Fluid and Electrolyte Balance in

Infants and Children

Joseph Chukwu and Eleanor Molloy

Keywords Phosphate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Fluid balance • Electrolyte balance • Acid-base Acid-Base Balance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
balance • Dehydration • Osmolality • Perioper- Acid-Base Balance Disorders . . . . . . . . . . . . . . . . . . . . . . . . . 13
ative management Perioperative Management in Infants and
Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Contents Intraoperative Management . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Postoperative Management . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Water Distribution in Infants and Children . . . . . . . . . . . 2 Fluid and Electrolyte Balance in Septic Shock . . . . 14
Water Homeostasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Insensible Water Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Total Parenteral Nutrition (TPN) . . . . . . . . . . . . . . . . . . . . . . 15
Disorders of Body Fluid Volume: Dehydration and Conclusions and Future Directions . . . . . . . . . . . . . . . . . 15
ECF Depletion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Volume Depletion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Cross-References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Fluid and Electrolyte Management . . . . . . . . . . . . . . . . . . . 5 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Electrolytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Sodium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Potassium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Introduction
Calcium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Magnesium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
During the time of rapid postnatal transition, for
example, term and preterm neonates have differ-
ent fluid requirements and electrolyte changes to
J. Chukwu (*) the older children and adults (Table 1). Age and
Clinical Research Unit, National Children’s Research
Centre, Our Lady’s Children’s Hospital, Dublin 12, Ireland gender are the most important determinants of
e-mail: joe.chukwu@gmail.com; josephchukwu@rcsi.ie this wide variation in fluid and electrolyte
E. Molloy requirements (Bianchetti and Simonetti 2009).
Department of Neonatology, Paediatrics, National Knowledge of the fluid and electrolyte composi-
Maternity Hospital, Dublin 2, Ireland tion and maintenance of homeostasis maintained
UCD School of Medicine and Medical Sciences, at the different stages of infancy and childhood is
University College Dublin, Dublin, Ireland essential to the effective management of fluid
Neonatology, Our Lady’s Children’s Hospital, Dublin 12, and electrolyte deficit in surgical pediatric
Ireland patients.
Paediatrics, Royal College of Surgeons in Ireland, Dublin,
Ireland
e-mail: elesean@hotmail.com

# Springer-Verlag GmbH Germany 2016 1

P. Puri (ed.), Pediatric Surgery,
DOI 10.1007/978-3-642-38482-0_16-1
2 J. Chukwu and E. Molloy

Water Distribution in Infants and Effective Circulating Volume (ECV)

Children
The body water composition varies throughout
infancy and childhood. While the infants’ total
body water is around 75%, it falls to 65–70% in
toddlers and falls further to 60% in the adolescents
as shown in Fig. 1 (Somers 2009). The total body
content in males is higher than in females by
2–10% after puberty (Greenbaum 2010b). About
two thirds of the total body water is within the
intracellular compartment; the rest is in the extra-
cellular compartment as shown in Fig. 2.
The extracellular fluid (ECF) compartment
consists of interstitial fluids which make up two
thirds of the ECF and the intravascular fluid
(plasma) accounts for the other third. The rest of
the ECF is transcellular fluid which includes the
peritoneal, synovial, cerebrospinal, and intraocu-
lar fluids. The body fluid compartments are deter-
mined by their electrolyte compositions. While
the sodium determines the ECF volume, potas-
sium regulates the ICF volume. Starling’s forces
control the partitioning of fluids into ECF and
ICF. The three mechanisms that control fluid dis-
tribution across capillary membrane are oncotic
pressure, hydrostatic pressure, and capillary per-
meability. Although albumin mass consists of
50% of total blood protein, it only accounts for
25% of the total oncotic pressure. Albumin is
anionic and attracts cations into the intravascular
compartment (Gibbs-Donnan effect). This is due
to the high intracellular concentration of non-
diffusible anions (Brandis). Water enters the cell
down to its concentration gradient. A second
Gibbs-Donnan effect is set up by the Na+/K+
ATPase in the cell membrane by preventing
sodium entry into the cell, sodium being the
impermeable to charged cation (Brandis 2001).
The arterial component of the intravascular vol-
ume perfusing the tissues at any particular time is
the effective circulating volume (ECV) (Bullock
et al. 2001; Somers 2009). However, the volume
of the arterial blood varies with the ECF volume;
hence, maintenance of both ECV and ECF vol-
umes is closely related. Since the ECF volume is
dependent on the state of its sodium content, ECF
volume is controlled by urinary sodium excretion
(Bullock et al. 2001). Volume receptors are
located in the carotid sinuses, the aortic arch,
and the kidney (Somers 2009). While the volume
receptors in the carotid sinuses and the aortic arch
control the ECV through the sympathetic nervous
and the natriuretic systems, the kidneys control
the ECV via the renin-angiotensin II-aldosterone
system (Skorecki and Brenner 1981; Patel 2009).
The effects of these responses result in the adjust-
ment of the glomerular filtration rate, peritubular
Starling forces, and renal microvascular hemody-
namics as well as the tubular flow rate, fluid
composition, and trans-tubular ion gradients
(Skorecki and Brenner 1981).
Serum Osmolality
Serum osmolality is defined as the concentration
of solute per weight of water. It is measured in
mosm/kg H20. The true (total) blood osmolality is
the sum of osmolalities of all blood solutes.
Sodium predominantly contributes to the plasma
osmolality. Other solutes that contribute to the
true osmolality include glucose, urea, and other
ions. Serum osmolality is not directly measured
but can be estimated by the following formula:
(sodium x2) þ glucose. This implies multiplying
the concentration of serum sodium (in mmol/l) by
two and adding this to the glucose concentration
(in mmol/l).

