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Morphine/nefopam/oxycodone Fetal megacystis and spontaneous bladder rupture following in-utero exposure: case report

A female fetus developed megacystis and spontaneous bladder rupture following in utero exposure to morphine, nefopam and oxycodone [duration of treatments to reactions onsets not stated;not all dosage and routes stated]. A 30-year-old pregnant woman, presented at 22 weeks of gestation. An ultrasound showed a eutrophic female fetus without any abnormalities. She had a history of mesenteric cystic lymphangioma and multiple bowel resections. At week 26, she presented with mild to moderate bowel occlusion and received parenteral nutrition supplements, resulting in rapid clinical improvement. Parenteral nutrition supplements were continued until the end of the pregnancy. At week 29, the mother was admitted for bilateral lumbar pain. Due to persistent pain and elevated serum creatinine, an internal ureteral bypass was performed with double J stents. Postoperative pain was treated with oral morphine, IV nefopam 120mg daily and immediate release oxycodone 5mg 4 times/day. At week 29 and day 4, a CT scan revealed significant uroperitoneum and bilateral pleural effusion. She also showed bilateral pleural effusion and acute renal failure, treated by thoracic drainage and bilateral nephrostomy. During her ICU stay, she developed painful uterine contractions, for which she received tocolytic treatment with atosiban. IV morphine was continued at a mean dose of 50mg of oxynorm/day for persistent lower back pain. Antenatal corticosteroid therapy was also administered. At this time, fetal heart rate (FHR) was normal. An ultrasound showed eutrophic fetus with estimated fetal weight [EFW] 1250g at week 29 and day 3 of gestation. The fetus had cephalic presentation, with a moderate excess of amniotic fluid and increased bladder volume. Enlarged fetal bladder was observed. At week 29 and day 5 (5 days following introduction of high-dose opioids in the mother), fetal megacystis increased and was accompanied by with pyelocaliceal dilatation. Three days later, an ultrasound showed voluminous fetal ascites as well as a small bladder with thickened walls. Morphologically, the fetal kidneys were normal. There was no anasarca or sign of fetal anaemia and the amniotic fluid index was normal. A possible spontaneous bladder rupture with urinary peritonitis was suspected. Due to absence of a clear cause, the morphine derivatives, which were administered to the mother for 8 days, were considered as a contributing factor to the fetal megacystis. Following discussion, anticipatory management was planned. The fetus was closely monitored with three FHR recordings every day and two ultrasounds every week. The mother and fetus remained stable for 9 days. The fetal bladder remained unchanged throughout monitoring. At week 31 and day 4, the mother went into spontaneous labor and received epidural anesthesia. The mother vaginally delivered a premature girl weighing 1700g, with moderate ischaemic anoxia. The girl had an Apgar scores of