WATER AND ELECTROLYTE BALANCE in normal and abnorm'

WATER AND ELECTROLYTE
BALANCE & IMBALANCE
DR. IVVALA ANAND SHAKER
PROFESSOR
DEPARTMENT OF BIOCHEMISTRY

FLUID AND
ELECTROLYTE
BALANCE &
IMBALANCE

The learner will be able to:
• Outline the body water compartments and their
composition.
• State the water balance in terms of input and output
• Define osmolality of extracellular fluid
• Compare the electrolyte composition of body fluids
• Explain the regulation of sodium and water balance by
Renin-Angiotensin system
• Classify the derangements in fluid and electrolyte balance
in terms of tonicity
• List the causes and features of Isotonic/ hypotonic/
hypertonic contraction and expansion of ECF
Specific Learning Objectives

The learner will be able to:
• Describe the distribution and regulation of intra and
extracellular cations (Potassium, magnesium and sodium)
• Describe the distribution and regulation of intra- and extracellular
anions (Phosphate and chloride)
• Explain the causes and features of derangements in electrolyte
composition
• Assessment of fluid and electrolyte balance in routine clinical
practice and interpretation of laboratory data
• Mention the composition of body fluids like milk, CSF and
amniotic fluid
• Explain the nutritional importance of milk
Specific Learning Objectives

INTRODUCTION
Fluid And Electrolyte Plays Vital Role In Maintaining
Homeostasis With In The Body.
Our Body Consists Of Two Type Of Fluid Intracellular
And Extracellular Fluid.
Fluid Is A Major Component Of Our Body It Serves A Vital
Role In Our Health, And In Normal Cellular Function By
Serving As A Medium For Metabolic Reactions With In The
Cell.
It Also Is The Transporter And Waste Products , A
Lubricant , An Insulator And A Shock Absorber

The body water compartments.
Water Balance

FUNCTIONS OF EXTRACELLULAR FLUID
Transport nutrients, electrolytes , oxygen to
cells andwaste products for excretion.
Hydrolyzes food for digestive process.
Regulates heat.
Lubricates and cushions joints and membranes .

MECHANISM CONTROLLING FLUID AND
ELECTROLYTE MOVEMENT
DIFFUSION: Diffusion is the movement of molecules from
an area of higher concentration to an area of lower
concentration .
FACILITATED DIFFUSION: In facilitated diffusion , one
molecule moves from an area of higher concentration
to an area of lower concentration with the help of some
carrier. E.g., glucose is transported into the cell with the
help of insulin as a carrier molecule.

MECHANISM CONTROLLING FLUID AND
ELECTROLYTE MOVEMENT
ACTIVE TRANSPORT: Active transport is a process in which
molecules are moved from an area of lower
concentration to an area of higher concentration and
they require external energy for movement against the
concentration gradient.
OSMOSIS: Osmosis is the flow of water between two
compartments separated by a membrane permeable to
water but not to solute. Osmosis requires no outside
energy for movement. Water moves from an area of low
solute concentration to an area of higher
concentration from the compartment that is more
diluted to side that is more concentrated.

ISOTONIC SOLUTIONS
Same solute concentration as blood.
If injected into vein, no net movement of
fluid.
Example: 0.9% NS Solution

HYPERTONIC SOLUTIONS
Higher solute concentration than RBC
If injected into vein, Fluid moves from
interstitial space INTO veins.
Eg: 5% Dextrose

AFFECTS OF HYPERTONIC SOLUTIONON
CELL
Cel
• The (solute)outside the cell is
higher thaninside.
• Water moves from low (solute)
to high(solute).
• The cellshrinks.
Cel
Shrunken
Cel
Shrunken
Cel

HYPOTONIC
SOLUTIONS
Lower solute concentration than
blood
If injected into vein, fluid moves
OUT of veins into tissues.

CE
L
AFFECTS OF
HYPOTONIC
SOLUTIONON
L
Cel
Cel
RupturedCel

Osmolarity- is concentration of all solutes per litre of
solution. (to pull water to it)
Osmolality- controls water movement & distribution
between and within body fluid compartments by
regulating concentration of fluid in each compartment. It
is determined by no. of dissolved particles per kg water.
(Na is main electrolyte)
Inc. Na(Hyperosmolality)
Dec. Na (Hypoosmolality)

TYPES OF FLUIDIMBALANCES
TYPES
FluidVolume
Excess
Extracellular
Fluid Volume
FluidVolume
Deficit
Excess (ECFVE)
Intracellular
FluidVolume
Excess
Extracellular
FluidVolume
Deficit
Intracellular
FluidVolume
Deficit
Third Space FluidShift

Intake per day Output per day
Water in
food
1250 ml Urine 1500 ml
Oxidation of
food
300 ml Skin 500 ml
Drinking
water
1200 ml Lungs 700 ml
Feces 50 ml
Total 2750 ml 2750 ml
Water Balance in the Body

The major factors controlling the intake are thirst and the
rate of metabolism.
The thirst center is stimulated by an
increase in the osmolality of blood, leading to increased
intake.
The renal function is the major factor controlling the rate
of output. The rate of loss through skin is influenced by the
weather, the loss being more in hot climate (perspiration)
and less in cold climate. Loss of water through skin is
increased to 13% for each degree rise in centigrade in body
temperature during fever.