Table 1 Calculation of daily maintenance fluid requirement and intravenous fluid infusion rate
Body weight (kg) Total daily maintenance fluid requirement in 24 h Intravenous fluid infusion rate (ml/h)
0–10 100 ml/kg 40
11–20 1,000 ml þ 50 ml/kg for each kg above 10 kg 40 þ (2 ml/kg/h for each kg weight above 20 kg)
>20 1,500 þ 20 ml/kg for each kg weight above 20 kg 60 þ (1 ml/kg/h for each kg weight above 20 kg)
Fluid and Electrolyte Balance in Infants and Children
Fig. 1 Total body water composition in the preterm,
infant, and the adolescent
Water Homeostasis
Sodium status determines volume status, while
water intake and excretion control maintain osmo-
lality. The two systems that regulate water balance
include the thirst mechanism which is stimulated
by increased plasma osmolality and the anti-
diuretic hormone (ADH, also called vasopressin)
secretion which is stimulated by decreased plasma
volume. ADH regulates urinary water loss by
increasing the renal reabsorption of water. Water
balance controls osmolality. The normal osmolal-
ity ranges between 285 and 295 mosm/kg. When
both volume depletion and increased osmolality
occur at the same time, maintenance of intravas-
cular volume takes precedence over maintenance
of osmolality (Greenbaum 2010b). The kidney is
the principal regulator of sodium balance by alter-
ation of the proportion of filtered sodium that is
reabsorbed (Greenbaum 2010b). Significant mor-
bidity and mortality are associated with volume
overload especially in critically ill children
(Greenbaum 2010b).
Insensible Water Loss
Insensible water loss represents about a third of
the total daily maintenance fluid requirements.
This loss occurs by evaporation through the skin
and the lungs. A febrile child loses an additional
3
Fig. 2 Body water distribution between the intracellular
fluid (ICF) and extracellular fluid (ECF) compartments in
the preterm neonate, the infant, and the adolescent
10–15% per one degree centigrade rise in temper-
ature above 38 centigrade through this means
(Greenbaum 2010b). Insensible water loss
through the lungs is increased in children who
are tachypneic and those with tracheostomy
tubes (Greenbaum 2010b).
Sweating
Sweating occurs in both infants and children.
Fluid lost through the sweat is not insensible as
it contains both salt and water. The normal sweat
chloride concentration is <40 mmol/l, but in
children with cystic fibrosis, a level >60 mmol/
l is diagnostic. However, causes of false-positive
sweat tests such as adrenal insufficiency,
eczema, nephrogenic diabetes insipidus, and
dehydration have to be taken into account in
interpreting the results of this test (Carter and
Marshall 2010).
Renal Blood Flow
Nephrons are functional in the fetus by 8 weeks of
gestation, but they continue to develop and mature
up to the 34th week when all the glomeruli are
present. The abdominal aorta provides the blood
supply to the kidneys through the left and right
renal arteries. The proportion of cardiac output
distributed to the kidneys increases from 15% to
18% in the first month of life to about 20–25% in
adulthood.
4 J. Chukwu and E. Molloy
Glomerular Filtration Rate
The glomerular filtration rate (GFR) is the rate at
which water and dissolved solutes in blood are
filtered into the kidneys. The GFR provides an
estimate of the renal function as this is determined
by an intact tubular function and glomerular fil-
tration (Mahan 2010). The normal range of GFR
is 80–125 ml/min/1.73m2. The GFR of the full-
term newborn is 40 ml/min/1.73m2, and this
increases rapidly within the first 2 years to reach
adult values of 100–120 ml/min/1.73 m2 and sta-
bilizes at this level (Mahan 2010). Indirect mea-
surement of GFR can be obtained by estimating
the endogenous creatinine clearance using a 24-h
urine collection (Lum 2002). The GFR can be
quickly estimated by measuring child’s length in
centimeters and plasma creatinine levels using the
formula outlined below (Lum 2002).
Ccr(ml/ min /1 . 73m2) = 0.55 
height (cm)/PCr(mg/dl) (Lum 2002)
ðCcr ¼ Creatinine clearance; PCr ¼ plasma creatinineÞ
In infants less than 1 year old, the factor should
be 0.45 instead of 0.55. However, estimating GFR
using such substituted measurements based on
serum creatinine or cystatin C clearance is not
good substitutes for a measured GFR (Becker
and Friedman 2013). The most accurate means
of measuring GFR is by inulin infusion – a sub-
stance which is not metabolized, reabsorbed, or
secreted by the renal tubules (Mahan 2010). Using
this method, the formula for calculating GFR is as
follows: GFR = [U] V/[P] ; (U = urinary concen-
tration of inulin; [P] = serum inulin concentration
and V = urine flow rate).
Disorders of Body Fluid Volume:
Dehydration and ECF Depletion
Volume Depletion
Volume depletion is any condition leading to
decreased effective circulating volume. In this
condition salt and water are lost. Examples
include vomiting, diuretics, bleeding, and
sequestration of fluid in the third space. Third-
space fluids are fluids that are still within the
body but are not in equilibrium with the vascular
fluids (Filston et al. 1982). This can occur in
children with pleural effusion, ascites, edema,
and severe sepsis. Estimation of the volume of
third-space fluid is difficult (Filston et al. 1982).
Dehydration
This implies mainly water loss resulting in hyper-
natremia, an increased serum osmolality, and
intracellular water depletion. The fluid balance is
altered due to fluid loss being greater than fluid
intake. In isotonic dehydration (mostly iso-
natremic), water and salt are lost in equal propor-
tions. In hypertonic (mostly hypernatremia),
water is predominantly lost, while in hypotonic
(always hyponatremic), a higher proportion of salt
than water is lost. The three main sites of fluid loss
are gastrointestinal (vomiting, diarrhea, blood
loss), the skin (burns, fever, CF), urine (diabetes
insipidus, diuretics, osmotic diuresis, diabetes
mellitus, alcohol, etc.). Prolonged decreased
fluid intake can also lead to dehydration, but this
is rare in infants and children. However, breast-
fed babies are more likely to be dehydrated due to
reduced fluid intake especially during the early
neonatal period when maternal breast milk pro-
duction is still low.
Risk Factors for Dehydration
Infants are more susceptible than older children
due to higher fluid turnover in the former com-
pared to the latter. Infectious diarrhea is more
common in infants than in older children. Infants
are not able to communicate their need for fluids
compared to older children. Infants and children
with some underlying medical or surgical condi-
tions such as gastroschisis and cyclical vomiting
syndrome are more prone to dehydration than
normal children.
Consequences of Dehydration
Dehydration results in decreased effective circu-
lating volume (#ECV), decreased perfusion, tis-
sue ischemia, acid-base balance disorders, and
eventually end-organ failure.
Fluid and Electrolyte Balance in Infants and Children
Symptoms and Signs of Dehydration
There are three groups of signs and symptoms
associated with dehydration (Bianchetti et al.
2009) which are those related to the manner of
loss (e.g., vomiting), symptoms related to the
disturbance of acid-base balance, and symptoms
related to the effects of volume depletion.
Degree of Dehydration
Most are accurately assessed by the degree of acute
weight change from baseline, but this parameter is
not always available at the initial presentation.
Since weight in children increases with age, using
a weight taken few weeks apart might not be an
option especially in younger children. If a recent
weight is available, the degree of acute weight loss
reflects the degree of fluids loss. One kilogram of
body weight loss equates one litre of fluid loss. In
reality however the degree of dehydration is
assessed clinically by a combination of history
and physical exam findings. The following signs
and symptoms in combination are useful for
assessing the degree of dehydration: dry mucous
membrane, sunken eyes, reduced urine output,
delayed capillary refill time, tachycardia, and
deep and/or rapid respiration (Table 2). In infants
whose anterior fontanelles are still open, a sunken
fontanelle is a useful sign for assessing the degree
of dehydration. Late signs in both infants and chil-
dren include decreased skin turgor and arterial
hypotension.
A four-item eight-point rating scale for
assessing the degree of dehydration has been
developed for children less than 4 years old
using a combination of general appearance, eyes,
mucous membrane, and the presence or absence
of tears (Goldman et al. 2008, Tables 3 and 4).
Laboratory Testing
These tests can confirm whether dehydration is
present or not and can detect associated electrolyte
and acid-base balance disturbances but are not
useful for assessing the degree of dehydration.
The following laboratory findings might point to
the presence of dehydration: decreased fractional
excretion of sodium, decreased urinary spot
sodium concentration <30 mmol/l, increased
5
urinary concentration >450 mosm/kg water, and
decreased serum bicarbonate <17 mmol/l. The
serum urea concentration is less useful for
assessing the degree of dehydration as it is
affected by intake and increased tissue
breakdown.
Fluid and Electrolyte Management
Infants and older children admitted to the hospital
who are unable to tolerate oral fluids require care-
ful management of fluid and electrolyte balance.
Additional care may be required for those requir-
ing surgical and medical procedure. Children with
underlying medical conditions such as diabetes
and heart or renal failure require special consider-
ation. Children in septic shock and trauma and
burn patients also require special attention. There-
fore, in planning the initiation of fluid therapy in
infants and children, these variables must be taken
into consideration (Tables 5 and 6). Consideration
should also be given to modifying any existing
local guidelines to the needs of each child’s fluid
and electrolyte requirements.
The major component of maintenance water
includes the total urine output in the last 24 h.
This accounts for about 60% of the total mainte-
nance water. Insensible loss through the skin and
the respiratory tract accounts for about 35% of the
maintenance fluid, while about 5% of the mainte-
nance fluid is lost through the stool. Maintenance
fluid should also be adjusted for ongoing losses
especially from the GI tract. Ongoing GI losses
occur through diarrhea, vomiting, gastrointestinal
drainage tubes, nasogastric tube, gastro-jejunal
tubes, intestinal mucocutaneous fistulae, etc.
Maintenance fluid therapy may need to be
decreased in the following circumstances: inap-
propriate ADH secretion, congestive heart failure,
oliguric renal failure, patent ductus arteriosus,
head trauma, and hypothyroidism The following
factors should be considered in assessing fluid and
electrolyte requirement in infants and older chil-
dren (Tables 7, 8, 9, and 10): recent acute weight
change, urine output, specific gravity and osmo-
lality, serum sodium and creatinine, blood urea,
6 J. Chukwu and E. Molloy

