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intracerebral_hemorrhage

Intracerebral hemorrhage

also known as cerebral hemorrhage.

Its a subtype of intracranial hemorrhage that occurs within the brain tissue itself, also called intraaxial hemorrhage.

Intraparenchymal hemorrhage (IPH) is one extension of intracerebral hemorrhage (the other is intraventricular hemorrhage (IVH)) with bleeding within brain parenchyma).

Epidemiology

Intracerebral hemorrhage causes 15% of strokes annually in the United States, and there is currently no effective therapy.

A systematic review of epidemiological studies reported intracerebral hemorrhage (ICH) incidence and mortality as unchanged over time; however, comparisons between studies conducted in different health services obscure assessment of trends.

Overall and fatal ICH rates have fallen in a large Australian population. Improvements in cardiovascular prevention and acute care may explain declining rates. There was no evidence of an increase in devastated survivors because the longer term mortality of 30-day survivors has not increased over time 1).

Types

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.

Spontaneous intracerebral hemorrhage, see Intracerebral hemorrhage and ruptured intracranial aneurysm

Traumatic intracerebral hemorrhage

Cerebral hemorrhage in infancy and childhood


Acute intracerebral hemorrhage

Chronic intracerebral hemorrhage.

Localization

Etiology

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. Non-traumatic can refer to increased excertion, tension or stress.

see Spontaneous intracerebral hemorrhage

see Traumatic intracerebral hemorrhage


In ischemic stroke or patients with TIA less than five cerebral microbleeds (CMBs) should not affect antithrombotic decisions, although with more than five CMBs the risks of future ICH and ischaemic stroke are finely balanced, and antithrombotics might cause net harm. In lobar ICH populations, a high burden of strictly lobar CMBs is associated with cerebral amyloid angiopathy (CAA) and high ICH risk; antithrombotics should be avoided unless there is a compelling indication 2).


MicroRNAs (miRNAs) are important regulators of translation and have been reported to be associated with the pathogenesis of numerous cerebrovascular diseases, including ICH.

A study explored the role of miRNA (miR)‑126 in ICH. Adult male Wistar rats were randomly assigned to ICH model and sham groups. ICH was induced by intracerebral injection of collagenase. The mRNA expression levels of miR‑126 in the two groups were determined. The miR‑126 lentivirus expression vector pWPXL‑miR‑126 or negative control vector was then constructed and delivered via intraparenchymal injection. Following transduction, behavioral testing (rotarod and limb placement tests), relative hemorrhagic lesion size, apoptotic cells and protein levels of vascular endothelial growth factor (VEGF)‑A and caspase‑3 were determined. The relative expression levels of miR‑126 were significantly decreased in the ICH group compared to the sham group (P=0.026). Overexpression of miR‑126 significantly improved the relative duration of stay on the rotarod at day 2 (P=0.029) and 3 (P=0.033), and statistically reduced the deficit score (P=0.036), the relative size of hemorrhagic lesion (P=0.019) and the number of apoptotic cortical neurons (P=0.024) compared with the sham group. Additionally, the protein levels of VEGF‑A were significantly elevated, however levels of caspase‑3 were downregulated by overexpression of miR‑126 compared with the negative control group. MiR‑126 therefore exhibits a protective role in ICH. Overexpression of miR‑126 protects against ICH, and may be involved in the process of angiogenesis and exhibit an anti-apoptotic effect 3).

Pathophysiology

Calcium is a key cofactor of the coagulation cascade and may play a role in the pathophysiology of intracerebral hemorrhage (ICH).

Hypocalcemia correlates with the extent of bleeding in patients with ICH. A low calcium level may be associated with a subtle coagulopathy predisposing to increased bleeding and might therefore be a promising therapeutic target for acute ICH treatment trials 4).

A recent increase in interest in the pathophysiology of ICH, has led to elucidation of the pathways underlying ICH-induced brain injury, pathways where intercellular and hematoma to cell signaling play important roles 5).

Diagnosis

Noncontrast computed tomography (NCCT) is the gold standard to detect intracerebral hemorrhage (ICH) in patients presenting with acute focal syndromes.

Diffusion-weighted magnetic resonance imaging (DW-MRI) may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke.

DW-MRI at b1000 has a diagnostic yield similar to Noncontrast computed tomography (NCCT) for detecting ICH and superior to NCCT for detecting ischemic stroke (IS). Therefore, DW-MRI may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke 6).

Intracerebral hemorrhage volume

Hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). Kothari et al., compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis.

The formula ABC/2 was used, where A is the greatest hemorrhage diameter by CT, B is the diameter 90 degrees to A, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness.

The ICH volumes for 118 patients were evaluated in a mean of 38 seconds and correlated with planimetric measurements (R2 = 9.6). Interrater and intrarater reliability were excellent, with an intraclass correlation of .99 for both.

Kothari et al., conclude that ICH volume can be accurately estimated in less than 1 minute with the simple formula ABC/2 7).

Scores

Treatment

As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can produce intracranial hypertension, which if left untreated can lead to coma and death.

The management of ICH has been influenced by the results of several major trials completed in the last decade. Developing evidence-based management strategies for ICH has been hampered by its diverse aetiology, high case fatality and variable cooperative organisation of medical and surgical care. Progress is being made through the conduct of collaborative multicentre studies with the large sample sizes necessary to evaluate therapies with realistically modest treatment effects.

Evidence based recommendations

A narrative review describes the major consequences of ICH and provides evidence-based recommendations to support decision-making in medical management 8).

Blood pressure management

Acute blood pressure management has been shown to be safe in the setting of acute ICH but there was no reduction in mortality with early blood pressure (BP) lowering, but uncertainty persists over whether potential benefits and harms vary according to the magnitude of BP reduction 9).

