Causes of Death in the Presence of Law Enforcement in Johnson County, Iowa, 2011-2020.

Objectives. To examine sudden and unexpected or trauma-related deaths that occurred in the presence of law enforcement in Johnson County, Iowa, between 2011 and 2020. Methods. We identified deaths in the presence of law enforcement using definitions from the National Association of Medical Examiners. We obtained data, including demographics, cause and manner of death, toxicology results, and circumstances and location of event leading to death, from comprehensive medical examiner investigative reports. Results. There were 165 deaths that occurred in the presence of law enforcement: 114 were from a known disease, and 51 were either trauma related or the sudden, unexpected initial presentation of a previously unrecognized disease. Three deaths occurred in the context of physical restraint by law enforcement. Suicide was the leading manner of death among trauma-related deaths; the means of suicide was predictable based on in-custody (hanging) or precustody (firearm) circumstances. Conclusions. Our findings highlight the potential role of medical examiners and coroners in improving completeness of data on reporting death in the presence of law enforcement to public health agencies. (Am J Public Health. 2024;114(6):642-650. https://doi.org/10.2105/AJPH.2024.307616).

Research, practice, and data informed investigations of child and youth suicide: A science to service and service to science approach.

BACKGROUND: Suicide rates for children and adolescents have been increasing over the past 2 decades. In April 2023, the National Institute of Mental Health (NIMH) convened a two-day workshop to address child and youth suicide. PURPOSE: The workshop focus was to discuss the state of the science and stimulate a collaborative response between researchers, death investigators, and data collection teams to build a science to service and service to science approach toward understanding - and ultimately preventing - this growing problem of child and youth suicide. HIGHLIGHTS: Topics that meeting participants highlighted as worthy of further consideration for research and practice were: increasing awareness among death investigators, medical examiners, and coroners that child suicide deaths under age 10 years do occur and should be investigated and documented accordingly; emphasizing the value of science based protocols for child and youth death investigations to enhance consistency of approaches; and articulating needs for postvention services to suicide loss survivors. OUTCOMES: The importance of collecting an accurate and complete cause and manner of death (i.e., unintentional, suicide, homicide, undetermined) among all child decedents, and demographic information such as race, ethnicity, and sexual/gender minority status was underscored as critical for enhanced surveillance. For prevention efforts, approaches to assessing and understanding suicidal thoughts and behaviors among diverse groups of children, and the variability in proximal and distal risk factors are needed to inform opportunities for preventive interventions for diverse communities. The need for consistent measures and processes to improve death investigations, fatality review committees, and coordination between data collection systems and agencies was also raised. PRACTICAL APPLICATIONS: Collaborations among researchers, death investigators, and data collection teams can help to fully describe the child and youth suicide crisis and provide actionable information for new research, and prevention and response efforts.

The National Association of Medical Examiners Position Paper: Second Autopsies.

ABSTRACT: Second autopsies are uncommon in the United States yet are of significant public value. A second autopsy may be sought when the first autopsy findings are disputed, considered biased, or inadequately communicated. Second autopsies are technically and interpretatively difficult and usually rely heavily on investigative information, first autopsy findings, and additional documentation from the first autopsy. Medicolegal second autopsies should be performed only by experienced, board-certified forensic pathologists. Pathologists performing second autopsies should acknowledge and disclose the limitations of second autopsies. The first autopsy pathologist should recognize the quality assurance value of a second autopsy and fully disclose autopsy documentation to the second autopsy pathologist, if permitted by jurisdictional law.

The Neuropathology of 1p36 Deletion Syndrome: An Autopsy Case Series.

1p36 deletion syndrome is the most common terminal deletion syndrome, manifesting clinically as abnormal facies and developmental delay with frequent cardiac, skeletal, urogenital, and renal abnormalities. Limited autopsy case reports describe the neuropathology of 1p36 deletion syndrome. The most extensive single case report described a spectrum of abnormalities, mostly related to abnormal neuronal migration. We report the largest published series of 1p36 autopsy cases, with an emphasis on neuropathologic findings. Our series consists of 3 patients: 2 infants (5-hours old and 23-days old) and 1 older child (11 years). Our patients showed abnormal cortical gyration together with a spectrum of neuronal migration abnormalities, including heterotopias and hippocampal abnormalities, as well as cerebellar hypoplasia. Our findings thus support the role of neuronal migration defects in the pathogenesis of cognitive defects in 1p36 deletion syndrome and broaden the reported neuropathologic spectrum of this common syndrome.

