EAR NOSE AND THROAT

NURSING
Prepared and presented
By
 COURSE OUTLINE:
Introduction and definition of ENT terminologies
Review of anatomy and physiology of the ear
History taking
Assessment of the auditory system
Evaluation of gross auditory activity
Diagnostic evaluation
Tests to detect vestibular problem
 Hearing loss and deafness
 Types and classification of hearing loss
 Assessment of hearing loss
 Clinical manifestations – early and late
 Risk factors for hearing loss
 Management of hearing loss
 Conditions of external ear
 Cerumen impaction
 Foreign bodies
 External otits media
 Conditions of the middle ear
 Tympanic membrane perforation
 Acute otitis media
 Serrous otitis media
  Chronic otitis media
 Otosclerosis
 Nursing care of a patient undergoing middle ear
surgery
 Conditions of the inner ear
 Motion sickness
 Meinieres disease
 Labyrinthitis
 Ototoxicity
 Acoustic neuroma
 The nose and paranasal sinuses
 Anatomy and physiology of the nose
 Functions of the nose
 Physical assessment of the nose and sinuses
Conditions of the nose
Epistaxis
Sinusitis
Rhinitis
Nasal polyps
Nasal fracture
Deviated septum
The throat
Tonsilitis and adenoiditis
Laryngitis
Cancer of the larynx
Peritonsillar abcess
Epiglottitis
Nursing process for a patient with partial
layngectomy
Terminologies in ENT
1. Acute otitis media – inflammation of the middle ear
lasting less than 6 weeks
2. Cholesteatoma – a benign tumor of the middle ear or
mastoid or both.can destroy structures of temporal bone
3. Chronic otitis media – repeated episodes of acute otitis
media causing irreversible tissue damage and
persistent tympanic membrane perforation.
4. Conductive hearing loss – loss of hearing in which
effective sound transmission to the inner ear is
obstructed.
5. Dizziness – altered sensation of orientation in space.
6. Endolymphatic hydrops – dilation of the endolymphatic
space of the inner ear.
7. Extoses – small, hard bony protrusions in the lower
posterior bony portion of the ear canal.
8. Labyrinthitis – inflammation of the inner ear
9. Vertigo – an illusion of movement in which the
individual or surroundings are perceived to be moving.
10. Tinitus – subjective perception of sound with internal
origin, unwanted noises in the ear
11. Menieres disease – a condition of the inner ear
characterised by a triad of symptoms i.e. episodic
vertigo, tinnitus, fluctuating sensorineural hearing loss
12. Middle ear effusion/serrous otitis media – effusion of
fluid in the middle ear without evidence of infection
13. Myringotomy – incision of the tympanic membrance
14. Ossiculoplasty – surgical reconstruction of the middle
ear bones to restore hearing.
15. Otalgia – ear pain
16. Otitis externa – inflammation of the external auditory
canal
17. Otorrhea – drainage from the ear
18. Otosclerosis – a condition characterised by
abnormal spongy bone formation around the stapes
20. Presbycusis – progressive hearing loss associated
with aging
21. Rhinorrhoea – drainage from the nose
22. Sensorineural hearing loss – loss of hearing due
to damage of the organ of hearing or cranial nerve
8 or both.
Review of anatomy and physiology of the ear
 It is the organ of hearing and balance/equilibrium.
Except the pinnae, the structures of the ear are within
the petrous portion of the temporal bone.
Its divided into three parts:
OUTER EAR
 Consists of the auricle or pinnae. Which is
composed of fibroelastic cartilage, covered with skin.
 The lobule/earlobe is the soft pliable part at the lower
extremity. The auricle collects the sound waves and
directs vi- brations into the external auditory canal.
 The external acoustic meatus/auditory canal is a
slightly ‘S’ shaped tube about 2.5cm long, extending
from the auricle to the tympanic membrane.
 It is lined with skin containing hairs.
 The lateral third has numerous sebaceous and
ceruminous glands. Ceruminous glands secrete
cerumen/wax – a sticky material containing
lysozyme and immunoglobins.
 Movements of the temporomandibular joint during
chewing and speaking massage the cartilagionous
meatus, moving the wax towards the exterior.
MIDDLE EAR
It is an irregularly shaped air filled cavity within the
petrous portion of the temporal bone. .Air reaches
the cavity through the eustachian or auditory tube,
which is about 4 cm long and lined with ciliated
epithelium. It connects the middle ear to the
nasopharynx and equalizes pressure on both sides
of the membrane.
It also drains the middle ear.
 In children it is shorter and wider thus making
children more susceptible to middle ear infections.
It is also more easily blocked by allergies,
enlarged adenoids or inflammation of the nose
and throat
 The tympanic membrane- completely
separates the external acoustic meatus from the
middle ear.
 it is oval in shape with three layers – outer
covering of hairless skin, middle layer of fibrous
tissue and an inner lining of mucous membrane.
 Normally it appears pearly grey and
translucent.
 The medial wall is a thin layer of temporal bone
with two openings, the round and oval window.
ct
The middle ear has three bones called
ossicles.
 Malleus: hammer shaped. Its handle is in
contact with the tympanic membrane and
the head forms a movable joint with the
incusIncus: is the middle anvil shaped bone.
Its bony articulates with the malleus & its
long process with the stapes. Its held to the
wall of the cavity by its short process.
 Stapes: it is the medial stirrup shaped bone.
Its head articulates with the incus and its
footplate fits into the oval window.
 INNER EAR
 It is filled with fluid. Between the bony labyrinth
and the membranous labyrinth is filled with
perilymph. The membranous labyrinth is filled
with endolymph.
 The vestibule is the expanded part nearest the
middle ear. It contains the oval and round window
in the bony labyrinth and the utricle and saccule
in the membranous labyrinth.
 The cochlea resembles a snail shell. transforms
mechanical energy into neural activity and
separates sounds into different frequencies
The cochlear duct has supporting cells and
specialised cochlear hair cells lying on the basilar
membrane, they contain auditory receptors that are
connected to the tectorial membrane. These cells
form the spiral organ/organ of corti.
Semicircular canals:
They are three, horse shoe shaped and lie in the
three planes of space.
They contain hair like nerve endings that are set in
motion by the fluid in the canals. contain sensory
receptor organs, arranged to detect rotational
movement.
They transmit information about the body’s position
to the brain.

Inner ear also consists of cranial nerve VII(facial

 Physiology of hearing:
Hearing is conducted over two pathways: air and
bone.
 Sound waves reach the inner ear through three
routes:
1. Through the ossicular chain from the tympanic
membrane to the oval window.(AIR)
2. Directly across the middle ear by means of air
waves.(AIR)
3. Bone transmission through the walls of the
external auditory canal to the inner ear.(BONE)

Sound waves enter through the external auditory

canal and strike the tympanic membrane which
vibrates at various speeds according to pitch
ct

 Ossicles in middle ear vibrate and transmit

vibrations to the oval window.
 Fluid in the cochlea is set in motion.
 Wavelike motion of fluid passes the
vibrations onto the tiny hair like nerve
endings(receptors) in the organ of corti and
subsequently converted to electrical energy
 The electrical energy travels through the
vestibulocochlear nerve to the central
nervous system, where it is analyzed and
interpreted in its final form as sound.
Balance and equilibrium
 Sense of static balance (when a person is at rest) is
centered in the utricle and saccule of the inner ear.
 Balance with movement is associated with the
semicircular canals.
 Balance depends on:-
Receptors in the ears (labyrinth-vestibular system)
Tactile skin receptors
Visual input (eyes)
Proprioceptors in muscles(muscles and joints)
Send info about equilibrium and balance to the brain
(cerebella)
for coordination and perception in the cerebral cortex.
