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الأحد، 31 أغسطس 2008

Prrolonged arterial hypotension due to propofol used for endotrachial intubation in a newborn infant



Prolonged arterial hypotension due to propofol used for endotracheal intubation in a newborn infant

Case presentation
During early pregnancy, the newborn’s mother had had malaria with hemolytic crisis but had recovered well under antimalarial treatment in Africa. Subsequent prenatal care in Switzerland revealed normalisation of pregnancy. At a gestational age of 37 4/7 weeks, an elective cesarean section (spinal anesthesia) was performed because of breech presentation. Apgar scores were 2 and 4 at 1 and 5 minutes, respectively, mainly due to poor respiratory effort. The newborn male infant was quickly intubated without medication. On transport to the regional hospital, there was accidental extubation. After arrival at the hospital, the cyanotic and apneic newborn received 8mg/kg propofol, 10 mcg/kg fentanyl and muscle relaxation and was reintubated.

On arrival at our neonatal critical care unit, the patient was deeply sedated with small pupils, spontaneous hypoventilation and with motor reaction only to painful stimulation. Birth weight, body length and head circumference were within normal range for age. In addition, there was arterial hypotension (MABP 25-30 mmHg), which was treated with volume 20ml/kg and dopamine 5 mcg/kg/min over 24 hours. His cardiovascular status remained otherwise completely normal. The patient was weaned from the ventilator within another 24 hours and showed no respiratory distress (FiO2 of 0.21 since admission). He never showed any signs of a systemic inflammatory response syndrome or of infection. Chest x-rays, head ultrasound and laboratory examinations (hemoglobin, leucocytes, electrolytes, renal function and plasmodium falciparum antigen) remained normal, except for a positive Coombs test due to AO-incompatibility. He went home at the age of 6 days with a normal neurologic and cardiopulmonary status.
DiscussionThe etiology of the infant’s poor respiratory effort immediately after birth remains unclear. The newborn might have suffered from side effects of maternal anesthesia. Neonatal encephalopathy due to maternal infection may present with bradypnea, but we would expect prolonged hypoventilation and additional signs of neonatal encephalopathy.

Prolonged arterial hypotension seen after the second endotracheal intubation however is most probably due to the medications used for intubation. Arterial hypotension seen after a single bolus of propofol is probably due to overdosing (maximal recommended dose is 3mg/kg bodyweight), limited hepatic clearance in the newborn infant, and fentanyl induced increase in propofol serum concentration (1-3).

Considering the increasing popularity of propofol (Disoprivan®) use in neonatal and pediatric anesthesia, it is important to remember the following facts:

1) The “propofol-infusion syndrome” does exist: it is rare but has a high fatality rate; propofol should therefore not be used for longtime sedation in neonatal or pediatric intensive care (4).

2) A single bolus of propofol reduces myocardial contractility and systemic vascular resistance (similar to thiopenthal). There is an increase in right-to-left shunting through fetal channels with worsening of cyanosis and pulmonary hypertension (5-8). Propofol should therefore not be used for intubation or sedation in conditions associated with cardiopulmonary compromise, such as newborns with respiratory distress syndrome, pulmonary hypertension, sepsis, cardiomyopathy or congenital heart disease. In these patients other medications for intubation have been shown to be much safer, such as ketamine or lowe dose benzodiazepines.

3) Recent studies suggest that there is propofol-related neurotoxicity (9-11).

In conclusion

despite the current unhibited enthusiasm for propofol, there are well documented and potentially lethal side-effects of propofol. This requires a differentiated approach to the use of propofol. Especially in the newborn infant, there is no place for propofol.

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