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Biomedical subjects

B G Stephens

Publications and source records attributed to B G Stephens.

At least 19 recordsLinked to original sources
PubMed2001

GHB. Club drug or confusing artifact?

GHB can be produced either as a pre- or postmortem artifact. The authors describe two cases in which GHB was detected and discuss the problem of determining the role of GHB in each case. In both cases, NaF-preserved blood and urine were analyzed using gas chromatography. The first decedent, a known methamphetamine abuser, had GHB concentrations similar to those observed with subanesthetic doses (femoral blood, 159 microg/ml; urine, 1100 microg/ml). Myocardial fibrosis, in the pattern associated with stimulant abuse, was also evident. The second decedent had a normal heart but higher concentrations of GHB (femoral blood, 1.4 mg/ml; right heart, 1.1 mg/ml; urine, 6.0 mg/ml). Blood cocaine and MDMA levels were 420 and 730 ng/ml, respectively. Both decedents had been drinking and were in a postabsorptive state, with blood to vitreous ratios of less than 0.90. If NaF is not used as a preservative, GHB is produced as an artifact. Therefore, the mere demonstration of GHB does not prove causality or even necessarily that GHB was ingested. Blood and urine GHB concentrations in case 1 can be produced by a therapeutic dose of 100 mg, and myocardial fibrosis may have had more to do with the cause of death than GHB. The history in case 2 is consistent with the substantial GHB ingestion, but other drugs, including ethanol, were also detected. Ethanol interferes with GHB metabolism, preventing GHB breakdown, raising blood concentrations, and making respiratory arrest more likely. Combined investigational, autopsy, and toxicology data suggest that GHB was the cause of death in case 2 but not case 1. Given the recent discovery that postmortem GHB production occurs even in stored antemortem blood samples (provided they were preserved with citrate) and the earlier observations that de novo GHB production in urine does not occur, it is unwise to draw any inferences about causality unless (1) blood and urine are both analyzed and found to be elevated; (2) blood is collected in NaF-containing tubes; and (3) a detailed case history is obtained.

Adult↗
PubMed2000

Toxicology and pathology of deaths related to methadone: retrospective review.

OBJECTIVES: To clarify the mechanisms and risk factors of methadone toxicity and to describe the findings of deaths related to methadone use Design Retrospective review of case notes in the records of the San Francisco Medical Examiner comparing the findings in cases where methadone was deemed the cause of death with findings in decedents where methadone was an incidental finding, and with 50 age-matched, disease and drug free, trauma victims. RESULTS: 38 cases out of the 3317 processed by our office during 1997-1998 were identified in which methadone had been detected. Cases were mostly male 28/38 (74%) and white, 28/38 (74%). In 17 of 38 cases death was deemed to have been caused by methadone toxicity. For the group the mean blood methadone concentration for all 38 patients, was 957 ng/ml SD = .681, SE = .14). The mean blood concentration of the main methadone metabolite (EDDP) was 253 ng/ml, SD = 529 ng/ml, SE = .089. The mean ratio of methadone in the blood to EDDP in the blood was 13.6:1 Values were not significantly different between cases in which methadone toxicity was the cause of death and in those in which it was an incidental finding. Cocaine, or the cocaine metabolite benzoylecgonine, was detected in the blood or urine of 16/38 cases (42%); morphine in one-third (13/38) and methamphetamine in only one. Pulmonary edema was evident in all cases, coronary artery disease in 9/38 (24%) and cirrhosis in 7/38 (18%) of the methadone users. Necrotizing fasciitis was the cause of death in 4 of the 38 methadone users (11%). Nationally, a sizeable percent of methadone deaths are from drugs diverted from treatment programs. CONCLUSIONS: The presence of methadone is often an incidental finding during postmortem examination which is unrelated to the cause of death. Postmortem measurements of methadone or its metabolite, or both, cannot be used in isolation to identify which deaths are associated with methadone toxicity.

Adult↗
PubMed1999

Does ethanol enhance cocaine toxicity?

