Fluid & Electrolyte Imbalance

Dr Simoonga Peter
 WHERE IS THIS WATER THAT IS SO
IMPORTANT FOUND???
• Generally 60% of body
consists of fluid.
• Fluid composition varies
with age, gender &
body fat.
• Distribution in body
compartments depends
on solute content of
each compartment.
 KEY ELEMENTS/TERMS

• Osmotic Pressure: The amount of hydrostatic

pressure required to stop the flow of water by
osmosis.

• Osmolality: Number of osmotically active

particles present per kilogram of water.
Measured using osmeter
Normal plasma Osmolality = 285-292
mOsm/kg
 KEY ELEMENTS/TERMS
• Osmolarity: Number of osmotically active
particles present per litre of water.
Calculated from lab data
Osmolality =2(Na⁺) + 2(K⁺) + Urea + Glucose
mmol/L.

• The effective plasma osmolarity (EPO) or

tonicity = 2[Na+ + K+] + [Glucose] mosmol/L.

• Osmolar Gap = Osmolality - Osmolarity

 WATER BALANCE
• Water intake = water
output ≈ 2500ml
• Factors that dictate
body water
requirement
 Amount needed for
proper osmotic
concentration
 Amount needed to
replace water losses.
•
 WATER BALANCE DISORDERS
• Disturbance of fluid balance (intake≠output)

FLUID DEFICIENCY →VOLUME DEPLETION

(HYOVOLEMIA)

FLUID EXCESS → VOLUME EXCESS (OVER

HYDRATION or HYPERHYDRATION)
 DEHYDRATION
• Dehydration means loss of water from the body.
 Pure (tissue) water loss – less common
 Depletion of Na and water – more common

• Can be hypotonic, isotonic or hypertonic

• It is important to identify which of these are present in a

clinical situation so as to administer the correct
replacement fluid.

• The quality of the therapy depends in part, on the state of

the kidneys and appropriateness of fluid used for
replacement.
CLINICAL FEATURES OF DEHYDRATION
• Decreasing BP/Postural
Hypotension
• Dry skin and mucous
membranes
• Sunken eyes and fontanels
• Circulatory failure – cold
and mottling of extremities
• Loss of skin turgor and
elasticity
• Delayed capillary refill.
• Altered LOC – lethargy,
confusion and coma.
• Increased thirst
 Body fluid compartment assessment
and fluid choice in dehydration
• Plasma Volume
 Pulse rate
 BP
 JVP
 CVP
• Interstitial Volume
 Edema
• Intracellular Volume
 Not so easy to assess clinically

Always remember to treat the

underlying cause of
dehydration
Disorders of Sodium Balance
 Regulation of sodium balance
• Kidney plays a predominant role.
• Renin -angiotensin -Aldosterone mechanism
effective circulating volume is the major stimulus
• Atrial Natriuretic peptide
increase in ECF, increase BP – stimulus
• Disorders can either be:
Decreased Na levels – hyponatremia
Increases Na levels – hypernatremia
 Hyponatremia
• Abnormally low serum sodium <136 mEq/L
• Usually accompanied by a decrease in plasma
osmolality.
• It is a very common disorder, occurring in up to
22% of hospitalized patients.
• Subdivided diagnostically into three groups,
depending on clinical history and volume status:
Hypovolemic
Euvolemic
hypervolemic
 CLINICAL FEATURES
• Symptoms depends upon the severity of
hyponatremia and the rate at which the sodium
concentration is lowered.
• Acute – develops in 48 hours or less. Subjected to
more severe degrees of cerebral edema
• Chronic- develops over 48 hours and brain
edema is less and is well tolerated.
• The signs and symptoms are due to increase in
volume of ICF and increase in volume of brain
cells rather than decrease in serum sodium.
 SIGNS AND SYMPTOMS OF
HYPONATREMIA
Central Nervous System
• Mild – Apathy ,Headache, Lethargy
• Moderate- Disorientation, Psychosis, Agitation, Ataxia
Confusion
• Severe-Stupor, Coma, Pseudobulbar palsy Tentorial
herniation , Cheyne-Stokes respiration, Death
Gastrointestinal System
• Anorexia, Nausea ,Vomiting
Musculoskeletal System
• Cramps, Diminished deep tendon reflexes
 DIAGNOSIS
• History and physical • Laboratory tests-
examination- to identify Provide important
hypovolemic hyponatremia initial clue in the
(diarrhoea, vomitting, burns) differential diagnosis
1. Plasma Osmolality
2. Urine Osmolality
• Radiologic imaging - to
3. Urine Sodium conc
assess whether patients have
4. Uric acid level
a pulmonary or CNS cause for
5. Serum potassium
hyponatremia. CT scanning of
6. Serum glucose
the thorax should be
considered in patients at high
risk small cell carcinoma
 TREATMENT
• Treatment needs to be individualized considering etiology,
rate of development, severity and clinical signs and symptoms

