Aneurysms of the visceral arteries are rare but important vascular lesions. Associated aneurysms are common. Because of the risk of rupture, often with a fatal outcome, an aggressive approach to the treatment of VAA is essential.

This report summarizes our experience with the use of cerebral spinal fluid drainage (CSFD) and naloxone for prevention of postoperative neurologic deficit (paraplegia or paraparesis). Methods: We reviewed 110 consecutive patients with 86 thoracoabdominal aneurysms and 24 thoracic aneurysms. The status of 47 patients (43%) was acute (rupture or dissection), and the status of 52 (47%) was Crawford type I or II. None of the patients had intercostal artery reimplantation. There were two patient groups for analysis of neurologic deficit risk. Group A (61 patients) received naloxone and CSFD, and group B (49 patients) did not. Results: One deficit occurred in group A and 11 deficits occurred in group B (p = 0.001). By multiple logistic regression analysis, the variables acute status, Crawford type II, or group B classification were significant factors for deficit risk. Use of the same logistic regression analysis on the subgroup of 47 patients with acute aneurysms and 33 patients with Crawford type 2 aneurysms confirmed the protective effect of combined CSFD and naloxone (group A) and that clinical presentation and extent of aorta replaced are the primary risk factors for development of deficit. To test this conclusion we developed a highly predictive model (correlation coefficient 0.997 with 16 series of thoracoabdominal aneurysms) for neurologic deficit. We applied our data to this model. Group B had the predicted number of deficits, and group A had substantially fewer deficits than predicted. Conclusions: We conclude that the combined use of CSFD and naloxone offers significant protection from neurologic deficits in patients undergoing thoracoabdominal and thoracic aortic replacement.

FPAES and CRECS occur in the same population with similar symptoms but require different treatment.

Intermittent claudication may occur in well-conditioned athletes because of an unusual form of popliteal artery entrapment that results from overtraining. These patients complain of calf muscle cramping, rapid limb fatigue, and occasional paresthesias on the plantar surface of the foot when running on inclines or when repetitive jumping is performed. Results of plethysmographic screening tests for popliteal entrapment are positive in these patients. Magnetic resonance angiography and intravenous digital subtraction angiography studies, however, do not demonstrate findings typical of anatomic popliteal entrapment. No evidence exists of aberrant positioning of the popliteal artery in foot neutral positioning, but with forced plantar flexion, the neurovascular bundle is deviated and compressed laterally. Surgical exploration of the popliteal fossa demonstrates no obvious musculotendinous abnormality. Symptoms of claudication and arterial compression are relieved by surgical release of the soleus muscle from its tibial attachments, resection of its fascial band, and resection of the plantaris muscle.

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