By

,

Esene Ignatius Ngene

SUBARCHNOID HAEMORRHAGE
REFERENCES BOOKS  Mark . S Greenberg et al.Handbook of Neurosurgery.Ed.6;27:781-834  Kenneth W. et al. Neurology and Neurosurgery Illustrated .Ed 4;p.273-300  Gilbert Dechambenoit.Manuel de Neurochirugie.p101-109  Robert A.Ratcheson et al.Ruptured Cerebral aneurysm perioperative management.Vol.6 My Search Engines http://www.dogpile.com/ http://www.google.com http://www.eu.ixquick.com/ http://www.quintura.com/ http://www.kartoo.com/ http://www.search-cube.com http://www.bib.ulb.ac.be/

SAH:INTRODUCTION

DEFINITION
• Extravasation of blood into the subarachnoid space.

• Represents about 10% of CVA.

SAH:INTRODUCTION

SAH:EPIDEMIOLOGY
INCIDENCE

Varies greatly b/n countries, from 2 cases/ 100,000 in China to 22.5/100,000 in Finland (1)
AGE (2) •Aneurysmal rupture is extremely rare in the first decade of life

• Incidence ↑ with age, occurring most commonly b/n 40 -60 yrs (mean age > 50 yrs)
SEX (2) •There is a clear female preponderance overall; SAH is ~1.6 times higher in F than M.

•Before age 40 F=M; > 40 there is an increasingly strong predominance of females
•SEASONAL VARIATION/ GEOGRAPHICAL FACTORS

1. Ingall T, Asplund K, Mahonen M, Bonita R. A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000;31(5):1054-1061. 2. 2.Hop JW et al. Stroke 1997; 28: 660-664 & Stroke 1998; 29: 798-804.

SAH:EPIDEMIOLOGY:RISK FACTORS FOR SAH (1)
Hypertension
Oral Contraceptives Substance abuse Pregnancy and Parturition LP &/or Cerebral angiography in pts with cerebral aneurysm Advancing age
Fibromuscular Dysplasia (FMD) Coarctation of the Certain conditions associated with aneurysms Aorta Familial Intracranial Aneurysm (FIA) Syndrome

Cigarette Smoking,

 Heavy Alcohol Use???
Cocaine-related SAH occurs in younger pts

Diurnal Variations in Blood Pressure

Autosomal Dominant Polycystic Kidney Disease

Bacterial endocarditis

1.Hop JW et al. Stroke 1997; 28: 660-664 & Stroke 1998; 29: 798-804.

SAH:EPIDEMIOLOGY:Natural History Of Ruptured Aneurysm
Of 100 pt with aneurysmal SAH treated conservatively

15 die before reaching hospital 85 15 die in the 1st 24H in hospital 24 Hrs 70 15 die between 24H and 2 wks 2Wks 55 15 die between 2wks and 2mths

SAH from Ruptured aneurysm carries a high initial mortality risk which gradually declines with time. Of the surivals of initial bleed, Rebleed and cerebral infarction are major causes of death

2 Mths

40 15 die between 2mths and 2yrs

2 Yrs

25

SAH:AETIOLOGY
SAH
TRAUMATIC

(Most Common)

SPONTANEOUS

10%

15%

5%

•Spinal AVM •Tumours •Blood Dyscrasias •Sickle Cell Disease •Drugs:Cocaine

70%

CAUSES of Spontaneous SAH
ANEURYSM AVM UNDISCOVERED OTHERS

CIRCLE OF WILLIS

SAH:PATHOPHYSIOLOGY • Intracerebral Vessels lie in Subarachnoid Space (SAS) giving off Perforating branchess to the brain tissue • Bleeding from these vessels &/or associated aneuryms occurs primarily into the SAS.
• Some intracranial aneurysms are embedded within the

brain tissue and when rupturedICH with/without SAH.
• The subarachnoid layer might give waySDH

BLOOD VESSEL

Dura Subdural Space
Arachnoid SUBARACHNOID SPACE Intracerebral Cortex

Pia

SAH:PATHOPHYSIOLOGY
• Aneurysmal RUPTURELEAKAGE of arterial blood into the SAS (less commonly into Epidural space and brain) • Rapid ↑ in ICP ↓CBF Disturbance of Consciousness • Fall in CBF ↓ Bleeding and Stop the SAH

