Surgical and demographic predictors of free flap salvage after takeback: A systematic review.

BACKGROUND: Microsurgical free tissue transfer (FTT) is a widely employed surgical modality utilized for reconstruction of a broad range of defects, including head and neck, extremity, and breast. Flap survival is reported to be 90%-95%. When FTT fails, salvage procedures aim at establishing reperfusion while limiting ischemia time-with salvage rates between 22% and 67%. There are limited data-driven predictors of successful salvage present in the literature. This systematic review aims to identify predictors of flap salvage. METHODS: A systematic literature review was conducted per PRISMA guidelines. Articles included in the final analysis were limited to those investigating FTT salvage procedures and included factors impacting outcomes. Cohort and case series (>5 flaps) studies up until March 2021 were included. Chi-square tests and linear regression modeling was completed for analysis. RESULTS: The patient-specific factors significantly associated with salvage included the absence of hypercoagulability (p < .00001) and no previous salvage attempts (p < .00001). Case-specific factors significantly associated with salvage included trunk/breast flaps (p < .00001), fasciocutaneous/osteocutaneous flaps (p = .006), venous compromise (p < .00001), and shorter time from index procedure to salvage attempt (R = .746). Radiation in the head and neck population was significantly associated with flap salvage failure. CONCLUSIONS: Given the complexity and challenges surrounding free flap salvage procedures, the goal of this manuscript was to present data helping guide surgical decision-making. Based on our findings, patients without documented hypercoagulability, no previous salvage attempts, fasciocutaneous/osteocutaneous flaps, trunk/breast flaps, and a shorter time interval post-index operation are the best candidates for a salvage attempt.

Effect of Nimodipine and Botulinum Toxin A on Peripheral Nerve Regeneration in Rats: A Pilot Study.

BACKGROUND: Peripheral nerve damage is a frequent problem, with an estimated 2.8%-5.0% of trauma admissions involving peripheral nerve injury. End-to-end, tension-free microsurgical repair (neurorrhaphy) is the current gold standard treatment for complete transection (neurotmesis). While neurorrhaphy reapproximates the nerve, it does not address the complex molecular regenerative process. Evidence suggests that botulinum toxin A (BTX) and nimodipine (NDP) may improve functional recovery, but mechanisms of action remain unknown. METHODS: This research investigates BTX and NDP for their novel capacity to improve neural regeneration in the setting of neurorrhaphy using a Lewis rat tibial nerve neurotmesis model. In a triple-masked, placebo-controlled, randomized study design, we compared functional (rotarod, horizontal ladder walk), electrophysiological (conduction velocity, duration), and stereological (axon count, density) outcomes of rats treated with: NDP+saline injection, BTX+NDP, Saline+placebo, and BTX+placebo. Additional controls included sham surgery +/- BTX. RESULTS: NDP+saline outperformed other treatment groups in the ladder walk. This group had the fewest deep slips (15.07% versus 30.77% in BTX+NDP, P = 0.122), and the most correct steps (70.53% versus 55.58% in BTX+NDP, P = 0.149) in functional testing. NDP+saline also had the fastest nerve conduction velocity (0.811m/s versus 0.598m/s in BTX+NDP, P = 0.126) among treatment groups. BTX+NDP had the highest axon count (10,012.36 versus 7,738.18 in NDP+Saline, P = 0.009). CONCLUSION: This study is the first to test NDP with BTX in a multimodal assessment of nerve recovery following neurotmesis and neurorrhaphy. NDP outperformed BTX+NDP functionally. Future work will focus on nimodipine in an effort to improve nerve recovery in trauma patients.

Brain Death Enhances Activation of the Innate Immune System and Leads to Reduced Renal Metabolic Gene Expression.

BACKGROUND: Brain death (BD)-associated inflammation has been implicated in decreased kidney allograft function and survival, but the underlying mechanisms have not been well distinguished from the conditions of critical care itself. We have developed a clinically translatable model to separate and investigate strategies to improve donor management and critical care. METHODS: Brain-dead (n = 12) and sham (n = 5) rhesus macaques were maintained for 20 hours under intensive care unit-level conditions. Samples were collected for immunophenotyping, analysis of plasma proteins, coagulation studies, and gene analysis for changes in immune and metabolic profile with comparison to naive samples (n = 10). RESULTS: We observed an increase in circulating leukocytes and cytokines, activation of complement and coagulation pathways, and upregulation of genes associated with inflammation in both brain-dead and sham subjects relative to naïve controls. Sham demonstrated an intermediate phenotype of inflammation compared to BD. Analysis of gene expression in kidneys from BD kidneys revealed a similar upregulation of inflammatory profile in both BD and sham subjects, but BD presented a distinct reduction in metabolic and respiratory processes compared to sham and naïve kidneys. CONCLUSION: BD is associated with activation of specific pathways of the innate immune system and changes to metabolic gene expression in renal tissue itself; however, sham donors presented an intermediate inflammatory response attributable to the critical care environment. The early onset and penetrating impact of this inflammatory response underscores the need for early intervention to prevent perioperative tissue injury to transplantable organs.

How Well Does Renal Transplantation Cure Hyperparathyroidism?

BACKGROUND: Most patients with end-stage renal disease will develop hyperparathyroidism (HPT). Transplantation reportedly resolves HPT in most cases. Currently, guidelines recommend a watchful waiting approach to HPT for the first 12 months after the transplantation to allow maximal allograft function. The purpose of our study is to examine the incidence and impact of HPT, defined as an elevated parathyroid hormone (PTH) level, after renal transplantation in a contemporary cohort. METHODS: Primary kidney transplantation was performed on 1609 patients from January 1, 2004, to June 6, 2012. Patients were stratified by timing of achieving normal serum PTH levels, and a multivariate logistic regression was constructed to determine predictive variables. Kaplan-Meier analysis was then performed on overall graft survival based on PTH normalization. RESULTS: Four hundred eighty-eight (30.3%) patients achieved normal PTH within 1 year posttransplant. Four hundred twenty-seven (26.6%) attained normal PTH between 1 and 2 years, with the remaining 694 (43.1%) categorized as having HPT. Patients achieving normal PTH within 12 months of transplantation had a significantly longer median graft survival (7.33 years) compared with those patients who normalized between 12 and 24 months (4.92 years, P < 0.001), and those with HPT (5.13 years, P < 0.001). Comparing normalization of PTH by 2 years to HPT patients, obesity (P < 0.001), months on dialysis (P < 0.001), and delayed graft failure (P = 0.006) were predictive of nonnormalization. Overall, allograft survival analysis revealed a survival advantage for patients who normalize PTH within 24 months of transplantation (P = 0.038). CONCLUSIONS: Renal transplant resolves HPT in 56.9% of patients at 2 years. Resolution within the first year portends longer graft survival. Therefore, earlier intervention for HPT should be considered.