Ventilatory response to CO2 in patients with epilepsy.

OBJECTIVE: Severe periictal respiratory depression is thought to be linked to risk of sudden unexpected death in epilepsy (SUDEP) but its determinants are largely unknown. Interindividual differences in the interictal ventilatory response to CO2 (hypercapnic ventilatory response [HCVR] or central respiratory CO2 chemosensitivity) may identify patients who are at increased risk for severe periictal hypoventilation. HCVR has not been studied previously in patients with epilepsy; therefore we evaluated a method to measure it at bedside in an epilepsy monitoring unit (EMU) and examined its relationship to postictal hypercapnia following generalized convulsive seizures (GCSs). METHODS: Interictal HCVR was measured by a respiratory gas analyzer using a modified rebreathing technique. Minute ventilation (VE ), tidal volume, respiratory rate, end tidal (ET) CO2 and O2 were recorded continuously. Dyspnea during the test was assessed using a validated scale. The HCVR slope (ΔVE /ΔETCO2 ) for each subject was determined by linear regression. During the video-electroencephalography (EEG) study, subjects underwent continuous respiratory monitoring, including measurement of chest and abdominal movement, oronasal airflow, transcutaneous (tc) CO2 , and capillary oxygen saturation (SPO2 ). RESULTS: Sixty-eight subjects completed HCVR testing in 151 ± (standard deviation) 58 seconds, without any serious adverse events. HCVR slope ranged from -0.94 to 5.39 (median 1.71) L/min/mm Hg. HCVR slope correlated with the degree of unpleasantness and intensity of dyspnea and was inversely related to baseline ETCO2 . Both the duration and magnitude of postictal tcCO2 rise following GCSs were inversely correlated with HCVR slope. SIGNIFICANCE: Measurement of the HCVR is well tolerated and can be performed rapidly and safely at the bedside in the EMU. A subset of individuals has a very low sensitivity to CO2 , and this group is more likely to have a prolonged increase in postictal CO2 after GCS. Low interictal HCVR may increase the risk of severe respiratory depression and SUDEP after GCS and warrants further study.

Report and Recommendations of the Association of Pathology Chairs' Autopsy Working Group.

Autopsy has been a foundation of pathology training for many years, but hospital autopsy rates are notoriously low. At the 2014 meeting of the Association of Pathology Chairs, some pathologists suggested removing autopsy from the training curriculum of pathology residents to provide additional months for training in newer disciplines, such as molecular genetics and informatics. At the same time, the American Board of Pathology received complaints that newly hired pathologists recently certified in anatomic pathology are unable to perform an autopsy when called upon to do so. In response to a call to abolish autopsy from pathology training on the one hand and for more rigorous autopsy training on the other, the Association of Pathology Chairs formed the Autopsy Working Group to examine the role of autopsy in pathology residency training. After 2 years of research and deliberation, the Autopsy Working Group recommends the following:Autopsy should remain a component of anatomic pathology training.A training program must have an autopsy service director with defined responsibilities, including accountability to the program director to record every autopsy performed by every resident.Specific entrustable activities should be defined that a resident must master in order to be deemed competent in autopsy practice, as well as criteria for gaining the trust to perform the tasks without direct supervision.Technical standardization of autopsy performance and reporting must be improved.The current minimum number of 50 autopsies should not be reduced until the changes recommended above have been implemented.

3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy) Intoxication in a Young Adult with Giant Coronary Aneurysms from Kawasaki Disease.

Kawasaki disease is an acute vasculitis of unknown etiology that usually occurs in children less than five years old. Coronary artery aneurysm due to arteritis is the most common cardiac complication. Chronic aneurysms are associated with an increased risk of developing luminal thrombosis and ischemic myocardial injury. We present a case of an 18-year-old male with a history of Kawasaki disease complicated by chronic giant aneurysms of the right and left coronary arteries. Serial echocardiographic studies and treadmill electrocardiogram stress tests as recent as 1.5 years before death revealed excellent cardiac function by clinical criteria. The decedent sustained a witnessed collapse after ingesting 3,4-methylenedioxymethamphetamine (MDMA) and ethanol. He was pronounced dead in the emergency department after unsuccessful resuscitative efforts. Autopsy revealed large aneurysms of the three main epicardial coronary arteries with extensive foci of severe stenosis by intimal fibrosis and organizing thrombus. Microscopic examination revealed multifocal severe myocyte hypertrophy. There were remote microinfarcts in the anterior and posterior aspects of the left ventricle and a recent, healing microinfarct in the posterior aspect of the left ventricle. Toxicology examination of postmortem femoral blood revealed MDMA, ethanol, and amiodarone. This case illustrates the residual, lasting effects of cardiac disease due to Kawasaki disease and a potential complication in the setting of use of an illicit stimulant, MDMA, an amphetamine derivative that produces sympathetic activation and cardiovascular effects including tachycardia, vasoconstriction, dysrhythmias, and coronary artery spasm. Kawasaki disease-related abnormalities of the heart likely resulted in a lower threshold for developing a fatal cardiac dysrhythmia under the circumstance of stimulant use.