SAH:CLINICAL PICTURE • HEADACHE • DIMINISHED CONSCIOUS STATE • MENINGISM • FOCAL NEUROLOGIC SIGNS • FUNDAL CHANGES

« Severity of Sx and Sy α to severity of bleeding »

SAH:CLINICAL PRESENTATION
• Most common Sx (present in 97% of pt)

• HEADACHE
• • • • DCL MENINGISM FOCAL NEUROLOGIC SIGNS FUNDAL CHANGES

• « Sudden onset of severe H/A in a pt

should be considered as SAH until proven otherwise »
• Sudden onset,Explosive « worst H/A ever » ↔« Blow to the head » . • Sentinel H/A =Warning H/A from aneurysmal enlargement or small leaks

(warning leak) !!!! May clear with Rx.

SAH:CLINICAL PRESENTATION
• HEADACHE

• Mild deteriorationApoplectic Death (Minor Hge) (Massive Hge)

• DCL
• • MENINGISM FOCAL NEUROLOGIC SIGNS • FUNDAL CHANGES

Mechanism:  Direct effect of SAH:  Mass effect associated with ICH
 Complications(Seizures,HCP,Brain damage due to ICH,diffused ischaemia ,Low CBF due to reduced Cardiac output)

SAH:CLINICAL PRESENTATION
• HEADACHE

• Develops within 6-24H • Due to blood in the SASmeningeal irritation:

DCL

• MENINGISM
• • FOCAL NEUROLOGIC SIGNS FUNDAL CHANGES

Nausea//Vomitting//Photophobia Nuchal Rigidity/+ve stretch signs • Downward extension into the cauda equina
Nerve root irritation Lumbago and Sciatic type of pain

SAH:CLINICAL PRESENTATION
• HEADACHE

DCL

• MENINGISM
• • FOCAL NEUROLOGIC SIGNS FUNDAL CHANGES

SAH:CLINICAL PRESENTATION

HEADACHE
DCL

• Mechanism:  Local pressure effect of aneurysm  Concomitant Intracerebral Hge

• •

MENINGISM FOCAL NEUROLOGIC SIGNS

 Cerebral Vasospasm

FUNDAL CHANGES

SAH:CLINICAL PRESENTATION:PRESSURE EFFECTS
OPTIC NERVE & CHIASMA
VISUAL FIELD DEFECT PITUITARY STALK or HYPOTHALAMUS INTRACAVERNOUS ANEURYSM
BASILAR ART. ANEURYSM

MIDBRAIN, PONS, CNIII

CN III CNIV
CNIV GANGLION

CNV1

Ophthalmoplegia & Facial pain

PcomA
CNIII Palsy

CAVERNOUS SINUS

SAH:CLINICAL PRESENTATION
• • • • HEADACHE DCL MENINGISM FOCAL NEUROLOGIC SIGNS

OPTIC FUNDI
 Papilloedema:Mild, Common 1st few days due to ICT (from HCP or Cerebral oedema)  Ocular haemorrhage (esp. In severe SAH)

• IntraRetinal haemorrhage(may surround fovea)
• Large Subhyloid (preretinal) →rupture into Vitreous Humour (Terson’s Syndrome) Permanent visual defect • Mechanism:Compression of retinal vein and

• FUNDAL CHANGES

retinochoriodal anastomoses by ↑ CSF
pressure causing venous tension and disruption of retinal veins.

SAH:CLINICAL PRESENTATION
• • • • HEADACHE DCL MENINGISM FOCAL NEUROLOGIC SIGNS

• FUNDAL

CHANGES

Clinical Grading Scales for SAH
Grade

.

Description

Hunt and Hess Scale
1 Awake,Asymptomatic or minimal headache and/or slight nuchal rigidity 2 Awake,Moderate to severe headache, nuchal rigidity, no neurological deficit

other than cranial nerve palsy
3 Drowsiness or confusion with (mild)/without focal deficit 4 Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances

5 Deep coma, decerebrate rigidity, moribund appearance
Hunt WE, Hess RM. “Surgical risk as related to time of intervention in the repair of intracranial aneurysms.” Journal of Neurosurgery 1968 Jan;28(1):14-20.

WFNS SAH GRADING SCALE
Scale for grading patients with a subarachnoid haemorrhage.

