Johan J. Dempers

Consent for autopsy research for unexpected death in early life.

Research in sudden death in fetuses (stillbirth) and infants (sudden infant death syndrome [SIDS]) is urgently needed, particularly in high-risk populations involving socioeconomic disadvantaged families. Essential to such research is the analysis of fetal and infant tissues at autopsy. Obtaining consent for donating autopsy tissues for research is especially problematic in socioeconomically disadvantaged populations in which mistrust of the medical establishment often exists. In this article, we present communication strategies for obtaining consent for research in autopsy tissues of stillbirth and SIDS cases in socioeconomically disadvantaged populations. Recommendations are provided about preparation for and the timing, setting, and content of the consent interview. The same lines of open and transparent communication delineated in this article are applicable to obtaining consent for the autopsy and autopsy research. Although the grief responses to the untimely death of the fetus or infant are universal and the recommendations of this essay are widely applicable to the general population, the expression of this grief and feelings toward autopsy-based research in socioeconomically disadvantaged populations may raise special issues that health care workers should be aware of when obtaining consent for research on autopsy-derived tissues.

Progressive Primary Pulmonary Tuberculosis Presenting as the Sudden Unexpected Death in Infancy: A Case Report

The classification of an unexpected infant death as the sudden infant death syndrome (SIDS) depends upon a complete autopsy and death scene investigation to exclude known causes of death. Here we report the death of a 4-month-old infant in a tuberculosis endemic area that presented as a sudden unexpected death in infancy (SUDI) with no apparent explanation based on the death scene characteristics. The autopsy, however, revealed progressive primary pulmonary tuberculosis with intrathoracicadenopathy, compression of the tracheobronchial tree and miliary lesions in the liver. This case underscores the clinical difficulties in the diagnosis of infantile tuberculosis, as well as the possibility of sudden death as part of its protean manifestations. The pathology and clinical progression of tuberculosis in infants differ from older children and adults due to the immature immune response in infants. This case dramatically highlights the need for complete autopsies in all sudden and unexpected infant deaths, as well as the public health issues in a sentinel infant tuberculosis diagnosis.

Profiling the approach to the investigation of viral infections in cases of sudden unexpected death in infancy in the Western Cape Province, South Africa.

BACKGROUND Sudden unexpected death in infancy is one of the main contributory factors to high infant mortality rates world-wide. Several risk factors, including viral infection, have been implicated in SUDI cases, but no single factor has been confirmed as the main cause of death. At the Tygerberg Medico-legal Laboratory, Cape Town, South Africa, investigation of lung tissue for viral infection forms part of an institutional protocol for the examination of cases of sudden unexpected death in infancy. METHODS Lung tissue from 82 cases of sudden unexpected death in infancy was collected over a 10 month period. Routine shell vial cultures and histological examination of the tissue were performed according to the standard institutional protocol on fresh and formalin-fixed tissue, respectively. In addition, real-time polymerase chain reactions and immunohistochemical staining for adenovirus, cytomegalovirus and respiratory syncytial virus were done on fresh and formalin-fixed lung tissue, respectively. RESULTS Huge variation was found in the number of positive cases confirmed by shell vial culture, real-time polymerase chain reaction and immunohistochemistry (0, 2 and 0 for adenovirus; 3, 29 and 2 for cytomegalovirus; and 0, 0 and 4 for respiratory syncytial virus, respectively). CONCLUSIONS In the absence of a National Protocol for investigation of sudden unexpected death in infancy, we conclude that the selection of viruses and routine diagnostic technique included in the institutional investigation protocol might be suboptimal and should be re-evaluated.

Linking mortuary data improves vital statistics on cause of death of children under five years in the Western Cape Province of South Africa.

Reducing child mortality requires good information on its causes. Whilst South African vital registration data have improved, the quality of cause‐of‐death data remains inadequate. To improve this, data from death certificates were linked with information from forensic mortuaries in Western Cape Province.

Hepatic hemangioendothelioma presenting as sudden unexpected death in infancy: A case report

The classification of an unexpected infant death as sudden infant death syndrome (SIDS) depends upon a complete autopsy, death scene investigation, and review of medical history to exclude known causes of death. Death from occult neoplastic disease in infancy is extremely rare but is within the broad differential diagnosis of SIDS. We report the sudden and unexpected death of a 1-month-old infant from a hepatic (infantile) hemangioendothelioma. The physiologic mechanism of death was likely cardiac failure induced by the circulatory demands of this large vascular tumor and respiratory compromise from diaphragmatic thoracic incursion. The clinical progression and pathology of these relatively common tumors of infant livers are extremely variable. This case dramatically illustrates the potential for fatal outcome of this tumor, as well as the need for autopsy to determine the cause of sudden and unexpected death in an infant.

The Institution of a Standardized Investigation Protocol for Sudden Infant Death in the Eastern Metropole, Cape Town, South Africa(,) (.)

