Abnormalities of Electrolytes

kibaru
 objectives
By the end of the session the student
should be able to

◦ Outline the common electrolytes, etiology

of excess or deficiency and treatment
 Potassium
Potassium is mostly contained in the
intracellular compartment.

serum potassium levels do not indicate the

total body potassium accurately.
Blood pH levels affect the
distribution of potassium between
the intracellular and extra cellular
compartments.
A low pH shifts potassium out of the
cell, while alkalosis drives potassium into
the cell.

A handy rule is that each 0.1 unit change

in pH results in a 0.3-0.6mEq/L change in
serum potassium.
The intracellular potassium concentration
affects cellular enzymes and intracellular pH.

 Low intracellular potassium raises the pH,

whereas high intracellular potassium lowers
the pH.

Potassium is necessary for maintaining cell

volume because of its important contribution
to intracellular osmolality
Potassium is plentiful in food.
 Dietary consumption varies
 1–2 mEq/kg is the recommended
intake.
The intestines normally absorb approximately
90% of ingested potassium.

 Most absorption occurs in the small intestine,

whereas the colon exchanges body potassium
for luminal sodium
There is some loss of potassium in sweat,
but this is normally minimal.

The colon has the ability to eliminate

some potassium.
Potassium is freely filtered at the glomerulus

 90% is reabsorbed before the distal tubule

and collecting duct, the principal sites of
potassium regulation.
Hypokalemia
Hypokalemia is defined as a serum
potassium level of < 3.5mEq/L.

Hypokalemia often results from

chronic diuretic use

 unreplaced electrolyte loss from NG

drainage.
CAUSES
TRANSCELLULAR SHIFTS  
   Alkalemia   
 Insulin   
 β-Adrenergic agonists e.g    Drugs/toxins
(theophylline, barium, toluene, cesium
chloride)
   Hypokalemic periodic paralysis congenital
    Thyrotoxic period paralysis
DECREASED INTAKE
Anorexia nervosa

EXTRARENAL LOSSES
    Diarrhea
    Laxative abuse
    Sweating    Sodium polystyrene sulfonate (Kayexalate)
 clay ingestion
Distalrenal tubular acidosis (RTA)
Proximal RTA
Ureterosigmoidostomy
Diabetic ketoacidosis
Tubular toxins: amphotericin, cisplatin,
aminoglycosides
Interstitial nephritis
Diuretic phase of acute tubular necrosis
Postobstructive diuresis
Hypomagnesemia
High urine anions (e.g., penicillin or
penicillin derivatives)
Emesis nasogastric suction
Chloride losing diarrhea
Cystic fibrosis
Low chloride formula
Posthypercapnia
Gitelman syndrome
Bartter syndrome
Loop and thiazide diuretics
◦ Adrenal adenoma or hyperplasia
◦ Glucocorticoid-remedial aldosteronism
◦ Renovascular disease
◦ Renin-secreting tumor
◦ 17α-hydroxylase deficiency
◦ 11β-hydroxylase deficiency
◦ Cushing syndrome
◦ 11β-hydroxysteroid dehydrogenase deficiency
◦ Licorice ingestion
◦ Liddle syndrome
RENAL LOSSES

◦ With metabolic acidosis

◦ Without specific acid-base disturbance
◦ With metabolic alkalosis
 Clinical Manifestations.

The heart and skeletal muscle are especially

vulnerable to hypokalemia

Hypokalemia makes the heart especially

susceptible to digitalis-induced arrhythmias such
as supraventricular tachycardia, ventricular
tachycardia, and heart block
The clinical consequences in skeletal
muscle include muscle weakness and
cramps.
Paralysis is a possible complication,
generally only at levels less than 2.5
mEq/L.
This usually starts with the legs, followed
by the arms.
Respiratory paralysis may require
mechanical ventilation.
 Some patients develop rhabdomyolysis; the
risk increases with exercise.
Hypokalemia slows gastrointestinal motility.
This manifests as constipation or, with levels
less than 2.5 mEq/L, ileus may occur.
Hypokalemia impairs bladder function,
potentially leading to urinary retention.
Hypokalemia causes polyuria and polydipsia by
two mechanisms: primary polydipsia and impaired
urinary concentrating ability, producing a
nephrogenic diabetes insipidus.

Hypokalemia stimulates renal ammonia

production, which is clinically significant if hepatic
failure is present because the liver cannot
metabolize the ammonia.
Chronic hypokalemia may cause kidney
damage, including interstitial nephritis and
renal cysts.

 In children, chronic hypokalemia, as in

Bartter syndrome, leads to poor linear growth.
ECGmanifestations:
Flattened T waves
Prolonged QT interval
Appearance of U waves
Treatment
Severe, symptomatic hypokalemia
receives more aggressive treatment.