History taking
 An otologic history includes:-
 Demographic data
 Chief complaint e.g. hearing loss, pain, tinnitus,
vertigo, dizziness, drainage, loss of balance.
 Frequency, duration, onset, precipitating factors
 Past medical history
 Childhood illnesses – otitis media, eardrum
perforations, mumps, measles, meningitis,
tonsillectomy, ear surgery
 Medications
 Ototoxicity drugs – aminoglycosides, quinine,
chemotherapeutic agents. Asprin causes tinnitus.
 Allergies
 Family history of hearing loss
 Social history – occupation, leisure activities &
hobbies.
Physical examination
1. Inspection and palpation
 Note size, configuration, inflammation, lumps,
lesions, cysts.
 Palpate and manipulate pinna to detect
tenderness, nodules or tophi (small, hard nodules
in the helix that are deposits of uric acid crystals
characterics of gout).
2. Direct observation
 Tilt head slightly to the opposite side while pulling
the pinnae up, back and out.
 Use penlight to inspect canal for abnormality –
excess wax, redness, scaliness, swelling, drainage
and cysts.
Assessment of the auditory system
1. Otoscopy – using an otoscope. It has a light source
and magnifying lens. Hold the otoscope in the right
hand, grasp auricle with opposite hand and gently pull
outwards to straighten the canal.
 Insert the speculum and observe.
 A normal tympanic membrane appears pearly grey
and translucent. It is positioned obliquely at the base
of the canal.
2. Whisper test – the examiner covers the untested ear
while testing the other ear.
 Whisper softly from a distance of 1-2 feet from the
unoccluded ear out of patients sight.
 Patients with normal hearing can repeat what is
whispered.
3. Weber test – it uses bone conduction to test
  A tuning fork is set in motion by striking it and is
placed on the patients vertex or forehead.
 A patient with normal hearing hears the sound
equally in both ears or describes the sound as
centred in the middle of the head.
 A patient with conductive hearing loss hears the
sound better in the affected ear.
 A patient with sensorineural hearing loss hears
the sound better in the normal/better hearing ear.
 It is useful in detecting unilateral hearing loss.
4. Rinne test- useful for distinguishing between
conductive and sensorineural hearing loss.
 A vibrating tuning fork is placed on the mastoid
bone, once the patient signals he does not hear
the sound, the fork is put 2 inches in front of the
ear.
  Normally, air conduction is audible longer than bone
conduction.
 In conductive hearing loss, bone conducted sound is
audible as long as or longer than air conducted sound.
 In sensorineural hearing loss the air conducted sound
is heard longer than the bone conducted sound.
 DIAGNOSTIC
5. Audiometry – it is the most important diagnostic tool.
 Types of audiometry –
I. Pure tone audiometry – the sound stimulus consists of
a pure or musical tone.
II. Speech audiometry- ability to hear and discriminate
sounds and words. The louder the tone before the
patient perceives it, the greater the hearing loss. The
patient wears earphones and signals when the tone is
heard.
 When evaluating hearing, three characteristics are
important:-
a) Frequency – refers to the number of sound waves
produced per second. it is measured per cycle or
Hertz(Hz) per second.
 a normal human ear perceives sound in frequencies
ranging from 20 – 20,000Hz.
 Frequencies from 500 – 2000 Hz are important in
understanding everyday speech and are referred to as
speech range/frequencies
b) Pitch – used to describe frequency of a tone. 100 Hz is
considered low pitch and greater than 10,000Hz high
pitch.
c) Intensity – measures the loudness of sound in
decibels(dB). It is the pressure exerted by sound. Hearing
loss is measured in decibels.
 Sound louder than 80dB is perceived by the human ear as
harsh and can damage the inner ear.
TESTS TO DETECT VESTIBULAR CONDITIONS
1. ROMBERG TEST – assesses the inner ear for balance.
 The client stands with the feet together, arms by the
side and eyes closed. Note the ability of the patient to
maintain upright posture with only minimal amount of
swaying.
 If the client loses balance, it is a positive Romberg,
indicating vestibular problems.
2. CALORIC TEST – used to determine if an alteration exists
in the vestibular origin of the vestibulococchlear nerve.
 With the client either seated or supine, instil water into
the external ear canal. Sometimes warm and cold water
are alternated. Test the affected side first.
 Normal response to this is
 Nystagmus (involuntary rapid rhythmic eye
movements)
 Feeling of falling
  Vertigo (feeling of spinning)
 Nausea
 Vomiting
 Decrease or absence of these response within three
minutes indicates abnormality.
Contraindications:
 Perforated ear drum
 Infection of the middle ear
NB: anticipate vomiting and provide an emesis basin.
3. ELECTRONYSTAGMOGRAPHY –electrodes are placed
near the clients eyes to assess for alterations in the
vestibular system.
 caloric test is performed while eye movements are
recorded on a graph. it assesess occulomotor and
vestibular systems and their corresponding
interaction.
HEARING LOSS
 It ranges from minor difficulty in understanding
words or hearing certain sounds to total deafness.
Types
A) Conductive hearing loss: Also called
transmission hearing loss.
 Conduction of sound waves to the organs of
hearing is disrupted.
 It is further classified as
a. Air conduction loss – due to a defect in the
external auditory canal
b. Bone conduction loss – due to a defect in the
bones of the middle ear.
Causes
1. Obstruction to the passage of sound through the
external auditory canal.
 Impacted cerumen
 Otomycosis
 Swelling of the canal walls(marked)
 Foreign body
2. Abnormalities of the tympanic membrane
 Perforation
 Thickening
 Retraction
 Scarring
3. Pathologic change in the middle ear which
interferes with the mobility of the ossicular chain.
 Otosclerosis(fixation of the ossicle)
  Secretions
 Granulations
 Otitis media
B) PERCEPTIVE/SENSORINEURAL HEARING LOSS
 Involves a disturbance of the organs of the inner ear
or the transmitting nerve.
 It is further classified as:
 Sensory – due to damage in the cochlea
 Neural – due to damage of the eighth cranial nerve
Causes:
1. Toxic neuritis of the acoustic branch of the auditory
nerve. May occur in mumps, influenza, diptheria,
rubella.
mumps is a common cause of unilateral deafness.
2. Trauma – blow or falls causing
 Concussions of the labyrinth
 Fractures of the base of the skull – injure
labyrinth
Industrial noise and gunfire
3. Drugs and poisons e.g quinine, salicylates,
aminoglycosides, arsenic, mercury, lead.
4. Meningitis – destroys the nerves
5. Old age – presbycusis
6. Tumors – acoustic neuroma
7. Meniere’s disease
8. Congenital predisposition
C) CENTRAL HEARING LOSS
 The brain is unable to intepret sound waves after
they have been transmitted.
 May occur in atherosclerosis or after CVA
 The deficit is in the auditory nucleus of the
D) FUNCTIONAL HEARING LOSS – No organic
cause is found and there is no damage to the
auditory nerve.
 It is believed to arise from psychological or
emotional conditions.
E) MIXED HEARING LOSS – when the patient has
both conductive and sensorineural hearing loss.
CLASSIFICATION OF HEARING LOSS
LOSS IN DECIBELS INTEPRETATION
0 – 15 decibels Normal hearing
16 – 25 Decibels Slight hearing loss
26 – 40 decibels Mild impairment
41 – 55 decibels Moderate impairment
56 – 70 decibels Moderately severe
impairment
71 – 90 decibels Severely impaired
Greater than 90 decibels Profoundly deaf
Clinical manifestations
Tinnitus
Inability to hear in groups
Answering questions inappropriately
Cupping hand around ear
Showing irritability with others
Increased volume of TV or radio
Later manifestations
speech deteroriation – slur words, speech may sound
flat, loud or soft.
