Intracranial Hemorrhage �  What Do Need to Know?

Kerry Brega, MD Associate Professor of Neurosurgery University of Colorado

Objectives � Know the common types of ICH. � Know how they can be differentiated. � Know when to suspect an ICH. � Know the necessary immediate medical

management. � Be aware of the common early

complications of ICH.

� Hypertensive hemorrhage � Amyloid angiopathy � Hemorrhagic conversion of CVA � Vascular malformation/ Aneurysm/

Cavernoma � Hemorrhagic tumor � Subdural hematoma � Venous sinus thrombosis

Diagnosis �  SUSPECT ICH WHEN---

�  Headache that is prominent complaint. 80% with ICH and only 25%with ischemic CVA

�  Among patients who can respond, 85% with aneurysmal SAH report sudden onset of the worst headache of their lives!

�  Nausea and vomiting 50% with ICH and 2% with ischemic CVA

�  Decreased level of consciousness-

�  These symptoms reflect increased intracranial pressure and are common to all types of ICH

Diagnosis ICH �  CT will identify and help classify the ICH

etiology. Each ICH type has a recognizable pattern. �  HTN- Small/end vessel (perforators) or

microaneuryms (Charcot-Bouchard) The bleeds are commonly located in Putamen, Thalamus, Pons, Cerebellum.

�  Amyloid Angiopathy- Protein deposition in small to medium cortical and leptomeningial vessels. (Not associated with systemic amyloidosis.) These bleeds tend to be more cortically located.

HTN Hemorrhage Location

Neurosurg Focus 15(4): Article 1; 2003

Hypertensive Stroke

Hypertensive Stroke

Cerebral Amyloid Angiopathy �  Can present single or mulitple spontaneous

intracerebral hemorrhages or as progressive dementia.

�  Usually in patients >60 years of age, thereafter increasing prevalence.

�  Younger patients in familial types. �  Correlation with Alzheimer Disease? �  30-40% recurrence rate on intracerebral

hemorrhage �  Hemorrhage usually in frontal or parietal cortical or

subcortical matter. Infrequently in basal ganglia, cerebellum or brain stem.

EMedicine.com

Amyloid Angiopathy

Hemorrhagic transformation of ischemic CVA � Occurs in about 10% � 2 types petichial or parenchymal

�  Petichial more common confined to the area of ischemia this may be due to leakage of blood cells through damaged capillaries without frank vessel rupture

�  Parenchymal hematomas are more likely due to vessel rupture and are larger

Hemorrhagic MCA infarct

Subarachnoid Hemorrhage �  42 year old woman presents to clinic with history of sudden

onset of the worst headache of her life 2 days ago. �  Headache largely resolved. �  Sentinel headaches as high as 20%. �  Ask about associated symptoms- Increased ICP and

meningismus. nausea/vomiting 77% stiff neck- 35%, photophobia brief loss of consciousness- 53% focal neurologic deficits including the cranial nerves radicular type leg pains or back pain

Work up for SAH �  CT scan reliable within first 3 days, the earlier

the better. But even if done within first 48 hours may miss up to 5%.

�  With a negative CT but a suspicious history or exam -> CTA or LP. CTA should reliably identify aneurysms above 2 mm in size. Role of CTA varies by institution.

�  Role of lumbar puncture varies by institution but recommended if CT negative and history is concerning. �  Presence of xanthrocromia

Subarachnoid

SAH/ CTA

Case 1

Hemorrhagic Tumor

Treatment �  Hurry! �  Treatment requires the same vigilance as the

ischemic strokes being evaluated for tPA. �  73% will increase in size over 3 hours. �  Up to 38% have hematoma expansion > 1/3

on repeat CT within 3 hours! Size matters! �  Mortalities range for 35-52% �  Approximately half in the first 48 hours!

Coagulopathies

�  Patients taking oral anticoagulants (OACs) �  12% to 14% of patients with ICH �  Goal is to get INR to 1.4 within 2 hours

�  Patients with qualitative or quantitative platelet abnormalities. Goal is >100,000

�  Recognition of an underlying coagulopathy provides an opportunity to target correction in the treatment strategy, Xa inhibitors and direct thrombin inhibitors

Review of Coagulation Cascade 22

Reversal of Oral Anticoagulants: Warfarin �  Vitamin K antagonist

�  inhibits coagulation factors II, VII, IX and X �  Half-life: 20-60 h (variable) �  Urgent reversal à reduce mortality, limit

hemorrhage expansion and improve outcomes �  Goal INR <1.5

�  Reversal Agents: �  Vitamin K (IV > PO > subq) �  FFP �  4-factor PCC (Kcentra)

Neurocrit Care. 2016; 24:6-46

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Direct Xa Inhibitors Xa Inhibitor Half-life

