Post Obstructive Diuresis

Post obstructive diuresis is excessive urine production, defined as urine output above 200 mL/h for 2 consecutive hours, or above 3 L in 24 hours (above 4 L daily in some definitions), following the relief of urinary tract obstruction. It occurs in about 50% of patients with relief of bilateral high grade obstruction and in a minority with unilateral obstruction. It is usually self-limiting within 24 to 72 hours but can cause dangerous volume depletion and electrolyte loss.

Two overlapping mechanisms operate:

• Physiological (appropriate) diuresis: excretion of retained salt, water and urea accumulated during obstruction, with a urea driven osmotic component. Output falls as volume and uraemia normalise. It rarely causes harm in a patient who drinks to thirst
• Pathological (inappropriate) diuresis: persistent loss of salt and water despite volume depletion, caused by tubular dysfunction. The recovering tubule shows reduced aquaporin-2 and sodium transporter expression (distal and collecting duct), impaired medullary concentration gradient, high circulating atrial natriuretic peptide, resistance to vasopressin and ongoing osmotic loss of urea. Urine is dilute or isotonic and sodium loss continues despite hypovolaemia

Risk factors are bilateral or solitary kidney obstruction, chronic high pressure retention with retained volume above 1 L, baseline serum urea above 40 mmol/L or creatinine above 300 micromol/L, volume overload before relief, diabetes, and large intravenous fluid replacement after relief.

• Urine output above 200 mL/h in the hours after catheterisation, stent or nephrostomy insertion, peaking in the first 24 hours
• Thirst, polyuria, postural hypotension, tachycardia, weight loss of more than 1 kg in 24 hours, dry mucous membranes
• Hyponatraemia (loss of sodium with water) or hypernatraemia (water loss in excess of salt, particularly with osmotic urea diuresis), hypokalaemia, hypomagnesaemia, hypophosphataemia, hypocalcaemia, metabolic acidosis
• Muscle weakness, cramps, arrhythmia from hypokalaemia and hypomagnesaemia; confusion from sodium disturbance
• Haematuria ex vacuo after rapid decompression

Red flags: urine output above 1 L in the first hour, systolic pressure below 90 mmHg, sodium below 130 mmol/L or above 150 mmol/L, potassium below 3.0 mmol/L, rising creatinine after relief, polyuria persisting beyond 48 hours.

• Monitor hourly urine volume and cumulative balance from the time of relief; weigh daily (twice daily in high risk patients).
• Bloods every 6 hours initially: sodium, potassium, urea, creatinine, bicarbonate, magnesium, phosphate, calcium, glucose; then 12-hourly.
• Urine sodium, potassium and osmolality at 6 and 24 hours: urine osmolality above 400 mOsm/kg with improving volume status suggests physiological diuresis; urine osmolality below 300 mOsm/kg with ongoing loss and hypovolaemia suggests pathological diuresis; urine sodium above 40 mmol/L despite hypovolaemia indicates salt wasting.
• Assess volume status: orthostatic blood pressure, capillary refill, inferior vena cava ultrasound.
• Exclude other causes of polyuria: hyperglycaemia, hypercalcaemia, diuretics, diabetes insipidus.

Differentials: osmotic diuresis from hyperglycaemia, diabetes insipidus, polyuric recovery phase of acute tubular injury, diuretic effect, over resuscitation.

Identify those needing monitoring

• Admit and monitor hourly for 24 to 48 hours any patient with bilateral obstruction, solitary kidney obstruction, urinary retention above 1 L, creatinine above 300 micromol/L or urea above 40 mmol/L.

Physiological diuresis

• Oral fluids to thirst; avoid mandatory intravenous replacement, which prolongs diuresis by supplying more salt and water to be excreted.
• Intravenous fluid only if oral intake is inadequate or the patient is hypovolaemic.

Pathological or hypovolaemic diuresis

• Replace 50% to 75% of the previous hour's urine output with 0.45% sodium chloride (use 0.9% sodium chloride if the patient is hypotensive or hyponatraemic with sodium below 130 mmol/L, or when urine sodium is above 100 mmol/L), hourly, adjusting every 4 to 6 hours to blood pressure, weight and electrolytes.
• Add potassium chloride 20 to 40 mmol in each litre when potassium is below 3.5 mmol/L (maximum rate 10 mmol/h peripherally; up to 20 mmol/h with cardiac monitoring in severe hypokalaemia below 2.5 mmol/L).
• Magnesium sulphate 8 mmol (2 g) intravenously over 1 hour for magnesium below 0.5 mmol/L, then 4 mmol twice daily; oral phosphate 250 to 500 mg elemental phosphorus (8 to 16 mmol) two to four times daily for phosphate below 0.6 mmol/L.
• Hypernatraemia (sodium above 145 mmol/L): replace free water using 5% glucose or oral water, lowering sodium no faster than 10 mmol/L in 24 hours.
• Hyponatraemia with sodium below 125 mmol/L: isotonic saline, with correction limited to 8 to 10 mmol/L in 24 hours.
• Monitor sodium every 4 hours if abnormal.

Treatment of refractory or prolonged diuresis

• If output remains above 200 mL/h beyond 48 hours with ongoing hypovolaemia, review for tubular dysfunction (nephrology), exclude diabetes insipidus and hyperglycaemia.
• Desmopressin has no role in physiological diuresis; consider only if diabetes insipidus is proven.
• Thiazide diuretics paradoxically reduce nephrogenic polyuria but are used only after specialist review.

Prevention of harm

• Decompression should not be slowed or staged, because staging does not reduce post-obstructive diuresis or haematuria ex vacuo.
• Avoid nephrotoxins and contrast after relief.

Recovery. Taper intravenous replacement to 25% of output then stop as output normalises and the patient drinks to thirst; check creatinine, sodium and potassium daily until stable. Urine concentrating defects can persist for weeks to months after prolonged obstruction.

Referral. Nephrology for pathological diuresis beyond 48 hours, creatinine not falling within 72 hours, persistent electrolyte disturbance.