SUBARACHNOID HEMORRHAGE
INTRODUCTION
🞂 Fourth most frequent cerebrovascular disorder
—following atherothrombosis, embolism, and primary intracerebral
hemorrhage, but one that is often disastrous
🞂 Non traumatic cases MC due to aneurysmal rupture
🞂 Saccular aneurysms also have been called "berry" aneurysms
🞂 They take the form of small, thin-walled blisters protruding from
arteries of the circle of Willis or its major branches
🞂 Their rupture causes a flooding of the subarachnoid space with blood
under high pressure
Subarachnoid hemorrhage
SAH Etiology- Non Traumatic
🞂 Aneurysmal Rupture : 80-85%
🞂 Non aneurysmal perimesencephalic haemorrhage : 10%
🞂 Arteriovenous Malformation/ Fistula
🞂 Intracranial vessel dissection
🞂 Venous Sinus thrombosis
🞂 Vasculitis
🞂 Coagulopathy
🞂 Drug abuse/ Cocaine use
🞂 Hypertensive crisis
Aneurysm
🞂 It is a focal outpouching from the wall
Introduction-Aneurysm
🞂 Prevalance 1-6%
🞂 1-2% of the population have
unruptured aneurysms
🞂 Any aneurysm can rupture,
although statistically larger (>1cm
– 4%) aneurysms are more likely to
do so.
🞂 Women>Men
🞂 Only about 20% of them rupture
during a lifetime
🞂 2-20/100,000 individuals/year
bleed
Introduction-Aneurysmal SAH
🞂 Incidence increases with age.
(Very rare in children)
🞂 Peak age is 55-60 years
🞂 More common in females
🞂 Multiple aneurysms in 20-30%
Introduction-Aneurysmal SAH
🞂 10-12% die before receiving medical attention
🞂 40-50 % of hospitalized pts.die within 1 month
🞂 Only 1/3rd of survivors have “good results”.
Pathological Features
-attenuated tunica media
-lack external elastic lamina
Risk Factors
🞂 Genetic factors
- heritable connective tissue disorders
-familial occurrence (7 to 20%)
Risk Factors
Cigarette smoking- strong association
- it decreases the effectiveness of α1-antitrypsin
Hypertension
Alcohol consumption
Hypercholesterolemia
Clinical Presentation – Aneurysmal rupture
🞂 Subarachnoid hemorrhage-most common
🞂 Mass Effect
🞂 Cerebral Ischemia
🞂 Asymptomatic Intracranial aneurysms
Premonitory Signs
• “Warning bleeds” are relatively common
• Sentinel headache 30-50%
• Early diagnosis prior to rupture will improve outcomes
• Unusual headache
• 50% of patients die within 48 hours
irrespective of therapy
Clinical Presentation
🞂 Subarachnoid Hemorrhage-
-Sudden onset severe headache
- nausea,vomiting and LOC
-Sentinel hemorrhage
O/E: Meningeal irritation
global/focal neurologic deficits
intraocular hemorrhage
Thunderclap headache
🞂 Reversible cerebral vasoconstriction syndrome
🞂 Cortical venous thrombosis
🞂 Arterial Dissection, ICH, ischemic stroke
🞂 Spontaneous intracranial hypotension
🞂 Pituitary apoplexy
🞂 Colloid Cysts
🞂 Acute meningitis
🞂 Acute HT crisis
🞂 Reversible posterior leukoencephalopathy
🞂 Primary thunderclap HA
Physical Findings in Patients with Subarachnoid Hemorrhage
Clinical Presentation
Edlow J and Caplan L. N Engl J Med 2000;342:29-36
Retinal haemorrhages
Clinical Presentation
🞂 Seizures
⭶ 6-16%
- common with anterior circulation aneurysms, esp- MCA
aneurysms
Clinical Presentation
🞂 Mass effect
⭶ Headache –most common
- Third nerve palsy or unilateral retro-orbital pain-internal
carotid- PCOM aneurysm
- Carotid-ophthalmic artery aneurysms may produce unilateral
visual loss or visual field defect
Clinical Presentation
🞂 Mass effect
-brainstem dysfunction
-trigeminal neuralgia
- cavernous sinus syndrome
- hypothalamic pituitary dysfunction
Grading of SAH
🞂 Hunt and Hess grading system
🞂 World Federation of Neurlogic Surgeons (WFNS) grading
system
HUNT AND HESS SCALE.