GI secretion Volume
in L
Sodium
mmol/L
Potassium
mmol/L
Chloride or
bicarbonate
mmol/L
Saliva 1.5 40 20 Chloride 40
Gastric juice 1.5 70–120 10 Chloride 100
Bile 1 140 5 Chloride 100
Pancreatic
juice
1.5–2 140 5 Bicarbonate
75–90
Intestinal
secretion
12 100-120 5-10 Bicarbonate
105
Gastrointestinal Secretions and their
Electrolyte Composition

Gamblegrams Showing Composition of Fluid Compartments

Solutes Plasma
mEq/L
Interstitial
fluid (mEq/L)
Intracellular
fluid (mEq/L)
Cations: 146 12
Sodium 140 5 160
Potassium 4 3 -
Calcium 5 1 34
Magnesium 1.5
Anions:
Chloride 105 117 2
Bicarbonate 24 27 10
Sulphate 1 1 -
Phosphate 2 2 140
Protein 15 7 54
Other anions 13 1 -
Electrolyte Concentration of body Fluid
Compartments

Since osmolality is dependent on the number of
solute particles, the major determinant factor is the
sodium.
Therefore sodium and water balance are dependent
on each other and cannot be considered separately.
It is maintained by the kidney which excretes either
water or solute as the case may be.

• Osmolarity
No. of moles/ mmoles of solute per liter of
solution
• Osmolality
No. of moles/ mmoles of solute per Kgm of
solvent Mainly determined by electrolytes

Osmolality
• Plasma – mainly contributed by Na
• ICF – mainly contributed by K
• Plasma osmolality
= 2 x [Na] + 2 x [K] + urea + glucose
• N value = 285 –295 m osmoles / kg

Solute Osmolality in mmol/kg
Sodium with anions 270 92%
Potassium with anions 7
Calcium with anions 3
Magnesium with anions 1
Urea 5
Glucose 5
Proteins 1 8%
292
Osmolality of Plasma

The difference in measured osmolality and
calculated osmolality may increase causing
an Osmolar Gap,
when abnormal compounds like ethanol,
mannitol, neutral and cationic amino acids etc
are present.

It is the term used for those extracellular solutes that
determine water movement across the cell membrane.
Permeable solutes such as urea and alcohol enter into the cell
and achieve osmotic equilibrium. Although there is increase
in osmolality, there is no shift in water.
On the other hand, if impermeable solutes like glucose,
mannitol, etc. are present in ECF, water shifts from ICF to
ECF and extracellular osmolality is increased.
So, for every 100 mg/dl increase in glucose, 1.5 mmol/L of
sodium is reduced (dilutional hyponatremia). Hence, the
plasma sodium is a reliable index of total and effective
osmolality in the normal and clinical situations.
Effective Osmolality

Crystalloids and water can easily diffuse across
membranes,
but an osmotic gradient is provided by the non-
diffusible colloidal (protein) particles.
The colloid osmotic pressure exerted by proteins is
the major factor which maintains the intracellular and
intravascular fluid compartments.
If this gradient is reduced, the fluid will extravasate
and accumulate in the interstitial space leading to
edema.

Total Osmotic Pressure : 5000 mm Hg
Effective Osmotic pressure: 25 mmHg
80% by albumin; 20% globulins

1. At equilibrium, the osmolality of extracellular
fluid (ECF) and intracellular fluid (ICF) are
identical.
2. Solute content of ICF is constant.
3. Sodium is retained only in the ECF.
4. Total body solute divided by total body water
gives the body fluid osmolality.
5. Total intracellular solute divided by plasma
osmolality will be equal to the intracellular
volume.
Summary of ECF and ICF

Hormones Regulating Water
Balance
•Aldosterone
•Renin – Angiotensin system
•ADH
•ANP

Aldosterone
• Mineralocorticoid
• From Zona glomerulosa of renal
cortex
• Causes Na+ reabsorption from renal
tubules
• K+ & H+ lost in urine

ADH (Vasopressin)
• From posterior Pituitary
• High plasma osmolality  stimulation of
Osmoreceptors
of hypothalamus
• Causes release of ADH
• Increases water reabsorption by DCT & CD of
kidneys
 1% rise in osmolality triggers ADH production,
which increases renal reabsorption of H2O
 Response also affected by volume loss (> 5%)

Mechanical ventilation,
drugs, anesthesia,pain

RENIN-ANGIOTENSIN-ALDOSTERONE.

Renin and Rennin are Different
Kidney secretes renin; it is involved in
fluid balance and hypertension.
Rennin is a proteolytic enzyme seen in
gastric juice, especially in children.

Pathway of Angiotensin Production.

