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Review : Diagnostic and

Treatment of Electrolyte
Disturbances
Calcarina F R Wisudarti

Electrolyte composition of body


fluid compartments
Electrolyte

ICF

Plasma

Interstitial

10

140

145

155

3.7

3.8

102

115

10

28

30

<0.01

1.2

1.2

Magnesium

10

0.8

0.8

Phosphate

105

1.1

1.0

Natrium
Kalium
Chloride
Bicarbonate
Calcium

Osmolality :concentration of a solution


which expressed in osmole per kg water
Osmolarity : concentration of a solution
which expressed in liter
Tonicity : describe the osmolarity of a
solution relative to plasma
Serum osmolality : 2 (Na) +
glucose/18+ BUN/2.8 + (serum
ethanol)/4.6 +
( unmeasured
osmoles )
Normal serum

Hypernatremia

Hypernatremia : serum natrium level > 145 mEq/L


Rare in patient with intact ADH, thirst mechanism and acces
to free water
Always associated with hyperosmolality
Causes :
Water
depletion :
Extrarenal loss :
( exposure , GIT
losses )
Renal loss :
Osmotic
diuresis,
diabetes
insipidus

Salt gain :
Hypertonic
saline
Sodium
bicarbonate

Diagnosis
Symptoms : pyrexia, restlessness,
irritability, drowsiness, lethargy,
confusion and coma.
Na serum exceeds 155 mmol/L
osmolarity
Diff Diagnose
(Urine
>330
mOsm/kg
)
800

Dehydration
Hypodipsia
Sodium intoxication

300 800

Osmotic diuresis
Partial or mild DI

< 300

Central or nephrogenic DI
Marini,2006

Diagnosis of DI : rise in urine


osmolality within 2 hours after
administration of 5 U aqueous
vasopressin sc or 1mcg DDVAP
> 50% increased in urine osmolality
central DI, while lesser rise
nephrogenic DI
Water deprivation test is risky .

therapy
Treatment of hypernatremia should addressed
on underlying cause and corrected the
hypertonicity
Reducing 1mmol/L/hour in acutely
hypernatremic patients ( in hours )
Reducing 0.5 mmol/L/hour in longer duration
hypernatremia.
Recommended target is 10 mmol/L reduction
per day.
If hemodynamic instability is present give
isotonic solution before replacing water deficit
If volume overload is present treat with diuretic
and 5 % dextrose.
McIlwaine,200
5

Fluid administration orally, enterally or


intravenously.
Formula :
Change in serum Na + =
infusate Na+ - serum Na+
TBW +1
Water deficit = TBW x ( 1 (140/sodium conc)

Aquaeous vasopressin 5 10 U im/sc q 4 to


6 hours or 2 mcg DDVAP q 12 hours for DI

Adrogue,2000

Dyalisis may be indicated ( in renal


failure patient )
Ongoing fluid and electrolyte loss
should be replaced
Neurologic status closely monitored

Hyponatremia
Serum Natrium < 135 mmol/L
Isotonic
hyponatremia
Hyperproteinem
ia
Hyperlipidemia

Hypotonic
hyponatremia
Hypovolemic
Hemorrhage
Vomiting
diarrhea
Isovolemic
Water
intoxication
SIADH
Hypervolemic
Heart Failure
CRF

Hypertonic
hyponatremia
Osmotic
agent :
Mannitol
Glucose
Starch

Diagnosis
Symptomps :nausea, vomiting,
lethargy, confusion,coma
Na< 125 changes in cognition and
motor function
Na < 120 confusion and seizure

Clinical approach
What is the serum osmolality ?
What is the intravascular volume status ?
What is the serum concetration of
sodium, albumin, lipid ?
What is the urinary volume,osmolality
and electrolyte composition ?
What medication and fluids is the patient
receiving ?
Is there evidence of renal disease ?
Is the patient edematous ?

Therapy
The pecific treatment depends on
acuteness, cause
Chronicand severity
Acute
symptomatic
hyponatremia

symptomatic
( > 48 h or
unknown )

3% saline
Loop diuretic
Correct no more
than 2 mEq/L
Correct no more
than 12 15
mEq/L/h over
first 24 h

3% saline
Loop diuretic
Correct no more
than 1.5 mEq/L
Correct no more
than 12 15
mEq/L/h 24 h
Correct to resolution
of symptomp
Close monitoring of
electrolytes and
neurologic status

Asymptomatic
hyponatremia
Treat underlying
cause
Euvolemia
Water restriction
Occasionally loop
diuretics
Hypovolemia
Normal saline
Hypervolemia
Salt and water
restriction
Loop diuretics for
some patients

Hyperkalemia
Serum kalium > 5mmol/L
Causes
K+

K+

K+

Clinical features
Parestesia, tingling, weakness,
flaccid paralysis
Cardiac arrythmia:
peaking T, flattening
P, prolongation PR int
widening QRS complex
sine wave

