Yoko Ihama

Characteristic features of injuries due to shark attacks: A review of 12 cases

Shark attacks on humans might not occur as often as is believed and the characteristic features of shark injuries on corpses have not been extensively reviewed. We describe the characteristic features of shark injuries on 12 corpses. The analysis of these injuries might reveal the motivation behind the attacks and/or the shark species involved in the attack. Gouge marks on the bones are evidence of a shark attack, even if the corpse is decomposed. Severance of the body part at the joints without a fracture was found to be a characteristic feature of shark injuries.

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.

Fatal propeller injuries: Three autopsy case reports

Most propeller injuries occur at water recreational facilities such as those with provision for water skiing, boat racing, skin and scuba diving. Propeller injuries resulting from nautical accidents can be fatal. The sharp blades of propellers rotating at high speeds cause multiple and serious injuries such as deep laceration, chop wounds, bone fractures and mutilation of extremities. We present the autopsy reports of three people who died after colliding with boat propellers.

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.

An autopsy case of commotio cordis from a motor scooter accident

A motor scooter carrying two 15-year-old boys collided with the back of an open, parked truck. The tailgate of the truck was down and in a horizontal position. At the autopsy of the driver, horizontal tramline bruises were found on the anterior chest, but the thoracic cage was intact. There was a transverse tear of the ascending aorta with adventitial hematoma, but significant bleeding was not found in the pericardial sac or the thoracic cavities. Therefore, it was obvious that cardiovascular collapse occurred immediately after the accident. Neither injuries nor diseases that would cause the instantaneous death were found on examination of the whole body. We determined that the driver died of commotio cordis due to blunt force to the anterior chest.

Temporal changes of the adrenal endocrine system in a restraint stressed mouse and possibility of postmortem indicators of prolonged psychological stress

We investigated temporal changes of adrenal endocrine systems through the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenomedullary (SA) axis in restraint stressed mice. Restraint stress for 1 day to 3 weeks caused a significant increase in serum levels of ACTH and glucocorticoids accompanied with an increase in adrenal weights, indicating activation of the HPA axis. Reflecting the overproduction of glucocorticoids, adrenal cholesterol content decreased. Moreover, adrenal gene expression involved in cholesterol supply, including scavenger receptor-class B type I, HMG-CoA reductase, and hormone-sensitive lipase, was increased over the same period. After 4 weeks stress, all of these changes returned to control levels. In contrast, adrenal gene expression of chromogranin A, which is cosecreted with catecholamine via the SA axis, was increased with 1 day to 2 weeks of stress, and decreased with 3-4 weeks of stress. Our results suggest that analyses of adrenal endocrine systems based on the combination of several markers examined here would be useful for not only proving prolonged psychological stress experience but also determining its duration.

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.

An autopsy case of suction injury

The right upper extremity of a 38-year-old man was entrapped in an underwater intake of a water duct of a dam reservoir, and he died despite being promptly rescued. His right upper extremity was swollen and exhibited purplish-red discolourations. The skin had numerous blisters and increased tension. Severe subcutaneous and muscle bleeding were observed in the right upper extremity. The circumference and volume of the right upper extremity were approximately 1.2 and 1.4 times, respectively, that the circumference and volume of the left upper extremity. The increase in weight of the right extremity was calculated to be approximately 2.1 kg; this finding indicates a severe decrease in the victims central blood volume. Furthermore, it is possible that much more than 2.1 kg of blood accumulated in the upper extremity upon exposure to vacuum pressure. We conclude that the victim died of circulatory collapse that was attributable to haemorrhage and re-distribution of blood as a result of vacuum pressure on the right upper extremity. Thus, we have examined the cause of death and the effects of vacuum pressure on the human body.

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.