Roger W. Byard

A Review of the Potential Forensic Significance of Traditional Herbal Medicines

Abstract:  Traditional herbal substances may contain highly toxic chemicals and heavy metals, in addition to naturally occurring organic toxins. These substances may cause illness, exacerbate pre‐existing ill health or result in death, particularly if taken in excess or in an unusual manner (e.g., injected rather than ingested). Lack of regulation of the content and quality of herbal medicines may result in contamination and adulteration with prescription medications. As there may be no history of the specific use of these products their contribution to death may not be fully appreciated during a standard autopsy. Even when their existence is known or suspected, it may be difficult to identify these substances on standard toxicologic screening. Herbal medicines may also be responsible for a range of symptoms and signs that may confuse the clinical presentation of cases. Given these issues the role of herbal medicines in forensic practice needs to be more clearly defined as deaths may be occurring where herbal medicines have made a significant, but as‐yet unrecognized, contribution.

Esophageal Causes of Sudden and Unexpected Death

ABSTRACT: Gastrointestinal conditions are uncommon causes of sudden and/or unexpected death as compared to cardiovascular diseases, motor vehicle trauma, or suicide, and may involve an array of fatal mechanisms. Lethal esophageal conditions are encountered even less often, the manifestations of which include acute upper airway occlusion from tumors or foreign material, intraluminal hemorrhage from vascular abnormalities, or perforation with fistula formation resulting in hemorrhage and sepsis. When encountered at autopsy, a particular condition may also be a manifestation of a disease that does not primarily involve the esophagus. For this reason, a detailed autopsy investigation is required for evidence of systemic or remote disease when lesions are found within the esophagus. In this report, possible life‐threatening esophageal conditions are reviewed with a description of lethal mechanisms, mention of rare associated diseases, and comment on difficulties that may arise at autopsy in the evaluation of such cases.

The association between body mass index and pulmonary thromboembolism in an autopsy population.

Abstract:  To evaluate the association between obesity and pulmonary thromboembolism (PTE) in a forensic context, 160 autopsy cases of fatal PTE were compared with age‐ and gender‐matched controls. The mean age of cases was 66 years (range 26–98 years; M/F 74:86). The mean body mass index (BMI) of cases with PTE was 30.88 (range 14.95–79.51), which was significantly higher than in the controls (mean BMI = 25.33; range 12.49–61.84) (p < 0.0001). Comparing the group with PTE with controls showed that five (3.1%) compared to 20 (12.5%) were underweight, 39 (24.4%) compared to 67 (41.88%) were of normal weight, 49 (30.63%) compared to 43 (26.88%) were overweight, 43 (26.88%) compared to 24 (15%) were obese, and 24 (15.0%) compared to six (3.75%) were morbidly obese. In each category of above‐normal BMIs, there were significantly greater numbers in the groups with PTE: overweight (p < 0.01), obese (p < 0.001), and morbidly obese (p < 0.0001).

Vitreous Humor Sodium Levels in Immersion Deaths

Abstract:  To determine whether vitreous humor sodium levels might be of use in evaluating deaths associated with immersion, samples of vitreous humor were prospectively evaluated at autopsy over a 4‐year period from 2006 to 2009. There were 19 cases of saltwater immersion (age range 9–76 years; mean age 44 years; M:F, 2.8:1) and 16 freshwater immersions (age range 2–81 years; mean age 27 years; M:F, 2.2:1). In the group of saltwater drownings, vitreous humor sodium levels were elevated, ranging from 145 to 184 mM (mean = 160.2 ± 9.9 mM), and in the cases of freshwater drowning, the levels were reduced, ranging from 73 to 148 mM (mean = 129.8 ± 17 mM; p < 0.0001). Alterations in electrolyte levels may have been because of hemoconcentration or dilution from electrolyte fluxes in the lungs, or from passive diffusion during immersion. This study has demonstrated that vitreous sodium level is an easily performed test that may be a useful adjunct to the investigation of possible immersion deaths.

Basal Renal Tubular Epithelial Cell Vacuolization and Alcoholic Ketoacidosis

Abstract:  Subnuclear renal tubular epithelial cell vacuolization is a marker for diabetic ketoacidosis. Whether it is because of hyperglycemia or of ketoacidosis is unclear. To examine the effect of ketoacidosis on renal cells in isolation, five cases of lethal alcoholic ketoacidosis without hyperglycemia were examined (vitreous humor β‐hydroxybutyrate: 6.42–8.75 mM, mean 7.66 mM; and glucose: 0.1–4.2 mM, mean 1.46 mM). Microscopic examination of the kidneys revealed basal vacuoles in three cases (60%). Seven control cases with acute alcohol toxicity without ketoacidosis (blood alcohol: 0.18–0.43%, mean 0.31%; and β‐hydroxybutyrate: 0.12–0.42 mM, mean 0.21 mM) did not have these changes. In this study, basal epithelial vacuolization was found only in cases with significant ketoacidosis. Although the numbers are small, the finding of basal renal tubular epithelial vacuolization in normoglycemic cases with elevated β‐hydroxybutyrate levels provide further evidence that disordered lipid metabolism may be involved in the pathogenesis of this phenomenon.

Further investigations into the speed of cerebral swelling following blunt cranial trauma.