Clinical significance of angiotensin converting enzyme
(ACE) inhibitors and its antagonists
Angiotensin converting enzyme (ACE) is a glycoprotein
present in the lung. ACE-inhibitors are useful in treating
edema and chronic congestive cardiac failure. Various
peptide analogues of angiotensin II (saralasin) and
antagonists of the converting enzyme (captopril) are useful
to treat renin-dependent hypertension. Angiotensin I is
inactive; II and III are active.

NATRIURETIC PEPTIDES
 Polypeptide hormone from rt. Atrium
 Stimulated by increased cardiac stretch
 Increases sodium loss and, as a result, increases
water excretion
 Decreases aldosterone production
 B-type (BNP) available in prescription form to
treat congestive heart failure

THIRST
 Most important factor in maintaining normal fluid
balance
 1% increase in osmolality causes thirst
 5% decrease in volume stimulates thirst
 Lack of access to water or poor thirst is the major
cause of hypernatremia
 Thirst contributes to hyponatremia in fluid loss,
edematous states
(triggered by low intravascular volume)

Decreased Volume of ECF Increased Osmolality
ofECF
Stimulates osmoreceptors in
hypothalmic thirst centre
Decreasedsaliva
secretion
Drymouth
Sensation ofthirst
Water abosrbed from
GIT
Increased amount of ECF Deccreased
Osmolality ofECF
Fig. Factors stimulating water intake through the thirst mechanism
HYPOTHALAMIC REGULATION
/THIRST

1. Hypo-osmolatiy and hyponatremia go hand in
hand.
2. Hypo-osmolality causes swelling of cells and
hyper-osmolality causes dehydration of cells.
3. Dilutional hyponatremia due to glucose or
mannitol increases the effects of hyperosmolity.
4. Fatigue and muscle cramps are the common
symptoms of electrolyte depletion.
Salient Features of Electrolyte Imbalance

1. Hypo-osmolality and hyponatremia go hand in hand.
2. Hypo-osmolality causes swelling of cells and hyper-osmolality
causes cell dehydration.
3. Hyponatremia of extracellular fluid causes symptoms when
associated with hyperkalemia.
4. Dilutional hyponatremia due to glucose or mannitol increases
the effects of hyperosmolality.
5. Fatigue and muscle cramps are the common symptoms of
electrolyte depletion.
6. Hypo-osmolality of gastrointestinal cells cause nausea, vomiting
and paralytic ileus.
Salient Features of Electrolyte Imbalance,
Especially in Cases of Patients on Fluids

1. Maintenance of intake-output chart, in cases of patients on IV
fluids. The insensible loss of water is high in febrile patients.
2. Measurement of serum electrolytes (sodium, potassium, chloride
and bicarbonate). This will give an idea of the excess, depletion
or redistribution.
3. Measurement of hematocrit value to see if there is
hemoconcentration or dilution.
4. Measurement of urinary excretion of electrolytes, especially
sodium and chloride.
Assessment of Sodium and Water Balance

DEHYDRATION
• Due to loss of water alone
• Due to loss of water & Na
3 types
• Isotonic contraction
• Hypotonic
• Hypertonic

Isotonic Contraction
• Cause – loss of fluid isotonic with plasma
- Loss of GI fluid – small intestinal
fistula, obstruction, paralytic ileus
- Recovery phase of renal failure
• Hypovolemia -  ed renal blood flow
- uremia, oliguria
Plasma Na normal
Hypotension in severe cases

Hypotonic Contraction
• Due to Na depletion
• Causes
- Infusion of large amounts of IV dextrose
- Deficiency of Aldosterone
• Hypo osmolality inhibits ADH – excessive
water loss – plasma Na & osmolality
restored – hypo osmolar contraction

• Water depletion without electrolyte loss
• Causes –
- Diarrhoea, vomiting
- Diabetes Insipidus
•  ed Na in plasma -  ed osmolality
•  ed renal blood flow – aldosterone secretion
– further Na retention & hypertension
Hypotonic Contraction

Treatment
• Oral supply of water
• IV administration of 5% glucose
• If electrolytes also lost, oral
supplementation or IV saline
infusion

Overhydration (Water
Intoxication)
•Due to retention of water
- Isotonic expansion
- Hypotonic expansion
- Hypertonic expansion

Isotonic Expansion
• Water & Na retention
• Causes
- Secondary to hypertension, cardiac
failure
- Secondary hyperaldosteronism
- Hypo albuminemia due to
nephrotic syndrome, protein
malnutrition

Hypotonic Expansion
• Predominant water excess
• Causes –
- Glomerular dysfunction
- Increased ADH
• High ECF volume inhibits Aldosterone –
Hyponatremia & low osmolality persists

• Retention of Na
• High plasma osmolality – ADH –
osmolality restored
• High aldosterone causes Na retention
• Associated Hypokalemia – Metabolic
alkalosis
• Cerebral cellular overhydration –
coma, death
Hypertonic Expansion

Abnormality Biochemical featuresOsmolality Hematocrit Plasma sodium
Expansion of ECF
Isotonic Retention of Na+,
water
Normal Low Normal
Hypotonic Relative water excessDecreased Low High
Hypertonic Relative sodium
excess
Increased Low High
Contraction of ECF
Isotonic Loss of Na+ and
water
Normal High Normal
Hypotonic Relative loss of Na+ Decreased High Low
Hypertonic Relative loss of
water
Increased High High
Disturbances of Fluid Volume

