Diabetes Insipidus

Definition | Aetiology | Pathophysiology | Risk Factors | Signs and Symptoms | Investigations | Management

Definition

Diabetes insipidus is a disorder of water balance caused by impaired secretion or response to antidiuretic hormone (ADH), leading to excessive urinary output and dehydration.

Aetiology

  • Central diabetes insipidus: due to inadequate ADH production from the hypothalamus or pituitary (e.g., traumatic brain injury, pituitary tumours, neurosurgery, meningitis).
  • Nephrogenic diabetes insipidus: renal resistance to ADH (e.g., chronic kidney disease, lithium toxicity, hypercalcaemia, hypokalaemia).
  • Gestational diabetes insipidus: increased metabolism of ADH by placental enzymes.
  • Primary polydipsia: excessive fluid intake leading to suppression of ADH secretion.

Pathophysiology

  • Inadequate ADH secretion (central DI) or renal resistance to ADH (nephrogenic DI) leads to reduced water reabsorption in the collecting ducts.
  • This results in excessive urine output (polyuria), dehydration, and compensatory thirst (polydipsia).
  • In chronic cases, hypernatraemia may develop due to excessive free water loss.

Risk Factors

  • Head trauma or neurosurgery.
  • Brain tumours affecting the hypothalamus or pituitary.
  • Chronic lithium therapy.
  • Electrolyte imbalances (hypercalcaemia, hypokalaemia).
  • Pregnancy (gestational DI).

Signs and Symptoms

  • Polyuria: excessive urine output (>3L/day).
  • Polydipsia: excessive thirst and fluid intake.
  • Nocturia: frequent urination at night.
  • Dehydration: dry mucous membranes, hypotension, tachycardia.
  • Hypernatraemia: in severe or untreated cases.

Investigations

  • Serum and urine osmolality: low urine osmolality (<300 mOsm/kg) with high serum osmolality (>295 mOsm/kg) suggests DI.
  • Water deprivation test: failure to concentrate urine suggests DI; response to desmopressin differentiates central from nephrogenic DI.
  • Serum sodium: may be elevated in dehydration.
  • Magnesium, calcium, and potassium: assess for electrolyte imbalances contributing to nephrogenic DI.
  • Pituitary MRI: indicated if central DI is suspected.

Management

1. Central Diabetes Insipidus:

  • Desmopressin (DDAVP): synthetic ADH analogue to reduce polyuria and polydipsia.
  • Fluid management: maintain adequate hydration.
  • Identify and treat underlying cause: e.g., surgical intervention for pituitary tumours.

2. Nephrogenic Diabetes Insipidus:

  • Thiazide diuretics: paradoxically reduce urine output by inducing mild volume depletion.
  • NSAIDs (e.g., indomethacin): enhance renal response to ADH.
  • Correct underlying cause: discontinue lithium, correct hypercalcaemia or hypokalaemia.

3. General Measures:

  • Encourage appropriate fluid intake to prevent dehydration.
  • Monitor serum sodium and osmolality regularly.

4. Referral:

  • Endocrinology: for specialist input in persistent or complex cases.
  • Nephrology: if nephrogenic DI is resistant to treatment.
  • Neurosurgery: if DI is secondary to pituitary or hypothalamic pathology.