Intraparenchymal hemorrhage – an overview sciencedirect topics brain anoxia

Intraparenchymal hemorrhage

Intraparenchymal hemorrhage (IH) arises commonly from deep penetrating cerebral arteries affected by lipohyalinosis, microaneurysm formation, and arteriosclerosis with severe degeneration of medial smooth muscle cells. As blood extravasates from the ruptured artery, neurologic deficit arises as adjacent brain tissue is disrupted, displaced, and compressed. The sites of predilection of IH are similar to those of lacunar infarction as in both cases the deep penetrating arteries are involved. These sites include commonly the putamen, thalamus, pons, and cerebellum.

IH usually occurs in the setting of chronic hypertension.

In the elderly it may also occur in association with cerebral amyloid angiopathy (CAA).Brain anoxia CAA is characterized by deposits of amyloid in the media and adventia of small and medium-sized cerebral arteries usually located in the superficial layers of the cerebral cortex and leptomeninges. The resultant cerebral hemorrhage is usually located superficially in one of the major brain lobes (so-called lobar hemorrhage). Lobar hemorrhage may also occur with other conditions including hypertension, bleeding disorders, and arteriovenous malformation. CAA increases with advancing age and is associated with histopathologic and clinical features of alzheimer’s disease.

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Intraparenchymal hemorrhage

ECG changes following intraparenchymal hemorrhage are similar to those of ischemic stroke and subarachnoid hemorrhage.Brain anoxia retrospective studies of patients with lobar and basal ganglia hemorrhages demonstrate ECG changes in 64–95% of cases ( goldstein, 1979; hays and diringer, 2006; maramattom et al., 2006; van bree et al., 2010). Repolarization changes are most characteristic and include qtc prolongation, nonspecific ST-T changes, and deeply inverted T waves. Prolonged qtc is frequently associated with hydrocephalus and insular cortex involvement ( van bree et al., 2010). Sinus bradycardia is a common arrhythmia found in patients with supratentorial intracerebral hemorrhage (ICH), while atrial fibrillation has been associated with brainstem hemorrhage ( talman, 1985). Although a common finding after ICH, ECG changes also do not consistently indicate that myocardial injury has taken place, and there is no clear association between mortality and the appearance or severity of ECG changes ( maramattom et al., 2006).Brain anoxia myocardial injury is observed in a small proportion of patients with intracerebral hemorrhage, likely as a result of an increase in sympathetic tone. The finding of troponin elevations may serve as an independent predictor of in-hospital mortality ( hays and diringer, 2006; sandhu et al., 2008; chung et al., 2009).

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Intracerebral hemorrhage

Bleeding directly into the substance of the brain is termed intraparenchymal or intracerebral hemorrhage ( fig. 7-4). It may occur as a complication of ischemic stroke, termed hemorrhagic conversion, or as the primary injury without preceding ischemia. Hypertension is the most important identified risk factor for intracerebral hemorrhage. More than 70 percent of patients with intracerebral hemorrhage have a history of hypertension, and the risk of hemorrhagic stroke is elevated 9.5-fold in the highest compared with the lowest quintile of systolic blood pressure. 60

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Intracranial hemorrhage is responsible for 10 to 15 percent of all stroke deaths but for more than one-third of the years of life lost before age 65 due to the younger age distribution of intra- cerebral hemorrhage. 53 case fatality rates are high, with 35 to 50 percent dead at 1 month and only 20 percent returning to independence at 6 months. 61 in the united states, an estimated 37,000 cases of intracerebral hemorrhage occur each year, with the total estimated cost of care exceeding $6 billion annually. 55

Other risk factors for intracerebral hemorrhage include age, race, substance abuse, anticoagulation, platelet dysfunction, and vascular and structural anomalies. Rates of intracerebral hemorrhage increase with age.Brain anoxia african americans have rates that are 40 percent higher than those of whites, with larger differences at younger ages. 62 cocaine and amphetamine use is associated with increased risk, particularly acutely, possibly because of transient severe hypertension. 60 abnormalities in clotting may account for an increased incidence of intracerebral hemorrhage with heavy alcohol use. Excessive anticoagulation and antiplatelet therapy also increase the risk of intracerebral hemorrhage. 63,64 thrombolytic agents used for ischemic stroke and myocardial infarction cause intracerebral hemorrhage in some cases. It may also occur with severe thrombocytopenia and platelet dysfunction.