Factor Acting through Effect
Extracellular
Osmolality
Thirst and ADH water intake;
reabsorption of
water from kidney
Hypovolemia Stimulation of thirst and
ADH
retention of
Water
-do- Stimulates Aldosterone retention of
Sodium
Expansion of ECF Inhibits Aldosterone ¯ reabsorption
of sodium
Hypo-osmolality Inhibits ADH Secretion ¯ reabsorption
of water
Control of Sodium and Water

Laboratory Tests of Fluid and Electrolyte Status
Serum
Sodium
Potassium
Chloride
Osmolality (freezing pt depress)
Urea, Creatinine
Urine electrolytes
Sodium excretion
Potassium excretion
Hematocrit

Urine Electrolytes
 Useful for determining cause of
electrolyte disorder
 Must interpret in light of volume status,
serum K+ of patient
 Random urine usually adequate by
calculating fractional excretion or TTKG

 In extrarenal sodium loss, > 99.5% reabsorbed
 With tubular damage, diuretics, adrenal
insufficiency,
volume overload, FENa increases, often > 5%
Sodium Excretion
x 100
PNa * UCr
UNa * PCr
FENa =

 In extrarenal potassium loss, maximum absorbed
is ~ 85-90%
 Potassium losses best described as trans-tubular K+
gradient (TTKG)
Potassium Excretion
PK * UOsm
UK * POsm
TTKG =
 TTKG > 8 = potassium loss,
< 2 = potassium retention

SODIUM
Sodium regulates the ECF volume. Total body sodium
is about 4,000 mEq. About 50% of it is in bones, 40%
in ECF and 10% in soft tissues. Sodium is the major
cation of ECF.
Sodium pump is operating in all the cells, so as to
keep sodium extracellular. This mechanism is ATP
dependent. Sodium (as sodium bicarbonate) is also
important in the regulation of acid-base balance.
Normal level of Na+ in plasma is 136–145 mEq/L and
in cells 12 mEq/L.

1. Cushing’s disease
2. Prolonged cortisone therapy
3. In pregnancy, steroid hormones cause sodium retention
4. In dehydration, when water is predominantly lost, blood volume
is decreased with apparent increased concentration of sodium
5. Exchange transfusion with stored blood
6. Primary hyperaldosteronism
7. Elderly patients with poor water intake, and inability to express thirst
8. Excessive intake of salt
9. Drugs:
Ampicillin
Tetracycline
Anabolic steroids
Oral contraceptives
Loop diuretics
Osmotic diuretics
Causes of Hypernatremia

Thirstmechanismis
stimulated
Increasetheintakeof
water

CLINICALMANIFESTATIONS
NEUROLOGICAL MANIFESTATIONS:
Lethargy, weakness
Irritability
Seizures, coma and death
Altered mental status
Decreased level of consciousness
Muscle twitching
Dry and sticky mucous membrane

ASSESSMENT
Heart rate and blood pressure.
Pulmonary edema.
Extreme thirst.
Decreased urine output.
Dry and flushed skin.
Dry and sticky tongue.
Skeletal muscle weakness.

1. Vomiting
2. Diarrhea
3. Burns
4. Addison’s disease (adrenalin sufficiency)
5. Renal tubular acidosis, reabsorption of sodium defective.
6. Chronic renal failure, nephritic syndrome
7. Congestive cardiac failure
8. Hyperglycemia and ketoacidosis
9. Excess non-electrolyte (glucose) IV infusion
10. Syndrome of inappropriate antidiuretic hormone and defective antidiuretic
hormone secretion
11. Pseudo- or dilutional hyponatremia, hyperproteinemia
12. Drugs:
Angiotensin converting enzyme inhibitors
Nonsteroidal anti-inflammatory drugs
Vasopressin and oxytocin
Chlorpropamide
Causes of Hyponatremia

Severe hyperlipidemia and
paraproteinemia can lead to low
measured serum sodium levels with
normal osmolality since
plasma water fraction falls. This
pseudohyponatremia is seen when
sodium is measured by flame
photometry, but not with ion selective
electrode.
Normotonic Hyponatremia:

Treatment of hyponatremia depends on cause,
duration and severity.
In acute hyponatremia, rapid correction is possible;
but in chronic cases too rapid correction may
increase mortality by neurological complications.
Effects of administered sodium should be closely
monitored, but only after allowing sufficient time for
distribution of sodium, a minimum of 4–6 hours.
Water restriction, increased salt intake, furosemide
and anti-ADH drugs are the basis of treatment for
hyponatremia.

