Neurology
Intracerebral Hemorrhage
Background
- Definition
- Hemorrhagic stroke characterized by bleeding into the parenchyma of the brain
- Aka intracranial hemorrhage
- General Information
- Ottawa SAH Rule being developed
- Not validated, requires further investigation
- Blood pressure reduction guidelines
Not
- standardized
- Controversy over aggressiveness of BP management
- Evidence is incomplete
- ICH represents 8-11% of acute strokes
- High morbidity/mortality
- Requires frequent re-evaluation
- Clinical presentation can evolve quickly
- Mainstays of Management
- Early detection
- CT (non-contrast) initial study of choice
- Minimizing secondary complications and ongoing injury
- BP management
- Reversal of anticoagulation
- Disposition for evaluation of early surgical intervention
- Epidemiology
- Incidence/Prevalence
- Incidence of stroke (both ischemic and hemorrhagic in 2010)
- 33 million globally
- Hemorrhagic strokes account for nearly a 1/3 of cases and 1/2 of deaths
- Twice as common as SAH
- Global incidence: 20 cases/100,000 people/year
- Men > women
- Asian and young-middle age African American > Caucasian
Pathophysiology
- Pathogenesis
- Bleeding into brain parenchyma
- Degenerative changes in penetrating arteries/arterioles lead to microaneurysm's, subsequent rupture
- Most commonly penetrating vessels of the MCA (2/3 affecting basal ganglia)
- Hematoma enlarges, causing local tissue injury, increased ICP
- Low blood flow state alters electrical conduction of neurons but initially leaves cell membranes intact, salvageable
- Once critical decrease in blood flow occurs, cell membrane destruction and irreversible damage occurs
- ICH is complicated by red cell lysis and edema leading to increased blood-brain barrier permeability which can lead to secondary injury
- Etiology/Risk Factors
- Nontraumatic intracerebral hemorrhage can be divided into primary and secondary
- Primary bleeds (85%)
- Related to chronic hypertension
- Amyloid angiopathy
- Secondary bleeds
- Bleeding diathesis
- Vascular malformations
- AV malformations
- Cavernous angiomas
- Cerebral aneurysms
- Aorto-venous fistulae
- Neoplasms
- Hemorrhagic conversion of an ischemic stroke
- Drug abuse
- Combine with other injuries to cause mass effect/herniation
- Contusions
- Other hematomas
- Edema around lesions
- Clinical effects depend on
- Size of hematoma
- Location
- If bleeding stops or is continuous
- Elderly
- Male sex
- Predilection is seen in African and Asian populations
- Japanese have high incidence of ICH
Diagnostics
- History/Symptoms
- Acute onset, unheralded
- Deficits develop over mins-hrs
- Occur during waking hrs
- Headache (50%)
- Acute onset
- "Worst headache of life"
- Thunderclap, pop, snap, or gunshot sound in head
- Exertional headache
- Fainting or passing out
- Seizure at onset
- Vomiting
- Declining mental status
- Cerebral hemorrhage clinically difficult to distinguish from cerebral ischemia
- PNH
- Hypertension
- Premorbid neurologic status
- Premorbid cognitive status
- Social Hx
- Alcohol abuse
- Drug abuse (cocaine)
- Family Hx
- Aneurysms
- AV malformations
- Physical Examination/Signs
- Clinically difficult to differentiate from ischemic stroke or SAH
- ABCs
- Neuro exam (focused)
- Note:
- Neuro exam may be normal initially (especially if SAH)
- Level of consciousness (LOC)
- Speech
- Cranial nerve (CN) function
- Motor function: tone, strength, pronator drift
- Sensory function: light touch, pain
- Cerebellar function: finger -to -nose, heel -to -shin
- DTRs
- Babinski's sign
- Look for signs of head trauma
- Fever
- Infectious vs central
- Central: associated with large and intraventricular bleeds
- A baseline severity score should be performed as part of the initial evaluation of patients with ICH:
