Establishing a Benchmark for Iatrogenic Hemodilution and Blood Transfusion in Long-Segment Spine Fusion Surgery.

STUDY DESIGN: Single-center retrospective cohort study. OBJECTIVE: To identify risk factors for transfusion during long-segment thoracolumbar fusion surgery and benchmark cutoffs that could be used by the operative team to guide the use of transfusion. SUMMARY OF BACKGROUND DATA: Perioperative transfusion for patients undergoing long-segment thoracolumbar fusion surgery is common. To date, no standardized intra- and perioperative management of transfusion administration has been defined. METHODS: Patients who underwent thoracolumbar fusion surgeries of 8 or more levels between 2015 and 2020 were identified. Patient demographics, surgical details, anesthesia and critical care records, and laboratory data were compared between patients who received intraoperative and postoperative blood transfusions and those who did not. Univariate and multivariate propensity-matched analyses were performed to identify independent predictors for blood transfusion, and ordinal analysis was performed to identify possible benchmark cutoffs. RESULTS: Among 233 patients identified who underwent long-segment fusions, 133 (57.1%) received a blood transfusion. Multivariate propensity-matched logistic regression showed that intravenous (IV) fluid volume was an independent predictor for transfusion (transfusion group 8051 mL vs. non-transfusion group 5070 mL, P<0.01). Patients who received ≥4 L total IV fluids were more likely to undergo transfusion than those who received <4 L (93.2% vs. 50.7%, P<0.01). Those receiving total IV fluids at a rate ≥60 mL/Kg (OR 10.45; 95% CI: 2.62-41.72, P<0.01) or intraoperative IV fluids at a rate ≥9 mL/Kg/hr (OR 4.46; 95% CI: 1.39-14.32, P<0.01) were more likely to require transfusions. CONCLUSIONS: IV fluid administration is an independent predictor for blood transfusion after long-segment fusion surgery. Limiting IV fluid administration may prevent iatrogenic hemodilution and decrease transfusion rates. These data can be used to create perioperative protocols with the goal of decreasing transfusion rates when not indicated and allowing earlier administration when indicated.

Surgical management of hepatocellular carcinoma after Fontan procedure.

The Fontan operation has successfully prolonged the lives of patients born with single-ventricle physiology. A long-term consequence of post-Fontan elevation in systemic venous pressure and low cardiac output is chronic liver inflammation and cirrhosis, which lead to an increased risk of hepatocellular carcinoma (HCC). Surgical management of patients with post-Fontan physiology and HCC is challenging, as the requirement for adequate preload in order to sustain cardiac output conflicts with the low central venous pressure (CVP) that minimizes blood loss during hepatectomy. Consequently, liver resection is rarely performed, and most reports describe nonsurgical treatments for locoregional control of the tumors in these patients. Here, we present a multidisciplinary approach to a successful surgical resection of a HCC in a patient with Fontan physiology.

Nuclear translocation of nuclear transcription factor-kappa B by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors leads to transcription of p53 and cell death in dopaminergic neurons.

We describe a new molecular mechanism of cell death by excitotoxicity mediated through nuclear transcription factor kappa B (NF kappa B) in rat embryonic cultures of dopaminergic neurons. Treatment of mesencephalic cultures with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) resulted in a number of changes that occurred selectively in dopaminergic neurons, including persistent elevation in intracellular Ca(2+) monitored with Fura-2, and a significant increase in intramitochondrial oxidation of dihydrorhodamine 123, probably associated with transient increase of mitochondrial permeability, cytochrome c release, nuclear translocation of NF kappa B, and transcriptional activation of the oncogene p53. Interruption of any of these steps by specific antagonists prevented neurite pruning and programmed cell death. In contrast, cell death was not prevented by caspase antagonists and only partly prevented by nitric-oxide synthase inhibitors. This signal transduction pathway might be a contributing mechanism in ongoing neuronal death in Parkinson disease.