Jack Garland

Neisseria meningitidis Isolated in Postmortem Vitreous Humor in a Death Due to Meningococcal Sepsis.

AbstractSepsis remains a difficult diagnosis at autopsy. With respect to meningococcal sepsis, a timely and definite diagnosis is critical because it requires public health department notification and the administration of prophylactic antibiotics to potential close contacts. A previous case series, in which both blood and cerebrospinal fluid were unavailable, suggested vitreous humor polymerase chain reaction might be a useful test in diagnosing meningococcal sepsis. We describe a fatal case of meningococcal sepsis where Neisseria meningitidis was detected in both vitreous humor and blood polymerase chain reaction, in addition to positive blood cultures. This gives further support to using microbiology of vitreous humor in suspected meningococcal sepsis, especially when microbiology samples are limited.

Post mortem tryptase cut-off level for anaphylactic death

Serum mast cell tryptase is used to support the diagnosis of anaphylaxis. The recommended clinical cut-off for total tryptase (<11.4μg/L) appears unsuitable in the post mortem setting due to largely unknown processes which result in significantly elevated levels in these samples. Consequently there is no widely accepted tryptase cut-off level for diagnosing an anaphylactic death. This 5-year retrospective study compared total tryptase levels in post mortem femoral blood in anaphylactic deaths and control. Univariate and multivariate analysis was used to assess the relative contribution of other factors (age, gender, post mortem interval, and presence of resuscitation) on post mortem tryptase levels. Nine anaphylactic deaths and 45 controls were identified. Receiver-operating characteristic (ROC) curve analysis identified an optimal cut-off of 53.8μg/L, with sensitivity of 89%, and specificity of 93%, for total post mortem tryptase in femoral blood to diagnosis anaphylaxis. No other factors showed any statistical significant contribution to post mortem tryptase elevation. Femoral total post mortem tryptase level of 53.8μg/L and above is a useful ancillary test in diagnosing an anaphylactic death.

Postmortem Vitreous Humor Magnesium Does Not Elevate in Salt Water Drowning When the Immersion Time Is Less Than an Hour

Background Elevation in postmortem vitreous humor sodium and chloride (PMVSC) in salt water drowning (SWD) when the immersion time is less than 1 hour (SWD1) is hypothesized to result from electrolyte changes in blood from salt water inhalation/ingestion during drowning. After approximately 1 hour after death, electrolytes may diffuse into the vitreous humor via the eye coverings. Another abundant element in salt water is magnesium, which is approximately 50 times higher in concentration than the blood and vitreous humor magnesium levels. Magnesium is able to diffuse across the eye coverings but not as easily through the blood-ocular barrier. With these properties, we hypothesize that postmortem vitreous magnesium (PMVM) would not be elevated in SWD1 but become elevated in SWD with immersion times greater than 1 hour (SWD>1). Aim The aim of this article was to investigate the differences in PMVM and PMVSC between nonimmersion deaths, SWD1, and SWD>1. Methods This is a 1-year retrospective study comparing PMVM and PMVSC in nonimmersion deaths, SWD1, and SWD>1. Results Postmortem vitreous magnesium is significantly higher in SWD>1 than SWD1 and nonimmersion deaths, with no significant difference between SWD1 and nonimmersion deaths. Postmortem vitreous humor sodium chloride is statistically higher in SWD1 and SWD>1 than nonimmersion deaths. Conclusions As a conclusion, PMVSC elevates and PMVM does not elevate in SWD1.

Lethal phlegmonous duodenitis

A recent case report titled ‘Lethal phlegmonous colitis’ by Gilbert and Byard highlighted this rare infectious condition involving the colon. As discussed, this phlegmonous inflammatory condition of the intestine is associated with viral or alcohol hepatitis, cirrhosis and immunosuppression, and runs a very fulminant course with high mortality. The post-mortem macroscopic findings of this condition involving the colon are described as ‘thickening of the caecum and ascending colon’, with likely no characteristic changes in the mucosal surface. The diagnosis is made on microscopy with oedema, florid acute inflammatory infiltration and organisms in the submucosa. It is, however, surprising that there is an even greater paucity of case reports in the forensic literature of this condition involving the stomach and small intestine, given that it more commonly involves the upper gastrointestinal tract. We would like to report another case of lethal phlegmonous inflammation involving the duodenum which had similar pathology and highlights the possible difficulties in diagnosing this condition at autopsy. The deceased was a 40-year-old man with significant background history of chronic alcohol abuse, diabetes mellitus type 2, high blood pressure, chronic pancreatitis, common bile duct stricture (awaiting stent insertion) and liver cirrhosis. He had been described to be ‘deteriorating’ leading up to his death. On the day of his death, he had multiple episodes of vomiting and subsequently became unconscious and passed away in the presence of ambulance staff. Apart from the significant chronic disease identified in keeping with the clinical history, phlegmonous inflammation of the duodenum was identified. At post-mortem, the duodenum was slightly discoloured and felt thickened, and histology confirmed phlegmonous duodenitis (Figure 1). The duodenal mucosa is commonly ‘discoloured’ at postmortem, giving a congested appearance which is often attributed to post-mortem bile staining. The thickness of the duodenal wall is difficult to assess at postmortem due to its anatomical position and surrounding structures. Therefore, the appreciation of this pathology in this region may be challenging, and the sampling and subsequent diagnosis is made by a high level of suspicion. It is our opinion that phlegmonous inflammation of the intestinal tract may be underappreciated at postmortem. We agree with Gilbert and Byards’s opinion that this condition should be considered at

Post mortem vitreous magnesium in adult population.

