Maki Fukasawa

A transnasal intracranial stab wound by a plastic-covered umbrella tip.

A 48-year-old man died from a transnasal intracranial stab wound caused by an umbrella. The track of the stab passed from the right nostril, through the sphenoid sinus, the left side of the sella turcica and anterior clinoid process, and finally reached the surface of the brain. The stab wound crossed the left internal carotid artery, causing an exsanguination and aspiration of blood into the airway, resulting in death. It is extremely rare that an umbrella tip used during a struggle would stab the nostril of the victim. Transnasal intracranial stab wounds can be overlooked and require sensitive handling.

Anaphylactic shock caused by sting of crown-of-thorns starfish (Acanthaster planci)

A 40s-year-old woman with previous history of injury due to contact with crown-of-thorns starfish, Acanthaster planci, was stung on the right middle finger. After immediately losing consciousness, she died 13 h after injury despite intensive medical treatment. Examination of the respiratory system revealed narrowing due to severe edema of the laryngopharynx, as well as alveolar hemorrhage, eosinophilic infiltration, and extensive neutrophil and eosinophil aggregation in the intravascular lumen of the lungs. Examination of the liver revealed severe diffuse hepatocellular necrosis and extremely high levels of liver transaminases, indicating severe liver damage. Based on these findings, we concluded that she had died from anaphylactic shock induced by circulation of crown-of-thorns starfish venom in the bloodstream. Injurious contact with the spine of the crown-of-thorns starfish can cause severe symptoms as well as systematic reactions, including anaphylaxis. To our knowledge, this is the first case of anaphylactic shock or death caused by human contact with the crown-of-thorns starfish reported in the English-language literature. Although rare, anaphylaxis due to injury by marine animals is potentially fatal. Saving lives requires providing education regarding prevention and enabling prompt response to possible anaphylaxis, including preparation of adrenaline for auto-injection.

Detection of imidacloprid in biological fluids in a case of fatal insecticide intoxication

Here, we describe a high-performance liquid chromatography/photodiode array detector method for the detection of imidacloprid in biological fluids in a case of suicide by ingestion of liquor mixed with Admire® Flowable insecticide (containing 20% imidacloprid). A plastic bottle containing a cloudy liquid (concentration of ethanol in the liquid was 150 mg/ml and that of imidacloprid was 50 mg/ml) was found near the decedent. The biological fluids collected at autopsy were prepared by deproteinization with acetonitrile. Zolpidem was used as an internal standard. The concentrations of imidacloprid in femoral blood and cerebrospinal fluid were 105 and 58.5 μg/ml, respectively. Ethanol was also detected in the samples, with concentrations of 1.0 mg/ml in femoral blood and 1.4 mg/ml in cerebrospinal fluid.

Morphologic investigation of injury caused by locally applied negative pressure in a rat model

Although some previous studies have reported patients who developed compartment syndrome or died because of locally applied negative pressure, no detailed investigation of pathologic changes caused by negative pressure-induced injury has been reported in the literature. The main purpose of this study was to examine the morphologic characteristics of injury caused by local negative pressure and correlate these with systemic changes. A total of 30 male Wister rats were used. Animals were randomly assigned to 6 groups. Negative pressure was applied to the right hindlimb of each animal in each group for periods of 0 (sham-operated), 30, 60, 90, 120, or 180 min using a vacuum pump. Macroscopic and microscopic changes induced by local negative pressure were already observed after 30 min and were exacerbated with time. The proportion of muscle degeneration was highest in the deep tissues, irrespective of exposure time. The observed increase in the weight of the injured hindlimb at 180 min was caused by an approximately 30% fluid shift to the hindlimb, demonstrating that the application of negative pressure to the hindlimb of rats can induce hypovolemic shock. We here reveal the morphologic changes induced by local negative pressure and discuss possible mechanisms of negative pressure-induced injury.

Investigation of an anatomically variant isolated bicuspid pulmonary valve: A case report

Introduction: We provide a discussion of the anatomical characteristics of the bicuspid pulmonary valve (BPV) in this paper. We performed an autopsy of an isolated BPV found in the heart of a deceased individual. The deceased was a man in his 60s and had no previous history of cardiovascular disease. The heart weighed 260 g and had mild right ventricular hypertrophy. The pulmonary valve had a fish-mouth-like shape that was convex to the pulmonary trunk and both cusps were thickened and hardened. The anterior and left semilunar cusps of the pulmonary valve were fused. Post-stenotic dilatation was noted. Conclusions : In comparing the present case with previous reports, we found that, in human BPVs, cusps are fused in at least 2 patterns.

