Subarachnoid Haemorrhage

Dr S Arun-CastroMBBS AKC PgDip

King’s College HospitalNeuro-ICU

Learning Objectives

• To understand the pathophysiology behind subarachnoid haemorrhage • To understand the steps taken to diagnose subarachnoid haemorrhage • To understand the treatment options for SAH

• To understand the ICU management of SAH

True or False? q1

1. The following are risk factors for a poor outcome post aneurysmal subarachnoidhaemorrhage (SAH):a. Male sexb. Presence of co-morbid conditionsc. Anterior circulation aneurysmd. World Federation of Neurosurgeons (WFNS) grade IV

True or False? q2

2. Proven therapies in the management of vasospasm include:a. Triple H therapyb. Oral nimodipinec. Antifibrinolyticsd. Balloon angioplasty

True or False? q3

3. The following statements are true:a. The ISAT study demonstrated a better outcome for coiled versus clippedaneurysmsb. The overall case mortality for SAH is 10%c. Intraoperative hypothermia improves neurological outcomed. CT is 100% sensitive in detecting aneurysms

Pathophysiology of SAH

• SAH may be spontaneous or traumatic • Spontaneous SAH are caused by Cerebral aneurysms ,AV malformations • Uncommon causes – neoplasms, dural AVM, venous angiomas, infectious aneurysms

Epidemiology of SAH• Incidence about

10/100,000/yr• Mean age of onset 51

years• 55% women

• men predominate until age 50, then more women

• Risk factors• cigarette smoking• hypertension• family history

800-900 patients undergo either endovascular coiling or surgical clipping each year in England

Case fatality rates for SAH• Population-based study in England • 24 hour mortality: 21%• 7 days: 37%• 30 days: 44%• Relative risk for patients over 60 years vs. younger = 2.95• NCEPOD : 25 % survival

Pobereskin JNNP 2001;70:340-3

Aneurysms

- 1-2% of the population have unrupturedaneurysms

- larger >1cm aneurysms :more likely

- Women>Men

- incidence increases linearly with age

- 10-15% of patients presenting with SAHhave multiple aneurysms

Common sites of aneurysms within the cerebral circulation. ACA - anterior cerebralartery; A com – anterior communicating artery; ICA – internal carotid artery; P comm. –posterior communicating artery; BA – basilar artery.

Clinical presentation

• “Worst headache in my life”• Neck stiffness• Photophobia• Often accompanied by a period of

unconsciousness • 50% do not awaken

diagnosis

Risk factors

On Examination

Investigation

• CT Brain without contrast Sensitivity decreases with time from onset

• CT scan is 90% sensitive within the first 24 hours• 80% sensitive at 3 days • 50% sensitive at 1 week

• CT also can detect intracerebral hemorrhage, mass effect, and hydrocephalus.

• A falsely negative CT scan can result from small-volume SAH.

Interpreting the CT• Distribution of SAH can provide information about the location of an aneurysm and prognosis

– Intraparenchymal hemorrhage may occur with MCA & PCAaneurysms.

– Interhemispheric and intraventricular hemorrhagesmay occur with ACA aneurysms.

Outcome is worse for patients with extensive clots inbasal cisterns than for those with a thin diffusehemorrhage

Diffuse SAH

MCA territory SAH

Florid SAH with early hydrocephalus

(ACLS text)

More subtle subarachnoid haemorrhage

interhemispheric fissure

Sylvian fissure

Negative CT but suspicious hx• If the history is strongly suggestive the CT is negative LP • Xanthochromia is a classic sign, but not present early on

• Angiography CT A or MRA to define the source of the bleed

• If multiple aneurysms : treatment targeted towards aneurysm

• adjacent to largest blood collection

• Sometimes there may be difficulty identifying the source

Clinical Grading Scales for SAH .../cont’d

Grade Description

World Federation of Neurological Surgeons Scale1 Glasgow coma scale 15, no motor deficit2 GCS 13 to 14, no motor deficit3 GCS 13 to 14, with motor deficit4 GCS 7 to 12, with or without motor deficit5 GCS 3 to 6, with or without motor deficit

Complications

Hydrocephalus first 24 hours -obstruction of CSF outflow in the ventricular system by clot

Rebleeding of SAH occurs in 20% of patients in the first 2 weeks. Peak incidence rebleeding = 1 day post SAH

- This may be from lysis of the aneurysmal clot

Vasospasm from arterial smooth muscle contraction is symptomatic in 36% of patients.