Fatigue – due to straining while listening to conversation
Indifference – disinterest as they cannot hear what is
said
Social withdrawl – keep to themselves as they don’t
hear what is said.
Insecurity – lack of self confidence, fear that they will
say the wrong things.
Indecision and procrastination - can’t hear thus they
doubt their ability to make decisions
Suspiciousness – hear part of conversations and
think others are talking about them.
False pride – conceal hearing loss by pretending not
to be interested in conversations.
Loneliness and unhappiness due to silence
Tendency to dominate conversation
Risk factors
Family history of sensory neural hearing loss
Congenital malformation of the ear esp. cranial
structure
Low birth weight less than 1.5 kgs

  Viral infections e.g. mumps, measles, chicken pox
 Age(old age)
 Exposure to loud noise
 Head trauma. Ear infections
 Malaria i.e celbral malaria &meningitis
MANAGEMENT
 It aims at restoring or assisting hearing, aural
rehabilitation and managing tinnitus.
1. Restore hearing:
 Provide antibiotics for bacterial infections & remove wax
 Acyclovir or oral corticosteroids for herpes virus infection
 Stop any ototoxic medications.This lessens the progress
of hearing loss or reverses the hearing loss.
2. Assist hearing
 Use of hearing aids which amplify sound.
 A hearing aid has: - a microphone which receives sound
waves from the air and changes them to electrical signals.
 An amplififier which increases the strength of
the electrical signal
Receiver / loudspeaker – which changes
electrical signals into sound waves.
Battery
3. Managing tinitus
 There is no proven treatment.
 Counsel the client and reassure
4. Aural rehabilitation
 Aims at maximising the hearing impaired clients
communication skills.
 Rehab is directed towards teaching more effective
use of other senses in communication e.g. vision.
 Speech or lip reading – involves integration of lip
movements, gestures, clues.
 Sign language – using hands to represent words or phrases.
 Non verbal aids – draw attention with hand movements.
Avoid chewing, careless expressions the patient may
misintepret
 Verbal aids – speak normally and slowly. Don’t exagerate
facial expression, use simple sentences, write difficult words
and avoid shouting and move closer to the better ear..
Implantable hearing devices:
1. Cochlear implant:- Type of hearing aid for profundly deaf
people.
2. contains a small computer chip which changes spoken word
to electrical impulses which are transmitted through the
auditory nerve endings in the cochlea to the brain where
they are intepreted.
3. Temporal bone stimulation:- for patients with conductive
hearing loss. It has an internal and external part. the external
part is above the ear and transmits sound to the inner device
which is implanted to the skull.
 Sound is transmitted to the inner ear through the
skull.
PREVENTION OF HEARING LOSS
1. Primary – aims at minimizing risks e.g. noise,
trauma, use of ototoxic drugs, and infection.
2. Secondary – early detection of hearing impairment
through screening and referral of any hearing
problems.
3. Tertiary – focuses on improvement of optimal
functioning through rehabilitation programmes.
CONDITIONS OF THE EXTERNAL EAR
IMPACTED CERUMEN
 Wax may form a solid plug or may be of a large amount
and blocks the external auditory canal.
Symptoms:
 Sense of blockage
 Conductive hearing impairment
 Otalgia
 tinnutus
Management:
1. removed by syringing/irrigating the outer ear with water
warmed to body temperature. The jet of water is aimed
above and behind the foreign body.
2. Manual removal of the wax using instruments i.e
cerumen curette or aural suction. Warm glycerine is
instilled 30 minutes before to soften the wax. Or mineral
FOREIGN BODY
A foreign body can either be animate or inanimate.
Determine the nature of the foreign body i.e food
stuff, insect, wood, plastic etc.
If the foreign body is a food substance, do not
attempt to irrigate as this will cause it to swell
leading to pain and possible injury to the eardrum.
If it is a small insect, shine a light, the insect may
be drawn to the light. Alternatively, apply a few
drops of mineral oil or glycerine and let the patient
lie on the affected side.
Visualise the foreign body and remove.
Do not attempt to remove an object without
visualising as this pushes it further in.
NB/irrigation,sunction and instrumentation are the
OTITIS EXTERNA/EXTERNAL OTITIS
It is inflammation or infection of the epithelium of
the auricle and external auditory canal
Causes
Water in the ear(swimmers ear)
Trauma to the skin of the ear canal
Causative organisms
Pseudomonas
Staphylococcus
Aspergillus
Clinical manifestations
Ear Pain
Discharge from external auditory canal
 Aural tenderness(not present in middle ear infections)
 Feeling of pressure & fullness inside the ear
 Fever
 Redness &swelling on outer ear(Cellulitis)
 Lymphadenopathy
 Pruritus
Otoscopy
 Ear canal is erythematous and edematous
 Discharge may be yellow or green, foul smelling
 Fungal infection – hairlike black spores may be visible.
Management
 Administer analgesics for pain i.e brufen,diclofenac
 Antibiotics specific to the causative organism e.g. CAF,
neomycin
 Antibiotic,cortcosteroid and fungal eardrops
Corticosteroids for inflammation
Warm moist compress for comfort
Fungal infections give nystatin
If fever and cellulitis is present give systemic
antibiotics.
Advice the patient to avoid cotton tipped
applicators to clean external auditory canal as they
may cause trauma which leads to infection.
Avoid getting ear canal wet, avoid swimming or
wear ear plugs when swimming.
CONDITIONS OF THE MIDDLE EAR
TYMPANIC MEMBRANE PERFORATION
It is caused by infection in the middle ear or by
trauma.
Sources of trauma include – skull fracture, explosive
injury, severe blow to the ears, foreign objects,
infections.
Management:
Most heal spontaneously within weeks after
rupture.
Some perforations may persist because scar tissue
grows over the edges of the perforation, preventing
extension of the epithelial cells across the margins
and final healing.
Incase of head injury or temporal bone fracture
For perforations that do not heal spontaneously
surgical intervention is required.
Tympanoplasty – surgical repair of the tympanic
membrane. It is based on:-
ACUTE OTITIS MEDIA
It is an acute infection of the middle ear lasting less
than six weeks.
Causes
Streptococcus pneumoniae
Haemophilus influenza
Moraxella catarrhalis
These organisms reach the middle ear after
eustachian tube dysfunction caused by
 obstruction related to URTI
Eustachian tube dysfunction due to inflammation of
surrounding structures e.g. sinusitis, adenoid
hypertrophy
Obstruction due to allergic reactions
Tympanic membrane perforation
Clinical manifestations
Otalgia relieved by perforation which can either be
spontaneous or therapeutic.
Drainage from the ear
Fever
Conductive hearing loss
Otoscopic examination- reveals a normal external
auditory canal. The tympanic membrane is
erythematous and often bulging.
Risk factors
Age i.e. less than one year
Chronic upper respiratory tract infections
Medical conditions that predispose to ear infections
e.g. Down’s syndrome, cleft palate.
Chronic exposure to second hand cigarette smoke
MANAGEMENT
Early and appropriate broad spectrum antibiotics
therapy – amoxycillin,augumentin ,clindamycin
erythromycin for 10 days.
Analgesics for pain.
If drainage occurs give antibiotic otic preparation.
Permanent hearing loss rarely occurs
Antihistamines for allergic reactions
Myringotomy or tympanotomy – incision of the
tympanic membrane. It is done to relieve pressure
and to drain serous or purulent fluid from the
middle ear thus relieving pain.
It is done under local anesthesia and microscope
guidance.
Drainage can be analysed for culture and
SERROUS OTITIS MEDIA/MIDDLE EAR EFFUSION/GLUE
EAR
Involves fluid in the middle ear without evidence of
active infection.
