1/11. Fatal child abuse by forced water intoxication.BACKGROUND: Although water intoxication leading to brain damage is common in children, fatal child abuse by forced water intoxication is virtually unknown. methods: During the prosecution of the homicide of an abused child by forced water intoxication, we reviewed all similar cases in the united states where the perpetrators were found guilty of homicide. In 3 children punished by forced water intoxication who died, we evaluated: the types of child abuse, clinical presentation, electrolytes, blood gases, autopsy findings, and the fate of the perpetrators. FINDINGS: Three children were forced to drink copious amounts of water (over 6 L). All had seizures, emesis, and coma, presenting to hospitals with hypoxemia (PO2 = 44 /- 8 mm Hg) and hyponatremia (plasma Na = 112 /- 2 mmol/L). Although all showed evidence of extensive physical abuse, the history of forced water intoxication was not revealed to medical personnel, thus none of the 3 children were treated for their hyponatremia. All 3 patients died and at autopsy had cerebral edema and aspiration pneumonia. The perpetrators of all three deaths by forced water intoxication were eventually tried and convicted. INTERPRETATION: Forced water intoxication is a new generally fatal syndrome of child abuse that occurs in children previously subjected to other types of physical abuse. patients present with coma, hyponatraemia, and hypoxemia of unknown etiology. If health providers were made aware of the association, the hyponatremia is potentially treatable.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/11. colchicine poisoning by accidental ingestion of meadow saffron (colchicum autumnale): pathological and medicolegal aspects.Although intoxications with colchicine, the alkaloid of colchicum autumnale (meadow saffron), are well known, in most cases the intoxications are evoked by oral or parenteral preparations traditionally used as medication against gout. The accidental ingestion of colchicum autumnale, on the other hand, is a rare event and has to our knowledge only twice been described in detail. We report a further case in which two persons confused this highly poisonous plant with wild garlic (allium ursinum), a popular spice in the Central European cuisine. While one person merely complained about a 3-day episode of nausea, vomiting and watery diarrhea, the second person died of multi-organ system derangements 48 h after the ingestion of the colchicum leaves. At autopsy hemorrhagic lung oedema, hypocellular bonemarrow, centrilobular fatty necrosis of the liver and necrosis of the proximal convoluted tubuli of the kidneys were observed. A colchicine concentration of 7.5 micrograms/ml was found in the bile whereas no substance was detected in the postmortem blood.- - - - - - - - - - ranking = 0.18181818181818keywords = intoxication (Clic here for more details about this article) |
3/11. Intramural hematoma of the esophagus: a complication of carbon tetrachloride intoxication with acute renal failure.Following a period of prolonged severe vomiting, an intramural esophageal hematoma could be demonstrated by endoscopy and by X-ray in a 21 year old patient with hepatic and renal failure after exposure to carbon tetrachloride. The hematoma resolved spontaneously. The intramural hematoma is thought to have developed from a microdissection of the esophageal wall in the presence of a hemorrhagic diathesis.- - - - - - - - - - ranking = 0.36363636363636keywords = intoxication (Clic here for more details about this article) |
4/11. ondansetron to prevent emesis following N-acetylcysteine for acetaminophen intoxication.We present a 17-year-old girl who developed persistent vomiting following acetaminophen overdose. Because of the amount of drug ingested (300 mg/kg acetaminophen) and the four-hour postingestion level (256 micrograms/ml), administration of N-acetylcysteine (NAC) was indicated. Emesis occurred immediately following the first three doses of NAC despite administering the drug by continuous nasogastric drip over one hour. Prior to the next attempt, ondansetron (0.15 mg/kg) was administered intravenously as an antiemetic. Thirty minutes following ondansetron, NAC was tolerated without further emesis. Although several antiemetics may have prevented further emesis, we chose ondansetron since, as a serotonin antagonist, it does not cause extrapyramidal side effects or sedation. In patients with potentially toxic drug ingestions, these side effects may be confused with or mask the adverse effects of the ingested drug, thereby interfering with the ongoing evaluation of the patient. Although not previously administered for this indication, ondansetron has several advantages over other antiemetic agents in the setting of an acute drug ingestion.- - - - - - - - - - ranking = 0.36363636363636keywords = intoxication (Clic here for more details about this article) |
5/11. A rare ingestion of the Black Locust tree.BACKGROUND: The Black Locust (robinia Pseudoacacia) tree contain toxalbumins, robin and phasin, that exert their toxic effects by inhibition of protein synthesis. Despite the potential dangers of Black Locust intoxication, reports of human toxicity after ingestion are rare. We report the first human intoxication of Black Locust bark in north america in over one hundred years. CASE REPORT: An eight-year-old male was brought to the emergency department 6 hours after chewing and expelling the Black Locust bark. He presented with emesis, which began approximately 2.5 hours after exposure. His vital signs were as follows: oral temperature, 97.5 degrees F; blood pressure, 128/75 mmHg; heart rate, 114 beats per minute; respiratory rate, 15 breaths per minute. Initial treatment included 4 mg i.v. ondansetron, which resolved the vomiting, one dose of activated charcoal, and intravenous fluids. He was then admitted to the intensive care unit (ICU) for observation of signs of toxicity. Laboratory findings were unremarkable except for a white blood cell of 18.4 K/uL and an elevated alkaline phosphatase of 183 U/L. The patient remained asymptomatic throughout his stay in the ICU and was discharged on the fifth day of admission with a normal white blood cell of 4.1 K/uL and an alkaline phosphatase of 251 U/L. CONCLUSION: patients with clinical toxicity following the ingestion of Black Locust are expected to do well with supportive care and observation.- - - - - - - - - - ranking = 0.18181818181818keywords = intoxication (Clic here for more details about this article) |
