腋臭手术中2%利多卡因局麻过量致死1例

某男 ,1 6岁 ,因患腋臭于某日在一乡镇卫生院行双侧腋臭手术。上午 8时 30分 ,医生先于右侧腋下注射2 %利多卡因 7支 (每支 5ｍｌ,1 0 0ｍｇ制剂 )后 ,切除毛囊区皮肤 ,止血缝合。 8时 5 5分患者诉头晕 ,但未引起手术者注意。继续于左侧腋下注射 2 %利多卡因 3支 ,9时 0 5分 ,在准备切除毛囊区皮肤时 ,患者突然抽搐 ,继而剧烈呕吐 ,吐出米汤等食糜样液体 ,量约 4 0 0ｍｌ,出现呼吸困难。术者立即停止手术 ,将患者侧卧 ,清除口腔呕吐物 ,症状无好转。此时患者呼吸极度困难 ,心音微弱。又给予人工呼吸、胸外心脏按摩、吸氧、插管、肌注药物等…     

腋臭手术中2%利多卡因局麻过量致死1例

某男,16岁,因患腋臭于某日在一乡镇卫生院行双侧腋臭手术.上午8 时30分,医生先于右侧腋下注射2%利多卡因7支(每支5ml,100mg制剂)后,切除毛囊区皮肤 ,止血缝合.8时55分患者诉头晕,但未引起手术者注意.继续于左侧腋下注射2%利多卡因3 支,9时05分,在准备切除毛囊区皮肤时,患者突然抽搐,继而剧烈呕吐,吐出米汤等食糜样液体,量约400ml,出现呼吸困难.术者立即停止手术,将患者侧卧,清除口腔呕吐物, 症状无好转.此时患者呼吸极度困难,心音微弱.又给予人工呼吸、胸外心脏按摩、吸氧、插管、肌注药物等抢救无效,于9时30分死亡.患者家属对死因提出疑问,引起医疗纠纷.     

An unusual fatal injury due to tyre burst: a case report

A 20 year-old male driver of a heavy duty crane, employed in an industry located in an industrial area on the outskirts of Delhi was fatally injured while repositioning an ill-fitted locking rim of a crane tyre (Fig. 1). The inner tube of the crane tyre had accidentally burst, dislodging the loose iron-locking rim, which hit the individual with a great force resulting in multiple injuries. He died on his way to the hospital.     

Death scene evaluation in a case of fatal accidental carbon monoxide toxicity

Exposure of humans to high concentrations of carbon monoxide can result in death, due to the formation of carboxyhaemoglobin (COHb), which impairs the oxygen carrying capacity of the haemoglobin. Carbon monoxide is responsible of a great number of accidental domestic poisonings and deaths throughout the world, particularly in homes that have faulty or poorly vented combustion appliances. A case is reported, in which a 21-year-old woman was found dead, due to carbon monoxide poisoning from a gas water heater, despite the puzzling evidence that the heater has been used for more than 10 years without any problem. An evaluation of the exposure to CO was performed, by measuiring the rate of production of CO from the heater, and using the Coburn-Forster-Kane equation to describe the kinetics of the poisoning process. The death was attributed to an accidental poisoning from carbon monoxide due to a sum of unfortunate circumstances.     

子宫内翻致死1例法医学鉴定分析

子宫内翻在妇产科临床中极为少见.因子宫内翻致死者罕见.笔者在实际工作中遇见一例,现报告如下:     

A fatal case of oleandrin poisoning

The study presents a case of fatal poisoning with oleander leaves in an adult diabetic male. After repeated vomiting, and gastrointestinal distress the patient was admitted at the hospital with cardiac symptoms 1h after the ingestion. Urine samples were assayed immunochemically and by GC-MS for drugs of abuse and for general toxicological screen. Blood was analyzed for alcohol and volatiles by static head space GC-MS. Blood and oleander leaves were analyzed by LC-MS/MS for oleandrin and related compounds, the main cardiac glycosides of Nerium oleander. Oleandrin was detected by LC-MS/MS in the blood sample at a concentration of approximately 10 ng/ml. Another cardiac glycoside with pseudo-molecular ion of m/z 577, a likely structural isomer of oleandrin, was also detected in the blood and oleander leaves. However, by using the response as a function of concentration for oleandrin, this cardiac glycoside was roughly estimated at a concentration of approximately 10 ng/ml in the deceased blood. This would give a total fatal blood concentration of cardiac glycosides of about approximately 20 ng/ml in the deceased blood.     

A fatal case involving proparacaine.

A 16-year-old female died soon after inhaling proparacaine. Analysis of the tissues revealed an amphoteric compound consistent with a hydrolysis product prepared in the laboratory by reacting proparacaine with HCl in the presence of heat.     