and osmolality. In the hospitalized patient, the
fluid input and output chart should also be
assessed in order to estimate the fluid deficit.
Slower fluid resuscitation in African children suf-
fering from hypovolemic shock is more beneficial
than rapid fluid resuscitation in these individuals
as was demonstrated in the Fluid Expansion as
Supportive Therapy (FEAST) trial (Maitland et al.
2011).
Electrolytes
Sodium
Sodium is the main electrolyte of the ECF respon-
sible for the maintenance of intravascular volume
and osmolality. Sodium, chloride and bicarbonate
anions account for 90% of the ECF osmolality.
Serum sodium concentration is maintained by a
combination of water intake, insensible losses,
and urinary dilution. The normal range is
135–145 mmol/l.
Dysnatremia
Hyponatremia
Hyponatremia is defined as sodium level
<130 mmol/l. In this condition the effective
Table 2 Signs and symptoms of dehydration in infants
and children
Infants and children
Dry mucous membranes
Sunken eyes
Reduced urine output
Delayed capillary refill
Tachycardia
Deep þ/ rapid respiration
circulating level might be increased, normal, or
decreased. Hypovolemic hyponatremia occurs as
a result of volume depletion, while normo- or
hypervolemic may be due to volume dilution.
When the ECV decreases, vasopressin is released
as a result and this is the most common cause of
hyponatremia in children.
In dilutional hyponatremia, syndrome of inap-
propriate ADH secretion (SIADH) leads to
increased vasopressin secretion resulting in
water retention, volume expansion, and hypo-
natremia, while in hypovolemic hyponatremia,
fluid and electrolyte loss leads to decreased ECV
which in turn triggers vasopressin secretion, water
retention, and hyponatremia. In cerebral salt
wasting syndrome (CSWS) on the other hand,
increased renal salt loss leads to volume depletion
which in turn stimulates increased vasopressin
leading to volume depletion and hyponatremia.
The important distinguishing feature between
SIADH and CSWS is volume depletion in
CSWS compared to the relative volume overload
in SIADH. While CSWS is treated by volume and
salt repletion, SIADH is treated by fluid restriction
(Peruzzo et al. 2010).
SIADH is common in critically ill children.
The diagnosis of SIADH is based on the classic
criteria developed by Schwartz and Batter and
includes hyponatremia with hypo-osmolality
with continuing urinary sodium loss, urine that is
less maximally dilute, no clinical signs of volume
depletion, and the absence of other possible
causes of hyponatremia. The most common
causes of postoperative hyponatremia in children
are subclinical volume depletion and the admin-
istration of hypotonic fluids (Peruzzo et al. 2010).
Other causes include stress, pain, nausea, and
narcotics all of which stimulate ADH release.
The symptoms of hyponatremia include nausea,

Table 3 Clinical dehydration scale in children aged 1 month and 36 months (Bailey et al. 2010; Friedman et al. 2004;
Woolley and Burton 2009)
Characteristic Score 0 if present Score 1 if present Score 2 if present
General appearance Normal Thirsty, restless, sleepy, or irritable Drowsy, limp, comatose
Eyes Normal Slightly sunken Deeply sunken
Tongue Moist Sticky Dry
Tears Present Decreased Absent
Fluid and Electrolyte Balance in Infants and Children 7

headache, diplopia, falls, seizures, and coma. The Significant morbidity and mortality are associ-
complications of hyponatremia include cerebral ated with severe hypernatremia. The main com-
edema and osmotic demyelination. plications associated with hypernatremia
include dural sinus thrombosis, intracranial
Hypernatremia hemorrhage, osmotic demyelination, and
Hypernatremia is defined as serum sodium shrinkage of the brain cell. Treatment of this
>150 mmol/l. This is a relatively uncommon condition may result in cerebral edema (Hoorn
condition after the age of 2 weeks occurring in et al. 2012).
1 in 2,000 children admitted to hospital (Forman The management of hypernatremia includes
et al. 2012). Relative deficit of water with addressing the root cause by taking a good history
reduced thirst sensation and/or reduce intake of and performing adequate physical examination
water is the main cause of hypernatremia. How- and managing fluid volume and electrolyte
ever hypernatremia may result from excessive balance. Robertson et al. investigated the
sodium intake (Vogt et al. 2009). This is a rare “relationship between fluid management, changes
but potentially fatal cause of hypernatremia in in serum sodium and outcome in hypernatremia
children and results in much higher urinary associated with gastroenteritis” in South African
sodium: creatinine ratio and urinary fractional children and concluded that adverse outcome was
sodium excretion than other causes of hyper- neither independently associated with intravenous
natremia (Forman et al. 2012). fluid sodium concentration nor with the rate of fall
The risk factors for hyponatremia in infants of serum sodium (Robertson et al. 2007). How-
and children include excessive water GI loss as a ever, Fang et al. in a retrospective study in Chi-
result of gastroenteritis, systemic infection, nese children, investigated the factors in fluid
postoperative cardiac surgery, and chronic neu- management of hypernatremic dehydration
rological conditions (Forman et al. 2012). patients that could prevent the development of
cerebral edema and identified “too rapid a rate of
rehydration, an initial fluid bolus to rapidly
Table 4 Eight-point scale for assessing the degree of expand plasma volume and the severity of the
dehydration hypernatremia” as the major risk factors for the
Scores Degree of dehydration development of this complication (Fang et al.
0 No dehydration 2010). A slow rehydration rate over 48–72 h was
1–4 Some dehydration suggested as the best way to prevent this problem
5–8 Moderate to severe dehydration (Fang et al. 2010).

Table 5 Composition of commonly used intravenous fluids in infants and children (Melbourne 2012)
Naþ Cl K+ Lactate Ca++ Glucose
Type of fluid Indications for use (mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L) (gram/L)
0.9% NaCl Resuscitation fluid 150 150 – – – –
(normal saline) in shock and trauma
0.9% NaCl Maintenance fluid in 150 150 – – 5
with 5% sick children and in
dextrose children with
hyponatremia
Hartmann’s Intraoperative and 130 110 5 30 2 –
solution postoperative
maintenance fluid
10% dextrose Used for the – – – – – 10
in water treatment of
hypoglycemia
8 J. Chukwu and E. Molloy

Table 6 Indications for parenteral nutrition in infants and Table 8 Daily protein requirements in infants and chil-
children dren (Kraus 1998)
Bowel surgery Age group Protein requirement (g/kg/day)
Burns Infants 2.5–3.0
Trauma >1 year 1.5–2.0
Short bowel syndrome Adolescents 1.0–1.5
Intestinal pseudo-obstruction
Inflammatory bowel disease
Multiple organ failure Table 9 Daily lipid requirements in infants and children
Post-bone marrow transplantation Initiation 1 g/kg/day
Malnutrition – malignancy, cystic fibrosis, anorexia Advancement 0.5 g/kg/day
nervosa
Maximum requirement 2–3 g/kg/day

