OPEN repair of thoracoabdominal aortic aneurysms (TAAs) is associated with significant respiratory morbidity. Predisposing factors include older age, preexisting lung disease, duration of aortic cross clamping, and the development of diaphragmatic dysfunction.1–3Endovascular Stent graft implantation has been advocated as an alternative treatment of TAAs in high-risk patients.4We describe a patient in whom diaphragmatic paralysis and ventilator dependence developed after endovascular Stent grafting of a TAA. We discuss the possible pathogenesis of this finding and its implications on our understanding of diaphragmatic dysfunction after surgical TAA repair.

A 71-yr-old woman with history of cigarette smoking, hypertension, and hypercholesterolemia was admitted to our hospital with the diagnosis of a small, contained rupture of a TAA. She had recently undergone endovascular Stent grafting of an infrarenal aortic aneurysm at another institution and wished to have her TAA also repaired through an endovascular approach. After approval by our institutional review board (Massachusetts General Hospital, Boston, Massachusetts) for compassionate release of a thoracic Medtronic AVE (Santa Rosa, CA) aortic Stent graft system, she underwent endovascular TAA repair during general anesthesia. Five Stent graft components were positioned through the right femoral artery to extend from 4–5 cm distal to the left subclavian artery to the suprarenal abdominal aorta. A completion aortogram revealed no endovascular leaks and satisfactory blood flow to the celiac, superior mesenteric, and renal arteries.

The postoperative course was complicated by atrial fibrillation, renal failure necessitating hemodialysis, nosocomial pneumonia, and respiratory failure necessitating prolonged mechanical ventilation and a tracheostomy. After approximately 4 weeks, the patient’s pneumonia resolved, and she was tolerating pressure support ventilation. However, her tidal volumes seldom exceeded 250–300 ml with a pressure support of 12–14 cm H2O, and she persistently had dyspnea. Her maximum inspiratory pressure was −30 cm H2O. On physical examination, she used the accessory muscles of breathing. On discontinuation of ventilatory support, inward retraction of the abdomen during inspiration developed immediately, suggestive of diaphragmatic paralysis. Electromyography and nerve conduction studies excluded a sensorimotor polyneuropathy, neuromuscular junction dysfunction, and a spinal cord lesion.

To confirm our clinical diagnosis of diaphragmatic paralysis, we placed two balloon-tipped catheters (SmartCath® Esophageal Catheter; VIASYS Healthcare, Palm Springs, CA) during local anesthesia from the nose into the esophagus and stomach to evaluate changes in intrathoracic and intraabdominal pressure during unsupported breathing.5A pneumotachometer (Novametrix Medical Systems, Wallingford, CT) was attached to the tracheostomy tube. Flow and pressures signals were recorded with a VenTrak Respiratory Mechanics Monitoring System (Novametrix Medical Systems) using waveform acquisition software (Analysis-Plus; Novametrix Medical Systems). As shown in figure 1, during unsupported breathing, both esophageal and gastric pressures had a negative deflection during inspiration, a finding suggestive of diaphragmatic paralysis.6–8 

Fig. 1. Esophageal (  left ) and gastric (  right ) pressures. Positive flow represents inhalation, and negative flow represents exhalation. Both esophageal and gastric pressure decrease during inhalation, consistent with diaphragmatic paralysis. 

Fig. 1. Esophageal (  left ) and gastric (  right ) pressures. Positive flow represents inhalation, and negative flow represents exhalation. Both esophageal and gastric pressure decrease during inhalation, consistent with diaphragmatic paralysis. 

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Because of the patient’s wish to avoid prolonged respiratory and renal support, mechanical ventilation and hemodialysis were eventually withdrawn, and she died on the 53rd postoperative day. A postmortem examination was denied by the family.