- Findings (based on type of lesion):
- Putamen hemorrhage
- Contralateral hemiplegia and hemisensory loss, eye deviation toward hemorrhage, visual field deficits
- Possible aphasia or neglect
- Cerebellar hemorrhage
- Neck stiffness
- HA, vomiting, ataxia (View Video)
- Strength/sensation may be normal except for ipsilateral facial weakness
- Cannot look toward side of bleed
- Possible rapid clinical deterioration
- Thalamic hemorrhage
- Contralateral hemiparesis and hemisensory loss
- Small, nonreactive pupils with downward gaze
- Pontine hemorrhage
- If patient is awake, may experience facial palsy, deafness, dysarthria
- "Locked-in" state with small pinpoint pupils
- Usually fatal
- Poor prognostic factors:
- Decreased level of consciousness (LOC) on arrival
- Large intracranial hemorrhage
- Intraventricular hemorrhage
- Diagnostic Testing
- Laboratory Evaluation
- General trauma labs
- Glucose (finger stick)
- CBC
- Electrolytes
- Coagulation studies
- Troponin
- Elevated levels often present
- Creatinine
- Consider (not routinely recommended):
- Other studies
- NIH Stroke Scale (Open Calc)
- HAT Score for Predicting Post-tPA Hemorrhage (Open Calc)
- Intracerebral Hemorrhage Score (Open Calc)
- FUNC Score (Open Calc)
- Secondary Intracerebral Hemorrhage (sICH) Score (Open Calc)
- PHASES Score (Open Calc)
- ECG
- Rule out: ACS, Afib, other dysrhythmias (often present)
- Lumbar puncture
- Not routinely recommended
- Check for xanthochromia (with concern for ICH and negative CT)
- EEG monitoring
- Additional lab tests based on clinical judgment and considered differential
- Diagnostic Imaging
- Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH
- CTA and contrast-enhanced CT may be considered: risk for hematoma expansion (COR IIb; LOE B)
- CTA, CT venography, contrast-enhanced CT, contrast-enhanced MRI, MRA, MR venography, and catheter angiography
- Evaluate for underlying structural lesions (e.g., vascular malformations, tumors) when there is clinical or radiological suspicion (COR IIa; LOE B)
- CT scan (non-contrast)
- Initial diagnostic test of choice
- Most sensitive within 6 hrs (View image)
- Evaluate for evidence of hemorrhage
- Detects bleeds > 1 cm diameter
- High risk of hydrocephalus if blood present in the ventricles
- MRI
- Limited usefulness in ED setting
- Evaluate for structural lesions, tumors
- Questionable accuracy in acute hemorrhage
- May be as accurate as CT for acute
- More accurate for chronic and microbleeds
- MRI Axial (View image)
- MRI Sagittal (View image)
- CT angiography (CTA)
- High -quality imaging of larger arteries
- DSA Frontal (View image)
- Exclude aneurysm
- Consider for:
- Cause of bleeding not established
- Stable patients
- CT venography (CTV)
- Consider if CVST suspected (multifocal hemorrhages in nonarterial distributions)
- CXR
- Not routinely recommended
- Consider if other etiology suspected
Differential Diagnosis
- Subarachnoid hemorrhage
- Epidural hemorrhage
- Subdural hemorrhage
- Ischemic stroke
- Tumor +/- bleed
- Meningitis
- Cervical artery dissection
- Idiopathic intracranial HTN
- Amyloid angiopathy
- Bleeding coagulopathy
- Hypoglycemic episode
- Drug overdose
- Seizure
- Metabolic disturbance
- Shock
Treatment
- Acute Treatment
- ABCs, O2
- Ongoing airway monitoring
- Keep patient NPO
- 2 large-bore IV lines (if available)
- Maintenance fluids
- Isotonic crystalloids for dehydration
- Stop anticoagulant
- Coagulopathy
- Identify and reverse underlying coagulopathy if possible
- Newer anticoagulants may not have a reversal agent
- Serial neuro exams
- Monitor progression of symptoms
- Cardiac monitor
- Watch for dysrhythmias (common)
- Monitor & control:
- Blood pressure
- Glucose
- Intracranial pressure (ICP)
- Body temperature
- Intubation
- Patient may rapidly deteriorate