BACKGROUND The study of post mortem vitreous magnesium (Mg) is less common than sodium (Na), chloride (Cl) and potassium (K) in the forensic literature. There is no accepted normal range for post mortem vitreous Mg and the relationship between post mortem vitreous Mg levels and post mortem interval (PMI), other electrolyte levels, disease conditions, age and sex have not been fully established. AIM To investigate the relationship of post mortem vitreous Mg with age, sex, PMI, vitreous electrolyte levels and diabetic status. METHODS A retrospective study of 20 consecutive cases of diabetics and 20 non-diabetic adult deaths was performed. Spearman correlation and the permutation test were used to explore the relationship between post mortem vitreous Mg and continuous and categorical variables respectively. RESULTS The mean post mortem vitreous Mg was 1.03mmol/L (95%CI: 0.98-1.08mmol/L). The absolute Spearman correlation coefficients (rho) between post mortem vitreous Mg with PMI, age, and other vitreous electrolytes (Na, Cl, and K) ranged between 0.04-0.21 (p>0.19). Post mortem vitreous Mg was statistically higher in diabetics (mean difference: 0.08mmol/L; area-under-the-curve=0.65 on receiver-operator-characteristic curve). No statistical difference was demonstrated between sexes (p=0.92). CONCLUSIONS In our adult population, post mortem vitreous Mg did not correlate with age, PMI, other vitreous electrolytes (sodium, chloride and potassium) or sex. It was higher in diabetics, however had limited utility as a surrogate marker. Overall, post mortem Mg is steady in the early post mortem period with a mean of 1.03mmol/L.

Neck injury and conjunctival petechiae in a woman who underwent cardiopulmonary resuscitation and subsequently died from meningococcal sepsis

Cardiopulmonary resuscitation (CPR) can create a range of unusual lesions and injuries, which may complicate forensic evaluation. Although potentially sinister findings, neck injury and conjunctival petechiae may also be seen in patients who have undergone CPR. We report a case of an individual with subcutaneous bruising and hemorrhage in the deep structures of the neck and florid conjunctival petechiae at autopsy that can be explained by cardiopulmonary resuscitation and meningococcal sepsis.

Increased Epicardial Fat Thickness in Sudden Death From Stable Coronary Artery Atherosclerosis

Background Sudden death from stable coronary artery atherosclerosis (SCAA) is well recognized. However, individuals can have ischemic heart disease or coronary artery atherosclerosis but die of noncardiac causes. Recently, it has been recognized that increased epicardial fat is detrimental to normal heart function. We hypothesize that individuals who die of SCAA have increased epicardial fat. Aim The aim of this study was to investigate whether there is an increase in epicardial fat in individuals who suddenly died of SCAA. Methods This was a 1-year retrospective study comparing the average epicardial fat thickness using postmortem computed tomography scan between individuals who suddenly died of SCAA (SCAA group) with individuals who primarily died of natural noncardiac causes but had established ischemic heart disease or significant coronary artery atherosclerosis (NCC group). Results Average epicardial fat thickness was significantly higher in the SCAA group (8 ± 2 mm) than in the NCC group (6 ± 2 mm, P = 0.008). Conclusions Individuals who die of SCAA appear to have higher epicardial fat thickness. The increase in epicardial fat may have an additional detrimental effect to the heart predisposing sudden death in individuals with coronary artery atherosclerosis.

Hyperdensity of the Basilar Artery on Postmortem CT: A Potential Indicator for Basilar Artery Thrombosis.

AbstractBasilar artery thrombosis constitutes 1% of all types of stroke, carries a mortality rate of up to 90%, and is one of the rarer causes of sudden death. It leads to brain stem ischemia and commonly presents with impaired consciousness, cranial nerve palsy, hemiplegia or quadriplegia, and sudden collapse. Clinically, the diagnosis of basilar artery thrombosis is made on clinical symptoms, along with a hyperdense basilar artery in antemortem computed tomography (CT) scan. To our knowledge, whether a hyperdense basilar artery indicates basilar artery thrombosis on postmortem CT scan is not documented in the literature. We present a case report of a 55-year-old man who on postmortem CT scan showed a hyperdense basilar artery and was subsequently confirmed to be a fatal basilar artery thrombosis. We suggest that a hyperdense basilar artery on postmortem CT should prompt the pathologist to consider basilar artery thrombosis.