Complications• Neurologic deficits from cerebral ischemia peak at days 4-12.

• Hypothalamic dysfunction causes excessive sympathetic stimulation myocardial ischemia or labile BP

• Hyponatremia may result from cerebral salt wasting/ SIADH

• Pulmonary oedema – neurogenic and nonneurogenic

• HAP/VAP

Hydrocephalus• Caused by obstruction of CSF flow by clotted blood• Can occur early (EVD) or late (VP shunt)• Careful with drainage – reduction in ICP can increase the risk of rebleeding

SAH + Hydrocephalus • Temporal horns dilated• diffuse SAH • Blood in the 4th ventricle• Diffuse cerebral oedema

Rebleeding

• Within first 24 hours• Up to 20% of patients rebleed within 2

weeks• Main preventative measure is control of

blood pressure – beta blockers• Alternatively early clipping of the

aneurysm allows hypertensive and hypervolemic therapy to prevent vasospasm

Focus of Treatment in SAH

• Identifying and Rx causative lesion

•preventing re-bleeding

• Rx hydrocephalus

• Rx and preventing vasospasm

So Early or Delayed Surgery

• Early clipping – less rebleeding• But higher incidence of vasospasm

Worst time is day 7 to 10 (highest time for vasospasm)

So – before 3 days, after 10 days

Clip vs Coiling

• International Subarachnoid Aneurysm Trial(ISAT) Lancet 2002

• 2143 patients randomized to NS• clipping (n=1070) or endovascular coiling(n=1073)• Outcomes 1 year• 23.7% dependent or dead at 1yr coiled • 30.6% dependent or dead at 1 y clipped

Basilar artery aneurysm

before coiling

Basilar artery aneurysm

after coiling

Calcium Channel Blockers

• Nimodipine 60mg q6h x 24d• Reduces:– Neurologic deficit– Cerebral infarction– Mortality

Blood Pressure Control

• Maintain systolic BP >130mmHg• Use vasopressors if necessary – tomaintain CPP, and reduce ischemicpenumbra from vasospasm• Generally avoid vasodilators (exceptcalcium channel blockers)

Initial angiogramRepeat angiogram

showing vasospasm (small arrows)

Vasospasm in acute SAH

Vasospasm

•Up to 33%• Delayed until 48-72 h post SAH until 14d• Associated with larger clots and increasingage• Caused by local blood products• Compensated for by increase in BP tomaintain supply of nutrients• Nimodipine / nicardipine

The Fisher Grading of SAH as Demonstrated by CT scan(Relation of Cerebral Vasospasm to Subarachnoid Hemorrhage Visualized by Computerized Tomographic Scanning. CM Fisher et al. Neurosurgery, 6:1-9, 1980)

Group (Grade)12

3

4

DescriptionNo blood detectedA diffuse deposition or thin layer with all vertical layers of blood (interhemispheric fissure, insular cistern, ambient cistern) less than 1 mm thick)Localized clots and/or vertical layers of blood 1 mm or greater in thicknessDiffuse or no subarachnoid blood, but with intracerebral or intraventricular clots

Summary of the Relationship between the Amount of Subarachnoid Blood and the Development of Vasospasm(CM Fisher et al. Neurosurgery, 6:1-9, 1980)

VASPSPASM

SubarachnoidBlood

No.Cases None

Slight-Moderate Severe

Signs ofSevere Vasospasm

None 11 7 2 2 0

Diffuseonly

7 4 3 0 0

Clot or ThickLayer

24 0 1 23 23

Diffuse orNone, withCerebral ofVentricularBlood

5 3 2 0 0

TOTAL 47 14 8 25 23

Vasospasm HHH Therapy• Haemodilution– Hct 30-35%

• Hypertension– Noradrenaline– BP titration to CPP/exam

• Hypervolemia Colloid/crystalloid

True or False? q1

• 1. The following are risk factors for a poor outcome post aneurysmal subarachnoid

• haemorrhage (SAH):• a. Male sex• b. Presence of co-morbid conditions• c. Anterior circulation aneurysm• d. World Federation of Neurosurgeons

(WFNS) grade IV

• FTFT• Aneurysms are more common in females,

sex does not alter survival outcome. Risk• factors for an unfavourable outcome are;

age, poor neurological condition on admission,

• posterior circulation/>10mm size, comordity especially hypertension, blood in

• subarachnoid space on CT.

