Hypokalemia & Hypomagnesemia By Saurabh Tiwari

1. Hypokalemia
and
Hypomagnesemia

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. Causes of Hypokalemia
Decrease
Intake
Increase Loss
Redistribution into
Cells
A.Non-renal
B.Renal
Saurabh Tiwari

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. Causes of Hypokalemia
III. Increased Loss
A. Non-renal
1. Gastrointestinal Los (diarrhea)
2. Integumentary Loss (sweat)
B. Renal
Saurabh Tiwari

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. 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.  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. SIGNS & SYMPTOMS
 Fatigue
 Muscular weakness & paralysis
 Hyporeflexia
 Dyspnea
 Arrhythmia
 Predispose to digitalis toxicity
 Constipation
Saurabh Tiwari

10.  Risk of hyponatremia
 resultant confusion, headaches, &
seizures
 Irritable
 Nervousness
SIGNS & SYMPTOMS
Saurabh Tiwari

11. TREATMENT
Therapeutic goals:
to correct the K+ deficit
to minimize on going losses
Saurabh Tiwari

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. 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. 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. 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. 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. 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. 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. 3. Related to GI Mg loss
Diarrhea
Vomiting and nasogastric suction
Gastrointestinal fistulas and ostomies
Hypomagnesemia with secondary
hypocalcemia (HSH)
Saurabh Tiwari

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.  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. 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. 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.  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. 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. 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. 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. 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. Thank You
Saurabh Tiwari