A case of fatal intoxication from metformin

A case of fatal intoxication from metformin is presented. The decedent was an obese 58-year-old-woman with type II diabetes, in whom severe lactic acidosis secondary to metformin accumulation was precipitated by acute renal failure. She had been on metformin 500 mg twice a day. Postmortem blood was deproteinated with acetonitrile, washed with dichloromethane, and the resulting supernatant injected into high-performance liquid chromatography system. Separation was performed on a analytical 125 x 4 mm i.d. RP-8 column. The wavelength was set at 235 nm. The mobile phase was acetonitrile (40%), sodium lauryl sulfate, and sodium dihydrogen phosphate adjusted to pH 5.1 (60%) at a flow rate of 1.0 mL/min. The concentration of metformin in postmortem blood was 77.3 microg/mL. The qualitative result was also confirmed by LC/APCI/MS/MS analysis.     

Two fatal cases of selenium toxicity

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.     

A fatal case of pure ethanol ingestion

An adult male was found dead in a car with two empty bottles (500 ml x 2) labeled dehydrated ethanol (>99.5%, v/v). At autopsy, extensive pancreatic necrosis with severe hemorrhage was observed. High concentrations of ethanol were detected in blood (8.14 mg/ml), urine (8.12 mg/ml) and tissue specimens. The cause of death was determined to be an acute alcohol intoxication caused by ingesting approximately 1l dehydrated ethanol.     

A fatal case of pepper poisoning.

An 8 month old infant died as the result of administration of a traditional remedy, given orally as an infusion of a red powder. The symptoms on admission were coughing with diarrhoea and vomiting. Analysis of the powder using high-performance liquid chromatography (HPLC) confirmed the suspicion of capsaicin. Pepper preparations, which are used as traditional medicines, are highly toxic and their use on infants should be discouraged.     

A fatal case of mercuric cyanide poisoning

A 57-year-old pharmacist was found dead 11 days after his disappearance. At the autopsy, samples of blood, urine, gastric content were obtained. Presence of ethanol, cyanide and mercury were detected in some samples. Cyanide and mercury were identified and quantified using high-performance liquid chromatography with diode array detector (HPLC) in fluorescence mode and ICP with mass selective detector (ICP-MS) respectively. Whole blood concentrations of ethanol was 1.72 g/L. Cyanide and mercury concentrations in whole blood were respectively 0.16 and 3.8 mg/L. Concentrations of cyanide (27 mg/L) and mercury (150 mg/L) in gastric contents prove a massive oral ingestion of mercuric cyanide or mercuric oxycyanide occurred. In this case report, the death was attributed to the combined toxicity of cyanide and mercury.     

Acute fatal poisoning cases due to furathiocarb ingestion.

Seven cases involving acute fatalities due to ingestion of furathiocarb, a carbamate insecticide, are presented. Furathiocarb was detected in the gastric contents using thin layer chromatography (TLC) and gas chromatography/mass spectrophotometry (GC/MS), and quantified in the blood using a gas chromatograph equipped with a nitrogen-phosphorus detector (NPD). The fatal levels of furathiocarb in the blood ranged from 0.1 to 21.6 micrograms/ml.     

A fatal case of oral ingestion of benzine

A young woman committed suicide by ingesting benzine. We report the findings obtained at autopsy and the chemical analyses of the gastric contents, blood, and tissues in this case. Fatal concentrations of n-hexane, benzene, toluene and m-, p-xylene were detected. Pulmonary edema and hemorrhage were caused by the primary effect of the chemicals or secondarily by respiratory depression, suffocation due to volatile fluid, or heart failure. Mild hemorrhage around arterioles and venules in the brain cortex suggest hyperpermeability of the vessels. The fragmentation and waviness of the cardiac myofibrils indicate the presence of hypercontraction and possibly arrhythmia.     

A fatal case of oral ingestion of toluene

A 51-year-old male ingested orally a large quantity of toluene and died about 30 min later. The presence of toluene in body fluids and tissues was confirmed by gas chromatography and gas chromatography/mass spectrometry. Tissue distribution of toluene showed that the liver detected the highest content of toluene (433.5 micrograms/g), except for the stomach contents, followed by pancreas (88.2 micrograms/g), brain (85.3 micrograms/g), heart (62.6 micrograms/g), blood (27.6 micrograms/g), fat (12.2 micrograms/g) and finally cerebrospinal fluid (11.1 micrograms/g).     

A fatal case of poisoning with cantharidin.

A case of fatal poisoning due to voluntary ingestion of cantharides powder for aphrodisiac purposes is reported. Clinical history, autopsy and analytical findings are described. Blood and urine samples collected during the 30 h of survival, as well as the cantharides product, were analyzed by gas chromatography-mass spectrometry. On the basis of the percentage of the active principle measured in the powder, an ingested dose of 26-45 mg of cantharidin could be estimated.