ELECTROLYTE IMBALANCE

HYPER & HYPONATREMIA

Presented by
Dr. Selina Akhter
Batch: DA-20

Guided by
Prof. Dr. Mushfiqur
Rahman
Dept. of Anesthesiology,
SICU and pain medicine
BIRDEM General
Hospital
 INTRODUCTION
Electrolyte refers to any substance that produces an
electrically conducting solution when dissolved in a
polar solvent such as water

They can be divided into two groups:

I. cations (+ve)
II. anions (-ve)
Examples of electrolytes:
• Sodium
• Potassium
• Calcium
• Magnesium
• Phosphate
• Chloride
• Bicarbonate
 IMPORTANCE OF
ELECTROLYTES
Electrolytes play a vital role in monitoring homeostasis
with the body
They help to:
• Regulate heart and neurological function
• Fluid balance
• Oxygen delivery
• Acid base balance
 CAUSES OF ELECTROLYTE
IMBALANCE
Electrolyte imbalance can develop by consuming too little
or too much electrolytes as well as excreting too little or
too much electrolyte
Electrolyte imbalance are most often due to:
• Vomiting
• Diarrhea
• Not drinking enough fluid
• Excessive sweating
• Drugs such as diuretics and laxatives
• Liver and kidney problems
 SODIUM
• Sodium is the most potent cation in ECF
• In the 15 L of ECF in a 70 Kg person there is around 50 g
of sodium,90% of the body’s total sodium content
• Standard concentration of sodium is 136-145 mEq/L
• Daily requirement: 10-15g
• Distribution of sodium ions are mediated by Sodium-
potassium pumps and sodium potassium channels
 SOURCES
Main source is NaCl(salt) during cooking
Other sources are:
• Cheese
• Bread
• Egg
• Carrot
• Whole grains
• Radish
• Nuts
 FUNCTIONS

• Maintain of osmotic pressure of blood and other

tissue fluid
• Maintain normal water balance and distribution
• Regulation of acid base balance
• Preservation of normal irritability of muscles and
permeability of the cells
 SODIUM REGULATION
Two primary systems are especially involved in
regulating the concentration of sodium and
osmolarity of ECF fluid by kidneys:
i. The osmoreceptor-ADH system
ii. The thirst mechanism
 (-)
Increase in Extracellular osmolarity
osmoreceptor
Increase in ADH secretion

Increase in Plasma ADH

Increase in water permeability by DCT & CD

Increase in water reabsorption

Decrease in Extracellular osmolarity

Fig: Osmoreceptor- ADH feedback mechanism

 THIRST MECHANISM

Thirst is the major defense mechanism against

hyperosmolarity and hypernatremia because it is the
only mechanism that increases water intake

Activation of the osmoreceptor by increases in ECF

osmolarity induces thirst, stimulating the individual to
drink water

Conversely, Hypo osmolarity suppresses thirst

 HYPERNATREMIAIA
• Hypernatremia is defined as a serum sodium
concentration of more than 145 mEq/L (Normal
Sodium 135-145 mEq/L)

• It is characterized by a deficit of total body

water (TBW) relative to total body sodium levels
due to either loss of free water or infrequently
the administration of hypertonic sodium
solutions
 CONT.
• In healthy subjects, the body's 2 main defense
mechanisms against hypernatremia are thirst and the
stimulation of vasopressin release
• Hypernatremia is most commonly seen in debilitated
patients who are unable to drink, the very aged, the very
young, and patients with altered consciousness
• Much of the total body Na is stored in the skin, bone and
cartilage which serves as a reservoir
 CLASSIFICATION OF HYPERNATREMIA

