Cardiac Output, Venous Return, and Their Regulation
Critical care of the patient with acute subarachnoid hemorrhage.ppt
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
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
Pobereskin JNNP 2001;70:340-3
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
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
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
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
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)
26. Frequency of medical complications after SAH
(placebo arm of North American Nicardipine Trial)
0
50
100
150
200
250
300
350
pulm
onary
m
etabolic
infectious
G
I
cardiac
total
severe
fatal
Solenski et al CCM 1995;23:1007-1017
27. Death by primary cause
(87 deaths among 455 patients)
24%
23%
22%
19%
5%
7%
vasospasm
medical complications
rebleeding
direct effect of SAH
surgical complication
other
Solenski et al CCM 1995;23:1007-1017
28. Extracerebral organ dysfunction and neurologic
outcome after aneurysmal subarachnoid hemorrhage
0
50
100
150
200
250
C
N
S
respiratory
renal
hepatic
cardiac
hem
atologic
intact
dysfunction
failure
Gruber A et al.Crit Care Med 1999;27:505-14
N=242
29. Extracerebral organ dysfunction and neurologic
outcome after aneurysmal subarachnoid hemorrhage
0
10
20
30
40
50
60
70
80
90
100
C
N
S
respiratory
renal
hepatic
cardiac
hem
atologic
overall mortality rate
with organ failure
mortality rate with
single organ failure
mortality rate as part of
multiple organ failure
Gruber A et al.Crit Care Med 1999;27:505-14
31. Pulmonary complications after SAH
0
5
10
15
20
25
pulm
onary
edem
a
pneum
onia
atelectasis
A
R
D
S
other
% (N=455)
Solenski et al CCM 1995;23:1007-1017
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
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
0
5
10
15
20
25
30
fever UTI sepsis other
% (N=455)
Solenski et al CCM 1995;23:1007-1017
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
Bleck TP, Henson S. Crit Care Med 1992;20:S31
47. Etiology of fever in SAH patients
0
2
4
6
8
10
12
14
post-op
pneurm
onia
m
eningitis
line infection
drug
allergy
H
SV
'central'
febrile episodes
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 utility
Bleck TP BMJ 2000;321:239
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
Bleck TP BMJ 2000;321:239
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
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
