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• Maintain normothermia. Hypothermia during TAAA repair is thought to be protective for the spinal cord and for prevention of tissue ischemia. If the core temperature is below 36°C (96.8°F) postoperatively, it can result in coagulopathy due to increased blood viscosity and platelet dysfunction. Hypothermia can also cause myocardial ischemia, affect drug distribution, and is a major risk factor for surgical site infection (SSI).
• Maintain pulmonary function. Ventilatory support is needed in patients undergoing open repair for at least the first 24 to 48 hours. Monitor O₂ saturation and peak inspiratory pressures. Wean the patient as soon as possible to prevent complications such as ventilator-acquired pneumonia (VAP) and barotrauma. Reintubation is associated with a higher incidence of mortality. Adequate pulmonary toilette is essential.
• Maintain mean arterial pressure (MAP) as specified to avoid spinal cord ischemia (SCI) in patients undergoing TEVAR or open TAA repair. After a TAA repair, MAP is monitored closely and is often kept at greater than 80 mmHg. Hypotension causes decreased spinal cord perfusion and may lead to temporary or permanent paralysis from SCI. Perioperative hypotension (MAP <70 mmHg) was found to be a significant predictor of SCI. Therefore, careful monitoring and prompt correction of arterial pressure is essential in preventing the development of paraplegia. Paralysis after a TAA repair decreases the one-year survival rate to less than 50%. Preoperatively, a spinal drain is placed in patients undergoing both stent graft and open repair TAA to both avoid and treat this complication.
• Maintain adequate arterial blood pressure. Avoid hypotension. Identify the cause of the hypotension and treat it as quickly as possible to avoid complications such as MI and end organ damage due to malperfusion. Excessive bleeding in the retroperitoneum or chest cavity require emergency reoperation. In the immediate postoperative period, these patients require large amounts of fluids, often vasopressors, as well as blood administration. Maintain MAP as ordered.
• Monitor neurologic function. Frequent assessment of neurologic function, at least every 2 hours, allows for early detection and prompt intervention. Check for any asymmetry in spontaneous movement of the upper and lower or between the right and left lower extremities. There is only a two-hour window before irreversible damage occurs. Check spinal drain tubing for kinks and monitor drain function. If these changes occur, reduction of the CSF pressure by drainage fluid is useful.
• Monitor urine output. Abdominal compartment syndrome should be considered in the presence of oliguria and hypotension that is not responsive to fluids or pressors, increased abdominal girth, and increased ventilatory requirements. Easily overlooked or mistaken for other events, such as hypovolemia, the clinician must consider and be alert to this possibility. In this set of patients, the increased intra-abdominal pressure is the result of a prolonged operation and fluid resuscitation, resulting in edema of the abdominal organs, which then compress the inferior vena cava. This compression results in decreased preload and cardiac output, raised intrapleural pressure, and decreased lung compliance resulting in hypoventilation, hypoxemia, hypercapnia, and acute onset of renal insufficiency. Decrease in cardiac output results in more injury/ischemia to the intra-abdominal organs causing metabolic acidosis and rising lactate levels. A bladder pressure of over 20 to 30 mmHg is diagnostic. Treatment is emergency decompression laparotomy. Once the abdomen is decompressed, the intraabdominal pressure returns to normal, and there is resolution of the previously mentioned signs. The abdomen is packed and closed secondarily in a staged manner.