths can be felt by per-rectal examination
 Biopsy – using Yeoman’s forceps
 Proctoscopy – used to visualise the rectum, sigmoid colon and anal cavity
 Sigmoidoscopy – used to visualise rectum and sigmoid colon
 Ultrasound of abdomen – to look for any secondaries in the liver, ascites etc.
 CT scan – shows operability, local extension, size, lymph node status, uterus
involvement and presence of perforation
Differential diagnosis: -
 Tuberculosis
 Inflammatory stricture
 Amoebic granuloma
Treatment: -
 Surgery: -
o Abdomino-perineal resection (APR) (gold standard) – sigmoid, descending
colon and upper rectum are mobilised per abdominally. Anal canal and
perianal and perirectal tissues are dissected per anally. Colostomy is created
by suturing skin to mucosa
o Total mesorectal excision – since the mesorectum contains nodes and
lymphatics, clearance gives much better results
o Circumferential resected margin – a 5cm clearance of the mesorectum from
the primary tumour is important as tumour implants can only grow up to 4cm
from the primary tumour margin
o In females – partial vaginectomy with or without hysterectomy and bilateral
oophorectomy may needed in T4 lesions to achieve surgical resection
o In elderly – Hartman’s procedure is done since they are NOT fit for major
surgery. The rectal growth is resected and the upper end of the rectum is
closed completely. The proximal colon is brought out as end colostomy
 Chemotherapy

101) Haemorrhoids; Anal fissure

Haemorrhoids

Selfless medicosis - Haemorrhoids

 Def: - collections of tissue and vein cushions that become inflamed and swollen

Etiology: -

 Excessive straining due to chronic constipation or diarrhoea

 Increased intra ab pressure e.g., pregnancy, ascites (portal HTN)
 Congestion from a pelvic tumour
Pathophysiology: -

 Are cushions of submucosal tissue containing venules, arterioles + smooth muscle

fibres that located in the anal canal – part of normal anorectal anatomy
 Function = as part of continence mechanism + aid in complete closure of anal canal
at rest
 3 haemorrhoid cushions: - 3, 7 & 11

 Haemorrhoids are attached by smooth muscle + elastic tissue, but are prone to
displacement + disruption
 The effect of gravity, increased anal tone + effects of straining may make them bulky
+ loose thus protrude + form piles and are vulnerable to trauma + bleed readily from
capillaries

Classification: -

1. External: -located distal to the dentate (pectinate line) + covered with anoderm
o Richly innervated sympathetic – hence more painful
2. Internal: - located proximal to the dentate line + covered by insensate anorectal
mucosa – may prolapse + bleed
o Rarely become painful unless they develop thrombosis or necrosis
(strangulation, incarceration, severe prolapse)
o Graded based on degree of prolapse: -
 1st degree – no prolapse
 2nd degree – prolapse but spontaneously reduces
 3rd degree – prolapse but can be manually reduced
 4th degree – permanent prolapse cannot be reduced
3. Combined = combination of Ext + int
 The PECTINATE LINE (DENTATE LINE) = is a line which divides the upper two-thirds
and lower third of the anal canal. Developmentally, this line represents the hindgut-
proctodaeum junction

Clinical: -

 Irritation – pruritis ani, mucus discharge, perianal discomfort

 Damage to mucosa – bleeding = bright red
 Prolapse – usually after defaecation

Diagnosis: -

 DRE (Digital rectal exam)

 Proctoscopy – shows exact position of piles, number, degree and size
 Sigmoidoscopy or colonoscopy – should be done if suspect malignancy
 FBC – may indicate anaemia

DDX: -

 Rectal prolapse
 Perianal warts
 Carcinoma

Treatment: -

 For 1st & 2nd degree – lifestyle modifications

o Stool softeners
o High fibre + increased fluid
o Sitz bath – patient sits in warm water with the anal region dipped in water for
20 mins, and repeats it 2-3 times a day. It helps to decrease edema, pain and
promotes healing
 Surgery for above 2nd degree: -
o Rubber band ligation = band strangulates underlying tissue causing
scarring + prevent further bleeding
o Sclerosantis – 2ml of 5% phenol inj into pile above dentate line
o Infra-red coagulation – coagulates vessels
o Cryotherapy – high compliance rate
 Surgery = excisional haemorrhoidectomy – excision of piles + ligation of vesicle
pedicles
o Stapled haemorrhoidpexy – for prolapsing haemorrhoids may result in less
pain + decreased recovery time

