Gemma B.

Tiu, MD, FPPS, FPSN, FPNSP

 MAINTENANCE ELECTROLYTE REQUIREMENTS

♦ it is the aim of normal maintenance to provide an

amount that will neither induce maximal renal
conservation nor require excretion of a large
unwanted excess.

♦ electrolyte deficits are seen mainly in association

with excess GIT or urinary loss, but sweating
may also lead to considerable loss of electrolytes.

♦ the urine is the major source of electrolyte losses

in healthy children

♦ no loss occurs during ventilation.

 MAINTENANCE ELECTROLYTE REQUIREMENTS

♦ a generous estimation for electrolyte maintenance

therapy is 2.5mmol of Na+ and K+ per 100
calories expended (exceptions: sweating,
vomiting and diarrhea, surgical drainage tubes,
burns, diuretic therapy and renal electrolyte –
losing disorders).

♦ daily electrolyte requirements:

Na+ = 2.5 – 3.0 mmol/100 cal/day
K+ = 2.0 – 2.5 mmol/100 cal/day
Cl- = 4.5 – 5.5 mmol/100 cal/day
 HYPONATREMIA

A.) DEFINITION
- serum Na+ concentration <135 mmol/L

B.) PATHOPHYSIOLOGY
- hyponatremia reflects hypoosmolarity; either
solute loss or water retention can produce
hyponatremia; disturbances in the GFR, the
reabsorption of Na+ in proximal tubule, the
delivery of Na+ to the distal tubular diluting
segment and the levels of ADH can lead to
hyponatremia; the commonest electrolyte
disturbance observed clinically.
C.) CAUSES
1.) Deficit of TBW and larger deficit of total body
Na+ (ECF depletion)
a.) Renal losses: diuretic excess esp thiazides,
RTA, salt-losing nephritis,osmotic diuresis,
metabolic alkalosis

b.) Adrenal (mineralocorticoid insufficiency)

c.) GIT losses: vomiting, diarrhea,fistula tubes
d.) Third – spacing: burns, pancreatitis,
traumatized muscle, ascites, peritonitis,
effusions
e.) Excessive sweating
2.) Excess TBW with normal total body Na+
(modest ECF volume excess, no edema)

a.) SIADH

b.) Glucocorticoid deficiency

c.) Water intoxication (IV therapy,

psychogenic water drinking )

d.) Hypothyroidism
3.) Excess total body Na + and larger excess of
TBW (ECF volume excess, edema)

a.) Renal: NS, ARF, CRF

b.) Cardiac: CHF
c.) GIT: cirrhosis
D.) SIGNS AND SYMPTOMS

1.) NEUROLOGIC: caused by cerebral overhydration

Anorexia Clouded sensorium
Nausea Decreased sensorium
Vomiting Pathologic reflexes
Agitation Cheyne-Stokes respiration
Headache Hypothermia
Muscle cramps Pseudobulbar palsy
Seizures Muscle weakness

2.) CARDIOVASCULAR: in the volume-depleted

hyponatremic child, fluids shifts from the ECF to
the ICF compartment further aggravate volume
depletion; shock occurs at a greater degree of
TBW depletion as compared with hypertonic or
isotonic conditions.
E.) LABORATORY EVALUATION
1.) Serum electrolytes: Na+, K+, Cl-, HCO3-
2.) Serum and urine osmolalities
3.) Urinalysis (including specific gravity)
4.) Urine Na+
5.) Others as indicated by possible causes:
liver function tests for cirrhosis, BUN,
creatinine, serum albumin, glucose, etc.
F.) THERAPY

1.) Depends on the severity and duration of the

hyponatremia and the ECF volume category

that best describes the patient.