Table 10 Daily caloric requirements in infants and chil-

Table 7 Daily electrolyte requirements in infants and dren (Kraus 1998)
children (Kraus 1998)
Daily caloric requirements
Electrolyte/element Daily maintenance requirements Age group (years) (kcal/kg/day)
Sodium 2–4 mEq/kg/day 0–1 90–120
Potassium 2–3 mEq/kg/day 1–7 75–90
Calcium 0.46–2.32 mEq/kg/day 7–12 60–75
Magnesium 0.25–0.50 mEq/kg/day 12–18 30–60
Chloride 2–3 mEq/kg/day
Phosphate 1–2 mEq/kg/day

and leukocytosis. Redistributive hyperkalemia

Potassium
Potassium is the main intracellular fluid. Potas-
sium homeostasis is maintained by the Na þ K
ATPase which facilitates the transport of potas-
sium back into the cell against its concentration
gradient. The serum potassium concentration is
therefore maintained with in a very narrow range
of 3.5–5 mmol/l. Disorders of potassium metabo-
lism include hypokalemia or hyperkalemia.
Hyperkalemia
Hyperkalemia is defined as serum potassium
levels greater than 5.5 mmol/l. Mild hyperkalemia
is defined as serum potassium level between 5.5
and 6.0 mmol/l; moderate hyperkalemia is
between 6.1 and 6.9, while severe hyperkalemia
is greater than 7 mmol/l (Ahee and Crowe 2000).
Serum potassium level greater than 10 mmol/l is
fatal if not treated (Tran 2005).
Causes of hyperkalemia in children and infants
include pseudohyperkalemia due mainly to sam-
ple hemolysis but may also be due thrombocytosis
results from acidosis (serum potassium decreases
by 0.4 for each 0.1 point decrease in serum pH)
and rapid cell death in tumor lysis syndrome,
trauma, diabetes ketoacidosis, intravascular coag-
ulation, and rhabdomyolysis (Greenbaum 2010c;
Hoorn et al. 2012). Primary adrenal insufficiency
or unresponsiveness can also cause hyperkalemia.
In congenital adrenal hyperplasia due to 21-
hydroxylase deficiency, the male infants usually
present with salt wasting, metabolic acidosis,
hyperkalemia, and hypovolemia. This presenta-
tion is less common in affected female infants as
they are diagnosed and treated during the newborn
period (Greenbaum 2010c). Hyperkalemia can
result from both acute and chronic renal disease
due to reduced renal potassium excretion and
renal tubular acidosis type IV. Drugs that interfere
with the renin-angiotensin-aldosterone system
(mineralocorticoid receptor blockers) such as
spironolactone, antifungal drugs, heparin,
NSAIDs, succinylcholine, and beta-blockers can
cause hyperkalemia. Potassium-containing com-
pounds used during aggressive potassium
Fluid and Electrolyte Balance in Infants and Children
supplementation, blood transfusion, and medici-
nal herbs may also result in hyperkalemia.
Symptoms and Signs of Hyperkalemia
The most concerning feature of hyperkalemia is
the effect on the cardiac conducting system. The
main symptoms and signs of hyperkalemia
include muscle weakness and muscle cramps.
ECG changes start with tall peaked T waves,
followed by prolonged PR interval, loss of P
waves, widened QRS complex, and finally ven-
tricular fibrillation and a sine wave (Greenbaum
2010c). Death might result if hyperkalemia is not
treated. Muscle paralysis and cardiac arrhythmias
are the two main complications of hyperkalemia.
Treatment of hyperkalemia is aimed at preventing
or ameliorating these complications.
Diagnostic Tests
The diagnostic tests for hyperkalemia include
serum electrolytes, urea and creatinine, serum
bicarbonate, platelets, and white cell counts.
Other tests include urine potassium, urine creati-
nine, plasma renin, and aldosterone.
Treatment of Hyperkalemia
The two basic principles guiding the management
of life-threatening hyperkalemia include mem-
brane stabilization to block the effect of the excess
potassium on the myocyte transmembrane poten-
tial and cardiac conduction and reduction of extra-
cellular potassium levels (Hoorn et al. 2012).
The therapeutic approach depends on the serum
potassium level, associated ECG changes, and on
whether the condition is likely to worsen or not
(Greenbaum 2010c).
Intravenous calcium gluconate or calcium
chloride helps in stabilizing the cardiac membrane
and in reducing the risk of cardiac arrhythmias
associated with hyperkalemia. It is recommended
for serum K > 7 mmol/l with or without ECG
changes (Hoorn et al. 2012). This treatment does
not lower serum potassium levels. Insulin with
glucose helps to move the potassium from the
ECF to the ICF. It does reduce the plasma potas-
sium but not the total body potassium. Frequent
monitoring of serum potassium and glucose is
required during this treatment. β-2 adrenergic
9
agonists such as intravenous salbutamol can also
help shift potassium into the cells (Murdoch et al.
1991, while sodium bicarbonate also helps shift
potassium intracellularly. However, sodium bicar-
bonate administration is only recommended when
acidosis coexists with hyperkalemia. Loop
diuretics remove excess potassium from the
plasma. It is recommended if hypervolemia is
present.
Sodium or calcium polystyrene sulfonate is an
ion exchange resin that can either be administered
by mouth or per rectum. The main drawback is
that it takes approximately 4 hours to work and
that oral administration of calcium polystyrene
sulfonate in preterm neonates with suspected or
proven ileus is associated with increased risk of
intestinal obstruction (Ohlsson and Hosking
1987). In this group of patients, insulin and glu-
cose infusion is preferred over oral or rectal resin
administration (Vemgal and Ohlsson 2012).
Fludrocortisone can be given if there is associated
adrenal insufficiency. Patients with hyperkalemia
associated with chronic renal impairment may
require hemodialysis or hemofiltration to remove
the excess potassium. This can also be employed
in intensive care settings. In addition to the above
measures, potassium should be avoided in all the
fluids administered to this patient.
Hypokalemia
This is defined as serum potassium level
<3.5 mmol/l. Severe hypokalemia results when
serum potassium level is less than 2.5 mmol/l.
Causes of Hypokalemia
The four mechanisms that lead to hypokalemia in
children and infants include low potassium intake,
redistributive or transcellular shift, renal losses,
and non-renal losses. The most common causes
of hypokalemia in infants and children are diar-
rhea and vomiting. While potassium and bicar-
bonate are lost in diarrheal stools, only minimal
amounts of potassium are lost through vomits as
gastric fluids contain low concentrations of potas-
sium of about 10 mEq/l. However, the associated
chloride loss in gastric fluid leads to metabolic
acidosis and hypovolemia which results in
increased urinary loss of potassium. Other causes
10
of hypokalemia include redistributive hypokale-
mia which is due to alkalosis and hypothermia,
hypokalemic paralysis, and the administration of
drugs such as insulin and β-adrenergics like
salbutamol, Risperdal, and chloroquine (Greenlee
et al. 2009). Administration of loop diuretics also
leads to hypokalemia. Primary or secondary aldo-
steronism results in increased renal potassium
loss, metabolic alkalosis, sodium retention, and
hypertension. Hypomagnesemia, renal tubular
acidosis types I and II, eating disorders, laxative
abuse, and low-potassium intake are other causes
of hypokalemia.
Symptoms and Signs of Hypokalemia
The symptoms of hypokalemia include paresthe-
sia, muscle cramps, muscle weakness, and paral-
ysis which may occur at serum potassium levels
<2.5 mmol/l. Leg muscles are usually affected
first followed by the arm muscles (Greenbaum
2010c). The signs of hypokalemia are hyporeflexia
and ECG changes which includes flat of T waves,
