Transesophageal Echocardiographic Diagnosis of Carbon Dioxide Embolism During Minimally Invasive Saphenous Vein Harvesting and Treatment with Inhaled Epoprostenol

Gas embolism is a rare but potentially fatal complication of minimal access procedures in which carbon dioxide (CO2) is used. This complication occurred in approximately 1 of 7500 cases of laparoscopic surgery (1). Endoscopic saphenectomy is gaining popularity because it decreases morbidity compared with harvesting by the open technique (2,3) as well as improves functional and cosmetic appearance. Although safe, two cases of gas embolism during endoscopic saphenectomy have been published in the English literature (4,5). In one of these, the diagnosis was confirmed with intraoperative transesophageal echocardiography (TEE). In this case report, we describe a case of CO2 embolism during endoscopic saphenectomy where TEE was used to confirm the diagnosis and evaluate the hemodynamic consequences and to assess the effectiveness of inhaled epoprostenol during this uncommon complication. Case Report A 69-yr-old man with unstable angina was transferred from another hospital to the Montreal Heart Institute in September 2001 for coronary arteriogram. His medical history included morbid obesity, hypertension, mild asthma, and dyslipidemia. He was taking amlodipine, hydrochlorothiazide, oral nitrates, pravastatin, and enteric coated aspirin. Coronary arteriography showed a 70% occlusion of the left anterior descending artery and a 60% stenosis of the circumflex artery. Left ventricular function was described as normal on the coronary angiogram. The patient was then scheduled for endoscopic saphenous harvesting and coronary artery bypass graft (CABG) without extracorporeal bypass. The day of surgery, he received morphine 10 mg IM, midazolam 7 mg IM, inhaled albuterol, and sodium citrate 30 mL as premedication. Upon arrival in the operating room, systolic blood pressure was 120/60 mm Hg, and the heart rate was 65 bpm. General anesthesia was induced with sufentanil 70 μg, midazolam 2.8 mg, and pancuronium 10 mg. Central venous and pulmonary artery catheters were then inserted. Catheterization showed a normal systolic and diastolic pulmonary artery pressure (22/8 mm Hg), and the cardiac output was 4.8 L/min (cardiac index, 2.3 L · min−1 · m2). The initial blood gas values (pH value, 7.48 U; Po2, 474 mm Hg; Pco2, 35 mm Hg) were within normal limits. Initial TEE examination showed normal left and right ventricular systolic function. No patent foramen ovale was present. Concomitantly to sternotomy and the beginning of the internal thoracic artery dissection, a right lower thigh incision was performed for endoscopic saphenectomy. After identification of the internal saphenous vein and insertion of a port, a seal was achieved at the level of the knee, and CO2 insufflation was initiated at a flow of 2 L/min to obtain a pressure of 15 mm Hg. Soon after the beginning of the endoscopic dissection, systolic pulmonary artery pressure suddenly increased to 65 mm Hg, and the systemic blood pressure declined to 90 mm Hg (Fig. 1A). This was associated with ST changes in lead II and V5. Capnography showed an immediate increase of end-tidal CO2 to 54 mm Hg (Fig. 2). Simultaneously, numerous gaseous bubbles were seen with the TEE in the right ventricular chamber, the right atrium, the pulmonary artery, and in the inferior vena cava confirming the infradiaphragmatic origin of the emboli (see video loops). The four-chamber view showed a dilated right ventricle associated with septal shift and compression of the left ventricle (Fig. 3 and video loop). No paradoxical emboli were visualized, and ischemic changes were detected on the continuous two leads electrocardiogram (II, V).Figure 1: Systemic (SAP), pulmonary (PAP), and central venous pressure (CVP) during the episode of CO2 embolism (A) and after the use of epoprostenol (B). ECG = electrocardiogram.Figure 2: Capnographic data wave form summary. There was a sudden increase in end-tidal CO2.Figure 3: Echocardiographic 2D examination obtained from a four-chamber view. A dilated right ventricle (RV) compressing the left ventricle (LV) through the interventricular septum is seen. RA = right atrium; LA = left atrium.CO2 insufflation was immediately discontinued, and ventilatory rate and tidal volume were increased with an Fio2 = 1.0. Pharmacologic treatment was initiated consisting of nitroglycerine up to 83 μg/min, norepinephrine 20 μg/min, and inhaled epoprostenol 75 μg via a jet nebulizer (Ref 8901, Salter Labs, Arvin, CA) attached to the inspiratory limb of the ventilator near the endotracheal tube. Nebulization was achieved with a bypass flow of oxygen at 8 L/min. Five minutes after the initiation of treatment, ST segment increase normalized, and pulmonary artery pressures returned to normal values (Fig. 1B). No more gaseous bubbles were detectable using the TEE, and both left and right ventricular function returned to normal (see video loop). After