2.) When the level of the serum Na+ is not

severely depressed, most patients do not

show symptoms directly attributable to the

hyponatremia. Many of these patients will
not require specific therapy.
3.) Serum Na+ concentrations <120 mmol/L are
more frequently associated with serious
clinical signs and symptoms and must be partially
corrected immediately, even when the etiology
is not yet known. Correction of the serum Na+
concentration to 125 mmol/L, a level at which
symptoms of hyponatremia are usually relieved,
is recommended. Hypertonic saline solution
using either 3% (513mmol/L) or 5%
(855mmol/L) saline is administered for
approximately 4 hours.
Na+required = (Na+ desired – Na + actual)
x 0.6 x wt (kg)
4.) When the serum Na+ concentration is deemed
to be “safe” (125 mmol/L or greater), further
correction toward a normal serum concentration
should be continued during the next 24 – 48 hrs
with subsequent therapy based on the ECF
volume classification of the patient:

• For patients with ECF volume contraction,

isotonic saline (or isooncotic colloid solution) is
the appropriate therapy. In the presence of
shock, 20ml/kg isotonic saline is given rapidly for
1 hr and repeated as necessary until BP and
peripheral circulation return to normal.
b.) Patients with modest ECF volume excess (no
edema), generally require water restriction. In
simple water intoxication, the normal kidney
responds with maximal urinary dilution which,
when coupled with restriction of water intake, will
rapidly restore Na+ concentration to normal. Daily
free water administration may be reduced by 25 –
50%, depending on the chronicity and severity of
the hyponatremia.
 For patients with SIADH or acute water
intoxication who are seriously symptomatic, serum
Na+ concentration may be increased by giving IV
furosemide followed by hypertonic saline. Chronic
SIADH patients may not respond to water
restriction and lithium or demeclocycline that
inhibit ADH effect on the kidney is recommended.

Urine Na and K losses must be measured and

replaced IV while restricting water replacement to
a minimum. Monitor serum electrolytes frequently.
 HYPERNATREMIA

A.) DEFINITION: serum Na+ concentration > 145 mmol/L

B.) PATHOPHYSIOLOGY:
Reflects deficiency of water relative to total body Na
content and usually a disorder of water rather of Na
balance. There is either an absolute or relative water
deficit, which can occur in the face of normal, increased
or even decreased total body Na. It causes a shift of water
from the ICF to the ECF compartment, resulting in
cellular dehydration. The hypertonicity stimulates the
secretion of ADH and the sensation of thirst. Thirst is more
important as the body’s defense against hypernatremia
and hypertonicity than ADH. If ADH secretion is not
sufficient to correct the hypertonicity, thirst is stimulated in
the awake patient and leads to water drinking as long as
there is free access to water.
C.) CAUSES

1.) Pure Na excess (increased total body Na)

2.) Water deficit (normal body Na)

3.) Water deficit in excess of Na deficit

(low total body Na)
D.) DIAGNOSTIC AND THERAPEUTIC APPROACH

ASSESS CIRCULATING VOLUME

ECF Volume Modest Volume excess ECF Volume excess

depletion (no edema) (edema)

Urine Na+ Urine Na+ Urine Na+ Urine Na+

>20 mmol/L <10 mmol/L Urine Na+
<10 mmol/L >20 mmol/L
>20 mmol/L

Renal Extrarenal CHF

SIADH Renal
losses losses Cirrhosis
Water Intoxication failure
nephrosis

Correction of shock
Saline replacement Water Water restriction
Specific replacement restriction Specific replacement
therapy therapy
E.) SIGNS AND SYMPTOMS

1.) Neurologic: secondary to cellular dehydration

restlessness spasticity
irritability coma
lethargy seizures
muscular twitching, death
hyperreflexia, brain hemorrhages

2.) Others:

decreased skin turgor (becomes doughy)

high – pitched cry or wail
fever
hypocalcemia
hyperglycemia (transient, disappears over a 36-hr period)
avid thirst
G.) LABORATORY EXAMINATIONS

1.) Serum Na+, K+, Cl-, HCO3-, BUN, creatinine

2.) Liver function tests

3.) Serum osmolality
4.) Urinalysis
5.) Urine Na+, creatinine, osmolality
H.) THERAPY

1.) The primary goal is the restoration of serum

tonicity. The specific approach depends on the
patient’s ECF volume. When dehydration is
severe and shock is present or imminent,
regardless of serum Na concentration, plasma
volume should first be corrected.

