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Departments of Anesthesiology, Pediatric Cardiology, and Cardiac Surgery, Charité Hospital, Berlin, Germany
Address correspondence and reprint requests to Ulrich Döpfmer, MD, Lindenstrasse 30, 12589 Berlin, Germany. Address email to doepfmer{at}snafu.de
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Abstract |
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IMPLICATIONS: We report a case of lung bleeding and gas embolization during cardiac surgery that was successfully treated by temporary occlusion of the blood vessel feeding the affected lung lobe with a balloon dilating catheter and temporary selective ventilation of the contralateral lung without further surgical interventions.
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Introduction |
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We report a case of severe pulmonary hemorrhage and gas embolism into the left atrium during separation from cardiopulmonary bypass (CPB). We successfully treated this patient using a new management algorithm with localization of the bleeding pulmonary vein by selective wedge angiography and temporary occlusion of the artery feeding the affected lobe using a dilating catheter. Temporary one-lung ventilation prevented further gas embolism. No further surgical interventions were required.
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Case Report |
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For drug administration and pressure monitoring, the right internal jugular vein and the left femoral artery were cannulated. No pulmonary artery catheter was used. Transesophageal echocardiography (TEE) confirmed the preoperative findings, and no new pathology was detected. Normothermic CPB using a centrifugal pump was established through a double-staged right atrial cannula and a cannula in the ascending aorta with flows between 4.3 and 6.3 L per min and arterial blood pressure between 60 and 80 mm Hg. Cardiac ischemia lasted 65 min and intermittent antegrade blood cardioplegia was used. Through an intrapericardial incision of the upper right pulmonary vein, an 18F "vent" (Jostra, Hirrlingen, Germany) was inserted for about 15 cm aiming at the mitral valve, but positioning was not checked by TEE. Implantation of a 23-mm CarbomedicsTM (Sulzer Carbomedics Inc., Austin, TX) mechanical aortic valve was uneventful. This vent was removed before trying to re-establish pulmonary blood flow and the incision was closed. A new vent was inserted at the highest point of the ascending aorta, proximal to the aortic cannula, and that vent was draining 500 mL/min, according to our usual "de-airing" protocol after valve surgery. On recommencing ventilation and reducing drainage to the pump, lung compliance became very reduced and even hand ventilation became impossible. Approximately 1 L of blood was lost through the endotracheal tube on disconnecting the ventilator. Full CPB was recommenced and the endotracheal tube was changed to a 37F left sided BronchocathTM tube (Broncho-Cath, Mallinckrodt Medical, Athlone, Ireland). Fiberoptic bronchoscopy revealed the right lung as the source of bleeding. The precise site could not be determined as a result of loss of bronchoscopic visibility as soon as pulmonary blood flow was increased. By this time a further 1.5 L of blood was lost, and TEE revealed severe gas embolization into the left atrium, as soon as the right lung was ventilated.
After re-establishment of full bypass the decision was made to attempt to localize the bleeding site using fluoroscopy. A 6F wedge catheter was positioned into the right pulmonary artery through a femoral vein puncture using a mobile C-arm angiography unit with anteroposterior radiation. Selective wedge-angiography of the right upper, middle, and lower lobe pulmonary artery was performed by hand injecting 5 mL of contrast medium through the wedged catheter. Lower lobe angiography revealed contrast medium in the right main bronchus and admixture of gas bubbles to the pulmonary venous return once the lung was ventilated.
At this time the patient had received 12 U of packed red cells and the total bypass time was exceeding 4 h. Immediate surgical resection of the right lower lobe was judged to be excessively risky. Therefore it was decided to temporarily occlude the feeding pulmonary artery and wean the patient from CPB using one-lung ventilation. For this purpose, the wedge catheter was exchanged with a guidewire to a 10 mm diameter OptaTM balloon dilating catheter (Cordis Europa, LJ Roden, The Netherlands). This was filled with 8 mL of contrast medium at a pressure of roughly 6 atmospheres.