GRADE I
II

GCS 15
14-13

MOTOR DEFICIT -(no motor deficit)
-(no motor deficit)

III
IV V

14-13
12-7 6-3

+ (with motor deficit)
+/-(with or without motor deficit) +/-(with or without motor deficit)

*Cranial nerve palsies are not considered focal deficit

Teasdale GM, Drake CG, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers JC. A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies. J Neurol Neurosurg Psychiatry. 1988 Nov;51(11):1457.

SAH:COMPLICATIONS
INTRACRANIAL
• ICH,IVH,SDH • HCP

EXTRACRANIAL
• FEVER • ALTERATION IN RESPIRATORY

• CEREBRAL OEDEMA
• SEIZURES • REBLEEDING

FXN
• EFFECT ON CVS • FLUID & ELECTROLYTIC

• VASOSPASM↔CEREBRAL
ISCHAEMIA/INFARCTION

DISORDER
• GIT (STRESS ULCERS) • CMPLTN OF BEDRIDDENESS

REBLEEDING AND VASOSPASM ARE THE MOST DELETORIOUS COMPLICATIONS

SAH:COMPLICATIONS
• INTRACRANIAL
 ICH,IVH,SDH
 HCP  CEREBRAL OEDEMA  SEIZURES  REBLEEDING  VASOSPASM↔CEREBRAL ISCHAEMIA/INFARCTION

ICH,IVH,SDH
 Location of hge affect outcome.

 Pt with ICH &/or IVH have poorer outcome • ICH:Direct rupture of aneurysm into brain
2nd rupture of SAH into parenchyma • • • IVH:Deleterious influence on pt’s outcome SDH: Rare.Due to rupture of arachnoid matter EFFECT: ↑ICP due to mass effect & acute HCP

SAH:COMPLICATIONS
•       INTRACRANIAL ICH,IVH,SDH HCP CEREBRAL OEDEMA SEIZURES REBLEEDING VASOSPASM↔CERE BRAL ISCHAEMIA/INFARCTI ON
HYDROCEPHALUS:Immediate and Delayed
ACUTE HCP:Timing:D0-D3 Due to interference of CSF flow via Aqueduct,V4 and SAS Rx:Emergency ventricular draining Delayed HCP:Timing: After D10 post initial bleed Due to leptomeningeal fibrosis (arachnoid granulations) Rx: Ventricular shunting

CEREBRAL OEDEMA
Increased Na+ and water content of brain

Mech: Vasogenic// Cytotoxic// Interstitial
SEIZURES

Acute LOC with abnormal tonic &/or clonic motor activity
Common in the early hours of SAH Mech:Acute ↑ICP immediately after rupture Cortical irritation by SAH Vasospasm

SAH:COMPLICATIONS

    

INTRACRANIAL
ICH,IVH,SDH HCP CEREBRAL OEDEMA SEIZURES REBLEEDING

REBLEEDING
 Used to be most feared cmpltn b/c mortality>50%  Rebleed increases with H& H grade

 LP might increase risk
 Effects mores severe than initial bleed:LOC,Death x2> Initial bleed

VASOSPASM↔CEREBRAL
ISCHAEMIA/INFARCTION

 Suspected in pt with sudden deterioration of consciousness
 Prevention: Early Rx (surgery or endovascular)  Role of antifibrinolytics uncertain

%chance of Rebleed within the 1st M6 of icitus
70
60 ICAS: Risk falls with time but never drops below 3.5% per year

% CNAHCE OF REBLEED

50 40 30 20 10

0
0 10 20 30 40 50 60 70 80

Days since First Bleed Adapted from Winn,Richard,Jane 1977 Annals of Neurosurgery

SAH:COMPLICATIONS
INTRACRANIAL
 ICH,IVH,SDH
 HCP

VASOSPASM↔CEREBRAL ISCHAEMIA/INFARCTION

Arterial vasospasm(VSP) leading to Delayed Cerebral
Ischaemia most impt cause of disability and death(13%) Pathology: Poorly understood. Hb break down

 CEREBRAL OEDEMA
 SEIZURES  REBLEEDING  VASOSPASM↔CEREBRAL ISCHAEMIA/INFARCTION

products????
Onset: D3 Max: D6-8 Resolve:D12 Pt with ICH or IVH or absence of blood on CT run no

risk of VSP
Types:
Clinical VSP: Delayed Ischaemic Neurologic Deficit

Radiographic:Angiographic VSP:↓ØVx

SAH:COMPLICATIONS:EXTRACRANIAL
PYREXIA:Due to ↑ metabolic rate or

Ischaemic hypothalamic insult
Infx (RTI or UTI)

