Electrolyte Disorders

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ElectrolyteDisorders

Patho-physiology

  • A change in serum electrolyte concentrations can be either due to a change in input, output or trans-compartmental shift
  • Changes in input are affected by enteral or parenteral intake (including TPN)
  • Changes in output is controlled by the kidneys but significant losses can occur via the GIT or skin.

Slide1

Renal excretion or transcompartmental shifts are the main homeostatic controls in response to changes in serum electrolyte concentration.  This is assisted by the signalling effect of different hormones.

Sodium concentration is also controlled by the regulation of thirst via osmoreceptors in the hypothalamus.

Electrolyte Major compartmental body store Hormone
Sodium Extra-cellular space ADH (but thirst mechanism is important in normal homeostasis)
Potassium Intra-cellular space Aldosterone
Calcium, Magnesium, Phosphate Bone PTH

Since sodium is predominantly an extra-cellular electrolyte, its concentration is very sensitive to body water content.   Therefore in the above schematic, the intake, loss and movement of water (in addition to sodium) has a significant impact on sodium concentration.

Therefore, the patho-physiology of electrolyte disturbances can be due to:

The overwhelming effects of

  1. Changes in input
  2. Changes in output

and/or Disorders in homeostatic controls

  1. Alterations in renal function
  2. Disorders of endocrine function

Clinico-pathological Correlation

Disorders of electrolytes have differing effects on excitable tissue.  Depending on magnitude and rate of change, symptoms can be mild and non-specific to severe and life-threatening.  Find below the serious manifestations.  Muscular weakness can be significant enough to impair respiration.  Effects on cardiac tissue can range from changes in ECG to clinically significant arrhythmias.

Slide2

As a major contributor to extracellular osmolality, serum sodium has a significant effect on cellular volume.  This has implications in closed compartments such as the brain.

Slide3

The General clinical approach 

  • Is it a clinical emergency? CNS, CVS, Resp or Neuro-musc effects (or mild, moderate abnormality)
  • Review volume status (dehydrated, hypovolaemic, oedematous)
  • Review GIT intake and output (oral intake, drug composition, vomiting, diarrhea)
  • Review Parenteral fluids (IVT, TPN)
  • Review Skin losses (sweating/burns +++)
  • Review Medication list
  • Check Renal function and urine output
  • Compare with recent results for rate of change
  • Consider renal tubular or endocrine dysfunction – perform urine electrolytes (see below)
  • Consider specific endocrine tests if cause not obvious
  • If asymptomatic/mild symptoms – address cause and monitor in an outpatient setting
  • If moderate symptoms – as above in an inpatient setting
  • if severe symptoms – seek specialist opinion and rapidly correct life-threatening abnormalities, address cause, admit to ICU

 

With multiple abnormalities – evaluate each abnormality individually and attempt to find a unifying explanation

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