1. Hyponatremia (<135 mmol/L)
2. Decreased osmolality (<270 mosm/kg)
3. Urine sodium >20 mmol/L
4. Urine osmolality >100 mosm/kg
Diagnostic Criteria for Syndrome of
Inappropriate Antidiuretic Hormone
Secretion

P
A
THOPHYSIOLOGY
Etiological Factors
As ECF concentration of Na Dec.
Na conc. Gradient (diff.) b/w ECF& ICF Dec.
Osmolality (Hypo- osmolality)
Osmosis (Water shift from ECF to ICF)
Intracellular Edema (Cellular Swelling)
Less Na. present to move across excitable membrane

Decreased Serum Osmolality
Delayed membrane depolarisation
Hyponatremia
Further Electrolyte imbalances(K, Ca, Cl)
Uncorrected Hypovolemic
Hyponatremia
Uncorrected Hypervolemic
Hyponatremia
Shock ECF volume excess
Convulsions & Coma Edema

Total body potassium(K+) is about 3500 mEq, out of which
75% is in skeletal muscle. Potassium is the major
intracellular cation, and maintains intracellular osmotic
pressure.
The depolarization and contraction of heart require
potassium. During transmission of nerve impulses, there is
sodium influx and potassium efflux; with depolarization.
After the nerve transmission, these changes are reversed.
The intracellular concentration gradient is maintained by the
Na+- K+ ATPase pump.
POTASSIUM

Requirement
Potassium requirement is 3–4 g per day.
Sources
Sources rich in potassium, but low in
sodium are banana, orange, apple,
pineapple, almond, dates, beans, yam and
potato. Tender coconut water is a very
good source of potassium.

Hyperkalemia is characterised by flaccid
paralysis, bradycardia and cardiac arrest,
ventricular arrythmia and ventricular
fibrillation..
ECG shows elevated T wave, widening of
QRS complex and lengthening of PR interval.
Hyperkalemia

Hyperkalemia
 First exclude artifactual hyperkalemia:
 Hemolysis
 Delayed separation (if refrigerated)
 EDTA contamination
 Fist clenching/relaxing during draw
 True hyperkalemia usually due to:
 Decreased excretion (renal insufficiency,
hypoaldosteronism)
 Increased intake
 Shift of potassium out of cells

Hyperkalemia
 Medications that cause hyperkalemia usually
inhibit renin/ aldosterone system:
 Renin production: NSAIDS, -blockers
 ACE inhibitors
 AGII-receptor blockers
 Heparin (its preservative, chlorbutanol,
inhibits aldosterone production)
 Potassium-sparing diuretics

Release From Cells
 Occasional cause of hyperkalemia
 Most commonly due to acidosis, insulin
deficiency
 Less commonly due to cell lysis (hemolytic
anemia, rhabdomyolysis, tumor lysis);
usually requires decreased renal
excretion as well before hyperkalemia
develops

1. Decreased renal excretion of potassium
Obstruction of urinary tract
Renal failure
Deficient aldosterone (Addison’s)
Severe volume depletion (heart failure)
2. Entry of potassium to extracellular space
Increased hemolysis
Tissue necrosis, burns
Tumor lysis after chemotherapy
Rhabdomyolysis, crush injury
Excess potassium supplementation
Malignant hypertension
Causes of Hyperkalemia

3. Redistribution of potassium to extracellular
Metabolic acidosis
Insulin deficiency (diabetes mellitus)
Tissue hypoxia
4. Transmembrane shift
5. Pseudohyperkalemia
Factitious (K+ leaches out)
Improper blood collection (hemolysis)
Thrombocytosis (>400 million/mL)
Leukocytosis (>11 million/mL)
6. Hyperkalemic periodic paralysis
7. Drugs
Spiranolactone, ACE inhibitors, Beta blockers Cyclosporine,
Digoxin
Causes of Hyperkalemia

Hypokalemia
 True hypokalemia usually due to:
 Increased excretion
 Decreased intake
 Shift of potassium into cells
 Laboratory tests of limited use in
determining cause; TTKG > 10 confirms
increased renal excretion as pathogenetic

Plasma potassium level is below 3 mmol/L. A value
less than 3.5 mmol/L is to be viewed with caution.
Mortality and morbidity are high.
Signs and symptoms: muscular weakness, fatigue,
muscle cramps, hypotension, decreased reflexes,
palpitation, cardiac arrythmias and cardiac arrest.
ECG waves are flattened, T wave is inverted, ST
segment is lowered with AV block.
This may be corrected by oral feeding of orange
juice.
Hypokalemia

1. Increased renal excretion
Cushing’s syndrome
Hyperaldosteronism
Hyper reninism, renal artery stenosis
Hypomagnesemia
Renal tubular acidosis
Adrenogenital syndrome
17 alpha hydroxylase deficiency
11 beta hydroxylase deficiency
2. Shift or redistribution of potassium
Alkalosis
Insulin therapy
Thyrotoxic periodic paralysis
Hypokalemic periodic paralysis
Causes of Hypokalemia

3. Gastrointestinal loss
Diarrhea, vomiting, aspiration
Deficient intake or low potassium diet
Malabsorption
Pyloric obstruction
4. Intravenous saline infusion in excess
5. Drugs:
Insulin
Salbutamide
Osmotic diuretics
Thiazides, acetazolamide
Corticosteroids
Causes of Hypokalemia

1. Cardiac diseases
2. Administration of drugs such as diuretics, ACE
inhibitors,
NSAIDs
3. Diabetic ketoacidosis
4. Receiving large volume of I.V. fluids
5. Fluid loss (burns, total parenteral nutrition, diarrhea)
6. Renal impairment
7. Weakness of unknown etiology
When Potassium level should be checked?

