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Deaths associated with parachuting are very uncommon. However, these deaths do tend to be "high profile" in the traditional and social media. When forensic pathologists examine the deceased after a fatal parachuting incident, the anatomical cause of death is usually not in question. For most forensic pathologists, it is usually the case that we will have very limited knowledge of parachuting equipment or the mechanics of a typical successful parachute jump. As such, the investigation of the death should involve a multidisciplinary approach with an appropriate expert providing the formal forensic examination of the parachuting equipment. We have endeavored to describe, in simple terms, the usual components of a typical parachute rig, a précis of the sequence of events in a routine skydive and BASE jump, and the various types of malfunctions that may occur. Last, we present a case report of a BASE jump fatality to illustrate how an expert examination of the BASE jumper's gear aided the medicolegal investigation of the death with some important aspects in the forensic examination of the jumper's equipment.

Postmortem computed tomography (CT) scanning is a routine examination in the medicolegal death investigation of every deceased person admitted to the Victorian Institute of Forensic Medicine. Pulmonary CT angiography is a standard clinical investigation for suspected pulmonary thromboembolism. To the best of our knowledge, a study of postmortem CT pulmonary angiography has not been previously reported in the English-speaking forensic literature. We present our findings on 13 cases of suspected massive pulmonary thromboembolism where forensic pathologists assessed postmortem CT pulmonary angiography, which were then correlated with conventional postmortem examinations.

We present a case of smothering of a 2-year-old male infant by his schizophrenic mother who was having a psychotic episode. In addition to the initial autopsy findings of conjunctival petechial hemorrhages, facial linear abrasions and bruises, and mucosal abrasions and bruises, expert odontologic examination revealed indentations of the cusps of central incisors and molars, providing additional evidence of smothering. The postmortem and toxicological examination revealed features of forced quetiapine administration. The case presented is the first case of forced administration of quetiapine described. Our case also highlights the value of expert forensic odontological examination.

The authors present the case of a 39-year-old woman with Gardner syndrome who died from marked hyponatremia and hypokalemia. Gardner syndrome is a rare variant of the familial adenomatous polyposis syndrome in which the affected individual develops thousands of polyps within the gastrointestinal tract, with a 100% risk of eventual malignant change. Individuals with Gardner syndrome also develop a variety of extra gastrointestinal abnormalities. In the case presented, a woman with a clinical history of Gardner syndrome who had previously undergone a total colectomy with ileorectal anastomosis presented to the hospital with a recent history of sore throat, fever, diarrhea, and abdominal pain. The symptoms were considered clinically to be due to a viral gastroenteritis. She was admitted to the hospital, where she had episodes of collapse believed to be vasovagal in origin. She suffered a cardiorespiratory arrest and died 24 hours after admission. After her death, electrolyte estimation performed on blood taken shortly before death revealed severe hyponatremia and hypokalemia. Postmortem examination showed the gastric mucosa to be virtually covered by innumerable adenomatous and hyperplastic polyps. Fewer polyps were seen within the small bowel. There was no evidence of malignancy. The features were consistent with Gardner syndrome. Hyponatremia and hypokalemia have been described in patients with villous adenomas and in familial adenomatous polyposis syndromes associated with numerous colonic polyps. The cause of death in this case was considered to be hyponatremia and hypokalemia associated with florid gastric polyps in a woman with Gardner syndrome. Viral gastroenteritis contributed to the death by causing further electrolyte depletion. To the best of the authors' knowledge, death in Gardner syndrome has not been described as attributable to such metabolic disturbance, in particular in those who have only gastric, small bowel, and rectal polyps remaining after total colectomy.

Hypotensive hemorrhagic necrosis of the basal ganglia and brainstem has only occasionally been described. Three such cases are reported. Cardiac arrest had occurred in all cases, and it took at least 1 hour to restore adequate circulation. The patients remained comatose for 2 days to 2 weeks until death. Persistent hypotension causing ischemia in the distribution of deep perforating arteries is considered to have been the key underlying mechanism. Hemorrhage is thought to have been caused by extravasation of red blood cells through damaged blood vessels.

Autopsy numbers in Australian hospitals have declined markedly during the past decade despite evidence of a relatively static rate of demonstrable clinical misdiagnosis during this time. The reason for this decrease in autopsy numbers is multifactorial and may include a general lack of clinical and pathologic interest in the autopsy with a possible decline in autopsy standard, a lack of clinicopathologic correlation after autopsies, and an increased emphasis on surgical biopsy reporting within hospital pathology departments. Although forensic autopsies are currently maintaining their numbers, it is incumbent on forensic pathologists to demonstrate the wealth of important information a carefully performed postmortem examination can reveal. To this end, the Pathology Division of the Victorian Institute of Forensic Medicine has instituted a program of minimum standards in varied types of coroner cases and commenced a system of internal and external audit. The minimum standard for a routine, sudden, presumed natural death is presented and the audit system is discussed.