Diaphragmatic dysfunction after open TAA repair has been generally attributed to the surgical dissection of the diaphragm. A “diaphragmatic-sparing” technique has been developed in an attempt to limit damage to the diaphragm by preserving its central tendinous portion.9However, even its use has not decreased the long-term pulmonary morbidity after open TAA repair, which remains between 20 and 40%.2,3Our report is important because it describes the occurrence of diaphragmatic paralysis after endovascular Stent grafting of a TAA in the absence of any surgical manipulation of the lung or chest wall.

With endovascular Stent grafting, avoidance of the lung and chest wall trauma associated with an open approach should minimize perioperative respiratory morbidity. However, acute respiratory failure still occurs in 5–14% of patients undergoing this procedure, and its etiology is unclear.4,10 

Based on our current report, we postulate that acute respiratory failure after endovascular Stent grafting of a TAA may result from compromised perfusion to the diaphragm. The blood supply to the diaphragm derives from branches of the internal mammary arteries, the lower thoracic aorta, and the upper abdominal aorta or celiac trunk.11A decreased blood supply from one or more of these sources may significantly compromise diaphragmatic function, as has been reported after harvesting of bilateral internal mammary arteries for coronary bypass surgery.12In the current patient, the extent of Stent grafting could have occluded the phrenic arteries originating from the thoracic or upper abdominal aorta or both. It is also possible that the blood supply to the phrenic nerves was compromised; however, such large nerves are well vascularized by their vasa vasorum and should be less susceptible to selective ischemic damage.

Phrenic nerve injury has also been described as a complication of central venous cannulation. The current patient had both internal jugular veins cannulated at different times. However, we do not believe that either cannulation caused her complication because (1) she never showed signs of phrenic nerve paralysis such as acute dyspnea or elevation of a hemidiaphragm immediately after central line placement; (2) nearly all cases reported in the literature occurred after traumatic placements, whereas our placements were uneventful; and (3) the current patient had unequivocal evidence of bilateral diaphragmatic paralysis (see below), and it is unlikely that she sustained two separate occurrences of phrenic nerve paralysis after line placement.13 

The possibility of ischemic injury to the diaphragm after TAA repair is significant not only as an unexpected complication of endovascular Stent grafting, but also because it would have implications regarding open repair. Similar to ischemic injuries to the spinal cord, ischemic injury to the diaphragm could occur during prolonged thoracic aortic cross clamping, independent of the technique used to dissect the diaphragm. This possibility is supported by the finding of Engle et al.  2that the diaphragmatic-sparing technique does not decrease the long-term rate of reintubation, tracheostomy, and prolonged mechanical ventilation after open TAA repair.

Diaphragmatic paralysis is a clinical diagnosis based predominantly on an accurate physical examination. In a spontaneously breathing patient with a patent airway, diaphragmatic paralysis produces a paradoxical inward retraction of the abdomen during inspiration. This phenomenon must be distinguished from similarly dyssynchronous breathing patterns that can be seen with upper airway obstruction and with the active contraction of the expiratory muscles at end-exhalation that can occur during respiratory distress of various causes.14Although a careful physical examination, including palpation of the abdomen to detect contraction of the oblique muscles, should suggest the correct diagnosis, measurement of the gastric pressure, as we report here, is useful in the diagnosis of diaphragmatic paralysis by demonstrating the occurrence of a negative deflection of the gastric pressure during inhalation.

Confirmation of diaphragmatic paralysis can be attempted using direct fluoroscopy, electromyography, measurement of the transdiaphragmatic pressure, or measurement of the individual intrathoracic and intraabdominal pressures. We chose intrathoracic and intraabdominal pressure measurement because it is simple, has been clinically validated,7,8and can be used in patients who are able to maintain spontaneous breathing only for a short time.

In summary, we have described a patient in whom ventilator dependence developed with diaphragmatic paralysis after endovascular Stent grafting of a TAA. We postulate that this complication resulted from ischemic injury to the diaphragm at the time of Stent graft placement. This case report is clinically significant because (1) it describes a risk factor for respiratory failure and ventilator dependence after endovascular Stent grafting of a TAA, and (2) it proposes a mechanism of diaphragmatic dysfunction (vascular compromise) that may pertain to both endovascular and open TAA repair.

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