PARAPLEGIA is a well-recognized complication of thoracic aortic aneurysm (TAA) repair, but rarely occurs after abdominal aortic aneurysm (AAA) repair. 1,2In most reported cases of postoperative paraplegia, it is difficult to identify the exact time of onset for the event, the factors that may have contributed to the development of spinal cord ischemia, or whether therapeutic interventions were effective. In the case described in this article, the delayed onset of paraplegia in the postoperative period after repair of a suprarenal AAA temporally followed an episode of hypotension, suggesting that the neurologic deficit was caused by hypoperfusion. Acute diagnosis and interventions directed to increase spinal cord perfusion by increasing arterial pressure and decreasing lumbar cerebrospinal fluid (CSF) pressure were immediately effective in reversing paraplegia, and led subsequently to full neurologic recovery.

Case Report

A 76-yr-old, 58-kg man was hospitalized for elective repair of a 5.5 × 7 cm suprarenal AAA. The patient's medical history was notable for hypertension, mesenteric artery stenosis, and infrarenal aortobifemoral bypass graft repair with right nephrectomy 12 yr ago. Aortic angiography demonstrated absence of the inferior mesenteric artery, occlusion of the celiac and superior mesenteric arteries, and ostial stenosis of the left renal artery.

An epidural catheter was inserted into the T7–T8 thoracic vertebral interspace. General anesthesia was induced by thiopental, fentanyl, and cisatracurium. Anesthesia was maintained with inhaled isoflurane, cisatracurium, and a continuous infusion of bupivacaine 0.05% and fentanyl 2 μg/ml at a rate of 6 ml/h via  the epidural catheter. The right radial artery and pulmonary artery pressures were monitored. The aneurysm was approached through a left retroperitoneal incision. After the intravenous administration of heparin 5,000 USP units and mannitol 25 g, the aorta was cross-clamped at the level of the diaphragm. A 20 mm Dacron graft (Sulzer Vascutek Gelweave™, Sulzer Vascutek, Austin TX) was interposed between the proximal end of the previous infrarenal aortic bifurcation graft and the aorta at the level of celiac artery. A 6 mm Dacron graft was used to bypass the superior mesenteric artery. The aorta was cross-clamped for 40 min. At the end of surgery, protamine 25 mg was administered intravenously. The hemoglobin concentration of the patient was 10.5 g/dl. His trachea was extubated in the operating room, and the patient had normal motor strength in all four extremities.

Neurologic assessment performed upon admission to the intensive care unit (ICU) verified intact motor and sensory function in all extremities. Forty-five minutes after arrival to the intensive care unit the patient's mean arterial pressure (MAP) decreased from 78 mmHg to 48 mmHg (fig. 1). Shortly thereafter, the patient reported weakness and loss of sensation in the lower extremities. Examination by a neurologist demonstrated flaccid paralysis and paraplegia extending to the T10 thoracic dermatome. MAP was increased to 75 mmHg by discontinuing the epidural infusion and increasing dopamine to 6 μg · kg−1· min−1intravenously. In addition, phenylephrine 50 μg intravenous bolus, 250 ml of packed red blood cells, and 5.5 l of normal saline were administered. After the arterial pressure increased, the patient was able to move his left leg weakly. Intravenous norepinephrine 3–6 μg/min and intravenous epinephrine 3–4 μg/min−1were then started in an effort to keep the MAP in the range of 95–105 mmHg. A 0.7 mm ID lumbar CSF drainage catheter (MoniTorr ICPTM, Clinical Neuro Systems, Exton, PA) inserted 7 cm into the subarachnoid space via  a 14-gauge Tuohy needle at the L3–L4 vertebral interspace measured a lumbar CSF pressure of 12 mmHg (fig. 1). Clear CSF, 15 ml was immediately drained, and 10 ml of CSF was drained every hour for a lumbar CSF pressure greater than 10 mmHg. Bilateral lower extremity motor strength and sensation gradually recovered and returned to normal over the next 60 min. The arterial pressure improved, permitting the discontinuation of norepinephrine, epinephrine, and a reduction of the dopamine dose to 3 μg · kg−1· min−1. Neurologic examination 7 h later demonstrated normal symmetrical motor strength in the lower extremities, no sensory deficits, and hyperreflexia. The lumbar CSF catheter was occluded 48 h later and then removed at 72 h after surgery. There were no further episodes of paraplegia, and the patient was discharged 23 days after the operation with no neurologic deficits.