- Be ready to intubate early
- Perform neuro exam before intubating
- Decrease brain edema if present
- Consult neurosurgery
- Surgical assessment and procedural intervention
- Medical/Pharmaceutical
- BP control
- For ICH patients presenting with SBP between 150-220 mmHg and without contraindication to acute BP treatment
- Acute lowering of SBP to 140 mmHg is safe (COR I; LOE A)
- Can be effective for improving functional outcome (COR IIa; LOE B)
- For ICH patients presenting with SBP > 220 mmHg
- Consider aggressive reduction of BP with a continuous IV infusion and frequent BP monitoring (COR IIb; LOE C)
- AVOID rapid swings in blood pressure
- Do not reduce MAP by > 20%
- Reduce BP slowly over 3-6 hrs
- Reducing BP too much or too quickly may cause hypotensive events (syncope)
- Beta-blockers
- Labetalol: 5-20 mg bolus every 10-15 min; infusion 2 mg/min (max 300 mg/day)
- Esmolol: 250 mcg/kg bolus loading; infusion 25-300 mcg/kg/min
- CCBs
- ACE-I
- Vasodilators
- Hydralazine
- Bolus 5-20 mg every 30 min
- Infusion 1.5-5 mcg/kg/min (if pregnant)
- Nitroglycerin: Infusion 20-400 mcg/min (signs of heart failure of ACS)
- Nitroprusside
- Infusion 0.1-10 mcg/kg/min
- If refractory HTN, high risk of side effects including hypotension
- May increase ICP
- Analgesia and sedation
- For unstable patients requiring intubation and ventilation (see RSI)
- Always perform neuro exam before intubating
- Titrate to minimize pain and minimize increases in ICP
- Pre-treatment medications
- Lidocaine
- 1.5 mg/kg IV to max of 100 mg 3 min prior to RSI
- Does blunt catecholamine release but unclear the effect on ICP (no good studies)
- Con: No evidence that pre-treatment lowers mortality
- Pro: Little harm from one dose
- Fentanyl
- 1 mcg/kg IV 3 min prior to RSI
- Also blunt catecholamines leading to decrease HR and BP but unclear if lowers ICP
- Con: No evidence that pretreatment lowers mortality
- Pro: Little harm from one dose, and likely the analgesic of choice post RSI and ETT placement
- RSI Medications: no specific recommendations
- Post RSI and ETT placement
- Analgesics: fentanyl, alfentanil, morphine
- These medications/sedation may have blood pressure lowering effects
- Sedatives: Propofol, Thiopental, Versed
- Continuous neuromuscular paralysis not recommended prophylactically (increases risk of pneumonia and masks seizure activity)
- If refractory (ICP elevation not responding to medical management): reducing muscle activity can lower ICP
- Ventilation
- 100% O2 at 10-12 breaths/min
- Tidal volume 10 cc/kg
- Avoid hyperventilation
- Reduces ICP only short-term
- Reserved for cases with impending edema
- Reverse anticoagulation
- Revised guidelines
- If ICH with INR elevated because of VKA: Withhold VKA, receive therapy to replace vitamin K–dependent factors and correct the INR, receive IV vitamin K
- PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP
- rFVIIa is not recommended for VKA reversal in ICH
- rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo
- Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or rivaroxaban was taken < 2 hrs earlier
- Hemodialysis might be considered for dabigatran
- Protamine sulfate may be considered to reverse heparin in acute ICH
- Stop Anticoagulant
- Warfarin reversal:
- Heparin reversal:
- If thrombocytopenia (< 100,000)
- Consider platelet transfusion
- Seizure
- Prophylaxis
- Benefit of routine prophylaxis not clear; not recommended
- Indicated for patients who have had a seizure
- Phenytoin 20 mg/kg IV
- Levetiracetam 500-1,500 mg IV
- Active seizure
- If seizures persist
- Continuous EEG monitoring if available should be started
- Cerebral edema
- Raise head of bed to 30 degrees
- Hyperventilate
- Goal: pCO2 28-32 mm Hg for short periods only
- Mannitol