Complications: -

 Constipation, infx, stricture, bleeding

Anal fissures
Selfless medicosis - Anal fissures

 Def: - a tear in the anoderm (thin pale, shiny sq ep covering lower half of anal canal)
distal to dentate line
 In younger pts – 15-40yrs
 1/350 adults – M=F

Etiology: -

 History of: -
o Constipation (Trauma from passage of hard stools)
o Diarrhea – substances cause irritation
o IBS etc

Classification: -

1. Acute
o Deep tear in the lower anal skin with severe sphincter spasm w/o edema or
inflammation
o Presents with severe pain + constipation
2. Chronic
o It has got inflamed, indurated margin with scar tissue
o Can causes repeated infection fibrosisabscess formationfistula
o Chronic fissures is less painful than acute one
o Can cause complications like abscess, fistula formation
3. Primary
4. Secondary

Pathophysiology: -

 Summary: - woundspasmvasoconstriction (poor wound

healing)ischemiapain
 Tear in anoderm causes spasm of internal anal sphincter – pain, increased tearing,
decreased blood to anoderm
 This cycle of pain, spasm + ischaemia contributes to development of poorly healed
wound = chronic fissure
 it occurs in the midline, posteriorly (more common in males), but can also occur in
the midline anteriorly more common in females).

Clinical: -

 Tearing pain with defaecation

 Not much blood like haemorrhoids
 Intense + painful + spasm

Diagnosis: -
  DRE not recommended as can cause severe pain!!! If necessary, perform under
anaesthesia

Treatment: -

 Conservative 1st line txt: -Focus on breaking cycle of pain, spasm + ischaemia
o Stool softeners – bulk forming laxatives
o Nitrate ointment – to cause local vasodilation
 Ca2+ channel used rather than nitrates nowadays
o Botulism toxin – to reduce spasm
o Local anaesthesia – lidocaine
 Surgical = lateral internal sphinctercetomy = procedure of choice
o Surgically divide internal fibers of sphincter to relax overall
 Anal advancement flap – flap over wound if not healing at all

102) Prolapse of the anus and rectum

 Def: -It is a circumferential descent of the rectum through the anal canal
 Affects women more
 In 15% patients, there is associated vaginal vault prolapse
Causes: -
 In infants
o Decreased sacral curvature and decreased anal canal tone
o Diarrhoea, cough, malnutrition
 Chronic constipation with straining
 Pudendal nerve damage – cause pelvic floor weakness and anal sphincter weakness
 Multiple childbirths – multiple birth injuries to the perineum results in damage to
the perineal nerve supply
 Increased intrabdominal pressure – due to chronic cough
Classification of anal prolapse: -
! 1. Complete – more than >3.5cm
o Full thickness (all rectal layers) Posterior of
rectum through the anus.
2. Partial – mucosal; most common; <3.75cm
o Haemorrhoidal disease upon palpitation
only double layer
3. Hidden/ Concealed -internal
o Rectal wall intussusception but doesn’t protrude.
Partial rectal prolapse (more common)
 Only the mucosa and submucosa of the rectum descends and NOT more than
3.75cm
 There is NO descent of the muscular layer
 Clinical features: -
 o History of mass per anum, which can be observed when patient is straining in
squatting position
 PER ANUM = through the anus !
o It is pink in colour and circumferential
o It differs from piles in that piles are NOT circumferential and are plum-blue
coloured (NOT PINK)
 Treatment: -
o Correct constipation in the child
o Submucosal injections of 10ml of 5% phenol in almond oil, under general
anaesthesia – created aseptic inflammation which results in tethering of the
mucosa to the underlying muscular coat
o Thiersch wiring
o Goodsall’s operation – excision of the prolapsed mucosa by its base
Complete rectal prolapse
 It is due to weakened levator ani and supporting pelvic tissues !
 Descent is always more than 3.75cm (generally 10-15cm) and involves all layers of
the rectum (including the muscular layer)
 The mucosa is thickened, ulcerated, bleeds and is incarcerated below the level of
anal verge
 It is often associated with uterine prolapse
 Clinical features: -
o Complete descent of rectum as mass per anum circumferentially, which is red !
in colour
o The mass is usually reducible and painless. However, incarcerated or
infected rectal prolapse is painful
o Can be associated with uterine prolapse
o Faecal incontinence (75% cases) – due to anal sphincter disruption and
prolapse rectal mucosal
o Bleeding
 Diagnosis – confirmed by observing the patient during straining in squatting
position
 Treatment: -
o Control the prolapse, restore continence and prevent constipation
o Rectopexy – fixing the rectum to the sacrum using sutures after complete
mobilisation of the rectum

