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• Hypokalemia is defined as serum potassium level < 3.5 mEql/L.

• It is associated with ten fold increase in mortality rates due to adverse effect on cardiac rhythm, blood pressure and cardiovascular morbidity rate.

• Systemic hypomagnesemia also can cause treatment resistant hypokalemia due to combination of reduced cellular uptake of potassium and exaggerated renal secretion.

ETIOLOGY

1. Decreased intake

• Starvation

• Clay ingestion

2. Redistribution into cells

• Acid-base : Metabolic alkalosis

• Hormonal : Insulin, beta adrenergic activity, and thyroid hormone promote, Na+, K- ATPase mediated cellular uptake K+. It can also occur in the setting of hyperthyroidism, with periodic attacks of hypokalemic paralysis.

• Insulin

• Increased β₂ adrenergic sympathetic activity : Post MI, head Injury

• β Adrenergic agonists : Bronchodilators , tocolytics

• αAdrenergic antagonists

• Thyrotoxic Periodic Paralysis

• Anabolic state

  • Vitamin B12 or folic acid supplementation (red blood cell production)

  • Granulocyte-macrophage colony stimulating factor supplementation (white blood cell production)

  • Total parenteral nutrition

• Others

  • Pseudohypokalemia : It can be due to invitro cellular uptake of K+ after venipuncture.

  • hypothermia,

  • familial hypokalemic periodic paralysis

  • Barium toxicity : systemic inhibition of “ leak” K+ channels.

3. Increased loss

• Nonrenal

  • Gastrointestinal loss (diarrhea)

  • Integumentary loss (sweat)

• Renal

  • Increased distal flow: diuretics, osmotic diuresis, salt-wasting nephropathies

  • Increased secretion of potassium :

1. Mineralocorticoid excess: primary hyperaldosteronism, secondary hyperaldosteronism (malignant hypertension, renin secreting tumors, renal artery stenosis, hypovolemia), congenital adrenal hyperplasia, Cushing’s syndrome, Bartter’s syndrome

2. Apparent mineralocorticoid excess : Genteic deficiency or inhibition of 11 beta-dehydrogenase-2 , Liddle's Syndrome

• Distal delivery of non-reabsorbed anions: vomiting, nasogastric suction, proximal (type 2) renal tubular acidosis, diabetic ketoacidosis, glue-sniffing (toluene abuse), penicillin derivatives

• Other: amphotericin B, Liddle’s syndrome, hypomagnesemia

Clinical Manifestation

• Severe hypokalemia 2.5 mEq/L : muscle weakness.

• ECG: U waves ; flattening or T wave inversion ; Prolongation of QT interval

• Cardiovascular : Hypertension, Orthostatic hypotension, potentiation of digitalis toxicity, dysarrhythmia.

• Neuromuscular :Malaise, Weakness, hyporeflexia, cramps, paresthesia, paralysis,rhabdomyolysis.

• GI: Ileus

• Renal:Increased ammonia production, Urinary concentration defects,metabolic alkalosis, nephrogenic diabetes insipidus, Glucose intolerance.

MANAGEMENT

• Mild hypokalemia is not necessary to correct .

• It can be corrected orally.

• IV correction is for less than 3.

• Through peripheral line 10 to 20 mEq can be given per hour, amounts of 40 -100 mEq/hr can be given to selected patients with paralysis or life threatening arrythmias.

• Amounts of more than 40 mEql is given via central line.

AVAILABILITY

• It is available as oral & parenteral preparation.

• IV preparation is available as ampules. Each ampule contains 20mEql of potassium in 10ml.

• Syp. Potklor 15ml contains 20mEql (Potassium chloride)

How to calculate potassium deficit ?

• It is been found that if hypokalemia is due to potassium deficit then a potassium deficit of 10% of the total body potassium stores is expected for every 1 mEq/L decrease.

• For example a 70kg man with K+ of 2.5; his total body stores =70*50=3500.(Normal k+ content in body is 50mEq/kg) 10% of it is 350mEql. That means he is deficit of 350mEq which has to be supplemented.

Mild to Moderate potassium depletion

• Potassium levels of 3.0 – 3.5 mEq/L is corrected using oral supplements.

• In patients with liver disease and heart disease aldosterone antagonist can be added to prevent urinary loss of potassium.

Moderate Hypokalemia

• 20 – 40 mEq/l is supplemented through peripheral line. Max 50 -60mEq/L.

Severe Hypokalemia (<2.5mEql)

• In general, maximum rate of correction is 10 to 20 mEq/hr; although as much as 40 -100 mEq/hr has been given to selected patients with paralysis or life threatening arrythmias.

• When infusing large volumes even in hypokalemia patients they must be monitored closely for any arrythmias.

Magnesium Deficiency & Hypokalemia

• Magnesium depletion has inhibitory effects on muscles NaK ATPase activity reducing influx into muscle cells and causing a secondary kaliuresis. It also causes increased K+ secretion by the distal nephron, due to reduction in magnesium dependdent intracellular block of K+ efflux through the secretory K+ channel of principal cells.

5% Dextrose & K+ supplementation

• Dextrose is not recommended as a diluent because dextrose can lead to release to insulin which will cause the shift of potassium intracellularly hence aggrevates hypokalemia.

• Transient reduction of serum potassium 0.2- 1.4mEq/l if 20 mEq K+/L of 5% dextrose is infused.

Notes

A rise in pH by 0.1 will cause 0.5 mEq/l decrease in serum K+ .

A approx drop of 0.5 mEq/L will cause a potassium of 175 mEq.

Potassium chloride V/S Potassium bicarbonate/citrate

• Potassium chloride more rapidly raises the plasma potassium concentration. The chloride gets retained in the ECF and maintains the electrical neutrality, thereby maximizing the rise of plasma potassium whereas bicarbonate enters the cell more rapidly than does chloride.

• In patients with hypokalemia and metabolic alkalosis (diuretic therapy, vomiting & hyperaldosteronism) hydrogen loss accompanies potassium loss . So chloride must be supplemented so as to correct both optimally.

• Potassium bicarbonate or citrate is preferred in hypokalemia with acidosis (RTA and chronic diarrheal state).

Why there is hypokalemia in vomiting ?

• Loss of gastric or intestinal secretions from any cause vomiting, diarrhea, laxatives or tube drainage is associated with potassium wasting and possibly hypokalemia.

• Loss of gastric secretions leads to metabolic alkalosis & raises the plasma bicarbonate concentration .

• Once the filtered bicarbonate load is above its proximal tubular resporptive threshold, the sodium bicarbonate and water are delivered to distal potassium secretory site in the kidney.

• Secreted potassium combines with the negatively charged bicarbonate and is excreted in the final urine leading to hypokalemia.

• A combination of hypovolemia- induced aldosterone release will lead to increased loss of potassium.

• In diarrhea potassium is lost through intestinal loss.

Note

• Catecholamines acting via beta 2 adrenergic receptor, promote potassium entry into the cells by increasing NA+/K+-ATPase activity. As a result, transient hypokalemia can occur with stress induced release of epinephrine, as in acute illness, coronary ischemia, alcohol withdrawal.

Reference

• Harrisons principle of medicine

• Tintinalli

• The ICU

Updated on 27/3/2014