FLUID AND ELECTROLYTE

BALANCE
PRESENTED BY: Dr. ODOCH JOB YUBU, MMED 1, ORTHOPAEDIC
MODERATED BY: Dr. NJERU
OUTLINE
• Introduction
• Distribution of body fluids
• Body fluid balance homeostasis
• Serum and Urine osmolality
• Electrolyte homeostasis (Sodium, potassium and chloride)
• Diabetes Insipidus Vs SIADH
• Regulatory mechanisms of body fluid and electrolytes (ADH, RAAS)
• Patient hydration status assessment (clinical and laboratory)
Introduction
• Water and electrolytes are constantly exchanged with the environment, and
their body content depends on the balance between intake and loss.
• Water (a solvent), is the largest single component of the body
• The main function of water is to act as a lubricant, facilitate cellular
metabolism, and also a transport medium
• Total Body Water (TBW) of an average man (70kg) = 60% of body weight
• TBW % depends on age and gender. Decreasing as the age increases.
• Adipose tissue has low H2O % compared to other tissues around (at about
10%)
• Water and electrolytes can pass through the capillary walls.
Introduction
FLUID COMPARTMENTS AND DISTRIBUTION
Total body water (TBW) is in 2
main functional compartments:
1. Extracellular Fluid (ECF) = 1/3
• Plasma
• Interstitial Fluid
• Trancellular fluid
2. Intracellular Fluid (ICF) = 2/3
Mainly in Skeletal muscle mass
FLUID BALANCE HOMEOSTASIS
• The body’s ability to maintain a stable balance of fluids, ensuring the
correct volume and composition of body fluids to support normal
physiological function e.g., cellular function, BP regulation & overall
metabolic processes.
• This ensures input vs. output equilibrium.
• This is achieved through the coordinated action of several systems,
including:
FLUID BALANCE HOMEOSTASIS
• Kidneys: Regulate the retention or excretion of water and
electrolytes. Adjusting urine concentration according to the body’s
needs
• Antidiuretic Hormone (ADH): Helps the kidneys retain water by
increasing the permeability of the tubules to water
• Aldosterone: Regulates sodium reabsorption and potassium
excretion, indirectly affecting water retention and blood volume
• Thirst mechanism:
• CVS System:
FLUID BALANCE HOMEOSTASIS
Fluid balances ….. Input and
output equilibrium.
NB. Disruption in fluid balance can
lead to conditions like;
dehydration, overhydration, or
electrolyte imbalances affecting
various organs and systems in the
body.
SERUM AND URINE OSMOLALITY
• Osmolarity: the concentration of
a solution/body fluids expressed
as the total number of solute
particles per liter.
• Osmolality: the concentration of
a solution/body fluids expressed
as the total number of solute
particles per kg
• Serum value 280-300 mOsm/kg
• Urine value 250-900 mOsm/kg
SERUM AND URINE OSMOLALITY
Principal determinants of osmolality are : Na+, glucose and urea (BUN)

