Fetal malrotation with midgut volvulus: Prenatal diagnosis and planning.

Introduction: Malrotation of the intestinal tract is a congenital malformation commonly found either incidentally or after affected individuals develop signs and symptoms of intestinal obstruction. Malrotation is prone to midgut volvulus that can cause intestinal obstruction and lead to ischemia and necrosis requiring emergent surgical intervention. Rare instances of in utero midgut volvulus have been reported in the literature and carry a high mortality given the difficulty in establishing a diagnosis prior to development of signs of intestinal ischemia and necrosis. Advancements in imaging have made it possible to diagnose in utero malrotation earlier, raising the question of optimal timing of delivery, especially in cases of prenatally diagnosed midgut volvulus. In these cases, the risks of premature birth must be weighed against the risks of fetal intestinal ischemia and potential fetal demise. Case presentation: This case report details an interesting presentation of intestinal malrotation with suspected midgut volvulus found on prenatal imaging at 33 weeks and 4 days' gestation. This prompted delivery of the infant at 34 weeks and 2 days' gestation with urgent operative management, within 3 hours of life, after diagnosis was confirmed postnatally. Intraoperatively, the infant was confirmed to have midgut volvulus without bowel ischemia, the intestines were reduced, and a Ladd procedure was performed without incident. The infant recovered postoperatively without complication, tolerated advancement to full volume feeds and was discharged on day of life 18. Conclusion: Successful management of fetal malrotation with midgut volvulus may be accomplished by early access to a multi-disciplinary team of professionals, prompt postnatal confirmation of diagnosis, and urgent correction to minimize the risk of complications.

Trimethoprim/Sulfamethoxazole-Induced Severe Lactic Acidosis: A Case Report and Review of the Literature.

Propylene glycol (PG) is used as a solvent in numerous medications, including trimethoprim/sulfamethoxazole (TMP/SMX) and lorazepam, and is metabolized in the liver to lactic acid. Cases of lactic acidosis related to PG toxicity have been described and always involved large doses of benzodiazepines and PG. We present the first case of severe lactic acidosis after a 3-day course of TMP/SMX alone, involving allegedly safe amounts of PG.A 31-year-old female with neurofibromatosis and pilocytic astrocytoma, receiving temozolomide and steroids, was admitted to the intensive care unit for pneumonia and acute respiratory failure requiring intubation. Her initial hemodynamic and acid-base statuses were normal. She was treated with intravenous TMP/SMX for possible Pneumocystis jirovecii pneumonia and was successfully extubated on day 2. On day 3, she developed tachypnea and arterial blood gas analysis revealed a severe metabolic acidosis (pH 7.2, PCO2 19 mm Hg, bicarbonates 8 mEq/L) with anion gap of 25 mEq/L and lactate of 12.1 mmol/L. TMP/SMX was discontinued and the lactate decreased to 2.9 mmol/L within 24 hours while her plasma bicarbonates normalized, without additional intervention. The patient never developed hypotension or severe hypoxia, and her renal and liver functions were normal. No other cause for lactic acidosis was identified and it resolved after TMP/SMX cessation alone, suggesting PG toxicity.Although PG-related lactic acidosis is well recognized after large doses of lorazepam, clinicians should bear in mind that TMP/SMX contains PG as well and should suspect PG toxicity in patients developing unexplained metabolic acidosis while receiving TMP/SMX.