ELECTROLYTE INBALANCE

Patria Adri Wibhawa

Clinical Rotation Student
Internal Medicine – Medical School of
Christian university of Indonesia, jakarta
 HYPONATREMIA

Defined as an abnormally low serum sodium

concentration (135 mEq/L)
 Etiology and classification
• I. Pseudohyponatremia
– A. Hyperlipidemia  High lipid serum and normal
osmolality
– B. Hyperglicemia  Finding hyponatremia and
hyperglicemia with normal or elevated serum
osmolality
• II. Hyponatremia with increased body total sodium
 This is a state in which an excess of total body
sodium and an event greater excess of total body
water  Edema, ascites or both. Serum osmolality is
low  CHF, Cirrhosis hepatic, SN
III. Hyponatremia with decreased total body
sodium
 Condition associated with both sodium and
water depletion are characterized by the
abcense of edema or ascites  Symptom and
sign  tachycardia, decreased sentral venous
pressure, a high hematocrite elevated serum
total protein may be present
• A. Decreased Urin sodium concentration (10
mEq/L), Ussualy associated with :
• a. Decreased chloride concentration
1. GI losses
- Vomiting or nasogatric suction or both
- Diarrhea
2. Exessive respiration with replacement of water
but not of the sodium losses
3. Volume depletion without replacemennt of loss
fluid and electrolyte after diuretic therapy
 • B. Increaesd urin sodium concentration (10
mEq/L)
Causes include adenocortical insufficiency and
salt losing nephropathy
4. Hyponatremia with normal Total body sodium
The disorders include in this category are not
associated with edema or volume depletion
A. Hypothyroidism or glucocorticoid deficiency may be
associated with euvolemic hyponatremia
• B. SIADH
 This condition may be idiopathic or may associated
with one of the following disorder, diseases of the
central nervous system (Stroke, meningitis),
Pulmonary diseases ( TBC, pneumonia), drugs
(Chlorpropamide, narcotics, barbiturates, vincristine,
antidepressants and clofibrate).
1.Criteria for diagnosis :
a. Hypotonicity of the body fluids
b. Urin osmolality greater than 100 mOsm/kg of water
c. Normal renal, adrenal, and thyroid function
d. Increased urinary excretion of sodium (30mEq/L)
e. Elevated serum concentration of ADH
f. Reversal of the syndrome by adequate fluid restriction
2. Comment  When a steady state is reached, some of the
abnormality described may not be present
 Diagnostic approach
• Once the diagnosis of hyponatremia is made,
the serum sodium lever should be rhececked
and the serumm osmolality determined
1. If the serum osmolality is normal or high in
the presence of confirm hyponatremia, the
possibility of hyperlipidemia or hyperglicemia,
or both should be investigated
2. If the serum osmolality is low, confirming the diagnosis of
true hyponatremia, The satus of the extracelluler fluid
volume should be assesed.
A. The presence of edema, ascites, rales, and S3 gallop, or
increaed jugular venous pressure indicate an excess of
total body sodium.
B. Postural pulse and BP changes, decreased skin turgor, dry
mucous membranes or decreased JVP indicate decreased
total body sodium
C. In the absence of signs of either increased or decreased
total body sodium TSH and cortisol should be checked
before entertaining the diagnose of SIADH
 Therapeutics
• A. Total Body Water ( Hypovolemia)
1. If Volume depleted, use NaCL 0,9 % (154 mEq/L)
2. Calculate sodium deficit :
- Target sodium = 125-135 mEq/L (130 mEq/L)
- Sodium deficite = 0,6 x weght in Kg ( desired Na – actual
Na)
- Correct at a rate not > 0,5 mEq/L/hours
 Give the patient 50% of calculated amount of sodium in
the first 8 hours and the other 50% in the next 16 hours
- Use normal saline, do not give hypotonic fluids until
serum sodium is more than 125 mg/L
3. Correct potassium deficit also
 Hypokalemia
• Definition
 As an abnormality low serum potassium
concentration (3,5 mEq/L)
 Etiology
• I. Non renal causes
A. Decreased pottasium intake
B. GI Losses of pottasium
1. Associated with alcalosis and volume depletion
a. Gastric suctioning and vomiting
b. Chronic laxative abuse ( maybe associated with
acidosis or normal PH as well)
2. Associated with acidosis
a. Diarrheal states ( including villous adenoma or
Zollinger-Ellison)
b. Ureterosigmoidostomy
II. Renal causes
A. Pottasium wasting associated with metabolic
acidosis
1. Renal tubular acidosis
2. Postobstructive uropathy
3. Diuretic phase of acute tubular necrosis
4. Chronic pyelonephritis
B. Pottasium wasting associated with metabnolic
akalosis
1. Diuretic therapy ( Furosemide, ethacrynic acid,
thiazides)
2. Disorder with increased aldosteron secretion and
hipertension ( Primary aldosteronism, renovascular
hypertension, essensial hypertension with vomiting
and diarrhea, diuretic therapy, oral contraception,
steroid therapy)
3. Disorder with increased aldosteron without
hypertension