Results due to negative pressure in the middle ear
secondary to eustachian tube obstruction, which
can occur with:-
Radiation therapy
Barotrauma – sudden pressure changes e.g.
deep sea diving, airplane descent.
Eustachian tube dysfunction from URTI or
allergy.
Carcinoma – nasopharyngeal cancer
obstructing the tube.
Clinical manifestations:
Conductive hearing loss

Popping or crackling noises – occur as the
eustachian tube attempts to open
Otoscopy: tympanic membrane is dull
 air bubble may be visualised
MANAGEMENT
No treatment is necessary unless infection occurs.
If significant hearing loss occurs, a myringotomy is
done and a ventilatory tube inserted.
Low dose corticosteroids to reduce edema of the
E.T incase of barotrauma.
Valsalva maneuevor, forcibly opens the E.T by
increasing nasopharyngeal pressure must be done
cautiously as it may worsen the pain or cause
tympanic membrane perforation.
Teach methods of opening the E.T e.g yawning,
CHRONIC OTITIS MEDIA/ chronic suppurative otitis media
It is repeated episodes of acute otitis media causing
irreversible tissue damage and persistent tympanic
membrane perforation.
It damages the tympanic membrane, destroys the
ossicles and may sometimes involve the mastoid.
Clinical manifestations:
Varying degrees of hearing loss.
Persistent or intermittent foul smelling otorrhea
Pain – in case of acute mastoiditis. Postauricular
area is tender and may be edematous and
erythrematous.
Nausea
Dizziness
Tympanic membrane perforation
Otoscopy: may show perforation
Cholesteatoma can be identified as a white
mass behind the tympanic membrane or
coming to the external canal through a
perforation.
Cholesteatoma is an ingrowth of the skin of the
external layer of the ear drum into the middle
ear. The skin forms a sac that fills with
degenerated skin and sebaeous materials. The
sac can attach to the structures of the middle
ear, the mastoid or both.
Causes:
Staphylococcus aureus
Streptococcus
Proteus
Pseudomonas
Diagnosis
1. History and Physical exam
2. Otoscopy – shows a perforated T.M
3. Culture of drainage
4. Mastoid xray to rule out mastoiditis
5. Sinus xray
6. MRI or CT scan temporal lobe to check for bone
destruction secondary to cholesteatoma.
Compications:
 Cholesteatoma
 Hearing loss
 Facial paralysis
 Lateral sinus thrombosis
 Subdural abcess
 Mastoiditis
 Labyrinthitis
Medical management:
 Suctioning the ear under otoscopic guidance.
 Dry the ear by wicking – roll a piece of clean
absorbent cloth into a wick and insert into the ear.
Leave for 1 – 2 minutes, remove and replace with
another wick. Repeat until the wick is dry.
 Antibiotic drops or powder for purulent discharge. 2%
acetic acid or boric acid, 5% CAF, systemic antibiotics
only in acute infections
Surgical management:
1. Tympanoplasty – surgical reconstruction of the
tympanic membrane. It aims at establishing middle
ear function by closing the perforation, preventing
2. Ossiculoplasty – surgical reconstruction of the
middle ear bones to restore hearing. Ossicles are
reconnected using prosthesis made of stainless
steel thus reestablishing the sound conduction
mechanism.
3. Mastoidectomy – it aims at removing
cholesteatoma and creating a dry /non infected
ear.
 It is done through a postauricular incision.
Infection is eliminated by removing mastoid air
cells. There is risk of injury to the facial nerve.
OTOSCLEROSIS
It is a condition characterised by abnormal spongy
bone formation around the stapes.
It results from the formation of new abnormal
spongy bone especially around the oval window
resulting in fixation of the stapes.
The stapes does not vibrate thus sound cannot be
transmitted.
It is more common in women and is worsened by
pregnancy.
It is a hereditary condition.
Clinical manifestations
Progressive conductive or mixed hearing loss
Tinnitus
Bone conduction is better than air conduction in the
Management:
Sodium flouride to mature abnormal spongy growth
and prevent breakdown of bony tissue.
Amplification with a hearing aid
Calcium gluconate and vitamin D to retard bone
resorption.
Stapedectomy- removal of the stapes
superstructure and part of the foot plate and
inserting a tissue graft and a suitable prosthesis.
Before surgery ensure that the client is free from
infection.
Pre and post op audiograms are performed to test
hearing acuity levels.
Post op the client should lie on the non operated
ear with the head of the bed elevated. This reduces
edema and prevents dislodgement of the
On discharge the patient is adviced to avoid
straining(exercise, lifting), to blow the nose gently,
one nostril at a time, avoid air travel for one month
and sneeze with the mouth open to prevent rupture
of the oval window.
MASTOIDITIS
It is inflammation of the mastoid process secondary
to repeated middle ear infection.
An inadequately treated infection reappears after
two or more weeks after initial episode of otitis
media.
Clinical manifestations:
Tenderness and swelling over the mastoid process
Ear pain
Conductive hearing loss
Fever
Discharge
Protrusion of the pinnae
Diagnosis
History and physical exam
CT Scan mastoid process – mastoid air cells filled
with fluid.
Management
Systemic antibiotics
Surgical drainage of the abscess or mastoidectomy
due to recurrent or persistent tenderness, fever,
headache and discharge.
Complication
deafness
Brain abscess
death
NURSING PROCESS FOR A PATIENT UNDERGOING
MASTOID SURGERY
Assessment:
 Health history – describe the ear condition,
infection, otalgia, otorrhea, hearing loss, vertigo.
 Duration and intensity, causes, previous
treatment, all medication the patient is taking,
allergies, family history of disease.
 Physical assessment – erythema, edema,
otorrhea, lesions.
Nursing diagnosis
1. Anxiety related to surgical procedure, potential
hearing loss, potential taste disturbance, potential
loss of facial movement.
2. Acute pain related to mastoid surgery
3. Risk for infection related to surgery and surgical
4. Disturbed auditory perception related to ear
disorder, surgery, packing of the ear.
5. Risk for trauma related to impaired balance or
vertigo during the immediate post op period.
6. Disturbed sensory perception related to potential
damage to the facial nerve.
7. Impaired skin integrity related to ear surgery and
incision sites
8. Deficient knowledge about mastoid disease,
surgical procedure and post op care.
Interventions
9. Reduce anxiety – reinforce the information
discussed with the surgeon.
 Encourage patient to discuss any anxieties or
concerns.
3. Prevent infection – impregnate the external
auditory canal through wick/packing with
antibiotic solution.
 Prophylactic antibiotics are administered
 Prevent water from entering the external
auditory canal for 6 weeks. A cotton ball with
insoluble substances e.g. petroleum jelly is
placed loosely in the ear canal to prevent water
from contaminating the external auditory canal.
4. Improving hearing and communication – hearing
in the operated ear may be reduced for several
weeks because of edema, accumulation of blood
and tissue fluid in the middle ear and dressings or
packing.
 Reduce environmental noise
 Face the patient when speaking
  Use non verbal clues e.g. facial expression,
pointing, gestures.
 Instruct family on effective ways to
communicate with the patient.
5. Prevent injury – vertigo may occur if the
semicircular canals are traumatized.
 Give antiemetics
 Antihistamines
 Provide safety measures e.g. assisted
ambulation to prevent injury/falls.
6. Preventing altered sensory perception – there is a
potential complication of facial nerve injury.
 Instruct the patient to report any evidence of
facial nerve injury/weakness such as drooping of
the mouth on the operated side, slurred speech,
decreased sensation and difficulty in
7. Promote wound healing – instruct the patient to
avoid heavy lifting, straining, exertion and nose
blowing for 2 – 6 weeks post op to prevent
dislodging of the prosthesis or the tympanic
membrane.