short PR interval, and U waves (Ford 2002).
Complications of Hypokalemia
Hypokalemia is associated with the following
complications: arrhythmias which may occur in
a child with coexistent heart disease (Greenbaum
2010c). The types of arrhythmia in hypokalemia
include ventricular fibrillation, ventricular and
atrial tachycardia, and premature ventricular con-
tractions. Ileus, respiratory failure (secondary to
the weakness of the respiratory muscles), glucose
intolerance, and rhabdomyolysis are other symp-
toms associated with hypokalemia (Jain et al.
2011). The risk of rhabdomyolysis is increased if
a child with hypokalemia embarks on exercise.
Investigations of Hypokalemia
The following investigations should be carried out
in a child with hypokalemia: serum electrolytes,
urea and creatinine, magnesium, and phosphate.
Blood gas should be done to determine the serum
bicarbonate levels as coexistent metabolic acido-
sis points to diarrhea as a possible cause, but other
conditions like proximal and distal renal tubular
acidosis have to be considered. Hypokalemic
J. Chukwu and E. Molloy
metabolic alkalosis indicates gastric losses, hyper-
aldosteronism, or diuretic administration as pos-
sible causes. Urinary potassium less than 20 mmol
might indicate gastrointestinal cause of hypokale-
mia, while a urinary level greater than 20 mmol
indicates renal losses (Hoorn et al. 2012). Occa-
sionally, urine potassium-to-creatinine ratio,
plasma renin, and aldosterone and thyroid func-
tion test might be required (Hoorn et al. 2012).
Blood pressure should be measured as coexistent
high blood pressure is associated with
hyperaldosteronism.
Treatment of Hypokalemia
History, examination, and investigations should
be undertaken to identify the underlying cause.
The main aim of therapy is to restore serum potas-
sium to normal. Treatment of hypokalemia is
influenced by the following factors: how low the
serum potassium level is, the child’s renal func-
tion, presence or absence of symptoms associated
with hypokalemia, whether the low potassium
level was due to redistributive causes, whether
the potassium loss is ongoing, and whether the
child is able to tolerate oral potassium supplemen-
tation (Greenbaum 2010c). Intravenous potas-
sium at a rate not exceeding 0.5 mmol/kg/h
should be administered if the child presents with
the following complications: profound muscle
weakness, cardiac arrhythmia, or respiratory dif-
ficulty or if the serum potassium level is very low
(Ford 2002). Otherwise oral potassium supple-
ments are usually sufficient to replenish the deficit
unless the child is vomiting, intolerant to oral
supplements, or is not allowed to take oral fluids
due to other medical or surgical indications. In
some cases, potassium supplementation may be
needed for a few weeks in order to correct the
deficit.
Serum potassium should be monitored regu-
larly while on potassium supplementation
although this might not be accurate in redistribu-
tive causes of hypokalemia. Coexistent hypo-
phosphatemia should be treated with a potassium
phosphate salt instead of the potassium chloride
salt. Ongoing losses should be corrected for espe-
cially in surgical patients and in other critically ill
patients.
Fluid and Electrolyte Balance in Infants and Children
Calcium
Serum calcium is closely regulated by the interplay
of skeletal, renal, and parathyroid factors which
include calcium-sensing receptors, vitamin D3,
and parathyroid hormone (Lietman et al. 2010).
Hypercalcemia
Most hypercalcemia is due to osteoclastic bone
resorption (Lietman et al. 2010). Hypercalcemia is
also a common complication of solid tumors (Sar-
gent and Smith 2010). Rarely, familial hypo-
calciuric hypercalcemia (also termed familial
benign hypercalcemia) can be the cause of hyper-
calcemia in children (Lietman et al. 2010). Inves-
tigations of hypercalcemia include serum urea and
electrolytes, calcium phosphate and magnesium,
vitamin D, PTH, and albumin. Measurement of
urinary calcium concentration might provide a
clue as to the etiology of hypercalcemia (Davies
2009). Asymptomatic hypercalcemia does not
require treatment. The main aims of treatment of
symptomatic hypercalcemia are to remove the
source of the excessive PTH secretion if possible
or to the excess serum calcium if removal of the
primary source is not possible (Davies 2009).
Hyperhydration and diuretics are the initial treat-
ment modalities for hypercalcemia (Cheung
2009). Bisphosphonate and calcitonin are used
to treat specific disorders associated with hyper-
calcemia. Recently new therapies have been
developed to treat hypercalcemia. These include
cathepsin K inhibitor, sclerostin, cinacalcet, and
bone morphogenetic protein 2 (Cheung 2009).
Treatment of hypercalcemia secondary to hyper-
parathyroidism is by parathyroidectomy (Lietman
et al. 2010).
Hypocalcemia
Hypocalcemia is one of the most common disor-
ders of mineral metabolism in children. The four
main causative mechanisms of hypocalcemia are
decreased intake or decreased absorption,
increased binding and sequestration, decreased
mobilization from the bones, and low serum pro-
tein (Marini and Wheeler 2010).
Mild hypocalcemia is usually asymptomatic as
long as the ionized calcium levels remain normal
11
(Marini and Wheeler 2010). The serum calcium
levels at which symptoms of hypocalcemia
develops are variable. Most of the symptoms are
due to irritability of the neuromuscular junction.
Cramps, paresthesia, and tetany are the most com-
mon symptoms. Others are seizures, hallucina-
tions, and headaches. Respiratory symptoms
such as dyspnea and stridor might develop if the
respiratory muscles are affected. The signs asso-
ciated with hypocalcemia include carpopedal
spasm, facial muscle hyperreflexia, and
papilledema. Laboratory investigations of hypo-
calcemia include serum calcium, phosphate, and
magnesium. Serum albumin, urea and electro-
lytes, PTH, and vitamin D levels are other labora-
tory investigations.
Magnesium
Magnesium is an important mineral involved in
maintaining bone health. Magnesium, like potas-
sium, is an intracellular cation required for many
biological processes. It catalyzes more than 300
enzyme systems and is involved in the generation,
storage, and transfer of energy in the body
(Gonzalez et al. 2009). Intracellular magnesium
modulates calcium and potassium channels in the
cardiac myocyte (Agus and Agus 2001).
Hypomagnesemia
This results mainly from the imbalance between
the absorption of magnesium from the GI and its
excretion from the kidneys (Gonzalez et al. 2009).
Increased GI or renal loss and redistribution mag-
nesium between the extracellular and intracellular
compartments are other causes of hypomagnese-
mia (Ayuk and Gittoes 2011). Symptomatic hypo-
magnesemia is usually associated with
hypocalcemia, hypokalemia, or metabolic acido-
sis (Ayuk and Gittoes 2011). Other electrolyte
abnormalities associated with hypomagnesemia
include hyponatremia and hypophosphatemia.
Drug-induced hypomagnesemia is associated
with diuretic and proton pump inhibitor therapy.
Symptoms of hypomagnesemia are tremors, tet-
any, seizures, nystagmus, and paresthesia. The
ECG changes associated with the condition
12
include prolonged QT interval, torsades de
pointes, and ventricular fibrillation (Foglia et al.
2004).
The consequences of hypomagnesemia
include cardiac arrhythmias, which usually results
from unrecognized coexistent hypokalemia, insu-
lin resistance, and nervous disturbance (Ayuk and
Gittoes 2011). Administering anesthetic agents to
patients with hypomagnesemia may increase the