Intracerebral hemorrhage may result from and occur in brain tumors, such as glioblastoma multiforme and in metastatic melanoma, choriocarcinoma, renal cell carcinoma, and bronchogenic carcinoma.Brain anoxia cerebral amyloid angiopathy, a vasculopathy common in the elderly, is associated with lobar hemorrhages, often centered at the gray-white junction. Other punctate hemorrhages may be apparent on gradient-echo MR images ( fig. 7-5), supporting the diagnosis. Arteriovenous malformations, abnormal complexes of arteries and veins in brain parenchyma, account for 5 percent of intracerebral hemorrhages. 60 cavernous malformations are dense collections of thin-walled vascular channels and appear to be the cause of intracerebral hemorrhage in 5 percent of autopsies 64; they are not apparent on angiography but have a “popcorn” appearance on MR images, with a hyperintense core surrounded by hypointense hemosiderin from previous small hemorrhages ( fig. 7-6).Brain anoxia aneurysms may produce intracerebral hemorrhages when blood is directed into the brain, and these rarely are mistaken for primary hypertensive hemorrhages.

Primary hypertensive intracerebral hemorrhage was thought to be caused by chronic vascular injury, resulting in formation of microscopic aneurysms, first characterized by charcot and bouchard in 1868. Advances in pathologic tissue preparation have raised doubts about the frequency and importance of microscopic aneurysms, which may actually represent complex vascular coils. 65 more recently, fibrinoid necrosis of small arteries has been proposed as the initial step in intracerebral hemorrhage. 66 brain injury occurs because of compression of surrounding tissue and from the direct toxic effects of blood.Brain anoxia mass effect from the hematoma may lead to uncal, subfalcine, tonsillar, or transtentorial herniation, depending on location, and death may ensue.

Clinical presentation depends on the location and size of the hemorrhage ( table 7-3). Nearly all intracerebral hemorrhage is characterized by the sudden onset of neurologic deficits, progressing over minutes and accompanied by headache, often with alteration of consciousness. Deterioration due to surrounding edema, hydrocephalus, or continuing or recurrent hemorrhage often occurs within the first 24 hours but may be delayed by days.

Prognosis is multifactorial. Hemorrhage volume, most easily measured by halving the product of the length, width, and depth on axial head CT images, is a powerful predictor of mortality, with 80 percent 30-day mortality in those with volumes greater than 60 ml, and 22 percent mortality in hemorrhages less than 30 ml. 67 mortality is much greater in those with intraventricular extension of blood. 68 hydrocephalus due to intraventricular extension or cerebrospinal fluid (CSF) outflow obstruction predicts in-hospital mortality: 51 percent of those with and 2 percent of those without hydrocephalus died in one series. 69 lower glasgow coma scale scores, greater age, location, and blood pressure or pulse pressure are other independent predictors of mortality.Brain anoxia simple multivariable prediction models have been developed and validated. 70,71

Urgent head CT is required in patients with suspected intracerebral hemorrhage. MRI is as sensitive as CT for detecting hemorrhage and is more sensitive for detecting an underlying structural etiology, but the rapidity, availability, and ease of interpretation of CT favor its initial use. Contrast-enhanced head CT scan may show evidence of persistent hemorrhage at the time of presentation, a sign associated with poor prognosis. 72 vascular imaging is required whenever aneurysmal subarachnoid hemorrhage is possible, such as in cases with a large amount of subarachnoid blood, and should be considered for all patients without a clear etiology who would be surgical candidates.Brain anoxia early MRI may be indicated if a structural etiology is suspected, but findings are often obscured by the hemorrhage, and a scan delayed by 4 to 8 weeks may provide more useful information if urgent diagnosis is unnecessary. MRI is useful in diagnosing cavernous malformations and may suggest cerebral amyloid angiopathy.

Treatment is generally supportive, although surgical intervention is indicated in some cases. Severe hypertension is common after intracerebral hemorrhage, in part because it is a response to elevated intracranial pressure and brain injury. In patients with a systolic blood pressure of 150 to 220 mmhg, acute lowering of systolic blood pressure to 140 mmhg is probably safe. Current consensus guidelines suggest treating with antihypertensive medications for systolic blood pressure greater than 180 mmhg or mean arterial pressure greater than 130 mmhg, though clinical trials to determine optimal blood pressure control after intracerebral hemorrhage are ongoing. 61 increased intracranial pressure may lead to coma and is treated with extraventricular drainage, osmotherapy, or hyperventilation.Brain anoxia

Surgical evacuation of primary intracerebral hemorrhages is commonly performed when there is posterior fossa hemorrhage with a risk of brainstem compression or when there is evolving neurologic deterioration in patients with lobar hemorrhages and other prognostic signs are favorable. A large, international trial randomized 1,033 subjects with supratentorial hemorrhage to receive early surgical evacuation of the hematoma or initial conservative treatment followed by surgical evacuation only if it was necessitated by neurologic deterioration. There was a favorable outcome at 6 months in 26 percent of those allocated to early surgery as compared with 24 percent in those allocated to initial conservative treatment ( P=0.89).Brain anoxia in subgroup analysis, it appeared that early surgery was more effective than conservative therapy when the hematoma was 1 cm or less from the cortical surface. Additional trials will be needed to resolve the issue of early surgical benefit for superficial hematomas. 73

After the acute period, aggressive treatment of hypertension is indicated. In addition to reducing cardiovascular disease and ischemic stroke, one study has shown that treating hypertension reduces the risk of intracerebral hemorrhage by more than 50 percent. 74

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Intraventricular hemorrhage

Infants born preterm are at an increased risk of intraventricular and intraparenchymal hemorrhage, which adversely affects their neurodevelopmental outcomes. 51,192 extravasation of blood normally contained within the cerebral intravascular space into the parenchymal ventricular space represents complete disruption of the BBB.Brain anoxia hence, understanding the pathophysiology of impaired BBB function is of vital importance in perinatal medicine because premature infants are at high risk of brain hemorrhages.