8. Teach the patient self care – instruct about
prescribed meds
 provide information about expected effects and
potential side effects of the medication.
 Instruct on activity restriction
 Prompt reporting of complaints e.g. infection,
facial nerve weakness, taste disturbance.
CONDITIONS OF THE INNER EAR
MOTION SICKNESS
Is a disturbance of the equilibrium caused by
constant motion e.g. in a vehicle, merry go round or
a ship. the brain senses movement but eyes can’t
perceive the movement.
Clinical manifestations
Sweating,Pallor,Nausea, Vomitingdizziness
Management
Antihistamines e.g. dimenhydrinate. It relieves
nausea and vomiting by blocking the conduction of
the vestibular pathway of the inner ear.
Anticholinergics e.g. scopolamine – it antagonises
the histamine response.S/E dry mouth, drowsiness
Look outsidethe car while travelling, take a front
MENIERE’S DISEASE
It is abnormal inner ear fluid balance caused by
malabsorption in the endolymphatic sac or in the
endolymphatic duct.
Clinical manifestations
Fluctuating, progressive sensorineural hearing loss
Tinnitus or roaring sound in the ear
Feeling of pressure or fullness in the ear
Episodic, incapacitating vertigo accompanied by
nausea and vomiting
Types
Cochlear – fluctuating progressive sensorineural
hearing loss associated with tinnitus and aural
tenderness in the absence of vestibular symptoms.
Vestibular- characterized by occurrence of episodic
Management:
Low sodium diet(200mg/day)
Limit foods high in salt
Give plenty of fresh fruits, vegetables and whole
grains.
Limit alcohol intake as it may change the volume
of inner ear fluid and worsen symptoms.
Eat meal and snacks at regular intervals
Avoid aspirin as it increases tinnitus and dizziness
Pharmacotherapy
Antihistamines to suppress the vestibular system
Tranquilizers e.g. diazepam in acute cases to help
control vertigo.
Antiemetics e.g. promethazine to control nausea
and vomiting and the vertigo because of the
antihistamine effect.
Surgical management aims at eliminating the
attacks of vertigo.
Endolympahtic sac decompression or shunting –
equalises the pressure in the endolympatic
space. A drain is inserted through a post auricular
incision.
Middle and inner ear perfusion – ototoxic
medication (streptomycin or gentamycin) are
administered to the patient by infusion into the
middle and inner ear. They destroy the vestibular
function and decrease vertigo . There is risk of
significant hearing loss.
Vestibular nerve sectioning – the nerve is cut thus
preventing the brain from receiving input from
the semicircular canals
LABYRINTHITIS
Inflammation of the inner ear either due to bacteria
or virus.
Viral causes:
Mumps
Rubella
Influenza
Bacterial is as a complication of otitis media. The
bacteria get to the middle ear through the oval or
round window.
Head injury, allergy, URTI
Clinical manifestations
Sudden onset vertigo with nausea and vomiting
Sensorineural hearing loss
Tinnitus
Management:
For bacterial labyrithitis – intravenous antibiotics
Fluid replacement therapy
Antihistamines
Antiemetics
Viral labyrinthitis treatment is based on the
symptoms.
OTOTOXICITY
 Due to adverse effects of medication on the cochlear,
vestibular apparatus or cranial nerve VIII.
 Most cause irreversible hearing loss except aspirin and
quinine
 High doses of aspirin cause bilateral tinnitus.
 IV meds especially aminoglycosides are the most
common cause of ototoxicity and destroy the hair cells
of the organ of corti.
Prevention
1. Counsel patients on side effects of these meds.
2. Use with caution in patients at high risk of
complications i.e. children, elderly, pregnant, patients
with kidney or liver problems and patients with current
hearing disorders.
3. Monitor hearing on those receiving long term IV
Selected ototoxic substances
Diuretics i.e furosemide
Aminigycosides
Asprin
Antimalarial agents i.e quinine
Chemotherapeutic agents i.e cisplastin
Alcohol
Metals i.e mercury
ACOUSTIC NEUROMA
Slow growing benign tumors of cranial nerve VIII,
usually arising from the Schwann cells of the
vestibular portion of the nerve.
Occurs where the nerve enters the internal auditory
canal or temporal bone from the brain.
Clinical manifestations:
Unilateral tinnitus
Sensorineural hearing loss
Mild intermittent vertigo
Diagnosis
History and physical exam
Vestibular tests
Audiometry
Management:
Surgical removal of tumor.
These tumors don’t respond well to radiation or
chemotherapy
Complications of surgery include:
>facial nerve paralysis
>cerebrospinal fluid leakage
>meningitis
>cerebral edema
THE NOSE AND NASAL CAVITY
Anatomy and physiology:
It is divided into two equal parts by a septum. The
posterior bony part of the septum is formed by the
perpendicular plate of the ethmoid bone and the
vomer.
Anteriorly it consists of hyaline cartilage.
The roof is formed by the cribriform plate of the
ethmoid bone, the sphenoid bone, frontal and nasal
bones.
The floor – roof of the mouth with the hard palate
anteriorly and soft palate posteriorly.
It is lined with highly vascular ciliated columnar
epithelium which contains the mucus secreting
goblet cells.
Posterior nares – openings from the nasal cavities
into the the pharynx.
Paranasal sinuses – are cavities in the bones of the
face and cranium which contain air. There are tiny
openings between the paranasal sinuses and the
nasal cavity.
They are lined with mucus membrane continuous
with that of the nasal cavity.
The main sinuses are:-
Maxillary sinuses – in the lateral walls
Frontal and sphenoidal - in the roof
Ethmoidal - in the upper part of the lateral walls.
The sinuses are used in speech resonance and they
lighten the skull.
Nasolacrimal ducts extend from the lateral walls of
the nose to the conjunctival sacs of the eyes. They
Functions of the nose
Warms air – due to the high vascularisation
Filters and cleans air – the hairs trap particles and
smaller particles adhere to the mucus.
Humidification
Olfaction – nerve endings in the cribriform plate
convey impulses to the olfactory nerves.
ASSESSMENT OF THE NOSE AND PARANASAL
SINUSES
Inspect the external nose for lesions, asymmetry or
inflammation
Examine the internal structures of the nose – the
patient tilts back and the tip of the nose is pushed
back. Note the mucosal colour, swelling, exudate
or bleeding.
Inspect the inferior and middle turbinates
Palpate the frontal and maxillary sinuses for
tenderness
Transilluminate to check for fluid or pus – light does
not go through if present.
NB: transillumination is passing a strong light
through a bony area to inspect sinuses.
RHINITIS
It is a group of disorders characterised by
inflammation and irritation of the mucus
membranes of the nose.
It can be acute, chronic or allergic.
Causes:
Change in temperature
Odors
Infection – common cold
Systemic diseases
Drugs e.g cocaine
Foreign bodies
Medication e.g. nasal decongestants
foods
Clinical manifestations
Rhinorrhea – excessive nasal drainage/ runny nose
Nasal congestion
Sneezing
Pruritus of the nose, roof of the mouth, throat eyes
and ears
Headache especially if sinusitis is present
Management:
identify the cause
Antihistamines for sneezing pruritus and rhinorrhea
e.g chlopheniramine, cetrizine
Oral decongestants for nasal congestion
Saline nasal spray acts as a decongestant and
liquefies mucus.
Nurse in a warm well ventilated environment to
ensure fresh air and prevent spread of infection to
others.
Give pleny of hot fluids to soothe the throat and
rehydrate.

ASSIGNMENT:read and make notes on viral

rhinitis(common cold)
EPISTAXIS (NOSEBLEED)
It is hemorrhage from the nose caused by rupture
of tiny distended vessels in the mucus membrane
of the nose.
