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
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