Aborted cancer surgery at a single tertiary cancer center: Rates, reasons, and outcomes.

BACKGROUND: Surgical resection is typically necessary for curative-intent treatment of most solid organ cancers. However, even with meticulous preoperative evaluation, operative procedures are occasionally aborted. The incidence, outcomes, and long-term prognoses of aborted cancer surgery have not been thoroughly investigated. METHODS: All oncologic operations performed at a single tertiary cancer center between 2011-2021 were retrospectively queried; natural language processing of operative reports was used to identify aborted cancer surgeries. Surgical indications, clinicopathologic characteristics, short- and long-term outcomes, and palliative care involvement were retrospectively reviewed from the electronic medical record. RESULTS: Overall, 345 patients underwent aborted cancer surgery for a rate of 36 patients per year. The most common cancers were pancreatic (28%), biliary (14%), and colorectal (9%). The most commonly aborted operations were pancreatoduodenectomy (34%) and hepatectomy (22%). Most operations were aborted due to unanticipated tumor unresectability (47%) and occult metastatic disease (43%). Sixty percent of patients returned to cancer-directed therapy; 9% underwent successful reattempt at resection. The median overall survival of all patients after aborted surgery was 13.6 months (95% confidence interval, 11.2-16.0 months). Those who returned to oncologic therapy had longer survival (18.6 months vs 5.4 months, P < .001). Palliative care consultation was received by 34% and 13% of patients overall and within 30 days of surgery, respectively. CONCLUSION: Aborted cancer surgery was associated with poor outcomes, particularly in patients with aggressive cancer types and those who did not receive further cancer-directed therapy. Future studies should identify interventions such as palliative care consultation that may improve patient-centered outcomes.

ATP-mediated increase in H+ flux from retinal Müller cells: a role for Na+/H+ exchange.

Small alterations in extracellular H+ can profoundly alter neurotransmitter release by neurons. We examined mechanisms by which extracellular ATP induces an extracellular H+ flux from Müller glial cells, which surround synaptic connections throughout the vertebrate retina. Müller glia were isolated from tiger salamander retinae and H+ fluxes examined using self-referencing H+-selective microelectrodes. Experiments were performed in 1 mM HEPES with no bicarbonate present. Replacement of extracellular sodium by choline decreased H+ efflux induced by 10 µM ATP by 75%. ATP-induced H+ efflux was also reduced by Na+/H+ exchange inhibitors. Amiloride reduced H+ efflux initiated by 10 µM ATP by 60%, while 10 µM cariporide decreased H+ flux by 37%, and 25 µM zoniporide reduced H+ flux by 32%. ATP-induced H+ fluxes were not significantly altered by the K+/H+ pump blockers SCH28080 or TAK438, and replacement of all extracellular chloride with gluconate was without effect on H+ fluxes. Recordings of ATP-induced H+ efflux from cells that were simultaneously whole cell voltage clamped revealed no effect of membrane potential from -70 mV to 0 mV. Restoration of extracellular potassium after cells were bathed in 0 mM potassium produced a transient alteration in ATP-dependent H+ efflux. The transient response to extracellular potassium occurred only when extracellular sodium was present and was abolished by 1 mM ouabain, suggesting that alterations in sodium gradients were mediated by Na+/K+-ATPase activity. Our data indicate that the majority of H+ efflux elicited by extracellular ATP from isolated Müller cells is mediated by Na+/H+ exchange.NEW & NOTEWORTHY Glial cells are known to regulate neuronal activity, but the exact mechanism(s) whereby these "support" cells modulate synaptic transmission remains unclear. Small changes in extracellular levels of acidity are known to be particularly powerful regulators of neurotransmitter release. Here, we show that extracellular ATP, known to be a potent activator of glial cells, induces H+ efflux from retinal Müller (glial) cells and that the bulk of the H+ efflux is mediated by Na+/H+ exchange.