(Salt losing nephropathy, juxtaglomerular
hyperplasia)
4. Disorder with normal or decreased aldosteron
and hypertension ( Cushing syndrom )
 Symptom and sign
1. Most symptom are non specific
anorexia, nausea, vomiting, abdominal
distension, ileus, weakness, decreased deep
reflexes, and depressed sensorium.
2. The ECG finding include lowering, flattening,
notching, or inversion of the T wave, prominent
U, depression of the S-T segment and arrhytmia.
3. Nephrogenic diabetes insipidus, rhabdomyolysis,
and aggravation of hepatic coma may also occur
 Diagnosis approach
I. Patient with hypokalemia require a through
investigation to determine whether the pottasium loss
is the result of renal or extra renal mechanism.
II. Renal origin  24 hours urinary excretion of
Pottasium should be measured while the patient is on
a reguler salt intake
• <20 mEq/24 hours  Excellent evidence
• > 20 mEq/24 hours especially 60 mEq/24 hours 
Suggestive of renal pottasium wasting
III. In patient with both metabolic alcalosis and
pottasium wasting, volume depletion may
cause the abnormal state to persist.
 Therapy
1. Oral ruote Oral pottasium should be given
preferably asdiluted liquid with or after meals or as
tablet, which must be swallowed and not allowed
to
dissolve in the mouth.
 Oral Kalium 0,75 gm (10mEq) 2-3 days
 Oral KCL solution 15-30 cc
(1gm KCL = 14 mEq k+)
2. Intravenous route
Max : 10-20 mEq/Hours.
Higher rate of infusion may be administered if
the clinical situation warrants a more rapid
correction of the hypocalemia.
 20-40 mEq in 1 L of saline or dextrose
solution
 Hypocalsemia
• Definition
Hypocalsemia exists when the total serum
calcium value is less than 8,5 mg/100mL.
 Approximately 50% of calcium in blood is bound
mainly to albumin and globulins
 The ionized calcium concentration is 5 mg/dL
and this fraction is biologically active
 Concurrent measurement of albumin is
indicated in order to show total serum calcium
 ETIOLOGY
• The most common cause of hypocalcemia is
surgically induced hypoparathyroidism.
• Therefore, if a thyroidectomy scar is present,
the diagnosis is usually obvious.
• A history of antecedent illness, past GI
surgery, or known underlying renal disease
may elucidate the cause in other case.
• I. Hypoparathyroidism
A. Surgically induced, partial or complete
Most common
B. Idopathic
C. Transient hypoparathyridism of infancy
(newborn)  Usually partial
D. Bioinactive parathyroid hormon (PTH)
• II. Reduction in serum albumin
A. Malabsorption states
B. Short bowel syndrome
C. Chronic liver disease and liver failure
D. Nephrotic syndrom
E. Malnutrition
• III. Pancreatitis
• IV. Renal disease
A. Renal tubular dysfunction
B. Acute tubular necrosis
C. Chronic renal failure
• V. Rickets and osteomalasia
• VI. Pseudohyparathyroidism, types I and II
• VII. Hypoparathyroidism in association with
other disease states, which may be familial
A. Addison’s disease
B. Pernicious anemia
C. Candidiasis
• VIII. Medullary carcinoma of the thyroid,
sporadic, familial, or in men
• IX. Hyperphosphatemia
• X. Other vitamin D-related disorders
 Symptoms
• Usually occur when the total serum calcium
value is below 7,5 mg/ 100mL, but they
sometimes occur at higher levels when there
has been a rapid decrease in the serum
calcium concentration.
• The symptomps are generally those of
neuromuscular irritability.
 Symptoms
I. Numbness and tingling of the face, hand, and
feet
II. Muscle cramps in the arms, hands, abdomen,
legs and feet
III. Increased number of stools or diarrhea
IV. Headaches, usually frontal, irritability, anxiety
V. Difficulty in breathing, particularly noisy
breathing during exercise or sleep
VI. Seizures, which are common, in infants this may
be the only complaint
VII. Decreased vision
VIII. Nail growth abnormalities and infections,
delay in “cutting” teeth
IX. Dry skin, often infected
X. Weight problem
A. Weight loss in association with chronic
systemic disease
B. difficulity in losing weight in
pseudohypoparathyroidism
XI. Bone growth abnormalities or pain (rickets
and osteomalacia)
 Sign
• Sign of neuromuscular irritability occur most
often.
• The following findings may be noted on physical
examination:
1. Thyroidectomy scar
2. Dry skin
3. Abormal or infected nails
4. Cataracts
5. Chovstek’s sign
6. Trousseau’s sign
7. Crowing noises during sleep
8. Seizure disorder  may be the finding in infants
9. Hypotension
10. Bone pain or bone abnormalities, including
abnormal growth, bowing and brachydactylia
11. Goiter if present may suggest medullary
carcinoma of the thyroid, chronic thyroiditis or
graves disease
 Diagnostic Approach Hypocalcemia

• Initial Investigation
 The most common
 THERAPY
• Medication : Is to correct the deficiency’s with
IV calcium ( Ca.Gluconas/ Chloride 10%) or
peroral (Ca.Gluconas/Carbonate); Can give
with vit D in a higher dose