FLUID AND

ELECTROLYTE
IMBALANCE
DR MUKTA SHARMA
 Water is the most abundant constituent in the body, comprising approximately 50% of
body weight in women and 60% in men.
Total body water is distributed in two major compartments: 5575% is intracellular and
2545% is extracellular fluid which is further subdivided into intravascular (plasma water)
and extravascular (interstitial) spaces in a ratio of 1:3.
Fluid movement between the intravascular and interstitial spaces occurs across the
capillary wall and is determined by Starling forces, i.e., capillary hydraulic pressure and
colloid osmotic pressure.
BODY FLUID AND ELECTROLYTE DISTURBANCES

Volume Changes: Hypovolemia

Hypervolemia
Concentration changes: Hyponatremia
Hypernatremia
Composition Changes: Acid/base Balance
Potassium Abnormalities
Calcium Abnormalities
Magnesium Abnormalities
HYPONATREMIA

Sodium is the most abundant positive ion of ECF compartment and is critical in determining ECF and
ICF osmolality
Normal Amount: 135-145meq/l
Signs and symptoms are seen : <120meq/l
Disorder of sodium mainly effects ECF volume resulting in hypovolemia or edema rather than the
alteration in plasma sodium concentration
CNS: confusion, lethargy, stupor, headache, seizure, coma
GI: nausea, vomiting
Skeletal system: muscle twitching
 Causes of hyponatremia

Hypovolaemic (sodium Renal sodium losses

deficit with a relatively Diuretic therapy (especially
smaller water deficit) thiazides)
Adrenocortical failure
Gastrointestinal sodium
losses
Vomiting
Diarrhoea
Skin sodium losses
Burns

Euvolaemic (water Primary polydipsia

retention alone) Excessive electrolyte-free water
infusion
SIADH
Hypothyroidism

Hypervolaemic (sodium Congestive cardiac failure

retention with relatively Cirrhosis
greater water retention) Nephrotic syndrome
Chronic renal failure (during free
water intake)
MANAGEMENT OF HYPONATREM IA

Critically dependent on its rate of development, severity and underlying cause.

If developed rapidly (over hours to days), and there are signs of cerebral oedema such as
obtundation or convulsions, sodium levels should be restored to normal rapidly by infusion
of hypertonic (3%) sodium chloride.
A common approach is to give an initial bolus of 100 mL, which may be repeated once or
twice over the initial hours of observation, depending on the neurological response and rise
in plasma sodium.
 On the other hand, rapid correction of hyponatraemia that has developed slowly (over
weeks to months) can be hazardous, since brain cells adapt to slowly developing hypo-
osmolality by reducing the intracellular osmolality, thus maintaining normal cell volume
Under these conditions, an abrupt increase in extracellular osmolality can lead to water
shifting out of neurons, abruptly reducing their volume and causing them to detach from
their myelin sheaths. The resulting myelinolysis can produce permanent structural and
functional damage to mid-brain structures, and is generally fatal. The rate of correction of
the plasma Na concentration in chronic asymptomatic hyponatraemia should not exceed
10 mmol/L/day, and an even slower rate is generally safer.
MANAGEMENT

Sodium deficit is calculated using the formula

deficit= (135-plasma NA+)X0.6X body wt. followed by a calculation of the required rate.
Corrected slowly over 24-48hours. 1/3rd in the first 8hours. 1/3rd is given in the next
16hours and the remaining 1/3rd over subsequent 24hours.
For every 100mg% of increase in sugar above normal, the serum sodium decreases by
1.6meq/l therefore hyperglycemia must be excluded as a cause of hyponatremia before
starting treatment.
HYPERNATREMIA

Serum sodium > 145mmol/lit, (>160mmol/lit severe)