SEIZURES • occur in 5-15% of pts with SAH. CVS
Mech: ↑catecholamines and derangement of autonomic heart control by hypothalamic insultEcg ∆S,ventricular Dysfxn,and Hypertension« Reactive hypertension » ie ↑BP in a pt with no h/o HBP .Normalises within days RESPIRATORY EFFECTS

Neurogenic and /or Cardiogenic oedema
FLUID AND ELECTROLYTIC DISTURBANCES

Most HYPONATRAEMIA due to SIADH or Cerebral wasting syndrome.

SAH:INVESTIGATION APPROACH
CT BRAIN:
• • • Non-contrasted CT Brain confirms Dx in 95% if done with 48H of bleed FINDINGS: Hyperdensity in SAS (disappears by D7) A).widely distributed  (interhemispheric//sylvian//Basal Cistern)  Over cortical sulci  Within ventricles B) More localized aiding identification site of aneurysm Within Interhemispheric fissure (AComA) Within Sylvian (MCA aneurysm) C) Associated lesions:ICH//HCP D) « Perimesencephalic » pattern E) FISCHER’s CLASSIFICATION

SAH:INVESTIGATION APPROACH

SAH:INVESTIGATION APPROACH

Subarachnoid blood filling the right cerebral sulci (arrow), (a)

CT Scan non-contrast showing blood in basal cisterns (SAH) – so called “Star-Sign” (b)

SAH:INVESTIGATION APPROACH

FISHER GRADE
The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan:

GRADE
1 2

DESCRIPTION
No hemorrhage evident. Subarachnoid hemorrhage less than 1mm thick.

3

Subarachnoid hemorrhage more than 1mm thick.

4

Subarachnoid hemorrhage of any thickness with intraventricular hemorrhage (IVH) or parenchymal extension.

SAH:INVESTIGATION APPROACH
LUMBAR PUNCTURE
• Done if –ve CT,usu +ve in 1st 12H ,CSF xanthochromic and doesn’t clot!!! ANGIOGRAPHY:DIGITAL//CTA///MRA • DIGITAL ANGIO= gold standard (femoral catherization,4Vx angio ,all incidences) • IND for immdiate angiography:Hematoma with mass effect Decision for urgent op (depends on school of thought) • CI:B/n D4-10 WHY????? • ANGIO –ve Vasospasm??? Dural AV Fistula (do ECA arteriography), Spinal angioma (Dx:MRI) In 10-20% cases arteriography is Normal:Repeat test at W2 and M3 IF –ve SAH of undefined cause: usually Peromesencephalic (Good prognosis) MRI Not routine. More sensitive than CT if done several days in detecting multiple aneurysm.

SAH:MANAGEMENT:GOALS
1.PT STABILIZATION(NEUROLOGIC +CARDIOPULMONARY) 2.PREVENTION OF REBLEEDING  Early Surgery (or Endovascular Rx)  Control of Hypertension  Antifibrinolytics* 3.VASOSPASM • A.Prevention Hypervolaemia +Hemodilution Vasodilators Calcium Channel Blockers • B.Therapy Hypertension Angioplasty 4.TREATMENT OF SYMPTOMATIC HCP • Ventriculostomy// VP Shunting 5.PREVENTION OF SEIZURES AND SYSYTEMIC COMPLICATIONS

SAH:MANAGEMENT:PROTOCOL
1.ICU admission 2.EVALUATION:  Airways,Breathing, Circulation  Glasgow Coma Scale  Hunt & Hess Grading 3.MONITORING  CBC  PT/PTT/PLATELETS  Glucose  Liver Function Test  Renal Fxn Testx ,Electrolytes 4.AIRWAYS PROTECTION  Pulse oximetry  Arterial blood gases  Blood pressure  Inputs and outputs (hourly)  Endotracheal intubation/Ventilation*  Central IV Line (pass fluids //monitor CVP)  Foleys Cather  NGT* ( Feeding!)

