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Hypokalaemia

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  • Chapter 19: Clinical Biochemistry and Metabolic medicine Potassium Homeostasis Hypokalaemia
  • Hypokalaemia

Hypokalaemia

Hypokalaemia

on 09 Oct, 2023
  • Date09 Oct, 2023

Clinical features 

  • Mild ( K+ 3.0–3.5 mmol/L): asymptomatic.
  • Muscle: muscular weakness, tiredness. 
  • Heart:
    • ventricular ectopic beats, arrhythmias,
    • arrhythmogenic effects of digoxin may be potentiated. 
  • Gut: Paralytic ileus. 
  • Kidney: 
    • renal tubular damage (hypokalemic nephropathy)
    • acquired nephrogenic diabetes insipidus → resulting in polyuria and polydipsia.

 

SAQ. A 28 years old male came with repeated weakness of all four limbs. You reviewed his investigation profile for the last 1 year and found that there is persistent hypokalemia. How will you clinically evaluate and investigate this patient to reach the diagnosis? 

 

Recurrent and/or Persistent hypokalemia: D/D

  • Drug induced: Diuretics, Corticosteroids, beta agonist, laxative abuse, 
  • Conn syndrome
  • Cushing’s Syndrome
  • Renal artery stenosis
  • Renal tubular acidosis – eg Sjogren syndrome, Wilson disease etc
  • Persistent diarrhea, vomiting 
  • Intestinal fistula
  • Liddle’s syndrome 
  • Gietleman’s syndrome
  • Hypokalemic periodic  paralysis 

 

Clinical Evaluation

  • medications (e.g., laxatives, diuretics, antibiotics), 
  • diet and dietary habits (e.g., licorice)
  • symptoms that suggest a particular cause (e.g., periodic weakness, diarrhea).

 

History Examination Possible diagnosis
  • Early Onset HTN 
  • Difficult to control with drugs
  • High BP
  • hypertensive retinopathy
  • Conn’s syndrome
  • Early Onset HTN 
  • Difficult to control with drugs
  • High BP
  • Renal bruit
  • hypertensive retinopathy
  • Renal artery stenosis
  • Weight Gain
  • Acne, hirsutism 
  • Moon face 
  • Proximal Myopathy
  • hypertension
  • Cushing syndrome
  • Drug cause – corticosteroids
  • History related to CTD Eg: 
  • Dry mouth, dry eye
  • Dental caries, LN
  • Small joint arthritis
  • Sjogren syndrome
  • H/O jaundice, weakness, 
  • abdominal distension, 
  • family history
  • jaundice, hepatomegaly, splenomegaly
  • ascites, tremor-rigidity-bradykinesia
  • KF ring, 
  • Wilson disease (RTA)
  • Past/ treatment history:
  • Ureterosigmoidostomy
  • NG suction, diarrhea
  • Recovery from renal obstruction, ATN

 

Investigation

Initial:

  • electrolytes, BUN, creatinine,
  • serum osmolality,
  • Mg2+, Ca2+,
  • complete blood count, and
  • urinary pH, osmolality, creatinine, electrolytes
  • Urinary calcium
  • TSH, FT4

 

Investigation  Finding 
  • CBC
  • Leukocytosis → Cushing syndrome 
  • S electrolyte, Bicarbonate
  • Plasma renin activity (PRA)
  • Serum aldosterone
  • Aldosterone renin ratio (ARR)
Renin

  • low → mineralocorticoid excess
  • high → other causes of hypokalemia. 
  • ARR: > 50→ suggestive of primary hyperaldosteronism 
  • stop anti HTN medication (ACEI, ARB, spironolactone, beta blocker→ false negative result may occur) 
  • Urinary electrolytes

 

  • urine potassium→ high (>30 mmol/24 hrs) → renal loss
  • urine potassium→ low (< 20 mmol/24 hrs) → GIT loss
  • urine chloride → <30 mmol/L → vomiting 
  • urine chloride → >40 mmol/L → diuretic therapy; tubular disorder such as Bartter or Gitelman syndromes. 
  • ABG analysis 
  • acidosis → RTA, lower GIT loss of potassium 
  • alkalosis → all other causes 
  • S. calcium, S magnesium
  • Urinary calcium/Cr molar ratio
  • hypocalcemia → loop diuretics
  • hypomagnesemia → loop diuretics, thiazide, bartter, Gitelman
  • Urinary calcium:
    • high → loop, Bartter 
    • low → thiazide, Gitelman
  • ECG
  • Features of hypokalemia 
    • T wave- flat, inversion;
    • ST –  depression;
    • U wave
    • P wave – peak; PR –  prolonged
To identify the underlying cause
  • USG of abdomen with doppler
  • Renal angiogram
  • Renal artery stenosis 
  • Adrenal mass → adenoma, hyperplasia, carcinoma 
  • F/O CLD, Ascites, Splenomegaly→ Wilson disease 
  • Intestinal obstruction (paralytic ileus) → cause / effect
  • CT abdomen with adrenal protocol
  • Adrenal neoplasm 
  • CXR
  • Lung mass → ectopic ACTH
  • SGPT, S ceruloplasmin 
  • Wilson disease
  • Colonoscopy
  • Villous adenoma
  • Urine for drug analysis
  • Occult diuretic use

 

Patients with Liddle’s syndrome classically manifest severe hypertension with hypokalemia, unresponsive to spironolactone yet sensitive to amiloride.

 

Management 

The goals of therapy in hypokalemia are to prevent life-threatening and/or serious chronic consequences, to replace the associated K+ deficit, and to correct the underlying cause and/or mitigate future hypokalemia

  • Treatment of the cause, if possible. 
  • If the problem is redistribution of potassium into cells, reversal of the process.
    • correction of alkalosis, stop beta agonist etc
  • Potassium replacement: 
    • slow-release potassium chloride tablets
  • acute condition:
    1. IV potassium chloride. 
    2. The rate of administration depends on the severity of hypokalaemia; presence of cardiac or neuromuscular complications. 
    3. generally not exceed 10 mmol of potassium per hour. 
    4. with severe, life-threatening hypokalemia, infusion rates up to 20 mmol/hr with continuous cardiac monitoring. 
  • In presence of metabolic acidosis: 
    • alkaline salts of potassium (potassium bicarbonate) orally. 
  • If hypomagnesemia: 
    • replacement of magnesium 
  • Potassium-sparing diuretics, such as amiloride: correction of hypokalemia, hypomagnesaemia and metabolic alkalosis, especially when renal loss of potassium is the underlying cause.
  • Frequent plasma potassium monitoring to avoid hyperkalemia 
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