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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.

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Presentation on theme: "Critical care of the patient with acute subarachnoid hemorrhage William M. Coplin MD FCCM Associate Professor of Neurology and Neurological Surgery Medical."— Presentation transcript:

1 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

2 Internal carotid artery Posterior communicating artery aneurysm

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4 Epidemiology of SAH Incidence about 10/100,000/yrIncidence about 10/100,000/yr Mean age of onset 51 yearsMean age of onset 51 years 55% women55% women –men predominate until age 50, then more women Risk factorsRisk factors –cigarette smoking –hypertension –family history

5 Case fatality rates for SAH Population-based study in England with essentially complete case ascertainmentPopulation-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

6 Conditions associated with aneurysms Aortic coarctationAortic coarctation Polycystic kidney diseasePolycystic kidney disease Fibromuscular dysplasiaFibromuscular dysplasia Moya moya diseaseMoya moya disease Ehlers-Danlos syndromeEhlers-Danlos syndrome

7 Subarachnoid hemorrhage Diagnostic approachesDiagnostic approaches Aneurysm managementAneurysm management –surgical –endovascular Critical care issues –rebleeding –neurogenic pulmonary edema –vasospasm and delayed ischemic damage –hydrocephalus –cerebral salt wasting –medical complications

8 Diagnostic approach to SAH Wide range of symptoms and signsWide range of symptoms and signs CT scanningCT scanning Limited role of lumbar punctureLimited role of lumbar puncture AngiographyAngiography –conventional vs. spiral CT vs. MRA –identification of multiple aneurysms –SAH without aneurysm

9 Florid SAH with early hydrocephalus (ACLS text)

10 More subtle subarachnoidhemorrhage interhemisphericfissure Sylvian fissure

11 Subhyaloid hemorrhage Flame and dot hemorrhages

12 Aneurysm management SurgicalSurgical –early surgery (first 3 days) becoming standard –large dose mannitol (electrolyte disturbances) –microsurgical technique EndovascularEndovascular –choice of cases for coiling –anesthesia or sedation issues usually requires NMJ blockadeusually requires NMJ blockade

13 Guglielmi detachable coil

14 Basilar artery aneurysm before coiling

15 Basilar artery aneurysm after coiling

16 Complications of aneurysmal SAH rebleedingrebleeding cerebral vasospasmcerebral vasospasm volume disturbancesvolume disturbances osmolar disturbancesosmolar disturbances seizuresseizures arrhythmias and other cardiovascular complications CNS infections other complications of critical illness

17 “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

18 11:40 PM

19 Critical care issues: rebleeding Unsecured aneurysms: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)Antifibrinolytic therapy (e.g., aminocaproic acid) –may be useful between presentation and early surgery Blood pressure managementBlood pressure management –labetalol, hydralazine, nicardipine AnalgesiaAnalgesia Minimal or no sedation to allow examinationMinimal or no sedation to allow examination

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21 Critical care issues: vasospasm and delayed ischemic damage Potential mechanismsPotential mechanisms –oxyhemoglobin/nitric oxide –endothelins DiagnosisDiagnosis –clinical –transcranial Doppler flow velocity monitoring –electrophysiologic –radiologic

22 Initial angiogram Repeat angiogram showing vasospasm (small arrows) Vasospasm in acute SAH

23 Critical care issues: vasospasm and delayed ischemic damage ProphylaxisProphylaxis –clot removal –volume repletion prophylactic volume expansion not usefulprophylactic volume expansion not useful –nimodipine 60 mg q4h x 14 days relative risk of stroke reduced by 0.69 ( ).relative risk of stroke reduced by 0.69 ( ). nicardipine mg/kg/hr isequivalentnicardipine mg/kg/hr is equivalent

24 Critical care issues: vasospasm and delayed ischemic damage Potential neuroprotective strategiesPotential 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)

25 Critical care issues: vasospasm and delayed ischemic damage ManagementManagement –volume expansion –induced hypertension –cardiac output augmentation dopamine or dobutaminedopamine or dobutamine intra-aortic balloon pumpintra-aortic balloon pump –angioplasty –papaverine –erythropoetin?

26 Frequency of medical complications after SAH (placebo arm of North American Nicardipine Trial) Solenski et al CCM 1995;23:

27 Death by primary cause (87 deaths among 455 patients) Solenski et al CCM 1995;23:

28 Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage Gruber A et al.Crit Care Med 1999;27: N=242

29 Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage Gruber A et al.Crit Care Med 1999;27:505-14

30 Competing concerns

31 Pulmonary complications after SAH Solenski et al CCM 1995;23:

32 Critical care issues: neurogenic pulmonary edema Symptomatic pulmonary edema occurs in about 20% of SAH patientsSymptomatic pulmonary edema occurs in about 20% of SAH patients –detectable oxygenation abnormalities occur in 80% Potential mechanisms:Potential mechanisms: –hypersympathetic state –cardiogenic pulmonary edema –neurogenic pulmonary edema ManagementManagement

33 Neurogenic pulmonary edema in SAH radiographic pulmonary edema occurs in about 23% of SAH patientsradiographic pulmonary edema occurs in about 23% of SAH patients –up to 80% have elevated AaDO 2 –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 sphinctersneurogenic 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

