Diabetes insipidus
Pathophysiology
ADH
Synthesised in hypothalamus
Released from post pituitary in response to:
Incr plasma osmolality (>1% from set point 285)
Hypovolaemia (overides osmotic regulation, allowing kidney to conserve water)
Angiotensin II
Pain, stress, emotion, exercise
Promotes water reabsorption in the kidneys
Activates V2 receptors on principal cells in the collecting duct
Via 2nd messenger cAMP, inserts aquaporin water channels into the luminal membrane
Water is conserved in excess of solutes and a small volume of hyperosmotic (concn) urine is excreted
Leads to decreased plasma osmolality, creating a negative feedback loop and cessation of ADH release
Consequences of head injury
Reduced ADH synthesis or release may occur in head injury - neurogenic DI
Inability to concentrate urine results in production of large volumes of dilute urine, dehydration and hypernatraemia
Direct trauma
Oedema/inflammation
Vascular insufficiency
Diagnosis
History
Polyuria
Polydipsia
Thirst
May be masked in head injured patients
Examination
Dehydration if patients are unable to drink freely or thirst mechanisms are impaired
Investigations
Hypernatraumia
Plasma ADH concn down
Plasma and urine osmolality
If urine output low and osmolality high, then both ADH secretion and the renal response are present (cause most likely extrarenal water loss)
If both urine output and urine osmolality are high - osmotic diuresis is suspected
Response to Desmopressin (1mcg IV) - differentiates between neurogenic and nephrogenic DI. Causes concn of urine in patients with neurogenic DI
If urine output is high and urine osmolality isless than plasma osmo, then the cause is due to ADH secretion or abnormal response to ADH
Imaging: Brain CT/MRI to determine cause
Response to fluid restriction: Inability to concentrate urine in DI