M/C mechanism is renal water loss
Patients with hypernatremia generally have reduced cerebral function, either as a primary
problem or as a consequence of the hypernatremia itself, which results in dehydration of
neurons and brain shrinkage. In the presence of an intact thirst mechanism and preserved
capacity to obtain and ingest water, hypernatremia may not progress very far. If adequate
water is not obtained, dizziness, confusion, weakness and ultimately coma and death can
result.
 CAUSES:
Hypovolaemic (sodium Renal sodium losses
deficit with a relatively Diuretic therapy (especially osmotic
greater water deficit diuretic, or loop diuretic during
water restriction)
Glycosuria
Gastrointestinal Na losses
Colonic diarrhoea
Skin sodium losses
Excessive sweating

Euvolaemic (water Diabetes insipidus (central or

deficit alone nephrogenic)

Hypervolaemic (sodium Enteral or parenteral feeding

retention with relatively IV or oral salt administration
less water retention Chronic renal failure (during water
restriction)
TREATMENT

Allow water orally

Calculate free-water deficit: [(Na+ 140)/140] X TBW
Administer deficit over 4872 h, without decrease in plasma Na+ concentration by >10
mM/24 h
Isotonic saline for initial correction of ECF deficit, once deficit gets corrected give
hypotonic saline
DISORDERS OF POTASSIUM BALANCE

major intracellular cation

the steep concentration gradient for potassium across the cell membrane of excitable
cells plays an important part in generating the resting membrane potential and allowing
the propagation of the action potential that is crucial to normal functioning of nerve,
muscle and cardiac tissues.
CAUSES OF HYPOKALEMIA

I. Decreased intake III. Increased loss

A. Starvation A. Non renal
B. Clay ingestion 1. Gastrointestinal loss (diarrhoea)
II. Redistribution into cells 2. Integumentary loss (sweat)

A. Acid-base balance- Metabolic alkalosis B. Renal

B. Hormonal Insulin 1. Increased distal flow and distal Na+ delivery:
diuretics, osmotic diuresis, salt-wasting nephropathies
C. Anabolic state
2. Increased secretion of potassium
1.Vitamin B12 or folic acid administration (red
blood cell production)
2. Total parenteral nutrition
D. Other
1. Pseudohypokalemia
2. Hypothermia
Clinical features: Fatigue, myalgia and episodic muscle weakness
Hypotonia , paralytic ileus, abdominal distension, hypoventilation, metabolic alkalosis
ECG: flattening or inversion of T waves
Prominent U wave
ST depression and prolonged QU interval
TREATMENT

Treatment of hypokalaemia involves first determining the cause and then correcting this where possible. If the
problem is mainly one of redistribution of potassium into cells, reversal of this (for example, correction of
alkalosis) may be sufficient to restore plasma potassium without providing supplements. In most cases, however,
some form of potassium replacement will be required. This can generally be achieved with slow-release
potassium chloride tablets, but in more acute circumstances intravenous potassium chloride may be necessary.
The rate of administration depends on the severity of hypokalaemia and the presence of cardiac or
neuromuscular complications, but should generally not exceed 10 mmol of potassium per hour

Oral potchlor (KCL) is prefrerred. If i.v has to be gven then rate should not be <20mmol/hr and ECG
monitoring is a must.
HYPERKALEMIA

I. Intra- to extracellular shift: Acidosis 2.Volume depletion

II. Inadequate excretion : A. Inhibition of the renin-
angiotensin-aldosterone axis;
1. Angiotensin-converting enzyme (ACE)
inhibitors
2. Angiotensin receptor blockers (ARBs)
3 Blockade of the mineralocorticoid receptor:
spironolactone
Others:
A Drugs: nonsteroidal anti-inflammatory drugs
(NSAIDs), cyclooxygenase 2 (COX2) inhibitors, -
blockers, cyclosporine, tacrolimus
B Chronic kidney disease, advanced age
C injury, sepsis, hemolyis

B. Decreased distal delivery

1. Congestive heart failure
 Clinical Features: weakness, flaccid paralysis, hypoventilation, arrythmia, Metabolic
acidosis
ECG: TALL t-waves
In moderate hyperkalemia prolonged PR interval and QRS
Loss of P wave in severe cases, ventricular fibrillation and asystole at pot>8
TREATMENT