GOALS of THERAPY:
1. To raise the plasma sodium concentration at a slow rate
2. To replace sodium or potassium deficit or both
3. To correct underlying etiology

BASIC PRINCIPLES OF CORRECTION:

• Rapid correction is indicated in acute (<48hours) symptomatic
or severe hyponatremia.(serum Na <120 mEq/L)
• In chronic cases patients are at little risk, however rapid
correction can lead to demylination. Use slower acting
therapies like water restriction
 Hypernatremia
• Plasma Na+ > 145 mEq / L
• Total body Na content is high with respect to
water
• Common cause – excessive water loss - Cells
dehydrate
• Considerably less common than
hyponatremia.
• Hypernatremia nonetheless is associated with
mortality rates as high as 40–60%.
 CLINICAL FEATURES
• The symptoms of hypernatremia are predominantly
neurologic.
• Altered mental status is the most common
manifestation, ranging from mild confusion and
lethargy to deep coma.
• The sudden shrinkage of brain cells in acute
hypernatremia may lead to parenchymal or
subarachnoid haemorrhages and/or subdural
hematomas; encountered primarily in paediatric and
neonatal patients
• Osmotic damage to muscle membranes also can lead
to hypernatremic rhabdomyolysis
 DIAGNOSIS
HISTORY AND PHYSICAL EXAMINATION:
• The history should focus on the presence or absence of thirst,
polyuria, and/or an extrarenal source for water loss, such as
diarrhoea
• The physical examination should include a detailed neurologic exam
and an assessment of the ECFV; patients may be hypovolemic, with
reduced JVP and orthostasis
• Accurate documentation of daily fluid intake and daily urine output
LAB INVESTIGATIONS:
• Measurement of serum and urine osmolality in addition to urine
electrolytes
 The appropriate response to hypernatremia and a serum osmolality
>295 mosmol/kg is an increase in circulating AVP and the excretion
of low volumes (<500 mL/d) of maximally concentrated urine, i.e.,
urine with osmolality >800 mosmol/kg
Diagnostic Approach
 MANAGEMENT
A two-pronged approach:
 Addressing the underlying cause
 Correcting the prevailing hypertonicity

RATE OF CORRECTION:
 Hypernatremia that developed over a period of
hours (accidental loading)
Rapid correction improves prognosis without cerebral
edema
Reducing Na+ by 1 mmol/L/hr appropriate

 Hypernatremia of prolonged or unknown duration

a slow pace of correction prudent
maximum rate 0.5 mmol/L/hr to prevent cerebral edema
A targeted fall in Na+ of 10 mmol/L/24 hr
Disorders of potassium Balance
 POTASSIUM BALANCE
• Potassium is the major intracellular cation.
• ECF [K⁺] is 3.5-5.0 mmol/L, whereas ICF is about 150
mmol/L.
• Total dietary intake of K+ is 40-120 mmol/day.
• 90% of it is absorbed in GI tract
• Sudden rise in plasma K+ is prevented by :
 Shift of K+ into the cell by insulin.
 Excess K+ excreted in urine.
• Renal excretion is the major route for elimination of
dietary and other sources of K+ excess.
 HYPOKALEMIA

• Serum K+ < 3.5mEq/L

• Beware if Pt Diabetic
insuline pushes K+ into cells
in DKA H+ replaces K+
Common Causes
 EFFECT OF HYPOKALEMIA AND
THEIR CLINICAL FEATURES

• Clinical features of K⁺ depletion vary greatly

between individual patients

• Severity depends on degree of hypokalemia.

