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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
23
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
24
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
25
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