CLINICAL GRADING OF SUBARACHNOID HEMORRHAGE
Grade I - Asymptomatic or with mild headache
Grade II-Moderate or severe headache, nuchal rigidity
Grade III-Confusion, drowsiness, or mild focal deficit
(discounting third nerve palsy)
Grade IV-Stupor or hemiparesis, early decerebrate
rigidity
Grade V-Deep coma, extensor posturing
WFNS Grading
Grade GCS Clinical
examination
1 15 No motor deficit
2 13-14 No motor deficit
3 13-14 Motor deficit
4 7-12 With or without motor
deficit
5 3-6 With or without motor
deficit
Diagnostic studies
🞂 Subarachnoid hemorrhage- CT scan,LP
🞂 Intracranial aneurysm – CTA, MRA, DSA
CT scan in SAH
CT scan Brain
🞂 hydrocephalus
🞂 recurrent subarachnoid hemorrhage
🞂 intracerebral hematoma
🞂 postoperative hemorrhage
🞂 brain edema or infarction caused by vasospasm
Giant Aneurysms
Diagnosis of SAH
🞂 CT scan head-positive in up to
- 95-100% in 12-24 hours
- 80% in 3 days
- 70% in 5 days
- 50% at1 week
- 30% at 2 weeks
MRI is not sensitive in acute bleed
MRI
Diagnosis of SAH
🞂 CT may be normal in about 5%
🞂 Lumbar puncture:uniformly blood stained.
-3 test tube test
-supernatant xanthochromia
Supernatant xanthochromia
Diagnosis of SAH
🞂 Lumbar puncture- positive in
100% in 12 hrs to 2 weeks
>70% after 3 weeks
40% after 4 weeks
Cause of SAH
CT Angiography-obtaining
images acquired during
the arterial phase of
contrast opacification
🞂 Demonstrate aneurysms
as small as 2 to 3 mm
🞂 Useful for surgical
planning
🞂 Also a screening tool in
populations at high risk
CT Angiogram
Diagnostic Evaluation
🞂 Magnetic Resonance
Angiography-
⮚ Takes ½ to 1 hour
⮚ Detects aneurysms >3 to 5
mm
⮚ MRI detects thrombosed
aneurysms
⮚ Screening modality
Diagnostic Evaluation
🞂 Intra-Arterial Angiography- (DSA)
“gold standard”
🞂 Mortality -<0.1%
🞂 Total neurological morbidity - 1%
🞂 Permanent neurological morbidity -0.5%.
MCA aneurysm
ACOM ANEURYSMS-
Giant ICA aneurysm
Large ophthalmic aneurysm
3D Rotational angiogram
Perimesencephalic bleed
Predictors of Outcome
🞂 Age
🞂 Clinical grade
🞂 Amount of blood in subarachnoid space (Fischer’s Grade)
Initial Management
🞂 Absolute bed rest with HOB at 30 degrees
🞂 Bedrest in a quiet room
🞂 Analgesia- short-acting and reversible agent(fentanyl) Pain is
associated with a transient elevation in blood pressure and increased
risk of rebleeding
🞂 Sedation (used with caution to avoid distorting subsequent
neurologic evaluation) with a short-acting benzodiazepine such as
midazolam
🞂 Hourly neurological assessments
🞂 Strict input and output monitoring
🞂 Monitoring BP, oxygen saturation
🞂 Comatose pts intubation and ventilation
🞂 Seizure prophylaxis- Phenytoin
🞂 Steroids - Glucocorticoids may help reduce the head and neck ache
caused by the irritative effect of blood ; no good evidence that they
reduce cerebral edema, are neuro protective, or reduce vascular
injury , and their routine use therefore is not recommended
🞂 Stool softeners
🞂 Ca channel blocker : Nimodipine60 mg PO every 4 h
🞂 Antifibrinolytics - may be considered in patients in whom treatment
cannot proceed immediately;reduce incidence of aneurysmal
rerupture but may also increase the risk of delayed cerebral
infarction and DVT
INVESTIGATIONS
🞂 Hemoglobin, serum electrolytes and glucose, and arterial
gases
🞂 ECG
🞂 Liver function
🞂 Coagulation profile
🞂 Chest examination and radiography are necessary to