• Symptoms seldom occur unless the plasma

[K⁺] is <3 mmol/L.
 EFFECT OF HYPOKALEMIA AND
THEIR CLINICAL FEATURES
Renal
Neuro muscular
a. Skeletal muscle weakness : - Poly urea (Nephrogenic) diabetic
- fatigue insipidus.
- Myalgia - Increased ammonia production.
- Muscular weakness in lower
- Increased bicarbonate
extremities.
reabsorption.
b. Smooth muscles – paralytic ileus.
3. Hormonal
c. Respiratory muscle weakness –
hypoventilation. - Decreased insulin secretion.
d. Tetany - Decreased aldosterone
e. Rhabdomyolysis secretion.
- Insulin resistance.
ECG FEATURES OF HYPOKALEMIA
• ECG changes of hypokalemia are due to delayed ventricular repolarisation
and do not correlate well with plasma potassium concentration.

Early changes include

1. Flattening or inversion of the T wave
2. Prominent U wave
3. ST segment depression
4. Prolonged Q.U. interval

Severe potassium depletion may result in

1. Prolonged PR interval
2. Decreased voltage and widening of the QRS complex
3. An increased risk of ventricular arrhythmias especially in patients with
myocardial ischemia or left ventricular hypertrophy.
 TREATMENT
• The therapeutic goals are to correct the potassium
deficit and to minimize ongoing losses.

• It is generally safer to correct hypokalemia via oral

route.

• In severe hypokalemia or those unable to take

anything by mouth intra venous replacement
therapy with Kcl may be required.

• The rate of infusion should not exceed 20 mmol/hr

unless paralysis or malignant ventricular arrhythmia
are present.
 HYPERKALEMIA
• Defined as a plasma potassium >5.0 mmol/L
• Occurs commonly as a result of either potassium
release from cells or decreased renal loss.
• Iatrogenic hyperkalemia may result from over zealous
parenteral potassium replacement or in a patients
with renal insufficiency.
• Beware:
Diabetics – Insulin deficiency pushes K+ outside cells.
Pseudohyperkalemia
 CLINICAL FEATURES
• Hyperkalemia is often asymptomatic until plasma [K+]
is >6.5 to 7.0 mEq/L and may lead to fatal cardiac
arrhythmia hence it is called a silent Killer.
• Vague muscular weakness is usually first symptom of
hyperkalemia.
• Severe hyperkalemia can lead to hyporeflexia, gradual
paralysis in the sequence:
Leg → Trunk → Arms → Face → Respiratory
• Paralysis usually spares the muscles supplied by cranial
nerves and patients remain alert and apprehensive
until cardiac arrest and death occurs.
 CLINICAL FEATURES
• The most serious effect of hyperkalemia is cardiac toxicity, which
does not correlate well with plasma [K⁺].
• Earliest ECG changes – Peaked T wave.

Serum [K+] ECG findings

6-7 mEq/L ● Tall peaked T waves
7-8 mEq/L ● Loss of P waves and progressive
widening of QRS complex.
8-10 mEq/L ● QRS merges with T waves forming sine waves
9 mEq/L ● Antrioventricular dissociation, ventricular
tachycardia or fibrilation or asystole.
 TREATMENT
• The need to treat hyperkalemia, how urgently and how aggressively,
depends on degree of clinical status.

EMERGENCY TREATMENT.
• Potentially fatal hyperkalemia (serum potassium >7.5mmol/L).
• Profound weakness, absence of P wave, QRS widening or ventricular
arrhythmia on ECG needs urgent treatment.

Principle :
A) antagonism of membrane effects hyperkalemia – Inj.Calcium gluconate.
B) Potasium movements into the cells:
 inj. Insulin and glucose.
 Inj. sodium bicarbonate.
 beta 2 adernergic agonsit e.g. salbutamol
C) Removal of potassium from the body:
 Loop or thiazide diuretics
 Cation exchange resin (Keyxalate)
Disorders of chloride Balance
 Hyperchloremia
• Causes:
 Dehydration
 Cushings syndrome
 Severe diarrhea - HCO₃- loss & comp retention of Cl-
 Renal tubular acidosis

• Often presents as hyperchloremic acidemia with

paradoxical alkaluria

• Rx: stop NaCl & replace with hypotonic crystalloids