mwebazavictor1997@gmail.com

1. INTRA CRANICAL HEMORRHAGE
presentation by Mwebaza Victor MBchB
CT scan of a spontaneous intracranial hemorrhage, leaking
into the lateral ventricles
A cerebral hemorrhage (also spelled haemorrhage) is a type of intracranial hemorrhage that occurs
within the brain tissue. 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 and
may be caused by increased exertion, tension or stress.[1]
A cerebral hemorrhage is an intra-axial hemorrhage; that is, it occurs within, rather than outside, the
brain tissue. 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%.[2]

2. Signs and symptoms
Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by
the area of the brain that is damaged by the bleed.[3] Other symptoms include those that indicate a rise
in intracranial pressure caused by a large mass putting pressure on the brain.[3] 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. Another common symptom is a patient can collapse. Some people may
experience continuous bleeding from the ear. Some patients may also go into a coma due to before the
bleed is noticed.
Causes.
Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital
admissions for stroke.[4] High blood pressure raises the risks of spontaneous intracerebral hemorrhage
by two to six times.[1] 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,[5][6][7] 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.[8]
Risk factors for ICH include:[9]
Hypertension (high blood pressure)
Diabetes mellitus
Menopause
Cigarette smoking
Excessive alcohol consumption
Severe migraine
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.

3. Diagnosis
Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been
proved to be effective in diagnosing intracranial vascular malformations after ICH.[10] So frequently, a
CT angiogram will be performed in order to exclude a secondary cause of hemorrhage[11] 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.[11]
Treatment
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.
Medication
One review found that antihypertensive therapy to bring down the blood pressure in acute phases
appears to improve outcomes.[12] Another review found an unclear difference between intensive and
less intensive blood pressure control.[13] The American Heart Association and American Stroke
Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg.[14]
Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also
increases the risk of thromboembolism.[15] It thus overall does not result in better outcomes in those
without hemophilia.[16]
Mannitol is effective in acutely reducing raised intracranial pressure.
Acetaminophen may be needed to avoid hyperthermia, and to relieve headache.[15]
Frozen plasma, vitamin K, protamine, or platelet transfusions are given in case of a coagulopathy.[15]
Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.[15]
H2 antagonists or proton pump inhibitors are commonly given for stress ulcer prophylaxis, a condition
somehow linked with ICH.[15]

4. Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids
haven been found to increase mortality rates and are no longer recommended.[17][18]
Glibenclamide (Glyburide), while not currently an FDA approved treatment, is being studied as a
promising treatment for preventing secondary brain injury and cerebral edema post-hemorrhage or
infarction.
Surgery
Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a structural vascular lesion or
lobar hemorrhage in a young patient.[15]
A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding
invasive surgical procedures.[19]
Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages,
although successful reports are limited.[15]
Other treatment
Tracheal intubation is indicated in patients with decreased level of consciousness or other risk of airway
obstruction.[15]
IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.[15]
Prognosis
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the
injury occurs in the brain stem.[2] 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.[5] 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.[5][20]
For spontaneous ICH seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the insult,[1]
and half of the deaths occur in the first 2 days.[21] 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.[22]
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.[23] A

5. human postmortem study shows that inflammation occurs early and persists for several days after
ICH.[24] New area of interest are the Mast Cells.[25]
Epidemiology
It accounts for 20% of all cases of cerebrovascular disease in the US, behind cerebral thrombosis (40%)
and cerebral embolism (30%).[26]
It is two or more times more prevalent in black patients than it is in white patients.[27]
References
1 2 3 4 5 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.
doi:10.1186/1471-2377-7-1. PMC 1780056. PMID 17204141.
1 2 Sanders MJ and McKenna K. 2001. Mosby's Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head
and Facial Trauma." Mosby.
1 2 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.
doi:10.1161/CIR.0b013e31828124ad. PMID 23239837.
1 2 3 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.
↑ 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.

6. ↑ Josephson, Colin B; White, Philip M; Krishan, Ashma; Al-Shahi Salman, Rustum (1 September 2014).
"Computed tomography angiography or magnetic resonance angiography for detection of intracranial
vascular malformations in patients with intracerebral haemorrhage". The Cochrane Library 9: CD009372.
doi:10.1002/14651858.CD009372.pub2. PMID 25177839. Retrieved 16 September 2014.
1 2 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.
↑ 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. PMID 25239836.
↑ 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. PMID 26242330.
↑ Hemphill JC, 3rd; Greenberg, SM; Anderson, CS; Becker, K; Bendok, BR; Cushman, M; Fung, GL;
Goldstein, JN; Macdonald, RL; Mitchell, PH; Scott, PA; Selim, MH; Woo, D; American Heart Association
Stroke, Council; Council on Cardiovascular and Stroke, Nursing; Council on Clinical, Cardiology (July
2015). "Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for
Healthcare Professionals From the American Heart Association/American Stroke Association.". Stroke; a
journal of cerebral circulation 46 (7): 2032–60. PMID 26022637.
1 2 3 4 5 6 7 8 9 eMedicine Specialties > Neurology > Neurological Emergencies > Intracranial
Haemorrhage: Treatment & Medication. By David S Liebeskind, MD. Updated: Aug 7, 2006
↑ 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 : official journal of the Neurosurgical Society of Australasia
17 (6): 685–93. doi:10.1016/j.jocn.2009.11.020. PMID 20399668.
↑ 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

