- During mild polyuria (2–3 mL/kg per hour) where resolution is expected, replacement of the previous hour’s urine output with appropriate fluid (usually IV 5% dextrose, IV 0.18% saline/4% dextrose or nasogastric water in ICU) whilst closely monitoring plasma and urinary osmolality and electrolytes may suffice.
Overadministration of dextrose solutions may cause hyperglycaemia, hyperosmolality and osmotic diuresis.
- Severe (>3 mL/kg per hour) or persistent polyuria merits ADH/AVP or DDAVP administration.
DDAVP is a selective V2 receptor agonist and is therefore less likely to cause hypertension. It’s long-acting and resistant to breakdown by vasopressinases.
Daily dose rates of 1–4 micrograms in a single or divided dose by intravenous, intramuscular or subcutaneous administration. Oral and intranasal formulations also exist.
ADH (vasopressin) may be administered subcutaneously or by intravenous infusion.
- In the acute situation, an ADH infusion (0.1–3 U/h) can be conveniently titrated against urine output before conversion to longer-acting DDAVP.
- ADH and DDAVP dose requirements are often higher during the acute onset of CDI – this may reflect loss of medullary interstitial hypertonicity, competitive antagonism at V2 renal receptors by biologically inactive ADH precursors released from the damaged hypothalamic-pituitary tract, or both.
The dose of ADH or DDAVP used is the minimum dose required to achieve acceptable control of urine output. Excessive administration may cause water retention and hypo-osmolal syndromes.
Other drugs may also reduce the polyuria of CDI, provided there is some residual ADH synthesis, include; chlorpropamide, clofibrate and carbamazepine. They are all reported to both enhance ADH release and renal responsiveness to ADH.