6/11. carbamazepine toxicity following Oxybutynin and dantrolene administration: a case report.OBJECTIVE: To report a case of carbamazepine toxicity following the administration of Oxybutynin and dantrolene. STUDY DESIGN: A case report. SETTING: The Spinal rehabilitation Department, Loewenstein Hospital, Raanana, israel. methods: A patient with C6D tetraplegia who sustained intoxication because of drug interaction is presented. She had been treated by carbamazepine 1000 mg/day for neuropathic pain for 2 years without clinical or laboratory signs of toxicity. After administration of Oxybutynin concomitantly with an increase in the dose of dantrolene, she presented the clinical symptoms and laboratory finding of carbamazepine intoxication. Trying to adjust the treatment to the patient's requirements, carbamazepine together with Oxybutynin and dantrolene was readministrated in lower doses. RESULTS: The combination of these drugs, even small doses, caused toxicity. Adding dantrolene and Oxybutynin elevated the blood level of carbamazepine, possibly by inhibition of cytochrome P450. CONCLUSION: A possible pharmacokinetic interaction between dantrolene and Oxybutynin should be borne in mind when considering carbamazepine medication for a patient with a spinal cord lesion.- - - - - - - - - - ranking = 0.18181818181818keywords = intoxication (Clic here for more details about this article) |
7/11. Acute renal failure associated with an accidental overdose of colchicine.CASE SUMMARY: A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis a, B, C and hiv viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l. DISCUSSION: The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.- - - - - - - - - - ranking = 0.27272727272727keywords = intoxication (Clic here for more details about this article) |
8/11. Interaction between carbamazepine and fluvoxamine.In 3 patients the addition of fluvoxamine to a constant dosage of carbamazepine (CZP) caused a substantial rise of plasma CZP accompanied by symptoms of intoxication. As this drug combination may occur increasingly in the future, this probably pharmacokinetic interaction is of practical relevance.- - - - - - - - - - ranking = 0.090909090909091keywords = intoxication (Clic here for more details about this article) |
9/11. iron poisoning.iron poisoning continues to be a major toxicologic problem, with major impact on the gastrointestinal and circulatory systems. Failure to recognize the severity of iron intoxication may result in an inappropriate level of intervention. By using estimates of the total body burden of iron, clinical symptoms, and the serum iron concentration, an appropriate decision can be made to initiate aggressive chelation therapy with deferoxamine. In severe intoxication, the use of intravenous deferoxamine is indicated, along with supportive care, with particular attention to maintaining the intravascular volume. Other important measures include correction of acidosis and disorders of coagulation and replacement of blood components when there is evidence of gastrointestinal hemorrhage. Under rare circumstances in which large numbers of iron tablets are present in the gastrointestinal tract, surgical removal may be indicated. In addition, measures such as hemodialysis and exchange transfusion should be reserved for those unusual poisonings in which more conservative therapy is unsuccessful. In rare cases of iron intoxication, late sequelae such as hepatic necrosis and gastrointestinal scarring with obstruction may occur. The prompt recognition and initiation of management of children with acute iron poisoning is the single most critical element in decreasing the morbidity and mortality associated with these products.- - - - - - - - - - ranking = 0.27272727272727keywords = intoxication (Clic here for more details about this article) |
10/11. delta-aminolevulinic acid dehydratase deficiency porphyria (ADP) with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a 69-year-old woman.delta-aminolevulinic acid dehydratase deficiency porphyria (ALAD porphyria, ADP) with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a 69-year-old woman is reported. The patient was admitted to our hospital complaining of slight cough with low-grade fever, and treated with piperacillin sodium, resulting in complete resolution of the symptoms, following a diagnosis of bronchopneumonia. Thereafter, however, she began to complain of vomiting, abdominal pain, facial numbness and paresis of the extremities with gait disturbance, and became comatose with hyponatremia (serum Na concentration 119 mEq/L) in a few days. Laboratory tests revealed an antidiuretic hormone (ADH) level of 13.5 pg/mL, plasma osmolality 218 mOsm/KgH2O, urinary osmolality 429 mOsm/KgH20, urinary Na concentration > 20 mEq/L, and no abnormalities of thyroid, adrenal or renal function. Neither edema nor dehydration was evident. These data indicated the presence of SIADH. No abnormalities suggestive of malignant or infectious diseases such as lung cancer, pneumonia and guillain-barre syndrome were evident from laboratory and roentgenographic findings. As the cause of SIADH, therefore, porphyria was suspected. Metabolites and activities of enzymes in the heme biosynthetic pathway were examined, and very low activity of delta-aminolevulinic acid dehydratase (ALA-D) (0.14 mumol PBG/mL RBC/h) was found. The patient was neither an alcoholic nor a heavy smoker, and she had no past history of heavy metal intoxication, photosensitivity or tyrosinemia. On the basis of these data and clinical features, she was diagnosed as having ADP. We consider this to be the first case of ADP reported in japan.- - - - - - - - - - ranking = 0.090909090909091keywords = intoxication (Clic here for more details about this article) |
| | Next -> |