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In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.
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PMID:[Electrolyte metabolism and emergency]. 688 72

We treated 13 adult patients with acute leukemia or chronic myelocytic leukemia (CML) in blast phase using succinylated Acinetobacter glutaminase-asparaginase (SAGA) administered on a daily dose schedule. SAGA reduced the peripheral blast count in two patients with acute lymphoblastic leukemia and two with blastic CML; however, no patient achieved either complete or partial remission. Marked central nervous system toxic effects (encephalopathy and coma) were observed, limiting treatment in patients whose disease appeared responsive; this effect finally prompted early discontinuance of the trial. Other toxic effects observed included nausea, hyperglycemia, and respiratory alkalosis. Hypersensitivity reactions to the enzyme were not seen. Pharmacologic analyses showed that prolonged blood glutamine depletion was achieved only by daily enzyme administration; however, we noted the importance of performing amino acid analysis on blood which was deproteinized immediately following phlebotomy. Our results demonstrate excessive central nervous system toxicity when glutaminase-asparaginase is administered on a daily schedule. Because of this effect, we propose that future trials of similar enzymes be limited to short courses of enzyme therapy, possibly with the addition of antimetabolites or amino acid analogs, which could enhance the antitumor effect without increasing toxicity.
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PMID:Clinical evaluation of succinylated Acinetobacter glutaminase-asparaginase in adult leukemia. 704 29

50% of hospitalized medical emergency cases are cardiological and respiratory emergencies. Myocardial infarction, cardiogenic shock, ventricular arrhythmias and left ventricular failure often cause sudden death occurring within 1 or 2 hours. Therefore immediate management is necessary already in the prehospital phase of cardiovascular events. This does also apply for acute respiratory failure due to obstructive ventilatory disorders. Acute exacerbations of chronic obstructive pulmonary disease frequently are masked and may be misinterpreted as encephalopathy or alcohol withdrawal syndrome. Sedation may be dangerous. Also neuroglucopenic syndrome and hyperosmolar coma are occasionally interpreted wrongly. Thyrotoxic crisis, adrenal crisis and hypercalcemia are characterized by lethargy, mental disturbance and weakness, by dehydration, myopathy, nausea, constipation, diarrhea or tenesms or arrhythmias. In this situation of varied symptoms the most important action is to think of endocrine emergency, which may have multiple etiologies.
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PMID:[Cardiovascular emergencies--endocrine and metabolic crises. Practical hints for the physician in emergency service]. 711 36

Succinylated Acinetobacter glutaminase-asparaginase (SAGA) has broader antitumor activity than Escherichia coli L-asparaginase in experimental systems; moreover, drug resistance does not develop in tumor cell lines initially sensitive to this enzyme. We have investigated the pharmacology and toxicology of SAGA after both single-dose and serial daily dose injections in 20 adult patients. Glutaminase activity in plasma after i.v. injection of single doses did not follow simple first-order kinetics (half-life during the initial 24 hr was 21 +/- 9 hr. A linear relation was observed between increasing doses of SAGA and resultant levels of plasma enzyme activity and blood glutamate. Assay of whole blood which had been deproteinized immediately following phlebotomy showed that single doses of SAGA lowered glutamine only transiently to nondetectable levels; serial daily doses were required to achieve and maintain continuous glutamine depletion. Reversible depression of the central nervous system, ranging from encephalopathy to coma, occurred in a dose-related manner and was dose limiting. Other prominent reactions included respiratory alkalosis, hyperglycemia, nausea, and vomiting. Transient antitumor effects were noted in two patients with solid tumors and in two patients with leukemia. SAGA causes considerable neurotoxicity in adults which requires close patient monitoring. Phase II studies in leukemic patients are in progress.
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PMID:Phase I evaluation of succinylated Acinetobacter glutaminase-asparaginase in adults. 743 89

