Intraoperative lobar torsion producing pulmonary infarction

Intraoperative lobar torsion producing pulmonary infarction

Intraoperative lobar torsion producing pulmonary infarction John G. Schuler, M.D., Boston, Mass. SporadiC reports of gangrene of a segment, lobe, or ...

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Intraoperative lobar torsion producing pulmonary infarction John G. Schuler, M.D., Boston, Mass.

SporadiC reports of gangrene of a segment, lobe, or entire lung have appeared in the literature. These infarcts have occurred as a result of blunt trauma to the chest,"- 1~, 18, III torsion due to hiatus hernia," or torsion of an accessory lobe." Lobar gangrene has also been described as a complication of pulmonary resection 1,", 10, 13, 1" and pneumonolysis." Recently, intraoperative torsion of the middle lobe occurred in a patient undergoing right upper lobectomy. This resulted in infarction of the middle lobe, which probably would have progressed to gangrene had not emergency resection been performed, Because pulmonary infarction caused by transient intraoperative torsion has not been described, to my knowledge, it seems worthwhile to present this experience and to review the subject of pulmonary torsion and gangrene. Case report A. K., a 58-year-old woman with a persistent density in the right upper lobe (Fig. 1, A and B) and a history of heavy cigarette smoking, underwent a right thoracotomy on March 29, 1972. There was a firm, 3 em. mass in the posterior segment of the upper lobe, extending into the apical segment. The tumor appeared grossly to be malignant, and a lobectomy was necessary for total biopsy, Three segmental veins of the upper lobe were From the Fifth (Harvard) Surgical Service, Boston City Hospital, Overholt Thoracic Clinic, and New England Baptist Hospital, Boston. Mass, 02090, Received for publication Jan. 8, 1973.

identified and ligated as were the segmental arteries. While the vessels were being exposed, the middle lobe was rotated 180 degrees about its bronchovascular pedicle. It remained in this position during the hilar dissection, perhaps 10 minutes. The abnormal position was then recognized and corrected. The lobe aerated readily and did not appear ischemic or congested. After completion of the upper lobectomy, the middle lobe remained in its normal position once expanded. It did not appear necessary to anchor the lobe to the lower lobe. Postoperatively, the patient complained of constant pain in the right chest and back which seemed more severe than customary. Except for a pulse rate of 120 beats per minute, she spent an uneventful night. On the first postoperative morning, the pulse rate had risen to 140 beats per minute, and the systolic blood pressure had fallen to 90 mm. Hg. She was cyanotic, with labored, grunting respirations, and still complained of unremitting, crushing chest pain. Breath sounds were absent over the right chest, although copious secretions were audible in the trachea. She was treated by endotracheal intubation, suction of a large volume of bloody secretions, and administration of oxygen and intravenous fluid. Her color improved and the blood pressure rose, although she remained critically ill. X-ray study of the chest showed incomplete expansion of the remaining right lung with marked opacification of the upper two thirds of the right thoracic cavity (Fig. 2). An infarcted right middle lobe was suspected, and emergency re-exploration was undertaken. The middle lobe was found to be greatly enlarged, occupying approximately 60 per cent of the right thoracic cavity. It was airless, blue-black, and engorged. The lobe was not twisted about its bronchovascular pedicle, and the middle lobe veins and segmental artery were intact. Patency of the pulmonary vessels could not be determined at surgery. Neither had been occluded by ligature.

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Fig. 1. A, Preoperative chest x-ray film showing persistent right upper lobe density. B, Right anterior oblique x-ray film of apex of right lung showing preoperative infiltrate.

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The lower lobe was mottled but well aerated. The middle lobe was resected, and fresh thrombus was observed in the pulmonary vein. Examination of the resected middle lobe revealed an acute hemorrhagic infarct (Fig. 3). The pulmonary vein contained fresh thrombus, and the pulmonary and bronchial arteries were patent. Postoperatively, the patient's course was stormy. The left lung had been flooded previously, and secretions were retained on both sides (Fig. 4). She required steroids, antibiotics, and tracheostomy before her condition stabilized. After gradual improvement, she was discharged on the twentysixth hospital day with the tracheostomy closed but with some residual dyspnea on mild exertion. A chest x-ray film 5 months later was normal (Fig. 5).

Discussion

Fig. 2. Chest x-ray film, taken on the first postoperative day, showing incomplete expansion and opacification of remaining right lung and early pulmonary edema of left lung.