1. Serum potassium estimation
2. Urine potassium: Low value (<20 mmol/L) is seen in
poor intake, GIT loss or transmembrane shift. High (>40 mol/L)
is seen in renal diseases.
3. Sodium and osmolality of spot urine: Low sodium
(<20 mmol/L) and high potassium indicate secondary
hyperaldosteronism. If urine osmolality is low (30–600) and a
value of urinary potassium of 60 mmol/L indicate renal loss. On
the other hand if urine osmolality is high (1,200), the same
value of potassium excreted in urine indicates low renal
excretion around 15 mmol/L.
4. ECG in all cases
5. Special tests: Aldosterone, plasma renin, cortisol and 17
hydroxyprogesterone.
Laboratory Evaluations for Potassium Abnormalities

Aim is to stop the loss and evaluation at frequent intervals.
Supplement adequate potassium (200 to 400 mmol for
every 1 mmol fall in serum potassium). In acute cases,
intravenous supplementation may be given; but only in
small doses (not more than 10 mmol/h). Serum potassium
should be checked every hour throughout the therapy. If
Magnesium is low, supplement it. Correct alkalosis. Even
after normal level is reached, daily potassium assay for
several days is to be continued.
Treatment of Hypokalemia

Intake, output and metabolism of sodium and chloride
(Cl–) run in parallel. The homeostasis of Na+, K+ and Cl– are
inter-related. Chloride is important in the formation of
hydrochloric acid in gastric juice.
Chloride ions are also involved in chloride shift.
Chloride concentration in plasma is 96–106 mEq/L. Chloride
concentration in CSF is higher than any other body fluids.
Since CSF protein content is low, Cl– is increased to maintain
Donnan membrane equilibrium. Excretion of Cl– is through
urine, and is parallel to Na+. Renal threshold for Cl– is about
110 mEq/L. Daily excretion of Cl– is about 5–8 g/day.
CHLORIDE

1. Dehydration
2. Cushing's syndrome. Mineralocorticoids
cause increased reabsorption from kidney
tubules.
3. Severe diarrhea leads to loss of bicarbonate
and compensatory retention of chloride.
4. Renal tubular acidosis.
Hyperchloremia is seen in

1. Excessive vomiting. HCl is lost, so plasma Cl—
is lowered.
There will be compensatory increase in plasma
bicarbonate. This is called hypochloremic alkalosis.
2. Excessive sweating.
3. In Addison's disease, aldosterone is diminished,
renal tubular reabsorption of Cl— is decreased,
and more Cl— is excreted.
Causes for Hypochloremia

The cystic fibrosis transmembrane conductance
receptor
(CFTR) chloride conducting channel is involved in
cystic
fibrosis. In cystic fibrosis, a point mutation in the
CFTR gene results in defective chloride transport.
So water moves out from lungs and pancreas. This
is responsible for the production of abnormally
thick mucus. This will lead to infection and
progressive damage and death at a young age.
Chloride Channels

Magnesium (Mg++) is the fourth most abundant cation in
the
body and second most prevalent intracellular cation.
Magnesium is mainly seen in ICF. Total body magnesium is
about 25 g, 60% of which is complexed with calcium in
bone. One-third of skeletal magnesium is exchangeable
with serum.
Magnesium orally produces diarrhea; but intravenously it
produces central nervous system (CNS) depression.
Magnesium

The requirement is about 400 mg/day for men and
300 mg/day for women. Doses above 600 mg may cause
diarrhea. More is required during lactation. Major sources
are cereals, beans, leafy vegetables and fish.
Normal Serum Level of Magnesium
Normal serum level Mg++ is 1.8–2.2 mg/dL. Inside the
RBC, the magnesium content is 5 mEq/L. In muscle tissue
Mg++ is 20 mEq/L. About 70% of magnesium exists in
free state and remaining 30% is protein-bound (25% to
albumin and 5% to globulin).
Requirement of Magnesium

• Mg++ is the activator of many enzymes requiring ATP.
Alkaline phosphatase, hexokinase, fructokinase,
phosphofructo-kinase, adenylcyclase, cAMP dependent
kinases, etc. need magnesium.
• Neuromuscular irritability is lowered by magnesium.
• „
Insulin-dependent uptake of glucose is reduced in
magnesium deficiency. Magnesium supplementation
improves glucose tolerance.
Functions of Magnesium

1. Cardiac arrhythmia
2. Resistant hypokalemia
3. Pregnancy with preeclampsia
4. Tetany not responding to calcium therapy
When to Test for Serum Level of Magnesium?

