The major disadvantage of intermittent dialysis is the frequent occurrence of hypotension, sometimes requiring premature discontinuation of the treatment. Dialysis hypotension can usually be attributed to preload reduction because rapid ultrafiltration exceeds fluid recruitment from the interstitium. In turn, the plasma refilling rate is adversely affected by rapid decreases of serum osmolality with intracellular fluid shifts. Acetate and bio-incompatible membranes also contribute to hypotension by induction of inappropriate vasodilatation. Reduction of myocardial contractility is mostly attributable to hypoxemia or acidosis. Convective solute removal (regardless of the ultrafiltration rate, small solute clearance, buffer, and membrane) appears to be hemodynamically better tolerated than diffusion. The mechanism underlying diffusion-related hypotension has not been elucidated. Possible explanations are increased diffusive removal of a small-molecular-weight substance (e.g. an inhibitor of NO synthase leading to increased NO synthesis and vasodilatation) or decreased diffusive removal of a vasodilating middle molecule (e.g. calcitonin gene-related peptide, atrial natriuretic peptide, parathyroid hormone).
In hemodynamically unstable patients, dialysis-induced hypotension can be attenuated by slow ultrafiltration (ultrafiltration controllers), promotion of plasma refilling by infusion of human albumin or the use of high-sodium dialysate, sequential ultrafiltration and dialysis (temporal segregation of ultrafiltration and solute removal), and using biocompatible membranes and bicarbonate (Tabled). Intermittent hemofiltration uses convective solute transport resulting in improved hemodynamic tolerance (no diffusion-related hypotension). However, despite these modifications, intermittent techniques will probably never reach the excellent hemodynamic tolerance of the continuous renal replacement techniques.
S^JïïiiI UraTiraiOfl ïtf i^ss Table 2 Prevention of dialysis-related hypotension
Rapid removal of osmotically active solutes from the extracellular compartment leads to an increase in cerebral water content (dialysis disequilibrium with headache, nausea, vomiting, and hypertension, eventually progressing to arrhythmias, confusion, tremor, seizures, coma, and death). The disequilibrium syndrome can be attenuated by adding solute (sodium, glucose, mannitol) to the dialysate and by initiation of dialysis before the urea has reached too high a level. In patients with pre-existing cerebral edema, intermittent dialysis can lead to life-threatening increases in intracranial pressure.
Hypoxemia during dialysis results from acetate-induced hypoventilation (only in spontaneously breathing patients) or from the use of bio-incompatible membranes. Intermittent hemodialysis may delay the recovery of renal function because of recurrent periods of hypotension (loss of autoregulation in the injured kidney) or because of the insufficient removal or generation of nephrotoxic mediators by low-flux bio-incompatible membranes. The hemodynamic intolerance to fluid removal often limits nutritional support. The requirement for specialized equipment and trained nursing staff is another limitation of intermittent dialysis.
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