Aneurysmal Subarachnoid Hemorrhage in the ICU

Chris Horn, MD

Neuro Intensivist

WellStar Kennestone Hospital

FYI

• This is more of a handout that covers a majority of topics an provides references then the actual presentation that you will see.

• If you have any interest at all in this topic and only want one review to read then read the one cited below – Critical Care Management of Patients Following

Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care (2011) 15:211–240

• Even with a consensus statement treatment of these patients remains variable

Making the diagnosis

• History and physical exam – Risk factors – LOC ?

• CT Head w/o contrast – Decrease of sensitivity with time

• LP – Xanthrochormia 12hrs -2 weeks – Lab technique (2)

• CT Angiogram of Head – A little better sensitivity for aneurysms <5mm

• Cerebral angiogram – Roughly 20% will be negative – Repeat cerebral angiogram to pick up the <5%

Risk Factors

Modifiable Non- modifiable

Cigarette smoking Previous SAH

HTN Polycystic Kidney Disease

Moderate to heavy EtOH consumption Connective tissue disease

Cocaine use Moya Moya

Endocarditis ( formation of mycotic aneurysms)

AVM

Fibromuscular Dysplasia

Dissection

Neurofibromatosis 1

Pseudoxanthoma Elasticum

Family History (two 1st to 3rd degree relatives )

Grade Exam Mortality (%)

Mortality (%) (27)

Mean Glascow Outcome Scale

1 Asymptomatic, mild HA, some nuchal rigidity

1 3.5 4

2 CN Palsy, moderate to severe HA, severe nuchal rigidity

5 3.2 4

3 Mild focal deficit, lethargy, confusion 19 9.4 3

4 Stupor, moderate to severe hemiparesis, early decerbrate rigidity

40 23.6 2

5 Deep coma, decerebrate rigidity, moribund appearance

77 70 2

Hunt and Hess Grade

Grade GCS Major Focal Deficit (Aphasia, Hemiparesis)

Associated Mortality %

Mean Glascow Outcome Scale

1 15 - 5 4

2 13-14 - 9 4

3 13-14 + 20 3

4 7-12 +/- 33 2

5 3-6 +/- 77 2

World Federation of Neurological Surgeons Grade

0%

5%

10%

15%

20%

25%

30%

35%

40%

1 2 3 4

Percentage of Delayed Cerebral Infarct

Fisher Score

Modified Fisher

Fisher Score (4, 5) 1- No SAH 2- Diffuse Thin 3- Diffuse Thick or localized clot 4- No SAH or diffuse thin with IVH and/or ICH Modified Fisher Score (3)- 0- No SAH 1- Thin blood no IVH 2- Thin blood +IVH 3- Thick blood no IVH 4- Thick blood + IVH

Initial Complications

• Re- bleeding(5, 6) – Associated with high mortality (~50% immediately and

another 30% die from subsequent complications) and morbidity

– Risk • 4% in 24 hours • 20% in 2 weeks • 50% in 6 months

– Treatment • Early securing of aneurysm • Antifibrinolytics • HTN control • Seizure prophyalxis

Initial Complications

• Hydrocephalus (1,7) – Can be communicating or non communicating – Acute development occurs in roughly 20%- 30% – Delayed development (after 3 days) is less common

occuring <5% – Chronic development (>1 week) of hydrocephalus

occurs in 10- 20% – Treatment

• External Ventricular Drain – Triggers for placing and management can be variable – Directed by CT scan and clinical exam – Grade 3 and above

Initial Complications

• Cardiac complications (1, 8-14) – Abnormalities on EKG, Biomarkers, Wall Motion

Abnormalities (WMA) • 50- 70% will have one or a combination • EKG within 48 hours

– P wave abnormalities, prolonged QT, ST, T wave abnormalities

• Tn and CK MB typically rise in 24 -48 hours • WMA as early as 3 hours • Possible link to higher mortality and morbidity

– Arrhythmias • Roughly 5- 10% • More commonly Tachy arrhythmias, brady arrhythmias, PAC, PVC

– Treatment • Supportive care- pressors, inotropes, balloon pump

Delayed Neurological Deterioration (DND) (1)

• Any clinically detectable neurological deterioration in a aSAH patient following initial stabilization except new bleeding.

• Possible causes – Delayed Cerebral Ischemia

– Vasospasm

– Cerebral edema

– Fever

– Hyponatremia

Delayed Neurological Deterioration (DND)

• Delayed Cerebral Ischemia (DCI) (1)

– Any neurological deterioration presumed related to ischemia that persist for an hour and cannot be explained by other physiologic abnormalities.

