Index
Module 10 • Neurology
Neurocritical Care
57%
Data Tables
Neurocritical Care
Keaton S. Smetana ~2 min read Module 10 of 20
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Neurocritical Care

B.Diagnosis/Pathogenesis
1

Serial neurologic examination

2Vital signs
3

NIH Stroke Scale and/or GCS score

Table 13. SAH Severity Scale Scores

Score Range

Comments

Hunt and Hess

0 (no symptoms) to 5 (moribund)

Best correlated with risk of mortality

World Federation

of Neurological

Surgeons

1 (GCS score 15, no deficit) to 5 (GCS score 3–6)

Integrates risk of mortality and

motor dysfunction

Fisher

1 (no blood visualized) to 4 (diffuse SAH, ICH,

or intraventricular hemorrhage present)

Best correlated with risk of

vasospasm

C.Imaging (Stroke 2023;54:314-70)
1

CT scan of brain

2Lumbar puncture when CT scan of brain is negative for blood
3

Digital subtraction (β€œconventional”) angiography

4

May use CT angiography or magnetic resonance angiography if conventional angiography is unavailable

5

Transcranial Doppler, often daily during peak vasospasm risk period

D.Medication History – To identify agents that might produce coagulopathy or hypertension
E.Laboratory and Other Tests
1

INR

2CBC
3

Troponin

4

ECG (electrocardiogram)

5

Echocardiogram

F.

Causes – Typically caused by cerebral aneurysm. Modifiable risk factors for SAH:

1

Hypertension

2Smoking
3

Illicit drug use

G.Clinical Impact
1

Sudden death: Around 22%–26% of patients die before hospitalization. Inpatient mortality 13.1% in

2018 (United States).

2Vasospasm and delayed ischemic neurologic deficits

Presence of blood in subarachnoid space elicits a chemical meningitis-type inflammatory response

and results in hemolysis of subarachnoid blood.

Vasospasm (persistent vasoconstriction) occurs, reducing distal cerebral blood flow.

Typical course is 3–14 days, but can occur out to 21 days post ictus.

ii.

Vasospasm risk peaks at around 7–10 days.

Several mechanisms of pathogenesis

Inflammatory infiltration

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