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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

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

slide2

Internal carotid artery

Posterior

communicating artery

aneurysm

epidemiology of sah
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
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
Conditions associated with aneurysms
  • Aortic coarctation
  • Polycystic kidney disease
  • Fibromuscular dysplasia
  • Moya moya disease
  • Ehlers-Danlos syndrome
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

Subarachnoid hemorrhage
diagnostic approach to sah
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
slide9

Florid SAH with

early hydrocephalus

(ACLS text)

slide10

More subtle

subarachnoid

hemorrhage

interhemispheric

fissure

Sylvian fissure

slide11

Subhyaloid hemorrhage

Flame and dot hemorrhages

aneurysm management
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
complications of aneurysmal sah
rebleeding

cerebral vasospasm

volume disturbances

osmolar disturbances

seizures

arrhythmias and other cardiovascular complications

CNS infections

other complications of critical illness

Complications of aneurysmal SAH
slide17

“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
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
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
Vasospasm in acute SAH

Repeat angiogram

showing vasospasm

(small arrows)

Initial angiogram

critical care issues vasospasm and delayed ischemic damage1
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 damage2
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 damage3
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
Frequency of medical complications after SAH(placebo arm of North American Nicardipine Trial)

Solenski et alCCM 1995;23:1007-1017

extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage
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 hemorrhage1
Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage

Gruber A etal.Crit Care Med 1999;27:505-14

pulmonary complications after sah
Pulmonary complications after SAH

Solenski et alCCM 1995;23:1007-1017

critical care issues neurogenic pulmonary edema
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
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
slide34

Neurogenic

pulmonary

edema

after SAH

PCWP=12

CI=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

Conditions associated with neurogenic pulmonary edema
mechanisms of 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 edema1
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
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 edema1
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
Metabolic complications after SAH

Solenski et alCCM 1995;23:1007-1017

infectious problems in sah patients
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
Infectious complications after SAH

Solenski et alCCM 1995;23:1007-1017

etiology of fever in sah patients
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 patients1
Etiology of fever in SAH patients

Bleck TP, Henson S. Crit Care Med 1992;20:S31

evidence based medicine
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
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
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 patients1
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
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
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
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 hydrocephalus
Critical care issues: hydrocephalus
  • Diagnosis
    • clinical
    • radiologic
  • Management
    • ventriculostomy
      • infection reduction
    • shunting
critical care issues other medical complications
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)
sah prognosis
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
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