Corinne L. Fligner

Suicide in the home in relation to gun ownership

BACKGROUND It has been suggested that limiting access to firearms could prevent many suicides, but this belief is controversial. To assess the strength of the association between the availability of firearms and suicide, we studied all suicides that took place in the homes of victims in Shelby County, Tennessee, and King County, Washington, over a 32-month period. METHODS For each suicide victim (case subject), we obtained data from police or the medical examiner and interviewed a proxy. Their answers were compared with those of control subjects from the same neighborhood, matched with the victim according to sex, race, and age range. Crude and adjusted odds ratios were calculated with matched-pairs methods. RESULTS During the study period, 803 suicides occurred in the two counties, 565 of which (70 percent) took place in the home of the victim. Fifty-eight percent (326) of these suicides were committed with a firearm. After excluding 11 case subjects for various reasons, we were able to interview 80 percent (442) of the proxies for the case subjects. Matching controls were identified for 99 percent of these subjects, producing 438 matched pairs. Univariate analyses revealed that the case subjects were more likely than the controls to have lived alone, taken prescribed psychotropic medication, been arrested, abused drugs or alcohol, or not graduated from high school. After we controlled for these characteristics through conditional logistic regression, the presence of one or more guns in the home was found to be associated with an increased risk of suicide (adjusted odds ratio, 4.8; 95 percent confidence interval, 2.7 to 8.5). CONCLUSIONS Ready availability of firearms is associated with an increased risk of suicide in the home. Owners of firearms should weigh their reasons for keeping a gun in the home against the possibility that it might someday be used in a suicide.

The Use of Antibodies Targeted Against the Neurofilament Subunits for the Detection of Diffuse Axonal Injury in Humans

Axonal injury is a common feature of human traumatic brain injury. Typically, damaged axons cannot be recognized unless a patient survives the injury by at least 10-12 hours (h). Limitations associated with the use of the traditional silver methods have been linked with this inability to recognize early posttraumatic reactive axonal change. Recently, we reported that antibodies targeting the neurofilament subunits proved useful in recognizing early traumatically induced axonal change in traumatically brain-injured animals. Accordingly, in the present communication, we employed antibodies to detect at the light microscopic level the 68 kD Nf-L and 170-200 kD Nf-H neurofilament subunits in head-injured patients who survived the traumatic event for periods ranging from 6 h to 59 days. Antibodies targeting all of the above-described subunits revealed a progression of reactive axonal change. Antibodies to the 68 kD subunit proved most useful, as they were not complicated by concomitant immunoreactivity in surrounding nuclei and/or dendritic and somatic elements. These immunocytochemical strategies revealed, at 6 h postinjury, focally swollen axons which appeared intact. By 12 h, this focal swelling had progressed to disconnection, with the immunoreactive swelling undergoing further expansion over 1 week postinjury. These findings demonstrate the utility of the previously described immunocytochemical strategies for detecting reactive axonal change in brain-injured humans, particularly in the early posttraumatic course. More importantly, these methods also demonstrate in humans that reactive axonal change is not necessarily caused by traumatically induced tearing.

Direct sampling of cystic fibrosis lungs indicates that DNA-based analyses of upper-airway specimens can misrepresent lung microbiota

Recent work using culture-independent methods suggests that the lungs of cystic fibrosis (CF) patients harbor a vast array of bacteria not conventionally implicated in CF lung disease. However, sampling lung secretions in living subjects requires that expectorated specimens or collection devices pass through the oropharynx. Thus, contamination could confound results. Here, we compared culture-independent analyses of throat and sputum specimens to samples directly obtained from the lungs at the time of transplantation. We found that CF lungs with advanced disease contained relatively homogenous populations of typical CF pathogens. In contrast, upper-airway specimens from the same subjects contained higher levels of microbial diversity and organisms not typically considered CF pathogens. Furthermore, sputum exhibited day-to-day variation in the abundance of nontypical organisms, even in the absence of clinical changes. These findings suggest that oropharyngeal contamination could limit the accuracy of DNA-based measurements on upper-airway specimens. This work highlights the importance of sampling procedures for microbiome studies and suggests that methods that account for contamination are needed when DNA-based methods are used on clinical specimens.