The rate for the sudden infant death syndrome (SIDS) in Cape Town, South Africa, is estimated to be among the highest in the world (3.41/1000 live births). In several of these areas, including those of extreme poverty, only sporadic, nonstandardized infant autopsy, and death scene investigation (DSI) occurred. In this report, we detail a feasibility project comprising 18 autopsied infants with sudden and unexpected death whose causes of death were adjudicated according to the 1991 NICHD definitions (SIDS, n = 7; known cause of death, n = 7; and unclassified, n = 4). We instituted a standardized autopsy and infant DSI through a collaborative effort of local forensic pathology officers and clinical providers. The high standard of forensic investigation met international standards, identified preventable disease, and allowed for incorporation of research. We conclude that an effective infant autopsy and DSI protocol can be established in areas with both high sudden unexpected infant death, and elsewhere. (SUID)/SIDS risk and infrastructure challenges.

Review of immunological and virological aspects as contributory factors in Sudden Unexpected Death in Infancy (SUDI)

Currently in South Africa research into sudden unexpected death in infancy (SUDI) is limited. The causes of sudden infant death syndrome (SIDS) remain obscure despite full medico-legal investigations inclusive of autopsy, scene visit and ancillary studies. Viral infections play an important role as a multitude of respiratory viruses have been detected in autopsy specimens and are implicated in these deaths. The specific contribution of viruses in the events preceding SIDS still warrants deciphering. Infancy is characterised by marked vulnerability to infections due to immaturities of the immune system that may only resolve by the age of 24 months. Routine viral screening of all SUDI cases at Tygerberg Forensic Pathology Service (FPS) Mortuary in Cape Town focuses on only a portion of respiratory viruses from lung and liver tissue. This review highlights important virological and immunological aspects regarding investigations into the infectious nature of SUDI, including the lack of national standardised guidelines for appropriate specimen collection at autopsy and subsequent laboratory analysis.

Henssge nomogram typesetting error.

The Henssge nomogram technique for estimation of post mortem interval (PMI) utilizing body cooling is used worldwide by forensic pathologists (FPs) who may photocopy the nomogram from a popular source such as the textbook Knight’s Forensic Pathology [1, 2] to calculate the PMI. The relationship of the components of the nomogram to each other is crucial for accurate calculations. Any alteration from the exact spatial layout will result in significant error. In recent cases, different FPs determined the PMI independently and observed significantly divergent answers for each case. Careful scrutiny of the calculation process showed that the only variable in the processes was that nomograms were copied from two different sources: one from Forensic Pathology by Knight and Saukko (FPKS3) [1], and the other from Knight’s Forensic Pathology (KFP2) [2]. The latter version is similar to that in the 1 edition of this text, as well as in a paper by Henssge et al. [3]. In one high-profile case, the ambient temperature was 24 C and the rectal temperature (RT) 33 C. With corrective factors, the nomogram in KFP2 showed the PMI as just over 19 h, while the nomogram in FPKS3 gave an estimated PMI of 16 h 30 min. Using the same values in an electronic version of the equation resulted in a PMI estimation of 19 h 10 min. This represents a 13 % difference in PMI between the nomograms in KFP2 and FPKS3. Careful study of the two versions of the nomogram led us to discover differences in the typesetting of the diagrams. This was visually illustrated by superimposition of the two scanned nomograms in KFP2 and FPKS3 (Fig. 1). These variations suggest to us that the nomograms printed in the textbooks mentioned are not exact replicas of the original. We do not believe that the nomogram published in the original journal [4] suffers from these spatial defects, as similar results are found when results from this nomogram are compared to those from the calculation. However, it is suggested by some, and we strongly recommend, that the nomograms reproduced in any printed format be used cautiously, and at least be correlated with a different source and/or an electronic version of the equation. These electronic resources based on the original Henssge equation are available as, among others, a web based resource [5], and Apple and Blackberry apps in the respective e-markets. The editors are aware of this problem (personal communication—email communication with Bernard Knight) and we understand that any future editions will contain a note regarding this.

Serotonin Receptors in the Medulla Oblongata of the Human Fetus and Infant: The Analytic Approach of the International Safe Passage Study

The Safe Passage Study is an international, prospective study of approximately 12 000 pregnancies to determine the effects of prenatal alcohol exposure (PAE) upon stillbirth and the sudden infant death syndrome (SIDS). A key objective of the study is to elucidate adverse effects of PAE upon binding to serotonin (5-HT) 1A receptors in brainstem homeostatic networks postulated to be abnormal in unexplained stillbirth and/or SIDS. We undertook a feasibility assessment of 5-HT1A receptor binding using autoradiography in the medulla oblongata (6 nuclei in 27 cases). 5-HT1A binding was compared to a reference dataset from the San Diego medical examiner’s system. There was no adverse effect of postmortem interval ⩽100 h. The distribution and quantitated values of 5-HT1A binding in Safe Passage Study cases were essentially identical to those in the reference dataset, and virtually identical between stillbirths and live born fetal cases in grossly non-macerated tissues. The pattern of binding was present at mid-gestation with dramatic changes in binding levels in the medullary 5-HT nuclei over the second half of gestation; there was a plateau at lower levels in the neonatal period and into infancy. This study demonstrates feasibility of 5-HT1A binding analysis in the medulla in the Safe Passage Study.