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Hypokalemia & Hypomagnesemia


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Hypokalemia & Hypomagnesemia By Saurabh Tiwari

Published in: Healthcare

Hypokalemia & Hypomagnesemia

  1. 1. Hypokalemia and Hypomagnesemia
  2. 2. Hypokalemia  Serum level below 3.5–5.0 mEq/L  Caused by vomiting, diarrhea, diuretics, gastric suctioning  Hypomagnesaemia  Muscle weakness, polyuria Saurabh Tiwari
  3. 3. Causes of Hypokalemia Decrease Intake Increase Loss Redistribution into Cells A.Non-renal B.Renal Saurabh Tiwari
  4. 4. Causes of Hypokalemia I. Decreased intake A. Starvation B. Clay Ingestion II. Redistribution into Cells A. Acid-Base (Metabolic Alkalosis) B. Hormonal (Insulin, Beta agonist, Alpha antagonist) C. Anabolic State (folic acid) D. Other (Hypothermia, Pseudo hypokalemia) Saurabh Tiwari
  5. 5. Causes of Hypokalemia III. Increased Loss A. Non-renal 1. Gastrointestinal Los (diarrhea) 2. Integumentary Loss (sweat) B. Renal Saurabh Tiwari
  6. 6. Cause of Hypokalemia in the patient  Gastrointestinal losses diarrhea (secretory)  Urine potassium level less than 20 mEq/L suggests gastrointestinal loss  Stool has a relatively high potassium content, and fecal potassium losses could exceed 100 mEq per day with severe diarrhea. Saurabh Tiwari
  7. 7. Gastrointestinal Loss  Hypokalemia is also due to increased K+ renal excretion  Loss of Gastric contents results in volume depletion and metabolic alkalosis, both of which promotes kaliuresis Saurabh Tiwari
  8. 8.  Stimulates aldosterone release=augments K+ secretion by principal cells  There is an increase in distal delivery of NaHCO3 which enhances the electrochemical gradient favoring potassium loss in urine. Gastrointestinal Loss Saurabh Tiwari
  9. 9. SIGNS & SYMPTOMS  Fatigue  Muscular weakness & paralysis  Hyporeflexia  Dyspnea  Arrhythmia  Predispose to digitalis toxicity  Constipation Saurabh Tiwari
  10. 10.  Risk of hyponatremia  resultant confusion, headaches, & seizures  Irritable  Nervousness SIGNS & SYMPTOMS Saurabh Tiwari
  11. 11. TREATMENT Therapeutic goals: to correct the K+ deficit to minimize on going losses Saurabh Tiwari
  12. 12.  It is safer to correct hypokalemia via oral route in order to prevent rebound hyperkalemia if given IV  The plasma potassium concentration should be monitored frequently when assessing the response to treatment Saurabh Tiwari
  13. 13. Emergency Treatment of Hypokalemia A. Estimated Potassium Deficit  serum K <3 mEq/L= K deficit >300 mEq  serum K <2 mEq/L= K deficit >700 mEq Saurabh Tiwari
  14. 14. B. Indications for Urgent Replacement  ECG abnormalities consistent with severe K+ depletion  myocardial infarction  hypoxia  digitalis intoxication  marked muscle weakness  respiratory muscle paralysis. Saurabh Tiwari
  15. 15. IV infusion - for severe hypokalemia or those who cannot take oral supplementation - peripheral vein = 40 mmol/L (preferred) central vein = 60 mmol/L - rate of infusion  20 mmol/hr - mixed in NSS  Continuous ECG monitoring  Serum potassium determination every 3-6 hoursSaurabh Tiwari
  16. 16. Non-Emergency Treatment of Hypokalemia  attempts should be made to normalize K+ levels if <3.5 mEq/L  oral supplementation is significantly safer than IV  KCL elixir, 1-3 tablespoon every day Saurabh Tiwari
  17. 17. Hypomagnesemia  Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood.  Hypomagnesemia is not necessarily magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa. Saurabh Tiwari
