Ellen de Kort

139 Blood pressure after propofol in neonates 8 Hypotension in the preterm infant has been associated with mortality, cerebral injury such as intraventricular hemorrhage and periventricular leukomalacia, and long-term neurologic sequelae. 16,20-24 The question rises, however, if every infant with low blood pressure needs treatment for hypotension. Blood pressure is only one aspect of cardiovascular status and may not directly correlate with tissue perfusion. Infants with hypotension in the absence of biochemical or clinical signs of shock presumably have adequate tissue oxygen delivery, a phenomenon indicated as permissive hypotension. 15 It has been shown that infants with permissive hypotension who did not receive treatment for hypotension had similar outcomes as normotensive patients. 25 A recent French population-based cohort study, however, showed that preterm infants below 29 weeks’ gestation who were treated for hypotension in the first 72 hours of life had significantly higher survival rates without major morbidity and a lower rate of severe cerebral abnormalities, compared to infants with hypotension who were untreated. 26 These conflicting results indicate that the importance of hypotension in the preterm population is still to be elucidated. Despite the statement that the hemodynamic status of the patients needed to be sufficiently stable to administer propofol, seven patients were hypotensive before the start of propofol. Besides this, nine patients received propofol while being at risk for hemodynamic insufficiency based on sepsis or NEC as underlying illness. Inclusion of these (possible) hemodynamically instable patients could have influenced the results and could have magnified the effect of propofol on blood pressure. Our analysis on the influence of hemodynamic status on the effect of propofol on blood pressure, however, shows that the effect of propofol on blood pressure is not different between patients who are presumed to be hemodynamically stable and patients who are presumed to have an increased risk of hemodynamic failure based on sepsis or NEC. Although caution with the interpretation of the results is warranted because of the small patient numbers, these data suggest that the tolerance for propofol in hemodynamically stable patients is not different from hemodynamically compromised patients. It should also be kept in mind that these results could also indicate that the hemodynamically stable patients in group 1 were not as hemodynamically stable as they were presumed to be. In our initial analysis we showed that a propofol starting dose of 2.0 mg/kg provided effective sedation in 86% of patients, compared to 4% and 13% of the patients receiving a starting dose of 1.0 mg/kg or 1.5 mg/kg respectively. 14 Solely based on the sedative effect of propofol, a starting dose of 2.0 mg/kg of propofol would be the best strategy. However, despite an equal incidence of hypotension compared to the 1.0 mg/kg starting dose, a dose of 2.0 mg/kg had a much more profound decrease in blood