Unexpected Death of a Child with Complex Febrile Seizures-Pathophysiology Similar to Sudden Unexpected Death in Epilepsy?

Febrile seizures are usually considered relatively benign. Although some cases of sudden unexplained death in childhood have a history of febrile seizures, no documented case of febrile seizure-induced death has been reported. Here, we describe a child with complex febrile seizures who died suddenly and unexpectedly after a suspected seizure while in bed at night during the beginning phases of sleep. She was resuscitated and pronounced brain dead 2 days later at our regional medical center. Autopsy revealed multiorgan effects of hypoperfusion and did not reveal an underlying (precipitating) disease, injury, or toxicological cause of death. Although a seizure was not witnessed, it was suspected as the underlying cause of death based on the medical examiner and forensic pathologist (author Marcus Nashelsky) investigation, the post-resuscitation clinical findings, and multiple aspects of the clinical history. The child had a history of complex febrile seizures that had previously caused apnea and oxygen desaturation. She had two febrile seizures earlier on the same day of the fatal event. Interestingly, her mother also experienced a febrile seizure as a child, which led to respiratory arrest requiring cardiorespiratory resuscitation. This case suggests that in a child with complex febrile seizures, a seizure can induce death in a manner that is consistent with the majority of cases of sudden unexpected death in epilepsy (SUDEP). Further work is needed to better understand how and why certain individuals, with a history of epilepsy or not, die suddenly and unexpectedly from seizures. This will only occur through better understanding of the pathophysiologic mechanisms underlying epileptic and febrile seizures and death from seizures including SUDEP.

Acid-sensing ion channel 1 and nitric oxide synthase are in adjacent layers in the wall of rat and human cerebral arteries.

Extracellular acidification activates a family of proteins known as acid-sensing ion channels (ASICs). One ASIC subtype, ASIC type 1 (ASIC1), may play an important role in synaptic plasticity, memory, fear conditioning and ischemic brain injury. ASIC1 is found primarily in neurons, but one report showed its expression in isolated mouse cerebrovascular cells. In this study, we sought to determine if ASIC1 is present in intact rat and human major cerebral arteries. A potential physiological significance of such a finding is suggested by studies showing that nitric oxide (NO), which acts as a powerful vasodilator, may modulate proton-gated currents in cultured cells expressing ASIC1s. Because both constitutive NO synthesizing enzymes, neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS), are expressed in cerebral arteries we also studied the anatomical relationship between ASIC1 and nNOS or eNOS in both rat and human cerebral arteries. Western blot analysis demonstrated ASIC1 in cerebral arteries from both species. Immunofluorescent histochemistry and confocal microscopy also showed that ASIC1-immunoreactivity (IR), colocalized with the smooth muscle marker alpha-smooth muscle actin (SMA), was present in the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA) and basilar artery (BA) of rat and human. Expression of ASIC1 in cerebral arteries is consistent with a role for ASIC1 in modulating cerebrovascular tone both in rat and human. Potential interactions between smooth muscle ASIC1 and nNOS or eNOS were supported by the presence of nNOS-IR in the neighboring adventitial layer and the presence of nNOS-IR and eNOS-IR in the adjacent endothelial layer of the cerebral arteries.

Four postmortem case reports with quantitative detection of the synthetic cannabinoid, 5F-PB-22.

