Aortic Cross-Clamping

The relative effects of suprarenal and infrarenal aortic cross-clamping (see Chapter 52 ) on renal function in patients undergoing major vascular surgery have been studied.^[19] Regardless of the position of the aortic cross-clamp, RBF is decreased to 50% of normal during surgical preparation of the aorta, presumably because of direct compression or reflex spasm of the renal arteries. After release of the suprarenal cross-clamp, RBF increases above normal (reflex hyperemia), but the GFR remains depressed to a third of control for up to 2 hours. After 24 hours, the GFR is still only two thirds of control. Tubular functions (concentrating ability, sodium and water conservation) are markedly impaired, but urine flow is maintained. Myers and Moran^[114] observed that these changes resemble an attenuated form of acute tubular necrosis. In the aforementioned study, all patients received mannitol pretreatment, which probably limited the tubular insult because oliguria was uncommon and recovery was relatively rapid. However, cross-clamp times longer than 50 minutes were associated with prolonged depression of the GFR and transient azotemia.^[19]

Infrarenal aortic cross-clamping may also impair RBF and GFR by inducing decreases in cardiac output in response to increased systemic vascular resistance. ^[115] Atheromatous embolism of the renal arteries may be induced by cross-clamping or manipulation in areas of dense aortic plaque. Partial or complete cortical necrosis may occur but is usually irreversible.

Renal Protection during Aortic Cross-Clamping

Mannitol has been used for more than 40 years to provide renal protection during aortic cross-clamping.^[116] Its protective effects have been clearly demonstrated in animal models of ischemic acute tubular necrosis,^[117] but few prospective controlled human studies have been conducted. Low-dose dopamine has commonly been used during major vascular surgery. In a canine study of thoracic aortic cross-clamping, RBF, GFR, and urine flow remained impaired for a considerable time after cross-clamp release. This delay was not prevented by prophylactic dopamine.^[72] In a human study of infrarenal cross-clamping, Paul and coworkers^[118] compared diuretic therapy with a combination of mannitol and dopamine versus fluid loading with saline to a pulmonary artery occlusion pressure of 12 to 15 mm Hg. Although mannitol and dopamine substantially increased urine flow and sodium excretion during cross-clamping, they were no better than saline in attenuating residual GFR depression after cross-clamp release.