2.) When urine output is present or has been

reestablished, hypotonic fluids are given to
bring Na concentration to normal.
Recommended rate of reduction of serum
Na concentration is 10 – 15 mmol/L daily.
a.) Volume to give in 48 hrs
- calculate fluid deficit by clinical means
- estimate 48 hrs worth of maintenance water
- add fluid deficit and maintenance needs for
48 hrs; if the child has significant on going
losses, these must also be included

b.) Glucose content: use 2-3% to prevent possible

problems with hyperglycemia from arising later.

c.) Na content: allow 80-100 mmol/L for the deficit

fraction of fluid and none for the maintenance
portion, the resultant concentration is usually
20-35mmol/L
d.) K content: generally, the maximal safe
amount for an IV infusion is about
40mmol/L, given when the child is
urinating.
e.) Anion content: advised amount of Na+ plus
K+ equals 60-75 mmol/L of cation.

f.) Calcium content: 1 amp 10% Ca

gluconate/500 ml of infusate

g.) Rate of administration: administer 1/4 of

volume/hr for 48 hrs; in an infant, the
usual
volume will be 275 – 350 ml/kg/48 hrs, or

about 6-7ml/kg/hr.
 HYPOKALEMIA

A.) DEFINITION:
- serum K+ concentration <3.5 mmol/L

B.) CAUSES:
1.) Hypokalemia without K+ deficit (shift from
ECF to ICF or redistribution hypokalemia)
a.) Insulin
b.) B2 catecholamines
c.) Alkalosis (metabolic/respiratory)
d.) Familial hypokalemic periodic paralysis
2.) Hypokalemia with K+ deficit

a.) Poor dietary intake

b.) External losses:
Diarrhea
Protracted vomiting
Laxative abuse
Ureterosigmoidostomy
Obstructed or long ileal loop
Excessive sweating
c.) Renal losses
Tubular diseases (drugs, cystinosis)
Diuretic abuse
RTA
DKA
Excessive mineralocorticoid effect
- Primary hyperaldoteronism
- Bartter’s Syndrome
- Cushing’s Syndrome
Non – absorbable anions
Leukemias
C.) SIGNS AND SYMPTOMS
1.) Neuromuscular : most important clinical
manifestations
a.) Ileus
b.) Muscle weakness
c.) Areflexia
d.) Tetany
e.) Autonomic insufficiency : orthostatic
hypotension
f.) Encephalopathy in patients with liver disease
2.) Cardiac
a.) Arrhythmias
b.) ECG changes: flattened T waves, U waves,
S – T segment depression, arrhythmias
(atrial and ventricular premature beats)
3.) Renal
a.) Concentrating defect (vasopressin –
resistance observed in chronic cases)
b.) Polydipsia, polyuria
c.) Edema and Na+ retention
d.) Increased renal ammonia production
e.) Hypokalemic nephropathy: cellular
vacuolization in the proximal tubule
(can revert with K+ repletion) and
interstitial fibrosis

4.) Rhabdomyolysis

5.) Vasoconstriction
6.) Hormonal
a.) Decreased aldosterone secretion
b.) Decreased insulin release

7.) Metabolic
a.) Hyperglycemia (from impaired insulin
release)
b.) Negative nitrogen balance

8.) Neuropathic
a.) Depression
b.) Apathy
c.) Confusional states
D. LABORATORY EVALUATION

1.) Serum Na+, K+, Cl-, HCO3-

2.) Serum BUN, glucose, creatinine
3.) ABG
4.) Urinalysis
5.) Urine Na+, K+, Cl-, Osmolality
6.) Others: ECG, plain abdominal X-ray,
UGI series
E. THERAPY
1.) Mild hypokalemia occurring in asymptomatic
persons may not require specific therapy.
Hypokalemic patients treated with digitalis
glycosides should be given K+ supplements.

2.) Replacement usually can be accomplished

by the oral route, done slowly (over days)
and started once urine flow is confirmed.

