Clinical diagnosis versus autopsy diagnosis in head trauma

The correct and complete diagnosis is essential for the adequate care and the favourable clinical evolution of the patients with head trauma. Purpose: To identify the error rate in the clinical diagnosis of head injuries as shown in comparison with the autopsy diagnosis and to identify the most common sources of error. Material and method: We performed a retrospective study based on data from the medical files and the autopsy reports of patients with head trauma who died in the hospital and underwent forensic autopsy. We collected: demographic data, clinical and laboratory data and autopsy findings. To quantify the concordance rate between the clinical diagnosis of death and the autopsy diagnosis we used a 4 classes classification, which ranged from 100% concordance (C1) to total discordance (C4) and two classes of partial discordance: C2 (partial discordance in favour of the clinical diagnosis- missing injuries in the autopsy reports) and C3 (partial discordance in favor of the necroptic diagnosis- missing injuries in the medical files). Data were analyzed with SPSS version 20.0. Results: We analyzed 194 cases of death due to head injuries. We found a total concordance between the clinical death diagnosis and autopsy diagnosis in 30.4% of cases and at least one discrepancy in 69.6% of cases. Increasing the duration of hospitalization directly correlates with the amount of the imaging investigations and these in turn correlates with an increased rate of diagnosis concordance. Among the patients with stage 3 coma who associated a spinal cord injury, we found a partial diagnosis discordance in 50% of cases and a total discordance in 50% of cases, possibly due to the need for conducting emergency imaging investigation and the need for surgical treatment. In cases with partial and total discordant diagnosis, at least one lesion was omitted in 45.1% of the cases. The most commonly omitted injuries in C2 cases were subdural hematoma, intracerebral hematoma and ventricular hemorrhage (21.6%). In C3 cases the most frequently omitted injuries were subarachnoidian hemorrhage and skull base fractures (17.9%). Conclusions: The clinical cause of death is not always concordant with the autopsy diagnosis. Autopsy may identify the inconsistencies in diagnosis, the injuries frequently skipped and the factors favoring the discordance rate between the clinical death diagnosis and the autopsy diagnosis, making it a valuable tool for improving the clinical care of the patients with head trauma

Bleeding after Hysterectomy: Recommendations and What to Expect

Bleeding after gynecological surgery remains an infrequent life-threatening complication, demanding appropriate medical and surgical management. Classified as early/“reactionary” and delayed/secondary, unexpected postoperative hemorrhage may arise regardless of the route or subtype of hysterectomy. Timely recognition and prompt intervention to arrest bleeding are essential strategies for the suitable outcome of the patient. The present chapter presents an overview on different aspects of bleeding after hysterectomy such as incidence rate, risk factors, mechanisms, and management techniques aiming to expand knowledge and skills in recognizing and treating this unpredicted potentially serious problem. Furthermore, we intend to offer a guide toward standardizing treatment practice across bleeding issues following hysterectomy considering clear recommendations and algorithms

The Complement System, T Cell Response, and Cytokine Shift in Normotensive versus Pre-Eclamptic and Lupus Pregnancy

Successful pregnancy requires an immunological shift with T helper CD4+ bias based on disbalance Th1/Th17 versus Th2/T regulatory (Tregs) required to induce tolerance against the semi-allogeneic fetus and placenta and to support fetal growth. Considered a pregnancy-specific hypertensive disorder, pre-eclampsia is characterized by multifaceted organ involvement related to impaired maternal immune tolerance to paternal antigens triggered by hypoxic placental injury as well as excessive local and systemic anti-angiogenic and inflammatory factor synthesis. Both systemic and local Th1/Th2 shift further expands to Th17 cells and their cytokines (IL-17) complemented by suppressive Treg and Th2 cytokines (IL-10, IL-4); alterations in Th17 and Tregs cause hypertension during pregnancy throughout vasoactive factors and endothelial dysfunction, providing an explanatory link between immunological and vascular events in the pathobiology of pre-eclamptic pregnancy. Apart from immunological changes representative of normotensive pregnancy, lupus pregnancy is generally defined by higher serum pro-inflammatory cytokines, lower Th2 polarization, defective and lower number of Tregs, potential blockade of complement inhibitors by anti-phospholipid antibodies, and similar immune alterations to those seen in pre-eclampsia. The current review underpins the immune mechanisms of pre-eclampsia focusing on local (placental) and systemic (maternal) aberrant adaptive and innate immune response versus normotensive pregnancy and pregnancy in systemic autoimmune conditions, particularly lupus