As noted earlier, pulmonary gangrene is a rare occurrence. Most cases have resulted from torsion of the lung after chest trauma or from inadvertent direct injury to pulmonary vessels during surgery. Intraoperative torsion of a lobe resulting in infarction has not previously been described. Therefore, I reviewed the subject of pulmonary gangrene

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Fig. 3. Photomicrograph of resected infarcted middle lobe showing intra-alveolar hemorrhage and severe vascular congestion .

and tor sion of the lung although gangrene had not yet developed in the case presented in this report. Much has been written about the experimental production of pulmonary gangrene. Yet the roles of the pulmonary and bronchial circulations have not been precisely defined. The significance of the bronchial arteries in maintaining viability of the lung has been stressed many times. Mathes" found that it was virtually impossible to interrupt the bronchial circulation by stripping peribronchial tissue since the vessels form profuse anastomoses in the bronchial submucosa. Ellis:' showed that bronchial artery obstruction in dogs produced infarction and ulceration of the proximal bronchus only. The pulmonary artery maintained tissue viabilit y distal to the hilum. The fact that pulmonary artery ligation is usually well tolerated," 9 , ' 0 with only an occasional case of infarction, " is doubtless due to the presence of the bronchial circulation. Mathes? and Liebow' described dilatation of bronchial vessels following pulmonary artery ligation. Ligation of the pulmonary artery in the first stage of a two-stage pneumonectomy does not produce infarction.

Rienhoff, ' 0 describing the first stage, cautioned that accidental interruption of the bronchial system would". , . in the presence of ligation of the pulmonary artery, result in necrosi s of the lung. " He did not present evidence to support this statement. Dargent" reported a case of pulmonary artery ligation which resulted in autolysis of a lobe to which there was no demonstrable bronchial circulation, providing further evidence of the importance of the bronchial system in pulmonary artery insufficiency. Mathes" and Swan-" found that pulmonary vein ligation produced a hemorrhagic, firm pulmonary parenchyma but not an infarction . Wyatt," as well, showed that vein ligation produced engorgement of the lung with extravasation of blood but without necrosis. Despite the case reported by Chambers and Sweeny ,' in which lobar gangrene appeared to follow pulmonary venous occlusion, it is difficult to ascribe the infarcted lobe reported in this paper to pulmonary vein thrombosis alone. Yet this was the sole pathologic finding in the blood supply of the lobe. As pre viously noted, experimental pulmonary vein ligation has been employed as

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Fig. S. Chest x-ray film 5 months after discharge. Fig. 4. Chest x-ray film, I day after re-exploration, showing full exp ansion of right lung with marked pulmonar y edem a of left lung .

a treatment for tuberculous cavitation, again without infarction." Thus it seems likely that the factor of torsion was important in the pathogenesis of the lobar infarction in our patient. During this torsion, both bronchial and pulmonary systems, as well as the bronchus, were presumably compromised. This brief period of significant, perhaps complete, ischemia may have precipitated injury, including bronchial artery spasm , which progressed to infarction once pulmonary vein thrombosis supervened . Obstruction of the bronchus itself, causing distal pooling of secretions, may have been an added significant injury. Mathes? showed that pulmonary artery occlusion with simultaneous bronchial obstruction produced infection and necrosis . Recognition of lobar or segmental gangren e may be difficult. Thirty-one reported cases of pulmonary gangrene resulting from torsion or intraoperative injury were reviewed, although in some the data were

fragmentary. Eighteen cases involved the upper lobes, 3 involved the lower lobes, 6 the middle lobe or lingula, and in 4 the lung lobes were indeterminate. In 25 of these pati ents, either an air leak or incomplete expan sion of the lung occurred. Consolidation or a "honeycomb" or "ground-glass" appearance was found on chest x-ray study in 9 patients. Other findings noted, although less frequently, were fever ( 6 patients), bloody or malodorous sputum, and foul chest tube drainage. Five of the 31 patients died. Pre vention or prompt recognition of postoperative pulmonary gangrene will naturally reduce the morbidity from this complication. During hilar dissection, care should be taken to avo id direct injury to remaining pulmonary vessels. As the interlobar or intersegmental fissure is developed, the position of the remaining lung should be noted to prevent intraoperative torsion. If the remaining lobes or segments are unusually mobile, they should be sutured lightly together to lessen the likelihood of postoperative torsion.

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Summary

A case of middle lobe infarction resulting from intraoperative torsion of the lobe is reported. The pathophysiology of pulmonary gangrene has been reviewed, and the probable mechanism responsible for lobar infarction in this report is presented. The available literature on postoperative and posttraumatic pulmonary gangrene has been summarized, and methods for preventing this complication are suggested. I would like to express my gratitude and appreciation to Dr. Richard H. Overholt for his assistance and suggestions in preparation of this report. I also wish to thank the Departments of Pathology of the New England Baptist and New England Deaconess Hospitals for their evaluation of the specimens and Dr. David P. Boyd for his suggestions in preparing this paper. REFERENCES

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