Fatal poisoning with blue vitriol

Cases of fatal poisoning with cupric compounds are relatively rare in everyday life and are not covered much in forensic literature. A case was encountered of fatal poisoning with a blue vitriol solution introduced into the uterine cavity in order to interrupt a pregnancy. A 39-year-old woman brought to the hospital by ambulance complained of pain in the lumbar region and profuse bloody genital discharge, which had appeared 3 days earlier. She believed she was 2 months pregnant and denied artificial interruption of the pregnancy. Upon examination, her condition was grave: a weak pulse of 80; blood pressure 100/60. The abdomen was soft, the liver and spleen not enlarged. Pasternak symptom was negative. The uterus was soft, painless and enlarged to 9 weeks of pregnancy. The uterine cervix was clean, the orifice closed. Discharge was profuse and bloody. The diagnosis was that she was 9 weeks pregnant and had a missed criminal abortion. Scraping out the uterus and corresponding therapy to control bleeding were ineffective. An operation was performed--extirpation of the uterus. However, despite the steps taken, the bleeding did not stop, and the patient's condition continued to worsen. 10 hours after being admitted to the hospital, she died. During forensic investigation, diffused, violet-colored cadaverous spots were discovered. Extensive subcutaneous hemorrhage was detected around the areas of injection. The skin covering was edematous; when pressed with a finger, areas of depression remained. There was about 250 ml of watery blood in the abdominal cavity. Internal organs were anemic. There were multiple subpleural, subepicardial, subcapsular, intraorgan and intramuscular micro- and macro-punctate hemorrhages; bleeding into the mucosa of the gastrointestinal tract and urinary tracts; and cerebral and pulmonary edema. Forensic histological examination showed acute circulatory disturbance with perivascular and peridiapedetic hemorrhage; concentrations of aggregated and hemolyzed erythrocytes in the small vessels and capillaries; cerebral, pulmonary and stromatic edema. In the kidneys there was coaugmentation of renal glomeruli; epithelial necrosis of part of the coiled ducts; lower epithelium in places had pigment grains; primarily in openings of straight ducts there were pigment cylinders; extreme plethora of the surrounding area, and infiltration from annular cells and polynuclears. Forensic chemical analysis showed 12.8 mg of copper; 6.6 mg in the uterus and 5.6 mg in the kidneys. From data obtained it can be concluded that the patient died from cupric compound poisoning, complicated by interruption of the pregnancy and uterine hemolytic hemorrhage. It was later established that during the month before being admitted to the hospital the patient introduced a solution of blue vitriol into the uterine cavity to interrupt the pregnancy.     

Fatal poisoning with sodium chloride

This is an account of accidental fatal poisoning of a psychiatric patient following the use of a saline emetic for suspected chlorpromazine poisoning.     

Fatal verapamil poisoning

A case of fatal verapamil poisoning is reported. The pathologic and toxicologic findings are discussed.     

Fatal cocaine poisoning

A case of lethal cocaine poisoning after parenteral application is described. The results of the quantitative gas chromatographic determination in blood, liver, urine, stomach contents and muscle are reported.     

Fatal bromethalin poisoning

Bromethalin is a neurotoxin found in some rodenticides. A delusional 21-year-old male presented to a hospital with altered mental status the day after ingesting a bromethalin-based rodenticide. He died 7 days after his self-reported exposure to c. 17 mg bromethalin (equivalent to 0.33 mg bromethalin/kg). His clinicopathologic course was characterized by altered mental status, obtundation, increased cerebrospinal fluid pressure, cerebral edema, death, and diffuse histologic vacuolization of the white matter in the central nervous system seen on microscopic examination at autopsy. The presence of a demethylated form of bromethalin in the patient's liver and brain was confirmed by gas chromatography with mass spectrometry. Clinical signs and lesions observed in this patient are similar to those seen in animals poisoned with bromethalin. This case illustrates the potential for bromethalin ingestion to result in fatal human poisoning.     

Fatal propane-butane poisoning

Two lethal poisonings by butane and propane are described, and the corresponding concentrations in the body fluids and organ tissues are evaluated. One case appeared to be an accident after deliberate inhalation for butane, one was a suicide. The mechanism of the inhalation could be reconstructed in both cases. The concentrations in the biological material agreed well with observations in similar cases.     

Fatal diltiazem poisoning

The diagnosis at postmortem examination and the results of the chemical analysis in a case of a diltiazem intoxication are presented. Two metabolites were identified as desacetyldiltiazem and N-desmethyldiltiazem.     

Fatal colchicine poisoning

In two cases, after i.v. injections of colchicine serum concentrations of 170 ng/ml and 240 ng/ml were found before death. Colchicine was extracted from serum with the aid of Extrelut extraction columns and analysed using HPLC. Urine was also analysed and the findings were confirmed by drawing a UV-curve for colchicine using the stop-flow method. In one case, colchicine was still detectable in urine 10 days after injection.     

Fatal outcome of poisoning with ethylene glycol

After an act of violence, a delinquent swallowed about 250 ml ethylene glycol (EG) - probably to commit suicide before being arrested. During an interrogation by the police he appeared to be inebriated. A blood sample taken at this time did not contain ethanol but 5.1 g/l EG, as revealed by the analytical results. Only after a second examination was he taken to an intensive care unit in a hospital in spite of signs of pronounced intoxication after 12 h at the first examination. The patient died 30 h after taking EG without being effectively treated. The correct diagnosis, initiated by information from the poison control center, was made too late. At autopsy, findings were indicative of stage II of EG poisoning with a body burden of still 40-60 g EG. The mean rate of degradation in the blood was approximately 0.15 g/l per hour.     

Fatal poisoning by vanadium

We report here a fatal intoxication case involving ammonium vanadate. A 24-year-old woman was admitted to the Emergency Department for abdominal pain, nausea, vomiting, multiple daily diarrheas, hypoglycaemia (0.2g/L) and severe acute renal failure with glomerular filtration rate estimated at 21 ml/min. This patient had taken an undetermined amount of ammonium vanadate 12h after ingesting. She died next morning in the context of respiratory distress despite intensive care and oxygen therapy. The autopsy revealed widespread asphyxia syndrome and erosive gastritis. Determination of vanadium concentration in blood was carried out by means of mass spectrometer (ICP-MS) using rhodium ((103)Rh) as the internal standard. The vanadium concentration was 6.22 mg/L, corresponding to 6000 times higher than normal concentration in the general population. The latency and the brutality of clinical picture degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory process.