ICU Management of Subarachnoid Hemorrhage
Daryl R. Gress, M.D.
Louise Nerancy Chair of Neurocritical Care
Director of Neurocritical Care ,University of Virginia
Disclosures: Scientific Advisory Board Ornim
Subarachnoid Hemorrhage Management
SAH is complex and fulminate disease
•predictable potential complications
•need overall treatment strategy
•team approach necessary for optimal outcome
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
–small portion of overall stroke
–10-15/100,000
–30,000 cases per year in US
–4.5% of all stroke mortality
–25% of stroke-related years of life lost <65
Johnston Neurology 1998; 50:1413-18
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage
–acute mortality 30-50%
–survivors have 50% risk of disability
–factors
•age
•clinical status at presentation
•medical co-morbidities
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage- etiologies
–trauma
–aneurysm
–AVM
–hypertension
–bleeding dyscrasias, malignancies
–“angio-negative”
Subarachnoid Hemorrhage
Subarachnoid Hemorrhage- “angio-negative”
–10-20% of spontaneous SAH
–benign perimesencephalic
•small blood volume
•focal, interpeduncular, pre-truncal
–other•large blood volume, diffuse or
asymmetric pattern
•may not have “benign” low risk of
recurrence
Subarachnoid Hemorrhage
– perimesencephalic hemorrhage
Subarachnoid Hemorrhage Management
Subarachnoid Hemorrhage
Clinical Presentation:
–headache
–transient alteration in consciousness
–focal neurologic findings
–normal exam possible
–Up to 30 % misdiagnosed at initial presentation
–Mayer, et al. STROKE 1996 27:1558-63
Subarachnoid Hemorrhage Management
Subarachnoid Hemorrhage
Diagnosis:
–clinical suspicion
–non-contrast CT
–lumbar puncture
–MR- coronal FLAIR images may enhance
sensitivity
Subarachnoid Hemorrhage Management
Subarachnoid Hemorrhage
Emergency Treatment:
–control MAP- attempt to prevent re-bleed
IV labetolol, nicardipine, nitroprusside
preserve CPP
–anticonvulsants, short term?
–need for ventriculostomy?
–steroids not necessary
–neurocritical care unit admission
Subarachnoid Hemorrhage Management
Subarachnoid Hemorrhage-Treatment Decisions:
Prognosis related to initial Hunt/Hess score- I-V
also related to mechanism of brain injury
•hydrocephalus
•tissue destruction
•hypoxia/hypoperfusion
Subarachnoid Hemorrhage Management
Neurocritical care complications:
–neurogenic pulmonary edema
–aspiration pneumonia
–cardiac ischemic injury
–hyponatremia
–DVT and pulmonary embolism
–fever
Subarachnoid Hemorrhage Management
Critical Care Complications
–cardiac ischemia
•EKG changes common: diffuse T wave inversions
•arrhythmias: sinus arrest, ventricular
fibrillation/tachycardia
•CK and troponin leaks
•global ischemia: depressed LV function, stunned
myocardium
•focal ischemia if underlying coronary artery disease
–catecholamine excess and calcium injury
Subarachnoid Hemorrhage Management
Critical Care Complications
–cardiac ischemia
•Typically apical sparing involving base, sudden
onset, CK and troponin leaks
•Less commonly apical dilation, delayed onset, less
troponin spill, “Takasuba heart”
–Spontaneous improvement in LV function over days
Subarachnoid Hemorrhage Management
Critical Care Complications
–hyponatremia
•sodium can drop precipitously over hours
•typically appears several days after SAH, time course
similar to vasospasm
•cerebral salt wasting with increases in circulating
ANF
•some component of SIADH possible in some cases
Subarachnoid Hemorrhage Management
Critical Care Complications
–hyponatremia
•sodium supplement always the treatment, enteral or
parenteral, may review hypertonic saline
•fluid restriction never favored in setting of possible