Therapy
Treatment Mechanis
m

Dosage

Onset

Duration

Calcium

Cardiac cell
stabilizer

10 ml of 10%
solution

seconds

30 60 min

Regular
insulin

Shift K+ into
cells

10 U iv +
glucose 50 g

15 30
min

24h

Albuterol

Shift K+ into
cells

10 20 mg by
inhaler over 10
min

20 30
min

2-3 h

Sodium
bicarbonat
e

Shift K+ into
cells

In cases of
acidosis

delayed

__

Kayexalate
with
sorbitol

Removes K+
from body

Oral : 15 30 g
Enema : 30 50
g

1h

__

Loop
diuretics

Removes K+
from body

intravenous

1h

__

Hypokalemia
Serum kalium < 3,5 mmol/L
Causes : decrease intake, increased losses,
redistribution of Kalium
Urinary K, Cl and systemic acid base
status are required for determining
etology of hypo K

Clinical feature
Weakness, hypotonicity,
constipation, ileus, ventilatory failure
Cardiac arrhythmia
ST segmen depression
flattened or inverted
T, heightened U
prolonged QU interval

Treatment
In life threatening hypo K
replacement of K. Maximal infusion
rate 20 40 mEq/h with continuous
cardiac monitoring.
Oral supplementation, safer, produce
gradual increase.

Hypercalcemia
Rare in critically ill patient
Serum Calcium > 2,60 mmol/L ( 10,4
mg/dL)
Caused by bone resorption
Hyperparathyroid and malignancy
Prolonged immobilization, thiazide
diuretics

Clinical feature
Nausea, vomiting, abdominal pain
and ileus
Ca++ > 12 mg/dL may manifest
confusion,delirium,psychosis and
coma.
Hypotension, hypovolemia
shortened QT

Therapy
Volume expansion with saline ( reducing 13 mg/dL )
Loop diuretics ( reducing 4 5 mg/dL each
day )
Calcitonin and biphosphonates ( inhibition of
bone resorption )
Calcitonin 8 U q 12 h ( iv or sc )
Biphosphonates : Etidronate ( 7.5mg/kg/d in
250 NS for 4 h in 3 days ), Pamidronate (60
90 mg infusion for 2 4 h single dose ),
Zoledronic acid ( 4 mg iv over 15 min single
dose )

Hypocalcemia
Cause :
Decreased intake
Binding and sequestration of Ca :
phosphate, chelating agent (e.g EDTA ),
citrate, pancreatitis
Inability to mobilize bone calcium (PTH )
Decreased in serum protein
concentration. 1 g/dL albumin reduction
reduce calcium by 0.8 mg/dL.

Clinical feature
Neuromuscular irritability,
carpopedal spasm
Parestesia, cramp and tetany
CNS sign : seizures, papilledems,
hallicinations,confusion, depression
QT prolongation

Treatment
Critical threshold < 0.8 mmol/L.
Treatment of asymptomatic hypo Ca
( > 0.8 mmol /L ) is unnecessary.
10 % CaCl contain 27 mg/ml (1.36
mEq ) elemental Ca. 10% Ca gluc 9
mg/ml ( 0,46 mEq). 200 mg
elemental Ca is necessary to raise
serum Ca by 1 mg/dL.

Hypermagnesemia
Uncommon, unless large iv doses
infused or conventional doses given for
renal failure patients.
Clinical sign :
Mg > 4 mEq/dL hyporeflexia and
hypotension
Mg > 7 mEq/dL somnolence
Mg > 10 mg/dL heart block and
paralysis

THERAPY
Calsium gluconate ( 1 2 g ) iv
Isotonic saline and loop diuretic
Dyalisis

Hypomagnesemia
Normal total concentration ; 1.5 2.3 mg/dL
Caused by :
Inadequate Mg intake
starvation
Increased renal or gastrointestinal loss
amphotericin,aminoglycosides, diuretics,
diabetes, ATN
inflammatory bowel disease, diarrhea ,
vomiting, NGT losses, pancreatitis
Intracellular shift of Mg
Refeeding with glucose , amino acid, insulin,
cathecolamines, metabolic acidosis

Clinical sign
Neuromuscular : muscle cramp,
carpopedal spasm, muscle weakness,
fasciculations
Neurologic :Seizures, nystagmus,
delirium
Cardiovascular : flattened T, U and
prolonged QT, atrial and ventricular
dysrythmia

THERAPY
Evaluation of underlying disease
Administration of Mg :
Oral : Mg gluc ( 500mg =1.2 mmol )
Mg oxide ( 400 mg = 6 mmol )
IV : Mg sulphate ( 1 g = 4 mmol )
Mg chloride ( 1 g = 4.5 mmol )
For iv Mg replacement , bolus and continous
infusion or infusion alone are recommended
Torsades de pointes 1 2 g over 5 min
Urgent hypo Mg, bolus 2 3 g Mg SO4
followed by 10 g MgSO4 over next 5 hours