 Supplementation is more cautious if renal

function is decreased because of the
kidney's limited ability to excrete
excessive potassium
Oral potassium is safer
 The dose of intravenous potassium is 0.5-1
mEq/kg, usually given over 1 hr.
 Conservative dosing is generally preferred.

Potassium chloride is the usual choice for

supplementation
For patients with excessive urinary losses,
potassium-sparing diuretics are effective, but they
need to be used cautiously in patients with renal
insufficiency.
Hyperkalemia
Itis defined as serum potassium of
greater than 6meq/L in a nonhaemolyzed
sample.

The serum potassium level is normally

0.4 mEq/L higher than the plasma value,
secondary to release from cells during clot
formation.
 This phenomenon is exaggerated with
thrombocytosis because of potassium release from
platelets.
◦ For every 100,000/m3 increase in the platelet count, the
serum potassium increases by approximately 0.15 mEq/L.

This also occurs with the marked white blood cell

elevations sometimes seen with leukemia.
◦ Elevated white blood cells counts, typically greater than
200,000/m3, can cause a dramatic elevation in the serum
potassium concentration.
aetiology
SPURIOUS LABORATORY VALUE
 Hemolysis
Tissue ischemia during blood drawing
Thrombocytosis
Leukocytosis
INCREASED INTAKE
◦ Intravenous or oral
◦ Blood transfusions
TRANSCELLULAR SHIFTS
 Acidemia
 Rhabdomyolysis
 Tumor lysis syndrome
 Tissue necrosis
 Hemolysis/hematomas/GI bleeding
 Succinylcholine
 Digitalis intoxication
 Fluoride intoxication
Beta-adrenergic blockers
Exercise
Hyperosmolality
Insulin
deficiency
Malignant hyperthermia
Hyperkalemic periodic paralysis
Adrenal disorders
Acquired Addison disease
21-hydroxylase deficiency
3β-hydroxysteroid dehydrogenase
deficiency
Lipoid congenital adrenal hyperplasia
Adrenal hypoplasia congenita
Aldosterone synthase deficiency
Adrenoleukodystrophy
Other causes
 Urinary tract obstruction
 Sickle cell disease
 Kidney transplant
 Lupus nephritis
 Angiotensin-converting enzyme inhibitors
 Angiotensin II blockers
 Potassium-sparing diuretics
 Cyclosporin
 Nonsteroidal anti-inflammatories
 Trimethoprim
DECREASED EXCRETION
◦ Renal failure
◦ Primary adrenal disease
◦ Hyporeninemic hypoaldosteronism
◦ Renal tubular disease
◦ Medications
Clinical Manifestations
 The most import effects of hyperkalemia are due
to the role of potassium in membrane
polarization.
 The cardiac conduction system is usually the
dominant concern.
 Some patients have paresthesias, weakness, and
tingling
 but cardiac toxicity usually precedes these clinical
symptoms, emphasizing the danger of assuming that
an absence of symptoms implies an absence of
danger.
ECG changes in hyperkalemia include
peaked T-waves, widened QRS
configuration, supraventricular
tachycardia, ventricular tachycardia and
ventricular fibrillation
 treatment
-discontinuation of all potassium
administration

-Calcium gluconate 100-200mg/kg

(1-2ml/kg of 10% solution)
◦ is administered as a slow infusion over
5-10 minutes

it stabilizes the heart muscles

-insulin
is administered (with glucose to avoid
hypoglycemia)
◦ to drive potassium into the ICF compartment.

B agonists e.g ventolin nebulization-

◦ to drive potassium into the ICF compartment.

Medications are administered to enhance potassium

excretion including Frusemide 1mg/kg body weight
alkalinization is done either by hyperventilating or
by administering sodium bicarbonate 1-2meq/kg
intravenously.

 Sodium polystyrene sulfonate (kayexalate) 1g/kg

body weight PR.

Rapid potassium removal can be achieved by

dialysis or exchange transfusion
 Calcium
Total serum calcium levels in infants decline from values
of 10-11mg/dL at birth to 7.5-8.5mg/dL over the first 2-3
days of life.

Approximately 50% of total calcium is in the ionized form

and is the only biologically available form of calcium.
Ionized calcium values, rather than
total values correlate better with
calcium functions such as cardiac
contractility
 Hypercalcemia
Rarely seen in infants.

