Autopsy Standardized Mortality Review: A Pilot Study Offering a Methodology for Improved Patient Outcomes.

A standardized mortality review of hospital autopsies identified discrepancies between clinical diagnoses and autopsy findings, unexpected deaths, adequacy of diagnostic workup, presence of adverse event, and type of a quality issue if present. The standardized review elements were chosen based on a review of quality metrics commonly used by hospitals. The review was completed by the pathologist based on their initial autopsy findings. The final autopsy report was later reviewed to confirm the initial review findings. Major discrepancies in diagnosis were categorized as class I or II based on the modified Goldman criteria. Ninety-six hospital autopsy cases from January 2015 to February 2018 were included in the study. The overall major discrepancy rate was 27%. Class I discrepancies, where a diagnosis found at autopsy might have improved survival had it been made premortem, were identified in 16% of cases. Categories associated with increased discrepancy rates included unexpected deaths, inadequate workup, abnormal labs or imaging not addressed, and certain quality issues. Deaths not expected at admission but expected at the time of death, those with adverse events, those within 48 hours of a procedure, those within 48 hours of admission, those with physician-specific quality issues, and those with system or process issues were not significantly related to diagnostic accuracy.

Postmortem Diagnosis of Diabetic Ketoacidosis Presenting as the "Dead-in-Bed Syndrome".

OBJECTIVE: To report a case of a young male with type 1 diabetes mellitus found dead in his bed, initially assumed to have died from hypoglycemia (i.e., the "dead in bed" syndrome). However, his autopsy findings revealed that diabetic ketoacidosis (DKA) was the cause of death. METHODS: We present the laboratory and autopsy findings of the patient, highlighting the importance of laboratory analyses of the vitreous humor and microscopy of kidney tissue when investigating the cause of sudden death in patients with type 1 diabetes. RESULTS: A 25-year-old healthy male with type 1 diabetes on continuous subcutaneous insulin infusion therapy was found dead in his undisturbed bed. An autopsy included vitreous humor analyses. His results were as follows: glucose of 755 mg/dL (reference range 70-105 mg/dL), anion gap >36 mEq (reference range 4-12 mEq/L), elevated acetone at 66 mg/dL (reference range negative), which were consistent with DKA. Renal microscopy demonstrated subnuclear vacuoles in the proximal tubules, 1 of 2 lesions were described as an Armanni-Ebstein lesion, which is a postmortem finding in patients who die from diabetic coma. CONCLUSION: The most likely cause of death at home in young patients with type 1 diabetes is severe hypoglycemia. However, an autopsy of the present case confirmed DKA based on vitreous humor biochemistry and microscopic examination of the kidneys, which demonstrated the Armanni-Ebstein phenomenon. Analysis of the vitreous fluid and microscopic examination of the kidneys for the presence of Armanni-Ebstein lesion can be used to help determine the cause of death in patients with type 1 diabetes mellitus.

MCP-1and IL-1ß expression in the myocardia of two young patients with Type 1 diabetes mellitus and fatal diabetic ketoacidosis.

Convincing evidence exists for the early onset of diabetic cardiomyopathy and coronary artery disease (CAD) as distinct forms of cardiac disease in young patients with Type 1 diabetes mellitus (T1DM) and the pre-stages of T2DM, forms of dysregulated insulin signaling. Progression of both chronic cardiac conditions is mediated by oxidative stress and low grade inflammation. This study reports the expression of monocyte chemotactic protein-1 (MCP-1) chemokine and the interleukin (IL)-1ß inflammatory cytokine in two young patients with suboptimal metabolic control and fatal diabetic ketoacidosis (DKA), two age-matched overweight/obesity cases and two age-matched controls. In addition, markers of oxidative stress, apoptosis, collagen deposition and cardiomyocyte hypertrophy were studied. Significant expression of MCP-1 and IL-1ß was seen in the myocardia of the T1DM/DKA cases, with lesser amounts expressed in the overweight/obesity myocardia. All of the other markers except cardiomyocyte hypertrophy were expressed to a significantly greater extent in the T1DM/DKA and overweight/obesity cases in comparison to the age-matched controls. Cardiomyocyte hypertrophy was significantly greater in the overweight/obesity cases than in the T1DM/DKA or the control cases.

Guidelines for postmortem protocol for ocular investigation of sudden unexplained infant death and suspected physical child abuse.

