electrolyte imbalance for a surgical resident

1. ELECTROLYTE
IMBALANCE
Dr. Vignesh kumar
Ambedkar hospital

2. Composition in body
compartments
Electrolyte ECF (mEq/l) ICF (mEq/l)
Sodium 135-150 10-18
Potassium 3.5-5.0 120-145
Calcium 8.5-10.5 mg/dl
Magnesium 1.5-2.4 30-50
Chloride 95-108 2-6
Phosphate 2.5-4.5 mg/dl 25-60
http://www.globalrph.com/index.htm

3. Composition of GI secretions
(mEQ/l) Sodium Potassium Chloride Bicarbonate
Saliva 10 25 10 30
Stomach 60-90 10-30 100-130
Duodenum 140 5 100
Mixed
gastric
aspirate
120 10 100
Ileum 140 5 100 30
Colon 60 30 40
Stool 35 3-12 20
Pancreas 140 5 75 115
Bile 140 5 100 35
Bailey&Love 26th ed., Schwartz 9th ed.

4. POTASSIUM
 Primary intracellular ion
 Regulates cell excitability
 RDA : 4700 mg (0.6-0.8mEq/kg/day)
 Regulated be renin-angiotensin-
aldosterone axis
 Relation to acid base balance(buffer)
potassium decreases by 0.3 mEq/l
for every 0.1 increase in pH

5. ETIOLOGY
HYPERKALEMIA HYPOKALEMIA
 Increased intake
 Increased secretion
 Impaired excretion
 Inadequate intake
 Excessive excretion
 GI losses
 Misc

9. Treatment of hypokalemia
 Correction = 0.4× Body weight× deficit
 Oral / IV
 How much to correct?
 Peripheral/central line?
 Refractory cases?? Why?
 Co-existing hypokalemia and acidosis,
what to correct first?

10. Treatment of hyperkalemia
 Stop all oral and iv infusions of
potassium
 Stabilize the heart
 Role of bicarbonate??
 Short term measures
 Permanent measures

11. SODIUM
 Primary extracellular ion
 Vital for homeostasis and action potential
in the body
 Controls water movement in and out of
the vascular system
 Regulated by ADH
 RDA : 2400mg (1-2mEq/kg/day)
 Serum osmolality
◦ 2×Na + BUN/2.8 + glucose/18
◦ 2×Na + Bl urea/6 + glucose/18

13. Hyponatremia
 Hypotonic/hypertonic
 Every 100 gm fall in glucose,
1.6mEq/l fall in na (transient h-na)
 Renal/ extra renal
 Volume status
 ADH – H-na – osmalilty
 SIADH

15. Treatment of hyponatremia
 Correction = 0.6(m)/0.5(f) × deficit × BW
 Na <110 or neurological symptoms
◦ 3% NS until Na >120 or symptom free
◦ Rate of correction 0.25 mEq/l/hr or 8
mEq/l/day
◦ Seizures are present, correction can be upto
4-5 mEq/l in first hour
◦ Central pontine myelinosis
Hypovolemia Euvolemia Hypervolemia
Salt and water Water restriction Salt & Water restriction
IV saline Loop diuretics

16. Hypernatremia
 Volume status
 Renal / extra renal
 Diabetes insipidus
 Sr.osmalality
 Rare for a thristy person to end up
with hypernatremia

18. Treatment of hypernatremia
 Volume status
 Rate of correction
◦ Acute – max of1-2 m Eq/l/hr
◦ Chronic – max of 0.5 mEq/l/hr
◦ Max of 8 mEq/l/day
 Diabetes insipidus
Hypovolemia Euvolemia Hypervolemia
NS/2 and D5 Water or D5 Salt restriction
Loop diuretics with
water

19. CALCIUM
 Regulated by PTH and Calcitonin
 Vitamin D plays a role in absorption
 Coagulation cascade, neuromuscular
function
 Ionic 50%, protein bound 40%, anion
bound 10%
 RDA : 1-2g
 Ionic ca = total ca + [0.8×(4.5-albumin)]
 Relation to acid-base balance
◦ Acidosis decreases protein bound ca levels

20. ETIOLOGY
HYPOCALCEMIA HYPERCALCEMIA
 Post thyroid and neck
surgery
 Endocrine
 Renal failure
 Hyperphosphatemia
 Malignant disease
 Nutritional
 Blood transfusion
 Inflammatory conditions
 Endocrine
 Renal dysfunction
 Malignant disease
 Nutritional
 Granulomatous disease
 Inherited disorders

22. Chvostek’s sign

23. Trosseau’s sign (carpopedal
spasm)

24. Treatment of hypocalcemia
 10ml of 10% calcium gluconate(1 gm)
f/b calcium infusion if necessary (0.5-
1.5mg/kg/hr)
 Gluconate preferred over chloride
 Hyperphosphatemia correction
 Refractory cases? Why?
 Oral supplementation with vitamin D
 Teriparatide (synthetic PTH)

26. Treatment of hypercalcemia
 Treat the etiology – m/c parathyroid
adenoma
 Stop thiazide diuretics
 Saline diuresis with furosemide
 Inhibit bone resorption
(biphosphonates)
 Hemodialysis
 Calcitonin as short term measure
 Oral phosphates

27. MAGNESIUM
 Normal levels 1.5-2.4 m Eq/l
 Protein bound(30%), anion
bound(10%) and free(60%)
 Calcium channel antagonist and co
factor in ATP powered reactions
 Physiological test to detect tissue H-
Mg
 Mg is reabsorbed in Henle’s loop and
DCT
 RDA : 400mg

29. Hypomagnesemia
 40% of hypomagnesemics are
hypokalemic
 60% of hypokalemics are
hypomagnesemic
Hypomagnesemia
Slows ATP
production
Na+-K+ ATPase
Loss of intracellular
potassium
Loss of potassium in urine

30. Treatment of
hypomagnesemia
 1gm MgSo4 contains 0.1 g of
elemental magnesium
 8-12g IV over 24 hours f/b 4-6g IV for
the next three days
 Dose to be adjusted in renal
insufficiency
 Deep tendon reflexes, RR, Urine
output to be checked while giving Mg
correction

31. Hypermagnesemia
 Uncommon in the absence of renal
failure
 IV overdose are better tolerated than
oral overdose
 Neuromuscular blockade
 Calcium channel blockade
 ECG changes

33. Treatment of
hypermagnesemia
 Stopping Mg in patients with intact
renal function will suffice
 Calcium to stabilize the heart
 Saline diuresis with loop diuretics
 Dialysis for renal failure patients