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Cerebral Haemorrhage
Type of intracranial bleeding that occurs within the brain tissue itself
Intracerebral hemorrhage (ICH), also known as cerebral bleed and intraparenchymal bleed, is a sudden bleeding into the tissues of the brain, into its ventricles, or into both.[3][4][1] It is one kind of bleeding within the skull[3] and is one kind of stroke.[4]
Cerebral bleeding affects about 2.5 per 10,000 people each year.[2] It occurs more often in males and older people.[2] About 44% of those affected die within a month.[2] A good outcome occurs in about 20% of those affected.[2] Intracerebral hemorrhage, a type of hemorrhagic stroke, was first distinguished from ischemic strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.[6]
Signs and symptoms
People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed.[7] Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain.[7]
Intracerebral bleeds 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. Collapsing is another symptom. Some people may experience continuous bleeding from the ear. 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.[9]High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times.[8] 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,[10][11][12] 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.
Traumautic 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.
Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH.[15] So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[16] or to detect a "spot sign".
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.[16]
Location
When due to high blood pressure, intracerebral hemorrhages typically occur in the putamen (50%) or thalamus (15%), cerebrum (10-20%), cerebellum (10-13%), pons (7-15%), or elsewhere in the brainstem (1-6%).[17][18]
Treatment
Treatment depends substantially on the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction.[19]
One review found that antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes.[20] Other reviews found an unclear difference between intensive and less intensive blood pressure control.[21][22] The American Heart Association and American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg.[1] However, the evidence finds tentative usefulness as of 2015.[23]
Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.[19] It thus overall does not result in better outcomes in those without hemophilia.[24]
H2 antagonists or proton pump inhibitors are commonly given for to try to prevent stress ulcers, a condition linked with ICH.[19]
Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.[26][27]
A craniectomy may take place, where part of the skull is removed to allow a swelling brain room to expand without being squeezed.
Prognosis
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[29] 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.[10] 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.[10][30]
For spontaneous ICH seen on CT scan, the death rate (mortality) is 34-50% by 30 days after the insult,[8] and half of the deaths occur in the first 2 days.[31] 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.[32]
Intracerebral hemorrhage was first distinguished from strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.[6] 32nd United StatesPresidentFranklin D. Roosevelt died from cerebral hemorrhage in 1945.
Research
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.[34][35] A human postmortem study shows that inflammation occurs early and persists for several days after ICH.[36] Modulating microglial activation and polarization might mitigate intracerebral hemorrhage-induced brain injury and improve brain repair.[37] A new area of interest is the role of mast cells in ICH.[38][35]
^Tsivgoulis, G; Katsanos, AH; Butcher, KS; Boviatsis, E; Triantafyllou, N; Rizos, I; Alexandrov, AV (21 October 2014). "Intensive blood pressure reduction in acute intracerebral hemorrhage: A meta-analysis". Neurology. 83 (17): 1523-9. doi:10.1212/wnl.0000000000000917. PMID25239836. S2CID36315871.
^Ma, J; Li, H; Liu, Y; You, C; Huang, S; Ma, L (2015). "Effects of Intensive Blood Pressure Lowering on Intracerebral Hemorrhage Outcomes: A Meta-Analysis of Randomized Controlled Trials". Turkish Neurosurgery. 25 (4): 544-51. doi:10.5137/1019-5149.JTN.9270-13.0 (inactive 2021-01-16). PMID26242330.CS1 maint: DOI inactive as of January 2021 (link)
^Boulouis, Gregoire; Morotti, Andrea; Goldstein, Joshua N.; Charidimou, Andreas (1 April 2017). "Intensive blood pressure lowering in patients with acute intracerebral haemorrhage: clinical outcomes and haemorrhage expansion. Systematic review and meta-analysis of randomised trials". Journal of Neurology, Neurosurgery, and Psychiatry. 88 (4): 339-345. doi:10.1136/jnnp-2016-315346. ISSN1468-330X. PMID28214798. S2CID25397701.
^Ma, J; Li, H; Liu, Y; You, C; Huang, S; Ma, L (2015). "Effects of Intensive Blood Pressure Lowering on Intracerebral Hemorrhage Outcomes: A Meta-Analysis of Randomized Controlled Trials". Turkish Neurosurgery. 25 (4): 544-51. doi:10.5137/1019-5149.JTN.9270-13.0 (inactive 2021-01-16). PMID26242330.CS1 maint: DOI inactive as of January 2021 (link)
^Yuan, ZH; Jiang, JK; Huang, WD; Pan, J; Zhu, JY; Wang, JZ (June 2010). "A meta-analysis of the efficacy and safety of recombinant activated factor VII for patients with acute intracerebral hemorrhage without hemophilia". Journal of Clinical Neuroscience. 17 (6): 685-93. doi:10.1016/j.jocn.2009.11.020. PMID20399668. S2CID30590573.
^Roberts, Ian; Yates, David; Sandercock, Peter; Farrell, Barbara; Wasserberg, Jonathan (9 October 2016). "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. 364 (9442): 1321-1328. doi:10.1016/S0140-6736(04)17188-2. ISSN1474-547X. PMID15474134.
^Edwards, P; Arango, M; Balica, L; Cottingham, R; El-Sayed, H (2005). "Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months". Lancet. 365 (9475): 1957-9. doi:10.1016/s0140-6736(05)66552-x. PMID15936423.
^Sanders MJ and McKenna K. 2001. Mosby's Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
^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.