Salicylate poisoning remains a major clinical hazard, usually resulting from accidental ingestions in preschool children, suicidal overdoses in adults and teenagers, and therapeutically acquired intoxication in all ages. Alkalemia or acidemia, alkaluria or aciduria, hypoglycemia or hyperglycemia, and water and electrolyte imbalances may occur; nausea, vomiting, tinnitus, hyperpnea, hyperpyrexia, disorientation, coma, and/or convulsions are common. With chronic, therapeutically induced salicylism, these symptoms may be mistaken for symptoms resulting from the illness for which the salicylates were administered. For acute ingestions, the magnitude of the poisoning is clearly dose related. Blood level determinations are good prognostic indicators for acute ingestions but are of limited value in chronic, therapeutically induced salicylism. Fluid and electrolyte management is the mainstay of therapy. Diuresis, hemodialysis, and hemoperfusion are effective, but the latter two rarely are necessary.
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PMID:Acute and chronic effects of aspirin toxicity and their treatment. 746 27

Medical directors of North American hyperbaric oxygen (HBO) facilities were surveyed to assess selection criteria applied for treatment of acute carbon monoxide (CO) poisoning within the hyperbaric medicine community. Responses were received from 85% of the 208 facilities in the United States and Canada. Among responders, 89 monoplace and 58 multiplace chamber facilities treat acute CO poisoning, managing a total of 2,636 patients in 1992. A significant majority of facilities treat CO-exposed patients with coma (98%), transient loss of consciousness (LOC) (77%), ischemic changes on electrocardiogram (91%), focal neurologic deficits (94%), or abnormal psychometric testing (91%), regardless of carboxyhemoglobin (COHb) level. Although 92% would use HBO for a patient presenting with headache, nausea, and COHb 40%, only 62% of facilities utilize a specified minimum COHb level as the sole criterion for HBO therapy of an asymptomatic patient. When COHb is used as an independent criterion to determine HBO treatment, the level utilized varies widely between institutions. Half of responding facilities place limits on the delay to treatment for patients with only transient LOC. Time limits are applied less often in cases with persistent neurologic deficits. While variability exists, majority opinions can be derived for many patient selection criteria regarding the use of HBO in acute CO poisoning.
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PMID:Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. 777 95

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46

1. Seven adult cases of deliberate oral exposure to 'Savlon' liquid (chlorhexidine gluconate 0.3%, cetrimide 3%) are presented. 2. In six patients, the symptoms were relatively mild including nausea, vomiting, sore throat and abdominal pain. 3. One patient who had concomitantly taken 'Dettol' liquid was comatose and hypotensive at presentation and was complicated by aspiration pneumonia and adult respiratory distress syndrome (ARDS). She was ventilated for a total of 10 days and was hospitalised for 5 weeks. 4. The data from this study suggest that symptoms associated with Savlon poisoning are usually mild. When aspirated, Savlon together with 'Dettol' liquid can cause ARDS.
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PMID:Poisoning due to Savlon (cetrimide) liquid. 782 85

We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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PMID:Serotonin syndrome. 785 15

Since our last report on valproate (VPA)-related hepatotoxicity in 1988, 8 other children have died of VPA-associated liver failure in Germany and Switzerland. We compared the clinical course of these children with that of 6 children with a reversible outcome of severe hepatotoxicity related to VPA. Thirty-five percent of patients with fatal liver failure were normally developed, 23.5% were receiving VPA monotherapy, and 35.3% were aged < or = 2 years. The initial clinical symptoms of VPA-related hepatotoxicity were nausea, vomiting, apathy or coma, and increasing seizures in more than 50% of patients, in combination with febrile infections at onset of symptoms. As compared with the series of German patients reported in 1988, one third of the fatalities occurred after the first 6 months of therapy as compared with 6% in the 1988 series. Clinical symptoms and laboratory findings were the same in patients with reversible and with fatal outcome. Early or immediate withdrawal of VPA after the first signs of VPA-associated hepatotoxicity may be responsible for the increased number of children who recovered after VPA-related severe liver failure. The pathogenesis of liver failure during VPA treatment remains unknown; metabolic defects and cofactors such as polypharmacy or infections have become increasingly likely to contribute by depleting intracellular CoA. Worldwide, 132 patients have died of VPA-associated liver failure and/or pancreatitis. Because a group at risk for fatalities with VPA cannot be defined precisely, patients treated with VPA and their families must be made well aware of the clinical symptoms of hepatotoxicity such as apathy, vomiting, or increased seizure frequency, especially in the presence of febrile infections. Laboratory tests and clinical controls during the first 6 months of therapy should not be neglected.
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PMID:Severe hepatotoxicity during valproate therapy: an update and report of eight new fatalities. 792 43


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