exclude pneumonia
Complications in aneurysmal SAH
🞂 Hydrocephalus 🞂 Seizures
🞂 Rebleeding 🞂 Pulmonary complications
🞂 Vasospasm 🞂 Cardiac complications
🞂 Hyponatremia
Hydrocephalus
🞂 Frequency during the first 3 days- 20 to 30%
🞂 Caused by obstruction of CSF flow by clotted blood
🞂 Can occur early (EVD) or late (VP shunt)
🞂 Careful with drainage – reduction in ICP
🞂 Can increase the risk of rebleeding
🞂 With IVH - 35 to 65 %
🞂 EVD-Prolonged drainage-infection risk
🞂 Chronic hydrocepalus in 50% of acute cases
Rebleed
🞂 Most disastrous and disabling
🞂 Mortality rates-70 to 90 %
🞂 Prevention of rebleed is early intervention
Rebleed
🞂 First 24 hrs- 4-6 %
🞂 1-2 % per day for 2 weeks
( cumulative 20%)
🞂 30% rebleed by 30 days
🞂 50% rebleed by 6 months
🞂 There after 3% per year
Vasospasm
🞂 Delayed ischemic
neurlogic deficit-
🞂 Onset on the 3rd day
🞂 Peak 6_8 days
🞂 Resolves by 3 weeks
Vasospasm
🞂 Clinical Features
- delayed deterioration
- focal neurlogic deficits
-confusion, irritability
-fever
- raised ESR, TLC
Vasospasm
🞂 Diagnosis by (after ruling out other causes of detrioration)
- Transcranial Doppler studies
- Angiography
Transcranial Doppler
TCD
Sl Mean flow Clinical
no velocity implication
1 100 cm per suspicious
second
2 >120 cm per diagnostic of
second vasospasm
3 >=200 cm per Clinical
second deterioration
Vasospasm manangement
🞂 Nimodipine
🞂 Triple H Therapy (HHH)
Hypervolemia
Hemodilution
Hypertension
🞂 Intraoperative removal of blood clot
Triple-H
🞂 Hypervolemia: packed erythrocytes, isotonic crystalloid, and
colloid and albumin infusions in conjunction with vasopressin
injection. CVP 10-12 mm of Hg
🞂 Hemodilution - hematocrit should be maintained at 30-35%
🞂 Hypertension - Inotropes and dobutamine
Endovascular treatment of vasospasm- when
hyperdynamic therapy fails
🞂 Intrarterial vasodilator- Papaverine, Verapamil,
Nimodipine,Nicardipine
🞂 Angioplasty
Other Complications
🞂 Fluid and Electrolyte Disturbances
Hyponatremia -1/3 rd
Usually due to cerebral salt wasting
🞂 Clinical deterioration
Other Complications
🞂 Chest Infection
🞂 Neurogenic
pulmonary edema
Other Complications
🞂 Cardiac complications
- ECG changes – may mimick MI
- stunned myocardium –takustubo cardiomyopathy
Definitive treatment
🞂 Surgical Clipping
🞂 Endovascular coiling
•Aim :
To completely and permanently obliterate the aneurysm from circulation to prevent rebleed
Acom A Aneurysm
Coiling- GDC coils
ACA Aneurysm
Anesthesia Management
Goals of anesthesia management:
• Prevention of rebleeding associated with acute hypertension (laryngoscopy,
coughing etc.)
• Cerebral protection (cooling)
• Facilitation of surgery – “brain relaxation”(mannitol, propofol etc)
• Hypnosis, amnesia and analgesia
Accomplished with titrated:
– Thiopental / Propofol
– Fentanyl
– IV Lidocaine
– Vecuronium
– Phenylephrine and antihypertensives available (Labetalol / Nicardipine /
Sod. Nitroprusside)
Blood Pressure Control
• Maintain systolic BP >130mmHg
• Use vasopressors if necessary – to maintain CPP, and reduce
ischemic penumbra from vasospasm
• Generally avoid vasodilators (except calcium channel blockers)
Conclusion
🞂 SAH is a NEUROSURGICAL EMERGENCY
🞂 High index of suspicion is required
🞂 Immediate investigation with a CT scan +/-LP should be done.
🞂 Securing aneurysm early results in better outcome
THANK YOU