103) Traumatic, congenital and other diseases of the anus and rectum

Congenital diseases of the rectum and anus -Anorectal malformations (ARM)

 ARM
 It is due to imperfect fusion of the post-allantoic gut with the proctodaeum
 It can be divided into 2 main types: -
 1. Non-syndromic ARM
a. Non-syndromic ARM with fistula !
(i) Recto-perineal
(ii) Recto-urinary
(iii) Rectovaginal, recto vestibular
b. Non-syndromic ARM without fistula – imperforate anus
c. Non-syndromic complex fistula
2. Syndromic ARM
 Clinical features: -
o New-borns have inability to pass meconium
o Abdominal distention
o Features of intestinal obstruction and
o Improper anal dimple
o Flat bottom with no or poorly developed midline groove between the
buttocks
o Absence of anal opening
 Diagnosis: - Wag stein’s invertogram – a metal coin (marker) is strapped to the site
of the anus and x-ray is taken. Length between the rectal pouch and coin is
measured
 Treatment: -
o Anoplasty
o anal dilation
o anal membrane incision
Traumatic diseases of the rectum and anus
 Traumas are uncommon by can occur by falling in sitting posture onto a pointed
object, penetrating injury, sexual assault or sexual activity involving anal penetration
 Diagnosis: -
o Anus should be inspected and palpated
o Laparotomy – done if there is presence of tenderness or rigidity
o Water soluble enema or CT with rectal contrast
 Treatment: -
o Finger and speculum used and lower laparotomy done if penetration is
confirmed
 A laparotomy is a surgical incision (cut) into the abdominal cavity.
This operation is performed to examine the abdominal organs and aid
diagnosis of any problems, including abdominal pain.
o Intraperitoneal rupture – closed with suture
o Colostomy needed in left iliac fossa after closing laparotomy wound !
o If damage is severe, resection is considered using Hartman’s
procedure) resect the rectosigmoid with closure of the anal stump and
formation of end colostomy)
1. Driver’s bottom

!
  It is epithelium lined tract, located a short distance behind the anus, containing
hair and diseased granulation tissue
 Most common location – interbuttock sacral region
 Cause – it is due to penetration of hair through the skin into the subcutaneous
tissue
 It is commonly seen in jeep drivers and hairy men
 Pathology: -
o Hair penetrates the skin, causing dermatitis, infection and pustule
formation.
o The hair then gets sucked into the sinus by negative pressure, causing further
irritation and formation of granulation tissue.
o Pus forms
 Clinical features: -
o visible hair in the opening of the sinus, discharge, throbbing pain, tender
swelling just above the coccyx
 Treatment: -
o Patient lies on stomach with butt elevated. Give anaesthesia.
o Make excision and primary closure.
o All sinus tracks, unhealthy granulation tissue and hair is removed
2. Post anal dermoid
!
 Def: -It is a cystic soft tissue swelling in front of the lower part of the sacrum
and coccyx
 It is NOT often discovered unless it forms a sinus with the exterior or it becomes
inflamed
 It is easily palpable on rectal examination
 Differential diagnosis – anterior sacral meningocele (child cries and paralysis of
lower limbs and incontinence)
 Treatment – complete excision of the cyst and sinus