- 1 g/kg IV bolus, then 0.25-0.5 g/kg every 6 hrs
- Target plasma osmolality of 300-310
- Hypotonic fluids
- Contraindicated
- Mild hypernatremia should be tolerated
- Hypertonic saline
- May be used
- Shown to reduce ICP even in refractory cases
- No guidelines regarding concentration of administration
- Glucose control
- Maintain 140-180 mg/dL range
- Avoid hypo/hyperglycemia
- Barbiturate coma
- For refractory intracranial hypertension
- Involves significant risk and intensive monitoring, (NOT first line therapy)
- Corticosteroids should not be administered for treatment of elevated ICP in ICH (COR III; LOE B)
- Surgical/Procedural
- Potential ventriculostomy, craniotomy, evacuation
- Cerebellar bleed: limited space in this part of the brain; swelling leads to rapid compartment syndrome-like cell death
- Therapeutic cooling (aka therapeutic hypothermia) may be used
- Not first line therapy; studies show neuroprotection from cooling and worse outcomes with fever in ICH
- No evidence yet linking this therapy to benefit in ICH
- Note: high rate of complications with this therapy and risk for rebound IC hypertension
- Therapeutic cooling to 32-34°C may be used
- No benefit of expensive equipment vs ice packs and cold IVF
- Further Treatment
- Optimize cerebral perfusion
- Treat systemic shock
- Treat hypoxia
- Good general medical care
- Monitor ICP and arterial pressure
- Keep ICP < 20
- Keep CPP < 70
- Repeat head CT as needed
- Complications of Treatment
- Precipitous or large reduction in BP may result in
- Hypotension
- Significantly reduced cerebral perfusion pressure
- Worsening injury
- Hypoglycemic episode from glucose control
- Hypotension if barbiturate coma used
- Rebound ICP elevation risk with rapid cessation of therapeutic cooling or prolonged hyperventilation
- Standard risk of neuromuscular blockade if used
- Renal failure precipitation with hyperosmotic hypovolemic state from mannitol use
- Prevention
- DVT prophylaxis with compression stalking
- Should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission
- Graduated compression stockings are not beneficial to reduce DVT or improve outcome
- Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptomatic DVT or PE
- The decision between these 2 options should take into account several factors, including
- Time from hemorrhage onset
- Hematoma stability
- Cause of hemorrhage
- Overall patient condition
- Aspiration precautions
- Outpatient: hypertension control and cessation of smoking, heavy alcohol, or cocaine use
Follow-Up
- Hospital/ED Admission
- Admit all hemorrhagic CVA patients, ICU recommended
- Up to 52% mortality, most deaths within first 48 hrs
- OR for evacuation PRN increased ICP, edema
- Possible Consultations
- Neurology
- Neurosurgery
- Radiology
Prognosis
- Morbidity/Mortality
- Mortality
- 1 month: 40% (half in first 2 days)
- 1 year: 54%
- 5 years: 71%
- 10 years: 80%
- Among survivors, only 20% living independently at 6 months
- LOW if patient is conscious before surgery
- Up to 45% if patient unconscious
- HIGH mortality if:
- Bleed into ventricles
- Cerebellar hematoma
Prevention
- DVT prophylaxis with compression stalking
- Should have intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission
- Graduated compression stockings are not beneficial to reduce DVT or improve outcome
- Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptomatic DVT or PE
- The decision between these 2 options should take into account several factors, including
- Time from hemorrhage onset
- Hematoma stability
- Cause of hemorrhage
- Overall patient condition
- Aspiration precautions
- Outpatient: hypertension control and cessation of smoking, heavy alcohol, or cocaine use
References
- Barnett HJ, Mohr JP, Stein BM (Eds). Stroke pathophysiology, diagnosis, and management. Churchill Livingstone:Philadelphia 1998
