Infants are unable to sustain ventilation due to poorly developed ventilatory centers in the brainstem and inefficient respiratory mechanics. Premature infants are also at risk for respiratory distress syndrome due to impaired amounts or lack of surfactant. They may also develop intraventricular hemorrhage from rapid changes in blood pressure or cerebral ischemia from hypoperfusion due to impaired cerebral autoregulation. In addition, this population is at risk for left to right shunting via the ductus arteriosus soon after birth (within 3–5 days after birth). Premature infants born before 34 weeks gestational age have a decreased glomerular filtration rate (GFR). Even term neonates have only 40 % of an adult’s GFR at birth. In addition, there is decreased tubular reabsorption capacity and a relative inability to absorb water, salts, glucose, protein, phosphate, and bicarbonate. Hyperglycemia and glycosuria can act as an osmotic diuretic and cause obligatory sodium as well as free water loss. Hepatic catalyzing enzymes are less active in premature infants. Oxidizing, reducing, and hydrolyzing enzymes are relatively inactive. Conjugation enzymes (conjugation with acetate, glycine, sulfate, and glucuronic acid) are also less active except for sulfonation. Therefore, the metabolism of various drugs, particularly opioids, can be impaired. These enzymes mature between 6 and 12 months of age, to adult capacity. A regional anesthetic should be used whenever feasible. Opiates could be used with caution, in reduced doses, and the infant’s respiratory status should be closely monitored. I would hope to extubate if successful epidural analgesia is provided and minimal opiates are administered intraoperatively. Prior to placement of a caudal or epidural, radiological images of the spine (which almost certainly would already have been part of this child’s work-up) should be evaluated to ensure the anatomy is normal.