An experimental study of postmortem decomposition of methomyl in blood

Methomyl (S-methyl-1-N-[(methylcarbamoyl)oxy]thioacetimidate) is a carbamate pesticide. It has been noted that in some cases of methomyl poisoning, methomyl is either not detected or detected only in low concentrations in the blood of the victims. However, in such cases, methomyl is detected at higher concentrations in the vitreous humor than in the blood. This indicates that methomyl in the blood is possibly decomposed after death. However, the reasons for this phenomenon have been unclear. We have previously reported that methomyl is decomposed to dimethyl disulfide (DMDS) in the livers and kidneys of pigs but not in their blood. In addition, in the field of forensic toxicology, it is known that some compounds are decomposed or produced by internal bacteria in biological samples after death. This indicates that there is a possibility that methomyl in blood may be decomposed by bacteria after death. The aim of this study was therefore to investigate whether methomyl in blood is decomposed by bacteria isolated from human stool. Our findings demonstrated that methomyl was decomposed in human stool homogenates, resulting in the generation of DMDS. In addition, it was observed that three bacterial species isolated from the stool homogenates, Bacillus cereus, Pseudomonas aeruginosa, and Bacillus sp., showed methomyl-decomposing activity. The results therefore indicated that one reason for the difficulty in detecting methomyl in postmortem blood from methomyl-poisoning victims is the decomposition of methomyl by internal bacteria such as B. cereus, P. aeruginosa, and Bacillus sp.

Acute puerperal uterine inversion

A gravida 3, para 2, 42-year-old woman was admitted to a hospital for induced labor at 38 weeks and 3 days gestation. Twelve hours after an intravenous infusion of prostaglandin E2 as an oxytocic agent, a healthy female baby weighing 3.41 kg was spontaneously delivered. Placental delivery was prolonged; therefore, an obstetrician manually removed the placenta 1 h after childbirth. Blood loss was estimated to be 700 ml at the time of placental delivery. Vaginal bleeding continued, and the patient’s blood pressure was noted to be 60/48 mmHg with a heart rate of 144 beats/min 30 min after the placental delivery. Although a vasopressor and volume expander fluid (Hespander ) were administered intravenously, the patient’s state of shock persisted. Blood transfusion was initiated 9 h after childbirth when the total blood loss exceeded 2,500 ml. Nevertheless, the patient gradually lost consciousness as vaginal bleeding persisted. Uterine inversion was detected by ultrasonography and the total blood loss was estimated to be 3,550 ml 12 h after childbirth. She was immediately transferred to an emergency department, but experienced cardiopulmonary arrest in the ambulance. The patient died of hemorrhagic shock 15 h after childbirth. The decedent was 170 cm tall and weighed 63 kg. At the medico-legal autopsy, there was very slight postmortem hypostasis on the back. Abdominal palpation revealed that the uterine fundus was approximately 5 cm below the umbilicus, but the crater-like depression of the fundus was not clear. The external genitalia had some edema from the vaginal birth, but there was no injury to the perineum or birth canal. A large number of blood clots were present in the vagina. Vaginal palpation revealed that the fundal endometrium was exposed through the cervix. External examination revealed no injuries except those from clinical procedures. There was 700 ml of reddish ascites but no bleeding in the abdominal and pelvic cavity. The uterine fundus had a crater-like depression, which was 9.5 cm in depth (Fig. 1). The bilateral fallopian tubes and right ovarian artery were caught in this depression. The removed uterus weighed 1,080 g. The cervix was extended by the inverted fundus, and the fundal endometrium was exposed widely through the cervix (Fig. 2). The uterine cavity had 730 ml of clots and had become narrow because of fundus inversion. The endometrium showed no sign of placental retention or injury. The heart weighed 350 g, and slight bleeding was noted on the outflow tract of the left ventricle. The left and right lungs weighed 960 and 1,030 g, respectively, and severe edema was seen in the bilateral lungs. Macroscopic and microscopic examination of the lungs did not reveal pulmonary thromboembolism or amniotic fluid embolism. We concluded that the patient died of puerperal bleeding caused by uterine inversion after vaginal childbirth.