risk of cardiac arrhythmias (Gambling et al.
1988). Investigation of hypomagnesemia includes
urea and electrolytes, blood gas, serum calcium,
phosphate, and magnesium. Intravenous magne-
sium is the treatment of choice for symptomatic
hypomagnesemia (Ayuk and Gittoes 2011). Oral
magnesium therapy should be used in asymptom-
atic patients.
Hypermagnesemia
Hypermagnesemia is rare due to the closely regu-
lated magnesium metabolism (Samsonov 2009).
Renal failure and excessive magnesium ingestion
are the two main causes of hypermagnesemia
(Samsonov 2009). Patients with Epsom salt poi-
soning and laxative abuse and those being treated
with magnesium as a cathartic are at increased risk
of hypermagnesemia (Samsonov 2009). Other
causes of hypermagnesemia include tumor lysis
syndrome, milk-alkali syndrome, hypothyroid-
ism, and Addison’s disease.
Although mild hypermagnesemia is usually
asymptomatic, severe hypermagnesemia is
associated with the following symptoms: head-
ache, nausea, and vomiting. Drowsiness,
decreased tendon reflexes, bradycardia, hypo-
tension, and ECG changes (torsades de pointes,
arrhythmias, and prolonged QT) (Troung et al.
2010) are the signs associated with hyper-
magnesemia. The treatment of hyper-
magnesemia depends on the serum magnesium
levels and the severity of symptoms and signs.
Mild asymptomatic hypermagnesemia can be
treated by discontinuation of magnesium ther-
apy. Severe hypermagnesemia may require such
measures as forced diuresis, intravenous cal-
cium gluconate infusion, dialysis, and respira-
tory support (Samsonov 2009).
J. Chukwu and E. Molloy
Phosphate
Phosphate is a predominantly intracellular anion
involved in several metabolic processes in the
body such as in the generation of adenosine tri-
phosphate (ATP), nucleic acids, and cyclic aden-
osine monophosphate (cAMP) and in the
generation of the coagulation cascade.
Hypophosphatemia
The causes of hypophosphatemia are decreased
GI absorption, increased renal excretion, and
redistribution between intracellular and extracel-
lular compartments (Troung et al. 2010). Mild
hypophosphatemia may be asymptomatic, but
chronic severe hypophosphatemia may cause
myalgia and muscle weakness (Troung et al.
2010). Other symptoms of hypophosphatemia
include bone pain and decreased levels of
consciousness.
The investigation of hypophosphatemia
involves checking the urea, electrolytes, chloride,
creatinine, calcium, phosphate, blood pH and
bicarbonate, parathyroid hormone, and vitamin
D levels. Determining the urinary phosphate, cre-
atinine, and calcium levels can help determine the
etiology of the hypophosphatemia.
Treatment of Hypophosphatemia
Oral phosphate at a dose of 1–2 mmol/kg/day, in
two to four divided doses, is preferred to intrave-
nous supplementation in patients who can tolerate
oral therapy (Troung et al. 2010).
Hyperphosphatemia
Hyperphosphatemia is a rare condition seen
mostly in children with chronic renal failure. It is
generally asymptomatic but may be associated
with hypocalcemia due to the formation of cal-
cium phosphate complexes. These are deposited
in the skin and arterioles of patients with chronic
hyperphosphatemia.
Laboratory investigation of hyper-
phosphatemia includes serum urea, electrolytes
and creatinine, calcium, phosphate, and magne-
sium. Hyperphosphatemia is treated by treating
the underlying cause, limiting intake, and/or
Fluid and Electrolyte Balance in Infants and Children
removal of the excess phosphate using phosphate
binders (Covic and Rastogi 2013).
Acid-Base Balance
The normal values for pH in infants and children
(7.35–7.45) are similar to those in the neonates
and adults. The pH is closely regulated so that
cellular enzymes could function optimally.
While mild chronic deviations from the normal
range can be tolerated, extreme, rapid deviations
increase mortality. The acid-base balance is
maintained by the lungs, kidneys, and intracellu-
lar buffers (Greenbaum 2010a). The pCO2 is
maintained within the normal range of
35–45 mmHg by the rapid response of the lungs
to the central mechanism that senses changes in
pCO2, while the bicarbonate level is maintained
within the normal range by the ability of the
kidney to regenerate the bicarbonate utilized in
neutralizing organic acids generated by the body
(Greenbaum 2010a). Lactate and acid-base bal-
ance can be used as markers of cardiac output,
tissue oxygenation, and cellular perfusion in peri-
operative patients. However, in ill patients many
other factors can contribute to hyperlactatemia
and these factors need to be addressed as well.
Although persistent hyperlactatemia in postoper-
ative cardiac patients is associated with increased
morbidity and mortality, a single measurement of
serum lactate is not a good predictor of survival
(Allen 2011).
Acid-Base Balance Disorders
Acid-base balance disorders may be in the form of
acidosis (pH < 7.35) or alkalosis (pH > 7.45).
Metabolic or respiratory disorders can manifest as
acidosis or alkalosis. Mixed acid-base disorder
may result when both respiratory and metabolic
acid-base disturbance coexist. In this case two
primary processes are going on at the same time.
Compensatory mechanisms exist to counter acid-
base disturbance. The body attempts to restore the
pH to normal using the compensatory
13
mechanisms of the kidneys, lungs, and the intra-
cellular buffers.
Metabolic Acidosis
Metabolic acidosis results from a primary reduc-
tion in the serum bicarbonate levels with a resul-
tant decrease in the pH levels below 7.35.
Addition of organic acid from external sources,
altered body metabolic pathways, or rapid admin-
istration of normal saline may result in metabolic
acidosis. Hyperchloremic acidosis with normal
anion gap results from the loss of bicarbonate
ions from the GI or urinary tract. Diabetes
ketoacidosis results from the addition of
unmeasured acid and is therefore associated with
a widened anion gap (Ford 2002).
Metabolic Alkalosis
Metabolic alkalosis occurs if the pH is >7.45 and
the HCO3 is >35 mEq/l. Metabolic alkalosis may
be chloride responsive or chloride resistant. This
categorization is based on urinary chloride con-
centrations. While the urinary chloride concentra-
tion in the chloride-responsive metabolic alkalosis
is <15 mEq/l, the urinary chloride concentration
in the chloride-resistant type is >20 mEq/l.
Vomiting and diuretic therapy are the most com-
mon causes of chloride-responsive metabolic
alkalosis, while adrenal adenoma and Gitelman
syndrome cause chloride-resistant metabolic aci-
dosis with high blood pressure and without high
blood pressure, respectively (Greenbaum 2010a).
Perioperative Management in Infants
and Children
The Holliday-Segar equation for calculating
maintenance fluid requirements in the postopera-
tive period in infants and children was revisited
because of the frequent occurrence of hypo-
natremic dehydration using this method (Steurer
and Berger 2011). Isotonic fluids are
recommended in such situations of volume deple-
tion where it is anticipated that ADH secretion
will be stimulated (Steurer and Berger 2011).
The European Society for Paediatric
14
Anaesthesiology recommends intraoperative
fluids that is isotonic and contains 1–2.5% glucose
and bicarbonate precursors like lactate, acetate, or
malate (Sumpelmann et al. 2011). For replace-
ment of losses, fluids with similar compositions
as the lost fluid should be used. In replacing the
ongoing losses in surgical patients, consideration
should also be given to the surgical pathology, the
surgical procedure, and the child’s comorbid
conditions.