Treatment of hyperkalaemia depends on its severity and the rate of development. In the absence of
neuromuscular symptoms or ECG changes, reduction of potassium intake and correction of underlying
abnormalities may be sufficient. However, in acute and/or severe hyperkalaemia (plasma K > 6.57.0
mmol/L) more urgent measures must be taken
If ECG changes are present, the first step should be infusion of 10 mL 10% calcium gluconate to stabilise
conductive tissue membranes (calcium has the opposite effect to potassium on conduction of an action
potential).
Shift K into cells Inhaled 2-adrenoceptor agonist (e.g.salbutamol)
IV glucose (50 mL of 50% solution and insulin
IV sodium bicarbonate2
Remove K from body IV furosemide and normal saline3
HYPERCALCAEMIA

With normal/elevated (inappropriate) PTH levels: tertiary hyperparathyroidism, Lithium-induced

hyperparathyroidism, Familial hypocalciuric hypercalcaemia
With low (suppressed) PTH levels: Malignancy (e.g. lung, breast, renal, colonic and thyroid carcinoma,
lymphoma, multiple myeloma)
Elevated 1,25(OH)2 vitamin D (vitamin D intoxication, sarcoidosis, HIV)
Thyrotoxicosis
Pagets disease with immobilisation
Thiazide diuretics
Glucocorticoid deficiency
 Investigations: If PTH level are detectable or elevated in the presence of hypercalcaemia
then primary hyperparathyroidism is the most likely diagnosis.
Low urine calcium excretion indicates likely FHH, confirmed by testing for mutations in the
gene coding for the calcium-sensing receptor.
If PTH is low and no other cause is apparent, then malignancy with or without bony
metastases is likely
Management :Treatment of severe hypercalcaemia involves rehydration with normal saline.
Calcitonin acts rapidly and can be added for the first 2448 hrs in patients with life-
threatening hypercalcaemia. Bisphosphonates reduce serum calcium to normal within 5 days,
the effect lasting up to 4 wks.
HYPOCALCAEMIA

The most common cause of hypocalcaemia is a low serum albumin with normal ionised calcium concentration.

Clinical assessment: Tetany can occur if total serum calcium is < 2.0 mmol/L (8 mg/dL).
In children, a characteristic triad of carpopedal spasm, stridor and convulsions occurs.
Adults :tingling in the hands and feet and around the mouth.
When overt signs are lacking, latent tetany may be revealed by Trousseaus sign (inflation of a
sphygmomanometer cuff to more than the systolic BP causes carpal spasm)or Chvosteks sign (tapping over the
facial nerve produces twitching of the facial muscles).

Hypocalcaemia with hypophosphataemia (vitamin D deficiency) causes rickets in children and osteomalacia in
adults.

Management: .Injection of 20 mL of 10% calcium gluconate slowly into a vein will raise the serum calcium
concentration immediately.
DISORDERS OF ACIDBASE BALANCE

Patients with disturbances of acidbase balance may present clinically either with the effects
of tissue malfunction due to disturbed pH (such as altered cardiac and CNS function), or with
secondary changes in respiration as a response to the underlying metabolic change (e.g.
Kussmaul respiration during metabolic acidosis).
The clinical picture is often dominated by the cause of the acidbase change, such as
uncontrolled diabetes or primary lung disease.
Frequently, the acidbase disturbance only becomes evident when the venous plasma
bicarbonate concentration is noted to be abnormal, or when a full ABG analysis shows
abnormalities in the pH, PCO2 or bicarbonate.
 In metabolic disturbances, respiratory compensation is almost immediate; i.e. the
compensatory change in PCO2 is achieved soon after the onset of the metabolic
disturbance.
In respiratory disorders, on the other hand, a small initial change in bicarbonate occurs
as a result of chemical buffering of CO2, largely within red blood cells, but further
compensatory changes in bicarbonate occur via long term adjustments in acid secretory
capacity by the kidney, requiring days to weeks.
When clinically obtained acidbase parameters do not accord with the predicted
compensation shown, a mixed acid base disturbance should be suspected.
METABOLIC ACIDOSIS

