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Correspondence |
Temple, Texas
To the Editor:
We witnessed a case of a probable carbon dioxide (CO2) embolus during an otherwise routine laparoscopic cholecystectomy. The patient was a 32-yr-old, 82 kg, ASA Class II woman with a past medical history significant only for cholelithiasis and iron-deficiency anemia. Surgery proceeded uneventfully until dissection of the gallbladder from the liver bed. There was a sudden fall in arterial oxygen saturation (SaO2) to 68% and an abrupt drop in the end-tidal carbon dioxide (ETCO2) was noted. A switch to manual ventilation revealed a marked decrease in pulmonary compliance. The blood pressure (BP) dropped to 70/40 mmHg and the heart rate (HR) rose to 120 beatsmin-1. At that time, we were advised of brisk bleeding in the surgical field, which the surgeons were trying to control. The surgeon was notified of a probable CO2 embolus and the peritoneum was immediately decompressed. Volume replacement was accomplished with lactated Ringers solution and a synthetic colloid intravenously. Ephedrine, in divided doses, was used for blood pressure support. A laparotomy was performed to control the bleeding, which was due to a transected bridging vein between the liver and gallbladder. The patient rapidly recovered with a return of ETCO2 to 34 and normalization of airway pressure, SaO2, BP, and HR. The elapsed time from onset of symptoms to normalization of vital signs was only minutes. The patient did have a total blood loss of 2500 mL. The surgery was completed without any other untoward events and the postoperative course was uneventful.
Because of the symptoms and the sudden onset and resolution of the symptoms, we believe this patient experienced a CO2 embolus. The mechanism of entrainment of CO2 was through the tear in the bridging vein during gallbladder dissection. Since we didnt have a precordial Doppler or transesophageal stethoscope in place and no arterial blood gas was drawn, we have no confirmatory proof of an embolus, however, we believe that is the most likely explanation for this scenario. Another possible explanation is hypovolemic shock compounded by the increased intra-abdominal pressures during ip insufflation, leading to a dramatic decrease in venous return to the heart. Unfortunately, we will not be able to definitively diagnose the inciting event of this case, but it was truly an educational experience, reminding us that there are life-threatening complications around every "routine" corner.
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