Intracerebral Haemorrhage (ICH)


Intracerebral haemorrhage (ICH) is a life-threatening type of stroke Opens in new window, caused by bleeding within the brain tissue itself. A stroke occurs when the brain is deprived of oxygen and blood supply.

An ICH can occur close to the surface or in deep areas of the brain. Sometimes deep hemorrhages can expand into the ventricles – the fluid filled spaces in the center of the brain. Blockage of the normal cerebrospinal (CSF) circulation can enlarge the ventricles (hydrocephalus) resulting in these symptoms:

  • headache, nausea, and vomiting
  • lethargy or confusion
  • sudden weakness or numbness of the face, arm or leg, usually on one side
  • loss of consciousness
  • temporary loss of vision
  • seizures

Primary ICH is most commonly caused by long-standing hypertension induced small vessel disease. The site of hypertensive haemorrhage tends to occur in characteristic locations such as the basal ganglia, thalamus and cerebellum. Berry aneurysms most commonly arise around the Circle of Willis, hence ICH due to aneurismal rupture is often located around this area.

Secondary ICH may occur into an underlying lesion such as a tumor or infarct, and clinical deterioration may result — so called symptomatic ICH (SICH) — but this is not always the case.

The clinical presentation of primary ICH is typically of sudden onset of a neurologic deficit with associated headache, collapse/transient loss of consciousness, hypertension and vomiting. However, clinical features alone are unable to differentiate ICH from infarction, hence the requirement for brain imaging to confirm the diagnosis. Both CT and MRI (Using gradient echo sequences) are equivalent in the detection of ICH.

Medical Management

Primary ICH is a medical emergency with a high mortality of between 35% and 50%, with half of these deaths occurring in the first 2 days. There is also a very high risk of dependency. Haematomas can expand rapidly, and there is a significant risk of early neurological deterioration and increasing intracranial pressure (ICP).

Treatment of raised ICP in a setting of ICH involves a range of modalities similar to those used in head trauma. These include elevation of the head of the bed, analgesia, sedation, an osmotic diuretic such as mannitol and hypertonic saline, hyperventilation, drainage of CSF via ventricular catheter, and neuromuscular paralysis.

There is no good evidence regarding the management of hypertension in the setting of ICH sufficient to make firm recommendations. Guidelines have been published, but treatment should be individualized and take place in consultation with neurology/neurosurgery/intensive care specialists. Sudden falls in blood pressure and hypotension should be avoided, as they may aggravate cerebral ischaemia in the setting of raised ICP, which is often associated with ICH.

Early studies of the use of recombinant factor Vlla have shown promise when administered within 3 hours of stroke onset, showing a significant reduction in haematoma expansion and improved mortality. Steroids are not indicated in ICH. Anticonvulsant prohylaxis is common practice.

Management of ICH associated with anticoagulation or thrombolysis is a matter of urgency and should be done in consultation with a haematologist and a neurosurgeon. Agents such as protamine sulphat, vitamin K, prothrombin complex concentrate and FFP may be indicated. Factor Vlla normalizes the INR very rapidly, but with a greater potential for thromboembolism.

Surgical Management

Surgical management of ICH depends on the location, cause, neurological deficit and overall clinical state. Early neurosurgical consultation should be obtained. High level evidence for improved outcomes following drainage of supratentorial haematomas by craniotomy is lacking, but the procedure may be indicated in selected patients, particularly in those with lobar clots within 1 cm of the surface. In patients presenting in coma with deep haemorrhages, craniotomy is not recommended and may worsen outcomes. The presence of a cerebellar haematoma is a particular indication for surgery, with a potential for a good neurological recovery. A variety of other techniques, such as minimally invasive haematoma evacuation, are under investigation.

