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A cerebral haemorrhage (also spelled hemorrhage) (aka intracranial hemorrhage, cerebral hematoma, intracranial hematoma) is a subtype of intracranial hemorrhage that occurs within the brain tissue itself. It is alternatively called intracerebral hemorrhage (ICH). It can be caused by brain trauma, or it can occur spontaneously in hemorrhagic stroke. Non-traumatic intracerebral hemorrhage is a spontaneous bleeding into the brain tissue.
A cerebral hemorrhage is an intra-axial hemorrhage; that is, it occurs within the brain tissue rather than outside of it. The other category of intracranial hemorrhage is extra-axial hemorrhage, such as epidural, subdural, and subarachnoid hematomas, which all occur within the skull but outside of the brain tissue. There are two main kinds of intra-axial hemorrhages: intraparenchymal hemorrhage and intraventricular hemorrhages. As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can increase intracranial pressure, which if left untreated can lead to coma and death. The mortality rate for intraparenchymal bleeds is over 40%.
Signs and symptomsEdit
Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain. Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Some patients may also go into a coma before the bleed is noticed.
Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis. Infection with the k serotype of Streptococcus mutans may also be a risk factor, because of its prevalence in stroke patients and production of collagen-binding protein.
Risk factors for ICH include:
- Hypertension (high blood pressure)
- Diabetes mellitus
- Cigarette smoking
- Excessive Consumption of alcoholic beverages
Tramautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.
Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan. Frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign".
Treatment depends substantially of the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
- Antihypertensive therapy in acute phases. The AHA/ASA and EUSI guidelines (American Heart Association/American Stroke Association guidelines and the European Stroke Initiative guidelines) have recommended antihypertensive therapy to stabilize the mean arterial pressure at 110 mmHg. One paper showed the efficacy of this antihypertensive therapy without worsening outcome in patients of hypertensive intracerebral hemorrhage within 3 hours onset.
- Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.
- Mannitol is effective in acutely reducing raised intracranial pressure.
- Acetaminophen may be needed to avoid hyperthermia, and to relieve headache.
- Frozen plasma, vitamin K, protamine, or platelet transfusions are given in case of a coagulopathy.
- Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.
- H2 antagonists or proton pump inhibitors are commonly given for stress ulcer prophylaxis, a condition somehow linked with ICH.
- Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids haven been found to increase mortality rates and are no longer recommended. 
- A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.
- Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.
- Tracheal intubation is indicated in patients with decreased level of consciousness or other risk of airway obstruction.
- IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum.
For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult, and half of the deaths occur in the first 2 days. Even though the majority of deaths occurs in the first days after ICH, survivors have a long term excess mortality of 27% compared to the general population.
The inflammatory response triggered by stroke has been viewed as harmful in the early stage, focusing on blood-borne leukocytes, neutrophils and macrophages, and resident microglia and astrocytes. A human postmortem study shows that inflammation occurs early and persists for several days after ICH. New area of interest are the Mast Cells.
- ↑ 1.0 1.1 1.2 1.3 1.4 Yadav YR, Mukerji G, Shenoy R, Basoor A, Jain G, Nelson A (2007). "Endoscopic management of hypertensive intraventricular haemorrhage with obstructive hydrocephalus". BMC Neurol 7: 1. Template:Citation/identifier. Template:Citation/identifier. Template:Citation/identifier. http://www.biomedcentral.com/1471-2377/7/1.
- ↑ 2.0 2.1 Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
- ↑ 3.0 3.1 Vinas FC and Pilitsis J. 2006. "Penetrating Head Trauma." Emedicine.com.
- ↑ Go AS, Mozaffarian D, Roger VL, et al. (January 2013). "Heart disease and stroke statistics--2013 update: a report from the American Heart Association". Circulation 127 (1): e6–e245. Template:Citation/identifier. Template:Citation/identifier.
- ↑ 5.0 5.1 5.2 McCaffrey P. 2001. "The Neuroscience on the Web Series: CMSD 336 Neuropathologies of Language and Cognition." California State University, Chico. Retrieved on June 19, 2007.
