LAUSR

Post mortem diagnosis of sepsis, especially in the forensic field, is a problem that presents several difficulties. Those difficulties are often linked to the lack of complete and adequate health records that could suggest or demonstrate the falling of the patient into a septic state. Moreover, in sepsis, pathological findings in sepsis are often nonspecific, and they are often compatible with other different clinical pictures [1]. Other clinical pictures that could simulate pathological findings that are compatible with those found in sepsis, are generally those of a systemic inflammatory response syndrome (SIRS). The death of a sepsis-affected patient generally follows a circulatory shock in the course of a multi organ failure syndrome (MOFS). Pathological findings are generally related to a generalized hypoperfusion damage, or to the presence of a disseminated intravascular coagulation syndrome (DICS); specifically, it is often macroscopically evident a picture of myocardial ischemia, pulmonary and cerebral edema, spleen infarction and often of intestinal hemorrhages [2]. Often, autopsy findings and routine histology in cases of suspected fatal sepsis are nonspecific and unconvincing. In the setting of a Sepsis, one of the organs that are most susceptible of damage is the lung. In the pulmonary parenchyma it can be found a massive leukocyte invasion, driven by a complex net of inflammatory cytokines. Various immunohistochemical markers have been investigated in cases of sepsis, especially with regard to changes in the lungs. Immunochemical markers aimed against E-selectine, very late antigen 4 (VLA-4), intracellular adhesion molecule 1 (ICAM-1) and lactoferrine were tried. Other markers were directed against the vascular endothelial growth factor (VEGF) in order to show its reduction during sepsis [3]. Through the use of immunohistochemical techniques on samples of lung taken from patients that died from Sepsis, it was demonstrated the presence of macrophages that expressed CeC chemokine receptor type 2 (CCR2) and CX3C chemokine receptor 1 (CX3CR1), two proteins that mediate migration and chemotaxis, highlighting a strong macrophage tissue recruitment during the infection [4]. In another study, in patients deceased from sepsis related acute respiratory distress syndrome (ARDS), using immunohistochemistry, it was demonstrated a diminishing in the expression of the angiotensin converting enzyme and of the vascular endothelial cadherin (VE-Cadherin) [5,6]. Those techniques proved to be extremely useful, with very encouraging results, often very suggestive of a diagnosis of sepsis, but they were not entirely convincing, and today, we still do not have a welldefined indicator capable of driving a histological diagnosis of Sepsis. Molecules such as tumor necrosis factor alpha (TNFα), interleukin1 beta (IL-1 β) and interleukin-6 (IL-6) are found intermittently, or for short periods of time during an inflammatory response and during sepsis [7]. Procalcitonin on the other hand is found persistently elevated in sepsis and it’s not subject to down-regulation, and it does not diminish even after prolonged periods of stimulation.