  18. 18. Causes Hypomagnesemia 1. Related to decreased Mg intake Starvation Alcohol dependence Total parenteral nutrition 2. Related to redistribution of Mg from ECF to ICF Hungry bone syndrome Treatment of diabetic ketoacidosis Refeeding syndrome Saurabh Tiwari
  19. 19. 3. Related to GI Mg loss Diarrhea Vomiting and nasogastric suction Gastrointestinal fistulas and ostomies Hypomagnesemia with secondary hypocalcemia (HSH) Saurabh Tiwari
  20. 20. 4. Related to renal Mg loss Gitelman syndrome Classic Bartter syndrome (Type III Bartter syndrome) Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) Autosomal-dominant hypocalcemia with hypercalciuria (ADHH) Isolated dominant hypomagnesemia (IDH) with hypocalcemia Saurabh Tiwari
  21. 21.  Alcoholics and individuals on magnesium- deficient diets or on parenteral nutrition for prolonged periods can become hypomagnesemic without abnormal gastrointestinal or kidney function.  The addition of 4-12 mmol of magnesium per day to total parenteral nutrition has been recommended to prevent hypomagnesemia. DECREASED MAGNESIUM INTAKE Saurabh Tiwari
  22. 22. REDISTRIBUTION OF MAGNESIUM FROM ECF TO ICF  Hungry bone syndrome, in which magnesium is removed from the extracellular fluid space and deposited in bone following parathyroidectomy or total thyroidectomy or any similar states of massive mineralization of the bones  Hypomagnesemia may also occur following insulin therapy for diabetic ketoacidosis and may be related to the anabolic effects of insulin driving magnesium, along with potassium and phosphorus, back into cells. Saurabh Tiwari
  23. 23. GASTROINTESTINAL LOSSES  When the small bowel is involved, due to disorders associated with malabsorption, chronic diarrhea, or steatorrhea, or as a result of bypass surgery on the small intestine.  Patients with ileostomies can develop hypomagnesemia as there is some degree of magnesium absorption in the colon Saurabh Tiwari
  24. 24.  Hypomagnesemia with secondary hypocalcemia (HSH) is a rare autosomal-recessive disorder characterized by profound hypomagnesemia associated with hypocalcemia.  Pathophysiology is related to impaired intestinal absorption of magnesium accompanied by renal magnesium wasting as a result of a reabsorption defect in the DCT. Saurabh Tiwari
  25. 25. RENAL LOSSES  Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC), an autosomal-recessive disorder, there is profound renal magnesium and calcium wasting.  The hypercalciuria often leads to nephrocalcinosis, resulting in progressive renal failure.  Other symptoms reported in patients with FHHNC include urinary tract infections, nephrolithiasis, incomplete distal tubular acidosis, and ocular abnormalities Saurabh Tiwari
  26. 26. Bartter’s syndrome  Autosomal recessive disorder involving impaired Thick Ascending Limb salt reabsorption Gitelman syndrome  autosomal recessive disorder involving loss of function of the thiazide sensitive sodium-chloride symporter located in the distal convoluted tubule Saurabh Tiwari
  27. 27. TREATMENT Diet Can be used alone for mild  Mg Green vegetables, meat, seafood, nuts, seeds, legumes, whole grains, peanut butter, cocoa, and Spinach (probably one of the best sources) Mg replacement  Assess renal function – route of Mg elimination IV or IM  Because the kidneys are main route of excretion, make sure to watch BUN and Creatinine levels. Renal failure clients have problems with high Magnesium Saurabh Tiwari
  28. 28. The risk of hypomagnesemia can be summarized as follows:  2% in the general population  10-20% in hospitalized patients  50-60% in intensive care unit (ICU) patients  30-80% in persons with alcoholism  25% in outpatients with diabetes Saurabh Tiwari
  29. 29. Thank You Saurabh Tiwari