1. Calculated serum osmolality = 2Na + glucose/18 + BUN/2.8

2. Normal ECF and ICF osmolality: Maintained b/w 290 -310 mOsm/kg
3. Any change in osmotic pressure: redistribution of water
4. Isotonic change in volume: no net movement of water as long as
the ionic concentration is the same
SERUM AND URINE HOMEOSTASIS
• The regulation of various substances in the blood (serum) and urine
to maintain the body’s internal balance of fluids, electrolytes, pH, and
metabolic waste products
• This is primarily handled by the kidneys, which filter the blood,
remove excess substances, and reabsorb necessary ones, all while
producing urine
• Several hormones regulate both serum and urine composition, e.g.
Aldosterone, ADH, PTH, Atrial Natriuretic Peptide (ANP)
SERUM AND URINE HOMEOSTASIS
SERUM HOMEOSTASIS.
▪ The composition of blood serum is tightly regulated to ensure proper
physiological function
▪ Serum contains water, electrolytes, proteins (albumin and antibodies),
hormones, nutrients, and waste products.
Key processes in serum homeostasis include:
1. Electrolyte balance
2. Acid-Base balance
3. Water balance
4. Glucose and protein regulation
SERUM AND URINE HOMEOSTASIS
URINE HOMEOSTASIS
• Urine composition reflects the body’s need to remove waste products and
excess substances while conserving essential nutrients and water.
• The kidneys manage urine production and composition through the
process of filtration, reabsorption, secretion, and excretion:
1. Electrolyte excretion
2. Water reabsorption
3. Acid-base balance
4. Nitrogenous waste excretion
5. Glucose and protein in urine
ELECTROLYTE HOMEOSTASIS
• Normal level of electrolytes in • Daily requirement of electrolytes
the body
ELECTROLYTE HOMEOSTASIS
• The regulation and balance of electrolytes in the body, which are vital
for many physiological functions, including maintaining fluid balance,
nerve transmission, muscle contraction, and acid-base balance
• Key electrolytes involved in this process include; sodium (Na+),
potassium (K+), calcium (Ca2+), chloride (Cl-), bicarbonate (HCO3-),
and magnesium (Mg2+)
• Regulation of electrolyte levels is controlled primarily by the kidneys>
ELECTROLYTE HOMEOSTASIS
KEY ASPECTS OF ELECTROLYTE HOMEOSTASIS
1. SODIUM
Regulated by the renin-angiotensin-aldosterone system (RAAS) and Antidiuretic
hormone (ADH). Sodium is crucial for maintaining fluid balance and nerve function
2. POTASSIUM
Regulated by aldosterone, the kidneys, and the exchange of hydrogen ions (H+).
Potassium is essential for normal muscle function, especially in the heart, as well as
nerve signal transmission
3. CHLORIDE
Works closely with sodium to maintain osmotic balance and is also important for
acid-base balance.
4. Calcium, Bicarbonate, Magnesium
SODIUM
HYPONATREMIA: Serum Na < 135 mEq/L SIGNS AND SYMPTOMS
1. Dilutional
• High ECF volume
• Excessive oral fluid intake or IVF therapy
• Syndrome of inappropriate ADH
• Drugs:
antipsychotics, tricyclic antidepressantants, ACEI
• 2. Depletional:
• Decreased intake: low sodium diet
• GI losses from vomiting
• Prolonged nasogastric tube suctioning
• Diarrhea
• Diuretic use or primary renal disease
SODIUM
MANAGEMENT OF HYPONATRAEMIA
• Most cases can be treated with water restriction
• Severe cases need Na administration
• Symptomatic at levels < 120 mEq/L
• Neurologic symptoms: give 3% NS ( correct Na at a rate < 1mEq/l,
until 130mEq/l or neurological symptoms improve)
• Rapidly corrected can lead to Central Pontine myelinolysis
SODIUM
HYPERNATRAEMIA SIGNS AND SYMPTOMS
Etiology
• Loss of free water or gain of Na+
• Hypervolemic hypernatremia
• Iatrogenic (Na+ containing fluids)
• Mineralocorticoid excess
(hyperaldosteronism, Cushing syndrome)
SODIUM
MANAGEMENT OF HYPERNATRAEMIA
First, assess the volume status
• Treat hypovolemia with isotonic fluids
• Once volume is restored replace water deficit with a hypotonic solution : dextrose 5%, ¼ NS
5% Dextrose

• Slowly correct Na levels at a rate < 1mEq/h and 12 mEq/d (< 0.7 mEq/h in chronic
hypernatremia) This is to prevent cerebral edema

• Hypernatremia could lead to Water shifts from the intracellular to the extracellular space in
response to a hyperosmolar extracellular space, which results in cellular dehydration. This
can put traction on the cerebral vessels and lead to subarachnoid hemorrhage
POTASSIUM
• K+ is critical to cardiac and neuromuscular function Potassium decreases by
0.3 mEq/L for every 0.1 increase in pH above normal..
• Factors that influence K+ Homeostasis ( distribution in ICF and ECF)
• Surgical stress
• Injury
• Acidosis (pH=Acid-Base Status)
• Catecholamines
• Glycoregulatory mechamisms
• Tissue metabolism
• Normal serum K+: 3.5- 5.0 mEq/L
 POTASSIUM
1. pH (Acid-Base status)
A. Acidosis (Low pH)
• Acidosis promotes the movement of K+ ions out of the cells into the
Extracellular fluid (ECF).
• This occurs because H+ ions move into the cells to buffer the excess
acidity, and to maintain charge balance,
• K+ ions therefore, move out of cells, increasing serum potassium =
hyperkalemia
• Therefore, low pH leads to hyperkalemia
 POTASSIUM
1. pH (Acid-Base status)
B. Alkalosis (high pH)
In alkalosis, H+ ions move out of cells to counter the higher extracellular Ph,
which pulls K+ ions into cells, resulting in lower serum potassium
(hypokalemia)

