M. Shuja Tahir, M.
Abid Bashir
Faisalabad, Pakistan
Critical Care
FLUID AND ELECTROLYTES - 4
COMPOSITION CHANGES
POTASSIUM
PHYSIOLOGY
Potassium is the main intracellular
cation. Only 2% of total body
potassium is present in the ECF.
Normal serum levels of potassium
ranges from 3.3 - 4.5 mEq/L. Total
2.8 mEq/L ECF Potassium is only 63 mEq (4.5 x
14L in 70 kg adult) but even this little
amount is critical for cardiac and
neuromuscular functions.
Normal daily requirement of
potassium is 1 mEq/kg. Normal dietary
intake is 50 - 100 mEq/day. Most of
this intake (99%) is lost in urine. In
patients with renal failure, the problem
2.5 mEq/L is to get rid of extra potassium.
1% potassium is lost in stools. This loss
may be increased in diarrhea or
mucous producing tumors of the
colon.
In the kidneys H+ & K+ compete for
+
exchange with Na . In alkalosis,
2.0 mEq/L potassium is lost to conserve H+.
Similarly potassium also shifts to
intracellular fluid compartment in
exchange for H+ to compensate
alkalosis. In acidosis exactly opposite
happen.
Renal tubular excretion of potassium is
increased when large quantity of
1.7 mEq/L
sodium in the filtrate is available for
reabsorption. Therefore, potassium
ECG changes in should also be replaced to cover these
Hypokalemia increased losses while replacing fluids
for the treatment of hypovolemia.
144 April to June, 2010
IR-029
HYPOKALEMIA
Hypokalemia is defined as serum level
of potassium below 3.5 mEq/L.
CAUSES
Hypokalemia is unusual because of
large body stores and ample amount
of potassium in diet. Main causes of
hypokalemia are increased excretion
through kidneys or prolonged depri-
vation.
The main causes of hypokalemia can
be summarized as follows:
Increased Losses
! Increased renal excretion
! Diuretics
! Loss from GIT
! Diarrhoea
! Nasogastric aspiration
! Vomiting
! Entero-cutaneous fistulae
! Loss from skin
! Burns
Decreased Intake
! Prolonged starvation
! Anorexia
! Continuous parenteral fluids
without potassium for prolonged
periods (in presence of obligatory
urinary losses (20 mEq / day)
! Re-feeding syndrome (total
parenteral nutrition without pota-
ssium as potassium is incor-
porated in rapidly dividing cells).
Intracellular Shift
(Total potassium is same but ECF level
INDEPENDENT REVIEWS
falls because of shift to intra cellular
compartment).
! Metabolic alkalosis.
! Increased insulin infusion.
! Myocardial infarction.
! Hypothermia.
! Theophyllin.
! Total Parenteral Nutrition without
potassium.
CLINICAL FEATURES
Mild hypokalemia is asymptomatic.
Clinical features of hypokalemia are
because of failure of normal muscular
contractility.
These are ;
! Decreased tendon reflexes.
! Generalized weakness leading to
flaccid paralysis.
! Paralytic ileus.
These features may be masked when
the patient is dehydrated. Rehydration
without Potassium replacement may
further worsen hypokalemia.
ECG Changes
! Ectopics
! T - wave depression
! Prominent U wave
! Depressed ST segment
! Increased PR interval
! QRS Widening
TREATMENT
Principles of treatment include;
! To correct the deficit
! To treat the cause of hypokalemia
! To prevent further hypokalemia by
replacing daily requirement and
loss of potassium.
CORRECTION OF DEFICIT
Although potassium is main intra-
April to June, 2010 INDEPENDENT
cellular cation, still in the absence of
redistribution factors, decrease in
serum potassium gives some clue to the
total body potassium deficit. On an
average decrease in serum level of 1
mmol/L (mEq/L) shows a total
deficiency of 200-400 mEq. If serum
level falls below 2 mEq/L, the deficit is
about 1000 mEq.
This deficit is corrected with KCl at a
rate of 20-40 mEq/hr.
Following important precautions must
be observed in replacing potassium ;
! Renal function of the patient must
be adequate.
! Use of central venous line if
replacement has to be done at a
rate of more than 10 mEq/h.
! Proper cardiac monitoring should
be done during the replacement.
! Do not replace more than 40 mEq/
hour.
! Do not add more than 40 mEq of
potassium to one litre of solution.
TREATMENT OF CAUSE
The cause of hypokalemia has to be
treated e.g; diuretics should be
stopped or changed. Similarly alkalosis
if present, has to be corrected.