In January 2014, the US government temporarily designated 5F-PB-22, along with three other synthetic cannabinoids (AB-FUBINACA, ADB-PINACA and PB-22), into Schedule I. Over the course of a 4-month time period (July-October 2013), our laboratory quantitatively identified 5F-PB-22 in specimens obtained from four postmortem cases. We describe the four cases, to include pertinent autopsy findings and decedent histories, together with quantitative results for 5F-PB-22 determined in postmortem blood and antemortem serum. Samples were prepared via a liquid-liquid extraction at pH 10.2 into hexane : ethyl acetate. Instrumental analysis was achieved with liquid chromatography coupled with electrospray ionization tandem mass spectrometry operating in multiple reaction monitoring mode. Two ion transitions were monitored for the analyte of interest, and one ion transition was monitored for the internal standard. The observed concentration range of 5F-PB-22 is 1.1-1.5 ng/mL for three postmortem blood specimens and one antemortem serum specimen. Three of the decedents experienced abrupt, sudden death; however, one decedent expired after a rapidly deteriorating hospital course.

Recent Iowa trends in sudden unexpected infant deaths: the importance of public health collaboration with medical examiners' offices.

During the winter in 2008, Iowa experienced an increase in sudden unexplained infant deaths (SUIDs). SUIDs and infectious causes of infant deaths generally average 3 monthly (SD = 1.0) in Iowa. However, in January 2008, 9 infant deaths were reported to the Iowa Department of Public Health and the Iowa Office of the State Medical Examiner. Between January and March of 2008, joint investigation of 22 SUIDs was conducted. The investigations required the involvement of multiple medical examiners from various jurisdictions, testing for pathogens at the University Hygienic Laboratory, epidemiologic support from the Iowa Department of Public Health, and consultation with the Centers for Disease Control and Prevention. The preliminary hypotheses for the increase in the infant mortality included viral respiratory disease and/or possible novel respiratory viral infections being the cause. Collaboration between public health and the medical examiner offices resulted in timely assessment of the cases. While no single causative agent was responsible for the increase seen in the number of infant deaths, respiratory pathogens played a role in the deaths of 15 of 22 children.

Postmortem gastric perforation (gastromalacia) mimicking abusive injury in sudden unexplained infant death.

Gastromalacia is a postmortem autolysis of gastric tissue that can culminate in gastric perforation. This entity is well-recognized by pathologists but is rarely encountered by diagnostic radiologists. We are reporting a case of sudden unexplained infant death (SUID) in which a boy was found to have pneumoperitoneum on postmortem radiographs, subsequently proved by autopsy to be caused by postmortem gastric perforation resulting from gastromalacia. It is important for radiologists to recognize this entity so as not to mistake it for bowel perforation caused by antemortem pathology, including inflicted trauma.

Autopsy after traumatic death--a shifting paradigm.

OBJECTIVE: The role of autopsy in evaluating missed injury after traumatic death is well established and discussed in the literature. The frequency of incidental findings in trauma patients has not been reported. We believe that incidental findings are under recognized and reported by trauma surgeons. PATIENTS AND METHODS: This prospective, descriptive, cohort study was conducted at a Level 1 trauma center in a rural state. Four hundred ninety-six deaths over a 4-y period were identified from the trauma registry. Two hundred four complete autopsies were available for review. One thousand eighteen traumatic diagnoses were identified from 204 autopsies and corresponding medical records by trauma surgeons blinded to patient identity. The surgeons recorded missed diagnoses, incidental diagnoses identified at autopsy, and diagnoses known at the time of death confirmed by autopsy. RESULTS: The surgeons had a κ-score of 0.82-0.84. Forty-two patients (21% of patients) had 68 severe missed injuries; 67 patients (33% of patients) had 94 minor missed injuries. Twenty-eight patients (14%) had significant incidental findings including premature atherosclerosis, multiple endocrine neoplasia, tuberculosis, and others. CONCLUSIONS: The autopsy after traumatic death is more than a mechanism of quality control and teaching. A high proportion of patients will have incidental findings important to family members, and have public health importance. Systems need to be developed to review autopsy results with attention to identifying and communicating incidental findings. Given the incidence of significant missed injuries and incidental findings, the autopsy continues to have an important role in health care.

Nitroxidergic innervation of human cerebral arteries.

A dense network of nerves containing neuronal nitric oxide synthase is present in cerebral vessels from experimental animals. The nerves may regulate cerebrovascular tone, protect the brain from stroke, and contribute to cluster headaches in humans; but studies in humans have shown only modest nitroxidergic innervation of cerebral vessels. We tested the hypothesis that nerve fibers containing neuronal nitric oxide synthase richly innervate human cerebral arteries. We used immunohistochemical techniques at post mortem and found dense neuronal nitric oxide synthase nerve staining in human cerebral vessel walls consistent with participation of nitroxidergic fibers in human physiological and pathophysiological processes.

