hyperammonemia/oedeem

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Hyperammonemia-induced cytotoxic brain edema under osmotic opening of blood-brain barrier in dogs.

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Infusion of an ammonium acetate solution into dogs during mannitol-induced reversible opening of the blood-brain barrier (BBB) resulted in a marked rise in intracranial pressure with exclusion of Evans blue dye. This indicated cytotoxic brain edema. These findings suggest a role for hyperammonemia

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure.

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Taurine (Tau), an amino acid that abounds in brain, has been implicated in inhibitory neuromodulation and osmoregulation, the latter function being manifested by Tau release along with osmotically obligated water in response to brain tissue edema. A previous study (Hilgier and Olson: J. Neurochem.

The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema.

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Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. The underlying pathogenesis has

Brain expression of the water channels aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema.

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Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or

Intracranial Pressure Monitoring Demonstrates that Cerebral Edema Is Not Correlated to Hyperammonemia in a Child with Ornithine Transcarbamylase Deficiency.

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BACKGROUND Ornithine transcarbamylase deficiency (OTCD) is an inborn error of urea cycle resulting in increased plasma levels of ammonia and glutamine and cerebral edema. However, the underlying mechanism of brain cytotoxicity remains controversial. Our objective is to present an unusual acute

Venovenous hemodiafiltration and hypothermia for treatment of cerebral edema associated with hyperammonemia.

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We report a 50 hour old newborn with inborn urea cycle disorder and hyperammonia of 2320 umol/L. The pharmacological treatment of the first metabolic crisis was combined with venovenous hemodiafiltration and therapeutic hypothermia to rescue the patient from a life-threatening cerebral edema.

Brain edema and inflammatory activation in bile duct ligated rats with diet-induced hyperammonemia: A model of hepatic encephalopathy in cirrhosis.

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Studies of the pathogenesis of hepatic encephalopathy are hampered by the lack of a satisfactory animal model. We examined the neurological features of rats after bile duct ligation fed a hyperammonemic diet (BDL+HD). Six groups were studied: sham, sham pair-fed, hyperammonemic, bile duct ligation

Cerebral edema induced by hyperammonemia: a case report.

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[Cerebral edema with hyperammonemia in valpromide poisoning. Manifestation in an adult, of a partial deficit in type I carbamylphosphate synthetase].

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A case of cerebral oedema developed during an apparently common attempted suicide with valpromide is reported. The most conspicuous biochemical abnormality was hyperammonaemia. The oedema proved refractory to the standard medical treatment of intracranial hypertension, and decompressive craniectomy

Hyperammonemia, the Last Indication of High-Volume Hemodiafiltration in Adult and Children: A Structured Review.

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Ammonia is a neurotoxic molecule that causes cerebral edema and encephalopathy. Ammonia is either produced in excess or poorly purified during severe hepatic insufficiency, poisoning, infection, and inborn errors of metabolism. During continuous renal replacement therapy, ammonia clearance is

Fatal hyperammonemia after renal transplant due to late-onset urea cycle deficiency: a case report.

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We present a case of severe hyperammonemia with subsequent brain herniation in an adult man after renal transplantation. After successful surgery and an initially uneventful postoperative course, the patient developed significant mental status changes associated with seizure activity. His condition

A rare case of hyperammonemia complication of high-protein parenteral nutrition.

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Hyperammonemia is a metabolic derangement that can be potentially fatal. Primary hyperammonemia due to urea cycle enzyme deficiency is usually discovered in neonates but rarely can present in adulthood. Late-onset manifestations of urea cycle disorders can go unnoticed, until they become life

Late onset hyperornithinemia-hyperammonemia-homocitrullinuria syndrome - how web searching by the family solved unexplained unconsciousness: a case report.

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BACKGROUND Hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, a rare inherited urea cycle disorder, can remain undiagnosed for decades and suddenly turn into an acute life-threatening state. Adult presentation of hyperornithinemia-hyperammonemia-homocitrullinuria syndrome has rarely been

Lactate contributes to ammonia-mediated astroglial dysfunction during hyperammonemia.

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Even though ammonia is considered to underlie nervous system symptoms of dysfunction during hyperammonemia, lactate, which increases as a metabolic consequence of high ammonia levels, might also be a contributing factor. The data presented here show that NH4Cl (5 mM) mediates astroglial cell

Hyperammonemia, bane of the brain.

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Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the

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