Download - SAH for Neurology Residents
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ANEURYSMAL SUBARACHNOID HEMORRHAGE
Dhaval Shukla
Associate Professor
Dept of Neurosurgery,NIMHANS
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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
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Aneurysm• Focal outpouching from the arterialwall
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Epidemiology
• Prevalence of aneurysm 1-6%• Multiple aneurysm in 20 – 30%• Only about 20% of them rupture during a
lifetime– 10/1 lakh population / year (average)– India – 3-4 (hospital based studies)– High in Finland and Japan (15-30)– Low in France, China
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Risk factors for aneurysm formation
• Incidence increases with age – Peak at 50-60 years– Very rare in children
• Female gender (1.2 – 1.6 times more common)
• Hypertension
• Smoking• Genetic factors
– Connective tissue disorders (Marfan, Ehler Danlos Syndrome)– Polycystic Kidney Disease– Familial occurrence (7 to 20%)
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Natural History
• 10-12% die before receiving medical attention
• 40-50 % of hospitalized pts.die within 1 month
• Only 1/3rd of survivors have “good results”.
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Clinical features
• Sudden severe headache (Thunderclap)– 1 in 8 to 10 pts with sudden severe headache have SAH
• Nausea, vomiting• Meningismus• Altered consciousness / coma• Focal neurological deficit• Seizures (10-25%)• Prodromal symptoms – sentinel bleeds (50%)• Ocular haemorrhages
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Pitfalls in clinical diagnosis
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HUNT AND HESS SCALE.
I - Asymptomatic or with mild headache
II-Moderate or severe headache, nuchal rigidity
III-Confusion, drowsiness, or mild focal deficit (discounting third nerve palsy)
IV-Stupor or hemiparesis, early decerebrate rigidity
V-Deep coma, extensor posturing
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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
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Diagnostic studies
SAH– CT scan– Lumbar Puncture
Intracranial aneurysm– DSA– CTA
– MRA
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CT scan
• 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
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Fisher’s Grade
2
4
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Modified Fisher’s Grade
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CT
• Intraventricular Hemorrhage (IVH)
• Hydrocephalus
• Intracerebral hematoma (ICH)
• Brain edema
• Infarction caused by vasospasm
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Hydrocephalus IVH and ICH
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Pitfalls in CT diagnosis
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Lumbar puncture (LP)
• Positive in
o 100% in 12 hrs to 2 weeks
o >70% after 3 weeks
o 40% after 4 weeks
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Supernatant xanthochromia
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Pitfalls in LP diagnosis
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Importance of correct diagnosis !
• A disease of high morbidity and mortality
• Good grade patients are usually misdiagnosed
• Misdiagnosis ranges 25-50%
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DSA
• Digital Subtraction Angiography (DSA)
“gold standard”
• Mortality -<0.1%
• Total neurological morbidity - 1%
• Permanent neurological morbidity -0.5%.
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DSA
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DSA
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3D Rotational angiogram
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CT Angiogram (CTA)
Demonstrate aneurysms as small as 2 to 3
mm
• Useful for surgical planning
• A screening tool in populations at high risk
• Sensitivity 95 – 97%
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Magnetic Resonance Angiography-
Takes ½ to 1 hour
Detects aneurysms >3 to 5 mm
MRI detects thrombosed aneurysms
Screening modality
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Angiogram-negative SAH• 15 to 20%
– 65 % are prepontine or perimesencephalic
• Causes– Vasospasm– Hypoperfusion– Poor angiographic technique – Thrombosis
• Repeat angiography– Undetected aneurysms found in an additional 2–5% of cases
at 2–4 weeks
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Perimesencephalic bleed
• Venous hemorrhage• Younger• Non-hypertensive• Better grade • More in males• Prognosis good• Re-bleeding is rare• Delayed ischemic deficit
very few
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Initial Management
• Absolute bed rest with 30degrees head elevation
• Analgesia- short-acting and reversible agent
– Pain is associated with a transient elevation in blood pressure and
increased risk of rebleeding
• Sedation with a short-acting benzodiazepine such as
midazolam
– Use with caution to avoid distorting subsequent neurologic
