Tom Bleck - Subarachnoid haemorrhage: what matters? Tom Bleck gives an overview of the pertinent facts regarding the complications and management of aneurysmal subarachnoid haemorrhage (SAH). The complications of aneurysmal SAH can be divided into immediate, early and late. The risk of re-bleeding is maximal on the first day, it is fatal in 75% of patients and the best management is to secure the aneurysm by coiling or clipping. Blood pressure control is utilised widely but parameters are arbitrary and the data is scarce. Early complications (days 1 - 3) include early brain injury in its various forms, stress cardiomyopathy, neurogenic pulmonary oedema and cerebral salt wasting. The most important late complication (day 4 onwards) is vasospasm. Tom briefly discusses the mechanisms and manifestations of SAH-associated brain injury including ischaemia, blood brain barrier breakdown, sustained depolarisation, hydrocephalus, vasospasm, seizures, hyperglycaemia and fever. He goes on to discuss in more detail the management of vasospasm, the associated evidence and the importance of distinguishing between clinically detectable and subclinical vasospasm.

1. SNACC 2015:
Subarachnoid Hemorrhage:
What Matters?
Thomas P. Bleck MD MCCM FNCS
Professor of Neurological Sciences, Neurological Surgery, Internal Medicine, and Anesthesiology, Rush Medical College; and
Director, Clinical Neurophysiology, Rush University Medical Center
1

2. Disclosures
• I am a current member of the ABIM Critical Care Subspecialty
Exam Committee.
– To protect the integrity of Board Certification, ABIM enforces strict
confidentiality and ownership of exam content.
– As a member of an ABIM exam committee, I agree to keep exam
information confidential.
– As is true for any ABIM candidate who has taken an exam for
Certification, I have signed the Pledge of Honesty in which I have
agreed not to share ABIM exam questions with others.
– No exam questions will be disclosed in my presentation.

3. Standard disclosures
• Research support from NINDS, AHA, Zoll
• Consultant for USAMRICD (nerve agent protection)
• DSMB chair for Sage phase 3 trial of allopregnenolone in
RSE
• DSMB member for a trial of ketogenic diet in RSE
• DSMB chair for a trial of intraventricular nimodipine in
SAH
• Many of the treatments discussed are not approved by
the FDA

4. SAH: What matters?
1. Rapidly identify patients with aneurysmal
SAH and secure their aneurysm(s) quickly
2. Lower MAP before securing the aneurysm
but not afterwards
3. Detect and manage early complications
a. Stress cardiomyopathy
b. Neurogenic pulmonary edema
c. Cerebral salt wasting

5. SAH: what matters?
4. Detect vasospasm early
a. Clinical
b. Electrophysiologic
c. Sonographic
d. Radiologic
5. Manage clinical vasospasm aggressively
a. Augment pressure and flow
b. Angioplasty and IA vasodilators

10. Critical care issues: rebleeding
• Unsecured aneurysms:
– 9% – 17% rebleed on day 0, then
– 1.5%/day for next 13 days [ up to 36% 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

20. Radiographic diagnosis of vasospasm
• Only half of patients with angiographic vasospasm
have clinical findings related to the arteries involved
• DSA is currently the standard method
– Good definition of large and medium vessels
– Allows angioplasty and intra-arterial therapy
• CTA for the diagnosis of vasospasm is increasing in
use
– Distal spasm may be more difficult to detect by
CTA
• What about ‘microvasospasm?’

21. 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 0.69 (0.58-0.84)
– Probably neuroprotection rather than a vascular effect
• nicardipine 0.075 mg/kg/hr is probably equivalent

25. Stroke 2000

26. Critical care issues: vasospasm and
delayed ischemic damage
• Management
– volume expansion
• rarely achieved
– induced hypertension
– cardiac output augmentation
• dobutamine or milrinone
• intra-aortic balloon pump
– angioplasty
– verapamil or nicardipine (no longer use papaverine)
– intrathecal or intraventricular NO donors

27. Lancet 2012

32. Cerebral salt wasting:
pathophysiology
• volume depletion puts SAH patients at risk for
stroke from vasospasm
– Wijdicks et al (1985) showed that volume restriction
(as one would do for patients with SIADH) doubled
the rates of stroke and death attributable to
vasospasm

35. 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

41. 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)

42. Seizures in SAH patients
• patients developing delayed ischemia may
seize following reperfusion by angioplasty
• late seizures occur in about 3% of patients

48. 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

52. For slides email
tbleck@gmail.com