48
By, Esene Ignatius Ngene
By,Esene Ignatius Ngene
SUBARCHNOID HAEMORRHAGEREFERENCES
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
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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
Diurnal Variations in Blood Pressure
Pregnancy and Parturition
LP &/or Cerebral angiography in pts with cerebral aneurysm
Advancing age
Certain conditions associated with aneurysms
Cigarette Smoking,
Heavy Alcohol Use???
Cocaine-related SAH occurs in younger pts
Familial Intracranial Aneurysm (FIA) Syndrome
Autosomal Dominant Polycystic Kidney Disease
Fibromuscular Dysplasia (FMD)
Coarctation of the Aorta
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
85
15 die between 2mths and 2yrs
7024 Hrs
552Wks
402 Mths
25 2 Yrs
15 die before reaching hospital
15 die in the 1st 24H in hospital
15 die between 24H and 2 wks
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
SAH:AETIOLOGY
70%
10% 15% 5%
CAUSES of Spontaneous SAH
ANEURYSM AVM UNDISCOVERED OTHERS
•Spinal AVM•Tumours•Blood Dyscrasias•Sickle Cell Disease•Drugs:Cocaine
SAH
TRAUMATIC
(Most Common)
SPONTANEOUS
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 rupturedICH with/without SAH.
• The subarachnoid layer might give waySDH
Intracerebral Cortex
Dura
Subdural Space
Arachnoid
SUBARACHNOID SPACE
Pia
BLOOD VESSEL
SAH:PATHOPHYSIOLOGY
• Aneurysmal RUPTURELEAKAGE 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
• HEADACHE
• DCL
• MENINGISM
• FOCAL NEUROLOGIC SIGNS
• FUNDAL CHANGES
• Most common Sx (present in 97% of pt)
• « 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
• DCL
• MENINGISM
• FOCAL NEUROLOGIC
SIGNS
• FUNDAL CHANGES
• Mild deteriorationApoplectic Death
(Minor Hge) (Massive Hge)
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
• DCL
• MENINGISM
• FOCAL NEUROLOGIC SIGNS
• FUNDAL CHANGES
• Develops within 6-24H
• Due to blood in the SASmeningeal irritation:
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
• MENINGISM
• FOCAL NEUROLOGIC SIGNS
• FUNDAL CHANGES
• Mechanism:
Local pressure effect of aneurysm
Concomitant Intracerebral Hge
Cerebral Vasospasm
SAH:CLINICAL PRESENTATION:PRESSURE EFFECTS
BASILAR ART. ANEURYSM
MIDBRAIN,PONS,CNIII
PcomACNIII Palsy
CAVERNOUS SINUS
INTRACAVERNOUSANEURYSM
CN III
CNIV
CNIV
CNV1GANGLION
Ophthalmoplegia & Facial pain
OPTIC NERVE & CHIASMA
VISUAL FIELD DEFECT
PITUITARY STALK orHYPOTHALAMUS
SAH:CLINICAL PRESENTATION
• HEADACHE
• DCL
• MENINGISM
• FOCAL NEUROLOGIC SIGNS
• FUNDAL CHANGES
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
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 SCALEScale for grading patients with a subarachnoid haemorrhage.
GRADE GCS MOTOR DEFICIT
I 15 -(no motor deficit)
II 14-13 -(no motor deficit)
III 14-13 + (with motor deficit)
IV 12-7 +/-(with or without motor deficit)
V 6-3 +/-(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 universalsubarachnoid 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
• CEREBRAL OEDEMA
• SEIZURES
• REBLEEDING
• VASOSPASM↔CEREBRAL
ISCHAEMIA/INFARCTION
EXTRACRANIAL
• FEVER
• ALTERATION IN RESPIRATORY
FXN
• EFFECT ON CVS
• FLUID & ELECTROLYTIC
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
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
• INTRACRANIAL
ICH,IVH,SDH
HCP
CEREBRAL OEDEMA
SEIZURES
REBLEEDING
VASOSPASM↔CERE
BRAL
ISCHAEMIA/INFARCTI
ON
SAH:COMPLICATIONS
• INTRACRANIAL
ICH,IVH,SDH
HCP
CEREBRAL OEDEMA
SEIZURES
REBLEEDING
VASOSPASM↔CEREBRAL
ISCHAEMIA/INFARCTION
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
Suspected in pt with sudden deterioration of consciousness
Prevention: Early Rx (surgery or endovascular)
Role of antifibrinolytics uncertain
0
10
20
30
40
50
60
70
0 10 20 30 40 50 60 70 80
% C
NA
HC
E O
F R
EBLE
ED
Days since First Bleed
%chance of Rebleed within the 1st M6 of icitus
Adapted from Winn,Richard,Jane 1977 Annals of Neurosurgery
ICAS: Risk falls with time but never drops below 3.5% per year
SAH:COMPLICATIONS
INTRACRANIAL
ICH,IVH,SDH
HCP
CEREBRAL OEDEMA
SEIZURES
REBLEEDING
VASOSPASM↔CEREBRAL
ISCHAEMIA/INFARCTION
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
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
insultEcg ∆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 GRADEThe Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan:
GRADE DESCRIPTION
1 No hemorrhage evident.
2 Subarachnoid hemorrhage less than 1mm thick.
3 Subarachnoid hemorrhage more than 1mm thick.
4Subarachnoid hemorrhage of any thickness with intra-ventricular 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 –veVasospasm???
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:PROTOCOL1.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 bloodin SAS (low risk of vasospasm)
SAH:MANAGEMENT:PROTOCOL
Clipping PcomA Endovascular Occlusion PcomA with Guglielmi Detachable Coils.
SAH:MANAGEMENT:PROTOCOL
PROBLEM
VASOSPASM
SOLUTIONPREVENTION :
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/12H3L/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
PROBLEMSEIZURES
HCP
INFECTION
DVT
GIT
GUT
SOLUTION
PREVENTION :
Prophylactic anticonvulsants:PHENYTOIN LD & MD
Ensure IV P°≈15-30cmH2O (OverdrainingREBLEEDING!!!!)
Routine ATB to cover G+ and G- (protocol varies ):
Penicillins + Cephaosporins
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
↑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
HEADACHE :Analgesics: Perfalgan 1g /8H Narcotics: Fentanyl 50ug bolusAGITATION:Tranquilizers:eg Benzodiazepines
Midazolam (DORMICAN) 1-2mg and ↑according to need
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 20 10-15 6-10
III 25 10-15 10-15
IV 50 20-25 40-50
V 80 25-30 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.