Rivaroxaban (Xarelto)* 5-9 h, 11-13 h in elderly

Apixaban (Eliquis) 8-12 h

Edoxaban (Savaysa) 10-14 h

Fondaparinux 17-20 h *DH preferred DOAC

}  No reversal agent currently available }  Andexanet alpha

}  Consider 4-PCC 1500 units }  No standard dose recommendation in

literature }  Doses up to 50 units/kg Neurocrit Care. 2016; 24:6-46

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Reversal of Oral Anticoagulants: Direct Thrombin Inhibitor

�  Dabigatran (Pradaxa) �  Half life: 12-17h �  Lab test: n/a

� Consider INR, aPTT, Thrombin Time, ACT

�  Reversal Agent: Idarucizumab (Praxbind) �  Monoclonal antibody that binds free and thrombin-bound

dabigatran �  Onset: Immediate �  Duration: at least 24 hours �  Dosing: 5g IVP over 10 minutes (available as 2.5g in 50mL

vials)

Neurocrit Care. 2016; 24:6-46. Dabigatran Package Insert. 2015

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Seizure Prophylaxis �  2010 guidelines recommended against it but there has been no

change in use. �  Levetiracetum- fewer side effects- Study showed that dilantin

associated with worse outcomes at 3 months but not levetiracetum. Some studies with it showing improved cognitive outcomes at discharge and fewer seizures.

�  Typical dose 500 BID

�  Taylor S, Heinrichs RJ, Janzen JM, Ehtisham A. Levetiracetam is associated with improved cognitive outcome for patients with intracranial hemorrhage. Neurocrit Care. 2011;15:80-84

�  Szaflarski JP, Sangha KS, Lindsell CJ, Shutter LA. Prospective, randomized, single-blinded comparative trial of intravenous levetiracetam versus phenytoin for seizure prophylaxis. Neurocrit Care. 2010;12:165-172

Xa Inhibitors � Andexxa-4 Ongoing multicenter trial � Bind Xa inhibitors so they cannot interact

with Factor Xa

Blood Pressure

� Blood pressure (BP) is frequently ( often markedly) elevated in patients with acute ICH �  Stress activation of the neuroendocrine system

�  Sympathetic nervous system �  Renin-angiotensin axis �  Glucocorticoid system

�  Increased intracranial pressure � Hypertension may contribute adverse outcomes

due to �  Hematoma expansion- There is more than double the risk

of death and dependency in patient with SBP > 140-150 range in the first 12 hours.

�  Perihematoma edema

Blood Pressure

� Blood pressure (BP) is frequently ( often markedly) elevated in patients with acute ICH �  Stress activation of the neuroendocrine system

�  Sympathetic nervous system �  Renin-angiotensin axis �  Glucocorticoid system

�  Increased intracranial pressure � Hypertension may contribute adverse outcomes

due to �  Hematoma expansion- There is more than double the risk

of death and dependency in patient with SBP > 140-150 range in the first 12 hours.

�  Perihematoma edema

Treatment of SAH � All the same considerations apply.

�  Treat intracracranial pressure �  Control blood pressure �  Reverse any coagulopathy

�  Prevent Re-Bleed/ secure the aneursym ASAP � Clipping of coiling

Generic ICH orders �  Q 1 hour neuro checks- tell the nursing staff what

you are looking for. �  Remember that agitation and increases in BP are

early signs of increased intracranial pressure. �  HOB 30 degrees �  Control BP generally < 140 systolic �  Correct coags ASAP �  Prophylaxis for seizure Kepra (lobar bleeds) �  treat fevers �  Fluids/O2 to maintain normal status

When things are going badly � Neurologic decline

�  Protect airway/ control BP �  Expansion of the clot #1 MUST REPEAT A CT

SCAN �  Seizure �  Hydrocephalus �  Vasospasm �  Other metabolic

Obstructive Hydrocephalus

Craniotomy and supratentorial hematoma evacuation

Cochrane Database of Systematic Reviews 2007 Issue 2

Case 1 � HPI: 67 y.o. man in A fib on Xeralto,

presents to ED with history of headaches for 2 days and trouble with vision.

� PMHx: A fib, HTN,

� PE: headache not severe �  189/100, HR 87 �  A & O X3, no motor or sensory deficits �  Right homonymous hemianopsia

Case 1

Case 1 �  Immediate management?

� While in ED develops significant decline in mental status?

� Treatment? Additional work-up?

Case 1

Case 2 � HPI: 74 y.o. man with artificial valve,

pacer, DM, HTN, OSA on coumadin. Had a fall about a month ago without LOC. Has progressively increasing headaches and balance problems. Fell twice over last week.

� PE: A & O X 3, headache 5/10, pronation with LUE, otherwise intact

Case 2

Case 2

Case 3 •  32 y.o. female with sudden onset of left arm

weakness and poor coordination 12 hours prior to admission. Sx’s relatively stable since.

•  (+) history of HA starting 3-4 days ago “like a band across my forehead”. HA slowly progressive over last 24 hours with onset of nausea, stiff neck and photophobia.

•  Seen in outside ER with CT scan

CT (+) Gad