vasospasm
–spontaneous resolution of hyponatremia and return of
sodium homeostasis over several weeks
Subarachnoid Hemorrhage Management
Major Problems to Avoid:
–aneurysm re-rupture
–hydrocephalus
–vasospasm
Subarachnoid Hemorrhage Management
Re-Bleeding following aneurysmal SAH
•high risk 2-4% over first 24 hours
20% over 10-14 days
•early definitive aneurysm treatment always
preferred, even if vasospasm suspected
Johnston Ann Neurol 2000;48:11-19
Subarachnoid Hemorrhage Management
Hydrocephalus
•acute
-common at presentation
•sub-acute -develops over days
•chronic -appears as NPH after
weeks/months
ventriculostomy or VP shunt
increased brain compliance common
–altered relationship of ventricular size and
pressure
Subarachnoid Hemorrhage Management
Vasospasm
•predictable time course, day 4 to 14 following SAH
•predictable location, related to blood clot
•some individual variability
•Pathology
–hemoglobin, oxyhemoglobin likely spasmogen
–smooth muscle contraction
–inflammatory arteriopathy
Subarachnoid Hemorrhage Management
Vasospasm Management
•nimodipine
–small improvement in outcome in early
trials
–no clear angiographic effect
–may work as neuroprotectant
–can compromise blood pressure
–may need to reduce dose or delete to
preserve BP
Subarachnoid Hemorrhage Management
Standard Vasospasm Management
•triple H therapy
–hemodilution
–hypervolemia
–hypertension
Subarachnoid Hemorrhage Management
Vasospasm Management
•hemodilution
–rheologic effect
–O2 carrying capacity vs. viscosity
–optimal hematocrit ~30-35%
–rarely need for therapeutic phlebotomy
Subarachnoid Hemorrhage Management
Vasospasm Management
•hypervolemia
–increase preload
–augment cardiac function, cardiac output
–CVP or pulmonary artery catheter
monitoring
the debate:
Is cardiac output an independent variable in
determining cerebral perfusion ?
Subarachnoid Hemorrhage Management
Vasospasm Management
•Induced hypertension
–cerebral perfusion pressure = MAP - ICP
–phenylephrine most useful, norepinephrine
–target MAP depends on clinical status,
timing, evidence of vasospasm
Subarachnoid Hemorrhage Management
Vasospasm Management
•cerebral perfusion is key
•in spasm, blood flow is pressure dependent
–not directly related to volume
–not directly related to cardiac output
–firm belief in absence of adequate data
•much of morbidity related to volume overload
Subarachnoid Hemorrhage Management
Vasospasm Management
•vasospasm watch
–neurocritical care nursing
–CT angiography and CT perfusion
–transcranial Doppler
•titrate intensity of medical management
•maximize therapy to avoid ischemic deficits
Subarachnoid Hemorrhage Management
Vasospasm Management
•maximize therapy to avoid ischemic deficits
•if deficits, urgent need for angiography
–angioplasty
–intra-arterial calcium antagonists
–always consider ICP
Subarachnoid Hemorrhage Management
Vasospasm Management-something new?
•endothelin receptor antagonist?
•blockade of ETA or ETB prevent/reverse
vasospasm in canine models
•ET-1 appears as acute phase reactant in CSF
•in Phase II clinical trial, clazosentan led to
angiographic effect demonstrated without clear
clinical effect
Subarachnoid Hemorrhage Management
Vasospasm Management-something new?
•endothelin receptor antagonist?
–Conscious II, randomized Phase III trial in
surgically clipped aneurysms following SAH
–Conscious III, randomized Phase III trial in coiled
aneurysms following SAH
Subarachnoid Hemorrhage Management
Vasospasm Management-something new?
•Intravenous sodium nitrite
–Nitric oxide donor delivered to vascular
endothelium
–Vasodilator
–Marked effect in primate model of SAH vasospasm
–Phase I-II trial at UVA