Acute kidney injury (AKI) has significant prognostic implications for long-term outcomes in patients undergoing liver transplantation. In several retrospective studies, perioperative variables have been associated with AKI. These variables have been mainly associated with changes in creatinine concentrations over several days or months post-transplantation. To better define AKI, new markers have become available that help to identify patients at risk for renal injury within hours of a triggering insult. We prospectively enrolled liver transplant patients at our institutions to evaluate neutrophil gelatinase-associated lipocalin (NGAL), a marker of early renal injury, as a surrogate for AKI in patients undergoing liver transplantation. Blood was prospectively collected at predetermined time points from 59 patients at 2 institutions. The electronic anesthesia records and the hospital computer data system were reviewed for perioperative variables. Data collection included patient demographics, intraoperative variables such as fluid management, transfusion requirements, hemodynamics, and urine output. Subsequently, patients were grouped according to the presence of risk for developing AKI as defined by the RIFLE (risk, injury, failure, loss, and end-stage kidney disease) criteria. The difference between the NGAL concentration 2 hours after reperfusion and the baseline NGAL concentration was predictive of AKI in all patients, including patients with preexisting renal dysfunction. In patients with creatinine concentrations less than 1.5 mg/dL, a single NGAL determination 2 hours after reperfusion of the liver was associated with the development of AKI. Total occlusion of the inferior vena cava was associated with AKI. In conclusion, NGAL concentrations obtained during surgery were highly associated with postoperative AKI in patients undergoing liver transplantation. These findings will allow the design of larger interventional studies. Our findings regarding the impact of surgical techniques and glucose require validation in larger studies.

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S pinal muscular atrophy (SMA), an inherited motor neuron disease, causes progressive degeneration of the spinal cord anterior horn cells and leads to muscle atrophy, respiratory muscle insufficiency, and scoliosis. Although the disease is rare in parturients, when present, it causes multiple problems, including airway difficulties, respiratory compromise, and spinal abnormalities. Dexmedetomidine has been used to facilitate awake fiberoptic intubation but the effect of the drug in parturients is less known. This case report describes the successful use of dexmedetomidine to facilitate fiberoptic intubation in a parturient with SMA before cesarean delivery.The 35-year-old patient with SMA type III presented at 35 weeks of gestation for urgent cesarean section after premature spontaneous rupture of membranes. She had anemia, asthma, and severe restrictive lung disease and had previously undergone a thoracosacral spinal fusion. She had a Mallampati class 4 airway, with a 12-mm mouth opening, limited cervical spine movement, complete airway obstruction when her head was turned to the left, and severe scoliosis. She consented to awake fiberoptic intubation using dexmedetomidine for sedation to avoid benzodiazepines and opioids before delivery. She had normal cardiac function and an ejection fraction of 70%. Pulmonary function tests confirmed severe restrictive lung disease and a severe decrease in diffusing capacity. She was placed in the right lateral position with her head turned to the right to obtain maximal airway patency. Standard monitors and an intra-arterial catheter were used along with supplemental oxygen. Intravenous dexmedetomidine 1 mg/kg was administered over 10 minutes, followed by an infusion of 1 mg/kg/h. She became anxious during the initial intubation attempt so a bolus of dexmedetomidine, 0.5 mg/kg, was given. She was successfully intubated on the third attempt. A total of 1.84 mg/kg dexmedetomidine was administered over 38 minutes. The patient was hypertensive before initiation of dexmedetomidine and had normal to elevated blood pressures during the intubation attempts. She did become hypotensive after induction of general anesthesia, which was treated successfully with two 5-mg doses of intravenous ephedrine. Intermittent fetal heart tones were normal. Dexmedetomidine was discontinued once the endotracheal tube was secured and general anesthesia was induced with sevoflurane. A right internal jugular central venous catheter was placed under ultrasound guidance, but was technically difficult due to contractures and lack of mobility in the cervical spine. Rocuronium, 0.5 mg/kg, was administered to aid surgeons in positioning the patient to maximize exposure of the lower abdomen. The infant was delivered 4 minutes after skin incision and 68 minutes after the dexmedetomidine infusion was halted. At the time of delivery, the maternal central venous, umbilical arterial, and umbilical venous dexmedetomidine concentrations were 710, 540, and 543 pg/mL, respectively. The neonate's 1-minute and 5-minute A...

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