Germinal matrix hemorrhage progressing to intraventricular or intraparenchymal hemorrhage is the prototype of intracranial hemorrhage encountered in preterm infants. 193 germinal matrix capillaries have large diameters and thin basement membranes, and they lack direct contact with perivascular structures along a large proportion of their circumference, in contrast with capillaries within the cerebral cortex at same gestational age. 194 the blood vessel density and the percentage of blood vessel area are larger in the germinal matrix vessels than those of adjacent gray and white matter in autopsy material from fetuses and preterm infants born between 16 and 40 weeks of gestation, potentially predisposing to hemorrhage in the germinal matrix. 195

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The periventricular germinal matrix exhibits rapid angio­genesis, resulting in high metabolic demand, rapid endothelial turnover, and high vascularity. 196 deficiencies in any of the components of the BBB can weaken this vasculature and increase the propensity for hemorrhage. Current understanding suggests that paucity of pericytes, low fibronectin levels in the basal lamina, and reduced key intermediate filaments of the astrocytic end-feet contribute to fragility of the germinal matrix BBB, rendering this area of the brain vulnerable to hemorrhage. 196

Pericytes are particularly important in the development of intraventricular hemorrhage because they play a key role in angiogenesis, providing structural support to the vasculature, maintaining the BBB, and controlling the remaining cells of the NVU. 47,197,198 pericyte recruitment is regulated by ligand-receptor systems that include platelet-derived growth factor, sphingosine-1 phosphate, angiopoietin, and TGF-β. 199 TGF-β expression is reduced in the germinal matrix microvasculature, resulting in pericyte paucity and increased fragility of the germinal matrix microvasculature.Brain anoxia

The basal lamina comprises several constituents including fibronectin that contribute to the structural integrity of vasculature by virtue of its anchoring function. 200-202 fibronectin levels are significantly reduced in the germinal matrix vasculature compared with the cerebral cortex and white matter in premature infants. 203 TGF-β up-regulates fibronectin. Consequently, low levels of TGF-β in the germinal matrix result in decreased fibronectin germinal matrix levels. Thus, reduced fibronectin in the basal lamina of the germinal matrix may also contribute to vascular fragility in this brain region. 204,205

Astrocytes also contribute to BBB development; they regulate its function, provide structural integrity, and contribute to barrier permeability. 200 glial fibrillary acidic protein (GFAP) is a key intermediate filament of the astrocytic end-feet cytoskeleton. 206-208 GFAP provides structural integrity and mechanical strength to astrocyte end-feet.Brain anoxia consequently, reduced GFAP expression in germinal matrix astrocytic end-feet in conjunction with a paucity of pericytes and reduced basal lamina fibronectin contributes to the fragility of the germinal matrix vasculature and to its vulnerability to hemorrhage in premature infants. 209

Glucocorticoids are one of the most widely used prenatal pharmacologic treatments to accelerate fetal maturation. 210 several studies have confirmed that prenatal glucocorticoids reduce both severity and incidence of intraventricular hemorrhage. 210-212 the beneficial effects of prenatal glucocorticoids include stabilization of the microvasculature of the germinal matrix. Prenatal glucocorticoids suppress angiogenesis in the germinal matrix microvasculature and trim the nascent and fragile vasculature, stabilizing the BBB and thereby reducing the vulnerability to hemorrhage.Brain anoxia infants treated with prenatal glucocorticoids exhibit improved pericyte coverage of the germinal matrix vasculature, higher fibronectin levels, and larger amounts of GFAP in astrocyte end-feet of germinal matrix blood vessels than untreated infants. 203,213,214

Prenatal corticosteroid administration also results in decreased permeability of the BBB early in ovine gestation. 103,104,106 this decrease in permeability was associated with increased expression in key tight junction proteins such as claudin-1, claudin-5, and ZO-2 111 taken together, the decreased incidence of intraventricular hemorrhage in premature infants after prenatal glucocorticoid treatment 215 and the decreased permeability of the BBB in ovine fetus after glucocorticoid treatment of ewes 103,104,106 suggest that glucocorticoids may accelerate microvascular maturation with a beneficial effects on BBB function in the human fetus and premature infant.Brain anoxia in addition, endogenous increases in glucocorticoids may also contribute to accelerated maturation of the endothelial vasculature of the fetus and premature infant. 106

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