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SUBARACHNOID HAEMORRHAGE (SAH) DR. MAUSAMINBEN HATHIDARA

Subarachnoid hemorrhage

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subarachnoid hemorrhage- neurological emergency

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Page 1: Subarachnoid hemorrhage

SUBARACHNOID HAEMORRHAGE (SAH)

DR. MAUSAMINBEN HATHIDARA

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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%)

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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)

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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

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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

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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

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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

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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

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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

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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

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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

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SIGNS

MENINGISM (neck stiffness, kernigs and brudzinskis)

Hypertension

Focal neurological deficit

Ocular signs

Coma

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INVESTIGATIONS CT Scan

MRI

Lumbar Puncture

Angiography

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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

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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

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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)

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GRADE CLINICAL PRESENTATION

1 CONSCIOUS

2 DROWSY

3 DROWSY WITH DEFICIT

4 MAJOR NEURODEFICIT

5 MORIBUND

BOTTERELL ET AL

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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

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THANK YOU