3.) If the K+ deficit is severe and is causing

cardiac arrhythmias, rhabdomyolysis,
extreme weakness with quadriplegia, or
respiratory distress, IV replacement is
necessary.
4.) Guidelines on IV administration of K+
a.) Via a peripheral vein, no more than 40
mmol/L; higher doses will produce local
irritation to peripheral vein.
b.) Via a central vein: 80 mmol/L; careful patient
monitoring with continuous ECG tracings
c.) Quantitative rate of repair: not >0.2 – 0.3
mmol/kg/hr; for potentially life –
threatening cardiac arrhythmias or
respiratory paralysis, up to 1 mmol/kg/hr can
be given by infusion pump with ECG
monitoring in the ICU
d.) Choice of K+ salt to administer:
- as KCL in cases of alkalosis
- as KHCO3 in cases of metabolic acidosis
5.) When hypokalemia results from simple
transcellular shifts in response to alkalosis
without an accompanying K+ deficit, correction
of the pH is all that is required.

6.) The child with symptomatic hypokalemia should

be admitted for diagnostic work-up and therapy.
Any child with a serum K= less than 3.0 mmol/L
should also be admitted.
7.) In the treatment of hypokalemia, it has always
been recommended that K+ repletion be
started only after the patient has already
voided but in life threatening hypokalemias,
one can start K+ replacement.

8.) Hypokalemia may have multifactorial causes;

correction of the contributing factors such as
acidosis will decrease its severity.

9.) Frequent measurements of extracellular K+ are

necessary as correction proceeds.
 HYPERKALEMIA

A.) DEFINITION :
- serum K+ concentration >5.0 mmol/L

B. ) CAUSES:
1.) Pseudohyperkalemia
a.) Improper collection or handling of
blood sample.
b.) In vitro hemolysis
c.) Leukocytosis or thrombocytosis
2.) Increase K+ load
a.) Oral/IV supplementation
b.) K – containing salt substitutes
c.) Blood transfusions
d.) Endogenous cell breakdown

3.) Decreased renal excretion

a.) ARF or CRF
b.) Mineralocorticoid deficiency/resistance
c.) K – sparing diuretics

4.) Shift from ICF to ECF

a.) Metabolic/respiratory acidosis
b.) Mineralocorticoid and insulin deficiency
c.) Drug – induced
d.) Hyperkalemic periodic paralysis
C.) SIGNS AND SYMPTOMS

1.) Neuromuscular: paresthesias, weakness,

flaccid paralysis

2.) ECG changes: classic sine wave of

hyperkalemia

3.) Hormonal effects:

a.) Stimulates the release of aldosterone
insulin and epinephrine
b.) Rises glucagon
D.) LABORATORY EVALUATION

1.) Serum Na+, K+, Cl-, HCO3-, BUN,

creatinine, glucose

2.) ABG

3.) Urinalysis, urine Na+, K+, Cl-,

osmolality

4.) ECG
E.) THERAPY

Three mechanisms in the emergency Tx of

hyperkalemia:

1.) Reverse membrane effects by increasing the

threshold potential and allowing excitable cells
to repolarize and fire a signal again.
10% Ca gluconate 0.5 – 1 ml/kg BW in 2 – 10
minutes IV onset/duration of action: immediate
(30 – 60 minutes)
REMINDERS: need for ECG monitoring
discontinue if pulse rate <100/min
2.) Transfer K+ into cells

a.) 8.4% Na bicarbonate 1 – 2 mmol/kg BW in

10 - 30 minutes IV
Onset/duration of action: 5 minutes/1 -4 hrs.
REMINDER: may be used in the absence of
acidosis

b.) Glucose 0.5 – 1 g/kg + Insulin 0.1 U/kg IV in

15 – 30 minutes
Onset/duration of action: 30 – 60 minutes/hours
REMINDER: monitor blood glucose

c.) Salbutamol or other B2 agonist 4 mg/kg in 10 ml

water by nebulizer
or 2.5 mg if BW <25kg
5.0 mg if BW >25kg
3.) Enhance renal excretion of K+

a.) Na polystyrene sulfonate (Kayexalate)