Defined as total serum calcium concentration

>11mg/dL or an ionized calcium
concentration of > 5mg/dL(1.25mmol/L)
Hypocalcemia
More common and is defined as total serum
concentration < 7mg/dL or ionized calcium
concentration of <4mg/dL(1mmol/L).
Early onset hypocalcemia may occur
within first 3 days in premature infants
born to mothers with poorly controlled
diabetes or infants who experienced
perinatal asphyxia.
Lateonset hypocalcemia develops after the first
week of life

usuallyassociated with conditions with high

phosphate levels including:
 Hypoparathyroidism
 Maternal anticonvulsant use
 Vitamin D deficiency
Vitamin D deficiency usually resolves with
reduction of the renal phosphate load or
vitamin D supplementation.
Calcium supplementation should be given if
total serum calcium is < 6.5mg/dL

 or ionized calcium concentration is < 0.8-

0.9mmol/L
SODIUM METABOLISM

Sodium is the dominant cation of the and it is the principal

determinant of extracellular osmolality.

 Less than 3% of sodium is intracellular.

 More than 40% of total body sodium is in bone

the remainder is in the interstitial and intravascular spaces.

The low intracellular sodium concentration, about
10 mEq/L, is maintained by Na+,K+-ATPase, which
exchanges intracellular sodium for extracellular
potassium.

Sodium is absorbed throughout the gastrointestinal

tract, with limited regulation.
Mineralocorticoids increase sodium transport into
the body
◦ although this has limited clinical significance.

 The presence of glucose enhances sodium

absorption due to the presence of a co-transport
system.
◦ This is the rationale for including sodium and glucose in
oral rehydration solutions.
Excretion
 Sodium excretion occurs in stool and sweat
◦ Sweat contain has 5-40 mEq/L of sodium

kidney regulates sodium balance and is normally

the principal site of sodium excretion.
The excretion of sodium by the kidney is
not regulated by the plasma osmolality.

The patient's effective plasma volume
determines the amount of sodium in the
urine.
This is mediated by a variety of
regulatory systems, including the renin-
angiotensin- aldosterone system and
intrarenal mechanisms.

In hyponatremia or hypernatremia, the

underlying pathophysiology determines
the amount of urinary sodium, not the
serum sodium concentration.
hypernatremia
Hypernatremia is a sodium concentration
greater than 145 mEq/L or greater than
150 mEq/L

 Mild hypernatremia is fairly common in

children, especially among infants with
gastroenteritis.
Hypernatremia in hospitalized patients is frequently
iatrogenic
◦ caused by inadequate water administration
◦ or excessive sodium administration.

Moderate or severe hypernatremia has significant

morbidity due to
◦ underlying disease
◦ the effects of hypernatremia on the brain
◦ the risks of overly rapid correction.
Causes of Hypernatremia
EXCESSIVE SODIUM
◦ Improperly mixed formula
◦ Excess sodium bicarbonate
◦ Ingestion of seawater or sodium chloride  
◦ Intentional salt poisoning (child abuse or
Münchausen syndrome by proxy)
◦ Intravenous hypertonic saline   
◦ Hyperaldosteronism   
WATER DEFICIT   
 Nephrogenic diabetes insipidus  
 which resuits in tubular concentration defect.
   Acquired    X-linked
 Autosomal recessive
 Autosomal dominant
 Central Diabetes Insipidus   
 Acquired   
 Autosomal recessive
 Autosomal dominant    Wolfram syndrome
WATER DEFICIT
Increased insensible losses   
◦ Premature infants
◦ Radiant warmers   
◦ Phototherapy   
Inadequate intake
◦ Ineffective breast-feeding   
◦ Child neglect or abuse    Adipsia (lack of
thirst)
WATER AND SODIUM DEFICITS  
Gastrointestinal losses   
 Diarrhea
 Emesis/nasogastric suction
 Osmotic cathartics (lactulose)
Cutaneous losses  
◦   Burns   
◦ Excessive sweating   
Renal losses
◦    Osmotic diuretics (mannitol)   
◦ Diabetes mellitus   
◦ Chronic kidney disease (dysplasia and obstructive
uropathy)   
◦ Polyuric phase of acute tubular necrosis

 
Postobstructive diuresis
Clinicalfeatures:
1-Manifestations of the etiologic cause.
2- Polyuria, polydipsia, nocturia and function
and ureters, this is seen in patients with
DIABETIS INSIPIDUS.
3- Hypernatraemia occurs only if there
(hypothalamic lesion) or patients unable muscle
twitches, lethargy, weakness, seizures, coma or
death.

With hypernatraemia, there is a shrink of
brain cells leads to decrease in brain size
which if severe it may lead to rupture of
vessels with focal intracerebral or
subarachnoid

Ifpatient survives, brain cells will adapt

and regain size.
Usually the hypernatraemic patient is
hypovolaemic, we calculate the water
deficit by the equation:
water deficit (litre)=Plasma Na/140−1x
(0.6 X body weight)
 Usually the hypernatraemic patient is
hypovolaemic, we can calculate
the water deficit by the equation:
◦ Water deficit (litre)=Plasma Na/140−1x (0.6 X body
weight) or
◦ calculating the water deficit: body weight*0.6(1-
145/current sodium level
The water deficit could be given orally as water or
intravenous as 5% dextrose in water

If there is Na+ loss as well give D 5%/1/2 saline

(glucose 5% in half tonic saline) is given.
Because of the dangers of overly rapid
correction, hypernatremia should not be
corrected rapidly.