• Hypovolemic hypernatremia
• Euvolemic hypernatremia
• Hypervolemic hypernatremia
 HYPOVOLEMIC
HYPERNATREMIA
• These patients have lost both Na and water, but
the water loss is more
• Hypotonic losses can be renal (osmoticdiuresis) or
extra renal (diarrhea or sweat)
• In either case, patients usually manifest signs of
hypovolemia
 CAUSES OF HYPOVOLEMIC
HYPERNATREMIA
• Body fluid loss (eg, burns, sweating)
• Diuretic use
• Gastrointestinal loss (eg, vomiting, diarrhea, fistulas)
• Heat injury
• Osmotic diuresis (eg, hyperosmolar nonketotic coma,
enteral feeding)
• Post-obstructive diuresis
 EUVOLEMIC HYPERNATREMIA
• This group of patients generally manifests signs of
water loss without overt hypovolemia unless the water
loss is massive
• Total sodium content is generally normal
• Nearly pure water losses can occur via the skin,
respiratory tract, or kidneys. Occasionally transient
hypernatremia is observed with movement of water into
cells following exercise, seizures, or rhabdomyolysis
 CAUSES OF EUVOLEMIC
HYPERNATREMIA
• Central diabetes insipidus
• Nephrogenic diabetes insipidus
• Fever
• Hyperventilation/mechanical ventilation
• Hypodipsia
• Medications(eg,amphotericin,aminoglycosides,lithium,
phenytoin)
• Sickle cell disease
 DIABETES INSIPIDUS
• The most common cause of euvolemic
hypernatremia is diabetes insipidus
• Diabetes insipidus (DI) is characterized by marked
impairment in renal concentrating ability that is
due either to decreased ADH secretion (central DI)
or failure of the renal tubules to respond normally
to circulating ADH (nephrogenic DI)
 CENTRAL DIABETES
INSIPIDUS
Causes
• Lesion in or around the hypothalamus and the pituitary
stalk
• Brain death
• Following neurosurgical procedure
• Head trauma
 DIAGNOSIS

• Suggested by a history of polydipsia, polyuria (often >6

L/d), and the absence of hyperglycemia

• The diagnosis of central DI is confirmed by an increase in

urinary osmolality following the administration of
exogenous ADH
 TREATMENT
• Aqueous vasopressin (5–10 units S/C or I/M every 4–6 h) is
the treatment of choice for acute central DI.

• Vasopressin in oil (0.3 mL intramuscularly every day) is

longer lasting but is more likely to cause water
intoxication.
 CONT.
• Desmopressin (DDAVP), a synthetic analogue of ADH with
a 12- to 24-h duration of action, is available as an
intranasal preparation (10–40 mcg/d either as a single
daily dose or divided into two doses) that can be used in
both ambulatory and perioperative settings
 ANESTHETIC CONSIDERATION
• In the perioperative setting, the diagnosis of DI is
suggested by marked polyuria without glycosuria
and a urinary osmolality lower than
plasmaosmolarity

• The absence of thirst in unconscious individuals

leads to marked water losses and can rapidly
produce hypovolemia
 NEPHROGENIC DIABETES
INSIPIDUS
ADH secretion is normal but the kidney fail to respond to
ADH and urinary concentrating ability is impaired
Cause:
• congenital
• chronic kidney disease
• hypokalemia
 CONT.
• hypercalcemia
• Sickle cell disease
• hyperproteinemia
• some drugs (amphotericin B, lithium, demeclocycline,
mannitol)
 DIAGNOSIS AND TREATMENT
• The diagnosis is confirmed by failure of the kidney to
produce urine following the administration of exogenous ADH

• Treatment is generally directed at the underlying illness and

ensuring an adequate fluid intake.

• Volume depletion by a thiazide diuretic can paradoxically

decrease urinary output by reducing water delivery to
collecting tubules.

• Na and protein restriction can similarly reduce urinary

output
 CAUSES OF HYPERVOLEMIC
HYPERNATREMIA
• Cushing syndrome
• Hemodialysis
• Hyperaldosteronism
• Iatrogenic-hypertonic saline
• Salt ingesion
 CLINICAL MANIFESTATIONS OF
HYPERNATREMIA
Symptoms Signs
Polyuria Muscle twitching
polydipsia Hyper reflexia
orthostasis tremor
restlessness ataxia
irritability muscle spasticity
lethargy focal and general
seizures
death
 COMPLICATIONS
• Focal intracerebral or subarachnoid hemorrhage, seizures
and serious neurological damage are common,
particularly in children with acute hypernatremia when
plasma [Na+] exceeds 158 mEq/L