Metabolic acidosis occurs when an acid other than carbonic acid (due to CO2 retention)
accumulates in the body, resulting in a fall in the plasma bicarbonate.
The pH fall that would otherwise occur is blunted by hyperventilation, resulting in a
reduced PCO2.
If the kidneys are intact (i.e. not the cause of the initial disturbance), renal excretion of
acid increases gradually over days to weeks, raising the plasma bicarbonate and hence the
pH towards normal in the new steady state.
 Causes of metabolic acidosis are classified according to the anion gap, which is the
difference between the main measured cations [Na+ + K+ ] and the main measured
cations [Cl + HCO3 ]
This is normally 1216 mmol/L but increases when an acid accumulates accompanied by
a corresponding anion.
METABOLIC ACIDOSIS WITH INCREASED ANION
GAP
Diabetic ketoacidosis (accumulation of ketones with hyperglycaemia).
Lactic acidosis (shock or liver disease).
Renal failure.
Poisoning (aspirin, methanol, ethylene glycol).
METABOLIC ACIDOSIS WITH NORMAL ANION
GAP
GI base loss (loss of HCO3 in diarrhoea, small bowel fistula, urinary diversion
procedure).
Renal tubular acidosis (urinary loss of HCO3 in proximal RTA, impaired tubular acid
secretion in distal RTA).
Therapeutic infusion or poisoning with HCl or NH4Cl.
MANAGEMENT

Identify and correct the underlying cause.

As metabolic acidosis is frequently associated with sodium and water depletion,
resuscitation with appropriate IV fluids will often be needed.
Use of IV bicarbonate in this setting is controversial.
METABOLIC ALKALOSIS

Metabolic alkalosis is characterised by an increase in the plasma bicarbonate concentration

and the plasma pH.
There is a compensatory rise in PCO2 due to hypoventilation but this is limited by the
respiratory response to hypoxia.
Clinically, apart from manifestations of the underlying cause, there may be few symptoms or
signs related to alkalosis itself.
When the rise in systemic pH is abrupt, plasma ionised calcium falls and signs of increased
neuromuscular irritability, such as tetany, may develop.
CAUSES

The causes are best classified by the accompanying disturbance of ECF volume:
Hypovolaemic metabolic alkalosis (most common pattern):
Sustained vomiting acid-rich fluid is lost from the body, hypokalaemia stimulates renal H+ excretion.
Diuretics (not potassium sparing diuretics) increase acid loss into the urine.
Normovolemic (or hypervolemic) metabolic alkalosis:
Occurs when both bicarbonate retention and volume expansion are found together:
Corticosteroid excess (Conns syndrome, Cushings syndrome, corticosteroid therapy).
Overuse of antacids
MANAGEMENT

Metabolic alkalosis associated with hypovolaemia is treated with IV fluids, specifically

isotonic sodium chloride.
Replacement of potassium helps correct the hypokalaemia and its consequences in the
kidney.
In metabolic alkalosis associated with normal or increased volume, treatment should
focus on correcting the underlying cause.
RESPIRATORY ACIDOSIS

Respiratory acidosis occurs when there is accumulation of CO2 due to type II

respiratory failure .
This results in a rise in the PCO2, with a compensatory increase in plasma bicarbonate
concentration, particularly when the disorder is of long duration and the kidney has fully
developed its capacity for increased acid excretion.
RESPIRATORY ALKALOSIS

Respiratory alkalosis develops when there is a period of hyperventilation resulting in a

reduction of PCO2 and increase in plasma pH.
If the condition is sustained, renal compensation occurs, such that tubular acid secretion
is reduced and the plasma bicarbonate falls.