Hyponatremia gulidelines


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Hyponatremia gulidelines

  1. 1. HYPONATREMIA - GUIDELINES Dr. Ratan Jha (consultant nephrologist) Dr. Mohd Viquasuddin (dnb resident)
  2. 2. introduction • Diagnosis and management of hyponatremia is challenging • inappropriate treatment can be harmful. • is often missed, misdiagnosed or poorly managed • can cause substantial morbidity, mortality • No single treatment protocol so often mismanaged. • Rapid correction is frequently associated with increased morbidity and mortality. • Recently available vasopressin-receptor antagonists (Vaptans) are specific and more effective method to treat hyponatremia.
  3. 3. Prevalence & epidemiology • Most common electrolyte disorder • Affects 15 -30 % of hospitalized patients • Affects 7 % of ambulatory patients • Causes 1 million hospitalizations/ year • Higher incidence in cirrhosis and heart failure • Higher incidence in geriatric populations • Hospital acquired hyponatremia common
  4. 4. Risk factors • Primarily due to elevated Vasopressin (ADH) • ADH released due to elevated plasma osmolality and hypovolemia / hypotension • ADH cause excess water reabsorption • Etiology based on classification • 1. hypovolemic • 2. euvolemic • 3. hypervolemic
  5. 5. Hypovolemic hyponatremia • Decreased Total body water and Na , greater decrease in Na • Gastro-intestinal losses : diarrhea, vomiting • 3rd space losses : burns, pancreatitis, peritonitis, rhabdomyolysis • Renal losses : diuretics, mineralocorticoid deficiency. • osmotic diuresis : glucose, mannitol, urea • Salt losing nephropathies : interstitial nephritis, medullay cystic kidney disease, partial urinary tract obstruction, polycystic kidney disease.
  6. 6. Euvolemic hyponatremia • Increased Total body water with normal total body Na • Drugs : carbamazepine, clofibrate, opioids, cyclophosphamide, NSAID’s, oxytocin. • Disorders : addison’s disease, hypothyroidism,SIADH • Increased intake of fluids : primary polydipsia • Non-osmotic release of ADH : nausea, pain, emotional stress
  7. 7. Hypervolemic hyponatremia • Increased Total body Na with a greater increase in Total body water • Extra-renal disorders : cirrhosis, heart failure • Renal disorders : acute kidney injury, chronic kidney disease, nephrotic syndrome
  8. 8. Why neurological symptoms ? • Symptoms are primarily neurological • Reduction in ECF not responsible • increase in volume of ICF responsible • particularly in the volume of brain cells • Hyponatremia leads to hypoosmolality of ECF, so water moves into cells (ICF). • Swelling of brain cells in enclosed space with fixed volume of rigid skull leads to increased intracranial pressure resulting in reduction of cerebral blood flow causing hypoxic brain damage. • if left untreated, can lead to herniation of the brain stem into the foramen magnum
  9. 9. Chronic hyponatremia • hyponatremia lasting more than 48 hours or with an unknown duration • neurological symptoms are less • in gradually developing hyponatremia, brain cells compensate by cellular exit of solutes that promote water loss and lessen brain swelling • not necessarily “asymptomatic” • can cause osteoporosis due to increased bone resorption
  10. 10. Approach to Hyponatremia • requires a systemic and sequential approach • Step 1. History and examination. • Step 2. Assessment of serum osmolality to confirm diagnosis of true hypotonic hyponatremia and rule out misleading results (hypertonic hyponatremia and pseudo-hyponatremia). • Step 3. Approach to true hypotonic hyponatremia by assessment of volume status and urine sodium concentration. • Step 4. Laboratory tests to assess underlying causes of hyponatremia.
  11. 11. Step 1 • detailed history and examination needed • Vomiting, diarrhea with hypotonic fluid ingestion, recent surgery, improper IV fluid administration • Associated diseases (i.e. psychiatric illness, CHF, cirrhosis, renal failure) • Recent head injury, intracranial surgery, subarachnoid hemorrhage, stroke, brain tumor, meningitis or brain abscess can cause SIADH. • Cough, shortness of breath, or pleuritic chest pain should prompt consideration of respiratory causes of SIADH • Use of medications • Skin turgor, mucous membrane appearance and postural hypotension • Detection of ascites, peripheral edema, pulmonary rales and S 3 • Measuring blood pressure, JVP, CVP and PCWP
  12. 12. Step 2 • Measure plasma osmolality with osmometer • osmometer provides actual (correct) osmolality • Normal plasma osmolality is 280 - 295 mOsm/kg • low plasma osmolality (POsm < 280 mOsm/kg) confirms diagnosis • normal plasma osmolality (POsm 280–295 mOsm/kg) suggests isotonic pseudo hyponatremia : check for hyperproteinemia, hyperlipidemia • high plasma osmolality (POsm > 295 mOsm/kg) suggests hypertonic hyponatremia : check for hyperglycemia, mannitol therapy and contrast dyes.