The bleeding was efficiently stopped, as judged by repeat bronchoscopy. The tracheal lumen of the BronchocathTM tube was initially left open to atmosphere and subsequently 6 cm H2O of continuous positive airway pressure (CPAP) was applied. No gas embolization was visualized under either condition by TEE. Weaning from CPB after a total bypass time of almost 5 h and infusion of protamine was uneventful. The left lung was ventilated using FIO2 = 1.0 at a rate of 10 breaths per minute and pressures of 24 over 4 cm H2O, resulting in tidal volumes of roughly 470 mL. Initial arterial blood gas analysis showed a PO2 of 110 mm Hg with a PCO2 of 38 mm Hg and a pH of 7.38. The PO2 improved to 265 mm Hg and PCO2 increased to 41.4 mm Hg after application of CPAP to the nonventilated lung. Blood clotting was aggressively normalized by transfusion of 24 U of fresh-frozen plasma, 1000 U of cryoprecipitate, 2500 U of factor 13, 2 g of fibrinogen, and 2 pooled units of platelets, supplemented by 2000 U of antithrombin III to avoid hypercoagulation. The patient was transfused with 24 U of red blood cells in the operating room and almost 4 L of blood had been suctioned from the tracheobronchial tree. She was transferred to the intensive care unit (ICU) using one-lung ventilation with the inflated OptaTM balloon in position with the proximal end securely fixed to the skin in the groin. Figure 1 shows a radiograph taken immediately after ICU admission.
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The endobronchial tube was exchanged for an endotracheal tube after a further 20 h and sedation stopped. On regaining consciousness she developed transient proximal weakness of all four extremities with bilateral positive Babinski’s sign. A computed tomography (CT) scan of the brain and cervical spine was reported as normal, and there were no deficits of the cranial nerves or sensory losses. The neurological signs had almost completely subsided before we could arrange a magnetic resonance tomography scan and further investigations. She was weaned from mechanical ventilation on the second postoperative day and discharged from ICU 3 days later, when the findings of her neurological examination had normalized. Her hospital stay was prolonged to a total of 33 days as a result of patchy infiltrates in the right lower lobe with signs of systemic inflammation requiring antibiotic treatment for 18 days. She required repeated pleurocentesis for recurrent right pleural effusions. A CT scan of her thorax 5 months later showed full expansion of all lung lobes with no residual opacifications, and she had New York Heart Association stage I exercise tolerance.
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Discussion |
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The management of major intrapulmonary bleeding during cardiac surgery depends on the site of the vascular injury (as only proximal lesions are amenable to surgical repair) (1,5), the experience of the surgical team (in Germany cardiac and thoracic surgery develop into two separate specialities), and the preoperative status of the patient and his or her suitability for major pulmonary resections. Local conditions are important for treatment decisions because in many locations emergency rigid bronchoscopy is becoming a lost art (11). The current pulmonary, circulatory, and hemostatic condition of the patient are other issues to be considered.
If an alternative to an emergency resection is sought, we advise against extensive bronchial lavages with saline, as these are very likely to lead to an acute respiratory distress syndrome or similar conditions (5). Increased levels of positive end-expiratory pressure may lead to gas embolism (12). We recommend temporary obstruction of the feeding artery. Achieving this goal with an intravascular catheter has the dual advantages of concurrently being able to perform a diagnostic angiography (if the lesion is not positively localized by bronchoscopy) and avoidance of reopening the chest, if bronchoscopy reveals no recurrence of hemorrhage after careful reestablishment of pulmonary circulation to the affected lung.
Numerous case reports describe systemic gas embolism secondary to pulmonary trauma (13), the most frequent etiology being penetrating, blunt, or blast injury to the lung. The most important issue in avoiding gas entry into an injured pulmonary vein is the avoidance of large gradients between airway pressures and pressures in the pulmonary vein (13,14). We achieved this aim by selectively ventilating the contralateral lung and then applied only moderate levels of CPAP. The organs most liable to damage by systemic gas emboli are the central nervous system and the heart (15). We considered our patient to be reasonably well protected from systemic gas emboli by the vent in the aortic root, as the subjective assessment of gas bubble load by TEE revealed the usual findings after valve replacement or aneurysmectomy. At no time did she develop any signs of coronary gas embolism. We did not specifically search for cerebral gas embolism before diagnosing any neurological deficits, as hyperbaric therapy was not a treatment option for a patient on one-lung ventilation with multiple blood clots in the small airways of the nonventilated lung, making her liable to pulmonary decompression injury.
In summary we present a case of disastrous lung bleeding, associated with systemic gas embolization, most likely caused by a flexible, round tipped, plastic pulmonary vein vent crossing through the atrium from the upper into the lower lobe vein. This situation was managed successfully by temporary balloon occlusion of the feeding artery and temporary one-lung ventilation, without any further surgical intervention. This method of management may not always lead to a definite solution of the problem, but it should at least be able to temporize so that further steps such as surgical resections can be planned in a more controlled manner.
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This article has been cited by other articles:
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  G. Stratmann and J. L. Benumof Endobronchial Hemorrhage Due to Pulmonary Circulation Tear: Separating the Lungs and the Air from the Blood Anesth. Analg., November 1, 2004; 99(5): 1276 - 1279. [Full Text] [PDF]
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