Characteristics and prediction of cranial crush injuries in children.

This study documents four clinical cases of fatal crush injuries to children between 1.5 and 6 years of age with correlations between modeled stress and clinically observed fracture patterns. The clinical case fractures were concentrated in the basicranium, bridged the impact sites, and traversed the middle cranial fossa in the area of the spheno-occipital synchondrosis. The crushing forces from these cases were recreated on a simplified finite element model of a cranium by applying bilateral pressures to corresponding regions. Numerous trials were run to develop a representative pattern of principal stress directions. In all cases, the highest tensile stresses were located on the basicranium and corresponded to the observed fracture path(s). These results suggest that prefailure stress field diagrams may predict fracture propagation paths, although these will not be exact. Also, these analyses indicate that quasi-static bilateral loading of the cranium may lead to predictable fracture of the basicranium.

Value of ADAMTS13 activity and inhibitor in the postmortem diagnosis of thrombotic thrombocytopenic purpura.

BACKGROUND AND OBJECTIVES: Thrombotic thrombocytopenic purpura (TTP) is a clinical diagnosis that can be difficult to establish in severely ill patients. We report a case of fulminant TTP in a woman who died before receiving plasma exchange. An autopsy plasma sample was analyzed for ADAMTS13 activity and inhibitor for correlation with the diagnosis of TTP. Recognizing that hemolysis in postmortem blood samples could interfere with ADAMTS13 activity, plasma samples from four additional decedents not suspected of having TTP were analyzed and correlated with their autopsy results. The purpose of this study was to assess whether testing postmortem samples for ADAMTS13 is useful in the postmortem diagnosis of TTP. MATERIAL AND METHODS: Plasma samples from the index case and four non-TTP decedents were analyzed for ADAMTS13 activity, ADAMTS13 inhibitor levels, and plasma free hemoglobin (PFH). Autopsy tissues were evaluated for evidence of platelet microthrombi in all five cases. RESULTS: The ADAMTS13 activity level in the index patient was <4%, and the inhibitor level was 1.0 inhibitor unit. Microthrombi were prominent in the heart, kidneys, pancreas, and adrenal glands, consistent with the clinical diagnosis of TTP. ADAMTS13 activity levels in the four non-TTP decedents ranged from 4 to 82% (3/4 < or = 26%), and inhibitor was present in two of the four samples. Postmortem PFH levels in the four non-TTP decedents ranged from 64 to 3,917 mg/dL. No microthrombi were observed. CONCLUSION: Low postmortem ADAMTS13 activity and evidence of inhibitor can occur in decedents without clinical or histologic evidence of TTP. Postmortem ADAMTS13 activity levels may not be valid in establishing a diagnosis of TTP, and high inhibitor levels in this setting may be related to elevated PFH. Caution must be used in the interpretation of ADAMTS13 testing in the presence of hemolysis.

Rural versus urban trauma: demographic influences on autopsy rates.

BACKGROUND: The autopsy has long been considered the gold standard for quality assurance review. Studies characterizing autopsies have been completed in large urban centers, but there is a paucity of research regarding autopsies at rural trauma centers. This is problematic considering that a majority of preventable trauma deaths occur in rural areas and death rates for unintentional injuries in rural populations are higher than urban populations. Rural trauma centers have differing characteristics warranting further research into the demographic differences between rural and urban trauma patients and the effects on autopsy rates. MATERIALS AND METHODS: This is a demographic study of a rural trauma center, University of Iowa Hospitals and Clinics (UIHC), with the goal of identifying characteristics of trauma patients on whom autopsy was performed. Four hundred ninety-six deaths were identified from the trauma registry between January 2002 and May 2007 (231 of which were autopsied) and demographic data (including age, race, length of hospital stay, etc.) regarding these patients was gathered into a database. Univariate and multivariate linear regression models were used to analyze differences between autopsied and non-autopsied trauma patients. Autopsy rate and basic demographics were also compared with 2 recent reports from urban trauma centers. RESULTS: Autopsied patients were younger than non-autopsied patients (mean age 45 y versus 71 y; P < 0.0001) and have a shorter median length of hospital stay (1 d versus 4 d; P < 0.0001). Autopsy rates for patients with blunt trauma were lower than rates for patients with penetrating or burn trauma (42% versus 67% and 56%; P = 0.004). If patients died while on a subspecialty service, they were less likely to have an autopsy. Compared with urban centers, this rural trauma center had lower autopsy rates, higher rates of blunt trauma, a higher mean age of deceased patients, and a lower percentage of males. CONCLUSIONS: UIHC, a rural trauma center, has a number of demographic characteristics that make it unique from urban trauma centers: an older population, lower percentage of male trauma patients, higher rates of blunt trauma, and lower rates of penetrating trauma. All of these factors influenced the lower rate of autopsies completed at rural trauma centers. Within a rural trauma center, those patients less likely to receive autopsy were older patients, those who died after 48 h in the hospital, and patients who suffered blunt injuries. The demographics of trauma patients most likely to receive an autopsy tend to correspond with those of an urban trauma population, thus providing a demographic explanation for the variation in autopsy rates among trauma systems.

