1/8. Fatal hypernatremia after using salt as an emetic--report of three autopsy cases.Although a plethora of reports on life-threatening complications of salt emesis has been published since the early 1960s, salt is still used to induce emesis in cases of intoxication in the clinical as well as in the domestic setting. We report three cases of fatal hypernatremia after salt was used as an emetic. All fatalities were subjected to medico-legal autopsy at the Institute of Legal medicine in Hamburg, germany. In all cases, symptoms of cerebral damage such as seizures, fever and somnolence developed within hours after salt ingestion. All individuals were admitted to hospital before their deaths. Here, severe hypernatremia (up to 245 mmol/l) was detected, and all patients died under the clinical picture of cerebral edema despite intensive medical treatment. At autopsy, unspecific signs of a central regulatory failure were present. histology revealed crenated red blood cells and few venous microthrombi in internal organs. Neuropathological investigations yielded no specific results but confirmed fatal cerebral edema and excluded other cerebral causes of death. Viewing the results of clinical and post-mortem investigations together, death could clearly be attributed to excessive salt intake in all cases.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/8. Interpretation of the urine osmolality: the role of ethanol and the rate of excretion of osmoles.One purpose of this report is to illustrate that calculating the rate of excretion of osmoles in the urine can be of value in the differential diagnosis of hypernatremia and polyuria. A second purpose is to illustrate a clinical example where the osmolality of the urine did not reflect the lack of action of ADH. A patient with ethanol intoxication seemed to have central diabetes insipidus on clinical grounds. However, the osmolality of the urine was 287 mosm/kg H2O, a value which made this diagnosis unlikely. Since the concentration of ethanol in plasma was 119 mmol/L, we suspected that the urine contained an appreciable quantity of alcohol; this might obscure the lack of action of ADH. A study was performed to document the quantitative relationship between the concentrations of ethanol in plasma and urine. The concentration of ethanol in the urine was approximately 1.4-fold greater than in plasma. Using this correction factor, the osmolality of the urine adjusted for ethanol in the patient was only 120 mosm/kg H2O, a value more consistent with the diagnosis of central diabetes insipidus.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
3/8. hypernatremia due to repeated doses of charcoal-sorbitol.Hypernatremic dehydration due to unreplaced stool water losses often complicates the use of the osmotic cathartic lactulose in the treatment of hepatic encephalopathy. sorbitol, another osmotic cathartic commonly used in the treatment of drug intoxications, has been reported in the pediatric literature to induce severe hypernatremia, but there is only a rare case report in an adult. We report a dramatic case of severe hypernatremia secondary to repetitive administration of activated charcoal-sorbitol suspension for the treatment of phenobarbital intoxication in an adult. Based on our experience with this case, several recommendations are provided regarding management of drug intoxications with charcoal-sorbitol suspension, including meticulous attention to fluid-electrolyte balance, type of replacement fluid, and dosing of the suspension.- - - - - - - - - - ranking = 3keywords = intoxication (Clic here for more details about this article) |
4/8. indomethacin treatment in a patient with lithium-induced polyuria.lithium intoxication causes polyuria, central nervous system manifestations, and ultimately stupor progressing to coma. Moreover, polyuria leading to hypernatraemia itself can progress to convulsions and coma. We present a patient with lithium intoxication who remained polyuric, hypernatraemic and somnolent despite normal serum lithium concentrations. After institution of indomethacin orally, polyuria and hypernatraemia disappeared and patient regained consciousness.- - - - - - - - - - ranking = 2keywords = intoxication (Clic here for more details about this article) |
5/8. Management of salt poisoning in an extremely low birth weight infant.We present the first reported case of severe salt poisoning in an extremely low birth weight neonate. The salt poisoning was managed with the careful use of intravenous fluids, insulin to manage the severe hyperglycemia, and furosemide to induce a saline diuresis. The hypertonicity was normalized slowly over 3 days by following the corrected serum sodium (Na) (serum Na 2.7 mEq for every 100 mg/dl of glucose over 100). No neurological damage was seen in our patient during the development of the hypertonicity or its correction. This suggests that the premature brain can develop osmoprotective molecules if hypertonicity develops slowly over 2-3 days. Slow correction is therefore recommended to avoid the development of water intoxication during correction. Despite the development of mild reversible renal failure, a large saline diuresis was induced with furosemide, thereby avoiding the need for dialysis in our patient. The only complication was the development of necrotizing enterocolitis, which has not been previously reported in association with salt poisoning.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
6/8. Hyperphosphatemic hypocalcemic coma caused by hypertonic sodium phosphate (fleet) enema intoxication.We describe an elderly woman with a deep hyperphosphatemic hypocalcemic coma, hypernatremia, hypokalemia, metabolic acidosis, pancytopenia and respiratory and circulatory failure secondary to phosphate intoxication following the overdose administration of hypertonic sodium phosphate enema. The causes of increased colonic retention and absorption and decreased renal excretion are discussed. We recommend the use of the safer and less toxic cathartic medications or at least a very cautions use of such enemas in anyone with renal failure.- - - - - - - - - - ranking = 5keywords = intoxication (Clic here for more details about this article) |
7/8. The acidosis of exogenous phosphate intoxication.BACKGROUND: Severe hyperphosphatemia resulting from the use of laxatives and enemas with high levels of phosphate has been the subject of many case reports. These have generally focused on the hypernatremia and hypocalcemia that develop and become life-threatening. Less attention has been paid to the metabolic acidosis of phosphate intoxication. methods: In-depth analysis of a case of severe hyperphosphatemia and review of the literature for cases with sufficient data to permit correlation between the phosphate concentration, acidosis, and anion gap. RESULTS: Marked metabolic acidosis with a large increase in the anion gap was present in our patient. The correlation between these parameters and the plasma phosphate concentration was highly significant. Despite a paucity of data in most case reports, we did uncover other cases of anion gap-positive metabolic acidosis in patients with hyperphosphatemia. CONCLUSIONS: Among high-risk patients, including the elderly and debilitated, the presence of metabolic acidosis, hypernatremia, an increased anion gap, and low plasma calcium levels or a prolonged QT interval on the electrocardiogram should raise suspicion of phosphate intoxication.- - - - - - - - - - ranking = 6keywords = intoxication (Clic here for more details about this article) |
8/8. A case of severe hyperammonemia and unconsciousness following sodium valproate intoxication.Although valproic acid has gradually gained its popularity in the treatment of various seizure disorders, overdose of valproate is not common. An 18-y-old man with a history of epilepsy controlled by sodium valproate and clonazepam attempted suicide with an ingestion of 45 g sodium valproate. He presented to our service with drowsiness and irritability. Extremely high serum ammonia (623 ug/dL) and elevated serum valproate concentration (575 ug/mL) were found on admission. Several metabolic abnormalities, including hypernatremia, hypocalcemia and metabolic acidosis, as well as, increased serum transaminase levels were also recorded. With supportive measures, he became clear 24 h later and was discharged 6 d after ingestion. Serial follow-up of his serum valproate and ammonia levels disclosed a close relationship between these 2 measurables. After acute overdose of valproic acid, patients usually present with mild and generally reversible depression of the central nervous system. However, impairment of liver function, hyperammonemia, fluid-electrolyte disturbances, coma, seizures, hypotension and even death may occur following valproate overdose. Symptomatic and supportive measures are the mainstay in the treatment of valproic acid overdose. With prompt diagnosis and early institution of treatment, a complete recovery should be anticipated.- - - - - - - - - - ranking = 4keywords = intoxication (Clic here for more details about this article) |