• Chronic hypernatremia is usually better tolerated than the

acute form. After 24 to 48 h, intracellular osmolarity
begins to rise as a result of increases in intracellular
inositol and amino acid concentrations, and brain
intracellular water content slowly returns to normal
 TREATMENT OF
HYPERNATREMIA
• The treatment of hypernatremia is aimed at restoring
plasma osmolality to normal and correcting the
underlying cause
• Water deficits should generally be corrected over 48 h, as
rapid correction can cause cerebral edema
• Abnormalities in extracellular volume must also be
corrected
 CONT.
• Hypernatremic patients with decreased total body Na
should be given isotonic fluids to restore plasma volume
to normal prior to treatment with a hypotonic solution

• Hypernatremic patients with increased total body

sodium should be treated with a loop diuretic along with
intravenous5% dextrose in water
 CONT.
• Enteral free water administration is preferable
when feasible, but a hypotonic intravenous
solution such as 5% dextrose in water can also be
used
• In general, decreases in plasma sodium
concentration should not proceed at a rate faster
than 0.5 mEq/L/h
Figure- Algorithm for the treatment of hypernatremia
 ANESTHETIC CONSIDERATIONS

• Hypernatremia has been demonstrated to

increase the MAC value of inhalation agent

• Decreases in the volume of distribution for drugs

necessitate dose reductions for most intravenous
agents, whereas decreases in cardiac output
enhance the uptake of inhalation anesthetics
 CONT.
• Hypovolemia emphasize any vasodilation or cardiac
depression from anesthetic agents and predisposes
to hypotension and hypoperfusion of tissues

• Hypovolemia will be exacerbated by induction and

maintenance of anesthesia

• If possible, surgery should be delayed until the

hypernatremia (>150mEq/L) has been corrected
with associated symptoms
 HYPONATREMIA

• Hyponatremia may be defined as when serum

sodium concentration is < 135 mEq / L
• Hyponatremia invariably reflects water retention
from either an absolute increase in TBW or a loss
of sodium in relative excess to loss of water
• Hyponatremia also associated with transurethral
resection of the prostate
 CLASSIFICATION OF
HYPONATREMIA
• Hypovolemic hyponatremia
• Euvolemic hyponatremia
• Hypervolemic hyponatremia
 HYPOVOLEMIC
HYPONATREMIA
• Progressive losses of both Na and water eventually
lead to extracellular volume depletion
• As the intravascular volume deficit approaches 5% to
10%,nonosmotic ADH secretion is activated
• A major exception to the latter is hyponatremia
due to vomiting, which can result in a urinary
[Na+] greater than 20 mEq/L
 Cont.
• Fluid losses resulting in hyponatremia may be
renal or extra renal in origin
• Renal losses are most commonly related to
thiazide diuretics and result in a urinary [Na+]
greater than 20 mEq/L
• Extra renal losses are typically gastrointestinal
and usually are associated with a urinary [Na+] of
less than 10mEq/L
 CAUSES OF HYPOVOLEMIC
HYPONATREMIA
Renal
• Diuretics
• Mineralocorticoid deficiency
• Salt-losing nephropathies
• Osmotic diuresis (glucose, mannitol)
• Renal tubular acidosis
 CONT.
Extrarenal
• Vomiting
• Diarrhea
• sweating, burns
 EUVOLEMIC HYPONATREMIA
Euvolemic hyponatremia is a result of excess water
intake or excess water retention from nonosmotic ADH
release
Causes of Euvolemic hyponatremia are:
• Primary polydipsia
• Syndrome of inappropriate antidiuretic hormone
• Glucocorticoid deficiency
• Hypothyroidism
• Drug-induced
 SIADH
• SIADH is characterized by hyponatremia, low
plasma osmolarity and an inappropriate anti
diuresis that is urine osmolarity higher than
anticipated for the degree of hyponatremia

• SIADH is a condition of nonosmotic ADH release

associated with a variety of malignancies,
infections and drugs
 CAUSES OF SIADH

Pulmonary disease
• Pneumonia
• Tuberculosis
• Abscess
• Asthma
Malignancy
• Lung
• Gastrointestinal
• Genitourinary
 CONT.
CNS disease
• Hemorrhage
• Hematoma
• Infection
• Tumors
Drugs
• Chlorpropamide
• Carbamazepine
• SSRIs
• Antipsychotics
• Opioids
• NSAIDs
 CSW AND SIADH

• Cerebral salt wasting (CSW) is a syndrome of

inappropriate renal sodium wasting and
hyponatremia with polyuria and hypovolemia
that occurs with traumatic brain injury,
subarachnoid and neuro surgery
• Proposed mechanisms for this disorder include
excess secretion of natriuretic peptides and
altered sympathetic stimulation to the kidney
 CONT.