CAUSE AND MANNER OF DEATH IN FATALITIES INVOLVING METHAMPHETAMINE

We reviewed a series of deaths in which methamphetamine was detected in the decedents blood. Analysis of postmortem whole blood was performed by gas chromatography/mass spectrometry with a limit of quantitation of 0.05 mg/L. Methamphetamine was detected in 146 cases; 52 were drug caused, i.e., a death in which the direct toxic effects of the drug caused or contributed to the death, 92 were classified as drug related, i.e., a death in which the drug was demonstrated in the blood, but did not directly cause death. A large proportion of the deaths resulted from homicidal (27%) or suicidal (15%) violence. An examination of methamphetamine concentrations in drug related deaths (n = 92), suggests that the range of concentrations in the recreational abusing population is substantial (0.05-9.30 mg/L) but with a median concentration of 0.42 mg/L, and with 90% of that population having concentrations less than 2.20 mg/L. There was substantial overlap in methamphetamine concentration between drug related deaths and drug caused deaths, although the highest concentrations were seen in the unintentional (accidental or undetermined) drug caused deaths. Methamphetamine related traffic deaths (n = 17) showed patterns of driving behavior consistent with reports elsewhere, and showed blood methamphetamine concentrations ranging from 0.05-2.60 mg/L (median 0.35 mg/L). The data show that most methamphetamine deaths occur with blood concentrations greater than 0.5 mg/L, but can occur with levels as low as 0.05 mg/L, though usually in conjunction with other drugs or significant natural disease. Neither apparently toxic nor therapeutic concentrations should be used in isolation to establish conclusively whether a death was caused by methamphetamine; proper classification of deaths involving methamphetamine requires complete death investigation, including investigation of the scene and circumstances of death, and a complete autopsy.

β-Cell Loss and β-Cell Apoptosis in Human Type 2 Diabetes Are Related to Islet Amyloid Deposition

Amyloid deposition and reduced β-cell mass are pathological hallmarks of the pancreatic islet in type 2 diabetes; however, whether the extent of amyloid deposition is associated with decreased β-cell mass is debated. We investigated the possible relationship and, for the first time, determined whether increased islet amyloid and/or decreased β-cell area quantified on histological sections is correlated with increased β-cell apoptosis. Formalin-fixed, paraffin-embedded human pancreas sections from subjects with (n = 29) and without (n = 39) diabetes were obtained at autopsy (64 ± 2 and 70 ± 4 islets/subject, respectively). Amyloid and β cells were visualized by thioflavin S and insulin immunolabeling. Apoptotic β cells were detected by colabeling for insulin and by TUNEL. Diabetes was associated with increased amyloid deposition, decreased β-cell area, and increased β-cell apoptosis, as expected. There was a strong inverse correlation between β-cell area and amyloid deposition (r = -0.42, P < 0.001). β-Cell area was selectively reduced in individual amyloid-containing islets from diabetic subjects, compared with control subjects, but amyloid-free islets had β-cell area equivalent to islets from control subjects. Increased amyloid deposition was associated with β-cell apoptosis (r = 0.56, P < 0.01). Thus, islet amyloid is associated with decreased β-cell area and increased β-cell apoptosis, suggesting that islet amyloid deposition contributes to the decreased β-cell mass that characterizes type 2 diabetes.

Macrocyclic and Other Non–group 1 Gadolinium Contrast Agents Deposit Low Levels of Gadolinium in Brain and Bone Tissue: Preliminary Results From 9 Patients With Normal Renal Function

ObjectiveThe purpose of this study was to determine whether gadolinium (Gd) is deposited in brain and bone tissues in patients receiving only non–Group 1 agents, either macrocyclic or linear protein interacting Gd-based contrast agents, with normal renal function. Group 1 agents are linear agents most associated with nephrogenic systemic fibrosis that the US Federal Drug Administration has defined as contraindicated in patients at risk for this disease. Materials and MethodsThis study was institutional review board approved and Health Insurance Portability and Accountability Act compliant for retrospective review of records and also had signed autopsy consent authorizing use of decedents tissue in research studies. Tissue samples were collected from 9 decedents undergoing autopsy who had contrast-enhanced magnetic resonance imaging (MRI) with only single agent exposure to a non–Group 1 Gd-based contrast agent. Decedents with only noncontrast MRI or no MRI served as controls. Multiple brain areas, including globus pallidus and dentate nucleus, as well as bone and skin, were sampled and analyzed for Gd using inductively coupled plasma mass spectrometry. Gadolinium levels were compared between groups of decedents using the Mann-Whitney test and between brain and bone tissues of the same cases using the Wilcoxon signed-rank test. ResultsOf the 9 decedents, 5 received gadoteridol (ProHance; Bracco Diagnostics, Princeton, NJ), 2 received gadobutrol (Gadovist; Bayer Healthcare, Whippany, NJ), and 1 each had gadobenate (MultiHance; Bracco Diagnostics) and gadoxetate (Eovist; Bayer Healthcare). Gadolinium was found with all agents in all brain areas sampled with highest levels in globus pallidus and dentate. Bone levels measured 23 times higher (median) than brain levels (P = 0.008 for bone vs globus pallidus) and showed a significant correlation (r = 0.81, P = 0.022). In controls, Gd levels in the brain were at or below limits of measurement and were significantly lower compared with study cases (P = 0.005 for globus pallidus). ConclusionGadolinium deposition in normal brain and bone tissue occurs with macrocyclic and linear protein interacting agents in patients with normal renal function. Deposition of Gd in cortical bone occurs at much higher levels compared with brain tissue and shows a notable correlation between the two. Thus, the bone may serve as a surrogate to estimate brain deposition if brain Gd were to become a useful clinical or research marker.