2. Catecholamines (epinephrine and norepinephrine)

A. beta-adrenergic stimulation (especially beta receptors)
• Catecholamines like epinephrine stimulate beta-2 receptors,
• These activate the Na+/K+-ATPase pump and promote the uptake of K+
into cells, reducing serum K+ levels
POTASSIUM
2. Catecholamines (epinephrine and norepinephrine)
B. Alpha-adrenergic stimulation
Alpha adrenergic receptors, however, promote the release of K+ from
cells, which can increase serum potassium levels
 POTASSIUM
3. Glycoregulatroy mechanisms (Insulin and Glucose)
A. Insulin and K+ Homeostasis
1. Insulin promotes K+ uptake into cells
• When insulin is released in response to elevated blood glucose, it
stimulates the activity of the Na+/K+-ATPase pump, which drives K+
into cells
• This mechanism is particularly important post-meal , helping to
prevent hyperkalemia that could result from dietary K+ intake
 POTASSIUM
3. Glycoregulatroy mechanisms (Insulin and Glucose)
A. Insulin and K+ Homeostasis
2. Insulin deficiency (e.g., in Diabetes)
• Without sufficient insulin, K+ remains in the ECF, potentially leading
to hyperkalemia.
• This is why hyperkalemia is often seen in Diabetic Ketoacidosis (DKA),
where insulin deficiency is coupled with metabolic acidosis, both of
which contribute to high extracellular potassium
POTASSIUM
3. Glycoregulatroy mechanisms (Insulin and Glucose)
B. Hyperglycemia and Potassium Homeostasis
• In the absence of insulin, high blood glucose levels can lead to an
osmotic shift, where water moves out of cells, carrying K+ with it into
the extracellular fluid, which can raise serum K+ levels.
• Administering insulin to lower blood glucose in hyperglycemic states
can also lower serum K+, as insulin shifts K+ back into the cells along
with glucose.
POTASSIUM
HYPERKALAEMIA
Serum level > 5.5 mmol/L
• Excessive potassium intake
• Increased release from cells
• Impaired excretion
POTASSIUM
EFFECTS OF HYPERKALAEMIA
• GI: nausea, vomiting, intestinal
• colic, diarrhea
• Neuromuscular: weakness,
• ascending paralysis, respiratory
• failure
POTASSIUM
MANAGEMENT OF HYPERKALAEMIA
POTASSIUM
HYPOKALAEMIA
POTASSIUM
MANAGEMENT OF HYPOKALAEMIA
• Check Magnesium level first
• Asymptomatic patient with K > 3.0mEq/L,
oral K replacement may be sufficient.
• Rate of IV infusion should not
Exceed 40 mEq/hr
• May cause a burning sensation if given
in the peripheral intravenous line
• Low flow rate of 10 mEq/hr or add
small amount of lidocaine in the
solution to decrease discomfort
MAGNESIUM
An essential mineral involved in numerous biochemical processes crucial for
overall health and cellular function.
An overview of its key roles in the body
Magnesium as an Enzyme Cofactor
Role in muscle and nervous system function
Bone health
Cardiovascular health
Glucose and insulin metabolism
Electrolyte balance
Anti-inflammatory and antioxidant properties
DNA and RNA stability
MAGNESIUM
HYPERMAGNESEMIA
Normal plasma Mg: 0.75-1.0 mmol/L
• Causes Of hypermagnesemia
• Severe renal insufficiency
• Magnesium containing antacids and laxatives
• Signs & Symptoms
✔ Nausea and vomiting
✔ Weakness, lethargy, hyporeflexia
✔ Hypotension, cardiac arrest
MAGNESIUM
MANAGEMENT OF HYPERMAGNESEMIA
• Eliminate exogenous sources
• Correct volume deficits
• Correct acidosis
• Acute symptoms: calcium chloride 5-10 ml immediately to antagonize
• CVS effects
• Hemodialysis: if levels and symptoms persist
MAGNESIUM
HYPOMAGNESEMIA
•Common in hospitalized patients and critically ill
1. Alteration of intake
2. Starvation, alcoholism, prolonged IVF therapy
3. Increased renal excretion
4. Alcohol abuse, diuretic use, amphotericin B, primary
aldosteronism ,diarrhea, malabsorption, acute
pancreatitis
MAGNESIUM
MANIFESTATION OF HYPOMAGNESEMIA
• Signs & Symptoms
• Hyperactive reflexes
•Muscles tremors, tetany
• Positive Chvostek's and trousseau signs
• Delirium and seizures

