Electrolyte imbalance

Dr.sabah
 hyponatremia
• Hyponatremia, defined as a serum sodium
concentration below 135 mEq/L.
• is usually caused by a failure to excrete water
normally .
• In healthy individuals, the ingestion of water
does not lead to hyponatremia because
suppressed release of antidiuretic hormone
(ADH), also called vasopressin, allows excess
water to be excreted in a dilute urine
• Hyponatremia —
• almost always due to the oral or intravenous intake of
water that cannot be completely excreted. Normal
individuals can excrete more than 10 L of urine per day
(and more than 400 mL per hour) and therefore will not
develop hyponatremia unless water intake exceeds this
value, which occurs most often in psychotic patients with
primary polydipsia.
• Hyponatremia caused by massive water intake rapidly
resolves as soon as water intake stops, provided that the
ability to dilute the urine is intact.
• Persistent hyponatremia is associated
with impaired water excretion that is most
often due to an inability to suppress the
release of antidiuretic hormone (ADH) or to
advanced renal failure.
• The two major causes of persistent ADH secretion are
the
– syndrome of inappropriate ADH secretion (SIADH) and
– reduced effective arterial blood volume. The latter can be
due to true volume depletion (eg, diuretics, vomiting, or
diarrhea) or to decreased tissue perfusion in heart failure or
cirrhosis. In the last two disorders, the severity of the
hyponatremia parallels the severity of the underlying
disease.
• Hyponatremia due to water retention is typically associated
with a reduction in plasma osmolality and tonicity .
• This initially creates an osmotic gradient that favors water
movement from the ECF into cells and the brain.
• Water movement into the brain can lead to cerebral edema
and potentially severe neurologic symptoms, particularly if
the hyponatremia is acute.
• In addition, overly rapid correction of severe chronic
hyponatremia can lead to potentially irreversible
neurologic injury
 Clinical features of hyponatremia
• symptoms range from nausea and malaise,
with mild reduction in the serum sodium, to
lethargy, decreased level of consciousness,
headache, and (if severe) seizures and coma.
• Hyponatremia is classified according to volume
status, as follows:
• Hypovolemic hyponatremia: decrease in total body
water with greater decrease in total body sodium
• Euvolemic hyponatremia: normal body sodium
with increase in total body water
• Hypervolemic hyponatremia: increase in total
body sodium with greater increase in total body
water
 DIAGNOSIS
• urine osmolality
• Urine osmolality helps differentiate between
conditions associated with impaired free-
water excretion and primary polydipsia. A
urine osmolality greater than 100 mOsm/kg
indicates impaired ability of the kidneys to
dilute the urine.
• Determine th severity of hyponatremia:
• Severe hyponatremia serum sodium
concentration of <120 mEq/L .
• Moderate hyponatremia – A serum sodium
concentration of 120 to 129 mEq/L.
• ●Mild hyponatremia – A serum sodium
concentration of 130 to 134 mEq/L.
 Management of hyponatremia
determine the duration of hyponatremia — Therapy for
hyponatremia depends in part upon the acuity:
• Acute – If the hyponatremia has developed over a
period of less than 48 hour.
Acute hyponatremia usually results from parenteral fluid
administration in postoperative patients (who have
antidiuretic hormone [ADH] hypersecretion associated
with surgery) and from self-induced water intoxication.
• Chronic – If it is known that hyponatremia has been
present for more than 48 hours.
• The more acute the hyponatremia, the
greater the risk of complications and the
greater the need for aggressive therapy.
• The more chronic the hyponatremia and the
lower the serum sodium concentration, the
greater the risk of complications from
overaggressive therapy and the greater the
need for monitoring to avoid overcorrection.
 Goal of therapy
• in patients with severe hyponatremia, the goal
of initial therapy is to raise the serum sodium
concentration by 4 to 6 mEq/L in a 24-hour
period.
• In symptomatic patients with acute
hyponatremia or in patients with severe
symptoms, this goal should be achieved
quickly, over six hours or less.
• Hypertonic solution 3 percent sodium chloride
50 mL bolus of 3 percent saline can be safely
administered in a peripheral vein .