104) Paraproctitis and abscesses

Para-proctitis !
Paraproctitis
 Def: -It is an acute inflammation of para-rectal cellular tissue (peri-rectal fat)
 Damage to mucosa
 More common in males
Causes: -
 Infections (E. coli; strepto, staph, entero) – main cause
 Constipation
 Long sitting on chair
 Micro trauma of rectum anal canal mucosa
 Ulcerative colitis, Crohn’s, STDs
Classification: -
 Based in etiology: -
o Non-specific ! classification
o Post traumatic – due to micro-trauma
o Specific – due to bacteria
 According to inflammatory process: -
o Acute
o Chronic – fistula occurs here
o Recurrent
 Based on localization: -mainly asked
1. Subcutaneous – localised near anus; causes acute pain especially during
defecation
2. Submucosal – localised above the Morganii’s crypts or anorectal line
3. Ischiorectal – localised in deep layer of ischiorectal fossa fat & can spread up
to prostatic gland
4. Pelviorectal- localised behind the fundus; localised in levator sheath (at
supralevator region)
5. Intersphincteric -severe pain in rectum with radiation to sacrum

Etiology and pathogenesis: -

 Infection of tissue (cellulitis) surrounding the rectum usually arising from the
cryptoglandular epithelium, lining of the anal canal
 Infection of the glandular sections can become suppurative spread and form
different forms of abscess as well as fistulas
 Initially the abscess form in the inter-sphincteric space, then spreads to other
potential spaces such as inter-sphincteric space
 10% cases can be due to infection from another area e.g., trauma, HIV, TB, STDs
Clinical features: -
 Perianal pain – made worse by movement and increase perineal pressure from
sitting of defecation
 Patient with ischio-rectal abscess present with systemic fever, chills and severe peri-
rectal pain and fullness
 External signs can be erythema, induration or fluctuance (movable fluid-filled
structure)
 50% patients have swelling around the rectum and 25% patients have rectal or peri-
rectal drainage that can be bloody, purulent or mucoid
 Constipation can occur due to pain on defecation
 High fever, malaise, weakness, chills, headache – in acute stage
Complications: -
 Fistula formation – main
 Purulent melting of the urethra
 Purulent process to the scrotum followed by gangrene – in severe and chronic forms
Diagnosis: -
 Physical examination – small, erythematous well-defined fluctuant subcutaneous
mass near the anal orifice
 CT, ultrasound, MRI, endoscopy
Treatment: -
 Presence of abscess is an indication for incision and drainage
o Resection of fistula
o Syringectomy through intestinal lumen
o Ligature method
o Syringectomy of fistula with sphinctercetomy
 Conservative: -
o Antibiotics
o Anti-inflammatory drugs
o Warm bath with potassium permanganate !
o UHA therapy – ultra high electromagnetic
Anal abscesses
 Ano-rectal abscess
 Def: -Anal abscess is an acute manifestation of purulent infection in the peri-rectal
area
 On the other hand, anal fistulas are the chronic manifestation of purulent infection
in the peri-rectal area
Etiology and pathogenesis: -
 An anal abscess is a pus-filled cavity, that most commonly develops from an infected
anal crypt gland after obstruction and bacterial overgrowth
 Causes – inflammatory bowel disease e.g., appendicitis, radiation-induced proctitis,
malignancy
 30-60% cases can progress into fistulas, which are ductal connections between the
abscess and the anal canal or the perianal skin
 Treatment - it can heal spontaneously after drainage into the anal canal
 Classification of anorectal abscess – according to anatomical location: -
1. Peri-anal (most common)
2. Ischio-rectal !
3. Inter-sphincteric
4. Super-levator
5. Submucosal
Clinical features: -
 Anal abscess patients – anorectal pain, palpable tender mass on digital rectal
examination
 Anal fistula patients – visible perianal site draining pus and discomfort during
defecation
Diagnosis: -
 CT, MRI or anal ultrasound – only needed for extended abscesses or complex fistulas
 DRE
Treatment: -
 Definitive treatment needs surgery
 Abscesses are incised and drained followed by open wound healing
 Anal fistulas are treated with fistulotomy