OBJECTIVES: Results of in vitro and animal studies suggest that ethanol enhances cocaine toxicity. If so, then that this implies that in ethanol users, postmortem blood cocaine concentrations should be lower, or anatomic evidence demonstrable. METHODS: Drug concentrations and autopsy findings were compared in a sample of 72 accidental deaths, where only cocaine, cocaine metabolites, and ethanol were detected. Findings in ethanol positive (E+) and negative (E-) deaths were compared using multiple Student's t-tests and chi2 testing for categorical variables. RESULTS: There were 47 E-decedents and 24E+. Mean ages were similar (40.2 +/- 8.7 and 37.5 +/- 11.1 years respectively). Mean E was 0.113 (range 0.030-0.350 g/dL), and less than 0.080 g/dL in 50% of the cases. Concentrations of C and BE were not significantly different in E- and E+ groups (C = 1.40 +/- 3.6 mg/L, and 0.76 +/- 1.93 mg/L respectively, BE = 3.04 +/- 5.36 mg/L and BE 2.09 +/- 3.77 mg/L, P = 0.4621 and 0.4520). Organ weights were pathologically increased in both groups, but not significantly different. Body Mass Index (BMI) was less (23.9 vs 25.5), and heart weight was greater (449 vs 407 g) than predicted. Over half the decedents had demonstrable heart disease, and 11% died of brain haemorrhage, though the rate for both disorders was similar in each group. CONCLUSIONS: In two-thirds of the cocaine-related deaths studied, no ethanol was detected. When ethanol was present, no differences between the two groups were identified. The findings suggest that acute cocaine toxicity is not enhanced by ethanol cocaine interactions. However, ethanol concentrations were generally low, and it is possible that increased toxicity is apparent when much larger quantities of alcohol have been consumed.

Journal Article↗
PubMed1999

Use of liquid nitrogen to remove duct tape from a homicide victim.

Removal of duct tape or similar adhesive products from a homicide victim may be facilitated by rapidly chilling the tape surface with liquid nitrogen. Physical separation of tape layers can be performed using the same technique. Cyanoacrylate glue (i.e., "super-glue") may be used to preserve fingerprints on the outer surface of the tape for recovery, or other techniques may be used to recover fingerprints from the outer surface prior to tape removal.

Adhesives↗
PubMed1999

Methamphetamine-related deaths in San Francisco: demographic, pathologic, and toxicologic profiles.

A study was undertaken to develop demographic, toxicologic, and pathological profiles of methamphetamine-related deaths. Anatomic and toxicologic findings in 413 deaths where methamphetamine was detected were compared with findings in a control group of 114 drug-free trauma victims. The number of cases per year did not change significantly over the course of the study. Mean age was 36.8 years, but 11% were over the age of 50. Decedents were overwhelmingly male (85.2%) and Caucasian (75%). Blood concentrations of methamphetamine and amphetamine were indistinguishable in cases where methamphetamine was related to the cause of death (MR) and cases where it was not (non-MR) (2.08 vs. 1.78 mg/L, p = 0.65, and 0.217 vs. 0.19 mg/L, p = 0.82). Coronary artery disease, ranging from minimal to severe multivessel, was identified in 79 of the 413 drug users, but in only six of the 114 drug-free controls (p = 0.0004), and MR decedents had enlarged hearts compared with controls. There were also ten cases of subarachnoid and intracranial hemorrhage in the MR group. Abnormalities of the liver (34%) and lungs (24.7%) were frequent. In 65% of these cases, death was due to accidental methamphetamine toxicity. In the remaining cases, methamphetamine was an incidental finding. We conclude that, in our jurisdiction, neither the rate of detection nor the number of methamphetamine deaths has increased significantly in the past 13 years. Decedents are almost all Caucasian males, and many were approaching middle-age. Methamphetamine use is strongly associated with coronary artery disease and with subarachnoid hemorrhage.

Accidents↗
PubMed1998

Olanzapine-related fatality.

A 43-year-old male psychiatric outpatient died within hours of ingesting as much as 600 mg of olanzapine, a newer antipsychotic agent related to clozapine. Analysis of postmortem blood and urine by gas chromatography with nitrogen-selective detection yielded olanzapine concentrations of 1238 and 6987 micrograms/L, respectively, greatly in excess of levels expected following therapeutic administration of the drug. Based on the toxicology findings, the decedent's known history of suicide attempts, and the circumstances surrounding the death, this case was ruled a suicide by olanzapine overdosage.

Adult↗
PubMed1997

Homicidal poisoning by paraquat.

The determination of homicidal poisoning due to the oral administration of paraquat presents a unique challenge for both the clinician and the pathologist. Reported are four cases of homicidal paraquat poisoning, three leading to conviction and one possible, but unproved case. This study illustrates that intentional paraquat poisoning is not generally considered, even when physicians are faced with an atypical clinical course for inflammatory disease. The mechanism of action and symptoms of paraquat poisoning are presented, guidelines for when to suspect paraquat are given, and recommendations for treatment are outlined.

