Effect of intravenous propacetamol on blood pressure in febrile critically ill patients.

Study Objectives. To investigate the effect of intravenous propacetamol, a parenteral bioprecursor of acetaminophen, on systemic blood pressure in critically ill patients with fever, and to establish the prevalence and clinical significance of this effect. Design. Prospective, observational study. Setting. A six-bed medical-surgical intensive care unit (ICU) of a university-affiliated tertiary care hospital in Israel. Patients. Fourteen critically ill patients (aged 17–83 yrs) with sepsis and fever (body temperature ≥ 38°C) who received an intravenous infusion of propacetamol 2 g over 15–20 minutes every 6 hours as needed to reduce fever. Measurements and Results. Demographic data, including degree of sepsis, were collected at baseline (before propacetamol infusion). Blood pressure, heart rate, body temperature, and need for fluid or vasopressor therapy were recorded at baseline, at end of infusion, and at 15, 30, 45, 60, 90, and 120 minutes after propacetamol administration. The drug was administered on 72 occasions in the 14 patients. Mean ± SE systolic, diastolic, and mean arterial pressures recorded 15 minutes after propacetamol administration were significantly lower than baseline measurements: 123 ± 29 versus 148 ± 33, 62 ± 12 versus 70 ± 15, and 83 ± 16 versus 97 ± 19 mm Hg, respectively (p<0.05). In 24 (33%) of the 72 infusions, systolic blood pressure decreased to below 90 mm Hg and required intervention with fluid bolus administration on six occasions; a fluid bolus was accompanied by a dosage increase or initiation of a norepinephrine infusion on 18 occasions. No correlation, however, was noted between the degree of decrease in mean arterial pressure and decrease in temperature (r2=0.01), or the degree of decrease in mean arterial pressure and decrease in heart rate (r2=0.23), at each data collection time point, as measured by linear regression. Conclusion. Intravenous propacetamol, given in antipyretic doses, caused a significant decrease in blood pressure 15 minutes after administration in febrile critically ill patients. This drug-induced hypotension was clinically relevant in that interventions to control blood pressure were required. Thus, clinicians should be aware of this potential deleterious effect, particularly in specific populations such as critically ill patients.