105) Chronic fistulous paraproctitis

 Anal fistulas
 Def: -It is a chronic abnormal communication running outwards form the anorectal
lumen to an external opening on the skin of the perineum or buttock and rarely, the
vagina
 Etiology – E. coli, Staph. Aureus
Pathogenesis: -
 Paraproctitis is caused by several microorganisms penetrating into the cells from
the rectum through the anal glands, damaged mucous membrane and also through
haematogenous or lymphogenous pathway from neighbouring organs affected by
the inflammatory process
 Paraproctitis has direct damage to the mucosa of the rectum in the region of the
posterior wall of the anal canal, where wide and deep crypts are located, which are
the entrance gates of infection
 Each crypt opens up to 6-8 ducts of anal glands
 The infection spreads to the para-rectal cells and ultimately an abscess form
 The abscess can also occur due to diverticulitis or inflammatory pelvic disease
 Anal abscesses progress into fistulas which are ductal connections between the
abscess and the anal canal or the peri-anal skin
 Obstruction of the anal glands by thick debris results in stasis and bacterial
overgrowth and thus abscess formation
 Clinical features: -
 Intermittent purulent discharge, which can be bloody and painful
 Pain during defecation
Classification: -
1. Inter-sphincteric (70% cases) – it is found between the internal and external
sphincters
2. Trans-sphincteric – extends through the external sphincter into the ischio-rectal
fossa
3. Extra-sphincteric – passes from the rectum to the skin through the levator ani
4. Supra-sphincteric – extends from the inter-sphincteric plane through the
puborectalis, exiting the skin after transversing the levator ani

Diagnosis: -
 Digital rectal examination – fluctuant, indurated mass, pain with pressure
 Proctosigmoidoscopy – it is needed under anaesthesia
 Fistula probe with methylene blue for contrast
Treatment: -
 Fistulotomy – cut along the whole length of the fistula to open it
 Possible Seton placement – enables enough drainage and fibrosis
 Fibrin glue or fistula plug

106) Congenital diseases of the colon. Morbus Hirschsprung. Dolychosigma. Dolichocolon

Hirschsprung’s disease (congenital megacolon)

