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CRITICAL CARE AND TRAUMA

Acute Pulmonary Artery Embolism During Transcatheter Embolization: Successful Resuscitation with Veno-Arterial Extracorporeal Membrane Oxygenation

Ingrid Haller, MD^*, Agnes Kofler, MD^*, Wolfgang Lederer, MD^*, Andreas Chemelli, MD, and Franz J. Wiedermann, MD^*

From the Departments of *Anesthesiology and Critical Care Medicine, and Radiology, Innsbruck Medical University, Austria.

Address correspondence and reprint requests to Franz J. Wiedermann, MD, Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Austria. Address e-mail to franz.wiedermann{at}i-med.ac.at.

	Abstract

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Versatile particles from transcatheter embolization may accidentally enter the pulmonary circulation, causing severe pulmonary embolism. A 36-yr-old woman patient suffering from an arteriovenous malformation in the left shoulder underwent embolization with micro coils, N-butyl-2-cyanoacrylate/lipiodol and polyvinyl alcohol particles. During embolization, acute onset of tachycardia, hypotension, and decline in oxygen saturation indicated right ventricular failure and decreased pulmonary perfusion confirmed by angiography. As mechanical resuscitation failed to stabilize cardiocirculatory function, veno-arterial extracorporeal membrane oxygenation support was preformed until hemodynamic stability was regained. Extracorporeal membrane oxygenation should be considered for cases where pulmonary embolism causes right ventricular failure and circulatory arrest during transcatheter embolization.

	Introduction

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Arteriovenous malformations (AVM), a tangled collection of blood vessels with abnormal communications between the arterial and venous systems, may produce a perfusion shunt of sufficient magnitude to increase cardiac output.1,2 Treatment of AVMs is either by conventional surgery, endovascular embolization or radio surgery.3,4 Complications of endovascular treatment of AVMs comprise hemorrhage, and less frequently, embolism.2,5

	CASE DESCRIPTION

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A 36-yr-old woman, 60 kg and 173 cm, ASA status I, was scheduled for the second session of transarterial embolization at the department of radiology. The patient suffered from paresthesias in her left arm due to an AVM in her left shoulder. Physical examination and preoperative routine laboratory results were unremarkable. Magnetic resonance imaging (MRI) showed a large AVM of 15 x 6 cm in diameter, located in the supraclavicular region and subscapular adjacent to the thoracic wall, involving the subscapular muscle and the brachial plexus. Diagnostic angiography revealed a large high-flow AVM, with arterial supply from the suprascapular artery, lateral thoracic artery, subscapular artery, and drainage predominantly to the axillary vein. Anesthesia was induced with 150 mg propofol and 0.2 mg fentanyl and maintained with propofol (400 mg/h) and remifentanil (1 mg/h). Unfractionated heparin (2500 I.U., I.V.) was administered.

The transarterial access via the right femoral artery was uneventful, but placement of the microcatheter was more distant from the "nidus" than during the first embolization session. Flow reduction in the AVM using 50 to 60 micro coils, 2 to 3 mm in diameter, inserted with a microcatheter (Fasttracker 18), was moderate. Hence, the interventional radiologist decided to administer polyvinyl alcohol (PVA) particles with a size of 500 to 700 and predominantly 700 to 1000 microns, and 3 mL of N-butyl-2-cyanoacrylate (NBCA) diluted with lipiodol. During embolization, the patient's arterial blood pressure decreased to 65/40 mm Hg, whereas her heart rate started to increase to 148 bpm. Her saturation of peripheral oxygen declined to 95%, end-tidal CO₂ remained at 30 mm Hg; central venous pressure was 20 mm Hg.

The inspiratory oxygen concentration was kept at 1.0, and ephedrine and phenylephrine were administered to increase her blood pressure. The procedure was immediately stopped and additional unfractionated heparin (5000 I.U., I.V.) was administered. Pulmonary angiography confirmed the presumed diagnosis of acute pulmonary embolism (PE) and showed right ventricular dilation and decreased perfusion of pulmonary vessels (Fig. 1). Approximately 15 min after the first hypotensive episode, her heart rate increased to 165 bpm, arterial blood pressure decreased to 45/45 mm Hg and saturation of peripheral oxygen declined to 73%; end-tidal CO₂ was 25 mm Hg. Cardiopulmonary resuscitation (CPR) and epinephrine in repeated doses, total 10 mg, did not succeed in stabilizing her cardiocirculatory function. As a last resort, veno-arterial extracorporeal membrane oxygenation (ECMO) support was established within 1 h (inspiratory oxygen concentration of 0.8). Two hours after onset of PE, the patient was referred to the intensive care unit (arterial blood gas examination: pH: 7.22, base excess: –14.3, HCO₃: 12.4, CO₂: 41.2 mm Hg; saturation of peripheral oxygen: 99%; central venous pressure: 14 mm Hg; mean pulmonary arterial pressure: 40 mm Hg). Transesophageal echocardiography showed dilation of the right atrium and ventricle. Antithrombotic treatment was maintained with unfractionated heparin (400 I.U./h). ECMO supported oxygenation for 5 days until the patient's circulation was sufficiently restored.