• If patient is symptomatic we treat with a 100
mL bolus of 3 percent saline, followed, if
symptoms persist, with up to two additional
100 mL doses (to a total dose of 300 mL); each
bolus is infused over 10 minutes.
• Fluid restriction — Fluid restriction to below the
level of urine output is indicated for the treatment
of symptomatic or severe hyponatremia in
edematous states (such as heart failure and
cirrhosis), syndrome of inappropriate antidiuretic
hormone (SIADH), and advanced renal impairment.
• Restriction to 50 to 60 percent of daily fluid
requirements may be required to achieve the goal
of inducing negative water balance
• Administer isotonic saline to patients who are
hypovolemic to replace the contracted
intravascular volume.
•  loop diuretic may be beneficial in patients
with SIADH .
• Patients with syndrome of inappropriate
antidiuretic hormone (SIADH) secretion who
have very mild or absent symptoms and a
serum sodium above 120 mEq/L can be
treated with oral salt tablets in addition to
fluid restrictio
• Vasopressin receptor antagonists — An
alternative or possible addition to fluid
restriction and sodium chloride administration
in patients with hyponatremia is the use of an
ADH receptor antagonist 
 hypernatremia
• Hypernatremia —  sodum more than 145mmol/l
• Hypernatremia is strictly defined as a hyperosmolar
condition caused by a decrease in total body water (TBW)
• most often caused by the :
– failure to replace water losses due to impaired thirst or lack of
access to water. Eg: elderly patients
– It can also be induced by the intake of salt in excess of water or the
administration of a hypertonic salt solution.
– In contrast to hyponatremia in which water moves into the cells,
the increase in plasma tonicity in hypernatremia usually pulls water
out of the cells, resulting in a decrease in intracellular volume
• the development of hyperosmolality from the
water loss can lead to neuronal cell shrinkage
and resultant brain injury.
• Loss of volume can lead to circulatory
problems (eg, tachycardia, hypotension).
t
 Management of hypernatremia
• Acute symptomatic hypernatremia, defined as
hypernatremia occurring in a documented
period of less than 24 hours, should be
corrected rapidly.
• Chronic hypernatremia (>48 h), however,
should be corrected more slowly due to the
risks of cerebral edema during treatment.
• Five percent dextrose in water, intravenously, at
a rate of (approximately 1.35 mL/hour x patient's
weight in kg) or approximately 70 mL/hour in a
50 kg patient and 100 mL/hour in a 70 kg patient.
• Hypernatremic patients who are also
hypovolemic will require isotonic fluids to
expand the extracellular fluid volume.
• in stable patients, chronic hypernatremia may
also be corrected with oral rehydration
• The goal of water repletion in patients with
chronic hypernatremia is to lower the serum
sodium by approximately 10 mEq/L in 24
hours but to avoid correcting the serum
sodium by more than 12 mEq/L in 24 hours.
• patients with acute hypernatremia -  Acute
hypernatremia is uncommon, occurring in patients
with:
– salt poisoning.
– diabetes insipidus who acutely lose the ability to replace
their water losses (eg, a patient with diabetes insipidus
who undergoes surgery and does not receive adequate
intravenous water).
– patients being treated for severe hyperglycemia, whose
water losses from glycosuria are not adequately replaced
• The initial regimen in patients with acute salt poisoning or
diabetes insipidus is :
– Five percent dextrose in water, intravenously, at a rate of 3 to 6
mL/kg/hour.
– The serum sodium and blood glucose should be monitored
every two to three hours until the serum sodium is lowered
below 145 mEq/L.
– Once the serum sodium concentration has reached 145 mEq/L,
the rate of infusion is reduced to 1 mL/kg/hour and continued
until a normal serum sodium (140 mEq/L) is restored.
– Patients with central diabetes insipidus will also require 
desmopressin therapy
• patients with both acute hypernatremia and oliguric
acute kidney injury, hemodialysis or continuous renal
replacement therapy can be used to correct
hypernatremia and avoid volume overload
• The goal of this regimen is to lower the serum
sodium by 1 to 2 mEq/L per hour and to restore a
normal serum sodium in less than 24 hours.
 hyperkalemia
• Hyperkalemia is defined as a potassium level
greater than 5.5 mEq/L. 