7. ↑ 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. doi:10.1136/jnnp-2013-305200.
↑ Wang J (December 2010). "Preclinical and clinical research on inflammation after intracerebral
hemorrhage". Prog. Neurobiol. 92 (4): 463–77. doi:10.1016/j.pneurobio.2010.08.001. PMC 2991407.
PMID 20713126.
↑ 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. doi:10.1016/j.brainres.2010.04.033. PMC 2885522. PMID 20420814.
↑ 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. ISBN 0-8247-0104-6.
↑ Copenhaver BR, Hsia AW, Merino JG, et al. (October 2008). "Racial differences in microbleed
prevalence in primary intracerebral hemorrhage". Neurology 71 (15): 1176–82.
doi:10.1212/01.wnl.0000327524.16575.ca. PMC 2676986. PMID 18838665.
Further reading
Hemphill JC, 3rd; Greenberg, SM; Anderson, CS; Becker, K; Bendok, BR; Cushman, M; Fung, GL; Goldstein,
JN; Macdonald, RL; Mitchell, PH; Scott, PA; Selim, MH; Woo, D (28 May 2015). "Guidelines for the
Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From
the American Heart Association/American Stroke Association.". Stroke; a journal of cerebral circulation
46: 2032–60. doi:10.1161/STR.0000000000000069. PMID 26022637.
External links
Wikimedia Commons has media related to Cerebral hemorrhage.
Parent friendly information on IVH in premature babies from The Hospital for Sick Children
LPCH on Intraventricular
Information on brain haemorrhage from Headway - the brain injury association, a UK-based charity
providing information and support
Cerebrovascular diseases (G45–G46 and I60–I69, 430–438)
Brain ischemia/
cerebral infarction

8. (ischemic stroke/TIA)
TACI, PACI
precerebral: Carotid artery stenosis
cerebral: MCAACAAmaurosis fugax
Moyamoya disease
POCI
precerebral: Anterior spinal artery syndromeVertebrobasilar insufficiency Subclavian steal syndrome
brainstem: medulla Medial medullary syndromeLateral medullary syndromepons Medial pontine
syndrome/Foville'sLateral pontine syndrome/Millard-Gublermidbrain Weber'sBenediktClaude's
cerebral: PCALacunar strokeDejerine–Roussy syndrome
cerebellar
General
cerebral: Cerebral venous sinus thrombosisCADASILBinswanger's diseaseTransient global amnesia
Intracranial hemorrhage
(hemorrhagic stroke)
Extra-axial
EpiduralSubduralSubarachnoid
Cerebral/Intra-axial
Intraventricular
Brainstem
Duret haemorrhage
Aneurysm
Cerebral aneurysm Intracranial berry aneurysmCharcot-Bouchard aneurysm
Other/general
Cerebral vasculitis
Neurotrauma (S06, Sx4, T09.3–4, 850–854, 950–957)

9. Traumatic brain injury
Intracranial hemorrhageIntra-axial Intraparenchymal hemorrhageIntraventricular hemorrhageExtra-
axial Subdural hematomaEpidural hematomaSubarachnoid hemorrhageBrain herniationCerebral
contusionCerebral lacerationConcussion Post-concussion syndromeSecond-impact syndromeDementia
pugilisticaChronic traumatic encephalopathyDiffuse axonal injuryShaken baby syndromePenetrating
head injury
Spinal cord injury
Anterior cord syndromeBrown-Séquard syndromeCauda equina syndromeCentral cord
syndromeParaplegiaPosterior cord syndromeSpinal cord injury without radiographic
abnormalityTetraplegia (Quadriplegia)
Peripheral nerves
Nerve injury Peripheral nerve injuryWallerian degenerationInjury of accessory nerveBrachial plexus
injuryTraumatic neuroma
This article is issued from WikiMed Medical Encyclopedia - version of the Thursday, May 26, 2016. The
text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for
the media files.