The Electrolytes

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The Electrolytes

In chemistry, an electrolyte is any substance containing free ions that make the substance electrically conductive. The most typical electrolyte is an ionic solution, but molten electrolytes and solid electrolytes are also possible.
Commonly, electrolytes are solutions of acids, bases or salts.
Electrolyte solutions are normally formed when a salt is placed into a solvent such as water and the individual components dissociate due to the thermodynamic interactions between solvent and solute molecules, in a process called solvation. For example, when table salt, NaCl, is placed in water, the salt (a solid) dissolves into its component ions, according to the dissociation reaction
NaCl(s) → Na+(aq) + Cl−(aq)
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The Electrolytes
Serum sodium
Sodium is the main extracellular cation and is involved in fluid volume control and fluid movements as well as in resting memebrane potential.
Normal serum Na+: 135 – 148 mEq/L.

Normal total sodium content:
Adults: 1.09 g/kg lean body weight.
Neonates: 1.78 g/kg lean body wt.
Normal daily requirements: 1.5 – 2.0 mmol/Kg body wt.

In a 70 Kg man:
Total body sodium: 4000 mmol
ECF sodium: 2100 mmol
ICF sodium: :400 mmol
Bony skeleton: 1500 mmol
(- 700 mmol exchangable).

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Serum sodium

Determining total deficit or excess:

∆Na = (140 – SNa)TBW in mEq
Where:
∆Na = sodium deficit or excess
SNa = serum sodium
TBW = total body water = 60%body wt(Kg)

Determining serum deficit or excess:

∆Na = (140 – SNa) ECF in mEq
Where:
∆Na = sodium deficit or excess.
SNa = seum sodium.
ECF = ECF volume = 20% Bwt /Kg

Example:

A 65 kg patient with a serum Na of 120 meq\l.
The ECF Na deficit is :
(140-120 )x20%x65= 260 meq.
Each 500ml bottle of 0.9% contains 75meq Na.
The no. Of Nacl bottles: 260\75= 3.5.

Hyponatraemia

Aetiology

1- increased Na+ loss:
A- intestinal loss.
B- excessive sweating.
C- infusion of water or diluted salt in hypovolaemic or renal impaired kidneys pts.
D- addison”s disease , diuretics.
2- water excess:
a- inappropiate replacement of losses with low Na containing fluid .
b- bladder wash , bowel wash .
c- in approp ADH syndrome .

Hyponatraemia c\o

1- low urine output.
2- loss of skin turgor .
3- loss of weight .
4-low CNS pressure .normal or low Bp
5- signs & symptoms of water intoxication:
a- low serum Na b- mental confusion .
Disorientation ,convulsion lethergy ,muscle weakness & coma
6- oligouria .

MANAGEMENT HYPONATREMIA

1- restrict water intake .
2- correct Na orally or parentrally if the pt is dehydrated
3- hypertonic saline may be needed.

Hypernatraemia

Aetiology

1- Na excess.
2- Water depletion.
Na excess: causes:
A- excess steroids, either iatrogenic or in Conn’s or cushing’s syndrome.
B- excess use of hyperosmolar high protein tube feeding.
C- partial drowning in sea water.

Water depletion

: causes:

A- insufficient water replacement as in fever, burns,excess sweating in tropical countries.
B- pt too ill or lethargic to respond to thirst or unable to communicate their thirst as infants or comatose pts.
C- lesions of upper GIT which prevent swallowing
D- profuse watery diarrohea.
E- over administration of osmotic diuretics such as mannitol or excess diuresis as in diabetes insipidus.

Clinical features:

Pt present with severe thirst, confusion, lethargy or even coma and if not treated appropriately may be at risk of death.

Management of Hypernatremia

Rehydrate pts with appropriate fluids in the presence of water depletion: hypotonic solutions are used for gradual reduction in serum sodium concentration.
To determine how much water in liters is needed to bring back the serum sodium to normal determine excess sodium(∆Na) and divide into the expected serum Na concentration (140 mEq/L)
Example: if excess sodium was 150mEq/L, then the amount of water needed to bring Na concentration to normal: 150 /140 = 1.07 liters.
Avoid rapid fall in serum sodium which may otherwise cause cerebral oedema.
Diuretics are usefull in the presence of sodium excess in normally hydrated pts.

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Serum potassium

Normal serum K+ level:
- 3.8 – 5 mEq/L

Normal total K+ content:
- Adults: 2.65 g/Kg lean body wt
- Neonates: 1.90 g/Kg lean body wt

Daily excretion of potassium
- 50 – 60 mEq/L

Normal daily requirements:
- 1.0 mmol/Kg body wt

In a 70kg man

- total body potassium 3800 mmol
- ECF potassium 60 mmol
- ICF potassium 3740 mmol

In the absence of acid base disturbances serum K+ levels closely represent total K+
Acidosis may result in an outward shift of potassium fro cells into the ECF space with resultant hyperkalemia, whereas alkalosis has opposite effect with resultant hypokalemia.
Thus these changes in serum potassium secondary to changes in pH do not reflect the true situation regarding the body content of potassium.
However a loss of 10% of total body potassium gives a true drop of seru K+ levels from 4 to 3 mEq/ L at a normal pH.

Hypokalemia

aetiology:

1- excess loss of potassium from the body.
2- reduced intake of K+.
3- Redistribution.