Positional asphyxia during law enforcement transport.

Three cases of positional asphyxia are described that occurred while victims were in a prone position in rear compartments of police patrol cars. These deaths are attributed to positional asphyxia. Autopsy findings and specific scene and circumstantial correlations of the investigation are discussed with emphasis placed on the limitations of interpretation of the anatomic changes at autopsy. Language: en

Effects of alcohol intoxication on the initial assessment of trauma patients

STUDY OBJECTIVES To evaluate the influence of alcohol intoxication on the initial assessment and treatment of trauma patients. DESIGN A prospective study of 2,237 trauma patients 18 years of age or older admitted to a Level I trauma center over a 19-month period. RESULTS The study population was primarily male (78%) and white (73%) and had sustained blunt trauma (79%). One thousand fifty-three patients (47.1%) had positive blood alcohol concentration (BAC); median BAC in patients with any detectable alcohol was 179 mg/dL. When stratified by injury severity categories and compared with nonintoxicated (BAC less than 100 mg/dL) patients, intoxicated patients with an Injury Severity Score (ISS) of 1 to 15 were more likely to undergo the following: field and/or ED intubation (relative risk [RR], 2.22; 95% confidence interval [CI], 1.7 to 2.7); diagnostic peritoneal lavage (RR, 1.83; CI, 1.43 to 2.3); head computed tomography scanning (RR, 1.18; CI, 1.0 to 1.4); and intracranial pressure monitoring (RR, 1.41; CI, 0.74 to 2.7). The effects were less pronounced for those patients with an ISS of more than 15, except for intracranial pressure monitoring where patients with an ISS of more than 15 were 47% more likely to have intracranial pressure monitoring if intoxicated (RR, 1.47; CI, 1.2 to 1.9). CONCLUSION Acute intoxication appears to alter the initial assessment of injury severity, resulting in an increased use of invasive diagnostic and therapeutic procedures.

Drug use in trauma victims

We examined the prevalence and characteristics of drug use in a large sample of fatally and nonfatally injured trauma victims. Routinely collected urine specimens from 452 emergency room patients and 160 persons autopsied at the Medical Examiners Office (MEO) were analyzed for the presence of marijuana, cocaine, opiates and benzodiazepines using EMIT enzyme immunoassays. Blood alcohol levels were also measured. Tests were positive for at least one drug in 40.3% of the ER and 18.7% of the MEO samples. Marijuana was the most commonly detected drug in both groups. Specimens were more likely to be positive in younger persons and in males, and in victims of assaults and traffic accidents. Alcohol was present in the blood in more than one third of ER and MEO samples. Only 39.8% of ER samples and 52.3% of MEO samples were negative for both alcohol and drugs.

Imaging of the Diaphragm: Anatomy and Function

The diaphragm is the primary muscle of ventilation. Dysfunction of the diaphragm is an underappreciated cause of respiratory difficulties and may be due to a wide variety of entities, including surgery, trauma, tumor, and infection. Diaphragmatic disease usually manifests as elevation at chest radiography. Functional imaging with fluoroscopy (or ultrasonography or magnetic resonance imaging) is a simple and effective method of diagnosing diaphragmatic dysfunction, which can be classified as paralysis, weakness, or eventration. Diaphragmatic paralysis is indicated by absence of orthograde excursion on quiet and deep breathing, with paradoxical motion on sniffing. Diaphragmatic weakness is indicated by reduced or delayed orthograde excursion on deep breathing, with or without paradoxical motion on sniffing. Eventration is congenital thinning of a segment of diaphragmatic muscle and manifests as focal weakness. Treatment of diaphragmatic paralysis depends on the cause of the dysfunction and the severity of the symptoms. Treatment options include plication and phrenic nerve stimulation. Supplemental material available at http://radiographics.rsna.org/lookup/suppl/doi:10.1148/rg.322115127/-/DC1.