Temperature management

The results of the targeted temperature management after intracerebral hemorrhage clinical trial may provide additional information on the applicability of targeted temperature management after intracerebral hemorrhage 10).

Surgery

Outcome

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking.

It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause intracranial hypertension and potentially fatal brain herniation syndromes.

They have high rates of morbidity and rates of mortality of up to 50%. Initial hematoma size and subsequent hematoma expansion are among the most important predictors of poor outcome.

Efforts to improve clinical outcome through mitigation of hematoma expansion have so far been unsuccessful.

Data suggest that outcomes can be improved with standardized medical care.

A strong association exists between the amount of intraventricular hemorrhage (IVH) and poor outcome in intracerebral hemorrhage. An IVH volume of 5 to 10 mL emerges as a significant threshold for decision making on prognosis in these patients 11).

The ICH score is a simple and reliable clinical grading scale that is used for predicting the early mortality of patients with ICHs.

Neurological deterioration (ND) occurs frequently and predicts poor outcomes. Hematoma expansion and intraventricular hemorrhage in early ND, and cerebral edema, fever, and medical complications in later ND 12).

Complications

Brain abscess after intracerebral hemorrhage.

Intracerebral hemorrhage recurrence.

Inflammatory response mediates secondary brain injury during intracerebral hemorrhage (ICH).

Hematoma expansion is associated with poor outcome in intracerebral hemorrhage (ICH) patients. The spot sign and the blend sign are reliable tools for predicting hematoma expansion in ICH patients.

1)
Gattellari M, Goumas C, Worthington J. Declining rates of fatal and nonfatal intracerebral hemorrhage: epidemiological trends in Australia. J Am Heart Assoc. 2014 Dec 8;3(6):e001161. doi: 10.1161/JAHA.114.001161. PubMed PMID: 25488294.
2)
Wilson D, Werring DJ. Antithrombotic therapy in patients with cerebral microbleeds. Curr Opin Neurol. 2016 Nov 24. [Epub ahead of print] PubMed PMID: 27898582.
3)
Kong F, Zhou J, Zhou W, Guo Y, Li G, Yang L. Protective role of microRNA-126 in intracerebral hemorrhage. Mol Med Rep. 2017 Jan 19. doi: 10.3892/mmr.2017.6134. [Epub ahead of print] PubMed PMID: 28112373.
4)
Morotti A, Charidimou A, Phuah CL, Jessel MJ, Schwab K, Ayres AM, Romero JM, Viswanathan A, Gurol ME, Greenberg SM, Anderson CD, Rosand J, Goldstein JN. Association Between Serum Calcium Level and Extent of Bleeding in Patients With Intracerebral Hemorrhage. JAMA Neurol. 2016 Nov 1;73(11):1285-1290. doi: 10.1001/jamaneurol.2016.2252. PubMed PMID: 27598746.
5)
Egashira Y, Hua Y, Keep RF, Xi G. Intercellular cross-talk in intracerebral hemorrhage. Brain Res. 2015 Apr 8. pii: S0006-8993(15)00291-7. doi: 10.1016/j.brainres.2015.04.003. [Epub ahead of print] Review. PubMed PMID: 25863131.
6)
Keigler G, Goldberg I, Eichel R, Gomori JM, Cohen JE, Leker RR. Diffusion-weighted Imaging at b1000 for Identifying Intracerebral Hemorrhage: Preliminary Sensitivity, Specificity, and Inter-rater Variability. J Stroke Cerebrovasc Dis. 2014 May 1. pii: S1052-3057(14)00065-2. doi: 10.1016/j.jstrokecerebrovasdis.2014.02.005. [Epub ahead of print] PubMed PMID: 24795096.
7)
Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, Khoury J. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996 Aug;27(8):1304-5. PubMed PMID: 8711791.
8)
Schreuder FH, Sato S, Klijn CJ, Anderson CS. Medical management of intracerebral haemorrhage. J Neurol Neurosurg Psychiatry. 2016 Nov 16. pii: jnnp-2016-314386. doi: 10.1136/jnnp-2016-314386. [Epub ahead of print] Review. PubMed PMID: 27852691.
9)
Aiyagari V. The clinical management of acute intracerebral hemorrhage. Expert Rev Neurother. 2015 Dec;15(12):1421-32. doi: 10.1586/14737175.2015.1113876. Epub 2015 Nov 13. PubMed PMID: 26565118.
10)
Rincon F, Friedman DP, Bell R, Mayer SA, Bray PF. Targeted temperature management after intracerebral hemorrhage (TTM-ICH): methodology of a prospective randomized clinical trial. Int J Stroke. 2014 Jan 22. doi: 10.1111/ijs.12220. [Epub ahead of print] PubMed PMID: 24450819.
11)
Chan E, Anderson CS, Wang X, Arima H, Saxena A, Moullaali TJ, Heeley E, Delcourt C, Wu G, Wang J, Chen G, Lavados PM, Stapf C, Robinson T, Chalmers J, Huang Y; INTERACT2 Investigators. Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: intensive blood pressure reduction in acute cerebral hemorrhage trial results. Stroke. 2015 Mar;46(3):653-8. doi: 10.1161/STROKEAHA.114.008470. Epub 2015 Feb 12. PubMed PMID: 25677598.
12)
Lord AS, Gilmore E, Choi HA, Mayer SA; VISTA-ICH Collaboration. Time course and predictors of neurological deterioration after intracerebral hemorrhage. Stroke. 2015 Mar;46(3):647-52. doi: 10.1161/STROKEAHA.114.007704. Epub 2015 Feb 5. PubMed PMID: 25657190.
intracerebral_hemorrhage.txt · Last modified: 2018/04/04 18:39 by administrador