evaluation
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Initial Management• Hourly neurochecks
• Strict input and output monitoring
• Monitoring BP, oxygen saturation
• Comatose patients – Intubation and ventilation
• Seizure prophylaxis- Phenytoin
• Stool softeners
• Nimodipine (60mg q4h for 21 days)
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INVESTIGATIONS
• Hemoglobin, serum electrolytes, glucose, and arterial gases
• ECG
• Renal and liver function tests
• Chest radiography
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Specific problems in aneurysmal SAH
• Rebleeding
• Vasospasm
• Hydrocephalus
• Hyponatremia
• Seizures
• Pulmonary complications
• Cardiac complications
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Rebleed
• Most disastrous and disabling
• Mortality rates-70 to 90 %
• Prevention of rebleed is early intervention
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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
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Vasospasm
• Delayed ischemic neurlogic deficit-
• Onset on the 3rd day
• Peak 6_8 days
• Resolves by 3 weeks
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Vasospasm
• Clinical Features
- delayed deterioration
- focal neurlogic deficits
- confusion, irritability
- fever
- raised ESR, total WBC count
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Vasospasm management
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Hydrocephalus• Acute hydrocephalus occurs in 15% to 87%
– With IVH - 35 to 65 %– managed by external ventricular drainage (EVD)
• Chronic shunt-dependent hydrocephalus occurs in 8.9% to 48%– Chronic hydrocepalus in 50% of pts with Ac. HCP– Treated with ventricular shunt placement
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Seizures• Early 6% to 18%
• Delayed seizures 3% to 7%
• Risk factors– MCA aneurysm– Thickness of SAH– ICH– Rebleeding– Infarction– Poor neurological grade– History of hypertension
• Prophylactic anticonvulsants in the immediate posthemorrhagic period
• Routine long-term use of anticonvulsants is not recommended
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Medical Complicationsof SAH
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Cardiac Complications
• Hypertension treated requiring IV medication (27%)
• Hypotension requiring pressors (18%)
• Life-threatening arrhythmia (8%)
• Myocardial ischemia (6%)
• Successful resuscitation from cardiac arrest (4%)
• Troponin I elevation (20%-68%)– Regional wall motion
abnormalities (26%)
ECG Changes
• ST segment alterations (15%–67%)
• T-wave changes (12%–92%)
• Prominent U waves (4%–52%)
• QT prolongation (11%–66%)
• Conduction abnormalities (7.5%)
• Sinus bradycardia (16%)
• Sinus tachycardia (8.5%)
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Neurogenic stunned myocardium
• Most severe form of cardiac injury
• Transient lactic acidosis
• Cardiogenic shock
• Pulmonary edema
• Widespread T-wave inversions
• Prolonged QT interval
• Reversible left ventricular wall motion abnormalities
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Hyponatremia • 10% to 30%• Associated with onset of vasospasm• Cerebral salt wasting• Risk factors
– Poor clinical grade
– ACOMA aneurysm
– Hydrocephalus,
• Treatment– Aggressive volume resuscitation
– 3% saline
– Fludrocortisones
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Pulmonary complications
• Chest Infection
• Neurogenic pulmonary edema
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Definitive treatment• Microsurgical Clipping OR Endovascular coiling
should be performed as early as feasible in the majority of patients to reduce the rate of rebleeding
• Complete obliteration of the aneurysm should be achieved whenever possible
• Determination of aneurysm treatment, as judged by both neurosurgeons and endovascular specialists, should be a multidisciplinary decision based on characteristics of the patient and the aneurysm
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Coiling
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DACA Aneurysm Coiling
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Coiling or Clipping
• For patients with ruptured aneurysms
judged to be technically amenable to both
endovascular coiling and neurosurgical
clipping, endovascular coiling should be
considered
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Clipping preferred• Patients presenting with large ICH and MCA aneurysm • Aneurysm characteristics
– Wide neck– Blebs– Geometrically complex with incorporation of branch artery– Partially thrombosed – Giant
• Inability to navigate delivery system• Patients preference
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Coiling preferred
• In elderly
• In poor-grade
• Aneurysms of basilar artery
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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
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Outcome
• Age
• WFNS grade
• Fisher grade
• Size of aneurysm
• Severity of vasospasm
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