True or False? q2

•2. Proven therapies in the management of vasospasm include:

•a. Triple H therapy•b. Oral nimodipine•c. Antifibrinolytics•d. Balloon angioplasty

• 2. FTFF• Triple H therapy is often used for symptomatic

vasospasm, but has not been proven to be• effective. There is no evidence that balloon

angioplasty is better than medical treatment.• There is level 1 evidence that commencing oral

nimodipine at admission in all cases of• SAH will decrease development of vasospasm.

Antifibrinolytics (potential to decreases• rebleeding) do not improve outcome and may

increase thromboembolic risk.

• 3. TFFF• The outcome advantage for coiling comes from level 1

evidence, note it included patients• in mostly good neurological condition who had to be deemed

suitable for both treatments.• The overall fatality is nearer 50%. Mild intraoperative

hypothermia did not improve• outcome in the IHAST trial. CT may miss small/delayed

presentation SAH, and therefore• lumbar puncture may be indicated in some patients before the

diagnosis can be excluded.

True or False? q3

• 3. The following statements are true:• a. The ISAT study demonstrated a better

outcome for coiled versus clipped• aneurysms• b. The overall case mortality for SAH is 10%• c. Intraoperative hypothermia improves

neurological outcome• d. CT is 100% sensitive in detecting aneurysms

Colice 1985

• http://www.ncepod.org.uk/2013report2/downloads/Managing%20the%20Flow_FullReport.pdf

• Relation of Cerebral Vasospasm to Subarachnoid Hemorrhage Visualized by Computerized Tomographic Scanning. CM Fisher JP Kistler and JM Davis. Neurosurgery, 6:1-9, 1980

• Stroke Association. 2013. Stroke Statistics. www. stroke.org.uk • VanGijn J, Kerr R and Rinkel, JE. 2007. Subarachnoid

haemorrhage. The Lancet: 369(9558); 306-318• VanGijn J and Rinkel JE. 2001. Subarachnoid haemorrhage:

diagnosis, causes and management. Brain: 124; 249-278 •

Complications of aneurysmal SAH

• rebleeding• cerebral vasospasm• volume disturbances• osmolar disturbances• seizures

• arrhythmias and other cardiovascular complications

• CNS infections• other complications

of critical illness

Critical care issues: rebleeding

• Unsecured aneurysms:• 4% rebleed on day 0• then 1.5%/day for next 13 days [27% for 2 weeks]

• Antifibrinolytic therapy (e.g., aminocaproic acid)• may be useful between presentation and early surgery

• Blood pressure management• labetalol, hydralazine, nicardipine

• Analgesia• Minimal or no sedation to allow examination

Critical care issues: vasospasm and delayed ischemic damage

• Potential mechanisms• oxyhemoglobin/nitric oxide• endothelins

• Diagnosis• clinical• transcranial Doppler flow velocity monitoring• electrophysiologic• radiologic

Critical care issues: vasospasm and delayed ischemic damage•Prophylaxis

• clot removal• volume repletion

• prophylactic volume expansion not useful• nimodipine 60 mg q4h x 14 days

• relative risk of stroke reduced by 0.69 (0.58-0.84). • nicardipine 0.075 mg/kg/hr is equivalent

Critical care issues: vasospasm and delayed ischemic damage• Potential neuroprotective strategies

• tirilizad mesylate is an effective neuroprotectant in SAH, approved in 13 countries but not the US

• N-2-mercaptopropionyl glycine (N-2-MPG), approved for prevention of renal stones in patients with cysteinuria

• AMPA antagonists (e.g., topiramate)• NMDA antagonists (e.g., ketamine)

Critical care issues: vasospasm and delayed ischemic damage• Management

• volume expansion• induced hypertension• cardiac output augmentation

• dopamine or dobutamine• intra-aortic balloon pump

• angioplasty• papaverine• erythropoetin?