REPLACEMENT /PREVENTION
Potassium may have to be replaced for
prevention of hypokalemia in the
presence of continuous losses. The best
way of replacement is oral. 40-100
mEq potassium may be replaced
depending upon the deficiency and
daily losses.
In case of oral intolerance, severe
depletion or symptomatic patient,
potassium may be replaced
REVIEWS 145
 parenterally taking all the above
mentioned precautions.
It is safe to replace the upper limit of
daily GIT losses provided the renal
function is adequate. Potassium
replacement without indication has to
be avoided in oliguric patients and for
up to 12-24 days post-operatively.
6.5 mEq/L
HYPERKALAMIA
Hyperkalaemia is defined as serum
potassium level of 5.5 meq/L or more.
CAUSES
Renal Failure
It is the most important and most
common cause of hyperkalaemia.
Kidneys play a major role (99%) in
7.0 mEq/L
getting rid of extra potassium.
Iatrogenic
Administration of potassium in patients
with impaired renal functions leads to
hyperklamea. Massive blood trans-
fusions may also increase serum
potassium as stored blood has high
potassium because of hemolysis.
8.0 mEq/L
Excessive GIT Bleeding
Absorption of potassium takes place
from hemolysed blood in the gut.
Drugs
Digitalis
Succinyl choline
Shift of Intracellular Potassium To
ECF
9.0 mEq/L
! Acidosis
! Insulin deficiency
ECG changes in ! Tissue necrosis
Hyperkalemia
! Severe injury, trauma or surgical
stress
! Catabolic states
146 April to June, 2010
! Revascularization of severely
ischemic limb
! Intravenous haemolysis
! Sepsis
! Cell lysis after chemotherapy
! Rhabdomyolysis as in crush
syndrome
Spurious
Serum potassium levels are normal,
but if the blood sample is taken from a
strangulated limb (as if tourniquet is
applied for a long time before taking
blood sample), falsely high potassium
levels are observed (because of
potassium release from platelets and
WBCs).
CLINICAL FEATURES
Clinical features are because of hyper
excitability of tissues.
Gastrointestinal Tract
! Nausea
! Vomiting
! Cramps
! Diarrhea
Cardiovascular System
! ECG changes
! Elevated T wave
! Widening of QRS complex
! Decreased voltage of P wave
! Sinusoidal ECG pattern
! Heart blocks
Cardiac arrest may occur in diastole.
TREATMENT
Mild Hyperkalaemia
Administration of exogenous potas-
sium should be with held.
Drugs which may interfere with the
potassium metabolism should be
discontinued. they include:
INDEPENDENT REVIEWS
! Beta blockers.
! NSAIDs.
! ACE inhibitor.
! Potassium sparing diuretics.
Diuresis should be enforced using loop
diuretics.
Severe Hyperkalaemia
(Serum potassium > 6.5 meq/L). It is
an acute emergency. Treatment of
severe hyperkalaemia can be divided
into two phases.
Emergency measures can temporarily
shift the potassium into the cells,
lowering serum potassium levels. It
provides sufficient time for therapeutic
measures.
Temporizing Measures
Glucose + insulin
One of the physiological effects of
insulin is to take the potassium inside
cells. Therefore insulin can be used as a
temporary measure to deal with
hyperkalaemia. Glucose should be
infused at the same time to avoid
hypoglycaemia.
The regimens are ;
1. 5% dextrose water (0.5 g/kg) +
insulin (0.3 units/gm of glucose) as
infusion.
2. 25 gm Dextrose water with 6-10
unit of insulin as a bolus.
3. 10% dextrose water (100 ml) + 20
units of insulin + 45 m Eq
NaHCO3
NaHCO3
50-100 ml 8.4% NaHCO3 (1
mmol/kg) is given I/V over 3-5
minutes. It may be repeated after 10-
15 minutes.
April to June, 2010 INDEPENDENT
CALCIUM GLUCONATE
Calcium gluconate has no effect on
serum potassium levels but stabilizes
the neuromuscular membrane
minimizing the risk of fatal arrhythmias.
5-10 ml of 10% Ca gluconate is given
I/Vover 2-3 minutes.
It should not be given to patient on
digitalis as heart block may occur.
INHALED β-AGONISTS
Beta agonists may decrease serum
potassium temporarily for upto 2
hours, but may increase heart rate and
blood pressure.
