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Critical care of the patient with acute subarachnoid hemorrhage. William M. Coplin MD FCCM Associate Professor of Neurology and Neurological Surgery Medical Director, Neurotrauma & Critical Care Wayne State University Dr. Abdul-Monim Batiha. Internal carotid artery. Posterior
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Critical care of the patient with acute subarachnoid hemorrhage William M. Coplin MD FCCM Associate Professor of Neurology and Neurological Surgery Medical Director, Neurotrauma & Critical Care Wayne State University Dr. Abdul-Monim Batiha
Internal carotid artery Posterior communicating artery aneurysm
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
Case fatality rates for SAH • Population-based study in England with essentially complete case ascertainment • 24 hour mortality: 21% • 7 days: 37% • 30 days: 44% • Relative risk for patients over 60 years vs. younger = 2.95 Pobereskin JNNP 2001;70:340-3
Conditions associated with aneurysms • Aortic coarctation • Polycystic kidney disease • Fibromuscular dysplasia • Moya moya disease • Ehlers-Danlos syndrome
Diagnostic approaches Aneurysm management surgical endovascular Critical care issues rebleeding neurogenic pulmonary edema vasospasm and delayed ischemic damage hydrocephalus cerebral salt wasting medical complications Subarachnoid hemorrhage
Diagnostic approach to SAH • Wide range of symptoms and signs • CT scanning • Limited role of lumbar puncture • Angiography • conventional vs. spiral CT vs. MRA • identification of multiple aneurysms • SAH without aneurysm
Florid SAH with early hydrocephalus (ACLS text)
More subtle subarachnoid hemorrhage interhemispheric fissure Sylvian fissure
Subhyaloid hemorrhage Flame and dot hemorrhages
Aneurysm management • Surgical • early surgery (first 3 days) becoming standard • large dose mannitol (electrolyte disturbances) • microsurgical technique • Endovascular • choice of cases for coiling • anesthesia or sedation issues • usually requires NMJ blockade
rebleeding cerebral vasospasm volume disturbances osmolar disturbances seizures arrhythmias and other cardiovascular complications CNS infections other complications of critical illness Complications of aneurysmal SAH
“If it becomes at all doubtful, let me know, I will be just inside” Captain Edward Smith to second officer Lightoller who then signed over to Murdoch at 10:00 PM 9:20 PM
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
Vasospasm in acute SAH Repeat angiogram showing vasospasm (small arrows) Initial angiogram
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 isequivalent
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?
Frequency of medical complications after SAH(placebo arm of North American Nicardipine Trial) Solenski et alCCM 1995;23:1007-1017
Death by primary cause (87 deaths among 455 patients) Solenski et alCCM 1995;23:1007-1017
Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage N=242 Gruber A etal.Crit Care Med 1999;27:505-14
Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage Gruber A etal.Crit Care Med 1999;27:505-14
Pulmonary complications after SAH Solenski et alCCM 1995;23:1007-1017
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 pulmonary edema after SAH PCWP=12 CI=4.2
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 Conditions associated with neurogenic pulmonary edema
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
Managing neurogenic pulmonary edema • acute subarachnoid hemorrhage patients do not tolerate hypovolemia • volume depletion doubles the stroke and death rate due to vasospasm
Managing neurogenic pulmonary edema • supplemental oxygen and CPAP or PEEP • place pulmonary artery catheter and, if there is coexisting cardiogenic edema, lower the wedge pressure to ~ 18 mmHg • echocardiography may be useful to determine whether cardiac dysfunction is also present • NPE usually resolves in a few days
Metabolic complications after SAH Solenski et alCCM 1995;23:1007-1017
Infectious problems in SAH patients • important to distinguish saccular aneurysms from mycotic (frequently post-bacteremic) aneurysms • postoperative infections • postoperative meningitis may be aseptic, but this is a diagnosis of exclusion • particularly a problem in the SAH patient because the hemorrhage itself causes meningeal reaction • complications of critical illness • complications of steroid use
Infectious complications after SAH Solenski et alCCM 1995;23:1007-1017
Etiology of fever in SAH patients • Collected data on 75 consecutive SAH patients who had undergone clipping. • Complete data available for 52 patients. • 32 (61.5%) of the 52 patients had at least one fever (temp >38.3°C) • Total of 46 episodes • 22% of episodes had no diagnosable cause (“central’) • Fever was not associated with vasospasm • Nonsignificant trend toward inverse relationship, 2 = 2.33, p < 0.13 Bleck TP, Henson S. Crit Care Med 1992;20:S31
Etiology of fever in SAH patients Bleck TP, Henson S. Crit Care Med 1992;20:S31
Evidence-based medicine • a system of belief that stresses the need for prospectively collected, objective evidence of everything except its own utility Bleck TP BMJ 2000;321:239
Real evidence-based rating scale • class 0: things I believe • class 0a: things I believe despite the available data • class 1: RCCTs that agree with what I believe • class 2: other prospective data • class 3: expert opinion • class 4: RCCTs that don’t agree with what I believe • class 5: what you believe that I don’t Bleck TP BMJ 2000;321:239
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)