Critical care issues: neurogenic pulmonary edema• Symptomatic pulmonary edema occurs in about

20% of SAH patients• detectable oxygenation abnormalities occur in 80%

• Potential mechanisms:• hypersympathetic state• cardiogenic pulmonary edema• neurogenic pulmonary edema

• Management

Neurogenic pulmonary edema in SAH

• radiographic pulmonary edema occurs in about 23% of SAH patients• up to 80% have elevated AaDO2

• a minority of cases are associated with documented LV dysfunction or iatrogenic volume overload

• neurogenic pulmonary edema appears to be a consequence of the constriction of pulmonary venous sphincters• requires neural control; in experimental models, does not

occur in denervated lung

Neurogenic pulmonaryedemaafter SAH

PCWP=12CI=4.2

Conditions associated with neurogenic pulmonary edema

• Common:• subarachnoid

hemorrhage• status epilepticus• severe head trauma• intracerebral

hemorrhage

• Rare:• brainstem infections• medullary tumors• multiple sclerosis• spinal cord infarction• increased ICP from a

variety of causes

Mechanisms of neurogenic pulmonary edema• hydrostatic: CNS disorder produces a hypersympathetic state,

raising afterload and inducing diastolic dysfunction which cause hydrostatic pulmonary edema• 5/12 patients had low protein pulmonary edema

• (Smith WS, Mathay MA. Chest 1997;111:1326-1333)• Consistent with either neurogenic or cardiogenic

hypotheses

Mechanisms of neurogenic pulmonary edema• neurogenic: contraction of postcapillary venular

sphincters raises pulmonary capillary pressure without raising left atrial pressure• Abundant experimental evidence of neurogenic

mechanism• Clinical evidence mostly inferred from low PCWP and

early hypoxemia• structural: ‘fracture’ of pulmonary capillary

endothelium

Colice 1985

Managing neurogenic pulmonary edema• acute subarachnoid hemorrhage patients do not tolerate

hypovolemia• volume depletion doubles the stroke and death rate due to

vasospasm

Seizures in SAH patients

• about 6% of patients suffer a seizure at the time of the hemorrhage• distinction between a convulsion and decerebrate posturing

may be difficult • postoperative seizures occur in about 1.5% of patients despite

anticonvulsant prophylaxis • remember to consider other causes of seizures (e.g., alcohol

withdrawal)

Seizures in SAH patients• patients developing delayed ischemia may seize following

reperfusion by angioplasty• late seizures occur in about 3% of patients

Seizure management in SAH• seizures in patients with unsecured aneurysms may

result in rebleeding, so prophylaxis (typically phenytoin) is commonly given

• even a single seizure usually prompts a CT scan to look for a change in the intracranial pathology• additional phenytoin is frequently given to raise the serum

concentration to 20+ ug/mL• lorazepam to abort serial seizures or status

epilepticus

DVT in the SAH patient

• even after the aneurysm is secured, there is probably a risk of ICH in postoperative patients for 3 -5 days• therefore, we usually place IVC filters for DVTs

• we also use IVC filters for unsecured aneurysm patients• angioplasty patients can probably be anticoagulated

Nutrition in the SAH patient

• no useful clinical trials available• hyperglycemia may worsen the outcome of delayed

ischemia• ketosis appears to protect against cerebral ischemic

damage in experimental models• if patients are not fully fed during the period of

vasospasm risk, trophic feeding may be useful, and GI bleeding prophylaxis should be given

Critical care issues: other medical complications• Cardiac (almost 100% have abnormal ECG)

• QT prolongation and torsade de pointes• left ventricular failure

• Pulmonary• pneumonia• ARDS• pulmonary embolism (2% DVT, 1% PE)

• Gastrointestinal• gastrointestinal bleeding (4% overall, 83% of fatal SAH)