SAH:MANAGEMENT:PROTOCOL
PROBLEM
REBLEEDING

SOLUTION
PREVENTION OF REBLEEDING  By Obliteration of the aneurysm • Surgically (Microsurgical CLIPPING):EARLY • Endovascularly (COILING// INTRAANEURYSMAL BALLOONING)  Control of HYPERTENSION:Unsecured aneurysm ↓Systemic BP but risk of ischaemia due to hypotension IDEAL BP=160/90 accepted to be 150/90 If BP>200/100 Treat!  ANTIFIBRINOLYTICS* • Controversial • Indicated in pt with delayed surgery with little or no blood in SAS (low risk of vasospasm)

SAH:MANAGEMENT:PROTOCOL

Clipping PcomA

Endovascular Occlusion PcomA with Guglielmi Detachable Coils.

SAH:MANAGEMENT:PROTOCOL
PROBLEM
SOLUTION
VASOSPASM PREVENTION : Achieved by maintaining Cerebral Perfusion via induction of HEYERVOLAEMIA & HEMODILUTION AT NORMOTENSION THERAPY: For establised symptomatic vasospasm:TRIPLE-H THERAPY HYPERTENSIVE HYPERVOLAEMIC HEMODILUTION TARGET:
 HYPERTENSIVE BP=160/90  HYPERVOLAEMIC: cvp 7-10 cm H2O  HEMODILUTION:HCT =30-35%

 MEANS:IV Fluids: Crystalloids,Colloids,Blood,Drugs(Dopamine)  90% pt: N/S 500cc/8H + RL 500cc/8H +/- HETRIL 250cc/12H3L/D  Daily fluids guided by CVP (7-10cmH2O) & DUIRESIS (1ml/Kg/H)  Nimodipine(NIMOTOP) 30mg 60mg/4H
 Centrally acting vasodilator/antihypertensive  CI if BP<110/70 (risk of hypotension b/c it is not 100% selective!!)

SAH:MANAGEMENT:PROTOCOL
PROBLEM
SEIZURES

SOLUTION
PREVENTION : Prophylactic anticonvulsants:PHENYTOIN LD & MD Ensure IV P°≈15-30cmH2O (OverdrainingREBLEEDING!!!!)

HCP

INFECTION

Routine ATB to cover G+ and G- (protocol varies ): Penicillins + Cephaosporins

DVT GIT GUT

Prevented by PNEUMATIC COMPRESSION THIGH-HIGH STOCKING & EARLY MOBILZATION Routine prohylaxis for GIT hge & Ulcers with anti –H2 or PPI Infection: Use Foleys cather

SAH:MANAGEMENT:PROTOCOL
PROBLEM & SOLUTION HEADACHE :Analgesics: Perfalgan 1g /8H Narcotics: Fentanyl 50ug bolus AGITATION:Tranquilizers:eg Benzodiazepines Midazolam (DORMICAN) 1-2mg and ↑according to need
↑ICP Controversial.Brain Dehydration with Caution Mannitol (0.25mg/kg over 20min) (effect in 20min last for 4-6H) Rx Cause

ELECTROLYTES ABN HYPONATRAEMIA: SIADH↔Cerebral salt Wasting Sydrome (↑ADH) (Central elaboration of an ANF) Timing:D3-15 last 2 wks Fliud restriction but when Na+ < 115mEq/L give N/S 3%

PYSCHIATRIC ALTERATIONS:Specialist mgt CARDIOPULMONARY:Monitoring

REHABILITATION: Multidisciplinary

SAH:PROGNOSIS

• Prognostic factor:
Age Hunt and Hess Grade Fischer’ Grade Presence of pre-existing HBP or arteriopathies

Operative mortality=5-26% depends on H&H grade & Timing of Op

SAH:PROGNOSIS
GRADE (Hunt & Hess) Deterioration REEBLEED Mortality (%)

I

5

10-15

3-5

II
III IV V

20
25 50 80

10-15
10-15 20-25 25-30

6-10
10-15 40-50 50-70

Loren et al.Neurology Secrets.P.270

CONCLUSION
• SAHshould be suspected in someone with sudden severe headache that peaks within minutes and lasts more than an

hour • Main manifestations:Headache,↓Conscious State,meningism,focal Neurologic Signs,fundal Changes • Complications:InCranial and extracranial Rebleeding and Vasospam are most Fatal • Prognosis is better with early management.