1. Increased urinary loss (tubular necrosis)
2. Hyperaldosteronism, volume expansion
3. Familial hypomagnesemia
4. Increased intestinal loss Diarrhea, laxatives, ulcerative colitis
Nasogastric suction, vomiting
5. Liver cirrhosis
6. Malabsorption
7. Protein calorie malnutrition
8. Hypoparathyroidism
9. Toxemia of pregnancy
10. Drugs: thiazide diuretics
Aminoglycosides, Cisplatin,Amphotericin
Cyclosporin, Haloperidol
Causes of Hypomagnesemia

1. Excess intake orally or parenterally
2. Renal failure
3. Hyperparathyroidism
4. Oxalate poisoning
5. Rickets
6. Multiple myeloma
7. Dehydration
8. Drugs: Aminoglycosides
Antacids
Calcitriol
Tacrolimus
Causes of Hypermagnesemia

Milk is the only food for the growth of young
ones of all
mammals. The milk is secreted by the
mammary glands.
Milk holds a unique place as an almost
complete natural food from the point of view
of nutrition. The major nutrients lacking in
milk are iron, copper and vitamin C.
Milk

Constituent Human Cow Buffalo Goat
Water (%) 87.5 87.2 83.6 87.5
Total solids (%) 12.5 12.8 16.4 12.5
Proteins (g/dl) 1.1 3.3 4.3 3.7
Lipids (g/dl) 3.8 3.8 6.0 3.5
Carbohydrate(g/dl) 7.5 4.4 5.3 4.7
Calcium (mg/dl) 34 150 160 170
Composition of Milk

Synthesis of lactose in mammary gland is catalyzed by
lactose synthase. A galactose unit is transferred from UD
Pgalactose to glucose.
Lactase deficiency leads to lactose intolerance
Many infants develop diarrhea and skin manifesta-tions due to
lactose intolerance. (It may also be due to allergy to milk proteins).
These children are to be fed with lactose-free formulae or soybean
proteins.
Lactose Synthesis

Mineral Human milk
(mg/100 ml)
Cow's milk
(mg/100 ml)
Buffalo's Milk
(mg/100 mI)
Magnesium 2.2 13 10
Phosphorus 16 100 100
Sodium 15 58 58
Potassium 55 138 130
Chloride 43 100 60
Iron Negligible Negligible Negligible
Mineral content of Milk

It is secreted during the first few days after parturition.
Colostrum coagulates on heating, whereas fresh milk does
not.
This coagulum forms a surface film containing casein and
calcium salts. Colostrum is mildly laxative, which helps to
remove meconium from the intestinal tract of the infant. The
change from colostrum to milk occurs within a few days
after the initiation of lactation. The proteins present in
colostrum are predominantly immunoglobulins. In the case
of cow, these immunoglobulins are readily absorbed by the
calf, and give protection to the young animal.
Colostrum (Colostral Milk)

The cerebrospinal fluid (CSF) is found within the
subarachnoid space and ventricles of the brain, as well as
around the spinal cord. The fluid originates in the choroid
plexus and returns to the blood in the vessels of the lumbar
region.
The total volume of fluid is about 125 mL. It is a
transudate or ultra filtrate of plasma. The composition of
the fluid is given in Table 25.10. CSF has the chloride
concentration higher than the plasma. This is in accordance
with the Gibbs-Donnan equilibrium.
Cerebrospinal Fluid

The protein concentration is usually 10–30 mg/dL, out of
which about 20 mg/dL is albumin, and globulin is about
5–10 mg/dL. In bacterial infections of the meninges, the
protein concentration is increased. But in such cases, the
neutrophil cell count is also increased.
In viral infections, the protein concentration is not
significantly increased, but mononuclear cells are
abundant.
In brain tumors, albumin level is raised, but cell count is
normal; this is called albumin cytological dissociation.
Biochemical Analysis of Cerebrospinal Fluid

Normal level of glucose in CSF is 50–70 mg/dL, which is
lower than the plasma level. Hence estimation of plasma
glucose along with CSF glucose is always done to avoid
misinterpre-tation due to a change in the plasma glucose.
Elevated levels are seen in diabetes mellitus.
In bacterial meningitis, however, the glucose level is far
lower when compared to the plasma, because it is
metabolized by bacteria.
Glucose Level in Cerebrospinal Fluid

Disease Color and
appearance
Cell count Protein Sugar Coagulation
Normal Clear and
colorless
0-4 ´ 106/L 10-30 mg/dl 50-70 mg/dl Not seen
Bacterial
meningitis
(purulent
meningitis)
Opalescent or
turbid due to
high cell content
Markedly increased
polymorphs
Marked
increase
Marked
decrease
May clot on
standing
Tuberculous
meningitis
May be
opalescent
Lymphocytes and
mononuclear cells
Increased Low but not
very much
decreased
Cobweb type
coagulation
Viral
infection
Clear and
colorless
Increased Increased Normal Nil
Brain tumor Clear and
colorless
Within normal
range
Increased Low Solidifies
Sub-
arachnoid
hemorrhage
Blood stained in
fresh
hemorrhage
RBCs and WBCs Increased Not significant Nil
Composition of the Cerebrospinal Fluid in Health
and Diseases