  13. 13. Step 3 • classified into hypovolemic, hypervolemic and euvolemic • treatment protocols are absolutely different in all three categories • Volume status should be measured • Urinary sodium should be measured
  14. 14. Diagnostic criteria for SIADH • Essential diagnostic criteria for SIADH • • Decreased measured serum osmolality (<275 mOsm/kg H2O) • • Clinical euvolaemia. Exclude hypovolemia and hypervolemia • • Urinary osmolality >100 mOsm/kg H2O during hypo- osmolality • • Urinary [Na+] >40 mmol/L with normal dietary sodium intake • • Normal thyroid and adrenal function. Exclude renal failure and use of diuretic agents within the week prior to evaluation • • No hypokalemia, no acid base disorders
  15. 15. Diagnostic criteria for SIADH • Supporting diagnostic criteria for SIADH • • Serum uric acid <4 mg/dL • • Blood urea nitrogen <10 mg/dL • • Fractional sodium excretion >1%; fractional urea excretion >55%c • • Failure to improve or worsening of hyponatremia after 0.9% saline infusion • • Improvement of hyponatremia with fluid restriction
  16. 16. Step 4 • Check urine Osmolality with osmometer. • distinguishes between hyponatremia with normal water excretion and hyponatremia due to impaired water excretion • Urine osmolality below 100 mOsm/kg indicates that antidiuretic hormone (ADH) secretion is completely and appropriately suppressed • urine osmolality exceeding 100 mOsm/kg indicates impaired water excretion which reflects impaired renal diluting mechanism (SIADH)
  17. 17. Step 4 • urine osmolality and urine Na helps in differential diagnosis of the etiology of hyponatremia • Urine Na (>40) and urine osmolarity(>150) will be high in SIADH, adrenal insufficiency & cerebral salt wasting syndrome • Low Urine Na (<30) and high urine osmolarity (>150) indicate hypovolemia • Low values of serum uric acid and blood urea favour euvolemic hyponatremia • high values of serum uric acid and blood urea favour hypovolemic hyponatremia.
  18. 18. Step 4 • Specific etiologic tests • Blood sugar: To rule out hyperglycemia • Serum creatinine: To rule out renal failure • Serum protein: High in multiple myeloma and low in cirrhosis of liver • Serum triglycerides: To rule out pseudohyponatremia • Serum potassium: High in Addison's disease and low in person with diuretics therapy, diarrhea and vomiting. • Thyroid function tests: To rule out hypothyroidism • Adrenal functions: ACTH & ACTH stimulation tests to rule out Addison's disease. • Acid-base balance: Metabolic alkalosis occurs in diuretic use or vomiting. Metabolic acidosis occurs in diarrhea or laxative abuse and primary adrenal insufficiency. • Head CT scan and Chest X-ray to rule out cerebral salt wasting syndromes
  19. 19. management • manage underlying cause of hyponatremia • Acute symptomatic hyponatremia may be corrected relatively rapidly • serum sodium should not be raised more than 8-10 mEq in first 24 hours • Chronic asymptomatic hyponatremia should be corrected slowly • Rate of serum sodium correction may be 6-8 mEq in 24 hours.
  20. 20. Serum sodium <120 mEq/L – 1. Water restriction to raise s. Sodium level – 2. 3% saline (hypertonic saline) or – 3. Diuretic + oral salt – Correction with hypertonic saline is more predictable (accurate) – careful with management of hyponatremia and may require hospitalization and regular monitroing. – Once serum sodium reaches 120 mEq/L then vaptan may be initiated if underlying cause cannot be corrected
  21. 21. Serum sodium 120-135 mEq/L – Asymptomatic – water restriction initially, if not controlled – use vaptans – Symptomatic – water restriction initially along with vaptan – (as water restriction will not work for long term, compliance issue with water restriction)
  22. 22. Acute symptomatic --Fluid restriction – 3% sodium chloride (hypertonic saline) • If rate of correction is rapid use 5% dextrose • Acute asymptomatic (Less likely) • Fluid restriction
  23. 23. Chronic asymptomatic – Fluid restriction – Improve protein intake in elderly -- Data suggests chronic asymptomatic hyponatremia develop cognitive dysfunction, bone demineralization and likely to develop symptomatic hyponatremia chronic hyponatremia patients should be treated • – Severe hyponatremia should be treated • Fluid restriction • 3% saline (hypertonic saline) • If hyponatremia is persistent, vaptans may be started/added once serum sodium reaches >120 mEq/L with other interventions •
  24. 24. Use of vaptans in hyponatremia – Euvolemic and hypervolemic hyponatremia – Chronic symptomatic hyponatremia where underlying cause can not be corrected and long term treatment is required – Can be started once serum sodium >120 mEq/L – For initiating vaptan patient should be admitted for 3-4 days, i.e. Vaptan therapy should be initiated in hospital – Monitoring of serum sodium after discharge, initially at 3-4 days, then every 15 days for a month and then monthly monitoring till therapy is continued – Liver function should be monitored intially, at 15 days for 2-3 months and then every 3 monthly – Ensure proper intake (good quantity) of water (fluid) while patients are on vaptan – Vaptan (tolvaptan) is contraindicated if patient can not drink water/can not feel thirst – Vaptans produce good quanttiy of water loss
  25. 25. …. • thank you • The end