2-4 ml of 0.5% solution (10-20 mg) of
albuterol SO4 is given via nebulizer
Therapeutic Measures
Adequate Hydration With Strong Diuresis
Normal saline is given with loop
diuretics (frusemide)
Sodium/potassium Exchange Resins
Sodium polysterene sulfonate (Kay-
exalate) is used to exchange potassium
for sodium. Sodium is retained and
potassium is excreted as Potassium
polysterene sulfonate. It takes upto 24
hours after administration to lower the
serum potassium.
It may be given orally as 20-50 gm
resin in 100-200 ml of 20% sorbitol
every 4 hours.
It may also be administrated as
retention enema (20 gm in 50 ml 70%
sorbitol added to 100-200 ml of
water). It may has to be repeated every
1-2 hours initially. As the patient
stabilizes, the frequency may be re-
REVIEWS 147
 duced to 6 hourly. balance. It may be the last option to get
rid of extra potassium when other
Dialysis measures fail.
It helps to maintain the electrolyte

CALCIUM
CAUSES
M ost of calcium in the body is
present in the bones. Plasma
calcium is present in three forms;
!
!
Malnutrition.
Vitamin D deficiency.
! Hypoparathyroidism.
1. Bound to albumin(40%). ! Surgery (parathyroid, thyroid).
2. Free unionized form (complexed to ! Hypomagnesaemia (Impairs
freely diffusible compounds (15%). PTH secretion & functions)
3. Free ionized form(45%). This ! High GIT losses
unbound ionized form is physio- ! Short gut syndrome, vomiting,
Calcium Metabolism
logically active. diarrhoea
! Sequestration
Calcium plays major role in neuro- ! Pancreatitis
muscular transmission, muscle con- ! Rhabdomyolysis (crush
traction and coagulation. syndrome)
! Massive blood transfusions
Daily Ca intake is 500-1000 mg. (EDTA binds Ca)
Serum calcium levels are 8.9-10.3 ! Hypohosphataemia
mg% (2.23-2.57 mmol/L). ! Ionized to unionized shift
Ionized calcium is 4.6-5.1mg% (1.15- ! Acute alkalosis
1.27mmol/L). ! Hyperventilation
! Vomiting.
The calcium metabolism is controlled ! NaHCO3
by hormones (parathormone and Even after subtotal thyroidectomy tran-
calcitonin) and vitamin D. sient hypocalcaemia may occur for 48-
72 hrs which improves in next 2-3 days.
The unionized and ionized calcium are
in equilibrium. Alkalosis leads to CLINICAL FEATURES
ionized to unionized shift resulting in Neurological
decreased serum levels of ionized ! Circumoral numbness
calcium. Ionization and solubility ! Tetany
Causes of Hypocalcemia
decreases in alkaline urine leading to ! Carpopedal spasm (Trousseu's
stone formation. Acidosis has exactly sign)
opposite effect. ! Facial twitching on taping Facial
Nerve (Chevostek's sign)
HYPOCALCAEMIA ! Laryngeal spasm
Hyopcalcaemia is defined as serum ! Seizures (in extreme cases)
calcium levels below 8mg/dl. ! ECG changes
! Prolonged QT interval
! Ventricullar Arrythmias

148 April to June, 2010 INDEPENDENT REVIEWS

TREATMENT
Treatment depends upon severity of
symptoms and degree of hypo-
calcemia.
For severe symptomatic patients, a
bolus of 200mg elemental Ca (10-20
ml Ca gluconate 10%) is given in 10
minutes to abort tetany followed by 1-2
mg/kg/hr elemental Ca as infusion.
After improvement of symptoms/serum
levels dose may be reduced to 0.3-0.5
mg/kg/hr. Once normal, switch to oral
therapy.
Serum levels of K, Mg & P should also
be checked and corrected.
For asymptomatic patient and mild
hypocalcemia (serum calcium > 7.6
mg/dL) oral calcium can be replaced in
doses of 1-2 g/day.
For severe asymptomatic hypo-
calcemia (serum calcium < 7.6 mg/dL)
Vitamin D has to be added as 50,000
IU Calciferol or 0.4mg
dihydrocalciferol or 0 . 2 5 - 0 . 5 m g
1,25,dihydroxy vit D3
HYPERCALCAEMIA
Hypercalcaemia is defined as serum
calcium levels of more than
10.5mg/dl.
CAUSES
! Milk alkali syndrome.
! Vitamin D intoxication.
! Total Parenteral Nutrition.
! Thiazide Diuretics.
! Hyperthyroidism.
! Granulomatous disease.
! Demineralization of bone.
! Hyperparathyroidism.
! Malignancies.
