Acute Pancreatitis Presenting as Sudden, Unexpected Death

Institute of Legal Medicine and Forensic Sciences, Berlin, Germany.
American Journal of Forensic Medicine & Pathology (Impact Factor: 0.7). 10/2007; 28(3):267-70. DOI: 10.1097/PAF.0b013e3181425615
Source: PubMed


Acute pancreatitis represents a spectrum of disease, ranging from a mild, transitory illness to a severe, rapidly progressive hemorrhagic form, with massive necrosis and mortality rates of up to 24%. The reported incidence of acute pancreatitis diagnosed first at clinicopathologic autopsy ranges between 30% and 42%. To better describe outpatient fatalities due to acute pancreatitis that present as sudden, unexpected death, we retrospectively reviewed the autopsy files at the Institute of Legal Medicine, University of Hamburg, Germany, from 2000-2004. Individual cases were analyzed for sex, age, race, circumstances of death, social background of the deceased and previous medical history, seasonal occurrence of the disease, blood alcohol concentration at the time of death, body mass index, autopsy findings, histopathology, and etiology of acute pancreatitis. Among the 6178 autopsies carried out during the 5-year period evaluated, there were 27 cases of acute pancreatitis that presented as sudden, unexpected death. In all cases, the diagnosis was first made at autopsy. The male:female ratio was 1.7:1 and the mean age was 52 years (range, 30-91 years). Etiologies of acute pancreatitis included alcohol (n=19), gall stones (n=2), other identified etiologic factors (n=3), and idiopathic (n=3). Complications of acute pancreatitis included lung edema and/or acute respiratory distress syndrome, peritonitis, disseminated intravascular coagulation, and sepsis. At least 20 subjects (74%) had lived isolated, with no social contacts. Contrary to the clinical observations of a clear seasonal variation in the onset of acute pancreatitis, we found no correlation between death due to acute pancreatitis and a specific month or season. Many prior studies have suggested that the majority of deaths in severe acute pancreatitis occur in the late phase of the disease as a result of pancreatic sepsis. Conversely, in the present study, the majority of affected individuals died during the very early phase of the disease. While gallstones represent the main etiologic factor in most larger clinical series, biliary etiology seems to play only a minor role in outpatient deaths undergoing medicolegal autopsies. Data derived from medicolegal autopsy studies should be included in future population-based studies of acute pancreatitis.

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    • "However most of the cases have acute hemorrhagic pancreatitis which is not problematic to diagnose during the autopsy. There are also anecdotal cases of fatty necroses in lipomatous heart as a cause of sudden death in acute pancreatitis [3]. However it seems that underlying hearth/vascular/brain disease is an important prerequisite for sudden death in acute pancreatitis [4]. "

