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
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
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
• cerebral
vasospasm
• volume
disturbances
• osmolar
disturbances
• seizures
• arrhythmias and
other
cardiovascular
complications
• CNS infections
• other
complications of
critical illness
“If it
becomes
at all
doubtful,
let me
know, I
will be
just
inside”
9:20 PM
Captain Edward Smith
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
Initial angiogram
Repeat 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 (0.580.84).
• 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
total
severe
fatal
150
100
50
0
pu
lm
m
on
ar
y
et
ab
ol
ic
in
fe
G
ct
io
us
I
ca
rd
ia
c
Solenski et al CCM 1995;23:1007-1017
Death by primary cause
(87 deaths among 455 patients)
23%
22%
24%
7%
5%
vasospasm
medical complications
rebleeding
direct effect of SAH
surgical complication
other
19%
Solenski et al CCM 1995;23:1007-1017
Extracerebral organ dysfunction and neurologic
outcome after aneurysmal subarachnoid hemorrhage
250
200
150
intact
dysfunction
failure
100
50
0
ol
at
m
he
c
ia
rd
ca
l
ic
og
ry
to
tic
pa
he
na
re
S
ira
sp
re
N
C
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
50
40
30
20
10
0
overall mortality rate
with organ failure
mortality rate with
single organ failure
mortality rate as part of
multiple organ failure
y
ic
og
ol
at
m
he
c
ia
rd
ca
r
to
tic
pa
he
l
na
re
S
ira
sp
re
N
C
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
r
he
ot
y
ar
S
D
R
A
is
as
ct
ele
at
ia
on
a
m
em
eu
ed
pn
on
lm
pu
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:
– 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
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
I
D
m
ce
e
yt
ly
g
er
l
ro
ct
p
hy
ele
ia
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
5
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 >38.3°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
14
12
10
8
6
4
2
febrile episodes
0
'ce
l'
ra
nt
p
t-o
SV
gy
H
ler
al
n
ug
dr
tio
ec
nf
ei
lin
tis
gi
in
en
ia
m
on
rm
eu
pn
s
po
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)
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