 It is a congenital disease that occurs due to absence of ganglion cells (nerves) in the
Auerbach plexus in the colon, resulting in functional obstruction and megacolon
 The transitional zone proximal to it only contains a few ganglions cells
 It always involves the anus, internal sphincter and rectum
 It is a cause of neonatal intestinal obstruction
 It is associated with Down syndrome
Types: -
!
 It can be divided into 3 types: -
1. Ultrashort segment HD – only anal canal and terminal rectum is aganglionic
2. Short segment HD (80% cases) – anal canal and rectum is completely
involved
3. Long segment HD – anal canal, rectum and part of the colon is involved
4. Total colonic HD – anal canal, rectum and whole length of colon is involved
 It has 3 zones: -!!!!
1. Immobile spastic segment i.e., aganglionic zone
2. Middle transitional zone of 1-5cm with less ganglions
3. Hypertrophied dilated segment – normal ganglionic area
Clinical features: -
 In 90% cases, symptoms appear in early neonatal period (within first 3 days of birth)
and the child fails to pass meconium
 After introducing finger into the rectum, the child passes stool that is similar to
toothpaste after straining
 Abdominal distention with features of intestinal obstruction
 In children – stools are similar to goat pellets
 Constipation – passing stool after every 3-4 days
Diagnosis: -
 Rectal exam – shows tight sphincter with empty rectum
 X-ray of abdomen – shows intestinal obstruction
 Barium enema – shows extent of disease and three zones
 Biopsy of all three zones – to study the ganglions in the zones
 Anorectal manometry – shows absence of recto anal reflex in HD which is
diagnostic
Differential diagnosis: -
 Hypothyroidism
 Total neuronal dysplasia
 Acquired megacolon – rectum is loaded with stool
Treatment: -
 Nutritional supplementation
 Modified Duhamel operation – resection of upper part of rectum and a part of the
colon followed by anastomosis of the colon to the posterior part of the lower
rectum
 Removal of the aganglionic segment & perform a pull through surgery whereby the
healthy part of the intestine is brought down to the anus
o It is sometimes performed in steps where the neonate first undergoes a
surgery for a colostomy proximal to the aganglionic segment to decompress
the colon and allow the neonate to grow before the 2nd stage of the
procedure which is pull through when the child is over 10 kg
 o 3 types of pull through procedures: - basically anastomose ganglionic part to
anus
 Swenson’s procedure - aganglionic rectum is dissected and healthy
part is anastomosed to anus
 Duhamel procedure – rectum is left and ganglionic bowel us brough
to rectorectal space (ganglionic part is anastomosed to the rectum
posteriorly)
 Soave operation – endorectal removal of mucosa and bringing down
the ganglionic colon through – anastomosed at anus
Dolychosigma and Dolichocolon
 Def: -It is a congenital anomaly in which sigmoid colon is longer than normal
o Do not confuse with MEGACOLON = abnormally wide Large Intestine
 Sometimes the lengthening can be associated with distention = then called
MEGADOLICHOCOLON
 It results in faecal material being delayed in the intestinal lumen for longer and thus
violation of defecation and chronic constipation
 Othe complications like excessive looping can increase the possibility of an
incomplete/complete volvulus thus when this occurs, it should be treated
accordingly
Clinical: -
 Patient mostly asymptomatic
 Chronic constipation due to chronic colostasis
Diagnosis: -
 No universal criteria – some sources suggest a colon greater than 2 meters
 Often the diagnosis is done incidentally during colonoscopy or barium enema
Treatment: -
 Treatment of constipation by changing diet, increasing water intake and using
laxatives
 Treat volvulus surgically is present