Postmortem examination is a cornerstone in identifying the cause of unexplained sudden death in children. Even in cases of suspected or known abuse, an autopsy may help characterize the nature of the abuse, which is particularly important in the forensic autopsy of children in the first 3 to 4 years of life when inflicted neurotrauma is most common. Forensic examinations are vital in cases that might otherwise be diagnosed as sudden infant death syndrome. The ocular autopsy in particular may demonstrate findings that were not appreciated on antemortem clinical examination. This protocol for postmortem examination of the eyes and orbits was developed to promote more consistent documentation of findings, improved clinical and forensic decision making, and more replicable and coherent research outcomes.

Ocular manifestations of crush head injury in children.

AIMS: To review the ocular manifestations of crush head injuries in children. METHODS: Retrospective clinical and pathological reviews. Group 1: A total of 16 children admitted with crush head injuries from television tip over. Group 2: Nine autopsy findings in crush head injury. RESULTS: Group 1: A total of 11 children had fundus examination: three by neurosurgeons, eight by ophthalmologists. Scattered posterior pole preretinal and blot haemorrhages extending to mid equator region observed in one child. No evidence of traumatic retinoschisis or retinal folds in any patient. Group 2: All with multiple skull fractures and six with subdural haemorrhage. Posterior pole retinal haemorrhages in four children, extending to the ora serrata in one after motor vehicle accident. No child had retinal folds. Subinternal limiting membrane haemorrhages in three children. Optic nerve sheath haemorrhage in three children. CONCLUSIONS: Intraretinal and preretinal haemorrhages, predominantly in the posterior pole, can occur in crush injury to the paediatric head. Haemorrhage under the internal limiting membrane or extending to the ora serrata were only seen in situations where crush injury was part of a fatal trauma scenario related to motor vehicles. Retinal folds and the typical macular retinoschisis associated with abusive head injury were not observed.

Age of retinal hemorrhages by iron detection: an animal model.

Intraretinal hemorrhages have been found in some abusively injured infants and children. Intraretinal hemosiderin has been proposed as an indication of previous injury. The limits of the accuracy of the proposal have not been established. Experimental central retinal vein occlusion (CRVO) was produced in 20 eyes of adult rhesus monkeys as part of ongoing research by one of the authors (SSH). The animal experiments were conducted in accordance with a research protocol approved by the Animal Care Committee, University of Iowa. CRVO produced diffuse intraretinal hemorrhages. Clinical ocular examinations assessed the onset and time course of retinal hemorrhages. Enucleation specimens were used to assess hemosiderin in the retinas. Hemosiderin was detected within 2 days of induction of retinal hemorrhages. It was detected in only 4 of 11 eyes (36%) studied more than 1 week following induction of hemorrhages. In 2 eyes, hemosiderin was found 9 and 16.8 months after development of hemorrhages. Hemosiderin can represent organization of current hemorrhage rather than evidence of prior hemorrhage. This study does not allow specifying the duration of hemorrhages with greater precision than "more than 2 days prior to death," and that, only if there is no survival interval. Failure to detect hemosiderin does not exclude prior retinal hemorrhages.

Why do histology on retinal haemorrhages in suspected non-accidental injury?

The detailed documentation of ocular pathology has become an important component in the autopsy investigation of suspected cases of non-accidental injury in infants and young children. Careful histological examination of retinal haemorrhages is of critical importance, but there remains debate about the significance of some findings. This issue has been thrown into sharper relief by recent neuropathological studies questioning the mechanisms of some CNS findings. To discuss the importance of histological findings in the retina and their potential significance and specificity, we have invited contributions from authors in the USA and UK.

Prehospital cardiac arrest in diabetic ketoacidemia: why brain swelling may lead to death before treatment.

An adolescent is reported with type 1 diabetes mellitus and diabetic ketoacidemia (DKA) who died from brain herniation prior to treatment with intravenous fluids and intravenous insulin. The pathophysiology of raised intracranial pressure (ICP) and water intoxication is discussed. As DKA evolves, water and electrolyte losses are replaced by very hypotonic fluids taken orally, leading to a physiologic excess of free water that would cause brain swelling prior to treatment. Central nervous system acidosis may interfere with normal compensatory mechanisms that help prevent small increases in ICP. The pathophysiology of pre-treatment brain swelling has important implications for rehydration with intravenous fluids and treatment with insulin. Prevention of DKA is paramount as well as complete postmortem evaluation of patients who die from this disease.