related literatures:
    Adapted from: Textbook of Adult Emergency Medicine E-Book. Authored By Peter Cameron, George Jelinek, Anne-Maree Kelly, Lindsay Murray, Anthony F. T. Brown. References as cited include:
  1. Executive Committee of the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. Journal of the American Medical Association 1995; 273: 1421 – 1428.
  2. North American Symptomatic Carotid Endarterectomy Trial Collaborators (NASCET). Beneficial effects of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. New England Journal of Medicine 1991; 325: 445 – 453.
  3. Koutahri RU, Panciolli A, Liu T, et al. Cincinatti Pre Hospital Stroke Scale: reproducibility and validity. Annals of Emergency Medicine 1999; 33: 373 – 378.
  4. Goldstein LB, Samsa GP. Reliability of the National Institute of Health Stroke Scale: extension to non-neurologists in the context of a clinical trial. Stroke 1997; 28: 307 – 310.
  5. Rothwell PM, Giles MF, Flassmann E, et al. A simple score (ABCD) to identify individuals at high risk of stroke after transient ischaemic attack. Lancet 2005; 366: 29–36.
  6. Kidwell, CS, Chalela JA, Saver JL, et al. Comparison of MRI and CT for detection of acute intracerebral haemorrhage. Jounal of the American Medical Association 2004; 292: 1823–1834.
  7. The ESPRIT Study Group. Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT). Lancet 2006; 367: 1665–1673.
  8. CAPRIE Steering Committee. A randomized, blinded, control trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996: 348: 1329–1339.
  9. The Stroke Prevention by Aggressive Reduction in Cholesterol levels (SPARCL) Investigators. High dose atorvastatin after stroke or transient ischaemic attack. New England Journal of Medicine 2006: 355: 549–559.
  10. Duffy BK, Philips PA, Davis SM, et al. Evidence based care and outcomes of acute stroke managed in hospital specialty units. Medical Journal Australia 2003; 178: 318–323.
  11. International Stroke Trial Collaborative Group. The International Stroke Trial (IST): a randomized trial of aspirin, subcutaneous heparin, both, or neither among. 19435 patients with acute ischaemic stroke. Lancet 1997; 349: 1569–1581.
  12. CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST: randomized placebo controlled trial of early aspirin use in. 20000 patients with acute ischaemic stroke. Lancet 1997; 349: 1641–1649.
  13. Hoffman J. Tissue plasimogen activator (tPA) for acute ischaemic stroke: why has so much been made of so little? Medical Journal Australia 2003; 179: 333–334.
  14. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group (NINDS). Tissue plasminogen activator for acute ischaemic stroke. New England Journal of Medicine 1995; 333: 1581–1587.
  15. Albers GW. Intravenous tissue-type plasminogen activator for treatment of acute stroke: the Standard Treatment with Alteplase to Reverse Stroke (STARS) study. Journal of the American Medical Association 2000; 83: 1145–1150.
  16. Katzan IL, Furlan AJ, Lloyd LE, et al. Use of tissue type plasminogen activator for acute ischaemic stroke: the Cleveland Area Experience. Journal of the American Medical Association 2000; 283: 1511–1518.
  17. Wahlgren N, Ahmed N, Davalos A, et al. Thrombolysis with alteplase for acute ischaemic stroke in the Safe Implementation of Trombolysis in Stroke (SITS-MOST): an observational study. Lancet 2007; 369: 275–282.
  18. Broderick, JP, Connolly S, Feldman E, et al. AHA/ASA Guidelines for the management of spontaneous intracerebral hemorrhage in adults. ICH. Stroke 2007; 38: 2001.
  19. Mayer S. Brun MC, Begtiup K, et al. Recombinant Factor 7a for acute ICH. New England Journal of Medicine 2005; 352: 777–785.
  20. Vahedi K, Hofmijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomized controlled trials. Lancet Neurology 2007; 6: 215–222.
  21. Further Reading
    1. Rothwell PM. Atherothrombosis and ischaemic stroke. British Medical Journal 2007; 334: 379–381.
    2. Alberts MJ, Latchaw RE, Selman WR, et al. Brain Attack Coalition. Recommendations for comprehensive stroke centres: a consensus statement of the Brain Attack Coalition. Stroke 2005; 36: 1597–1616.
    3. Libman RB, Wirkowski E, Alvir J. Conditions that mimic stroke in the emergency department. Archives of Neurology 1995; 52: 1119–1122.
    4. Schriger DL, Kalafut M, Starkman S, et al. Cranial computed tomography interpretation in acute stroke. Physician accuracy in determining eligibility for thrombolytic therapy. Journal of the American Medical Association 1998; 279: 1293–1297.
    5. Adams HP Jr, Zoppo G, Alberts MJ, et al. AHA/ASA Guidelines for the early management of adults with ischaemic stroke. Stroke 2007; 38: 1655.
    6. Diener H, Bogousslavsky J, Brass LM, et al. on behalf ot the MATCH Investigators. Acetylsalicilic acid on a background of clopidogrel in high risk patients randomized after recent stroke or transient ischaemic attack: The Match trial results. Lance 2004; 364: 331–337.
    7. Sacco RL, Adams R, Albers G, et al. AHA/ASA Guidelines for the prevention of stroke with ischaemic stroke or transient ischaemic attack. Stroke 2006; 37: 577.
    8. Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and Refinement of a score to predict very early stroke risk after transient ischaemic attack. Lancet 2007; 369:283–292.