Hepatic Encephalopathy

Fraser, C. L.; Arieff, Allen I.

doi:10.1056/nejm198510033131406

Cited by 136 publications

(41 citation statements)

References 113 publications

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“…Information on blood pressure was not given in all cases, but the available data (17,20,22,24) (25). In such cases, greater osmotic shifts and over-hydration may occur and are likely to induce brain edema (25,27) (34), and is considered to be an important factor in the development of CPM (35). A patient with diabetes mellitus and chronic hepatitis C who developed a pontine lesion has also been documented in a previous case report (23).…”

Section: Discussionmentioning

confidence: 99%

Central Pontine Lesions Observed with MRI in Four Diabetic Patients

et al. 2008

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We report four diabetic patients with a central pontine lesion on magnetic resonance imaging (MRI). All patients also had hypertension, diabetic neuropathy and nephropathy, and three had chronic hepatitis C. Their neurological symptoms were disproportionately mild compared with the MRI features, which were of high intensity on T2-weighted images, but were less prominent on T1-and diffusion-weighted images. A subclinical pontine lesion was found in two patients who had undergone MRI previously. We consider that diabetes mellitus is an important factor for developing a pontine lesion with or without symptoms, probably in association with hepato-renal problems and hypertension.

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Section: Discussionmentioning

confidence: 99%

Central Pontine Lesions Observed with MRI in Four Diabetic Patients

et al. 2008

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“…Frequently, metabolic encephalopathies are produced by multiple causes, such as ethanol intoxication with phosphate depletion ( pernatremia with hepatic encephalopathy (2), hyponatremia with hypoxia (3), and carbon monoxide exposure with hypoxia (4).…”

Section: Introductionmentioning

confidence: 99%

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Vexler

Ayus²,

Roberts³

et al. 1994

J. Clin. Invest.

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Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia + hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na+-K+-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling. (J. Clin. Invest. 1994.93:256-264.)

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“…Hepatic failure disrupts the blood-brain barrier causing brain edema, which is the most commonfinding contributing to death in hepatic encephalopathy (14). In relation to acute renal failure, uremia can cause patchy cerebral white matter edema similar to the lesion in the present case (15).…”

Section: Discussionmentioning

confidence: 56%

Reversible White Matter Lesions in a Patient with Fulminant Hepatitis and Acute Renal Failure.

et al. 1994

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A 36-year-old man developed fulminant hepatitis and acute renal failure with profound hyponatremia (116 mEq/L). Emergent hemodialysis corrected the serum sodium to 136 mEq/L within 24 hours. He developed generalized convulsions ll days later. Magnetic resonance imaging (MRI) revealed a single large symmetrical lesion in the pons and extensive white matter lesions in the bilateral occipital, temporal, parietal and right frontal regions. These lesions showed marked resolution as the patient recovered. Fulminant hepatitis and acute renal failure could induce extensive edema in the cerebral white matter. Therefore, not all MRIabnormalities in the white matter after correction of hyponatremianecessarily reflect myelinolysis. (Internal Medicine 33: 360-362, 1994)

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Hepatic Encephalopathy

Cited by 136 publications

References 113 publications

Central Pontine Lesions Observed with MRI in Four Diabetic Patients

Central Pontine Lesions Observed with MRI in Four Diabetic Patients

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Reversible White Matter Lesions in a Patient with Fulminant Hepatitis and Acute Renal Failure.

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