Excess loss of K from the body

:causes:

a) excess loss of GIT secretions:
vomiting, nasogastric suction and intestinal fistulas. These are usually associated with alkalosisdue to chloride loss from upper GIT.
Loss of secretions from lower GIT occurs in diarrohea, excess use of purgatives and villous tumors of rectum.these are not associated with alkalosis
Excess loss of K from the body: causes:cont

b) excessive renal losses:
- K loosing diuretics.
- Osmotic diuresis.
- High dose corticosteroids.
- Hyperaldosteronism.
- Cushing’s syndrome.

2- Reduced intake of potassium:

- Prolonged administration of K free diets or fluids.
- anorexia.
- alcoholism

3- Redistribution:

- Insulin glucose therapy
- overcorrection of acidosis (alkalosis).

Hypokalemia clinical freatures

Personality changes.
Drowsiness & Later coma.
Cardiac arrythmias
Muscle weakness and hypotonia(skeletal and smooth) such as paralytic ileus & particularly cardiac muscle with ECG changes.
Muscle cramps and tetany 20 to hypocalcemia (due to alkalosis)
Reduced renal blood flow and GFR.
Aggravation of digoxin toxicity.

Hypokalemia management:

Mild hypokalemia (K+ 3.0 – 3.4) can easily be managed by increasing dietary intake with oral supplements of K.
Severe hypokalemia K+ less than 2.5 mmol/l should be corrected by IV therapy. IV potassium should not exceed 10 – 20 mmol/ hour and even less if there is oliguria.

Hyperkalemia

etiology

1- Increased body gains
- Iatrogenic: excessive K therapy.
2- Failure or reduced renal excretion:
- Reduced Na+/K+ & H+
- K sparing diuretics.
- Addisons disease.
- renal glomerular failure
- Salt depletion.
3- body redistribution.
4- secondary to acidosis
- diabetic.
- renal.
- severe tissue injury
- burns
- Crush injuries
- surgical trauma
A hemolyzed blood specimen gives a false rise in serum K level by 0.5 mEq/l. One unit of blood if hemolyzed contains 18mEq/l of K.
This also applies to hemolytic diseases such as hemolytic sickle cell crises.

Hyperkalemia clinical features

Bradycardia, hypotension and ECG changes.
Intestinal colics, nausea, vomiting and diarrohea.
Parathesia and muscle weakness.
Heart block cardiac asystole .

ECG changes in K disturbances

Hypokalemia:

Low flat or inverted T- wave, wide QRS comlexes, prolonged PR intervals , depressed ST segments, and high U – waves.

Hyperkalemia:

Diminished P waves, wide QRS complexes, short Q-T intervals. Tall peaked T- waves,arrythmias and heart block.

Hyperkalemia management

Dextrose infusion plus insulin: 50ml of 50% dextrose + 20 units soluble insulin will rapidly lower K levels .
Sodium lactate or bicarbonate: 100 mmol HCO3-(100 ml of 8.4% NaHCO3-( given IV will induce alkalosis and force K into cells.
Calcium gluconate:10ml 0f 10%Ca gluconate given IV slowly with ECG monitoring, counteract K effect on cardiac and conductive tissue.
Hemodialysis or peritoneal dialysis in chronic cases.

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Serum calcium

Normal serum levels:

4.3 – 5.3 mEq/L (8.5 -10.5 mg/100ml)

Daily requirements:

10mg /kg body wt

Total body calcium

Adults: 20.1 g/kg body wt
Neonates 9.20 g/kg body wt

In a 70 kg man

Total body calcium: 30160 mmol
ECF calcium : 35mmol(2.5 mmol/l)
ICF calcium : 125mmol(5mmol/l)
Bony skeleton : 30000 mmol

Hypocalcemia aetiology:

1- hypoparathyroidism.
2- malabsorption.
3- alkalosis.
4- acute pancreatitis.
5- renal failure.
6- small intestinal fistulas

Hypocalcemia clinical features

Numbness, tingling and hyperactive tendon reflexes.
Positive chvostek’s sign (facial twitching on tapping over the facial nerve.)
Abdominal cramps.
Tetany with carpopedal spasm
Convulsions
ECG changes prolongation of QT interval.

Management:

Calcium gluconate injections.
Treat alkalosis.
Treat the cause


Hypercalcemia aetiology

Hyperparathyroidism
Bone metastatic carcinoma,sp from breast
Acidosis
Osteoporosis
Renal tubular acidosis
Hypervitaminosis D
Sarcoidosis
Tumors secreting parathormone.

Hypercalcemia clinical features

1- bones: generalized osteoporosis, osteitis fibrosa cystica and bone cysts.
2- Abdominal groans: pancreatitis, peptic ulceration
3- Stones: renal tract stones& nephrocalcinosis.
4- Pshychic moans
5- Fatigue, muscle weakness and ↓reflexes
6- Anorexia,nausea, vomiting& constipation
7- Thirst, polyuria and nocturia
8- Corneal calcification
9- Lasitude, stupor or even coma

Investigations in hypercalcemia

High serum calcium.
Hypercalcuria
Hypophoshatemia
Hyperphosphaturia
Elevated seum alkaline phosphatase
Elevated serum parathyroid hormone > 0.5μgs/l.

Hypercalcemia differential diagnosis

Primary hyperparathyroidism
Sarcoidosis
Myelomatosis
Hyperthyroidism
Milk – alkali syndrome
Vitamin D intoxication
Immobilization with paget’s disease.

Hypercalcemia management

Emergency management
Saline drip (to cause a dilution)
Chelating agents (EDTA)
Steroids.
Sodium sulphate dialysis
Mithromycin

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Hyponatremia Tutorial
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