The goal is to decrease the serum sodium

by less than 12 mEq/L every 24 hr, a rate
of 0.5 mEq/L/hr.
Ifa child develops seizures from brain edema
secondary to overly rapid correction
◦ administration of hypotonic fluid should be stopped and
an infusion of 3% saline can acutely increase the serum
sodium, reversing the cerebral edema.
Normal saline is preferable to lactated
Ringer solution because the lower sodium
concentration of the lactated Ringer
solution can cause the serum sodium to
decrease too rapidly, especially if
multiple fluid boluses are given.
 Rarely the hypernatraemic patient is
hypervolaemic, in this situation

we have to give furosemide (lasix) and compensate

urine loss with either oral water or D 5% I.V.

 Treatment of the etiologic cause as DDAVP

intranasally for Central Diabetes Insipidus.
 Hyponatraemia
Definition:
Hyponatraemia is a state where plasma sodium
concentration is less than 135 mmol/L.

Hyponatraemia is the commonest electrolyte

abnormality in hospitalized patients.
Usually this is dilutional hyponatraemia due
to defective renal water excretion as a result
of excess secretion or potentiation of ADH
 causes
Hypovolaemic Hyponatraemic states:
• Diuretic therapy.
• Mineralocorticoid deficit (Addison's disease).
• Salt-losing nephropathy (analgesic nephropathy,
chronic
tubulo- interstitial nephritis, incomplete urinary
tract
obstruction, after recovery from acute
tubular necrosis and
after release of urinary obstruction).
• Gastrointestinal losses (diarrhea or
vomiting).
• Fluid loss in third space (peritonitis,
ileus, burn or crush injury).
In these conditions volume receptors are stimulated

with secretion of ADH which will then stimulate
water reabsorption from the distal nephron.
◦ This process will continue even with development of
hyponatraemia and hypoosmolality owing to the fact that
volume receptors are more potent than the osmoreceptors.
2. Hypervolaemic (oedematous) Hyponatraemic
states:
• Liver cirrhosis
• Congestive heart failure.
• Nephrotic syndrome
• Renal failure with water overload.
In these conditions, although total body water is
increased, the effective circulating blood volume is
decreased as the excess fluid is extravascular and is
interstitial.

The decreased effective circulating volume results

in excessive stimulation and secretion of ADH with
more water retention.
Euvolaemic (Normal volume) Hyponatraemic
States:
• Hormonal (Myxoedema, glucocorticoid deficiency
or exogenous ADH vasopressin).
• Massive water load (psychogenic polydipsia,
parenteral fluid or excessive water absorption
during bladder irrigation at transurethral
prostatectomy).
• Syndrome of inappropriate secretion of ADH
(SIADH)
• Essential hyponatraemia:
◦ Occurs mostly with chronic illness, under nutrition or
with T.B.

◦ There is a resetting of the osmostat (in the hypothalamus)

for lower level of osmolality and consequently lower
plasma sodium concentration.
Clinical Features of Hyponatraemia:
• Manifestations of hyponatraemia
depend greatly on the rate of its
development.
A very slowly progressive hyponatraemia
can be asymptomatic while acutely
developing hyponatraemia could be very
serious.

• With hyponatraemia, plasma will be
hypotonic while cells (especially brain
cells) will be hypertonic. To achieve
osmotic equilibrium, water will move
from plasma to cells with a consequent
cell oedema (brain oedema).
• Plasma sodium concentrations above 120 mmol/L
are usually well tolerated, while the majority of
patients will have severe cerebral dysfunction once
plasma sodium is below 110 mmol/L
◦ lethargy
◦ anorexia, nausea
◦ vomiting
◦ confusion
◦ disorientation
◦ convulsions
◦ coma and even permanent brain damage).
 Treatment of Hyponatraemia:
• In severe hyponatraemia, rapid correction with
hypertonic saline is contraindicated as it may
lead to fatal central pontine myelinolysis.

 It is wise to increase plasma sodium by only 5-

10 mmol/Litre per 24 hours.
This is achieved through the administration of
loop-diuretic and normal saline and in severe
cases, small amounts (100-200 ml) of hypertonic
(double strength i.e. 300 mmol/L) saline may be
infused.
Correction of the underlying cause in the
overloaded patient water restriction can be
combined with loop-diuretics as furosemide and
sometimes salt supplements.

In SIADH, lithium or demeclocycline may be

given to induce a renal concentration defect.