Pre- and post-fire pollutant loads in an urban fringe watershed in Southern California.

Post-fire runoff has the potential to be a large source of contaminants to downstream areas. However, the magnitude of this effect in urban fringe watersheds adjacent to large sources of airborne contaminants is not well documented. The current study investigates the impacts of wildfire on stormwater contaminant loading from the upper Arroyo Seco watershed, burned in 2009. This watershed is adjacent to the Greater Los Angeles, CA, USA area and has not burned in over 60 years. Consequently, it acts as a sink for regional urban pollutants and presents an opportunity to study the impacts of wildfire. Pre- and post-fire storm samples were collected and analyzed for basic cations, trace metals, and total suspended solids. The loss of vegetation and changes in soil properties from the fire greatly increased the magnitude of storm runoff, resulting in sediment-laden floods carrying high concentrations of particulate-bound constituents. Post-fire concentrations and loads were up to three orders of magnitude greater than pre-fire values for many trace metals, including lead and cadmium. A shift was also observed in the timing of chemical delivery, where maximum suspended sediment, trace metal, and cation concentrations coincided with, rather than preceded, peak discharge in the post-fire runoff, amplifying the fire's impacts on mass loading. The results emphasize the importance of sediment delivery as a primary mechanism for post-fire contaminant transport and suggest that traditional management practices that focus on treating only the early portion of storm runoff may be less effective following wildfire. We also advocate that watersheds impacted by regional urban pollutants have the potential to pose significant risk for downstream communities and ecosystems after fire.

Sudden death from hyponatremia and hypokalemia in a woman with Gardner syndrome.

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.

Issues in child homicides: 11 cases.

For a variety of reasons, child homicides are the most difficult cases for forensic pathologists. For example, the events are usually not witnessed, accidental explanations are offered, often there is more than one carer spanning the period over which the injuries might have occurred and there can be conflicting opinions between the various medical specialities. Eleven cases of fatal child abuse are presented to illustrate and briefly discuss particular difficulties. Reference is also made to interaction with the legal process and parallel difficulties the law has with fatal child abuse.

Audit in forensic pathology.

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.

Hypotensive hemorrhagic necrosis in basal ganglia and brainstem.

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.

Phaeochromocytomas discovered during coronial autopsies in Sydney, Melbourne and Auckland.

BACKGROUND: The diagnosis of phaeochromocytoma can be difficult and previous autopsy studies have found that many of these tumours are not recognised during life. AIM: To determine the incidence of phaeochromocytoma during coronial autopsies and the characteristics of the individuals concerned. METHOD: Review of coronial autopsy records from Auckland (1981-97), Melbourne (1991-97) and Sydney (1991-97). RESULTS: Twenty-two patients were found giving an incidence of 0.05% (one tumour per 2031 autopsies) with similar figures in each centre. Thirteen of the patients were men, 12 were overweight (body mass index >25 kg/m2) and three of the seven Auckland patients were Maori. Fourteen of the tumours were left-sided, one was extra-adrenal and none had metastasised. The one patient with bilateral tumours had multiple endocrine neoplasia syndrome type 2 (MEN-2) which had not been recognised during life. The heart weight was increased in 95% of the patients. The tumour may have contributed to the patient's death in up to 50% of the cases, although the true significance of these lesions as a cause of death remains unclear. Three patients died soon after general anaesthetics had been given for unrelated reasons. CONCLUSIONS: Even though phaeochromocytomas are uncommon, we fail to diagnose a significant number of these tumours during life. Methods are needed to increase the detection of phaeochromocytoma and to distinguish functional and non-functional tumours.

Comparison of antiepileptic drug levels in sudden unexpected deaths in epilepsy with deaths from other causes.

PURPOSE: (a) To compare postmortem antiepileptic drug (AED) levels in patients with sudden unexpected death in epilepsy (SUDEP) with those in a control group of subjects with epilepsy. If SUDEP patients more frequently had undetectable or subtherapeutic AED levels, this would suggest that compliance with AED treatment is poorer in this group and that poor compliance is a risk factor for SUDEP. (b) To determine whether a particular AED was detected more commonly in the SUDEP group, suggesting that this AED is associated with a higher risk of SUDEP. METHODS: A retrospective study of coronial cases was performed. Postmortem AED levels in 44 SUDEP cases and 44 control cases were compared. The control group consisted of epileptics who died of causes other than epilepsy, including natural disease (e.g., ischemic heart disease, accidents, and suicide). The AEDs measured included carbamazepine (CBZ), phenytoin, (PHT), valproate (VPA), phenobarbitone (PB), lamotrigine (LTG), clonazepam (CZP), and clobazam (CLB). The number of SUDEP and control cases in which CBZ only was detected were compared, as were the number in which PHT only was detected. RESULTS: Compared with the controls, the SUDEP group showed no difference in the number with no detectable AEDs (13 vs. 11), the number with subtherapeutic AEDs (10 vs. 13), and the number with therapeutic levels (21 in both groups). CBZ only was detected in 11 SUDEPs and 11 controls, and PHT only in five SUDEPs and 10 controls. CONCLUSIONS: Our study suggests the SUDEP group were no less compliant with AED treatment than the control group. This study does not support the hypothesis that poor compliance with AED treatment is a risk factor for SUDEP. There was no evidence that PHT or CBZ is associated with a higher risk of SUDEP.

Nontraumatic clostridial myonecrosis.

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.

Adrenocortical insufficiency.

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.

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.

Postmortem extravasation of blood potentially simulating antemortem bruising.

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.

Cerebral air embolism due to disconnection of a central venous catheter.

A case of cerebral air embolism complicating disconnection of a central venous catheter is presented. In the context of increasing use of central venous catheterization this case highlights the risk of cerebral air embolism associated with the use of central venous catheters. In this case there was no patent foramen ovale and air must have passed from the venous to the cerebral circulation through physiologic shunts in the lung. Possible means of entry of air with central venous catheters, pathogenetic mechanisms relating to cerebral air embolism, treatment and preventative measures are also discussed.

Involvement of codeine in drug-related deaths.

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.