1 g/kg/dose PO or per rectum diluted with
2 – 4ml of Sorbitol or 10% dextrose/g
resin every 4-6 hrs
Onset/duration of action; 60 minutes/hrs

b.) 0.9% NaCl 10 – 20 ml/kg IV in

45 – 60 minutes
Onset/duration of action: 30-60 min/hrs
 HYPOCALCEMIA

A.) DEFINITION:
- serum Ca++ concentration < 9.0 mg/dl
beyond the neonatal period

B.) PATHOPHYSIOLOGY:
A result of an inability to mobilize Ca from
bone into the ECF and IV compartments either
as a result of failure of secretion of adequate
amounts of PTH or an inadequate
responsiveness of end – organs to PTH despite
adequate secretion of the hormone.
C.) CAUSES:

1.) True hypoparathroidism

a.) Familial with or without multiple
endocrine abnormalities
(“autoimmune”)
b.) DiGeorge Syndrome
c.) Postsurgical
d.) Idiopathic
e.) Magnesium deficiency

2.) End – organ resistance to PTH

a.) Pseudohypoparathyroidism
b.) Insensitivity to c – AMP
3.) Abnormalities of vitamin D metabolite
a.) Primary Vitamin D deficiency (dietary, sunlight)
b.) Secondary Vitamin D deficiency
- malabsorption (Celiac disease, biliary Atresia, etc.)
- anticonvulsant therapy
c.) Primary Vitamin D resistance
(Familial Hypophosphatemic Rickets)
d.) Secondary Vitamin D resistance
- Fanconi Syndrome
- RTA

4.) Miscellaneous
a.) Hypoproteinemia
b.) Hypernatremic DHN
c.) Postacidotic tetany
d.) Diuretic abuse
e.) Phosphate loading
D. SIGNS AND SYMPTOMS
1.) Tetany
2.) Frank seizures
3.) Larygospasm
4.) Non- specific: vomiting, muscle weakness,
irritability, lethargy, bone pain, generalized
feeling of debilitation
5.) Neonate: apnea, poor feeding,
abdominal distension
6.) Early signs: spontaneous tonic contractions
of muscles of the upper and lower
extremities, carpopedal spasm
7.) ECG changes: prolongation of Q – T interval
with normal R-S-T segment and normal
T - waves
E.) LABORATORY EVALUATION

1.) Serum Ca++, phosphorus, alkaline

phosphate, Mg+, total protein, albumin,
PTH, pH, BUN, creatinine

2.) Urine Ca++, phosphorus, creatinine

3.) Others : ECG, skull and CXR’s, skeletal

survey
 F.) THERAPY

1.) If patient is symptomatic:

a.) Ca gluconate 10% (9.2mg elemental Ca/ml)
Dose: 0.5 – 1.0 ml/kg IV bolus administered
over 3 – 5 minutes under cardiac
monitoring. Stop infusion if heart rate
falls below 60/min.

b.) Maintenance Ca gluconate 10% should follow

IV bolus once symptoms are relieved.
Dose: 100 mg elemental Ca/kg/hr added to
the IV solution.
c.) Oral Ca supplements (50mg elemental Ca/kg BW/day)
Ca lactate (13% Ca by weight)
Ca gluconate (9 % Ca by weight)
Ca chloride (21% Ca by weight)
Dose: children up to 3 yrs: 10 – 25 ml
4 – 12 yrs: 30 – 45 ml
In severe Ca deficiency states, Ca may be given up
to daily doses of 75 ml. Fast – growing children may
require adult doses.

d.) When Mg deficiency is suspected or confirmed, give

Magnesium.
Dose: 0.25 mmol/kg or 0.125 ml/kg of 50% MgSO4
IM (1g of 50% MgSO4 contains 99 mg Mg or
about 4mmol).
2.) If patient is asymptomatic oral Ca
supplements should be given and patients
admitted for work – up.

