genitourinary disorders
Acute Kidney Injury (AKI)
Treatment of AKI
Immediate treatment of pulmonary edema and hyperkalemia Dialysis as needed to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms Adjustment of drug regimen for degree of renal dysfunction Usually restriction of water, sodium, phosphate, and potassium intake, but provision of adequate protein Possibly phosphate binders (for hyperphosphatemia) and intestinal potassium binders (for hyperkalemia) Life-threatening complications are addressed, preferably in a critical care unit. Pulmonary Edema is treated with oxygen, IV vasodilators (eg, Hyperkalemia is treated as needed with IV infusion of 10 mL of 10% is controversial, correction of the nonanion gap portion of severe Metabolic Acidosis (pH Hemodialysis None Severe electrolyte abnormalities cannot otherwise be controlled (eg, potassium>6 mmol/L) Pulmonary edema persists despite drug treatment Metabolic acidosis is unresponsive to treatment Uremic symptoms occur (eg, vomiting thought to be due to uremia, asterixis, encephalopathy, pericarditis, seizures) Bloodureanitrogen (BUN) and creatinine levels are probably not the best guides for initiating dialysis in acute kidney injury (AKI). In asymptomatic patients who are not seriously ill, particularly those in whom return of renal function is considered likely, dialysis can be deferred until symptoms occur, thus avoiding placement of a central venous catheter with its attendant complications. Nephrotoxic drugs are stopped, and all drugs excreted by the kidneys (eg,digoxin, some antibiotics) are adjusted; serum levels are useful. Daily water intake is restricted to a volume equal to the previous day’s urine output plus measured extrarenal losses (eg, vomitus) plus 500 to 1000 mL/day for insensible loss. Water intake can be further restricted for hyponatremia or increased for hypernatremia. Although weight gain indicates excess fluid, water intake is not decreased if serum sodium remains normal; instead, dietary sodium is restricted. Sodium and potassium intake is minimized except in patients with prior deficiencies or gastrointestinal losses. An adequate diet should be provided, including daily protein intake of about 0.8 g/kg. If oral or enteral nutrition is impossible, parenteral nutrition is used; however, in AKI, risks of fluid overload, hyperosmolality, and infection are increased by IV nutrition. Calcium salts (calcium carbonate,calcium acetate) or iron-based or synthetic phosphate binders before meals help maintain serum phosphate at<5.5 mg/dL (<1.8 mmol/L). 6 mmol/L in the absence of Hemodialysis (eg, if other therapies, such as diuretics, fail to lower potassium), a cation-exchange resin is prescribed when delayed onset of action of several hours is acceptable. An indwelling bladder catheter is rarely needed and should be used only when necessary because of an increased risk of Introduction to Urinary Tract Infections (UTIs) and urosepsis. In many patients, a brisk and even dramatic diuresis after relief of obstruction is a physiologic response to the expansion of extracellular fluid (ECF) during obstruction and does not compromise volume status. However, polyuria accompanied by the excretion of large amounts of sodium, potassium, magnesium, and other solutes may cause hypokalemia, hyponatremia, hypernatremia (if free water is not provided), hypomagnesemia, or marked contraction of ECF volume with peripheral vascular collapse. In this postoliguric phase, close attention to fluid and electrolyte balance is mandatory. Overzealous administration of salt and water after relief of obstruction can prolong diuresis. When postoliguric diuresis occurs, replacement of urine output with 0.45% saline at about 75% of urine output prevents volume depletion and the tendency for excessive free water loss while allowing the body to eliminate excessive volume if this is the cause of the polyuria. 