❑ Hypomagnesemia can lead to hypocalcemia, persistent hypokalemia

❑ When they coexist, prompt correction of Mg2+ , to restore the other
electrolytes
MAGNESIUM
MANAGEMENT OF HYPOMAGNESEMIA
▪ Mg level 0.5 -0.9 mmol/L
• Magnesium sulfate 0.25 mmol/L in NS 250 ml infused over 24 hr for 3
days
▪ Mg < 0.5 mmol/L
• Magnesium sulfate 0.5 mmol/l in NS 250 ml iv over 24 hr for 1 day,
then 0.25 mmol/l in NS 250 ml over 24 hr for 2 days
Asymptomatic and mild - Oral: milk of magnesia 15 ml ( 24.5
mmol/l ) q 24 hours and hold if diarrhea.
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
• Different organs regulate electrolyte and water balance in our body
• Different hormones and receptors play a vital role in electrolyte and
fluid balance
• (Lungs, Kidneys, liver, hypothalamus ,pituitary ,heart etc)
• Two main factors that trigger -ECF volume and ECF osmolarity
• Two main receptors -osmoreceptors (hypothalamus ) and
mechanoreceptors -baroreceptors that sense the blood pressure in
blood vessels.
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
OSMOTIC STIMULI

• osmoreceptors -receptors that detect and regulate changes in the

osmolality. These sensory receptors are found in the hypothalamus
and some in the kidneys

• Hypothalamus osmoregulation – The hypothalamus regulates blood

osmolarity by producing antidiuretic hormone (ADH) aka arginine
vasopressin which influences the reabsorption of water by the
kidneys ( V2 receptors in distal nephron )
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
• ADH secretion is triggered by; low
ECF volume, pain, dehydration,
high osmolarity and decreased by
increased ECF volume, Alcohol
• SIADH - high ADH from the
pituitary gland and other sources
leading to high water retention
• Diabetes insipidus - due to
diminished ADH secretion or
kidneys not responding to ADH
therefore leading to increased fluid
loss via urine
DIABETES INSPIDUS Vs SIADH
• Diabetes insipidus (DI) and Syndrome of inappropriate antidiuretic
hormone (SIADH) are 2 conditions involving the hormone antidiuretic
hormone (ADH), but they have opposite effects on water balance in
the body.
DIABETES INSPIDUS Vs SIADH
DIABETES INSIPIDUS (DI)
Pathophysiology
• DI occurs due to either insufficient ADH production
(central/neurogenic DI) or the kidneys’ inability to respond to ADH (
nephrogenic DI).
• This leads to excessive water loss in urine and the inability to
concentrate urine
DIABETES INSPIDUS Vs SIADH
DIABETES INSIPIDUS
Key Features
• Polyuria: up to 15-20 litres/day
• Polydipsia: to compensate for water loss
• Dehydration: due to the large urine output and in cases of insufficient
water intake
• Serum osmolality; increased, due to water loss and the resulting
concentration of solutes in the blood
• Urine osmolality: decreased (very dilute urine, low osmolality
• Serum sodium: hypernatremia due to excessive water loss
DIABETES INSPIDUS Vs SIADH
DIABETES INSIPIDUS
Diagnosis
• Water deprivation test: the patient will continue to produce large amounts
of dilute urine despite dehydration
• Desmopressin (ADH Analog) test: reduces urine output and increases urine
concentration. In nephrogenic DI, desmopressin has little or no effect
MANAGEMENT
• Central DI: Desmopressin (ADH REPLACEMENT)
• Nephrogenic DI: thiazide diuretics, low-sodium diet and NSAIDS to reduce
urine output
DIABETES INSPIDUS Vs SIADH
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION
(SIADH)
Pathophysiology
Occurs when too much ADH is produced, causing the kidneys to retain
water, leading to water overload and dilution of blood solutes
DIABETES INSPIDUS Vs SIADH
SIADH
Key Features
• Oliguria: due to water retention
• Fluid retention: causing dilutional hyponatremia
• No edema: despite water retention, peripheral edema is typically absent
because water is retained intracellularly
• Serum osmolality: decreased (diluted blood due to water retention)
• Urine osmolality: increased (concentrated urine despite low serum
osmolality)
• Serum sodium: hyponatremia due to water retention and dilution of
sodium
DIABETES INSPIDUS Vs SIADH
SIADH
Diagnosis
• Serum and Urine osmolality tests: serum osmolality will be low and
urine osmolality will be inappropriately high for the level of serum
osmolality
• ADH levels: elevated in SIADH
MANAGEMENT
• Fluid restriction, salt tablets, or hypertonic saline in severe cases.
• Medications such as vasopressin receptor antagonists (e. tolvaptan)
DIABETES INSPIDUS Vs SIADH
SUMMARY
DI results in excessive urination and hypernatremia, while SIADH leads
to water retention and hyponatremia
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
VOLUME STIMULI