April to June, 2010 INDEPENDENT
! Primary.
! Secondaries (metastasis).
! Multiple myeloma.
! Prolonged Immobilization.
! Sarcoidosis.
Hyperparathyroidism can be differenti- Carpal Spasm
ated from other causes of
hypercalcemia by raised levels of PTH.
In all other conditions, PTH is
depressed due to negative feedback of
hypercalcemia.
CLINICAL FEATURES
! Bones (bone Pains).
! Stones .
! Groans (abdominal cramps).
! Mental Moans (psychiatric Chevostek`s sign
problems).
! Weight loss / anorexia.
! Dehydration.
! Increased thirst.
! Adynamic ileus.
! Nausea, vomiting, constipation
! Altered mental status
! Somnambulance leading to
stupor leading to coma
! Diffuse weakness leading to
fatigue and lethargy
! Depression
! ECG Changes
! QT shortening
! Arrythmias
TREATMENT
Treatment should be accompanied
by strict monitoring. The principles
of treatment include restriction of
exogenous Ca intake, treatment of
underlying cause and correction of
volume deficit. Thiazide diuretics Causes of Hypercalcemia
should be stopped. Aggressive
measures are required in severe
cases. Critical level of calcium is
REVIEWS 149
 15mg/dl which may be lethal. This
is usually encountered in cancer
patients and patients on cytotoxic
therapy.
Saline + Loop Diuretics
250-500ml normal saline is infused
per hour along with 20mg lasix I/V
every 6 hours. The aim is to main-
tain output at 200-300 ml/ hr. The
rate of infusion and dose of diuretic
is adjusted and monitored accord-
ingly. KCl 20mEq and MgSO4 8-
16mEq (1-2g) may be added to
each liter of normal saline to
prevent magnesium and potassium
deficiency. Regimen may promote a
loss of 2gm Ca in 24hrs
Salmon Thyrocalcitonin
It is mainly used in hypercalcaemia
due to malignancy or hyperpara-
thyroidism. After a test dose of 1 IU
subcutaneously, 4 IU are given
subcutaneous or intramuscular
every 12 hours. It usually takes 6 to
10 hours to lower the serum cal-
cium. The dose may be doubled
after 48 hours if desired results are
not achieved to a maximum dose of
8 IU/kg 6 hourly. Adequate
hydration must be ensured to avoid
renal failure.
Palmidronate Disodium
It is also used in malignancy
induced Hypercalcemia. Adequate
hydration should be ensured. For
mild to moderate hypercalcemia
(12-13.5 mg%), 60 mg is give in
150 April to June, 2010
one liter of ½ saline, saline or
dextrose water over 24 hours. For
severe hypercalcemia, the dose is
90 mg. The dose can be repeated
after 7 days if required.
Plicamycin
The dose is 25 μg / kg / day. It is
also given in 1 Liter of Normal
saline or dextrose water over 4-6
hours once daily for 3-4 days. It
takes 1-2 days to lower serum
calcium which remains low for up to
one week.
Steroids
Prednisolone 40-80mg is given per
day. It decreases calcium absorp-
tion from the gastrointestinal tract
as well reabsorption from the
bones.
Haemodialysis
The haemodialysis may be required in
case of emergency as most of the
above mentioned measures take some
time to lower the serum calcium.
Parathyroidectomy
Emergency parathyroidectomy has to
be performed if medical measures fail.
Inorganic Phosphate
Inorganic phosphates decrease bone
re-absorption and form Calcium
Phosphate salts. These may be used in
emergency to lower the serum calcium.
These are used very cautiously as rapid
infusion may lead to tetany, acute renal
failure or hypotension. These should be
infused slowly over 12 hrs for no more
than 2-3 days.
INDEPENDENT REVIEWS
 MAGNESIUM
M
agnesium is mainly an
intracellular cation. It shares
some properties of potas-
sium and some of calcium. There is
no direct hormonal regulation of Mg
metabolism. Excretion is through the
kidneys.
Normal serum levels are 1.3 - 2.2 meq
/ L (0.65 - 1.1 mmol / L)
HYPOMAGNESEMIA
CAUSES
! Excessive Losses
! From GIT
! Diarrhoea
! Vomiting
! Malabsorpotion
! Biliary fistula
! From kidneys
! Marked diuresis
! Hyperaldosteronism
! Renal tubular acidosis
! Chronic Alcoholism
! Drugs
! Loop diureties
! Cyclosporine
! Cisplastin
! Aminoglycosides
! Shift into ICF compartment
! Acute MI
! Alcohol withdrawal
! Glucose containing solutions
! Redeposition into bone
! Trauma Patients
! After parathyroidectomy
CLINICAL FEATURES
Hypomagnesemia is usually accompa-
nied by hypokalaemia and hypo-
phosphatemia. Main problem is
hyperexcitability of neurological
tissues.
