Search

Remifentanil-induced hyperalgesia (RIH) is a part of a general opioid-induced hyperalgesia (OIH) syndrome, seemingly resulting from abrupt cessation of continuous remifentanil infusion at rates equal or exceeding 0.3 mcg/kg/min. The intricate mechanisms of its development are still not completely understood. However, hyperactivation of the N -methyl d -aspartate receptor system, descending spinal facilitation and increased concentration of dynorphin (a κ-opioid ligand) are commonly proposed as possible mechanisms. Several ways of prevention and management have been suggested, such as slow withdrawal of remifentanil infusion, the addition of propofol, pretreatment with or concomitant administration of ketamine, buprenorphine, cyclooxygenase-2 inhibitors (NSAIDs), methadone, dexmedetomidine. In clinical and animal studies, these strategies exhibited varying success, and many are still being investigated., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

The hypercoagulable state in liver transplant recipients that may manifest as abnormal thrombus formation in large vessel structures, such as cardiac chambers and the pulmonary arteries, poses a substantial threat for the patient and graft survival. Massive pulmonary embolism is a rare, albeit potentially lethal, complication that may occur at any stage of liver transplant surgery. In this study, we present the case of a major perioperative thromboembolic event in a liver transplant recipient that had taken place in the early post-transplant period during the second-look surgery that was then successfully treated by catheter-directed clot removal. We will attempt to identify potential factors that may have been associated with abnormal thrombus formation., (Copyright © 2020. Published by Elsevier Inc.)

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., Competing Interests: Conflict of interest None to declare.

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., Competing Interests: Conflict of interest: None to declare.

A case of stress (takotsubo) cardiomyopathy (TC) that occurred intraoperatively during liver transplantation surgery was identified by transesophageal echocardiography. Only a few cases of TC occurring during liver transplantation have been reported to date. Unlike other cases reported, TC occurred during the anhepatic stage of the liver transplantation, with subsequent complete recovery. Notwithstanding the large number of cases of TC in the perioperative settings reported worldwide, the exact reasons of this syndrome occurring intraoperatively as well as precipitating factors and conditions remain mostly unknown., (Published by Elsevier Inc.)

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., Competing Interests: Conflict of interest: None declared.

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., Competing Interests: Author Disclosure Statement: The authors report no conflicts of interest.

Introduction: Reperfusion is the most critical event during liver transplantation, and sustained leakage of acidic preservation solution from the liver graft contributes to marked hemodynamic instability. Recent laboratory studies with hepatocyte cultures have revealed that low pH may protect hepatocyte mitochondria against ischemia-reperfusion injury by inhibiting the mitochondrial permeability transition (MPT), the so-called "pH paradox." However, the clinical significance of this pH paradox theory remains largely unknown. In this study, we sought to determine whether there is an association between serum pH immediately prior to reperfusion and hemodynamic recovery after reperfusion and graft survival., Methods: We analyzed retrospective data from 527 patients who underwent Orthotopic liver transplantation between 2003 and 2008. All patients were allocated to one of two groups: pH ≤ 7.32 or pH > 7.32, as measured 5 min before reperfusion. Case-control matching was performed using the propensity score to adjust for background differences between the two groups. Data were analyzed using Student's t-test and the χ (2) test., Results: There were 85 patients in the pH ≤ 7.32 group and 385 patients in the pH > 7.32 group. The recovery of mean arterial pressure after hepatic artery reperfusion was significantly faster in the pH ≤ 7.32 group (slope of recovery: 0.0004 % vs. 0.0002 %/min, p = 0.041). Other parameters studied, including vasopressor dosage after reperfusion, did not show any statistically significant difference between groups., Conclusions: Our findings suggest that less aggressive treatment of acidosis with a slower rate of normalization of serum pH (from low to normal) after reperfusion promotes faster hemodynamic stabilization. These findings provide evidence to support the concept of the pH paradox, and may also substantiate the argument against the usage of alkalizing agents before reperfusion unless acidosis becomes clinically significant.

Decreases in endothelial nitric oxide synthase derived nitric oxide (NO) production during liver transplantation promotes injury. We hypothesized that preemptive inhaled NO (iNO) would improve allograft function (primary) and reduce complications post-transplantation (secondary). Patients at two university centers (Center A and B) were randomized to receive placebo (n = 20/center) or iNO (80 ppm, n = 20/center) during the operative phase of liver transplantation. Data were analyzed at set intervals for up to 9-months post-transplantation and compared between groups. Patient characteristics and outcomes were examined with the Mann-Whitney U test, Student t-test, logistic regression, repeated measures ANOVA, and Cox proportional hazards models. Combined and site stratified analyses were performed. MELD scores were significantly higher at Center B (22.5 vs. 19.5, p<0.0001), surgical times were greater at Center B (7.7 vs. 4.5 hrs, p<0.001) and warm ischemia times were greater at Center B (95.4 vs. 69.7 min, p<0.0001). No adverse metabolic or hematologic effects from iNO occurred. iNO enhanced allograft function indexed by liver function tests (Center B, p<0.05; and p<0.03 for ALT with center data combined) and reduced complications at 9-months (Center A and B, p = 0.0062, OR = 0.15, 95% CI (0.04, 0.59)). ICU (p = 0.47) and hospital length of stay (p = 0.49) were not decreased. iNO increased concentrations of nitrate (p<0.001), nitrite (p<0.001) and nitrosylhemoglobin (p<0.001), with nitrite being postulated as a protective mechanism. Mean costs of iNO were $1,020 per transplant. iNO was safe and improved allograft function at one center and trended toward improving allograft function at the other. ClinicalTrials.gov with registry number 00582010 and the following URL:http://clinicaltrials.gov/show/NCT00582010.

Ischemic insult to the splanchnic vasculature can jeopardize bowel viability and lead to devastating consequences, including bowel necrosis and gangrene. Although acute mesenteric ischemia (AMI) may occur at any age, the elderly are most commonly affected due to their higher incidence of underlying systemic pathology, most notably atherosclerotic cardiovascular disease. Treatment options include pharmacology-based actions, endovascular, and surgical interventions. AMI remains a life-threatening condition with a mortality rate of 60% to 80%, especially if intestinal infarction has occurred and surgical intervention becomes emergent. Early recognition and an aggressive therapeutic approach are essential if the usually poor outcome is to be improved. Anesthetic management is complex and must account for comorbid disease as well as the patient's presumptive acute deterioration. Blood pressure support typically involves careful, but often massive, fluid resuscitation and may also additionally require pharmacologic support.

In this review, we discuss the anesthetic implications of the new anticoagulant and antiplatelet drugs, focusing our discussion mainly on neuroaxial/regional anesthesia and central catheter placement issues. We offer practical recommendations for their use.

One hundred and two male and female patients, aged 65-85 years, have been examined. All of them had been subjected to urgent surgery for acute surgical pathology of the organs of hepatopancreatoduodenal area. Surgery was performed under one of the following anesthesia techniques: neuroleptanalgesia, epidural anesthesia (EA), combination of EA and endotracheal anesthesia. Changes in central hemodynamics, acid-base balance and oxygen balance parameters have been studied in the preoperative, intraoperative and early postoperative period. The advantages of a combined technique which ensures optimal conditions for the maintenance of circulatory and oxygen homeostasis have been proved.