Electrolyte imblance (shortly from Dr Ifrah) Flashcards Preview

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Causes of hyponatraemia

Hyponatraemia is overall due to water excess or sodium depletion: 

  • fluid loss 
  • renal disease
  • head trauma
  • hyperglycaemia 
  • heart failure 
  • drugs: IV dextrose, thiazides, loop diuretics


Presentation of hyponatraemia

  • anorexia
  • headache 
  • irritability
  • low GCS
  • seizures
  • increased risk of falls



  • serum osmolarity 
  • urine osmolarity 
  • urine Na


Management of hyponatraemia

- chronic

- acute

  • correct underlying cause 


Chronic /asymptomatic:

  • fluid restriction
  • demeclocycline → used when SIADH is a cause (MoA: increased urine volume, decreased urine osmolality, and reverted hyponatremia)


Acute /symptomatic: 

  • replace Na → max rise 4-6 mmol/l in 24 hrs
  • in emergency: hypertonic saline, furosemide



A possible complication of too quick treatment of hyponatraemia and how to avoid it


Osmotic demyelination syndrome (central pontine myelinolysis):

  • can occur due to over-correction of severe hyponatremia


  • To avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period


  • Symptoms usually occur after 2 days and are usually irreversible. Dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma. Patients are awake but are unable to move or verbally communicate, also called 'Locked-in syndrome’


Management of hypercalcaemia

  • fluids → rehydration with normal saline(3-4 litres/day) 
  •  bisphosphonates →take 2-3 days to work with the maximal effect being seen at 7 days


  • calcitonin - quicker effect than bisphosphonates


  • steroids in sarcoidosis


  • Loop diuretics (furosemide) → sometimes used in patients who cannot tolerate aggressive fluid rehydration

*diuretics should be used with caution as they may worsen electrolyte derangement and volume depletion



Features of hypercalcamia

  • 'bones, stones, groans and psychic moans'
  • corneal calcification
  • shortened QT interval on ECG
  • hypertension


Causes of hypercalcaemia

Two conditions account for 90% of cases of hypercalcaemia:

  • 1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients


  • 2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including; bone metastasesmyeloma, PTHrP from squamous cell lung cancer

Other causes include

  • sarcoidosis
  • vitamin D intoxication
  • acromegaly
  • thyrotoxicosis
  • Milk-alkali syndrome
  • drugs: thiazides, calcium containing antacids
  • dehydration
  • Addison's disease
  • Paget's disease of the bone


Causes of hypernatraemia

  • dehydration
  • osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
  • diabetes insipidus
  • excess IV saline


Features/presentation of hypernatraemia 

  • thirst 
  • lethargy
  • weakness
  • confusion 
  • come
  • seizures


Investigations in hypernatraemia 

  • serum and urine osmolarity 
  • urine Na


Management of hypernatraemia

  • encourage PO water
  • glucose 5% 


*avoid hypertonic solutions


Hypernatraemia should be corrected with great caution. Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death

  • rate of no greater than 0.5 mmol/hour correction is appropriate


Causes of hypokalaemia

Hypokalaemia with alkalosis

  • vomiting
  • thiazide and loop diuretics
  • Cushing's syndrome
  • Conn's syndrome (primary hyperaldosteronism)

Hypokalaemia with acidosis

  • diarrhoea
  • renal tubular acidosis
  • acetazolamide
  • partially treated diabetic ketoacidosis


  • Magnesium deficiency may also cause hypokalaemia →normalizing the potassium level may be difficult until the magnesium deficiency has been corrected


Features of hypokalaemia


  • muscle weakness, hypotonia
  • hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics

ECG features

  • U waves
  • small or absent T waves
  • prolonged PR interval
  • ST depression


ECG features of hypokalaemia 

ECG features

  • U waves
  • small or absent T waves
  • prolonged PR interval
  • ST depression


Management of hypokalemia 

  • replace K+ 
  • Mx depends on severity and ECG findings


Causes of hyperkalaemia

Causes of hyperkalaemia

  • acute kidney injury
  • drugs: potassium sparing diuretics, ACE inhibitorsangiotensin 2 receptor blockersspironolactoneciclosporinheparin
  • metabolic acidosis
  • Addison's disease
  • rhabdomyolysis
  • massive blood transfusion


ECG features associated with hyperkalaemia

ECG findings

  • Peaked or 'tall-tented' T waves (occurs first)
  • Loss of P waves
  • Broad QRS complexes
  • Sinusoidal wave pattern
  • Ventricular fibrillation


Features/symptoms of hyperkalaemia

  • weakness
  • paraesthesia
  • paralysis 
  • depressed tendon reflexes


Management of hyperkalaemia 

Stabilisation of the cardiac membrane

  • intravenous calcium gluconate

(does NOT lower serum potassium levels)

Short-term shift in potassium from extracellular to intracellular fluid compartment

  • combined insulin/dextrose infusion
  • nebulised salbutamol

Removal of potassium from the body

  • calcium resonium (orally or enema)
    • enemas are more effective than oral as potassium is secreted by the rectum
  • loop diuretics
  • dialysis
    • haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia


Definition of hypercalcaemia and hypocalcaemia 

Hypercalcaemia →      >2.6 mmol/L


Hypocalcaemia →    <2.1 mmol/L



Causes of hypocalcaemia


  • vitamin D deficiency (osteomalacia)
  • chronic kidney disease
  • hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
  • pseudohypoparathyroidism (target cells insensitive to PTH)
  • rhabdomyolysis (initial stages)
  • magnesium deficiency (due to end organ PTH resistance)
  • massive blood transfusion

Acute pancreatitis may also cause hypocalcaemia. Contamination of blood samples with EDTA may also give falsely low calcium levels


Management of hypocalcaemia 

  • acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
  • intravenous calcium chloride is more likely to cause local irritation
  • ECG monitoring is recommended
  • further management depends on the underlying cause


Features/ symptoms/signs of hypocalcaemia 

As extracellular calcium concentrations are important for muscle and nerve function many of the features seen in hypocalcaemia seen a result of neuromuscular excitability


  • tetany: muscle twitching, cramping and spasm
  • perioral paraesthesia
  • if chronic: depression, cataracts
  • ECG: prolonged QT interval

Trousseau's sign

  • carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • wrist flexion and fingers drawn together
  • seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people

Chvostek's sign

  • tapping over parotid causes facial muscles to twitch
  • seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people


ECG features seen in hypocalcaemia

  • prolonged QT and PR intervals
  • T wave inversion 
  • heart block 


Definition of: 



  • Hypermagnesemia   Mg > 1.1 mmol/L 


  • Hypomagnesemia Mg <0.6 mmol/L 


Causes of hypermagnesemia 

  • renal failure 
  • iatrogenic


Features of hypermagnesemia 

  • confusion
  • weakness 
  • respiratory depression 
  • AV block
  • cardiac arrest


ECG features of hypermagnesemia

  • prolonged QT and PR intervals 
  • T wave peaking 


Management of hypermagnesemia 

  • If Mg >1.75 mmol/L → CaCl IV bolus repeated if needed


  • saline diuresis with furosemide


  • haemodialysis