Common site is in the anterior septum, where 3
major blood vessels enter the nasal cavity i.e.
The anterior ethmoidal artery
The sphenopalatine artery
The internal maxillary branches
Risk factors
local infections – rhinitis
Systemic conditions e.g. hypertension
Drying of the mucus membrane especially in high
altitude
Tumors
Thrombocytopenia
Use of aspirin
Management:
Determine the site of bleeding(use nasal penlight or
speculum)
Apply direct pressure. The patient sits upright and
tilts the head forward(this prevents aspiration and
swallowing of blood) and pinches the nose for 5 –
10 minutes continuously.
Apply cold compress on the patients forehead. If
the source is not identified – pack the nose with
gauze impregnated with liquid paraffin, petroleum
jelly or antibiotic ointment
If bleeding persists, a cotton ball soaked in
vasoconstrictor solution(adrenaline, epinephrine) is
The pack may remain in place for 48 hours.
A balloon catheter may be used to arrest posterior
bleeding
Antibiotics are prescribed due to the risk of sinusitis
and toxic shock syndrome.
Nursing management
Monitor vital signs
Assist in the control of bleeding
Relieve patient anxiety
Teach on ways to avoid epistaxis – forceful
noseblowing, straining, high altitudes and nasal
trauma e.g. nose picking.
Teach how to apply direct pressure.
Refer if bleeding is uncontrolled ,patient requires
fluid replacement or blood transfusion
NASAL FRACTURE
It is the most common facial fracture
It may affect the ascending process of the maxilla
and the septum. the torn mucous membrane
results in a nose bleed
It is usually as a result of direct assault.
Clinical manifestations:
Pain
Bleeding from the nose internally into the pharynx
Swelling of the soft tissues adjacent to the nose
Periorbital ecchymosis(bruising)
Nasal obstruction
Deformity
Assessment:
Internal examination of the nose to rule out fracture
of the nasal septum and a sub mucosal septal
hematoma
Clear fluid draining from either nostril suggests a
fracture of the cribriform plate with leaking CSF. It is
differentiated from mucus through use of a
glucostick. CSF contains glucose.
Palpate for deviations of the bone
X-ray to rule out extension of the fracture to the
skull.
Management
Control bleeding by packing.
 Ensure patent airway and rule out cervical spine
fracture
Refer to a specialist after 3 -5 days to allow edema
to subside for reduction of fracture or rhinoplasty
to reshape the external appearance of the nose
especially where reduction is delayed past 7-10
days and bone healing begins
Nursing management:
Apply ice pack or cold compress. Keep the head
elevated.
The patient breathes through the mouth because of
the nasal pack thus give mouth rinses to help
moisten oral mucous membranes.
Analgesics e.g. NSAID’s
Advice patient to avoid sports activities for 6weeks
Complications
Hematoma, infection,abscess and avascular/septic
necrosis
NASAL POLYPS
Are benign mucus membrane masses that form
slowly in response to repeated inflammation of the
nasal mucosa.
They appear as bluish grayish projections in the
nares
Clinical manifestations:
Nasal obstruction
Nasal discharge
Speech distortion
Visible polyp
Management:
Removed by endoscopy or nasal surgery
Slow their growth by applying corticosteroids.
DEVIATED SEPTUM
A condition in which the size of the septum is not
proportional to the size of the nose or the septum is
deflected from the normal straight position of the
nasal septum.
Causes
Trauma to the nose
Congenital disproportion
Clinical manifestations:
Obstruction or nasal breathing
Nasal edema in cases of trauma
Dryness of the nasal mucosa
Bleeding incase of trauma
In cases of severe deviation, it may block the sinus
Management
Nasal septoplasty – surgical reconstruction and
proper alignment of the deviated septum.
SINUSITIS
Inflammation of the mucus membranes of the
sinuses.
ACUTE SINUSITIS
It is rapid onset infection in one or more of the
paranasal sinuses that resolves with treatment.
Subacute sinusitis: is persistent purulent nasal
discharge despite therapy with symptoms lasting
less than three months.
Sinusitis occurs due to blockage/obstruction of the
sinus cavities
It often follows a URTI or an exacerbation of allergic
Other conditions that block the normal flow of sinus
secretions:-
Abnormal structure of the nose
Enlarged adenoids
Tooth infection
Trauma to the nose
Tumors
Pressure of foreign bodies
Clinical manifestations:
Facial pain or pressure over the affected sinus
Nasal obstruction
Fatigue
Purulent nasal discharge
Fever
Headache
Ear pain
Sense of fullness
Dental pain
Decreased sense of smell
Early morning periorbital edema
Diagnosis
History and physical exam with emphasis on head
and neck.
Palpate the sinuses
Percuss sinuses – pain
Transillumination – there will be decreased
transmission of light
CT Scan
MANAGEMENT
The goals are to treat infection, shrink the nasal
mucosa and relieve pain.
Antibiotics – 1st line – amoxyl, ampicillin, septrin,
erythromycin
2nd line cefuroxime, augmentin. For those with
prolonged symptoms.
They are given for 10 – 14 days in serious
bacterial infection
Nasal decongestants or nasal saline spray –
improve patency of the openings of the sinuses and
improve sinus drainage. Maximum use of 3 – 4
days.
Antihistamines for allergy e.g. cetrizine
Heated mist and saline irrigation to open blocked
passages.
Nursing
Teach on signs of complications such as periorbital
edema and severe headache, nuchal rigidity.
Teach methods of promoting sinus drainage e.g
Humidification of the air at home and use of
steam inhalation
Warm compress to relieve pressure.
Increasing fluid intake
Avoid swimming, diving, air travel during acute
infection
Stop smoking
Side effects of nasal sprays – rebound congestion
Completion and correct use of antibiotics
Complications
Meningitis
Brain abscess
Osteomyelitis
CHRONIC SINUSITIS
It is due to prolonged, repeated or inadequately
treated acute sinus infection with symptoms lasting
more than three months. Irreversible mucosal
damage may occur.
Pathophysiology
Mechanical obstruction of the ostia of the frontal,
maxillary and anterior ethmoidal sinuses.
Obstruction prevents adequate draining and
resultant stagnation of secretions which provides an
ideal media for bacterial growth.
Blockage that persists for more than three weeks in
an adult may be due to:-
Infection
Allergy
Clinical manifestations:
Cough because of thick discharge constantly
dripping backwards into the nasopharynx.
Chronic hoarseness
Chronic headache – periorbital and facial pain
Mouth breathing – snoring and sore throat.
Decrease in smell and taste
Sense of fullness in the ears
Complications
Orbital cellulitis
Meningitis
Encephalitis
MANAGEMENT
Antibiotics – augmentin, clarythromycin. Macrolides
increase mucocilliary clearance and improve sinus
symptoms, decrease nasal secretions and polyp
size associated with chronic sinusitis.
Nasal decongestants / saline sprays
Antihistamines
Surgical management:
Endoscopy – to correct structural deformities that
obstruct the openings of the sinuses.
Excising and cauterising nasal polyps
Correcting deviated septum
Incising and draining the sinuses
Removing tumors
Nursing management
Teach gentle nose blowing as forceful blowing
increases symptoms
Increase environmental humidity
Take plenty of fluids
Apply local heat
Elevate the head of the bed to promote sinus
drainage
Importance of following medication regimen
Signs that require follow up.
THE PHARYNX
REVIEW OF ANAT & PHYSIO
It is a tube 12 -14 cm long. It extends from the base
of the skull to the level of the 6th cervical vertebra.
It lies behind the nose ,mouth and larynx. It is wider
in its upper end.
It is divided into three:-
Nasopharynx – it lies behind the nose, above the
level of the soft palate. On its lateral walls are the
2 openings for the auditory tubes. The posterior
wall has the pharyngeal tonsils which consist of
lymphoid tissue.
