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SIADH is caused by inappropriate secretion of ADH leading to water retention and dilutional hyponatremia. It is diagnosed based on low serum sodium, low serum osmolality, high urine osmolality, and elevated urine sodium. Treatment involves fluid restriction and sodium supplementation. Cerebral salt wasting and diabetes insipidus can cause similar hyponatremia but are distinguished based on clinical features and laboratory findings.
SIADH is caused by inappropriate secretion of ADH leading to water retention and dilutional hyponatremia. It is diagnosed based on low serum sodium, low serum osmolality, high urine osmolality, and elevated urine sodium. Treatment involves fluid restriction and sodium supplementation. Cerebral salt wasting and diabetes insipidus can cause similar hyponatremia but are distinguished based on clinical features and laboratory findings.
SIADH is caused by inappropriate secretion of ADH leading to water retention and dilutional hyponatremia. It is diagnosed based on low serum sodium, low serum osmolality, high urine osmolality, and elevated urine sodium. Treatment involves fluid restriction and sodium supplementation. Cerebral salt wasting and diabetes insipidus can cause similar hyponatremia but are distinguished based on clinical features and laboratory findings.
Water excretion is impaired Suppression of ADH is impaired Functions of ADH Increases permeability of water in the cells of the distal tubules by upregulating Aquaporin-2 channels (V2 receptors) Increases the permeability of collecting ducts to urea Increases SVR via IP3/Ca++ 2nd messengers on endothelium CNS effects like memory formation and circadian rhythm SIADH - causes Intracranial infection, stroke, hemorrhage, tumor, very common in SAH population (69%) Intrathoracic malignancy, abscess, PNA, effusion, PTX, chest wall deformity Drugs vasopressin, DDAVP, oxytocin, analgesics, antidepressants, amiodarone, antipsychotics, sulfonylureas, carbamazepine, cyclophosphamide Extracranial tumors small-cell lung CA, pancreatic CA HIV/AIDS Hereditary gain-of-function V2 receptor mutation Miscellaneous Guillan-Barre, nausea, stress, pain, acute psychosis Major surgery **** Idiopathic SIADH Hypothalamus receives feedback from:
decrease in blood volume will stimulate ADH secretion from posterior pituitary. SIADH - pathophysiology ADH-induced water retention Dilutional hyponatremia Volume expansion -> secondary natriuresis Sodium and water loss Potassium loss Result: Euvolemic hyponatremia Reduced serum osmolality Increased urine osmolality Increased urine sodium SIADH - diagnosis Laboratory Findings Na < 135 mEq/L Posm < 270 mOsm/kg Uosm > 300 mOsm/kg UNa > 25 mEq/L Low BUN Normal Cr Low uric acid Low albumin SIADH - treatment Treat the underlying cause, if known Fluid Restriction commonly 800-1000mL/d Correct Na+ deficit no more than 10mEq/L in 24 hours, 18mEq/L in 48 hours 0.9% NaCl 3% NaCl NaCl enteral tablets 2-3g TID Add a loop diuretic SIADH treatment Vasopressin receptor antagonists Promote aquaresis Tolvaptan, conivaptan Vaprisol (Conivaptan) Indicated in euvolemic or hypervolemic hyponatremia
Contraindicated in hypovolemic hyponatremia
V1a and V2 receptors
Causes aquaresis or excretion of free water
Demeclocycline or Lithium (diminished collecting
tubule response to ADH) Cerebral Salt Wasting Hyponatremia caused by impaired renal tubular function -> inability of kidneys to conserve salt Salt wasting leads to volume depletion Two theories: Impaired sympathetic neural input -> failure of aldosterone release -> no sodium resorption BNP release decreases sodium resorption, inhibits renin/aldosterone release, decreases autonomic outflow at level of brainstem Cerebral Salt Wasting Commonly occurs in subarachnoid hemorrhage population (7%) Carcinomatous, infectious meningitis Encephalitis Poliomyelitis CNS tumors CNS surgery usually within the first 10 days Cerebral Salt Wasting Diagnosis: Evidence of volume depletion Increased urine output Laboratory Findings Na < 135 mEq/L Low Posm Uosm > 300 mOsm/kg UNa > 40 mEq/L High BUN Increased Cr Low uric acid Increased albumin Cerebral Salt Wasting Treat with volume repletion 0.9% NaCl 3% NaCl is sometimes warranted Fludrocortisone Diabetes Insipidus The most common cause of hypernatremia in neurological population Deficient ADH Central DI occurs with hypothalamic-pituitary axis dysfunction or injury Nephrogenic DI diminished renal sensitivity to ADH Usually considered a euvolemic to hypovolemic state, depending on the patients thirst mechanism Diabetes Insipidus Diabetes Insipidus Typical Clinical picture: Polyuria Polydipsia Laboratory Findings Nocturia Na >145 mEq/L Posm > 285 mOsm/kg Uosm < 300 mOsm/kg UNa low Urine Spec. Grav. < 1.005 UOP > 3ml/kg/h Diabetes Insipidus Goal is to restore plasma volume and serum Na+ levels Patient with intact thirst mechanism Pitcher at bedside. Drink to thirst only! Severe forms Replace UOP 1:1 with 1/2NS DDAVP 5u SQ Q4-6h, commonly given orally/nasally
DDAVP will be ineffective if nephrogenic (HCTZ can be used)
Review SIADH CSW DI Serum Na+ < 135 mEq/L < 135 mEq/L > 145 mEq/L Urine Na+ > 25 mEq/L > 40 mEq/L < 25 mEq/L Serum Osm < 270 mOsm/kg < 270 mOsm/kg > 285 mOsm/kg Urine Osm > 300 mOsm/kg > 300 mOsm/kg < 300 mOsm/kg Urine O/P oliguria polyuria polyuria CVP normal/high low normal/low Plasma ADH high normal low Rx Fluid restrict, give Give volume, give Drink to thirst, Na+, vaprisol, Na+, DDAVP (central), demeclocycline fludrocortisone HCTZ (nephrogenic)