Electrolyte

1. Electrolyte
Presenter: Dr Hem narayan Amatya
Lumbini Medical College
Total no of slides =38 1

2. Contents
• Introduction
• Hyponatremia
• Hypernatraemia
• Hypokalemia
• Hyperkalemia
• Hypercalcemia
• Hypocalcemia
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3. Electrolyte
• Minerals in body fluids that carry an electric charge
• Six major electrolyte are:-
• •Sodium
• •Potassium
• •Calcium
• •Chloride
• •Phosphate
• •Magnesium
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4. Osmolar substance intracellular and
extra cellular
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5. Sodium
• RDA – 2.3 gm of NaCl/day(Dietary guideline
for Americans )
• Potential Na+ loss – sweat, urine, and GI
secretions
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6. Sodium
• Function
--Maintains osmolarity
– Influences water distribution
– Affects concentration, excretion and absorption of
potassium and chloride
– Aids nerve and muscle fiber impulse transmission
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7. Hyponatremia
• Mild (130–138 mEq/L)
• Moderate (120–130 mEq/L)
• Severe (<120 mEq/L)
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8. Classification
Hyponatremia
Volume status
Decreased oral
intake
Diuretics
Renal loss
Primary renal loss
High
Increased intake
Postoperative ADH
secretion
Normal
Hyperglycemia
SIADH
Water intoxication
Diuretics
Plasma Na+ ↓ by
1.4 mmol/L for
every 100 mg/dL
glucose concn
Low

9. Clinical features
Body System Hyponatremia
Central nervous
system
Headache, confusion,
hyperactive or
hypoactive deep tendon
reflexes, seizures,
coma, increased
intracranial pressure
Musculoskeletal Weakness, fatigue, muscle
cramps/
twitching
Gastro intestinal Anorexia, nausea,
vomiting, watery
diarrhea
Cardiovascular Hypertension and
bradycardia
if intracranial pressure
increases
significantly
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10. • Mild asymptomatic hyponatremia -requires no
treatment.
• Asymptomatic hyponatremia associated with
ECF volume contraction - Na repletion
(isotonic saline)
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11. • Hyponatremia associated with edematous
states - restriction of Na and water intake,
-promotion of water loss in excess of
Na, loop diuretics
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12. • In asymptomatic patients,
the plasma Na+ should't be raised > 0.5 to 1.0
mmol/L per h & >10 to 12 mmol/L over the first 24 h.
• Severe symptomatic hyponatremia
treated with hypertonic saline
Na + raised by 1 to 2 mmol/L per hour for the first 3
to 4 h or until the seizures subside.
• Too rapid correction - osmotic demyelination syndrome
(ODS) -flaccid paralysis, dysarthria, and dysphagia.
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13. Hypernatraemia
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14. Causes of hypernatraemia
latrogenic
Administration of hypertonic sodium solutions
• Insensitivity to ADH (nephrogenic diabetes insipidus)
Lithium ,Tetracyclines, Amphotericin B, Acute tubular
necrosis
• Osmotic diuresis
Total parenteral nutrition
Hyperosmolar diabetic coma
• Deficient water intake
• ADH deficiency - Diabetes insipidus
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15. Clinical manifestations
Body System Hypernatremia
CNS Restlessness, lethargy, ataxia, irritability,
tonic spasms, delirium, seizures, coma
Muskoskeletal Restlessness, lethargy, ataxia, irritability,
tonic spasms, delirium, seizures, coma
Cardiovascular Tachycardia, hypotension, syncope
Tissue Dry sticky mucous membranes, red
swollen tongue, decreased saliva and
tears
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16. Treatment
• Acess volume status first
• In hypovolemic -, offsetting the volume deficit
with isotonic fluids
• Nonhypovolemic- free water replacement with
hypotonic solutions
• acute hypernatremia- correction rate no more
than 1 to 2 mEq/hr
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17. • chronic hyponatremia, no more than 0.5
mEq/hr
• 8 mEq/day.
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18. Potassium
• average intake of potassium - 50 to 100 mEq/d
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19. Hypokalemia
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20. Etiology
• Inadequate intake
• Dietary, potassium-free intravenous fluids,
potassium deficient
• TPN
• Excessive potassium excretion
• Hyperaldosteronism
• GI losses
• Direct loss of potassium from GI fluid (diarrhea)
• Renal loss of potassium
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21. Clinical manifestations
• Fatigue, myalgia,
• muscular weakness of the lower extremities
• hypoventilation
• metabolic alkalosis
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22. • electrocardiographic changes -
flattening or inversion of the T wave,
prominent U wave,
ST-segment depression
Severe K+ depletion –
prolonged PR interval, widening of the QRS
complex, and ventricular arrhythmias
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23. Treatment
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• Potassium chloride is usually the preparation
of choice.