34 Neurogenicpulmonaryedema after SAH PCWP=12CI=4.2

35 Conditions associated with neurogenic pulmonary edema Common: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

36 Mechanisms of neurogenic pulmonary edema hydrostatic: CNS disorder produces a hypersympathetic state, raising afterload and inducing diastolic dysfunction which cause hydrostatic pulmonary edemahydrostatic: 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: )(Smith WS, Mathay MA. Chest 1997;111: ) –Consistent with either neurogenic or cardiogenic hypotheses

37 Mechanisms of neurogenic pulmonary edema neurogenic: contraction of postcapillary venular sphincters raises pulmonary capillary pressure without raising left atrial pressureneurogenic: 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 endotheliumstructural: ‘fracture’ of pulmonary capillary endothelium

38 Colice 1985

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41 Managing neurogenic pulmonary edema acute subarachnoid hemorrhage patients do not tolerate hypovolemiaacute subarachnoid hemorrhage patients do not tolerate hypovolemia –volume depletion doubles the stroke and death rate due to vasospasm

42 Managing neurogenic pulmonary edema supplemental oxygen and CPAP or PEEPsupplemental oxygen and CPAP or PEEP place pulmonary artery catheter and, if there is coexisting cardiogenic edema, lower the wedge pressure to ~ 18 mmHgplace 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 daysNPE usually resolves in a few days

43 Metabolic complications after SAH Solenski et al CCM 1995;23:

44 Infectious problems in SAH patients important to distinguish saccular aneurysms from mycotic (frequently post-bacteremic) aneurysmsimportant to distinguish saccular aneurysms from mycotic (frequently post-bacteremic) aneurysms postoperative infectionspostoperative 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 illnesscomplications of critical illness complications of steroid usecomplications of steroid use

45 Infectious complications after SAH Solenski et al CCM 1995;23:

46 Etiology of fever in SAH patients Collected data on 75 consecutive SAH patients who had undergone clipping.Collected data on 75 consecutive SAH patients who had undergone clipping. Complete data available for 52 patients.Complete data available for 52 patients. 32 (61.5%) of the 52 patients had at least one fever (temp >38.3°C)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 vasospasmFever 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

47 Etiology of fever in SAH patients Bleck TP, Henson S. Crit Care Med 1992;20:S31

48 Evidence-based medicine a system of belief that stresses the need for prospectively collected, objective evidence of everything except its own utilitya system of belief that stresses the need for prospectively collected, objective evidence of everything except its own utility Bleck TP BMJ 2000;321:239

49 Real evidence-based rating scale class 0: things I believeclass 0: things I believe –class 0a: things I believe despite the available data class 1: RCCTs that agree with what I believeclass 1: RCCTs that agree with what I believe class 2: other prospective dataclass 2: other prospective data class 3: expert opinionclass 3: expert opinion class 4: RCCTs that don’t agree with what I believeclass 4: RCCTs that don’t agree with what I believe class 5: what you believe that I don’tclass 5: what you believe that I don’t Bleck TP BMJ 2000;321:239

50 Seizures in SAH patients about 6% of patients suffer a seizure at the time of the hemorrhageabout 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 prophylaxispostoperative seizures occur in about 1.5% of patients despite anticonvulsant prophylaxis remember to consider other causes of seizures (e.g., alcohol withdrawal)remember to consider other causes of seizures (e.g., alcohol withdrawal)

51 Seizures in SAH patients patients developing delayed ischemia may seize following reperfusion by angioplastypatients developing delayed ischemia may seize following reperfusion by angioplasty late seizures occur in about 3% of patientslate seizures occur in about 3% of patients

52 Seizure management in SAH seizures in patients with unsecured aneurysms may result in rebleeding, so prophylaxis (typically phenytoin) is commonly givenseizures 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 pathologyeven 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 epilepticuslorazepam to abort serial seizures or status epilepticus

53 DVT in the SAH patient even after the aneurysm is secured, there is probably a risk of ICH in postoperative patients for 3 -5 dayseven 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 patientswe also use IVC filters for unsecured aneurysm patients –angioplasty patients can probably be anticoagulated

54 Nutrition in the SAH patient no useful clinical trials availableno useful clinical trials available hyperglycemia may worsen the outcome of delayed ischemiahyperglycemia may worsen the outcome of delayed ischemia ketosis appears to protect against cerebral ischemic damage in experimental modelsketosis 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 givenif patients are not fully fed during the period of vasospasm risk, trophic feeding may be useful, and GI bleeding prophylaxis should be given

55 Critical care issues: hydrocephalus DiagnosisDiagnosis –clinical –radiologic ManagementManagement –ventriculostomy infection reductioninfection reduction –shunting

56 Hydrocephalus after SAH

57 Critical care issues: other medical complications Cardiac (almost 100% have abnormal ECG)Cardiac (almost 100% have abnormal ECG) –QT prolongation and torsade de pointes –left ventricular failure PulmonaryPulmonary –pneumonia –ARDS –pulmonary embolism (2% DVT, 1% PE) GastrointestinalGastrointestinal –gastrointestinal bleeding (4% overall, 83% of fatal SAH)

58 What about steroids?

59 SAH prognosis Sudden death prior to medical attention in about 20%Sudden death prior to medical attention in about 20% Of the remainder, with early surgeryOf the remainder, with early surgery –58% regained premorbid level of function as high as 67% in some centersas high as 67% in some centers –9% moderately disabled –2% vegetative –26% dead

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