Postoperative paraplegia after AAA repair has an estimated incidence between 0.15–0.3%. 2Although the precise mechanism of paraplegia after aortic reconstruction remains to be established, factors that increased the risk in the case described were the presence of extensive peripheral vascular disease, previous replacement of the infrarenal aorta with a bifurcated graft, suprarenal position of the aneurysm, need for a supraceliac aortic cross clamp, and onset of hypotension in the immediate postoperative period. Investigators have suggested that the lumbar, iliolumbar, and lateral sacral arteries of the hypogastric and pelvic circulation are important sources of blood flow to vessels supplying the caudal portion of the spinal cord. 2–3In the presence of occlusive disease of the aortoiliac arteries, the hypogastric and pelvic circulation may be supplied by collaterals from the hypogastric, inferior mesenteric, or superior mesenteric arteries. 4Previous aortobifemoral bypass grafting with prior sacrifice of the inferior mesenteric artery and severe occlusive atherosclerotic disease of the mesenteric vessels in this patient were likely to have severely compromised the collateral blood supply to the spinal cord arising from the hypogastric and pelvic circulation. In this situation, it was likely that the further decrease in spinal cord perfusion as a consequence of hypotension was a primary event that contributed to the development of spinal cord ischemia in a watershed distribution. In previous reports, hypotension has also been implicated as a factor that contributed to ischemic infarction of the spinal cord. 5–8 

Combined general anesthesia and epidural analgesia with a very dilute concentration of local anesthetic permitted early neurologic evaluation and the immediate diagnosis of paraplegia caused by spinal cord ischemia. Clinical experience has indicated that continuous epidural infusion of bupivacaine 0.05% and fentanyl 2 μg/ml started during surgery produces satisfactory analgesia without impairment of motor function. 9Although epidural hematoma or local anesthetic-induced motor blockade were considered, the acute onset of paraplegia and complete sensory loss in the early postoperative period was most consistent with spinal cord ischemia.

Emergency treatment of paraplegia with vasopressor therapy to augment the arterial pressure and lumbar CSF drainage to decrease the lumbar CSF pressure was immediately initiated to increase the net spinal cord perfusion pressure. Lumbar CSF drainage to prevent postoperative paraplegia after aortic surgery has been advocated, but its effectiveness for the treatment of delayed onset postoperative paraplegia remains controversial. 2,10–15The specific use of vasopressor therapy for the treatment of spinal cord ischemia has not been studied, but the presumed ischemic etiology of the complication prompted its use. Norepinephrine and epinephrine were chosen in an effort to increase both the arterial pressure and cardiac output. Multiple vasopressor agents at relatively high doses were required initially to generate a MAP greater than 90 mmHg. Recovery of neurologic function coincided with the increased arterial pressure. It was possible that hypotension at the onset of spinal cord ischemia may have also been caused by ischemia-induced autonomic dysfunction as in the syndrome of spinal or neurogenic shock. Ischemia-induced autonomic dysfunction would explain also the need for vasopressor therapy during the event and the spontaneous recovery of arterial pressure after the return of neurologic function.

Cases of delayed onset of paraplegia in the postoperative period after AAA have been reported, but their frequency has been difficult to determine because not all patients have neurologic assessments immediately after surgery. 5,16–17In contrast to paraplegia detected upon emergence from general anesthesia, delayed onset of paraplegia indicates that the vascular supply to the spinal cord was not irreversibly damaged as a consequence of surgery. 15Delayed onset of paraplegia suggests that postoperative events such as hypotension, increased CSF pressure, or embolization, may have triggered the onset of neurologic dysfunction in patients at risk for spinal cord ischemia. 14–15Based on this pathophysiology, it is reasonable to predict that delayed onset paraplegia is reversible and will respond to treatment with interventions directed at increasing spinal cord perfusion. Full or partial recovery from delayed onset paraplegia after AAA or TAA repair has been reported, but standard treatment algorithms for this complication have not yet been developed or tested.

The events of this case challenge earlier presumptions that postoperative paraplegia is an unavoidable, unpredictable, and untreatable complication of aortic reconstruction. 2,10,14Although it was not possible to determine with certainty the precise mechanism of postoperative paraplegia and the relative contribution of individual treatment interventions, the additive effect of the treatment strategy to increase spinal cord perfusion pressure was temporally followed by the recovery of neurologic function. Considering the severity of this complication and its associated morbidity, early implementation of this treatment algorithm can be justified while awaiting additional evidence to support its clinical effectiveness.


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