A case of successful treatment of pylephlebitis in a patient with acute appendicitis

Pylephlebitis is a rare and potentially lethal complication of acute appendicitis. It leads to the development of liver abscesses and sepsis. Usually, this  complication is the result of late diagnosis. Only rare cases of successful treatment of pylephlebitis in the context of acute appendicitis are published in special literature.The aim of the demonstration is to analyze of the diagnosis and medical tactic mistakes as a case of pylephlebitis in a patient with acute appendicitis; show the possibilities of modern methods of diagnosis and treatment, which made it possible to achieve a success.The case of successful treatment patient with pylephlebitis was shown in the article. Late diagnosis of acute appendicitis was associated with the patient’s refusal and with some diagnostic and tactic mistakes that were analyzed. The case presented by jaundice, liver failure and fever. Thrombosis of portal vein diagnosed by U/S, CT scan with intravenous contrast on day 11 of the illness. Appendectomy was performed. Intensive care with extracorporeal therapy, antibacterial and anticoagulant therapy were also provided. Septic thrombosis  of portal vein was complicated by an abscess of the right lobe of the liver and sepsis. The case of successful treatment of patient with septic thrombosis of portal vein and superior mesenteric vein complicated by liver abscess and sepsis is considered in the article. Intensive therapy, extracorporeal detoxification and abdominal abscess drainage under the U/S control have resulted in a fully  repatency of portal vein that was confirmed by CT scan data

Point-of-care Platelet Function Tests: Relevance to Arterial Thrombosis and Opportunities for Improvement

© The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.Studies using whole blood platelet aggregometry as a laboratory research tool, provided important insights into the mecha- nism and modulators of platelet aggregation. Subsequently, a number of point-of-care (POC) platelet function tests (PFTs) were developed for clinical use, based on the concept that an individual’s thrombotic profile could be assessed in vitro by assessing the response to stimulation of platelet aggregation by specific, usually solo agonists such as adenosine diphosphate (ADP), collagen and thrombin. However, adjusting antiplatelet medication in order to improve the results of such POC PFTs has not translated into a meaningful reduction in cardiovascular events, which may be attributable to important differences between the POC PFT techniques and in vivo conditions, including patient-to-patient variability. Important limitations of most tests include the use of citrate-anticoagulated blood. Citrate directly and irreversibly diminishes platelet function and even after recalcification, it may result in altered platelet aggregation in response to ADP, epinephrine or collagen, and inter- fere with thrombin generation from activated platelets. Furthermore, most tests do not employ flowing blood and therefore do not assess the effect of high shear forces on platelets that initiate, propagate and stabilize arterial thrombi. Finally, the effect of endogenous thrombolysis, due to fibrinolysis and dislodgement, which ultimately determines the outcome of a thrombotic stimulus, is mostly not assessed. In order to accurately reflect an individual’s predisposition to arterial thrombosis, future mbotic status which overcome these limitations should be used, to improve cardiovascular risk prediction and uide pharmacotherapy.Peer reviewe