•  It can be difficult to diagnose clinically
because symptoms may be vague or absent.
• However, the fact that hyperkalemia can lead
to sudden death from cardiac arrhythmias
requires that physicians be quick to consider
hyperkalemia in patients who are at risk for 
 Signs and symptoms

Patients with hyperkalemia may be asymptomatic,

or they may report the following symptoms
(cardiac and neurologic symptoms predominate):
• Generalized fatigue
• Weakness
• Paresthesias
• Paralysis
• Palpitations
• Evaluation of vital signs is essential for determining the
patient’s hemodynamic stability and the presence of
cardiac arrhythmias related to hyperkalemia.  
• Additional important components of the physical exam
may include the following:
• Cardiac examination : extrasystoles, pauses, or bradycardia
• Neurologic examination : diminished deep tendon reflexes
or decreased motor strength
• In rare cases, muscular paralysis and hypoventilation may
be observed
• Signs of renal failure, such as edema, skin
changes, and dialysis sites, may be present
• Signs of trauma may indicate that the patient
has rhabdomyolysis, which is one cause of
hyperkalemia
 Electrocardiography
• Tall peaked T waves with a shortened QT
interval are usually the first findings 
• As the hyperkalemia gets more severe, there is
progressive lengthening of the PR interval and
QRS duration, the P wave may disappear, and
ultimately the QRS widens further to a sine
wave pattern. 
• ABC
• ntravenous access established and should be
placed on a cardiac monitor.
• In the presence of hypotension or marked QRS
widening, intravenous bicarbonate, calcium,
and insulin given together with 50% dextrose
may be appropriate
• Insulin administered with glucose
• Alkalinizing agents: Increases the pH, which
results in a temporary potassium shift from the
extracellular to the intracellular environment;
these agents enhance the effectiveness of
insulin in patients with acidemia
• Beta2-adrenergic agonists.
• Diuretics.
• Magnesium sulfate: Has been successfully
used to treat acute overdose of slow-release
oral potassium.
• Dialysis is the definitive therapy in patients
with renal failure or in whom pharmacologic
therapy is not sufficient. 
 hypokalemia
Hypokalemia is generally defined as a serum
potassium level of less than 3.5 mEq/L (3.5
mmol/L).
• Moderate hypokalemia is a serum level of 2.5-3.0
mEq/L
• severe hypokalemia is a level of less than 2.5
mEq/L. 
•  Hypokalemia is a potentially life-threatening
imbalance that may be iatrogenically induced.
 causes
• Inadequate oral intake of potassium
• Excess exceretion of potassium
– Mineralocorticoid excess (endogenous or
exogenous)
– Osmotic diuresis: Mannitol and hyperglycemia can
cause osmotic diuresis
– Increased gastrointestinal losses
– Drugs
– Genetic disorders
• Some drugs like:
• Diuretics
• Methylxanthines (theophylline, aminophylline, caffeine)
• Verapamil (with overdose)
• Quetiapine (particularly in overdose)
• Ampicillin, carbenicillin, high-dose penicillins
• Bicarbonate
• Antifungal agents (amphotericin B, azoles,
echinocandins) [16, 17]
• Gentamicin
 Signs and symptoms
• The symptoms of hypokalemia are nonspecific and
predominantly are related to muscular or cardiac
function.
• Weakness and fatigue (most common)
• Muscle cramps and pain (severe cases)
• Worsening diabetes control or polyuria
• Palpitations
• Psychological symptoms (eg, psychosis, delirium,
hallucinations, depression)
 managment
The goal of the treatment is :
• reduction of potassium losses
• Replenishment of potassium stores
• Evaluation for potential toxicities
• Determination of the cause to prevent future
episodes, if possible
• patients with a potassium level of 2.5-3.5 mEq/L
may need only oral potassium replacement
• If the potassium level is less than 2.5 mEq/L,
intravenous (IV) potassium should be given, with
close followup, continuous ECG monitoring, and
serial potassium levels
• The serum potassium level is difficult to replenish
if the serum magnesium level is also low