| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
Departments of *Anesthesiology and
Surgery, Montreal Heart Institute, Quebec, Canada
Address correspondence and reprint requests to André Denault, MD, FRCPC, Montreal Heart Institute, Department of Anesthesiology, 5000 Belanger St. East, Montreal, Quebec, H1T 1C8, Canada. Address e-mail to denault{at}videotron.ca
 |
Abstract |
|---|
 Top Abstract IntroductionCase ReportDiscussionReferences |
|---|
IMPLICATIONS: We describe a patient scheduled for coronary artery bypass who developed carbon dioxide (CO2) embolism with acute pulmonary hypertension during endoscopic saphenectomy. Transesophageal echocardiography was useful in the diagnosis of CO2 embolism and to assess response to inhaled epoprostenol.
|
Introduction |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
|
Case Report |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
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).
|
|
|
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 |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
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.
|
Footnotes |
|---|
|
References |
|---|
|
TopAbstractIntroductionCase ReportDiscussionReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  P. K. Sinha, A. Jayant, and B. Kumar The need for monitoring during endovascular vein harvesting Eur. J. Cardiothorac. Surg., January 1, 2008; 33(1): 137 - 137. [Full Text] [PDF]
|
|
|
|
|
|
E. V. Potapov, S. Buz, and R. Hetzer CO2 embolism during minimally invasive vein harvesting Eur. J. Cardiothorac. Surg., May 1, 2007; 31(5): 944 - 945. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Mommerot and L. P. Perrault Carbon dioxide embolism induced by endoscopic saphenous vein harvesting during coronary artery bypass grafting J. Thorac. Cardiovasc. Surg., December 1, 2006; 132(6): 1502 - 1502. [Full Text] [PDF]
|
|
|
|
 |
|
 C. A. Dias-Junior, A. Martineau, P. Couture, and A. Denault Pharmacologic Therapy of Acute Pulmonary Embolism * Response Anesth. Analg., January 1, 2004; 98(1): 266 - 267. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