• Vasospasm(1)

– Narrowing of blood vessels seen on a radiographic image or increased mean flow velocity on sonography

Delayed Neurological Deterioration (DND) (1)

• Vasospasm – Vasospasm seen in 70% of all aSAH patients after day 3 – Only roughly 30-40 % of these patients will continue on to

DCI – Time Course

• Between day 3-14 • Peaks around day 6-8

– Monitoring • Clinical exam • Trans Cranial Doppler • Other monitoring devices

– Licox -pbO2 – Micro dialysis – cEEG

Delayed Neurological Deterioration (DND) (1,15)

• A word about transcranial doppler …

– ~10% patient don’t have windows- meaning cant get a waveform

– Predictive of vasospasm not DCI

– MCAs are the most reliable when very high >200cm/sec or low <120 cm/sec

– Also helpful if significant increase in MFV

• Doubling in 24- 48 hours

Delayed Neurological Deterioration (DND)

• Vasospasm treatment

– Poiseuille Equation

= Length

= Viscosity

= Radius

= CPP

= CBF

HYPERTENSION/ HYPERVOLEMIA

HYPERVOLEMIA/ HEMODILUTION

Delayed Neurological Deterioration (DND)

• Vasospasm treatment (Cont.) – From Poiseuille equation comes triple H therapy – The H that appears to be the most helpful is Hypertension in regards

to improving cerebral blood flow – Increase sBP by at least 20mmHg , ceiling sBP 200-220mmHg or if the

symptoms resolve – Judicious use of IV fluids .

• Follow CVP, PADP, SVV, Echo/ IVC

– Intrathecal Cardene • shows improvement with mean flow velocity

– Angiography • IA vasodilators

– In difficult to examine patients further imaging is helpful to guide therapy. • CTA/P

Delayed Neurological Deterioration (DND) (16-19)

• The logical assumption is that DCI is dependent on vasospasm which is unfortunately not always true

• Although nimodipine has been shown to improve outcome it has not been shown to reliably reduce vasospasm

• Clazosentan ( endothelin antagonist) and nicardipine have also been shown to reduce the relative risk vasospasm but it does not translate into decrease infarcts and better recovery

No Vasospasm n=497

Hypoperfusion n= 46

Vasospasm n= 157

31 regions with hypoperfusion

but no proximal vasospasm

142 regions with vasospasm did not

exhibit hypoperfusion

15 regions with hypoperfusion and vasospasm

Above is a Venn diagram of 25 aSAH patients who have undergone PET scan and cerebral angiogram in relatively quick succession which showed that true hypoperfusion was not routinely associated with vasospasm. (20)

Delayed Neurological Deterioration (DND) (20,21, 24)

• DCI is more than just vasospasm

• Theories on other pathophysiologic states contributing to DCI – Early Brain Injury

• Intracranial circulatory arrest / cerebral edema

– Cortical Spreading Depression • Depolarization of grey matter that leads to

hypoperfusion from cortical vasoconstriction

– Microthombus formation

– Arteriolar constriction

Delayed Neurological Deterioration (DND)

• Fever (22,23)

– Fever is common among the Neurologically critically ill

– Up to 40% aSAH and typically not isolated (may persist for as long as 2 weeks)

– Generally 50% can be attributed to infectious sources (pulmonary, uti)

– Independently associated with death and severe disability

Primary Injury Axonal Damage

Direct Cell Membrane Damage Metabolic Stress

Break down of BBB Cortical spreading depression

Secondary Injury Glial swelling

Endothelial dysfunction Delayed neuronal damage

Cytokine release Increased inflammation

Excitotoxicity

FEVER Outcome

Delayed Neurological Deterioration (DND)

• Sodium regulation (1, 24, 25) – Hyponatremia

• 20-30% of aSAH – Cerebral salt wasting

» Catecholamine release and high sympathetic state with increase release of naturetic peptides

– SIADH

• Differentiated by volume status

• Associated with worse outcome

• Polyuria has also been shown to correlate with vasospasm onset

• Treatment – Goal is to maintain euvolemia therefore making fluid restriction difficult.

– Increase Na intake (PO, IV, NG/OG), Fludrocortisone,

Delayed Neurological Deterioration (DND)

• Global Cerebral Edema – Initial or delayed – Has been shown to be a predictor of poor outcome and

mortality – Global edema on admission

• Loss of consciousness at ictus • Poor grade

– Delayed global edema • Large aneurysm • Loss of consciousness at ictus • Use of vasopressors

– Treatment • Basic bedside manipulations hypertonic NaCl/ Mannitol

Sedation, TTM Burst suppression

Outcome (27-29)

• A recent retrospective review of a prospective collected database to determine reasons for aSAH patients death showed.. – Withdrawal driven by primary effects of initial bleed,

rebleeding and medical complications – Admission predictors of Mortality where age, LOC, GCS,

APACHE II, mFS and large aneurysm – While several hospital complications increase risk of dying,

