No abstract

Rare co-existance of disease or pathology Background:Congenital factor X deficiency is a rare inherited coagulopathy. Pregnancies in women with this disorder are often associated with adverse outcomes, including miscarriage, premature labor, and hemorrhage during pregnancy and in the peripartum period. The literature on this disorder is sparse and shows a limited number of successful pregnancies in women with factor X deficiency. Case Report:In this report, we present the case of a successful pregnancy and term delivery by elective cesarean section in a 39-year-old primigravida with congenital factor X deficiency. Medical management followed the recommendations of an interdisciplinary team comprising specialists in obstetrics, anesthesia, transfusion medicine, hematology, and neonatology. This high-risk pregnancy was successfully brought to term, and a healthy male neonate was delivered by elective cesarean section at 39 weeks' gestation. The patient's factor X deficiency (0.19 kIU/L) was treated using 4 units of solvent-detergent-treated fresh frozen plasma (SD-FFP) 1 h before the cesarean section, leading to hemostatic levels of factor X and an uneventful intraoperative course. Postoperatively, the patient's factor X levels were controlled daily and corrected using SD-FFP as needed, with no clinically significant blood loss. Conclusions:SD-FFP can be used to manage congenital factor X deficiency in the peripartum period and maintain perioperative blood loss within normal limits.

Free radicals mediated damage of phospholipids, proteins and nucleic acids results in subsequent neuronal degeneration and cell loss. Aim of this study was to evaluate the existence of lipid and protein oxidative damage and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in various rat brain structures 24 h after lateral fluid percussion brain injury (LFPI). Parietal cortex, hippocampus, thalamus, entorhinal cortex, and cerebellum from the ipsilateral hemisphere were processed for analyses of the thiobarbituric acid reactive substances (TBARS) and oxidized protein levels as well as for the SOD and GSH-Px activities. Immunohistochemical detection of oxidized proteins was also performed. Results of our study showed that LFPI caused significant oxidative stress in the parietal cortex and hippocampus while other brain regions tested in this study were not oxidatively altered by LFPI. GSH-Px activities were significantly increased in the parietal cortex and hippocampus, while the SOD activities remained unchanged following LFPI in all regions investigated.

Tumour lysis syndrome (TLS) is a group of pathophysiological processes caused by rapid degradation of tumour cells with subsequent release of intracellular contents into the extracellular space. It is characterized by the development of systemic metabolic disturbances with or without clinical manifestations. The process usually occurs in highly proliferative, large tumours after induction of cytotoxic therapy. Rarely, however, spontaneous TLS can develop, as well as signs of multiorgan failure triggered by an excessive metabolic load and sterile inflammation. The combination of the aforementioned is thus quite unique. Here, we present a 63-year-old male in which spontaneous TLS was accompanied with acute liver failure and delineated underlying nonHodgkin lymphoma. Initial laboratory findings included hyperkalaemia, hyperphosphataemia, hypocalcaemia, uraemia, and increased creatinine levels indicating the onset of TLS with acute kidney injury. Moreover, the patient showed signs of jaundice, coagulopathy, and hepatic encephalopathy. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous fluid therapy, allopurinol treatment, high flow continuous venovenous haemodiafiltration, and commencement of chemotherapy. The case highlights the possibility of TLS as a differential diagnosis in patients presenting with multiorgan failure and the importance of early detection of this potentially challenging and fatal diagnosis.

Chemical meningitis is a very rare but potentially devastating complication of spinal anaesthesia and analgesia. It can be provoked by intrathecal application of substances, such as local anaesthetics, or may occur as a result of the anaesthesia technique used. We describe, until now published, a case of 20-year-old primipara who received spinal analgesia with levobupivacaine for labor and delivery and developed generalized epileptic seizures and high fever. Laboratory tests showed an increased white blood cell count, elevated neutrophil granulocytes, and elevated C-reactive protein; the cerebrospinal fluid (CSF) analysis showed increased levels of proteins, lactate, leukocytes, and erythrocytes. A brain computed tomography (CT) and CT angiography scan did not reveal any pathological alteration. Microbiological analysis of CSF and blood cultures did not show any pathogen growth, and the patient was treated with antibiotics and corticosteroids. The patient later fully recovered and was discharged from the hospital.