24. • Severe hypokalemia - IV KCl.
40 mmol/L via a peripheral vein or 60 mmol/L
via a central vein.
The rate of infusion should not exceed 20
mmol/h unless paralysis or malignant
ventricular arrhythmias are present.
Ideally, KCl should be mixed in normal saline
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25. Hypercalcemia
• Normal level 8.5 to 10.2
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26. 26
Hypercalcemia- Causes
• Excessive PTH production
Primary hyperparathyroidism (adenoma, hyperplasia, rarely carcinoma)
Tertiary hyperparathyroidism (long-term stimulation of PTH secretion in
renal insufficiency)
• Hypercalcemia of malignancy
Overproduction of PTHrP (many solid tumors)
Lytic skeletal metastases (breast, myeloma) Excessive
• 1,25(OH)2D production
Granulomatous diseases (sarcoidosis, tuberculosis, silicosis)
Lymphomas
Vitamin D intoxication

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Hypercalcemia- Causes
• Primary increase in bone resorption
Hyperthyroidism
Immobilization
• Excessive calcium intake

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Clinical Manifestations -hypercalcemia
• Mild hypercalcemia (up to 11–11.5 mg/dL)
usually asymptomatic
vague neuropsychiatric symptoms –
trouble concentrating, personality
changes, or depression.
peptic ulcer disease
nephrolithiasis
fracture

29. • More severe hypercalcemia (>12–13 mg/dL),
lethargy, stupor, or coma
gastrointestinal symptoms (nausea, anorexia,
constipation, or pancreatitis).
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30. • electrocardiographic changes-
– bradycardia,
– AV block, and short QT interval;
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31. 31
Hypercalcemia: Treatment
• Initial therapy
volume expansion : 4–6 L of saline over the first
24 h,
• If there is increased calcium mobilization from
bone
Zoledronic acid
pamidronate

32. Hypocalcemia
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33. 33
Hypocalcemia - Causes
• Low Parathyroid Hormone Level
(Hypoparathyroidism)
Parathyroid agenesis
DiGeorge syndrome
Surgical Radiation
Infiltration by metastases or systemic diseases
Autoimmune Reduced parathyroid function

34. • High Parathyroid Hormone Levels (Secondary
Hyperparathyroidism)
Vitamin D deficiency
Renal insufficiency with impaired 1,25(OH)2D production
• Drugs
Calcium chelators
Inhibitors of bone resorption (bisphosphonates)
• Miscellaneous causes
Acute pancreatitis
Osteoblastic metastases
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35. 35
Clinical Manifestations
• Symptom :
paresthesias-caused by increased
neuromuscular irritability.
• On physical examination
Chvostek's sign
Carpal spasm (Trousseau's sign).

36. • Severe hypocalcemia –
seizures
carpopedal spasm
bronchospasm
laryngospasm
prolongation of the QT interval
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37. 37
Hypocalcemia: Treatment
• Acute, symptomatic hypocalcemia
calcium gluconate, 10 mL 10% wt/vol (90
mg or 2.2 mmol) intravenously, diluted in 50
mL of 5% dextrose or 0.9% sodium chloride,
given intravenously over 5 min.

38. • Chronic hypocalcemia- due to
hypoparathyroidism
• treated with
calcium supplements
vitamin D2 or D3
calcitriol
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