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subarachnoid hemorrhage- neurological emergency
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SUBARACHNOID HAEMORRHAGE (SAH)
DR. MAUSAMINBEN HATHIDARA
INTRODUCTION Subarachnoid hemorrhage (SAH) is a pathologic condition
that exists when blood enters the subarachnoid space
The most common cause of SAH is trauma
The most common cause of spontaneous SAH is an
aneurysmal bleed (65-80%)
EPIDEMIOLOGY
Incidence about 9-10/100,000/yrHigher in Japan (3 times) and FinlandMean age of onset 51 years (6th decade)Facts and figures
Men predominate until age 40, then more Men predominate until age 40, then more women (55%); some studies – 3:2 ratiowomen (55%); some studies – 3:2 ratio
Seasonal (winter/spring), diurnal (late morning) Seasonal (winter/spring), diurnal (late morning) and day (Sunday)and day (Sunday)
30 % rupture during sleep30 % rupture during sleep About 50 % of patients with an aneurysm have About 50 % of patients with an aneurysm have
warning prior to SAH (6-20 days)warning prior to SAH (6-20 days)
Case Fatality
The Overall case fatality varied from 32-67%
Population-based study in England with essentially
complete case ascertainment
24 hour mortality: 21%24 hour mortality: 21%
7 days: 37%7 days: 37%
30 days: 44%30 days: 44%
Pobereskin JNNP 2001;70:340-3
ETIOLOGYCATEGORY CAUSES
TRAUMA CLOSED, PENETRATING, ELECTRIC,ETC…
VASCULAR ANEURYSMS, ATHEROSCLEROSIS, AVM, VASCULITIDES
IDIOPATHIC BENIGN PERIMESENCEPHAIC SUBARACHNOID HEMORRHAGE
BLOOD DYSCRASIAS LEUKEMIAS, HEMOPHILIAS, THROMBOCYTOPENIAS
INFECTIONS DENGUE, LEPTOSPIROSIS, BACTERIAL MENINGITIS
TOXINS AMPHETAMINES, COCAINE, NICOTINE, ANTICOAGULANTS
NEOPLASMS GLIOMAS, MENINGIOMAS, HEMANGIOBLASTOMA, ETC
Risk Factors Hypertension Hypertension Cigarette smoking Cigarette smoking Oral contraceptives Oral contraceptives Alcohol consumption (debatable) Alcohol consumption (debatable) Diurnal variations in blood pressureDiurnal variations in blood pressure Pregnancy and parturition Pregnancy and parturition Slight increased risk during lumbar puncture Slight increased risk during lumbar puncture
and/or cerebral angiography in patient with and/or cerebral angiography in patient with cerebral aneurysm cerebral aneurysm
Slight increased risk with advancing age Slight increased risk with advancing age Following cocaine abuse Following cocaine abuse
PATHOPHYSIOLOGY
CEREBRAL BLOOD FLOW AND METABOLISM
RAISED ICT
IMPAIRED VASODILATORY AUTOREGULATIONVASOSPASM WITH GLOBAL ISCHEMIA
BLOOD (‘TOXIC’)BLOCKAGE OF THE ARACHNOID GRANULATIONS
SYMPATHETIC SURGE
MIPULMONARY EDEMA
CEREBRAL BLOOD FLOW/VOLUME/METABOLISM
CBF is globally decreased after SAH
Mean CBF decreases with time after SAH; it reaches a nadir in
10 to 14 days, after which it slowly increases toward normal,
In patients with poor grades, CBF and cerebral metabolism
may remain depressed for weeks ;
Cerebral blood volume was markedly increased in patients
with severe neurological deficits
INTRACRANIAL PRESSURE RESPONSES
Mean ICP was 10 mm Hg in patients with clinical grades 1 and
2, 18 mm Hg in patients with clinical grades 2 and 3, and
29 mm Hg in those with clinical grades 3 to 5.
Vasospasm, which was more common in patients with a poor
clinical grade and larger SAH, was associated with a
significant rise in ICP from a mean of 16 mm Hg in those
without vasospasm to 29 mm Hg in those with vasospasm
PRESENTATION HEADACHE :
The most common symptom (97%)
Usually severe ("the worst headache of my life) and sudden in
onset.
They may clear and the patient may not seek medical attention
(sentinel/warning bleeds) - in 30-60% of cases
Vomiting may be present
May pulsate towards the occiput and may sometimes be
percieved as neck pain
OTHER SYMPTOMS
Decreased consciousness and alertness
Eye discomfort in bright light (photophobia)
Mood and personality changes, including confusion and irritability
Muscle aches (especially neck pain and shoulder pain)
Nausea and vomiting
Numbness in part of the body
Seizure (1 in 14)
Stiff neck
Vision problems, including double vision, blind spots, or temporary
vision loss in one eye
SIGNS
MENINGISM (neck stiffness, kernigs and brudzinskis)
Hypertension
Focal neurological deficit
Ocular signs
Coma
INVESTIGATIONS CT Scan
MRI
Lumbar Puncture
Angiography
GRADING
GRADE SIGNS/SYMPTOMS SURVIVAL
1 Asymptomatic/Minimal headache or neck stiffness
70%
2 Moderate/severe headache with neck stiffness +/- CN palsies
60%
3 Drowsy/ minimal neurological deficit
50%
4 Stuporous with hemeparesis 20%
5 Comatose with decereberate posturing/response
10%
0 Unruptured aneurysm -
1a No Meningism but with fixed neurodificit
-
HUNT AND HESS IN 1968
GRADE CT APPEARANCE
1 NONE
2 < 1mm thickness
3 > 1mm thickness
4 Diffuse with parenchymal/ventricular extension
FISHERS
GRADE CT APPEARANCE
0 NONE
1 MINIMAL
2 MINIMAL WITH IVH
3 THICK
4 THICK WITH IVH
CLAASSENS MODIFICATION
GRADE GCS NEURODEFICIT
1 15 ABSENT
2 13-14 ABSENT
3 13-14 PRESENT
4 7-12 ABSENT/PRESENT
5 <7 ABSENT/PRESENT
WORLD FEDERATION OF NEUROSURGEONS (WFNS)
GRADE CLINICAL PRESENTATION
1 CONSCIOUS
2 DROWSY
3 DROWSY WITH DEFICIT
4 MAJOR NEURODEFICIT
5 MORIBUND
BOTTERELL ET AL
A newer grading by Ogilvy and Carter - to predict outcome
and gauge therapy
The system consists of five grades and it assigns one point
for the presence or absence of each of five factors:
Age greater than 50
Hunt and Hess grade 4 or 5;
Fisher scale 3 or 4
Aneurysm size greater than 10 mm
Posterior circulation aneurysm 25 mm or more
THANK YOU