April to June, 2010 INDEPENDENT
The symptoms are:
! Tremors
! Exaggerated reflexes
! Tetany
! Altered mental status in severe
deficiency
ECG changes are similar to that of
hypokalaemia. These are ;
! Depression of T wave.
! QRS Complex Widening.
! Increased PR and QT intervals.
! Ventricular arrythmias may
occur in patients on digitalis.
TREATMENT
Mg can be given orally or parenterally
depending upon the severity of the
situation. In acute emergency (serum
Mg < 1.0 meq/L or if the patient is
symptomatic)1-2 gm of MgSO4
(equivalent to 8-16m eq/L) is given as
an I/V bolus over five minutes, followed
by infusion of 1-2 gm hourly. Once the
patient is stabilized, the dose can be
reduced to a maintenance dose of 0.5-
1g /hour.
For asymptomatic patients, the dose of
parenteral MgSO4 is 50-100mEq /
day (6-12gm) for 3-5 days till the stores
are replenished.
It is important to note that I/V MgSO4 is
treatment of choice for patients of
torsades de pointes as well es
eclampsia and pre-eclampsia. For
maintenance, magnesium can be
given orally.
Oral magnesium is available in three
forms ;
REVIEWS 151

The author :
Muhammad Shuja Tahir
FRCS (Ed), FCPS (Hon)
is professor and head of the
department of Surgery at
Independent Medical
College Faisalabad.
shuja@iu-hospital.com
The author :
Muhammad Abid Bashir,
FCPS
is associate professor in
department of Surgery at
Independent Medical
College Faisalabad and
®
instructor of ATLS .
abidbashir@hotmail.com
152
! MgO2 available as 400mg tab,
equivalent to 241mg elemental
magnesium (20m eq).
! Magnesium gluconate (500mg
tab.) Eq. to 27mg or 2.3m eq,
magnesium.
! Mg chloride
HYPERMAGNESEMIA
! Hypermagnesemia is highly
infrequent
! In severe hypermagnesemia
clinical features are due to (over-
stable) / latent neuromuscular
membranes
These are ;
! Depressed tendon reflexes.
! Paralysis of voluntary muscles.
REFERENCES
1. Shires III, GT, Borber AB, Shires GT. Fluid &
Electrolyte management of the surgical
patient, In Shwortze I, Shires GT, Spencer
FC, Doly JM, Fisher JE, Galloway AC. (Ed).
Principles of surgery 7th Ed. 1999. Mc
Grath Hills New York PP 53-76.
2. Shires GT, Canizoro PC. Fluid, Electrolyte
management of surgical patient. In
sabiston DC (Ed). The text book of surgery.
The biological bases of modern surgical
practice 14th Ed. 1991. W.B Sanden Co.
Philadelphia PP 57-76.
3. Doly JM, Barie PS, Dudnch SI. Preparation
of the patient. In Nylium (Lm), Baker RJ,
April to June, 2010
! Hypotension.
! Sinus brady cardia.
! Prolonged PR, QT interval.
TREATMENT
Stop any exogenous magnesium
administration. In presence of normal
renal functions, normal saline is
administrated at a rate of 250-500
mg/ml along with 20mg frusenide I/V
every 6 hourly.
In life threatening conditions, as for
cardiac conduction abnormalities or
respiratory depression, 10-20ml of
10% Ca-gluconate can be adminis-
tered I/V over 5-10 minutes.
In case of renal failure, haemodialysis
has to be done to get rid of extra Mg.
Fischer JE. (Ed) Mastery of surgery 3rd Ed.
1997, Little Drown, Co. Boston. PP. 22-49.
4. Gnerlich JL, Buchman TA. Fluid,
Electrolyte, Acid base disorders. In
Klingensmith ME, Chen LE, Glasgow SC,
Goer TA, Melby SJ, (Eds) Washington
Manual of surgery 5th Ed. 2008.
Lippincott Williams & Wilkins,
Philadelphia. PP 71-91.
5. Steele RJC, Patients with metabolic
disorders. In Cuschieni A, Steelw RJC,
Moosa AR (Ed). Essential surgical practice
4th Ed. 2000. Butterworth Heinmann
Oxford PP. 205-14.
INDEPENDENT REVIEWS