DCI was not part of it

• The continued theme in outcome data of aSAH patients – Continued improvement 6 months out to a year. Even out

to 36 months improvement can still be seen

1. Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care (2011) 15:211–240 2.Williams A. Xanthochromia in the cerebrospinal fluid. Practical Neurology, 2004, 4, 174–175. 3. Frontera JA, Claassen J, Schmidt JM, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale. Neurosurgery 2006;59(1):21–27 4. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980 Jan; 6:1–9 5. Naidech AM, Janjua N, Kreiter KT, et al. Predictors and impact of aneurysm re-bleeding after subarachnoid hemorrhage. Arch Neurol 2005;62:410–416 6. Hillman J, Fridriksson S, Nilsson O, et al. Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study. J Neurosurg 2002;97(4):771–778 7. Germanwala AV, Huang J, Tamargo RJ. Hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurg Clin N Am. 2010 Apr;21(2):263-70 8. Ducruet AF, Albuquerque FC, Crowley RW, et al. Balloon-pump counterpulsation for management of severe cardiac dysfunction after aneurysmal subarachnoid hemorrhage. World Neurosurg. 2013 Dec;80(6):e347-52. 9. Kilbourn KJ, Ching G, Silverman DI, McCullough L, Brown RJ. Clinical outcomes after neurogenic stress induced cardiomyopathy in aneurysmal sub-arachnoid hemorrhage: a prospective cohort study. Clin Neurol Neurosurg. 2015 Jan;128:4-9. 10. Urbaniak K, Merchant AI, Amin-Hanjani S, Roitberg B. Cardiac complications after aneurysmal subarachnoid hemorrhage. Surg Neurol. 2007 Jan;67(1):21-8; discussion 28-9. 11. van der Bilt IA, Hasan D, Vandertop WP, Wilde AA, Algra A, Visser FC, Rinkel GJ. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009 Feb 17;72(7):635-42 12. van der Bilt IA, Hasan D, van den Brink RB, et al. SEASAH (Serial Echocardiography After Subarachnoid Hemorrhage) Investigators. Time course and risk factors for myocardial dysfunction after aneurysmal subarachnoid hemorrhage. Neurosurgery. 2015 Jun;76(6):700-5; discussion 705-6.

13. van der Bilt I, Hasan D, van den Brink R,et al.; SEASAH (Serial Echocardiography After Subarachnoid Hemorrhage) Investigators. Cardiac dysfunction after aneurysmal subarachnoid hemorrhage: relationship with outcome. Neurology. 2014 Jan 28;82(4):351-8. 14. Frontera JA, Parra A, Shimbo D, Fernandez A, et al. Cardiac arrhythmias after subarachnoid hemorrhage: risk factors and impact on outcome. Cerebrovasc Dis. 2008;26(1):71-8. 15. Vora YY, Suarez-Almazor M, Steinke DE, et al. Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery 1999;44(6):1237–1247 16. Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm—a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983;308(11):619–624 17. Macdonald RL, Higashida RT, Keller E, Mayer SA, et al. Randomized trial of clazosentan in patients with aneurysmal subarachnoid hemorrhage undergoing endovascular coiling. Stroke. 2012 Jun;43(6):1463-9. 18. Macdonald RL, Higashida RT, Keller E, Mayer SA, et al . Randomised trial of clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid hemorrhage undergoing surgical clipping (CONSCIOUS-2). ActaNeurochir Suppl. 2013;115:27-31. 19. Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology 1998;50(4):876–883 20. Dhar R, Diringer MN. Relationship between angiographic vasospasm, cerebral blood flow, and cerebral infarction after subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:161-5. 21. Naraoka M, Matsuda N, Shimamura N, Asano K, Ohkuma H. The role of arterioles and the microcirculation in the development of vasospasm after aneurysmal SAH. Biomed Res Int. 2014;2014:253746. 22. Badjatia, Neeraj. Hyperthermia and fever control in brain injury. Critical care medicine 37.7 (2009): S250-S257. 23. Fernandez A, Schmidt JM, Claassen J, et al. Fever after subarachnoid hemorrhage Risk factors and impact on outcome. Neurology. 2007 Mar 27;68(13):1013-9. 24. Chen S, Feng H, Sherchan P, et al. Controversies and Evolving New Mechanisms in Subarachnoid Hemorrhage. Progress in neurobiology. 2014;0:64-91

25. Brown RJ, Epling BP, Staff I, et al. Polyuria and cerebral vasospasm after aneurysmal subarachnoid hemorrhage. BMC Neurol. 2015 Oct 13;15:201.

26. Claassen J, Carhuapoma JR, Kreiter KT, Du EY, Connolly ES, Mayer SA. Global cerebral edema after subarachnoid hemorrhage frequency, predictors, and impact on outcome. Stroke. 2002 May 1;33(5):1225-32.

27. Lantigua H, Ortega-Gutierrez S, Schmidt JM, Lee K, Badjatia N, Agarwal S, Claassen J, Connolly ES, Mayer SA. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015 Aug 31;19:309. doi: 10.1186/s13054-015-1036-0. PubMed PMID: 26330064; PubMed Central PMCID: PMC4556224.

28. Wilson DA, Nakaji P, Albuquerque FC, McDougall CG,Et Al. Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design. J Neurosurg. 2013 Sep;119(3):606-12. doi: 10.3171/2013.4.JNS121287. Epub 2013 May 31

29. Navi BB, Kamel H, Hemphill JC 3rd, Smith WS. Trajectory of functional recovery after hospital discharge for subarachnoid hemorrhage. Neurocrit Care. 2012 Dec;17(3):343-7.