View larger version (133K): [in this window] [in a new window]   Figure 1. Angiography of the pulmonary circulation reveals missing peripheral pulmonary vessels due to bilaterally scattered microemboli. Acute dilation of right ventricle and pulmonary artery indicates pulmonary hypertension.

Computer tomography imaging displayed multiple micro-vascular pulmonary arterial lipiodol emboli with infiltration of the lungs and pleural effusion on both sides and light pericardial effusion (Fig. 2). Repeated chest radiograph examinations showed progressive streaky shadows and formation of atelectasis in basal areas of both lungs. One week after CPR, the patient developed pneumonia and was treated with metronidazol and ciprofloxacin.

View larger version (75K): [in this window] [in a new window]   Figure 2. Six days after embolization contrast medium enhanced computed tomography scans show the partially embolized arteriovenous malformation in the left thoracic wall. Hyperdense emboli (NBCA/lipiodol) mostly in the lower pulmonary arteries are still verifiable.

Cranial MRI for neurological evaluation of possible residuals of cardiac arrest and resuscitation was performed 12 days after CPR and showed no signs of any hypoxic lesions. Features of demyelization were unchanged as compared to the MRI scan prior to embolization.

Three weeks after resuscitation, the patient was transferred from the intensive care unit to a general ward. She survived without any neurological sequelae and was discharged from hospital 2 wk later having regained complete recovery of her cardiocirculatory performance.

	DISCUSSION

Top Abstract Introduction CASE DESCRIPTION DISCUSSION REFERENCES

 
A case is presented with acute PE after transcatheter embolization with micro coils, NBCA/lipiodol and PVA particles. Substances had accidentally passed through the AVM via macro-shunts to the pulmonary circulation, creating multiple microemboli and consequently acute right ventricular failure.

In endovascular embolization, the surgeon guides a catheter though the arterial network until the tip reaches the site of the AVM. The surgeon then introduces a substance that will plug the fistula, correcting the abnormal pattern of blood flow by forming thrombi. The materials used to create an artificial blood clot in the center of an AVM include fast-drying, biologically inert glues, fibered titanium coils, and tiny balloons. Since embolization usually does not permanently obliterate the AVM, it serves as an adjunct to surgery or to radiosurgery.

Endovascular embolic treatment of AVMs is not without risk. Pulmonary embolization complicating therapeutic transcatheter embolization of a cerebral AVM was reported by Leitman et al.6 Kjellin et al. hypothesized that inadvertent pulmonary migration of embolic material is rather common, even though it mostly goes unrecognized.7 With increasing use of interventional techniques, anesthesiologists working in interventional radiology must be aware of this potential complication and know advanced treatment strategies.

Death from massive PE is more frequent in patients with cardiac arrest requiring CPR. In addition, the absence of thromboemboli within the main pulmonary artery and the presence of multiple peripheral thrombi are a grave prognostic sign. In hemodynamically unstable patients, prompt surgical intervention with ECMO can be life-saving. In acute massive PE, the method was first reported in 1961.8 ECMO can compensate for cardiorespiratory failure while oxygenating blood that passes through a membrane oxygenator, and it can establish blood flow with the help of roller pumps, thus providing both cardiac and respiratory support. Cannulae are placed in large blood vessels either veno-arterial or veno-venous to provide access to the patient's blood. Anticoagulation is commonly achieved with heparin. In 13 of 21 patients eligible for ECMO and suffering from massive PE, the method was reported to be life-saving.9

In our patient, NBCA/lipiodol and PVA particles of 500 to 1000 microns had passed through the AVM and been filtered by the pulmonary circulation, creating multiple microemboli and consequently acute right ventricular failure. Although the presumed diagnosis of acute PE was confirmed by angiographic investigation, the anesthesiologist was reluctant to administer thrombolytics. The mechanism of impaired lung perfusion was assumed to be the combined consequence of obstructing particles, adjacent thrombi, and systemic vasospasm. At that time, it was not known whether lung perfusion would be able to recover, at least in part, after vessels were obstructed by numerous particles. ECMO was initiated to immediately improve oxygenation and possibly serve as a bridge to lung transplant if recovery failed. However, in our patient emergent ECMO decompressed the acutely overloaded right atrium and ventricle; it improved end-organ perfusion and maintained hemodynamic stability. When lung perfusion had spontaneously recovered over 5 days, weaning of ECMO support was uneventful. The authors recommend that ECMO be considered in the algorithm for management of massive PE after transarterial microcatheter embolization.

	ACKNOWLEDGMENTS

 
We express our gratitude to the teams of cardiac surgery, cardiothoracic anesthesiology, and intensive care medicine, Innsbruck University Hospital, for their excellent performance and care.

	Footnotes

 
Accepted for publication May 1, 2008.

	REFERENCES

Top Abstract Introduction CASE DESCRIPTION DISCUSSION REFERENCES

 

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