Adult↗
PubMed1996

Postmortem perianal findings in children.

The postmortem finding of anal dilation or an exposed pectinate line in children who have died under suspicious circumstances continues to raise the concern of possible sexual abuse. The following multicenter, collaborative study was designed to help address that question. Sixty-five subjects, ranging in age from birth to 17 years, were autopsied at three different sites. A standard protocol along with 35-mm cameras were used to record the results. Thirty-eight (58%) subjects were boys, and 27 (42%) were girls. Forty-two (65%) were white, 10 (15%) African-American, five (8%) Asian, three (5%) white Hispanic and five (8%) other. Fifty-seven (88%) were in Tanner stage I of secondary sexual development. Thirty-four (52%) died of natural causes, 26 (40%) from accidental injuries, three (5%) from other causes, and four (6%) as a result of a homicide. Forty-eight subjects (74%) had some dilation of the anal sphincters. In 21 children (32%), the entire anal canal, including the rectal ampulla, could be visualized. In another 21 (32%) subjects, the pectinate line was exposed. Only the outer portion of the anal canal opened in six children (10%), whereas 17 (26%) had no dilatation of the anus. Anal laxity led to flattened skin folds in 50 (77%), a shallow anal canal in 40 (62%), the exposure of both the pectinate line in 38 (59%), and the anal mucosa in 24 (37%). Venous congestion was present in 14 (22%), venous pooling in three (5%), erythema in six (9%), and increased pigmentation in eight (12%). Funneling was found in two (3%). Blood was present in three (5%), and an abrasion was discovered in one (2%). No fissures, lacerations, hemorrhoids, or scars were found in any of the children. Anal orifice size varied with the age of the child, the amount of traction applied to the buttocks, and a history of a CNS injury at the time of death. It is suggested, finally, that anal dilatation alone cannot be used a marker for prior sexual abuse and the exposure of the pectinate line should not be confused with tears or fissures of the anal verge. Further studies of children known to have been sodomized prior to death are required.

Anal Canal↗
PubMed1994

Driving under the influence of GHB?

A driver was found asleep behind the steering wheel of his car, and the vehicle was at rest in a traffic lane with the engine running. His manifestations included horizontal and vertical gaze nystagmus, muscle flaccidity, and severe ataxia. He admitted ingesting a white powder, which he identified as an amino acid, about 1 hour prior to discovery by police. A urine specimen collected approximately 1 hour after the traffic stop contained 1975 mg/L of gamma-hydroxybutyrate (GHB). We tentatively conclude that GHB may cause impairment of the psychomotor skills required for safe operation of a motor vehicle.

Adult↗
PubMed1993

Infant death in San Francisco 1989-1990.

This paper examines all of the unexplained and violent deaths of children less than one year of age in the City and County of San Francisco during the years 1989-1990. A total of 62 cases were collected and analyzed retrospectively. Among the cases we examined, 34 deaths were determined as SIDS, while seven were moded as accidents and two as homicides. The deaths were examined with respect to the following parameters: sex, race, age, height and weight, cause and manner of death, significant autopsy and microscopic findings; circumstances of death including place, the person discovering or reporting the death, the presence of siblings or previous child death in the family and previous illness in the same child. A particular stress is given to the definition and diagnosis of SIDS, according to the international literature, and to the criteria adopted to distinguish SIDS cases from accidents and homicides. A review of both the American and European literature shows that most articles do not include comparisons of data from both the autopsy and the scene. Additionally there is little standardization in the investigation and the extent of postmortem examinations performed. An international standardization of these methods appears necessary and the use of protocols to assure complete investigation and postmortem examination will allow more intensive evaluation of data. Here we give a brief presentation of the necropsy protocol for Sudden Unexpected Infant Death recently written and approved by the California Department of Health Services and used in the Chief Medical Examiner's Office in San Francisco.

Age Factors↗
PubMed1989

The seed queen.

Although many drugs are routinely used in medicine and therefore knowledge of them is potentially important in death investigations, the actual manufacture or composition of the individual tablets or capsules is not general forensic information. Some of this information is protected under laws dealing with manufacturing secrets, and some is patent information pertaining to methods of manufacturing. When tablets or capsules are part of the evidence from the victim, their appearance may not always be in the form that is expected. This case presents a misidentification of tablet material as "seeds" that resulted in a delayed diagnosis of the cause of death. The composition of the tablet material is discussed so that others may avoid this error.

Adolescent↗