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    ABSTRACT: Acute pancreatitis (AP) is a common disease. Mild disease resolves spontaneously in a few days. Severe forms of the disease can lead to local complications, necrosis, and abscesses in and around the pancreas. Systemic inflammation in severe AP is associated with distant organ failures. The aim of this study is to identify genetically determined prognostic factors involved in the clinical features of AP. The study employs a candidate-gene approach, and the genes are involved in trysinogen activation in the initiation phase of the disease, as well as in the systemic inflammation as the disease proceeds. The last study examines adipokines, fat-derived hormones characterized with the capacity to modify inflammation. SPINK 1 is a gene coding trypsin activation inhibitor. Mutations N34S and P55N were determined by minisequencing methods in 371 AP patients and in 459 controls. The mutation N34S was more common in AP patients (7.8%) than in controls (2.6%). This suggests that SPINK 1 gene mutation N34S is a risk factor for AP. In the fourth study, in 12 matched pairs of patients with severe and mild AP, levels of adipokines, adiponectin, and leptin were evaluated. Plasma adipokine levels did not differ between patients with mild and severe AP. The results suggest that in AP, adipokine plasma levels are not factors predisposing to organ failures. This study identified the SPINK 1 mutation N34S to be a risk factor for AP in the general population. As AP is a multifactorial disease, and extensive genetic heterogeneity is likely, further identification of genetic factors in the disease requires larger future studies with more advanced genetic study models. Further identification of the patient characteristics associated with organ failures offers another direction of the study to achieve more detailed understanding of the severe form of AP. Akuutti haimatulehdus on tavallinen akuutin vatsakivun syy. Lievä haimatulehdus paranee muutamassa päivässä. Vaikeaan haimatulehdukseen liittyy paikallisia komplikaatioita; kudoskuoliota ja paiseita haimassa ja sen ympärillä ja systeeminen tulehdusreaktio liittyy monielinvaurioon. Tämän tutkimuksen tarkoituksena on tunnistaa geneettisesti määräytyviä ennusteellisia tekijöitä akuutissa haimatulehduksessa. Tutkimuksen kandidaattigeenit liittyvät trypsinogeenin aktivaatioon taudin alussa ja systeemiseen tulehdukseen taudin edetessä. Viimeinen osatyö tutkii adipokiinien mahdollista osuutta systeemisen tulehduksen säätelijöinä. SPINK 1 koodaa trypsiinin aktivaation inhibiittoria. Tämän geenin mutaatiot N34S ja P55N määritettiin minise-kvensoimalla 371 akuuttia haimatulehdusta sairastavalta potilaalta ja 459 kontrollihenkilöltä. Mutaatio N34S oli tavallisempi akuuttia haimatulehdusta sairastavilla potilailla (7.8%) kuin kontrolleilla (2.6%). Tulehdusgeenipolymorfismit geeneissä TNF, HSPA1B, CD14 and IL-10 on liitetty kirjallisuudessa alkoholi-haimatulehduksen riskiin ja siihen että haimatulehdus kehittyy vaikeaksi. Tutkimuksen 397 akuuttia haimatulehdusta sairastaneelta potilaalta ja 310 kontrollihenkilöltä määritettiin genotyypit MALDI-TOF tekniikkaan perustuvalla menetelmällä. Eroja eri tutkimusryhmien välillä ei todettu. Hemostaattisen muutokset liittyvät tulehdukseen ja hyytymistä edistävät tekijät saattavat vahventaa tulehdusreak-tioita. Hyytymistä edistävä hyytymistekijä V Leiden mutaatio ja plasminogeenin aktivaation inhibiittori -1 4G/5G polymorfia määritettiin 397 haimatulehduspotilaalta ja 310 kontrollihenkilöltä. Tutkimusaineistossa näiden po-lymorfioiden alleelifrekvenssit eivät eronneet kontrolliaineistosta. Neljännessä osatyössä tutkittiin adipokiinien, adipokiinin ja leptiinin pitoisuuksia plasmassa lievää ja vaikeaa haimatulehdusta sairastavilla potilailla. Sairaalaan tulovaiheessa ei todettu eroja plasman adipokiini pitoisuuksissa potilailla joilla oli lievä tai vaikea akuutti haimatulehdus. Tuloksista voidaan päätellä että adipokiinit eivät vaikuta systeemiseen tulehdukseen akuutissa haimatulehduksessa. Tämän väitöskirjatyön tulokset osoittavat, että SPINK1 N34S mutaatio on riskitekijä akuuttiin haimatulehdukseen sairastumisessa. Akuutti haimatulehdus on monitekijäinen tauti ja taudin kulkuun vaikuttavien geneettisten tekijöiden tunnistaminen vaatii suuren potilasmäärän omaavia tutkimuksia ja tarkkaa tuntemusta muista tekijöistä jotka vaikuttavat taudin vaikeusasteeseen.
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    ABSTRACT: Acute pancreatitis is a protean disease which is usually mild and self limiting in most cases. The disease is severe and is associated with a high mortality in 5 - 20% of cases due to systemic complications culminating in multi-organ failure and shock. Acute pancreatitis (AP) in a subset of patients presents as sudden unexpected death and is diagnosed for the jirst time during autopsy. The majority of cases of sudden unexpected death can usually be attributed to a past history ofillness, clinicalfeatures or characteristic findings on postmortem examination. The forensic pathologist or the medical examiner faces the daunting task of determining the cause of death in those cases without any antecedent causes, suspected violence, suicide or homicide and with no clinical history of illness. Acutepancreatitis is not an uncommon cause of sudden death. We herein report jive cases of acute hemorrhagic pancreatitis from the Forensic Pathology Unit of University Malaya, Kuala Lumpur, Malaysia. Two patients presented as sudden death at home while three others died within 24 hours of hospitalization. All fivepatients had similar findings of acute hemorrhagic pancreatitis on post mortem examination. Pancreatitis associated organ failure was one of the most important determinants of mortality. Clinical correlates of organ failure included respiratory distress, hypotension and anuria. While biliary etiology represents the main cause in various clinical studies, it had an insignificant role in our five cases of sudden death undergoing medico-legal autopsy. Etiological factors included alcoholism in one and idiopathic causes in four patients. Autopsy based studies provide valuable information and a holistic approach to the study of acute pancreatitis.
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