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
 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
 Subarachnoid hemorrhage
Diagnostic Critical care issues
rebleeding
approaches
neurogenic pulmonary
Aneurysm edema
vasospasm and
management delayed ischemic
surgical damage
endovascular hydrocephalus
cerebral salt wasting
medical complications
 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
Flame and dot hemorrhages Subhyaloid hemorrhage
 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
Guglielmi detachable coil
Basilar artery aneurysm
before coiling
Basilar artery aneurysm
after coiling
 Complications of aneurysmal
SAH
rebleeding arrhythmias and
cerebral other
vasospasm cardiovascular
volume complications
disturbances CNS infections
osmolar other
disturbances complications of
seizures critical illness
 If it
becomes
at all
doubtful,
let me
know, I
will be
just
inside
Captain Edward Smith

9:20 PM to second officer

Lightoller
who then signed over to
Murdoch at 10:00 PM
11:40 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
Initial angiogram showing vasospasm
(small arrows)
 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
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)

350
300
250
200
150 total
severe
100
fatal
50
0
pulmonary
metabolic
infectiousGI cardiac

Solenski et al CCM 1995;23:1007-1017

Death by primary cause
(87 deaths among 455 patients)

23%

vasospasm
22% medical complications
24% rebleeding
direct effect of SAH
surgical complication
other

7% 19%
5%

Solenski et al CCM 1995;23:1007-1017

 Extracerebral organ dysfunction and neurologic
outcome after aneurysmal subarachnoid hemorrhage

250

200

150

100 intact
dysfunction
50 failure
0
CNS respiratory
renal hepatic cardiac hematologic

N=242 Gruber A et al.Crit Care Med 1999;27:505-14

 Extracerebral organ dysfunction and neurologic
outcome after aneurysmal subarachnoid hemorrhage

100
90
80
70
60 overall mortality rate
50 with organ failure
40 mortality rate with
30 single organ failure
20 mortality rate as part of
10
multiple organ failure
0
CNS respiratory
renal hepatic cardiac hematologic

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

Competing concerns
Pulmonary complications after SAH

25
20
15
10
5 % (N=455)
0
pulmonary
pneumonia
edema
atelectasis
ARDS other

Solenski et al CCM 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
 Conditions associated with
neurogenic pulmonary edema
Common: Rare:
subarachnoid brainstem infections
hemorrhage medullary tumors
status epilepticus multiple sclerosis
severe head trauma spinal cord infarction
intracerebral increased ICP from a
hemorrhage variety of causes
 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
Colice 1985
 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
30

25
20
15

10 % (N=455)
5

0
electrolyte hyperglycemia
DI

Solenski et al CCM 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

30

25

20

15
% (N=455)
10

0
fever UTI sepsis other

Solenski et al CCM 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 >38.3C)
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

14
12
10
8
6
4 febrile episodes
2
0
post-oppneurmonia
meningitis
line infection
drug allergy
HSV 'central'

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 dont agree with what I believe
class 5: what you believe that I dont

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)
 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
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
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
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

Diagnosis
clinical
radiologic
Management
ventriculostomy
infection reduction
shunting
Hydrocephalus after SAH
 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)
What about steroids?
 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