Oropharynx- it lies behind the mouth, from below
the level of the soft palate to the level of the
upper part of the body of C3. its lateral walls
  laryngopharynx – extends from the oropharynx
above and continues as the esophagus below.
 The pharynx is composed of three layers of
tissue:-
1. The mucous membrane lining – the mucous varies
slightly in different parts. In the nasopharynx it is
ciliated columnar epth, in the oropharynx and
laryngopharynx it is stratified squamous
epithelium.
2. Fibrous tissue – it forms the intermediate layer . It
is thicker in the nasopharynx where there is little
muscle and becomes thinner towards the lower
end where the muscle layer is thicker.
3. Muscle tissue – consists of several involuntary
constrictor muscles that play a part in the
mechanism of swallowing.
Functions
Passage for air and food
Warming and humidifying air
Taste – nerve endings for the sense of taste in the
epithelium of the oral and pharyngeal parts.
Hearing – eustachian tube equalises pressure
Protection – through tonsils
Speech – provide a resonating chamber for sound.
LARYNX / VOICE BOX
Extends from the root of the tongue and hyoid bone
to the trachea.
Lies infront of the laryngopharynx.
It is composed of several irregularly shaped
cartilages attached to each other by ligaments and
membranes.
The main cartilages are:-
1 thyroid cartilage
1 cricoid cartilage
2 arytenoid cartilages
1 epiglottis
The thyroid cartilage forms the laryngeal
prominence. It is incomplete posteriorly. Its upper
part is lined with stratified squamous epithelium
and its lower part with ciliated columnar epithelium.
The cricoid cartilage is shaped like a signet ring. It
is lined with columnar epithelium.
Arytenoid cartilages – are roughly pyramid shaped
hyaline cartilages. They form part of the posterior
wall of the larynx. It gives attachment to the vocal
cords and muscles. It is lined with ciliated columnar
epithelium.
The epiglottis is a leaf shaped fibroelastic cartilage
lined with stratified sqaumous epithelium. It closes
off the larynx during swallowing, protecting the
lungs from accidental inhalation of foreign objects.
The vocal cords are two folds of mucous membrane
with cord like free edges which extend from the
inner wall of the thyroid prominence anteriorly to
the arytenoid cartilages posteriorly.
When muscles are relaxed, vocal cords open and
are said to be abducted. In this position they
produce a low pitched sound.
When muscles controlling vocal cords are
contracted, vocal cords are stretched out tightly
across the larynx and are said to be adducted. They
produce a high pitched sound.
When not in use the vocal cords are adducted.
Functions
Production of sound
Speech
Protection of the lower respiratory tract
Passageway for air
Humidifying, filtering and warming air
Assessment of the throat
History – sorethroat, discharge from the throat,
sense of lump or swelling, dypnea, difficulty
swallowing, hoarseness, cough
Physical exam – ask client to open mouth wide, use
a tongue depressor to lower the tongue. View the
anterior and posterior pillars, palatine tonsils, uvula
and posterior pharynx. Inspect for colour, size,
symmetry, exudate and ulceration.
TONSILITIS AND ADENOIDITIS
Tonsils are composed of lymphoid tissue and are
situated on each side of the orophoarynx. Acute
infection of these glands is tonsillitis.
Adenoids or pharyngeal tonsils consist of lymphoid
tissue near the center of the posterior wall of the
nasophaynx.
Caused by Group A beta hemolytic streptococcus.
Manifestations;
Sore throat
Fever
Snoring
Difficulty swallowing
Mouth breathing
Foul smelling breath
Voice impairment
Noisy respirations
Nasal obstruction
Infection can spread to the middle ear through the
eustachian tube causing acute otitis media.
Management:
Antibiotics for bacterial infection – penicillins
Increased fluid intake
Analgesics
Salt water gargles
Surgery – tonsilectomy, adenoidectomy,
adenotonsilectomy.
Indications for surgery
Repeated episodes despite antibiotics
Hypertrophy of the tonsils and adenoids that could
cause obstruction and obstructive sleep apnea
Repeated attacks of purulent otitis media
Suspected hearing loss due to serous otitis media
that has occurred in association with enlarged
tonsils and adenoids.
Peritonsilar abscess that occludes the pharynx,
making swallowing difficult and endangering
patency of the airway.
Contraindications
age less than 5 years
Cleft palate – done after repair
Bleeding diseases
Active PTB
NURSING MANAGEMENT
Routine pre op care – consent, NPO for 6 hours
before surgery, pre op checklist, vital signs,
rehydrate patient, allay anxiety.
Give analgesics for pain
Warm water gargles to relieve pain and sooth the
throat.
Post op: nurse prone with the head turned to the
side to allow drainage from the mouth and the
pharynx
 do not remove the oral airway until the gag and
swallowing reflex have returned.
Apply an ice collar around the neck – this reduces
edema and hemorrhage.
If there is no bleeding give cold water and drinks to
the patient.
Advice the patient to avoid too much talking and
coughing as they will cause throat pain.
Inform the surgeon if the patient vomits blood, if
there is increased temperature or pulse.
Teach the family on how to observe for signs of
bleeding
To give saline solutions for mouthwash/gargle to
cope with the thick mucus and halitosis that may
present after surgery.
Explain that sorethroat , vomiting and stiff neck
may occur in the first 24 hours.
Liquid and semiliquid diet is given for several days.
Avoid spicy, hot, acidic and rough foods.
PERITONSILLAR ABSCESS
Is a collection of purulent exudate between the
tonsilar capsule and surrounding tissues.
It may develop after an acute tonsilar infection that
progresses to local cellulitis and abscess. It is
caused by beta hemolytic streptococcus.
In severe cases, the infection can spread over the
palate and to the neck and chest. Edema can cause
airway obstruction, which can become life
threatening and is a medical emergency.
Clinical manifestations
Fever
Trismus – inability to open the mouth due to spasm
of the muscles of mastication.
Drooling
Odynophagia – a severe sensation of burning,
squeezing pain when swallowing
Dysphagia – difficulty or pain while swallowing
Otalgia
Enlarged cervical lymph nodes
Swelling of the soft palate
Tonsilar hypertrophy
Dehydration
Management
Antibiotics - effective in the early stages and
resolves
Surgical management to prevent rupture and
aspiration
Fine needle aspiration of pus from the abscess
Incision and drainage
If the patient presents with acute airway
obstruction they may require intubation –
cricothyroidotomy or tracheotomy.
Pre op give warm saline gargles and mouthwashes
to provide relief.
Post op cool saline gargles at intervals of 1 – 2
hours for 24 – 36 hours.
Give plenty of fluids
LARYNGITIS
It is inflammation of the mucus membrane lining
the larynx accompanied by edema of the vocal
cords.
Causes
Voice abuse e.g. shouting
Exposure to dust, chemicals and other pollutants.
URTI
Changes in temperature
Smoking
Clinical manifestations
Hoarse voice
Aphonia – complete loss of voice
Severe cough – dry , sore throat.
Persistent urge to clear the throat
Management
Rest the voice
Avoid irritants – dust, smoking
Inhale steam. Menthol may be added to sooth the
throat.
For bacterial infection, provide antibiotics.
Increase fluid intake to thin the secretions
Chronic
Rest the voice
Eliminate any respiratory tract infection
Stop smoking and 2nd hand smoking
Topical corticosteroids or by inhalation eg
beclomethasone dipropionate
Advice the patient to stay in a well humidified
Teach on complications to report:-
Loss of voice with sore throat that makes
swallowing saliva difficult
Hemoptysis
Noisy respirations
Continued hoarseness after resting the voice for
more than 5 days.
