# Central Neurogenic Diabetes Insipidus > do not confuse with [[hyponatremia#Cerebral salt-wasting syndrome]], which is a state of hyponatraemia. > [!key points] > - Central neurogenic DI (CNDI) is characterised by an abnormal increase in urine output, an increase in fluid intake, and thirst due to decreased secretion of ADH, resulting in elimination of extracellular fluid. > - **Findings:** polyuria (dilute), low urine osmolality, elevated serum osmolality, and [[hypernatremia|hyper-na]] > - likely due to ↓ vasopressin > - **Treatment**: *DDAVP* (desmopressin) 1-2 mcg, IV fluids (sometimes 0.45% NaCl) and titrated to urine output ## Overview of CNDI - In *trauma patients*, CNDI usually is due to damage of the posterior part of the pituitary gland where ADH is stored and secreted.   - In patients with neurological conditions, CNDI is often associated with neurosurgery, tumors, ↑ ICP, brain death, and CNS infections such as meningitis or encephalitis. - CNDI occurs in up to 16% of all brain-injured patients and usually occurs 5 to 10 days after trauma. CNDI usually occurs in 3 phases: 1. First phase consists of polyuria due to the inhibition of ADH that lasts a few hours or up to several days. 2. Second phase (5–6 days) is characterised by near-normal urinary output because of the release of stored ADH. 3. Third phase is transient or permanent excessive urinary output due to depletion of stored ADH or loss of functioning of the cells that produce ADH.   If the lack of ADH is uncorrected in patients with TBI, ==CNDI results in severe dehydration and further worsening of electrolyte balance.== ## Signs and Symptoms Signs and symptoms of CNDI include: - *polyuria* (large volumes of dilute urine, 250 mL/h) - polydipsia (extreme thirst in patients who are awake and alert) - *hypovolemia* - [[hypernatremia]] Urinary specific gravity is less than 1.005 (normal, 1.005–1.030), urine osmolality is less than 200 mOsm/kg, serum osmolality is elevated (>295 mOsm/kg), the serum level of sodium is elevated (>145 mEq/L), and the urinary level of sodium is markedly decreased. Marked urinary losses of other electrolytes (potassium and magnesium) may occur simultaneously. Patients may also have weight loss of approximately 3% to 5% of body weight. Hypovolemia associated with CNDI in patients with TBI must be corrected. Other assessment findings may include indications of dehydration: confusion, irritability, poor skin turgor, dry mucous membranes, hypotension, and/or tachycardia. ## Diagnosis Diagnosis of CNDI in patients with TBI is based on clinical signs and symptoms and laboratory findings, specifically ==**polyuria**, low urinary specific gravity, low urine osmolality, **hypernatremia**, and elevated serum osmolality==. ## Treatment The goal in CNDI is to correct the ADH deficiency and restore fluid balance by promoting sodium and water reabsorption. - In the acute phase of CNDI, exogenous ADH is provided, and **fluid equivalent to the amount of urine output is given either orally, if the patient can tolerate adequate oral intake, or intravenously**. Patients with intact thirst centers who are able to take fluids orally are encouraged to drink as much as possible when thirsty to keep up with fluid losses. - In patients with TBI, complications from impaired level of consciousness, sensory and motor deficits, and dysphagia often preclude oral intake, and **intravenous solutions are required to meet the fluid demands**. Intravenous *hypotonic solutions* most often used to replace lost body fluids include 0.45% saline titrated hourly to *replace urine output*. ==Exogenous ADH==, either **desmopressin** (*DDAVP*), vasopressin, or lypressin, may be administered. *Desmopressin* can be administered nasally 5 to 2 μg/d in divided doses or parenterally 5 to 40 μg/d in daily divided doses. *Vasopressin* (aqueous Pitressin) can be administered intravenously 0.5 to 2 U every 3 hours for patients who have urine output of more than 300 mL/h for 2 consecutive hours.  A vasopressin infusion may become necessary, which can be started at 0.2 U/min and titrated to a maximum dose of 0.9 U/min.  Lypressin dosage is 5 to 20 U 3 to 7 times per day nasally # Nephrogenic diabetes insipidus aka "Argine vasopressing resistance" unlike neurogenic DI due to ↓ vasopressin, nephrogenic is due to resistance to vasopressin/ADH → decrease in ability of kidney to concentrate the urine by removing water **major ED causes** - [[​Lithium Toxicity]] - [[hypercalcaemia]] others: - polcystic kidney disease - amyloidosis - hypokalaemia - *post obstructive diuresis* - sickle cell