We describe three cases of nontraumatic clostridial myonecrosis seen at the Victorian Institute of Forensic Medicine. Nontraumatic clostridial myonecrosis is an uncommon and often fatal condition that requires immediate institution of appropriate medical and surgical therapy. It is most commonly caused by Clostridium perfringens and Clostridium septicum and is associated with gastrointestinal and hematologic malignancies, diabetes mellitus, and peripheral vascular disease. The clinical features include a rapidly evolving acute illness with severe pain, marked tachycardia, and brawny discoloration of the skin with bullae formation and crepitus, followed by hypotension and acute renal failure. Features at autopsy include reddish brown skin discoloration with bullae formation and necrotic skeletal muscle. Radiographs may be of use prior to the postmortem in detecting gas within the soft tissues. Gram stain and microbiologic culture are important in establishing a definitive diagnosis; although the major factors in suggesting the diagnosis are the recognition of the typical clinical history and macroscopic autopsy findings.

Primary adrenocortical insufficiency is a rare disease which may present with protean clinical symptoms and signs. At one end of the spectrum is the patient with a long clinical history with marked pigmentation and documented episodes of crises which may follow relatively minor viral illnesses. The other extreme is illustrated by patients with a rapid deterioration in health culminating in unexpected or unexplained death. In the latter instances, the forensic pathologist may well be involved, and the case will present a significant challenge to diagnosis. We report 5 cases of primary and secondary adrenocortical insufficiency seen at the Victorian Institute of Forensic Medicine in 1 year. One adult man presented as a case of sudden unexplained death. In 2 cases, the diagnosis of adrenocortical insufficiency was raised following postmortem examination and confirmed by the treating physician following further consultation. In the remaining 2 cases, the diagnosis was known prior to postmortem examination and the diagnosis confirmed.

Vertebral artery trauma is not commonly seen by forensic pathologists. The experience of vertebral artery trauma at the Victorian Institute of Forensic Medicine (30 cases) is summarized and reviewed in the light of the literature. Causes of vertebral artery trauma are discussed. In case 1, the history and timing of the injury raise the question as to whether the vertebral artery dissection occurred before the episode of trauma, that is, was spontaneous or resulted from trauma. Moreover, underlying vertebral artery disease was present, raising the question as to how much trauma was needed to cause vertebral artery dissection. In case 2, despite the history of head/neck trauma, a neurosurgeon considered the subarachnoid hemorrhage was spontaneous, due most likely to ruptured saccular aneurysm or arteriovenous malformation. In case 3, the vertebral artery rupture was not diagnosed in the setting of multiple injuries. Case 4 is an example of prolonged survival with delayed onset of symptoms following vertebral artery trauma. Case 5 is an example of the not uncommon scenario of homicidal vertebral artery trauma accounting for basal subarachnoid hemorrhage, rapid collapse and death. Cases 1 and 4 indicate that relatively normal activity may be possible following vertebral artery trauma in some cases (at least for a time). Cases 1 and 4 are also examples of intracranial vertebral artery dissection.

A case of florid postmortem extravasation of blood, potentially simulating antemortem bruising, is presented. A 98-year-old woman died in hospital, the cause of death being certified as congestive cardiac failure. After burial, it was apparent that the grave had been disturbed by crowbars and shovels. Exhumation was performed and autopsy revealed considerable apparent facial bruising as well as lacerations and fractures. There was no documentation by the medical or nursing staff of any injuries to the deceased preceding death. There was also no documentation of injury by the funeral directors. Subsequently, two men admitted to removing the body from the grave and mutilating it. Thus, what was apparently facial bruising was, in fact, postmortem extravasation of blood simulating antemortem bruising. The degree of extravasation was considered to be related to the severity of the injuries, loose subcutaneous tissues of the head and neck, and dependent position of the body upon return to the grave. This case demonstrates the degree of postmortem extravasation of blood that may occur in particular circumstances and may simulate antemortem bruising. In other circumstances, the postmortem extravasation of blood may well have led investigators to pursue inquiries regarding homicide.

The incidence and role of codeine in drug-related deaths in Victoria was investigated over a 5-year period. There were a total of 107 cases involving codeine, representing 8.8% of all drug-related deaths in this period in Victoria. There were only six fatalities in which codeine was considered the major poison. The mean (+/- SD) concentration of codeine in femoral blood was 4.0 +/- 2.3 mg/L (range, 2.1-8.0 mg/L). The mean concentration of free codeine was 1.3 +/- 0.9 mg/L (range, 0.4-2.8 mg/L). The remaining 101 cases involved a combination of codeine and other drugs. The mean total codeine blood concentration was 1.8 +/- 3.3 mg/L (range, 0.04-26 mg/L), which was significantly lower than in those cases where codeine was the major poison (p < 0.002). The mean concentration of free codeine was 0.82 +/- 4.9 mg/L (range, 0.02-9.0 mg/L), which was not significantly different (p > 0.05) from the six codeine-only cases. The most common drugs found in this group, other than codeine, were acetaminophen (62%), diazepam (46%), salicylate (20%), and ethanol (25%). The association of other psychoactive drugs in these deaths made the contribution of codeine difficult to assess. Free codeine concentrations > 0.4 mg/L and total codeine concentrations > 2.0 mg/L may be sufficient to cause death in the absence of any other contributing factors.