107) Acute surgical abdomen

 Shorter video – SOCCRATES mnemonic

 Longer but more detailed
 SURGICAL ABDOMEN = underlying etiology that requires an emergent evaluation
by a surgeon
 This topic is related to the diagnosis and treatment of acute abdominal pain
 Abdominal pain either sudden or gradual in onset, normally progresses in severity so
it becomes a prominent feature of a patient’s illness
History: -
 Careful and detailed history helps define the time of onset, location and any changes
in character with positions
 Pain
o Pain that lasts for more than 6 hours and is severe usually need surgery for
treatment of the underlying problem
o Pain that is sharp, severe and sudden in onset, waking the patient from sleep
or preventing them from functioning, often suggests a perforated viscus
o Pain in the upper abdomen is generally peptic ulcer disease, acute
cholecystitis or pancreatitis
o Pain in the lower abdomen is generally ruptured ovarian cyst or perforated
diverticulitis
o Character of the pain can also help differentiate diseases
 Pain from small bowel obstruction is a cramping, intermittent pain
 Pain from strangulation of pain is dull, constant pain
o Original location of the pain – change in position of pain can indicate acute
appendicitis
o Sudden burning pain in epigastrium – indicates perforated viscus
o Radiating pain – indicates acute cholecystitis, which radiates around the
right costal margin to the right scapula and shoulder
 Vomiting
o It is uncommon in perforated ulcer
o Common in acute cholecystitis
o Always occurs in small bowel obstruction and is recurrent and pain is relieved
by vomiting
o Pain precedes vomiting by 3-4 hours in patients with appendicitis
o Clear vomit – indicates pylorus
o Bile-stained vomit – indicates obstruction is distal to the entrance of common
bile duct into the duodenum
 Anorexia – associated with acute appendicitis
 Constipation and diarrhoea – profuse watery diarrhoea for 12 hours indicates
gastroenteritis
 Menstruation – accurate menstrual history is important in abdominal pain, including
cycle frequency and duration of period
Organ system review: -
 It is done to avoid overlooking an extra-abdominal cause of pain such as pulmonary
embolism or myocardial infarction
 Patients with systemic illness e.g., Lupus, nephrotic syndrome and sickle cell may
develop abdominal pain as a clinical feature of their illness and do NOT need surgery
 Anxious, pale, sweating, restless patient that complains about abdominal pain has
high probability of intra-abdominal disease or serious extra-abdominal disease with
pain referred to the abdomen
 Dehydration, sunken hollow eyes – indicates generalised peritonitis
Physical examination: -
 General appearance is noted – is patient anxious, pale, sweating, or lying quietly
supine in bed
 Position in bed is important – is patient lying down on the side or in fetal position
 Rapid heart rate with hypotension is caused by peritonitis
 Examination begins with visual inspection – previous scars, obvious masses,
abdominal defects
 Percussion – begin in the quadrant free of pain and be done lightly to avoid pain
 Auscultation – do all four quadrants. Pay attention to frequency and pitch of bowel
sounds
 Location of maximum tenderness – maximal tenderness in right lower point over
McBurney’s point indicates appendicitis
 Rectal examination – determine pelvic mass or peri-rectal abscess
 Rebound tenderness – indicates peritoneal irritation (quick release of examining
hand)
Diagnostic imaging: -
 X-ray, CT, ultrasound, arteriograms, urogram, radionuclide test
 Free intraperitoneal air – can be due to perforation of gastric or duodenal peptic
ulcer
 Abnormal calcific densities can be seen on x-ray – seen in gallstones, renal stones,
pancreatic stones
 Both supine and erect x-ray different views can be used to distinguish between
gastric outlet obstruction and colon obstruction
 CT detects gas in portal and mesenteric veins
 Ultrasound – diagnose acute cholecystitis and appendicitis
Lab tests: -
 Serum amylase levels – high in acute pancreatitis and pancreatic cystic disease
 Serum aspartate aminotransferase (AST) – high in acute hepatitis
 hCG – diagnose ectopic pregnancy
 Liver function tests with upper quadrant pain – indicates jaundice or hepatitis
Peritoneal diagnostic tap: -
 Used to determine the presence of intraperitoneal blood, fluid and pus
Non-surgical causes of abdominal pain: -
 Heart – acute pericarditis
 Lungs – pneumonia, pulmonary infarction
 GI – acute hepatitis, acute pancreatitis
 CNS – nerve root compression
108) Thromboembolic complications

1. Deep vein thrombosis (phlebothrombosis)

 3 factors that cause DVT are Virchow’s triad: -
1) Stasis
2) Hypercoagulability
3) Vessel wall injury
Causes: -
 After operation (most common) – 20% patients after surgery develop DVT
 Trauma – to the leg, ankle, thigh or pelvis
 Immobility – bed ridden patients, or person travelling for long period of time
 Obesity, pregnancy
 Oral contraceptives – oestrogen
 Antithrombin III deficiency, thrombophilia
 Recent myocardial infarction, heart failure
Clinical features: -
 Fever
 Severe pain and swelling in the calf and thigh
 Leg is tense, tender, warm, pale or bluish
 Positive Homan’s sign – passive forceful dorsiflexion of the foot with extended knee
causes tenderness in the calf
Diagnosis: -
 Venous doppler ultrasound
 Duplex scanning – shows non-compressible vein which is wider than normal

Treatment: -
 Rest, elevation of limb, bandaging the entire limb
 Anticoagulants – heparin and warfarin – initially give heparin for 7 days followed by
warfarin for 3-6 months
 Thrombolytics – streptokinase
Prevention/prophylaxis: -
 Apply pressure bandage to the legs (compression socks) after major surgeries and
elevate and massage the legs
 Low dose heparin in suspected cases and after major surgery
  Aspirin – prevents platelet aggregation
 Dextran
2. Pulmonary embolism
 It is due to DVT that gets detached and becomes pulmonary embolism
 Types: -!!!!
1) Small emboli – cause pulmonary hypertension of features of
bronchopneumonia
2) Medium emboli – lodge in the branches of the pulmonary artery and cause
chest pain, dyspnea and haemoptysis
3) Massive emboli – cause block at the bifurcation of the pulmonary artery and
cause sudden chest pain, severe dyspnea, shock and sudden death
Risk factors: -
 After surgery and trauma patients who are bedridden
 Obesity, pregnancy
 Varicose veins
Diagnosis: -
 Chest x-ray – shows hyperlucency in an area of oligemia (Westermarck sign)