- ↑ Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." Retrieved on 2008-01-16.
- ↑ Shepherd S. 2004. "Head Trauma." Emedicine.com. Retrieved on June 19, 2007.
- ↑ Kazuhiko Nakano et al.. "The collagen-binding protein of Streptococcus mutans is involved in haemorrhagic stroke". Nature Communications. http://www.nature.com/ncomms/journal/v2/n9/full/ncomms1491.html.
- ↑ Major Risk Factors for Intracerebral Hamorrhage in the Young Are Modifiable Edward Feldmann, MD; Joseph P. Broderick, MD; Walter N. Kernan, MD; Catherine M. Viscoli, PhD; Lawrence M. Brass, MD; Thomas Brott, MD; Lewis B. Morgenstern, MD; Janet Lee Wilterdink, MD Ralph I. Horwitz, MD. Published in Stroke. 2005;36:1881.
- ↑ Yeung R, Ahmad T, Aviv RI, Noel de Tilly L, Fox AJ, Symons SP. Comparison of CTA to DSA in determining the etiology of spontaneous ICH. Canadian Journal of Neurological Sciences. 2009 March; 36(2):176-180.
- ↑ Wada R, Aviv RI, Fox AJ, Sahlas DJ, Gladstone DJ, Tomlinson G, Symons SP. CT angiography ‘spot sign’ predicts hematoma expansion in acute intracerebral hemorrhage. Stroke. 2007 April; 38(4):1257-1262. Epub 2007 February 22.
- ↑ Fujii M et al. J Clin Neurosci 17:1136-9,2010 PMID 20541417
- ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 13.8 eMedicine Specialties > Neurology > Neurological Emergencies > Intracranial Haemorrhage: Treatment & Medication. By David S Liebeskind, MD. Updated: Aug 7, 2006
- ↑ Lancet. 2004 Oct 9-15;364(9442):1321-8.Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial.
- ↑ Lancet. 2005 Jun 4-10;365(9475):1957-9. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months.
- ↑ Cedars-Sinai Health System - Cerebral Hemorrhages Retrieved on 02/25/2009
- ↑ Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" Cooper P and Golfinos G. 2000. Head Injury, 4th Ed. Morgan Hill, New York.
- ↑ Guidelines for the Management of Spontaneous Intracerebral Hemorrhage in Adults
- ↑ Hansen, B.M.; Nilsson O.G.; Anderson H; et al. (Oct 2013). "Long term (13 years) prognosis after primary intracerebral haemorrhage: a prospective population based study of long term mortality, prognostic factors and causes of death". Journal of Neurology, Neurosurgery & Psychiatry 84 (10): 1150–1155. Template:Citation/identifier. http://jnnp.bmj.com/content/early/2013/05/27/jnnp-2013-305200.
- ↑ Wang J (December 2010). "Preclinical and clinical research on inflammation after intracerebral hemorrhage". Prog. Neurobiol. 92 (4): 463–77. Template:Citation/identifier. Template:Citation/identifier. Template:Citation/identifier.
- ↑ Wu H, Zhang Z, Hu X, Zhao R, Song Y, Ban X, Qi J, Wang J (2010). "Dynamic changes of inflammatory markers in brain after hemorrhagic stroke in humans: a postmortem study.". Brain Research 1342 (1342): 111–1117. Template:Citation/identifier. Template:Citation/identifier.
- ↑  Lindsberg e.a.: Mast cells as early responders in the regulation of acute blood–brain barrier changes after cerebral ischemia and hemorrhage
- ↑ Page 117 in: Henry S. Schutta; Lechtenberg, Richard (1998). Neurology practice guidelines. New York: M. Dekker. Template:Citation/identifier.
- ↑ Copenhaver BR, Hsia AW, Merino JG, et al. (October 2008). "Racial differences in microbleed prevalence in primary intracerebral hemorrhage". Neurology 71 (15): 1176–82. Template:Citation/identifier. Template:Citation/identifier. Template:Citation/identifier.
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