Both are characterized by elevated urine

sodium concentration, low serum osmolality,
and high urine osmolality
Patients with SIADH are usually euvolemic or
mildly hypervolemic, whereas patients with
CSW are hypovolemic, and thus treatments for
these two disorders are very different
 CONT.

• The treatment of SIADH is free water restriction,

and the treatment of CSW is volume and sodium
replacement with normal or hypertonic saline
• Demeclocycline , a tetracycline antibiotic that
antagonizes ADH activity at the renal tubules, is
often used as an adjunct in the treatment of
SIADH when water restriction alone is
insufficient
 HYPERVOLEMIC HYPONATREMIA
• Characterized by an increase in both sodium and
TBW
• When the increase in TBW is relatively greater than
the increase in total body sodium, hyponatremia
occurs
• Hyponatremia in these settings results from
progressive impairment of renal free water excretion
and generally parallels underlying disease severity
 CAUSES OF HYPERVOLEMIC
HYPONATREMIA
• Congestive heart failure
• Cirrhosis
• Nephrotic syndrome
 CLINICAL MANIFESTATIONS OF
HYPONATREMIA
• Patients with mild to moderate
hyponatremia ([Na+] >125 mEq/L) are
frequently asymptomat ic
• Serious manifestations of
hyponatremia are generally associated
with plasma sodium concentrations
less than 120 mEq/L
 CONT.
Symptoms Signs
Anorexia Abnormal sensation
Nausea Disorientation
Lethargy Agitation
Apathy Cheyne-stokes breathing
Muscle cramps Hypothermia
Pathologic reflexes
Pseudobulbar palsy Seizures
Coma
Death
 TREATMENT OF HYPONATREMIA

• Isotonic saline is generally the treatment of choice

for hypovolemic hyponatremic patients. Once the
ECF deficit is corrected, spontaneous water
diuresis returns plasma [Na+] to normal
• Water restriction is the primary treatment for
hyponatremic patients with euvolemic or
hypervolemic
 CONT.
• Acute, symptomatic hyponatremia requires prompt
treatment. In such instances, correction of plasma [Na+]
to greater than 125 mEq/L is usual sufficient to reduce
symptoms and signs
• Excessively rapid correction of hyponatremia has been
associated with neurological manifestation
• The following correction rates have been suggested: for
mild symptoms, 0.5 mEq/L/h or less; for moderate
symptoms, 1 mEq/L/h or less; and for severe symptoms,
1.5 mEq/L/h or less
 CONT.
• More rapid correction of hyponatremia can be
achieved by giving a loop diuretic with isotonic
saline. Even more rapid corrections can be
achieved with intravenous hypertonic saline (3%
NaCl)
• Hypertonic saline may be indicated in markedly
symptomatic patients with plasma [Na+] less than
110 mEq/L. Three percent NaCl should be
administered with caution
Figure-Algorithm for the treatment of hyponatremia
 ANESTHETIC CONSIDERATIONS

• Hyponatremia is the most common electrolyte

disorder which increases both perioperative
morbidity and mortality
• If possible , should be corrected before operation
• If case of urgent, treatment should continue
throughout ot and postoperative period
 CONT.
• Induction and maintenance of anesthesia on
patient with hypovolemic hyponatremia with risk
of hypotension
• Addition to fluid therapy, vasopressor and/or
inotropes may be needed
• Hypervolemic hyponatremic patients (CCF) should
be avoided fluid overload
 CONT.
• Patients undergoing transurethral resection
of the prostate can absorb significant
amounts of water from irrigation fluids (as
much as 20 mL/min) and are at high risk for
rapid development of profound acute water
intoxication
REFERENCES