The Impact of Fluid Balance on Acute Kidney Injury in Nontraumatic Subarachnoid Hemorrhage.

Background: Nontraumatic subarachnoid hemorrhage (SAH) can lead to poor neurologic outcomes, particularly when delayed cerebral ischemia (DCI) occurs. Maintenance of euvolemia following SAH is thought to reduce the risk of DCI. However, attempts at maintaining euvolemia often err on the side of hypervolemia. In this study, we assessed the relationship between fluid balance and acute kidney injury (AKI) in SAH patients, assessing hypervolemia versus euvolemia and their impact on AKI. Methods: In a quaternary care center, neuroscience intensive care unit we conducted a retrospective longitudinal analysis in adult patients who suffered a nontraumatic SAH. Results: Out of 139 patients, 15 (10.8%) patients developed an AKI while hospitalized, with 7 stage I, 3 stage II, and 5 stage III injuries. Acute kidney injury patients had higher peak sodium (150.1 mEq/L vs 142.7 mEq/L, 95% confidence interval [CI]: [2.7-12.1 mEq/L]), higher discharge chloride (109.1 mEq/L vs 104.9 mEq/L, 95% CI: [0.7-7.6 mEq/L]), and lower hemoglobin at discharge (9.3 g/dL vs 11.3 g/dL, 95% CI: [1.0-2.9 g/dL]). At 7 days, AKI patients had a fluid balance that was 1.82 L higher (P = .04), and 3.38 L higher at 14 days (P = .02), in comparison to day 3. Acute kidney injury was associated with significant mortality increases. This increase in mortality was found at 30 days from admission with a 9.52-fold increase, and at 60 days with a 6.25-fold increase. As a secondary outcome, vasospasm (19 patients, 13.7%) showed no association with AKI. Conclusions: Acute kidney injury following SAH is correlated with clinically significant hypervolemia, elevated sodium, elevated chloride, decreased urine output, and decreased hemoglobin at discharge-risk factors for all SAH patients. This study further elucidates the harm of hypervolemia and gives greater practical evidence to physicians attempting to balance the dangers of vasospasm and AKI.

Sepsis and the microcirculation: the impact on outcomes.

PURPOSE OF REVIEW: Advances in the treatment of septic shock have historically focused on resuscitation endpoints, mainly mean arterial pressure and cardiac output. As the definitions of sepsis and septic shock have shifted to focus on the diversity of causes of dysregulated host-response we have seen an emerging phenotype where tissue hypoxia persists despite adequate macrocirculatory parameters. Interest in the topic of microcirculation is re-emerging as validated bedside techniques for hemodynamic monitoring, such as video microscopes, are becoming available. We review the current understanding of how sepsis induced hypoperfusion with a focus on recent advances in monitoring the microcirculation, and how a proliferation of biomarkers and emerging therapeutic targets may impact future research. RECENT FINDINGS: Conventional hemodynamic monitoring systems fail to assess the microcirculation, and it's response to treatment. Lactate and venous oxygen saturations often drive biomarker-guided sepsis management. Visual assessments such as mottling and capillary refill time are often associated with predicting outcomes, but sometimes can have issues with inter-provider reliability. Microcirculatory damage can be observed sublingually and appears to have prognostic value. SUMMARY: Sepsis is associated with changes in the microcirculation that can lead to tissue hypoxia and organ dysfunction. Further studies are needed to validate the usefulness of microcirculatory bedside tools in guiding resuscitative efforts.

High-Dose Intravenous Ascorbic Acid: Ready for Prime Time in Traumatic Brain Injury?

Traumatic brain injury (TBI) is one of the leading public health problems in the USA and worldwide. It is the number one cause of death and disability in children and adults between ages 1-44. Despite efforts to prevent TBIs, the incidence continues to rise. Secondary brain injury occurs in the first hours and days after the initial impact and is the most effective target for intervention. Inflammatory processes and oxidative stress play an important role in the pathomechanism of TBI and are exacerbated by impaired endogenous defense mechanisms, including depletion of antioxidants. As a reducing agent, free radical scavenger, and co-factor in numerous biosynthetic reactions, ascorbic acid (AA, vitamin C) is an essential nutrient that rapidly becomes depleted in states of critical illness. The administration of high-dose intravenous (IV) AA has demonstrated benefits in numerous preclinical models in the areas of trauma, critical care, wound healing, and hematology. A safe and inexpensive treatment, high-dose IV AA administration gained recent attention in studies demonstrating an associated mortality reduction in septic shock patients. High-quality data on the effects of high-dose IV AA on TBI are lacking. Historic data in a small number of patients demonstrate acute and profound AA deficiency in patients with central nervous system pathology, particularly TBI, and a strong correlation between low AA concentrations and poor outcomes. While replenishing deficient AA stores in TBI patients should improve the brain's ability to tolerate oxidative stress, high-dose IV AA may prove an effective strategy to prevent or mitigate secondary brain injury due to its ability to impede lipid peroxidation, scavenge reactive oxygen species, suppress inflammatory mediators, stabilize the endothelium, and reduce brain edema. The existing preclinical data and limited clinical data suggest that high-dose IV AA may be effective in lowering oxidative stress and decreasing cerebral edema. Whether this translates into improved clinical outcomes will depend on identifying the ideal target patient population and possible treatment combinations, factors that need to be evaluated in future clinical studies. With its excellent safety profile and low cost, high-dose IV AA is ready to be evaluated in the early treatment of TBI patients to mitigate secondary brain injury and improve outcomes.

Cefepime challenge after piperacillin/tazobactam-induced thrombocytopenia.

Drug-induced thrombocytopenia (DITP) has been described as a sudden and severe hematologic complication of piperacillin/tazobactam. The proposed mechanism by which piperacillin/tazobactam causes DITP involves the formation of a covalent bond to platelet membrane protein thereby inducing a humoral immune response. Given the immunogenic nature of this adverse event and the structural similarities across beta-lactam antibiotics, the potential for cross-reactivity between agents within the class should be considered. However, the structural moiety of piperacillin/tazobactam responsible for this immunogenic response has not been identified-the relationship between structure and activity for this phenomenon remains unknown. Data on the safety and cross-reactivity of other beta-lactam agents in this setting is lacking. We report the first case of piperacillin/tazobactam DITP successfully challenged by the use of cefepime for the treatment of aspiration pneumonia. Further studies are needed to determine the structural moiety of piperacillin/tazobactam responsible for this immunogenic response and evaluate the safety of other beta-lactam antibiotics in this clinical setting.

Acute Respiratory Distress in the Operating Room and Prone Ventilation: A Case Report.

There have been many advances in the management of acute respiratory distress syndrome, a condition which Bellani et al, in the LUNG SAFE trial (Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure), found represents up to 10.4% of intensive care unit admissions and 23.4% of patients requiring mechanical ventilation, with an unadjusted intensive care unit and hospital mortality of 35.3% and 40%, respectively. Studies have shown that prone positioning can improve oxygenation in patients who are mechanically ventilated for acute respiratory distress syndrome. This case report describes an example in which intraoperative prone positioning improved oxygenation in a patient after aspiration of gastric contents on induction of general anesthesia.