• changes in plasma volume

can be detected and
regulated by different
organs in the body - like
kidneys,heart

• RAAS system ( organs

involved -lungs, liver,
adrenal cortex)
• Heart -Baroreceptors and
cardiac regulations via ANP
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
RAAS
The renin-angiotensin-aldosterone system (RAAS) involves several steps,
including:
1. When your blood pressure falls, your kidneys release the enzyme renin into
your bloodstream.
2. Renin splits angiotensinogen, a protein your liver makes and releases, into
pieces. One piece is the hormone angiotensin I.
3. Angiotensin I, which is inactive (doesn’t cause any effects), flows through
your bloodstream and is split into pieces by angiotensin-converting enzyme
(ACE) in your lungs and kidneys. One of those pieces is angiotensin II, an
active hormone.
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
RAAS
4. Angiotensin II causes the muscular walls of small arteries (arterioles) to
constrict (narrow), which increases blood pressure. Angiotensin II also
triggers your adrenal glands to release aldosterone and your pituitary gland
to release antidiuretic hormone (ADH, or vasopressin).
5. Together, aldosterone and ADH cause your kidneys to retain sodium.
Aldosterone also causes your kidneys to release (excrete) potassium through
your urine.
6. The increase in sodium in your bloodstream causes water retention. This
increases blood volume and blood pressure, thus completing the
renin-angiotensin-aldosterone system.
The renin-angiotensin-aldosterone system is also activated by other
hormones, including corticosteroids, estrogen and thyroid hormones.
FLUID AND ELECTROLYTE
REGULATORY MECHANISMS
BARORECEPTORS
• mechanoreceptors located in the arterial
walls,aortic arch, carotid sinus and vena
cava
• detect a decrease in arterial blood
pressure which leads to decreased
baroreceptor afferent nerve active
• signals are then processed by medullary
cardiovascular control pathways
• this will lead to increased sympathetic
and decreased parasympathetic activity
therefore HR, arterial vasoconstriction,
HYDRATION STATUS ASSESSMENT
Both clinical assessment and laboratory tests play a role in determining
the patient’s hydration status.
a. CLINICAL ASSESSMENT
• History and symptoms
• Physical examination
• Signs of severe dehydration
HYDRATION STATUS ASSESSMENT
b. LABORATORY ASSESSMENT
1. Serum electrolytes
2. Blood urea nitrogen (BUN) and creatinine
3. Hematocrit and hemoglobin
4. Serum osmolality
5. Urine osmolality and specific gravity
6. Urine output
7. Acid base balance
8. Plasma lactate levels
9. Urine sodium concentration
HYDRATION STATUS ASSESSMENT
COMBINING CLINICAL AND LABORATORY ASSESSMENTS
1. In dehydration, you expect to see signs like dry mucous
membranes, tachycardia, hypotension, and elevated lab markers
such as sodium, BUN, and hematocrit. Urine will be concentrated
with high specific gravity.
2. In overhydration, signs include edema, elevated JVP, and
hyponatremia, with dilute urine and low specific gravity
REFERENCES

• Review of Medical Physiology, by Ganog

• Colloids versus crystalloids for fluid resuscitation in critically ill people Sharon R
LewisMichael W Pritchard David JW , 03 August 2018
• Fluid and Electrolyte Management of the surgical patient, in Schwartzs Principles
of Surgery, 11th Ed, chap 3, p83-101 .
• Shock, Electrolytes and Fluids, in Sabiston Texbook of Surgery, 20th Ed, chap 4
Pg44-97.
• Managing physiologic changes in the surgical patient, in Essential Surgery 5TH Ed,
p 19-32
• G P Joshi, Intraoperative fluid management. Available on UPTODATE.
• N. Siparsky, Overview of Postoperative fluid therapy in adults. Available on
UPTODATE.
THANK YOU