Hydration status should be continuously moni-
tored in perioperative children. Weight, blood pres-
sure, pulse, capillary refill time, urine output, and
respiratory rate are some of the clinical parameters
used to assess hydration status. In addition strict
recording of the fluid input and output might be
necessary. The laboratory parameters include
blood urea, electrolyte and osmolality, urine spe-
cific gravity, osmolality, and electrolytes.
Intraoperative Management
Careful intraoperative fluid management and
monitoring minimize adverse hemodynamic
effects during and after surgery. Blood loss should
be minimized as much as possible since total
blood volume is relatively low especially in very
young infants. A seemingly small-volume loss in
such infants could cause major hemodynamic
instability. Other high-risk children are those
with preoperative anemia, those on anti-
thrombotic or antiplatelet therapy, and those
undergoing complex, emergency, or re-operative
surgeries (Vretzakis et al. 2011). Measures to
reduce blood loss in these high-risk patients
include autologous blood donation and
normovolemic hemodilution (Vretzakis et al.
2011). Intravascular monitoring of blood pressure
and central venous pressure should be undertaken
during major surgical procedures. Fluid losses
should be carefully documented.
Postoperative Management
Good preoperative and intraoperative fluid man-
agement obviates fluid and electrolyte problem
J. Chukwu and E. Molloy
postoperatively. Replacement of lost fluid during
the surgery may still be ongoing postoperatively.
Ongoing losses may occur from wounds, drain-
ages, fistulae, or postoperative hemorrhage. Mon-
itoring of the vital signs and the fluid input and
output should continue during the immediate
postoperative period. Oliguria, hypotension, and
transient renal impairment may occur. Serum
urea, electrolytes, creatinine, and glucose as well
urine specific gravity should be monitored.
SIADH is one of the complications to watch out
for. Hyperchloremic metabolic acidosis may arise
from the administration of normal saline so Ringer’s
lactate is preferable (Steurer and Berger 2011).
Fluid and Electrolyte Balance in Septic
Shock
Shock is defined as a state of acute cardiovascular
dysfunction in which the delivery of oxygen and
nutrients is insufficient to meet the metabolic
demands of the tissues. Clinically, in shocked
patients, the capillary refill time is greater than
2 s. Hypotension is a late sign which is present
only in decompensated shock in children. The
mortality rate is about 5–7%. Every hour delayed
in initiating appropriate measures to reverse the
shock state increases the mortality by 40%. Septic
shock in infants and older children is character-
ized by severe hypovolemia unlike septic shock in
adults which exhibits a hyperdynamic state
(Aneja and Carcillo 2011). Aggressive fluid resus-
citation is therefore required in children pre-
senting with septic shock. Vasoconstriction is a
common feature of septic shock in children unlike
adults. This is because of the limited cardiac
reserve in children. If vasoconstriction is pro-
longed, cardiac failure may result. Inotropes,
vasodilator, and in some cases ECMO may be
required to support cardiac function (Vretzakis et
al. 2011). Goal-directed therapy over 72 h – main-
tenance of normal blood pressure and Central
Venous (CV) oxygen saturations >70% –
decreases mortality from 40% to 12%. The basic
principles of therapy in septic shock are resusci-
tation, administration of antimicrobials, and
removal of the nidus of infection (Aneja and
Fluid and Electrolyte Balance in Infants and Children
Carcillo 2011). Antibiotics should be adminis-
tered within the first hour, and the infection source
should be removed as soon as possible (Carcillo et
al. 2009).
Surgical conditions predisposing children to
septic shock include intussusception and
Hirschsprung’s diseases with enterocolitis and
volvulus. Endotoxins produced by Gram-negative
bacteria are responsible for most of the clinical
manifestations of septic shock.
Clinical Manifestations
Management
Crystalloid boluses of 20 ml/kg are infused rap-
idly. Up to 60 ml/kg of resuscitation fluid may be
required. Normal saline is the preferred resuscita-
tion fluid. Appropriate antimicrobials should be
initiated as early as possible. In cold shock periph-
eral adrenaline may be required, while in warm
shock adrenaline should be infused centrally,
while vasodilators might be needed in children
with pulmonary hypertension or high systemic
vascular resistance (Aneja and Carcillo 2011).
Although maintaining tight glycemic control
might be harmful in adults with septic shock,
this issue has not been resolved in pediatric
shock. Hydrocortisone is recommended for chil-
dren with absolute cortisol deficiency. Mortality is
about 50% in children requiring conventional
extracorporeal membrane oxygenation (ECMO)
but can be improved by the use of central
ECMO (MacLaren et al. 2011).
Total Parenteral Nutrition (TPN)
Total parenteral nutrition is indicated in cases of
intestinal failure resulting from congenital enter-
opathies, massive intestinal surgical resections,
intractable diarrheas, and immune-mediated con-
genital diarrheal diseases (Kocoshis 2010,
Askegard-Giesmann and Kenney 2015, Table 6).
TPN is also indicated in pediatric oncology
patients especially those undergoing bone marrow
transplant (Copeman 1994). TPN can be given via
peripheral or central venous access.
15
Complications associated with TPN therapy
include sepsis and thrombosis. Adjunctive thera-
pies for short bowel syndrome, such as epidermal
growth factor (EGF), or glucagon-like peptide 2
(GLP-2) may lead to improved outcomes for
patients with such conditions in the future
(Kocoshis 2010).
Conclusions and Future Directions
Fluid and electrolyte management in children is
continuously evolving as the understanding of
fluid and electrolyte requirement is progressing.
Most of the current estimates of maintenance
fluids are based on very old studies involving
only very few subjects. Properly designed and
adequately powered studies are needed to further
advance the management of fluids and electro-
lytes in critically ill children.
Cross-References
▶ Fetal Surgery
▶ Metabolism
▶ Nutrition
▶ Preoperative Assessment
References
Agus MS, Agus ZS. Cardiovascular actions of magnesium.
Crit Care Clin. 2001;17(1):175–86.
Ahee P, Crowe AV. The management of hyperkalaemia in
the emergency department. J Accid Emerg Med.
2000;17:188–91.
Allen M. Lactate and acid base as a hemodynamic monitor
and markers of cellular perfusion. Pediatr Crit Care
Med. 2011;12(4 Suppl):S43–9.
Aneja R, Carcillo J. Differences between adult and pediat-
ric septic shock. Minerva Anestesiol. 2011;77
(10):986–92.
Askegard-Giesmann JR, Kenney BD. Controversies in
nutritional support for critically ill children. Semin
Pediatr Surg 2015;24(1):20–4.
Ayuk J, Gittoes NJ. How should hypomagnesaemia be
investigated and treated? Clin Endocrinol. 2011;75
(6):743–6.
Bailey B, Gravel J, Goldman RD, Friedman JN, Parkin PC.
External validation of the clinical dehydration scale for
16
children with acute gastroenteritis. Acad Emerg Med.
2010;17(6):583–8.
Becker J, Friedman E. Renal function status. AJR Am J
Roentgenol. 2013;200(4):827–9.
Bianchetti MG, Simonetti GD, Bettinelli A. Body fluids
and salt metabolism – part I. Ital J Pediatr. 2009;35
(1):36.
Brandis, K. Regulation of cell volume. Fluid Physiol.
2001. http://www.anaesthesiamcq.com/FluidBook/
fl6_2.php
Bullock J, Boyle III J, Wang M, editors. NMS physiology.
4th ed. Baltimore: Lippincott Williams & Wilkins;