 CT and MRI – can detect PE

 Pulmonary angiography – 100% diagnostic
 Doppler study – to rule out DVT
Treatment: -
 Thrombolytics – streptokinase
 Pulmonary embolectomy
 Treat DVT

109) Basic principles of laparoscopic surgery

 Laparoscopic cholecystectomy
Advantages of laparoscopic surgery: -
 Minimal scar of abdomen
 Shorter hospital stays and early return to work
 Faster post-operatively recovery
 Less painful than open surgery and trauma of access is very less
Instruments used: -
 Zero-degree laparoscope is used. Side viewing scopes are also used to have better
visualisation 30 degrees
 Cold light source – halogen lamp used
 Camera and video-monitor display
 CO2 insufflator – CO2 enters the peritoneal cavity producing a pneumoperitoneum.
This causes an increase in intraabdominal pressure
 Hooks and spatulas with cautery for dissection
 Endo staplers
 Suction-irrigation apparatus
 Different sized trocars – 10mm, 5mm
Technique: -
 Pressure bandages are applied to both legs to improve venous
return and decrease stasis
 Ryle’s tube and Foley’s catheter
 Pneumoperitoneum is created using Veress needle through an
umbilical incision.
o Pneumoperitoneum is created up to a pressure of
15mmHg which distends the abdominal cavity to give
proper visualisation of abdominal cavity
 Laparoscope is inserted through umbilical port (10mm). abdomen
is evaluated for any pathology
 3-4 additional ports are placed through trocars depending on the procedure done.
The ports are placed in a way to have proper triangulation of instruments for
dissection
Physiologic changes due to pneumoperitoneum: -
 CO2 causes hypercarbia, acidosis and hypoxia
 Pneumoperitoneum exerts pressure on the IVC and decreases venous return and
thus cardiac output
 Compromises respiratory function by compressing over the diaphragm impairing
pulmonary compliance
Complications: -
 CO2 narcosis and hypoxia
o NARCOSIS = a state of stupor, unconsciousness, or arrested activity produced
by the influence of narcotics or other chemical or physical agents
 IVC compression
 Bleeding
 Organ injury during port insertion e.g., major vessels, bowel, mesentery, liver
 Cautery burns to abdominal structures
Contraindications: -
 Bleeding disorders
 Peritonitis
 3rd trimester pregnancy
 Portal hypertension
 Compromised cardiac status
Laparoscopic surgeries: -
 Laparoscopic cholecystectomy
 Laparoscopic appendicectomy
 Laparoscopic inguinal hernia repair
 Diagnostic laparoscopy – tumour biopsy, infertility, staging malignancy
Laparoscopic cholecystectomy
 Indications: - gallstones, cholecystitis
 Technique: -
a) After pneumoperitoneum, the patient is placed in head up and slightly left
tilt position to make the bowels fall below and towards the left side
b) One 10mm trocar is inserted at the umbilicus and a laparoscope is inserted
c) One 10mm port is inserted in the epigastric region and two 5mm ports are
inserted in the right subcostal line for grasping the gallbladder and for
dissection
d) Calot’s triangle is dissected and the cystic duct and cystic artery are clipped
– the cystic artery, RHA, cystic lymph node of Lund, lymphatics, and
connective tissue make up the contents of Calot's triangle
e) Careful NOT to injure or clip the CBD or hepatic ducts
f) The gallbladder is separated from its bed using cautery and spatula and
removed through the epigastric port
g) The abdomen is drained and the patient is discharged after 2-3 days
Laparoscopic appendicectomy
 Indications – acute appendicitis
 Technique: -
a) One 10mm trocar is inserted at the umbilicus and a laparoscope is inserted
b) One 5mm port is inserted in the lower left abdomen and one 5mm ports is
inserted at the lower right abdomen region
c) The mesoappendix is clipped or cauterised
d) The appendix base is clipped using Roder knot and ligature