Amniocentesis is the process by which amniotic fluid is
collected for analysis. Examination of amniotic fluid is of
importance in prenatal diagnosis
Early gestation Preterm
Volume 450-1200 ml 500-1400 ml
Bilirubin <0.075 mg/dl <0.025 mg/dl
Creatinine 0.8-1.1 mg/dl 1.8-4.0 mg/dl
Estriol 10 mg/dl >60 mg/dl
L/S ratio <1:1 >2:1
Protein 0.6-0.24 g/dl 0.26-0.19 g/dl
Urea 18 6 mg/dl 30 11 mg/dl
Uric acid 3.71 mg/dl 9.92.2 mg/dl
Normal Composition of Amniotic Fluid
Amniotic Fluid

The lung maturity is assessed by measuring the lecithin/
sphingomyelin (L/S) ratio, which is an index of the
surfactant (surface tension lowering complex)
concentration in amniotic fluid. In late pregnancy, the cells
lining the fetal alveoli start synthesizing dipalmitoyl-
lecithin so that the concentration of lecithin increases,
whereas that of sphingomyelin remains constant. As a
result, as the fetal lung matures, the lecithin sphingomyelin
(L/S) ratio rises. An L/S ratio of 2 is taken usually as a
critical value.
Lung Maturity

CALCIUM
IMBALANCES
HYPOCALCEMIA HYPERCALCEMIA

HYPOCALCEMIA
4.5 meq/L or
Serum calcium below
8.5mg/dL.

ETIOLOGY
Inadequate dietary intake of calcium
Vitamin D deficiency
Malabsorption of fat in intestine
Metabolic acidosis
Renal failure with hyperphosphatemia, acute pancreatitis, burns, Cushing’s Disease,
hypoparathyroidism.
Medications- Magnesium sulfate.
Malignancy (Multiple Myloma)

CLINICAL MANIFESTATIONS
NEURO-
MUSCUL
AR
RESPIRATORY GI CV HEMATOLOGIC
• Tetany
Sympto
ms-
 Twitc
hing
arou
nd
mout
h,
 Tingling
and
numbnes
s of
fingers
 Facial spasm
 Convulsions
• Dyspnea
• Laryngeal
Spasm
• Increa
sed
perista
lsis
• Diarrhea
• Dysrhythmias
• Palpitations
• Prolong
ed
bleeding
time

MEDICAL MANAGEMENT
Determine and correct the cause of hypocalcemia.
Asymptomatic hypocalcemia- Oral calcium
gluconate, calcium lactate, calcium chloride.
Administer Calcium supplements 30 minutes before
meals for better absorption and with glass of milk
because Vitamin D is necessary for absorption of
Calcium from the intestine.

MEDICAL MANAGEMENT
I/V Calcium Gluconate or Calcium
Chloride(10%) – slowly to avoid
hypertension, bradycardia and other
symptoms.

DIETARY MANAGEMENT
Chronic/Mild Hypocalcemia: diet high in Calcium.
E.g: cheese, milk, spinach.
Hypocalcemia due to parathyroid deficiency- Avoid
foods high in phosphates. E.g: milk products,
carbonated beverages.

HYPERCALCEMIA
Serum calcium level more than 5.5 meq/L Or
11mg/dL.

ETIOLOGY
Metastatic Malignancy of- lung,
ovaries, prostate, bladder,
leukemia, kidney.
Hyperparathyroidism
Thiazide diuretic therapy
Prolonged immobilization
Excessive intake of calcium
supplements and Vitamin D.

CLINICAL MANIFESTATIONS
GI NEURO
-
MUSCU
LAR
CV RENAL MUSCUL
O-
SKELETA
L
• Anorexia
• Vomitting
• Consti
patio
n
• Deccre
ased
peristal
sis
• Mild-
Moderate
•
Hypercalcemia-
 Weakness
•
 Fatigue
 Depression
 Difficu
lty to
conce
ntrate
• Severe
Hypercalce
mia-
Dysrhythm
ias Heart
Block
• Polyuria
• Kidney
Stones
• R
e
n
al
fa
ilu
re
• Bone pain
• Fracture

LABFINDINGS
SerumCalcium->5.5meq/L(>11.5mg/dL)
ABG- pH <7.45,HCO3>26meq/L

MEDICAL MANAGEMENT
Correct the underlying cause.
prevent fluid
I/V NS (0.9%)+ Furosemide- is given rapidly to
overload, promote urinary calcium excretion.
Calcitonin- decreases- serum calcium- inhibit the effect of
PTH on osteoclasts and increasing urinary calcium excretion.
Corticosteroids- decrease calcium by competing with vitamin
D thus resulting in decreased intestinal absorption of calcium.

MEDICAL MANAGEMENT
Avoid or use in reduced dosage- calcium or vitamin D
supplements or calcium containing antacids if they are the
cause.
Etidronate disodium- reduces serum calcium by reducing
normal and abnormal bone reabsorption of calcium and
secondarily by reducing bone formation.

DIETARY MANAGEMENT
Oral fluids-
 Assisst in adequately hydrating the client
 Flushing excess calcium through the kidney.

12/31/2023 177
Parul Institute of Medical Sciences and
Research
Thank You!

WATER AND ELECTROLYTE BALANCE in normal and abnorm'

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