2001.
Carcillo JA, Kuch BA, Han Y, et al. Mortality and func-
tional morbidity after use of PALS/APLS by commu-
nity physicians. Pediatrics. 2009;124:500–8.
Carter ER, Marshall SG. Cystic fibrosis. In: Marcdante KJ,
Kliegman RM, Jenson HB, et al., editors. Nelson essen-
tials of pediatrics. 6th ed. Philadelphia: Saunders
Elsevier; 2010. p. 521–2.
Cheung M. Drugs used in paediatric bone and calcium
disorders. Endocr Dev. 2009;16:218–32.
Copeman MC. Use of total parenteral nutrition in children
with cancer: a review and some recommendations.
Pediatr Hematol Oncol. 1994;11(5):463–70.
Covic A, Rastogi A. Hyperphosphatemia in patients with
ESRD: assessing the current evidence linking out-
comes with treatment adherence. BMC Nephrol.
2013;14:153.
Davies JH. A practical approach to problems of hyper-
calcaemia. Endocr Dev. 2009;16:93–114.
Fang C, Mao J, Dai Y, et al. Fluid management of hyper-
natraemic dehydration to prevent cerebral oedema: a
retrospective case control study of 97 children in China.
J Paediatr Child Health. 2010;46(6):301–3.
Filston HC, Edwards 3rd CH, Chitwood Jr WR, Larson
RM, Marsicano TH, Hill RC. Estimation of postopera-
tive fluid requirements in infants and children. Ann
Surg. 1982;196(1):76–81.
Foglia PE, Bettinelli A, Tosetto C, Cortesi C, Crosazzo L,
Edefonti A, Bianchetti MG. Cardiac work up in pri-
mary renal hypokalaemia-hypomagnesaemia
(Gitelman syndrome). Nephrol Dial Transplant.
2004;19(6):1398–402.
Ford D. Fluid, electrolyte, & acid-base disorders & therapy.
In: Hay Jr W, Hayward A, Levin M, Sondheimer J,
editors. Current pediatric diagnosis & treatment. 16th
ed. New York: Lange Medical/McGraw-Hill; 2002. p.
1280–8.
Forman S, Crofton P, Huang H, Marshall T, Fares K,
McIntosh N. The epidemiology of hypernatraemia in
hospitalised children in Lothian: a 10-year study show-
ing differences between dehydration, osmoregulatory
dysfunction and salt poisoning. Arch Dis Child.
2012;97(6):502–7.
Friedman JN, Goldman RD, Srivastava R, Parkin PC.
Development of a clinical dehydration scale for use in
children between 1 and 36 months of age. J Pediatr.
2004;145(2):201–7.
J. Chukwu and E. Molloy
Gambling DR, Birmingham CL, Jenkins LC. Magnesium
and the anaesthetist. Can J Anaesth. 1988;35
(6):644–54.
Goldman RD, Friedman JN, Parkin PC. Validation of the
clinical dehydration scale for children with acute gas-
troenteritis. Pediatrics. 2008;122(3):545–9.
Gonzalez EP, Santos F, Coto E. Magnesium homeostasis.
Etiopathogeny, clinical diagnosis and treatment of
hypomagnesaemia. A case study. Nefrologia. 2009;29
(6):518–24.
Greenbaum L. Acid-base disorders. In: Marcdante KJ,
Kliegman RM, Jenson HB, et al., editors. Nelson essen-
tials of pediatrics. 6th ed. Philadelphia: Saunders
Elsevier; 2010a. p. 136–40.
Greenbaum L. Fluids and electrolytes. In: Marcdante KJ,
Kliegman RM, Jenson HB, et al., editors. Nelson essen-
tials of pediatrics. 6th ed. Philadelphia: Saunders
Elsevier; 2010b. p. 123–5.
Greenbaum L. Potassium disorders. In: Marcdante KJ,
Kliegman RM, Jenson HB, et al., editors. Nelson essen-
tials of pediatrics. 6th ed. Philadelphia: Saunders
Elsevier; 2010c.
Greenlee M, Wingo CS, McDonough AA, Youn JH, Kone
BC. Narrative review: evolving concepts in potassium
homeostasis and hypokalemia. Ann Intern Med.
2009;150:619–25.
Hoorn EJ, Tuut MK, Hoorntje SJ, van Saase JL, Zietse R,
Geers AB. Dutch guideline for the management of
electrolyte disorders – 2012 revision. Neth J Med.
2012;71(3):153–65.
Jain VV, Gupta OP, Jajoo SU, Khiangate B. Hypokalemia
induced rhabdomyolysis. Indian J Nephrol. 2011;21
(1):66.
Kocoshis SA. Medical management of pediatric intestinal
failure. Semin Pediatr Surg. 2010;19(1):20–6.
Kraus DM. Pediatrics nutrition. PMPR 652
Pharmacoceutics II. 1998. Retrieved from www.uic.
edu website: http://www.uic.edu/classes/pmpr/
pmpr652/Final/krauss/pedsnutrition.html.
Lietman SA, Germain-Lee EL, Levine MA. Hypercalce-
mia in children and adolescents. Curr Opin Pediatr.
2010;22(4):508–15.
Lum GM. Kidney and urinary tract. In: Hay Jr W, Hayward
A, Levin M, Sondheimer J, editors. Current pediatric
diagnosis & treatment. 16th ed. New York: Lange
Medical/McGraw-Hill; 2002. p. 693–716.
MacLaren G, Butt W, Best D, Donath S. Central extracor-
poreal membrane oxygenation for refractory pediatric
septic shock. Pediatr Crit Care Med. 2011;12(2):133–6.
Mahan JD. Nephrology and urology. In: Marcdante KJ,
Kliegman RM, Jenson HB, et al., editors. Nelson essen-
tials of pediatrics. 6th ed. Philadelphia: Saunders
Elsevier; 2010. p. 607–10.
Maitlan K, Kiguli S, Opoka RO, et al. FEAST trial group.
Mortality after fluid bolus in African children with
severe infection. N Engl J Med. 2011;364(26):2483–95.
Marini JJ, Wheeler AP, editors. Critical care medicine – the
essential. 4th ed. Philadelphia: Lippinkott Williams and
Wilkins; 2010.
Fluid and Electrolyte Balance in Infants and Children
Melbourne, The Royal Children’s Hospital. Intravenous
fluids: IV fluids for children beyond the neonatal
period. 2012. Retrieved 03/07/2013, from http://www.
rch.org.au/clinicalguide/guideline_index/Intravenous_
Fluids/.
Murdoch IA, Dos Anjos R, Haycock GB. Treatment of
hyperkalaemia with intravenous salbutamol. Arch Dis
Child. 1991;66(4):527–8.
Ohlsson A, Hosking M. Complications following oral
administration of exchange resins in extremely low-
birth-weight infants. Eur J Pediatr. 1987;146(6):571–4.
Patel S. Sodium balance-an integrated physiological model
and novel approach. Saudi J Kidney Dis Transpl.
2009;20(4):560–9.
Peruzzo M, Milani GP, Garzoni L, et al. Body fluids and
salt metabolism – part II. Ital J Pediatr. 2010;36(1):78.
Robertson G, Carrihill M, Hatherill M, Waggie Z, Reyn-
olds L, Argent A. Relationship between fluid manage-
ment, changes in serum sodium and outcome in
hypernatraemia associated with gastroenteritis. J
Paediatr Child Health. 2007;43(4):291–6.
Samsonov D. Abnormalities in magnesium metabolism. In:
Kiessling S, Goebel J, Somers M, editors. Pediatric
nephrology in the ICU. Berlin: Springer; 2009. p. 69–84.
Sargent JT, Smith OP. Haematological emergencies man-
aging hypercalcaemia in adults and children with
haematological disorders. Br J Haematol. 2010;149
(4):465–77.
Skorecki KL, Brenner BM. Body fluid homeostasis in man.
A contemporary overview. Am J Med. 1981;70
(1):77–88.
17
Somers M. Fluids and electrolyte therapy in children. In:
Avner E, Harmon W, Niaudet P, Yoshikawa N, editors.
Pediatric nephrology. 5th ed. Berlin: Springer; 2009. p.
325–53.
Steurer MA, Berger TM. Infusion therapy for neonates,
infants and children. Anaesthesist. 2011;60(1):10–22.
Sumpelmann R, Becke K, Crean P, Johr M, Lonnqvist PA,
Strauss JM, Veyckemans F. European consensus state-
ment for intraoperative fluid therapy in children. Eur J
Anaesthesiol. 2011;28(9):637–9.
Tran HA. Extreme hyperkalaemia. South Med J. 2005;98
(7):729–32.
Troung TR, Grant R, Langlois V. Renal complications. In:
Abla O, editor. Handbook of supportive care in pediat-
ric oncology. 1st ed. Toronto: Jones and Bartlett; 2010.
p. 267–88.
Vemgal P, Ohlsson A. Interventions for non-oliguric hyper-
kalaemia in preterm neonates. Cochrane Database Syst
Rev. 2012;5:CD005257.
Vogt B, Berwert L, Burnier B. Hypernatremia. Ther
Umsch. 2009;66(11):753–7.
Vretzakis G, Kleitsaki A, Aretha D, Karanikolas M. Man-
agement of intraoperative fluid balance and blood con-
servation techniques in adult cardiac surgery. Heart
Surg Forum. 2011;14(1):E28–39.
Woolley WL, Burton JH. Pediatric acute gastroenteritis:
clinical assessment, oral rehydration and antiemetic
therapy. Pediatr Health. 2009;3(2):191–7.