- Perry JJ, Stiell IG, Sivilotti MA, et al. Clinical Decision Rules to Rule Out Subarachnoid Hemorrhage for Acute Headache. JAMA. 2013;310(12):1248-1255
- Perry JJ, Stiell IG, Sivilotti MA, et al. Sensitivityof computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343:d4277
- Edlow JA, Panagos PD, Godwin SA, Thomas TL, Decker WW; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2008;52(4):407-436
- Broderick J, Connolly S, et al. Guidelines for the management of spontaneous intra- cerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 38:2001, 2007
- Kidwell CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for detection of acute intracerebral hemorrhage. JAMA 2004;292:1823
- Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2010;41:2108
- Ohwaki K, Yano E, Nagashima H, et al. Blood pressure management in acute intracerebral hemorrhage: relationship between elevated blood pressure and hematoma enlargement. Stroke 2004;35:1364
- Garg RK, Liebling SM, Maas MB, et al. Blood pressure reduction, decreased diffusion on MRI, and outcomes after intracerebral hemorrhage. Stroke 2012;43:67
- Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 2013;368:2355
- Anderson CS, Huang Y, Arima H, et al. Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT). Stroke 2010;41:307
- Broderick JP, Brott TG, Duldner JE, et al. Volume of intracerebral hemorrhage. A powerful and easy-to-use predictor of 30-day mortality. Stroke 1993;24:987
- Zia E, Engström G, Svensson PJ, et al. Three-year survival and stroke recurrence rates in patients with primary intracerebral hemorrhage. Stroke 2009;40:3567
- Franke CL, van Swieten JC, Algra A, van Gijn J. Prognostic factors in patients with intracerebral haematoma. J Neurol Neurosurg Psychiatry 1992;55:653
- Crocco TJ, Tadros A, Kothari RU. Chapter 99, Stroke. Rosen’s Emergency Medicine 2010. 1333-45
- Diringer MN, Zazulia AR. Osmotic therapy: fact and fiction. Neurocrit Care. 2004;1:219-233
- Broderick JP, Conolly S, Feldmann, et al. REPRINT: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage in Adults: 2007 Update: A Guideline From the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Circulation 2007; 116:e391-e413
- Adams JG. Emergency Medicine: Clinical Essentials, 2nd ed., Philadelphia, PA:Elsevier-Saunders, 2012;Chapter 103
- Edlow J, Selim M. Neurology Emergencies, 1st ed., New York, NY:Oxford University Press, 2010;Chapter 4
- Linn J, Bruckmann H (2009) Differential diagnosis of nontraumatic intracerebral hemorrhage. Klin Neuroradiol 19:45-61
- Rogers RL, Scalea T, Wallis L, Geduld H. Vascular Emergencies: Expert Management for the Emergency Physician, 1st ed., Cambridge University Press, 2013;Chapter 3
- Manji H, Wills A, Kitchen N, Dorwood N, Connolly S, Mehta A. Oxford Handbook of Neurology, 1st ed., Oxford University Press, 2007;Chapter 7
- Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 8th ed, McGraw-Hill Education, 2016;Chapter 14
- Walls RM, Hockberger RS, Gausche-Hill M. Rosen's Emergency Medicine - Concepts and Clinical Practice, 9th ed, Philadelphia, PA;Elsevier-Saunders, 2018;Chapter 91
- Linn J, Bruckmann H (2009) Differential diagnosis of nontraumatic intracerebral hemorrhage. Klin Neuroradiol 19:45–61
- American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, and Council on Clinical Cardiology. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage
A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. May 28, 2015;46(7):2032-2060
- Intracerebral Hemorrhage. StatPearls [Internet]. Available at: https://www.ncbi.nlm.nih.gov/books/NBK553103/. [Accessed June 2024]
Contributor(s)
- Minckler, Michael, MD
- Bouska, River, MD, MPH
- Drummond, Brian, MD
- Ballarin, Daniel, MD
Updated/Reviewed: June 2024