1. Description of the problem

Generally polyuria is defined as a urine output of > 3 L/day. However, some experts feel that any “inappropriately high” urine output to the physiologic state can be considered as polyuria.

Polyuria can quickly deplete any given patient’s intravascular volume leading to hypotension and organ hypoperfusion. So early recognition, followed by replacement of volume losses with simultaneous efforts to identify the cause and rectify it should be undertaken. Common causes of polyuria in hospitalized patients include hyperglycemia, diabetes insipidus, recovering phase of acute kidney injury, or iatrogenic due to diuretics (mannitol, furosemide).

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Clinical features

Clinical features include high urine output with other signs of intravascular volume depletion, including dry mucous membranes, poor skin turgor, delayed capillary refill, tachycardia and hypotension. Patients may exhibit altered mentation from the inciting cause such as severe hyperglycemia or hypercalcemia or as a result of severe hypernatremia from water diuresis.

Patients with primary polydipsia can exhibit severe hyponatremia with altered mentation. Cardiac arrhythmias from hypokalemia and or hypomagnesemia can also occur.

Key management points

Key management principles include:

  • Maintenance of airway and breathing when compromised

  • Intravascular volume repletion

  • Diagnostic evaluation of underlying reason of polyuria

  • Treatment of the underlying cause

  • General supportive care

2. Emergency Management

  • Emergency management should always start with assessment and maintenance of airway if patient is obtunded or comatose.

  • If patient presents with seizures due to extreme dyselectrolytemias, benzodiazepines (lorazepam) should be administered and patient placed in left lateral position to prevent aspiration. If altered mentation is prolonged, intubation should be considered. Anti-epileptic therapy is generally not advised if the seizure is purely triggered by a dyselectrolytemia.

  • If focal neurologic deficits are present, neuro imaging should be considered to rule out a stroke (cerebral arterial or venous thrombosis). Note that dyselectrolytemias alone do not lead to focal neurologic deficits.

  • Early aggressive volume resuscitation with isotonic fluids (0.9% saline or lactated Ringer’s) should be initiated. In a hypotensive patient only isotonic fluids should be used irrespective of serum sodium level.

  • Electrocardiogram should be done in all patients, both to look for signs of coronary ischemia/infarction from severe dehydration and arrhythmias from dyselectrolytemias.

Management points not to be missed
  • Ensure patient airway

  • Assess severity of hypovolemia and degree of compensation

  • Obtain 2 large-bore IV lines

  • Start isotonic fluid boluses with 0.9% saline or lactated Ringer’s (250-500 ml aliquots over 15-30 min) and assess response and tolerance

  • Send appropriate diagnostic tests to establish cause of polyuria

  • Monitor serum sodium, potassium and magnesium levels frequently and maintain homeostasis

  • General supportive care including prophylaxis for deep venous thrombosis

  • Desmopressin nasal spray 5-20 mcg once or twice a day

  • Desmopressin injection 1 mcg subcutaneous route every 12 hours

  • Hydrochlorothiazide 25-50 mg oral route once or twice a day

3. Diagnosis

Diagnosis of polyuria is often done looking at the urine output chart of the patient. History is key in diagnosing some causes of polyuria, including hereditary disorders, lithium toxicity and hyperglycemic hyperosmolar states.

The following step-wise approach will assist in identifying the etiology of polyuria:

  • Thorough history and clinical examination

  • Measurement of urine and serum osmolality

  • Serum sodium, potassium, glucose, calcium and magnesium

  • Calculate urine total electrolyte excretion: {2 x (urine sodium + urine potassium)} x total urine volume in 24 hours. If total urinary electrolyte excretion is more than 600 mosm/day then an electrolyte-induced solute diuresis should be diagnosed.

  • A water deprivation test can distinguish central vs. nephrogenic DI

  • Urine osmolality – If < 250 mosm/L suggests a hypotonic urine usually from either psychogenic polydipsia or diabetes insipidus (DI) (central or nephrogenic).

  • Serum osmolality will help distinguish between psychogenic polydipsia and DI (hypotonic in the former and hypertonic in the latter)

  • If urine and serum osmolality both are high, it suggests a solute-induced diuresis as a cause of polyuria

  • Calculating total electrolyte excretion will differentiate between electrolyte vs non-electrolyte induced solute diuresis.

Confirmatory tests

Plasma osmolality: 275-285 mosm/L


Urine output is determined by water intake and water excretion. Water intake is primarily controlled by thirst, which is stimulated by decreased intravascular volume or blood pressure and increased plasma osmolality.

Primary determinant of water excretion is the anti-diuretic hormone (ADH). ADH acts on specific receptors in the basolateral membrane of the collecting duct and increases permeability for water reabsorption by inserting water channels on the luminal membrane. ADH secretion is stimulated again by low intravascular volume and high plasma osmolality, with intravascular volume status being the more potent stimulus.

Polyuria hence happens when there is increased intake overwhelming the renal water excretory capacity (psychogenic polydipsia), or by decreased ADH secretion in response to stimuli (central DI) or resistance to ADH at the collecting tubule (nephrogenic DI).

Hence in patients with psychogenic polydipsia, free water restriction is the treatment of choice. In patients with central DI replacement of ADH in the form of nasal desmopressin spray should be done. Nephrogenic DI is treated with a combination of free water restriction and thiazide diuretics. In patients with solute diuresis, treatment of the underlying cause and replacement of intravascular volume are the mainstay of treatment.


Epidemiology of polyuria in the critically ill patients is ill-defined. When the intravascular volume depletion is not corrected adequately in a timely manner, it can lead to significant morbidity and mortality. The dyselectrolytemias associated with polyuria, including hypernatremia, severe hypokalemia and hypercalcemia, can all lead to increased adverse events including encephalopathy and cardiac arrhythmias.

Special considerations for nursing and allied health professionals.


What's the evidence?


Kamel, KS, Ethier, JH. “Urine electrolytes and osmolality: when and how to use them”. Am J Nephrol. vol. 10. 1990. pp. 89-102. (Discusses the role of urine electrolytes and a user's guide to apply them in clinical practice.)

Diagnostic approach

Oster, JR, Singer, I. “Polyuria of solute diuresis”. Arch Intern Med. vol. 157. 1997. pp. 721-9. (Good overview on solute diuresis.)

Narins, RG, Riley, LJ. “Polyuria – simple and mixed disorders”. Am J Kid Dis. vol. 2. 1991. pp. 237-41. (Good review on polyuria.)


Kanno, K, Sasaki, S. “Urinary excretion of aquaporin-2 in patients with diabetes insipidus”. New Engl J Med. vol. 332. 1995. pp. 1540-5. (Describes the importance aquaporins in DI.)