Pancreatic resections in renal failure patients: is it worth the risk?

Background. Chronic kidney disease affects 20 million US patients, with nearly 600,000 on dialysis. Long-term survival is limited and the risk of complex pancreatic surgery in this group is questionable. Previous studies are limited to case reports and small case series and a large database may help determine the true risk of pancreatic surgery in this population. Methods. The American College of Surgeons National Surgical Quality Improvement Program database was queried (2005-2011) for patients who underwent pancreatic resection. Renal failure was defined as the clinical condition associated with rapid, steadily increasing azotemia (rise in BUN) and increasing creatinine above 3 mg/dL. Operative trends and short-term outcomes were reviewed for those with and without renal failure (RF). Results. In 18,533 patients, 28 had RF. There was no difference in wound infections, neurologic or cardiovascular complications. Compared to non-RF patients, those with RF had more unplanned intubation (OR 4.89, 95% CI 1.85-12.89), bleeding requiring transfusion (OR 3.12, 95% CI 1.37-14.21), septic shock (OR 8.86, 95% CI 3.75-20.91), higher 30-day mortality (21.4% versus 2.3%, P < 0.001) and longer hospital stay (23 versus 12 days, P < 0.001). Conclusions. RF patients have much higher morbidity and mortality after pancreatic resections and surgeons should consider this before proceeding.

The reactions of myoglobin, normal adult hemoglobin, sickle cell hemoglobin and hemin with hydroxyurea.

The kinetics of the reaction of hydroxyurea (HU) with myoglobin (Mb), hemin, sickle cell hemoglobin (HbS), and normal adult hemoglobin (HbA) were determined using optical absorption spectroscopy as a function of time, wavelength, and temperature. Each reaction appeared to follow pseudo-first order kinetics. Electron paramagnetic resonance spectroscopy (EPR) experiments indicated that each reaction produced an FeNO product. Reactions of hemin and the ferric forms of HbA, HbS, and myoglobin with HU also formed the NO adduct. The formation of methemoglobin and nitric oxide-hemoglobin from these reactions may provide further insight into the mechanism of how HU benefits sickle cell patients.