critical care of the patient with acute subarachnoid hemorrhage

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

4. 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

5. 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

6. Conditions associated with aneurysms Aortic coarctation Polycystic kidney disease Fibromuscular dysplasia Moya moya disease Ehlers-Danlos syndrome

7. Subarachnoid hemorrhage Diagnostic approaches Aneurysm 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 signs CT scanning Limited role of lumbar puncture Angiography conventional vs. spiral CT vs. MRA identification of multiple aneurysms SAH without aneurysm

12. 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

13. Guglielmi detachable coil

14. Basilar artery aneurysm before coiling

15. Basilar artery aneurysm after coiling

16. Complications of aneurysmal SAH rebleeding cerebral vasospasm volume disturbances osmolar disturbances seizures arrhythmias and other cardiovascular complications CNS infections other complications of critical illness

19. 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

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

22. Vasospasm in acute SAH

23. 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

24. 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)

25. 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?

27. Death by primary cause (87 deaths among 455 patients)

28. Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage

29. Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage

30. Competing concerns

31. Pulmonary complications after SAH

32. 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

33. 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

35. 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

36. 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

37. 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

41. Managing neurogenic pulmonary edema acute 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 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

43. Metabolic complications after SAH

44. 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

45. Infectious complications after SAH

46. 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

47. Etiology of fever in SAH patients

48. Evidence-based medicine a system of belief that stresses the need for prospectively collected, objective evidence of everything except its own utility

49. 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

50. 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)

51. Seizures in SAH patients patients developing delayed ischemia may seize following reperfusion by angioplasty late 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 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

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 days therefore, we usually place IVC filters for DVTs we also use IVC filters for unsecured aneurysm patients angioplasty patients can probably be anticoagulated

54. 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

55. Critical care issues: hydrocephalus Diagnosis clinical radiologic Management ventriculostomy infection reduction shunting

57. 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)

58. What about steroids?

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