Alexander A. Vitin, Leonard Azamfirei and Dana Tomescu
A comprehensive analysis of published cases of Takotsubo cardiomyopathy, occurred in liver transplant recipients in the perioperative period, has been attempted in this review. Predisposing factors, precipitating events, potential physiological mechanisms, acute and post-event management have been discussed.
Alexander A. Vitin, Leonard Azamfirei, Dana Tomescu and John D. Lang
Lactic acidosis (LA) in end-stage liver disease (ESLD) patients has been recognized as one of the most complicated clinical problems and is associated with increased morbidity and mortality. Multiple-organ failure, associated with advanced stages of cirrhosis, exacerbates dysfunction of numerous parts of lactate metabolism cycle, which manifests as increased lactate production and impaired clearance, leading to severe LA-induced acidemia. These problems become especially prominent in ESLD patients, that undergo partial hepatectomy and, particularly, liver transplantation. Perioperative management of LA and associated severe acidemia is an inseparable part of anesthesia, post-operative and critical care for this category of patients, presenting a wide variety of challenges. In this review, lactic acidosis applied pathophysiology, clinical implications for ESLD patients, diagnosis, role of intraoperative factors, such as anesthesia- and surgery-related, vasoactive agents impact, and also current treatment options and modalities have been discussed.
Introduction. Cirrhotic patients have been considered for decades to have a pro-haemorrhagic pattern and were treated as such based on the results from standard coagulation tests. The aim of our study was to determine the effects of platelet count and fibrinogen levels on rotational thromboelastometry (ROTEM) parameters.
Methods. We prospectively included 176 patients with End-Stage Liver Disease (ESLD) admitted to our Intensive Care Unit prior to liver transplantation. Collected data consisted of severity scores, liver, renal and standard coagulation tests, fibrinogen levels, platelet counts and ROTEM parameters. Four ROTEM assays were performed (ExTEM, InTEM, ApTEM and FibTEM) and the following parameters included: CT – clotting time, CFT – clot formation time, MCF – maximum clot firmness, ML – maximum lysis, alpha angle, TPI – thrombin potential index, MaxV - maximum velocity of clot formation (MaxV), MaxVt - time to MaxV, MCE - maximum clot elasticity and AUC - area under the curve.
Results. Statistical analysis demonstrated a linear correlation between platelet counts and ExTEM TPI (R2 linear =0.494), ExTEM MaxV (R2 linear =0.253), ExTEM MCE (R2 linear = 0.351) and ExTEM MCF (R2 cubic = 0.498). Fibrinogen levels correlated linearly with ExTEM MCF (R2 linear = 0.426), ExTEM TPI (R2 linear = 0.544), ExTEM MaxV (R2 linear = 0.332), ExTEM MCE (R2 linear = 0.395) and non-linearly with ExTEM CFT (R2 cubic = 0.475).
Conclusion. Fibrinogen levels and platelet counts had an important effect on both standard and derived ROTEM parameters. Further analysis is required in order to determine clinically oriented cut-off values below which severe coagulopathy would develop.
Alexandra Lazăr, Anca Meda Georgescu, Alexander Vitin and Leonard Azamfirei
In recent years, a new form of medicine has become increasingly significant, namely, personalised medicine (PM). PM is a form of care in which treatment is tailored for an individual patient.
PM is about using multiple data sets to create a digital human mapping. A person’s biological traits are determined by the interactions of hundreds of genes and gene networks, as well as external factors such as diet and exercise. Combining and then investigating these multiple databases with powerful statistical tools, allows a new understanding of how genetic intricacy drives health and disease and so leads to a closer personalised medical approach that targets each individual’s unique genetic make-up.
Sepsis is a systemic inflammatory response to infection, ranging from systemic inflammatory response syndrome (SIRS) to septic shock and multiple organ dysfunction syndromes (MODS). Sepsis is the most common cause of death in intensive care patients. Treatments in an ICU may need to be adapted to the continuous and rapid changes of the disease, making it challenging to identify a single target. PM is thus seen as the future of sepsis treatment in the ICU.
The fact that individual patients respond differently to treatment should be regarded as a starting point in the approach to providing treatment. The disease itself comes secondary to this concept.
Anca Meda Georgescu, Bianca Liana Grigorescu, Ioana Raluca Chirteș, Alexander A. Vitin and Raluca Ștefania Fodor
Sepsis is an injurious systemic host response to infection, which can often lead to septic shock and death. Recently, the immune-pathogenesis and genomics of sepsis have become a research topic focusing on the establishment of diagnostic and prognostic biomarkers. As yet, none have been identified as having the necessary specificity to be used independently of other factors in this respect. However the accumulation of current evidence regarding genetic variations, especially the single nucleotide polymorphisms (SNPs) of cytokines and other innate immunity determinants, partially explains the susceptibility and individual differences of patients with regard to the evolution of sepsis. This article outlines the role of genetic variation of some serum proteins which have the potential to be used as biomarker values in evaluating sepsis susceptibility and the progression of the condition.
Ioana Raluca Chirteș, Dragos Florea, Carmen Chiriac, Oana Maria Mărginean, Cristina Mănășturean, Alexander A Vitin and Anca Meda Georgescu
Background: Known also as Osler’s triad, Austrian syndrome is a complex pathology which consists of pneumonia, meningitis and endocarditis, all caused by the haematogenous dissemination of Streptococcus pneumoniae. The multivalvular lesions are responsible for a severe and potential lethal outcome.
Case report: The case of a 51-year-old female patient, with a past medical history of splenectomy, is presented. She developed bronchopneumonia, acute meningitis and infective endocarditis as a result of Streptococcus pneumoniae infection and subsequently developed multiple organ dysfunction syndromes which led to a fatal outcome. Bacteriological tests did not reveal the etiological agent. The histopathological examination showed a severe multivalvular endocarditis, while a PCR based molecular analysis from formalin fixed valvular tissue identified Streptococcus pneumoniae as the etiologic agent.
Conclusions: The presented case shows a rare syndrome with a high risk of morbidity and mortality. Following the broad-spectrum treatment and intensive therapeutic support, the patient made unfavourable progress which raised differential diagnosis problems. In this case, the post-mortem diagnosis demonstrated multiple valvular lesions occurred as a result of endocarditis.