3.) In all cases, milk should be changed to a

low – phosphate milk (human or modified
cow’s milk).
 HYPERCALCEMIA

A.) DEFINITION:
- serum Ca++ concentration >11 mg/dl

B.) PATHOPHYSIOLOGY:
Due to either increased intestinal absorption
of Ca++ or increased mobilization of Ca++
from bone with or without increased
absorption from the intestinal tract. PTH
increase bone resorption and vitamin D
increases intestinal Ca++ reabsorption.
C.) CAUSES:

1.) Primary hyperparathyroidism

a.) Adenoma, carcinoma
b.) Hyperplasia
c.) MEN

2.) Secondary hyperparathyroidism

a.) Malabsorption and Vitamin
D deficiency
b.) CRF
c.) Following kidney transplantation
3.) Neoplastic disease
a.) Malignant tumor with metastasis to the bones
b.) Tumors secreting humoral nonparathyroid –
like substances
c.) Tumors secreting PTH – like substances
d.) Multiple Myeloma and other
lymphoproliferative diseases
(“osteoclast – activating factor”)
4.) Hypervitaminosis D
5.) Hypervitaminosis A
6.) Sarcoidosis and TB
7.) Hyperthyroidism
 8.) Adrenocortical insufficiency

9.) Infantile hypercalcemia

10.) Immobilization

11.) Milk – Alkali Syndrome

12.) Use of Ca – ion exchange resins

13.) Hypercalcemia associated with ARF

14.) Thiazide – induced hypercalcemia

D. SIGNS AND SYMPTOMS
1.) Neurologic
a.) Headache, irritability, lethargy, fatigue
b.) Weakness, seizures, coma
c.) Hyporeflexia, behavioural changes

2.) GIT
a.) anorexia, nausea, vomiting, constipation
b.) DHN

3.) Cardiovascular
a.) Bradycardia
b.) HPN
c.) Short Q – Tc interval in the ECG
4.) Renal
a.) Polydipsia, polyuria
b.) Hypokalemia,aminoaciduria,
nephrocalcinosis, nephrolithiasis

5.) Dermatologic
a.) Pruritus
b.) Band keratopathy, ectopic calcification
E.) LABORATORY EVALUATION

1.) Serum Ca++, phosphorus, alkaline

phosphatase, total protein, albumin,
creatinine, PTH, vitamin D

2.) Urine Ca++, phosphorus, creatinine

3.) Others: ECG, skull and abdominal x-rays,

skeletal survey, IVP

4.) Unexplained hypercalcemia: work – up

for hidden malignancy
F.) THERAPY

1.) For symptomatic patients, initial emergency

treatment is the infusion of saline at a rate
2x the maintenance followed by bolus
injections of furosemide 1 – 2 mg/kg every
6-8 hrs; management depends on a
normally – functioning kidneys.

2.) In patients with no pre – existing cardiac

disease, the subsequent amount of saline
may be given at 2 – 3x the daily
maintenance requirements until serum
Ca++ returns to normal. May be guided
also by the state of hydration of the
patient.
3.) Hypercalcemic crisis requires hospitalization
in the ICU

4.) For vitamin D intoxication, infuse PO4

or SO4 salts followed by oral prednisone
(1-2 mg/kg/day).

5.) In malignancy, mithramycin at 25 ug/kg IV

be given.

6.) For acute oliguric renal failure, peritoneal or

hemodialysis is indicated.
THANK YOU!
1.) Either solute loss or water retention can
produce hyponatremia.

(a) True
(b) False
2.) One of the causes of hypernatremia is
water deficit with normal body sodium.

(a) True
(b) False
3.) A 6 – month old infant with Loose
Bowel Movement for 3 days was
brought in because of abdominal
distention. PE on the abdomen
revealed no bowel sounds heard.

a.) Hyponatremia
b.) Hypokalemia
c.) Hypernatremia
d.) Hyperkalemia
4.) Which drug enhances renal excretion of
potassium in hyperkalemia?

(a) Na polystyrene sulfonate

(b) Na bicarbonate
(c) Salbutamol
(d) All are correct
5.) A patient with DiGeorge Syndrome was
rushed in because of difficulty of
breathing. PE showed carpopedal
spasms of the fingers.

Impression:

a.) Malingering
b.) Hypocalcemia
c.) Hyponatremia
d.) Hypokalemia