Fatal abusive head trauma cases: consequence of medical staff missing milder forms of physical abuse.

OBJECTIVES: Missed diagnosis of child abuse may lead to chronic abuse with potential for death. This paper reports 3 such cases. METHODS: This is a retrospective chart review of 38 cases diagnosed as abusive head trauma between January 1, 2004 and December 31, 2006 at a university hospital. We sought to identify fatal cases with a past medical history of physical abuse that was missed by the medical staff. RESULTS: Three cases (7.9%) had a past medical history of physical abuse that was missed by the medical staff. Infants were 2 males and 1 female. Their ages were 2.5, 3.5, and 6 months, respectively. Missed abuse episodes involved rib fractures, a metaphyseal tibial fracture, and a shaking episode, respectively. The intervals that had elapsed between the missed and the fatal abuse episodes were 24 hours, 12 days, and 6 weeks, respectively. Perpetrators of fatal head trauma were all biological fathers. One plead guilty, and 2 were convicted of involuntary manslaughter. The infants were in the care of the perpetrators of the fatal abuse episodes at the time the missed abuse episodes occurred. CONCLUSIONS: Physicians assessing children, especially infants, should be alert to indicators of abusive trauma to recognize abuse early on. Including abusive trauma in the differential diagnostic list and taking appropriate steps to rule out or confirm the diagnosis are of paramount importance in establishing child protective services and preventing further abuse and neglect that may at times be fatal.

A homozygous mutation in human PRICKLE1 causes an autosomal-recessive progressive myoclonus epilepsy-ataxia syndrome.

Progressive myoclonus epilepsy (PME) is a syndrome characterized by myoclonic seizures (lightning-like jerks), generalized convulsive seizures, and varying degrees of neurological decline, especially ataxia and dementia. Previously, we characterized three pedigrees of individuals with PME and ataxia, where either clinical features or linkage mapping excluded known PME loci. This report identifies a mutation in PRICKLE1 (also known as RILP for REST/NRSF interacting LIM domain protein) in all three of these pedigrees. The identified PRICKLE1 mutation blocks the PRICKLE1 and REST interaction in vitro and disrupts the normal function of PRICKLE1 in an in vivo zebrafish overexpression system. PRICKLE1 is expressed in brain regions implicated in epilepsy and ataxia in mice and humans, and, to our knowledge, is the first molecule in the noncanonical WNT signaling pathway to be directly implicated in human epilepsy.

Evaluation of serum cortisol in the postmortem diagnosis of acute adrenal insufficiency.

Normal adrenocortical activity is necessary for electrolyte regulation and the maintenance of cardiovascular function. Although chronic adrenal insufficiency generally presents with the gradual onset of a set of characteristic symptoms and signs, the more sudden loss of adrenal activity can present with acute, rapidly progressive cardiovascular dysfunction that can be fatal if not recognized and treated promptly. We herein describe a patient who had most of his adrenal tissue removed during resection of metastatic renal carcinoma, conventional clear cell type, with much of the remaining adrenal tissue undergoing necrosis during or shortly after surgery. Although the patient appeared to be stable and progressing adequately well, he died suddenly 2 days postoperatively. When the gross autopsy findings suggested the possibility of adrenal insufficiency, clinical laboratory assessment of adrenocortical activity was sought. Analysis of stored antemortem serum samples and of blood obtained at autopsy demonstrated a progressive decrease in cortisol levels which, in this stressed postsurgical patient, proved fatal. The use of both antemortem and postmortem blood in the demonstration of acute adrenal insufficiency at autopsy is discussed.