Treatment of Renin-Angiotensin-Aldosterone System Dysfunction With Angiotensin II in High-Renin Septic Shock.

Endothelial dysfunction is common in septic shock and has been shown to impair angiotensin converting enzyme and the renin-angiotensin-aldosterone system (RAAS). Dysregulation of this pathway, which can be measured with plasma renin activity (PRA), is important not only because RAAS dysfunction is associated with increased mortality but also because treatment with angiotensin II (Ang-2) has been shown to decrease mortality. In this case series of 2 patients, serial PRA levels identified septic shock patients with RAAS dysfunction. The patients were treated with Ang-2, an angiotensin type 1 receptor agonist, which resulted in significant improvements in hemodynamics and PRA levels during treatment.

Impact of Preoperative Platelet Count on Bleeding Risk and Allogeneic Transfusion in Multilevel Spine Surgery.

STUDY DESIGN: This was an observational cohort study of patients receiving multilevel thoracic and lumbar spine surgery. OBJECTIVE: The aim of this study was to identify which patients are at high risk for allogeneic transfusion which may allow for better preoperative planning and employment of specific blood management strategies. SUMMARY OF BACKGROUND DATA: Multilevel posterior spine surgery is associated with a significant risk for major blood loss, and allogeneic blood transfusion is common in spine surgery. METHODS: A univariate logistic regression model was used to identify variables that were significantly associated with intraoperative allogeneic transfusion. A multivariate forward stepwise logistic regression model was then used to measure the adjusted association of these variables with intraoperative transfusion. RESULTS: Multilevel thoracic and lumbar spine surgery was performed in 921 patients. When stratifying patients by preoperative platelet count, patients with pre-operative thrombocytopenia and severe thrombocytopenia had a significantly higher rate of transfusion than those who were not thrombocytopenic. Furthermore, those with severe thrombocytopenia had a higher rate of red blood cells, fresh frozen plasma, and platelet transfusion than those with higher platelet counts. Multivariate logistic regression found that preoperative platelet count was the most significant contributor to transfusion, with a platelet count ≤100 having an adjusted odds ratio (OR) of transfusion of 4.88 (95% confidence interval [CI] 1.58-15.02, P = 0.006). Similarly, a platelet count between 101and 150 also doubled the risk of transfusion with an adjusted OR of 2.02 (95% CI 1.01-4.04, P = 0.047). The American Society of Anesthesiologists classification score increased the OR of transfusion by 2.5 times (OR = 2.52, 95% CI 1.54-4.13), whereas preoperative prothrombin time and age minimally increased the risk. CONCLUSION: Preoperative thrombocytopenia significantly contributes to intraoperative transfusion in multilevel thoracic lumbar spine surgery. Identifying factors that may increase the risk for transfusion could be of great benefit in better preoperative counseling of patients and in reducing overall cost and postoperative complications by implementing strategies and techniques to reduce blood loss and blood transfusions. LEVEL OF EVIDENCE: 2.

When All Else Fails: Novel Use of Angiotensin II for Vasodilatory Shock: A Case Report.

Angiotensin (AT) II is an endogenous hormone that acts on venous and arterial smooth muscle to cause vasoconstriction. Recent trials have sparked great interest in its ability to be used as a vasopressor for catecholamine-refractory hypotension. Herein, we describe the successful use of AT II in a patient with a colonic perforation with septic shock refractory to conventional treatment. After AT II initiation, there was an immediate reduction in catecholamine requirement, and the patient survived.

A quantitative trait locus on chromosome 18 is a critical determinant of excitotoxic cell death susceptibility.

C57BL/6J (B6) and FVB/NJ (FVB) mice are phenotypically distinct in their susceptibility to seizure-induced cell death after kainate administration. Previous studies using quantitative trait loci (QTLs) mapping established that the distal region of mouse chromosome 18 contains a gene(s) that is probably responsible for the difference in seizure-induced cell death susceptibility between two inbred strains, B6 and FVB, that are relatively resistant and susceptible, respectively, to seizure-induced cell death. The genetic locus has been mapped to a approximately 12-centimorgan region of chromosome 18, designated as seizure-induced cell death 1 (Sicd1). In order to confirm the Sicd1 QTL, we have developed congenic mouse strains containing the relevant donor segment from the resistant B6 strain on the susceptible FVB background, also referred to as the FVB.B6-Sicd1 congenic strain. Congenic and FVB littermate controls were tested in a seizure-induced cell death paradigm. The presence of B6 chromosome 18 alleles on an FVB genetic background conferred protection against seizure-induced cell death, as compared with FVB littermate controls. To further localize the Sicd1 QTL, new congenic lines carrying overlapping intervals of the B6 segment were created [interval-specific congenic lines (ISCLs)-1-4] and assessed for seizure-induced cell death phenotype. All of the ISCLs exhibited reduced cell death associated with the B6 phenotype, as compared with the parental FVB strain. The most dramatic of these, ISCL-4, showed a nearly four-fold reduction in the extent of seizure-induced cell death. This suggests that ISCL-4 contains the putative gene(s) of the Sicd1 QTL.