altered sodium and water homeostasis hypernatremia

• Normal serum sodium is 135-145 mmol/l
• Revision

  Total body water: Men - 60% water (42 litres), Women - 55% water (38 litres)
• Hyponatraemia

  • Low serum sodium <135 mmol/l
  • Commonest electrolyte abnormality seen in 20-30% of hospital admissions
  • Can be fatal
  • Usually caused by an excess of water and is dilutional
• Water transfer between compartments

  1. Controlled through ion exchange

  2. Passively through hydrostatic and osmotic pressure
• volumes in Compartments

  • Intracellular 30 litres
  • Interstitial 9 litres
  • Vascular 3 litres
• Fluid IV solution

  • 0.9% saline (hypertonic)
  • 4% dextrose, 0.18% saline (hypotonic)
• Volume status

  • Normal total body water is 55-60% (euvolaemic/normovolaemic)
  • Volume depletion is hypovolaemic
  • Volume overload is hypervolaemic
• Clinical signs of hypovolaemia

  • Postural hypotension, supine hypotension
  • Tachycardia
  • Absence of jugular venous pulse at 45°
  • Reduced skin turgor/dry mucosa
  • Oliguria
  • Organ failure
• Clinical signs of hypervolaemia

  • Hypertension
  • Tachycardia
  • Raised jugular venous pressure at 45°
  • Gallop rhythm (3rd heart sound)
  • Peripheral and pulmonary oedema
  • “Third space gains” (peritoneal space, joint space…)
  • Organ failure
• Causes of hypovolaemic hyponatraemia

  1. Diseases - Haemorrhage, vomiting, diarrhoea, burns, diuretic state, sequestration, miscellaneous renal disease, heat exposure, Addison’s disease

  2. Iatrogenic - Diuretics, stoma/fistula, gastric aspiration
• Common causes of euvolaemic hyponatraemia include:

  • Hypotonic IV fluids
  • hypothyroidism
  • SIADH
• 3 classical causes of hypervolaemic hyponatraemia:

  • Heart failure
  • liver failure
  • nephrotic syndrome
• Heart failure causes reduced cardiac output, which leads to:

  1. reduced effective circulation volume

  2. reduced organ perfusion

  3. RAAS and ADH stimulation
• SIADH is the excessive secretion of ADH and excessive/inappropriate water resorption, leading to sodium dilution and euvolaemic hyponatraemia
• Central pontine myelinolysis

  1. Devastating/fatal condition associated with rapid correction of hyponatraemia

  2. Related to water fluxes into and out of the brain

  3. Commoner in alcoholism and malnutrition
• Causes of ectopic ADH secretion

  • Malignancy: small cell lung cancer, pancreas, bladder, prostate, etc.
  • non-malignant: TB, pneumonia
• SIADH can occur due to drugs e.g., thiazide diuretics, carbamazepine, amitriptyline
• Hyponatraemia

  1. Not suppressed by reduced tonicity

  2. Water reabsorption is excessive (and inappropriate)

  3. Sodium is diluted

  4. Hyponatraemia results
• Causes of SIADH

  • Pituitary hypersecretion/direct effect
  • Ectopic secretion
  • Drugs
• Pituitary hypersecretion causes of SIADH

  • Neurological: meningitis, encephalitis, head injury, stroke etc.
• Diabetes Insipidus due to ADH is insufficient/inactive causes

  • Diuresis continues unabated
  • Free water loss occurs
  • Sodium is concentrated
  • Hypernatremia occurs
  • No/failed feedback mechanism
• Treatment of hypernatremia

  1. Can be very difficult

  2. Hydration tends to simply cause polyuria

  3. Synthetic ADH (DDAVP) works for cranial DI (supra normal dose may work for nephrogenic DI)

  4. NSAID's might help
• Causes of cranial/central DI

  • Non/reduced synthesis of ADH: pituitary tumour, head injury, meningitis, genetic, idiopathic
• Causes of nephrogenic DI

  • Reduced tubular response to ADH due to drugs (lithium), or could be inherited
• hypovolaemic hyponatraemia occurs due to excessive sodium losses and the controlled water losses are insufficient to concentrate sodium back up
• the type of hyponatraemia depends on the volume of water lost and concentration of sodium therein
• water is lost through the kidneys, gut, lungs and skin
• clinical signs of hyponatraemia can be generated when there is a difference in the relative size of fluid compartments from normal
• Hyponatraemia can be associated with three volume status

  • euvolaemic
  • hypovolaemic
  • hypervolaemic
• euvolaemic hyponatraemia is dilutional, meaning water is being evenly distributed across all compartments diluting the salt
• In hypervolaemic hyponatraemia the water gains exceed the sodium gains
• In heart failure the physiological correcting mechanisms kick in, because hypovolaemia exceeds tonicity
• The correcting mechanisms for heart failure result in :

  • sodium retention (aldosterone)
  • water retention (aldosterone and ADH)
  • hyponatraemia results from dilution
  • fluid overload worsens left ventricular functioning
  • hypovolaemia continues to win over hyponatraemia
  • the vicious cycle worsens
  • this is maladaptive responce (happening for the right reasons but is not good)
• SIADH is not suppressed by the reduced tonicity
• treatment of hypovolaemic hyponatraemia includes:

  • restoration of volume state (give blood if necessary, crystalloid, 0.9% saline)
  • cessation of diuretics
  • steroids for Addison’s disease
• treatment for hypervolaemic hyponatraemia include:

  • diuretics (usually loop diuretics, furosemide…)
  • fluid restriction
  • treatment of underlying cause (e.g., heart attack)
• treatment of euvolaemic hyponatraemia include:

  • treat the underlying cause (stop hypotonic IV fluids, thyroxine replacement)
  • fluid restriction (down to 500ml/day)
  • rarely, demeclocycline can be given
• Recommended rate of correcting hyponatraemia to avoid central pontine myelinolysis:

  • 4-10 mmol/l/day if asymptomatic
  • 8-12 mmol/l/day if symptomatic
  • with careful monitoring/observation
• Causes of hypernatremia

  • water loss (fever, hyperventilation,DI)
  • reduced water intake (iatrogenic, psychological in elderly, infants, apathetic, stroke, coma, confusion ect.)
  • high sodium intake (iatrogenic: concentrated foods, emetics-high sodium drugs)
• investigation of hypernatremia

  • history
  • examination
  • non-specific tests
  • take note of: urinary sodium concentration and serum and urine osmolality