The administration of citrated blood products during massive transfusion requires calcium salt administration to prevent citrate toxicity and to maintain ionized calcium values. The literature does ...not provide adequate guidance for the amount of calcium required during massive transfusions during liver transplantation. This study was conducted to provide guidance on calcium salt replacement during a massive transfusion in liver transplant patients, with a focus on the phase of transplantation during which citrate metabolism was minimal.
An observational retrospective chart review.
An academic single-institution study of hospitalized patients.
One hundred thirty-two patients after liver transplantation.
The study authors observed documented measurements of ionized calcium and observed the ratio of calcium salts to citrated bank blood products in patients undergoing liver transplantation with complete data sets. They also observed the effect of continuous venovenous hemofiltration on the distribution of ionized calcium values.
Prereperfusion, an average of 1.09 g CaCl2/L of citrated blood was administered to maintain ionized calcium in the normal range. Postreperfusion, less CaCl2 was administered, and a rebound of ionized calcium occurred. Prereperfusion, continuous venovenous hemofiltration reduced the number of ionized calcium values outside of 2 standard deviations, meaning fewer values were critically low.
With massive transfusions up to 67 liters (approximately 13 blood volumes), 1.09 g CaCl2/L citrated blood maintained ionized calcium in the normal range in the absence of citrate metabolism. This ratio may have value in empiric treatment when ionized calcium measurements are unavailable, and massive transfusion rates exceed metabolic capacity.
Almost three-quarters of all heart failure patients who are older than 65 have heart failure with preserved ejection fraction (HFpEF). The proportion and hospitalization rate of patients with HFpEF ...are increasing steadily relative to patients in whom heart failure occurs as result of reduced ejection fraction. The predominance of the HFpEF phenotype most likely is explained by the prevalence of medical conditions associated with an aging population. A multitude of age-related, medical, and lifestyle risk factors for HFpEF have been identified as potential causes for the sustained low-grade proinflammatory state that accelerates disease progression. Profound left ventricular (LV) systolic and diastolic stiffening, elevated LV filling pressures, reduced arterial compliance, left atrial hypertension, pulmonary venous congestion, and microvascular dysfunction characterize HFpEF, but pulmonary arterial hypertension, right ventricular dilation and dysfunction, and atrial fibrillation also frequently occur. These cardiovascular features make patients with HFpEF exquisitely sensitive to the development of hypotension in response to acute declines in LV preload or afterload that may occur during or after surgery. With the exception of symptom mitigation, lifestyle modifications, and rigorous control of comorbid conditions, few long-term treatment options exist for these unfortunate individuals. Patients with HFpEF present for surgery on a regular basis, and anesthesiologists need to be familiar with this heterogeneous and complex clinical syndrome to provide successful care. In this article, the authors review the diagnosis, pathophysiology, and treatment of HFpEF and also discuss its perioperative implications.
We sought to investigate the biological effects of pre-reperfusion treatments of the liver after warm and cold ischemic injuries in a porcine donation after circulatory death model.
Donation after ...circulatory death represents a severe form of liver ischemia and reperfusion injury that has a profound impact on graft function after liver transplantation.
Twenty donor pig livers underwent 60 minutes of in situ warm ischemia after circulatory arrest and 120 minutes of cold static preservation prior to simulated transplantation using an ex vivo perfusion machine. Four reperfusion treatments were compared: Control-Normothermic (N), Control- Subnormothermic (S), regulated hepatic reperfusion (RHR)-N, and RHR-S (n = 5 each). The biochemical, metabolic, and transcriptomic profiles, as well as mitochondrial function were analyzed.
Compared to the other groups, RHR-S treated group showed significantly lower post-reperfusion aspartate aminotransferase levels in the reperfusion effluent and histologic findings of hepatocyte viability and lesser degree of congestion and necrosis. RHR-S resulted in a significantly higher mitochondrial respiratory control index and calcium retention capacity. Transcriptomic profile analysis showed that treatment with RHR-S activated cell survival and viability, cellular homeostasis as well as other biological functions involved in tissue repair such as cytoskeleton or cytoplasm organization, cell migration, transcription, and microtubule dynamics. Furthermore, RHR-S inhibited organismal death, morbidity and mortality, necrosis, and apoptosis.
Subnormothermic RHR mitigates IRI and preserves hepatic mitochondrial function after warm and cold hepatic ischemia. This organ resuscitative therapy may also trigger the activation of protective genes against IRI. Sub- normothermic RHR has potential applicability to clinical liver transplantation.
In bacterial meningitis, death and long-term neurological sequelae are caused jointly by several factors. Despite highly qualified intensive care and effective antibacterial therapy mortality rates ...remain high. Beta-lactam antibiotics, currently used for initial therapy of bacterial meningitis, lead to a rapid lysis of bacteria with a consecutive profound release of proinflammatory bacterial cell wall components, causing a substantial burst of meningeal inflammation. The only approved adjunctive therapy so far is corticosteroids. The use of nonbacteriolytic, protein-synthesis inhibiting antibiotics in experimental models of pneumococcal meningitis appeared to be a promising therapeutic approach towards neuroprotection by diminishing the inflammatory process.