hemodynamic stabilization and progressive weaning of inotropic support, the saphenous vein was removed by the open technique, and the two CABGs were completed uneventfully without extracorporeal bypass. Postoperatively, the patient had an uneventful course. He was tracheally extubated approximatively 8 h after surgery. No focal or diffuse neurologic sequelae were noted, and the patient was discharged home the fourth postoperative day. Discussion Massive gaseous embolism is a rare but serious complication of endoscopic procedures. Prompt diagnosis and treatment is crucial. Immediately stopping CO2 insufflation, hyperventilation of the patient with a Fio2 = 1.0, and inotropic support of hemodynamic function are the baseline of treatments of this condition. Other treatments included Trendelenburg position and central venous pressure increase. Aspiration of gas from the right ventricle via a central venous catheter may relieve a gas lock in severe cases. Cardiopulmonary bypass has been used for refractive hemodynamic instability. Although not routinely used during these procedures, TEE is the most sensitive method to diagnose and guide treatment when a gaseous embolism occurs. We also found that inhaled epoprostenol was efficient in the treatment of pulmonary hypertension secondary to CO2 embolism and was beneficial in the hemodynamic stabilization, enabling the surgeon to complete the off-pump CABG procedure. The internal saphenous vein used for CABG is usually harvested by the open technique. Many complications have been reported with this technique, including skin necrosis, dehiscence, and wound infection (6). Endoscopic saphenous vein harvesting has been proposed in these patients. Several authors have noted an overall decrease in morbidity associated with this procedure (2,3). However, CO2 embolism remains a risk factor, as demonstrated in our case report. The incidence of this complication during endoscopic saphenectomy is unknown. Only two cases have been reported in the English literature (4,5). The mechanisms of CO2 embolism usually involve absorption into the circulation, CO2 being highly soluble in blood, or, more seriously, direct entry of gas into the vascular bed generally via an injury to a vessel, particularly in the presence of relative hypovolemia. In the second mechanism, manifestations of CO2 embolism are through a gas-lock effect causing obstruction to right ventricular ejection, right and left cardiac failure, paradoxical embolism with or without patent foramen ovale, arrhythmia, pulmonary hypertension, systemic hypotension, and cardiovascular collapse. Embolization of CO2 in the pulmonary arterioles can also trigger cytokine release, platelet and neutrophil activation, with subsequent pulmonary vasoconstriction, bronchospasm, and pulmonary edema (7). This patient’s systolic and diastolic pulmonary artery pressures remained high despite treatment with large doses of IV nitroglycerin. Several authors have reported their experience using epoprostenol in the treatment of pulmonary hypertension (8–13). Our patient received a 75-μg dose of inhaled epoprostenol with the intent to diminish the pulmonary artery pressure. The dose was based on our experience with this medication (13). The pulmonary arterial pressure returned to normal values soon after its administration (Fig. 1B). Epoprostenol is available rapidly, is easier to use compared with nitric oxide, and has the advantage of diminishing the pulmonary arterial pressure without causing marked systemic hypotension such as occurs with IV vasodilators. In our previous experience with CO2 embolism (4), the off-pump bypass procedure had to be converted to CABG with extra-corporeal circulation. It is possible that the favorable response observed in the treatment of pulmonary hypertension with use of inhaled epoprostenol may have prevented us from using extra-corporeal circulation for circulatory support. CO2 embolism should be suspected when an increase in end-tidal CO2 is followed by a decrease in cardiac output and hypotension. TEE is the most sensitive method to detect gas embolism (14). Its use during cardiovascular procedures makes early detection of CO2 embolization prompt and easy. In this case, TEE clearly identified CO2 originating from the inferior vena cava, confirming its origin from the lower extremities. It also showed gas in the right ventricle and main pulmonary artery and documented right ventricular failure, interventricular septal shift toward the left ventricle, and a decrease in left ventricular dimension. This is the second case reporting the use of the TEE for detection of gaseous embolism during endoscopic saphenectomy. However, in this patient, the hemodynamic management was guided by the use of TEE. Disappearance of gas embolism and return to normal cardiac function after the administration of epoprostenol were also documented before the decision to continue the off-pump CABG procedure was finalized.

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