Abstract:  An anesthetized sheep model of traumatic brain injury (TBI) has been developed to assess early changes in intracranial pressure (ICP) following closed head injury. Immediately after TBI, a transient (<10 min) hypertensive response occurred, followed by significant and prolonged systemic hypotension. ICP demonstrated a biphasic response, being seven times baseline values of 8 ± 2 mm Hg 10 min after injury, decreasing to 25 ± 2 mm Hg by 30 min, and then increasing to values exceeding 30 mm Hg by 4 h postinjury. ICP was always significantly higher than baseline values, which combined with hypotension, reduced cerebral perfusion pressure to less than 60% of normal. This early and sustained increase in ICP after craniocerebral trauma acutely alters cerebral perfusion pressure and brain oxygenation and provides a potential pathophysiological explanation for immediate clinical manifestations in humans following significant TBI.

Lower Extremity Deep Venous Thrombosis with Fatal Pulmonary Thromboembolism Caused by Benign Pelvic Space‐Occupying Lesions—An Overview

Abstract:  Venous stasis predisposes to thrombosis. One hundred and sixty cases of fatal pulmonary thromboembolism were reviewed to determine how many cases had deep venous thromboses associated with venous blood flow reduction caused by external pressure from benign pelvic masses. Three cases were identified, representing 2% of cases overall (3/160): a 44‐year‐old woman with a large uterine leiomyoma (1048 g); a 74‐year‐old man with prostatomegaly and bladder distension (containing 1 L of urine); and a 70‐year‐old man with prostatomegaly and bladder distension (containing 3 L of urine). Although a rare cause of fatal deep venous thrombosis and pulmonary thromboembolism, space‐occupying pelvic lesions can lead to extrinsic pressure on adjacent veins reducing blood flow and causing stasis and thrombosis. Individuals with large pelvic masses may, therefore, be at increased risk of pulmonary thromboembolism from deep venous thrombosis, particularly in the presence of concurrent risk factors such as immobility, thrombophilias, malignancy, and significant cardiopulmonary disease.

Letter to the Editor—Quality Assurance in Disaster Victim Identification (DVI) Exercises

Disaster victim identification (DVI) exercises involve the coordinated identification of human remains following a mass disaster. The number of victims involved can vary from under 10 in a light aircraft crash to thousands, as in the World Trade Center attack of 2001. Bodies may be intact or fragmented, fresh or putrefied, and there are a number of issues that arise in terms of jurisdiction, recording of data, and security. One of the recurring problems in DVI incidents that involve multiple agencies is the potential for misidentification because of failure to establish clear practice guidelines and lines of authority at the earliest possible opportunity, inadequate or idiosyncratic initial examinations, failure to follow protocols, and failure to ensure adequate quality assurance reviews (1). Each step of the identification process, from locating bodies at the scene to formal acceptance of identifications at Reconciliation Panel Meetings requires an internal audit. Each body or part needs to have a unique identifier, and this should be able to be tracked through the entire process of fingerprint, pathology, dental, and DNA examinations. In our experience, this is not always the case, and a large amount of time in the later stages of large DVI exercises is spent in re-examining and sampling bodies and parts that may have been examined multiple times before—a very time-consuming and costly process. A way to highlight the effectiveness of a DVI exercise would be to focus on the number of cases ⁄ specimens that had to be re-examined to correct failures in procedures. This ‘‘Correction of Failures Index’’ could be measured quite simply as the total number of cases ⁄ specimens that had to undergo re-examination as a percentage of the total number of cases ⁄ specimens examined. An exercise where most cases have had to be re-examined would give a CF index close to 100% indicating inefficient practice, whereas an exercise with minimal errors requiring very few re-examinations would be close to 0%. The lower the index, the more effective has been the exercise. The CF index could provide a simple way to assess the overall effectiveness of an exercise and also to monitor activity during specific times of the process, to determine when errors were most likely to occur, or be discovered. Examining teams with high CF indices could be identified early in the process and steps taken to focus on specific issues that would require correction or modification. The desirable range and application of an effective CF index will only be established by trialling this in the field. As each disaster will be different, it is quite likely that the denominator may also be different, representing complete bodies in one instance or fragmented body parts in another.

Caustic Ingestion—A Forensic Overview

The ingestion of corrosive substances may produce severe burns to the upper aerodigestive tract and stomach, particularly if the pH is greater than 12 or less than two. There is a biphasic age grouping with adult cases most often involving self‐harm and pediatric cases accidental ingestion. Three cases are reported to demonstrate characteristic features following the ingestion of potassium hydroxide, glacial acetic acid and Lysol®, respectively. All deaths were due to the effects of caustic burns to the upper aerodigestive tract, esophagus and stomach with perforation and/or hemorrhage. The extent of injuries in these cases depends on the nature, amount, and concentration of the agent and on the exposure time. A point to note at autopsy is that tissue damage may also occur from postmortem exposure. Typical injuries involve perioral, limb, and trunk burns, with extensive aerodigestive liquefactive/coagulative necrosis causing hemorrhage and perforation.

Alcohol Intoxication May Exacerbate the Effects of Blunt Cranial Trauma Through Changes in Brain Free Magnesium Levels

Abstract:  Moderate to high levels of alcohol decrease brain intracellular free magnesium concentration, a factor known to be critical in brain injury. Phosphorus magnetic resonance spectroscopy was used to examine changes to brain free magnesium concentration after blunt cranial trauma in alcohol‐intoxicated rats. Rats exposed acutely or chronically to alcohol sufficient to increase blood alcohol levels to between 150 and 350 mg/dL demonstrated a brain free magnesium level that was 20–50% less than in nonintoxicated animals (p < 0.01). After injury, brain free magnesium levels declined more rapidly and to a greater extent in alcohol‐affected animals than in nonintoxicated control animals (p < 0.001). As both preinjury depletion of magnesium and degree of magnesium decline after brain injury have been associated with poor recovery, these findings suggest that moderate to severe alcohol intoxication may predispose the brain to a worse outcome by reducing brain free magnesium levels, both before and after injury.