Hypokalaemia
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Hypokalaemia is defined as a serum potassium concentration < 3.5 mmol/L. It is one of the most common electrolyte abnormalities encountered in clinical practice.
Classification:
- Mild: 3.0 – 3.4 mmol/L.
- Moderate: 2.5 – 2.9 mmol/L.
- Severe: < 2.5 mmol/L.
Pathophysiological Importance
Potassium is the major intracellular cation. It determines the Resting Membrane Potential. Hypokalaemia causes hyperpolarisation of cells, making them less excitable (muscle weakness) but paradoxically increasing cardiac foci excitability (arrhythmias).
Clinical Scenario: The Weak Hiker
A 22-year-old female presents with profound generalized weakness after a weekend of hiking. She is unable to stand. History reveals she has been having palpitations and 'anxiety attacks' for months. BP is 160/95.
Key Teaching Points
- Profound weakness + Hypertension + Hypokalaemia suggests **Conn's Syndrome** (Primary Hyperaldosteronism) or **Thyrotoxic Periodic Paralysis**.
- Check Renin:Aldosterone Ratio.
- The weakness is due to hyperpolarisation of skeletal muscle membranes.
- Emergency replacement is needed, but check Magnesium too!
- Prevalence: Found in ~20% of hospitalized patients.
- Risk Groups: Patients on diuretics (thiazides/loop), eating disorders, alcoholics.
Mechanism 1: Redistribution (Shift into cells)
- Insulin: Drives K+ into cells (used therapeutically in hyperkalaemia).
- Beta-agonists: Salbutamol, Adrenaline (stress response).
- Alkalosis: H+ exits cells to buffer blood; K+ enters to maintain electroneutrality.
- Refeeding Syndrome: Anabolic surge drives K+, Mg, PO4 into cells.
- Familial Hypokalaemic Periodic Paralysis.
Mechanism 2: Renal Loss (Urine K > 20 mmol/L)
- Diuretics: Thiazides (block Na/Cl -> more Na to distal tubule -> exchanged for K). Loop diuretics.
- Hyperaldosteronism: Conn's syndrome, Renal Artery Stenosis. (Aldosterone sucks Na in, spits K out).
- Cushing's Syndrome: Cortisol has mineralocorticoid activity.
- Magnesium Deficiency: Mg keeps the ROMK channel closed. Low Mg opens it, causing K leak.
- Renal Tubular Acidosis (Type 1 & 2).
- Bartter / Gitelman Syndromes: Genetic tubulopathies mimicking diuretics.
Mechanism 3: Gastrointestinal Loss (Urine K < 20 mmol/L)
- Vomiting: Loss of H+ causes alkalosis -> Renal K loss. (Direct K loss in vomit is small).
- Diarrhoea: Direct loss of K+ (stool K is high).
- Laxative abuse.
- Villous Adenoma: Mucus-secreting tumour (McKittrick-Wheelock syndrome).
Musculoskeletal
Cardiovascular
Gastrointestinal
Renal
- Vitals: Arrhythmia? Hypertension (Conn's/Cushing's)?
- Neurology: Test power (proximal weakness). Reflexes may be reduced.
- Hydration status.
First Line
- U&Es: Confirm level. Check Creatinine.
- Magnesium: Vital. If Mg is low, K cannot be corrected.
- Blood Gas:
- Alkalosis: Suggests Vomiting, Diuretics, Conn's.
- Acidosis: Suggests Diarrhoea or RTA.
- ECG: Look for U waves, prolonged QT.
Second Line (Finding the cause)
- Urine Potassium: (Spot or 24h).
- Low (<20): GI loss.
- High (>20): Renal loss.
- Renin / Aldosterone: If hypertensive.
- Cortisol: If cushingoid.
Goal: Replace potassium safely. Oral route is safer and preferred unless severe or NBM.
1. Mild/Moderate (2.5 – 3.4 mmol/L)
- Oral Replacement:
- Sando-K: Effervescent tablets. Contains KCl. (12 mmol K+ per tablet). Typically 2 tabs TDS.
- Slow-K: Modified release.
- Dietary: Bananas, oranges, spinach, tomatoes (slow effect).
- Review diuretics (can they be stopped? or switch to K-sparing like Spironolactone/Amiloride).
2. Severe (< 2.5 mmol/L) or Symptomatic
- IV Potassium Chloride:
- Alert: Potassium is a lethal drug if given rapid bolus (cardiac arrest).
- Peripheral Line: Max concentration 40 mmol/L. Max rate 10 mmol/hour. (Painful/Phlebitis).
- Central Line: Can give stronger concentrations (e.g. 20-40 mmol in 50ml or 100ml) at max 20-40 mmol/hour with Cardiac Monitoring.
- Magnesium: Give IV Magnesium Sulphate if Mg low.
3. Chronic Management
- K-sparing diuretics (Amiloride, Spironolactone).
- Correct underlying cause (e.g., Conn's adenoma removal).
Disease-Related
- Cardiac Arrest (VF/VT).
- Respiratory Failure (muscle weakness).
- Paralytic Ileus.
Treatment-Related (Hyperkalaemia)
- Overshoot is common, especially if renal function is impaired.
- Rebound hyperkalaemia in redistribution (e.g. DKA treatment) - once acidosis/insulin is fixed, K moves back out.
- Generally excellent if treated.
- Sudden cardiac death is the main mortality risk.
- Resuscitation Council UK: Guidelines on peri-arrest arrhythmias (electrolytes).
- NICE Guideline CG174 (IV Fluids): Guidance on potassium supplementation in maintenance fluids.
What is Potassium? Potassium is a salt (mineral) that is vital for the electrical signals in your heart and nerves.
Why is mine low? Common causes are:
- Fluid loss: Severe vomiting or diarrhoea.
- Water tablets (Diuretics): These make kidneys flush out potassium.
- Low intake: Rarely a cause unless you are starving.
What are the symptoms? You might feel weak, tired, or have muscle cramps. If it gets very low, it can cause the heart to beat irregularly (palpitations).
How do we fix it?
- Mild: We give you supplements (fizzy tablets) and ask you to eat potassium-rich foods (bananas, potatoes).
- Severe: We give a drip into your vein. We have to do this slowly because giving it too fast is dangerous for the heart.
- Unwin RJ, et al. Hypokalemia: Diagnosis and Treatment. J Am Soc Nephrol. 2011;24:14-25.
- NICE. Intravenous fluid therapy in adults in hospital [CG174]. 2013 (Updated 2017).
- Kjeldsen K. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 2010;15(4):e96–e99.