CANCER OF THE LARYNX
It is a malignant tumor in and around the larynx.
It is mostly a sqaumous cell carcinoma
Predisposing factors
Carcinogens – tobacco, alcohol, asbestos, smoking,
tar products, cement dust e.t.c
Straining the voice
Chronic laryngitis
Age more than 60years
Family predisposition
History of alcohol abuse
Signs and symptoms
Hoarse voice for more than 2 weeks – harsh, raspy,
low pitched
Persistent cough
Sore throat
Pain and burning in the throat esp. consuming hot
liquids or citrus juices.
Lump may be felt in the throat.
Later symptoms
Dysphagia
Dyspnea
Unilateral nasal obstruction or discharge
Persistent hoarseness
Foul breath
Metastasis: weight loss, cervical lymphadenopathy,
Categories
Supraglottic – involves the false vocal cords
Glottic – involves the true vocal cords
Subglottic – downward extension of the disease
from the vocal cords.
Diagnosis
History and physical exam
Laryngoscopy
Histology of tumor sample
Management
Radiation – for early stages or together with surgery
& chemo
Surgery – laryngectomy – surgical removal of part
or all of the larynx and surrounding structures.
Partial laryngectomy – remove part of the larynx,
Supraglottic laryngectomy – remove the hyoid
bone, glottis and false vocal cords. Tracheostomy
tube is left in place until glottic airway is
established. Enteral feeds are given until healing
occurs. Aspiration is a potential complication.
Voice is preserved though it may change.
Hemilaryngectomy – remove one true cord, one
false cord and the tumor. Pt has NGT and
tracheostomy for several days post op, there is
high risk of aspiration. Voice changes but airway
and swallowing remain intact.
Total laryngectomy – remove all laryngeal
structures – hyoid bone, epiglottis, cricoid
cartilage and 2 or 3 rings of the trachea. Voice
changes and a permanent tracheostomy is
inserted.
Speech therapy – pre op counsel the patient on loss
of voice and alternative methods of
speech/communication e.g writing, lip reading,
esophageal speech, artificial larynx etc.
NURSING CARE OF PATIENT UNDERGOING
LARYNGECTOMY
ASSESSMENT
Health history- hoarseness, sorethroat,
dypnea, dysphagia, pain or burning in the
throat.
Physical examination-thorough head and neck
examination with emphasis on patient airway.
Palpate neck for swelling or adenopathy.
General state- nutritional status and BMI
Pre operative evaluation by a speech therapist
Family Social history- history of cancer in the
family, history of alcohol intake.
Assess the psychological readiness of the
patient and the family.
NURSING DIAGNOSES
Deficient knowledge about surgical procedure
and post-op care
Anxiety and depression related to the
diagnosis of cancer and impending surgery.
Ineffective airway clearance related to excess
mucus production secondary to surgical
alteration of the airway.
Impaired verbal communication related to
anatomical deficit secondary to removal of the
larynx and to edema.
Imbalanced nutrition less than body
requirements related to inability to ingest food
secondary to swallowing difficulties.
Disturbed body image and low self esteem
Nursing diagnosis continued
Self care deficit related to pain, weakness,
fatigue, musculoskeletal impairment
secondary to surgical procedure.
Pain
Potential for complications- respiratory
distress (hypoxia, airway obstruction, tracheal
edema), hemorrhage, infection, aspiration
NURSING INTERVENTIONS
Teach the patient pre operatively.
Clarify misconceptions of disease, nature of
surgical procedure and its effect on speech.
For complete laryngectomy make the
patient understand that the natural voice
will be lost but special training can provide
a means of communication.
Review equipment and treatments for post
op care with the patient and family. Teach
important coughing and deep breathing
exercises and assist the patient to perform
a return demonstration.
INTERVENTIONS continued

Reduce anxiety and depression

Provide the patient and the family with
opportunities to ask questions and verbalise
feelings.
Arrange for someone post laryngectomy to
visit the patient.
Active listening to the patient and providing
an environment that promotes open
communication and allows patient to
verbalise feelings.
Nursing interventions
• Maintain a patent airway
– Position the patient in fowlers or semi-fowlers
position after recovery from anaesthesia. It
reduces surgical edema and promotes lung
expansion.
– Observe patient for restlessness, dyspnea…
– Assess/ auscultate lung sounds
– Use with caution drugs that depress respiration e.g
opiods. However ensure adequate pain relief as
pain may cause shallow breaths and ineffective
cough.
– Encourage to turn, cough and take deep breaths.
Suction to remove excess secretions.
– Early ambulation to prevent atelectasis,
pneumonia and DVT
Perform laryngectomy tube care (similar to
tracheostomy care).assignment: review
tracheostomy care.
Clean stoma daily with saline solution or
prescribed solution. Frequently patient coughs
up large amounts of mucus through this
opening. To prevent excess mucus production
ensure the air is humidified.
Laryngectomy tube may be removed after
stoma is well healed, within 3 – 6 weeks.
Teach how to clean and change tube.
Promoting alternative communication methods
Establish means of communication
E.g place a call bell within easy reach of the
patient
Writing material, insert IV in the opposite hand
Hand signals
Give adequate time as this method of
communication takes time and can be frustrating
to the patient.
Promote adequate nutrition and hydration
Post op the patient may be NPO for several days.
Alternative feeding and hydration methods are
used.
IV fluids, enteral feeding through NGT or
gastrotomy tube, parenteral nutrition.
When starting oral feeds, start with thick liquids
 Observe for and report difficulty in swallowing.
Appetite may be altered for sometime due to loss
of sense of smell as taste and smell are closely
related.
Pt should avoid sweet food to increase salivation
& reduce appetite.provide mouth wash to the pt
Monitor weight ,lab findings ,vs
Promoting positive body image and self esteem.
Due to disfiguring surgery and loss/altered
communication pattern.
Encourage patient to express feelings and
counsel or refer to a support group.
Promoting self care management
Encourage participation and provide positive
reinforcement
Monitoring and managing potential complications
Hypoxia causes:- restlessness, initial increase in
BP followed by hypotension and somnolence.
Cyanosis is a late sign.
Immediately rule out obstruction by having the
patient cough or breath in deeply.
Reposition to ensure an open airway.
Administer oxygen as prescribed.
Prepare always for possible intubation and
mechanical ventilation.
Hemorrhage – notify the surgeon incase of active
bleeding at the surgical site, drains or trachea.
Monitor vitals for changes – increase in pulse,
decrease in BP, rapid deep respirations, cold
clammy skin may indicate active bleeding.
Give IV fluid and blood components
Manage shock
Infection – monitor for signs of infection e.g.
increase in temperature and pulse, change in
type of wound drainage, increased areas of
redness or tenderness at surgical site, purulent
drainage, odor, increased wound drainage.
Administer antibiotics and culture drainage
Wound breakdown – caused by infection, poor
wound healing, radiation therapy or tumor
growth. It can create an emergency as the carotid
artery is close to the stoma site and may be
eroded and rupture.
observe stoma site for wound breakdown,
hematoma, bleeding and report to surgeon.
Aspiration – risk due to depressed cough,
sedating effects of anaesthesia and analgesics,
alteration in the airway, impaired swallowing and
 During tube feedings position the head of the bed
at 30 degrees or higher and remain so for 30 -45
minutes after feeding.
Check tube position before each feed.
Teaching
Tracheostomy and stoma care. Importance of
humidification at home, avoid air conditioned air
as it may be too cold or too dry.
Hygiene and safety measure in the shower to
prevent water entering the stoma. No more
swimming.
Signs of infection
Handwashing before and after tracheostomy
care. Proper disposal of mucus and soiled
dressing.
Perform oral care regularly to avoid halitosis and