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Fluid and electrolytes

Bitseat Woldegebriel, Peds PCCM


Introduction
Total body water (TBW) as percentage of body weight varies with age & sex
• 80 % in premature infants
• 70 to 75 % in term infants
• 65 to 70 % in toddlers
• 60 % after 1 year of life
• 50% for females
• Percent of TBW decreases
• High fat content in overweight children
• During dehydration

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Compartments of TBW

• Distributed in the body in 2 compartments


• ECF- 1/3 of TBW & 20- 25% of body weight
• Interstitial
• Intravascular/ Plasma
• ICF- 2/3 of TBW and 30- 40%
of body weight

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Electrolyte Composition

• Composition of solutes in ICF


& ECF are very different

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Osmolality
Measure of solutes in given amount of solvent
ICF and ECF are in osmotic equilibrium
Plasma osmolality is normally 285-295 mOsm/kg
It can be estimated by calculation:
Osmolality = 2 ×[Na]+[glucose]/18 +[BUN]/2.8
Glucose and blood urea nitrogen (BUN) are measured in
mg/dL
Effective osmolality (tonicity) reflects the concentration of solutes that do
not easily cross cell membranes
Effective osmolality can be calculated as follows:
Effective osmolality = 2 ×[Na]+[glucose]/18
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Cont’d

Difference b/n measured serum osmolality and calculated serum


osmolality is called osmolal gap; usually caused by
Unmeasured osmoles
Pseudohyponatremia

Osmolal gap of more than 10 is abnormal

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Regulation of Osmolality & Volume
Plasma osmolality and the intravascular volume is controlled by
independent systems
Water balance, which determines osmolality
RAAS

Sodium balance, which determines volume status


Osmo-receptor, ADH

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Fluid Therapy
• Maintenance therapy

• Replacement Fluids

• Deficit therapy

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Maintenance Therapy
• Used in child who can’t be fed enterally

• Composed of solution of H20, glucose, Na+ and K+

• Don’t provide adequate calories, protein, fat, minerals, or vitamins

• Doesn’t provide electrolytes such as Ca +2, PO4, Mg+2 & bicarbonate

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Cont’d

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Cont’d
• Maintenance Electrolyte Needs  
• In children, the daily requirements are:
• Sodium = 2 to 3 mEq/100 mL of water/ day
• Potassium = 1 to 2 mEq/100 mL of water/day

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What fluid to use
• D5 ½NS +20meq kcl; in child who doesn’t have volume depletion

• D5 NS(0.9%) +20meq kcl; for children with volume depletion

• Isotonic saline or RL ;in postop and in patients with gastroenteritis.

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Management of Dehydration
• What is DHN
• Classification?
Introduction
Assessment
• Does the child have diarrhoea?
• If no, do not check for dehydration, move on to assess priority signs
• Is the child lethargic?
• Not interested in surroundings, sleepy, confused, ‘V’ or less on AVPU
• Does the child have sunken eyes?
• Ask mother –sunken, dark rings, wrinkled
• Is the child able to drink ?
• Just we can ask the mother whether the child is able to drink or not
and decide accordingly
• Does the skin pinch take longer than 2 seconds to go back?
.
Treatment of severe DHN
• Assess for shock – if present treat shock first
• Assess nutritional status
• In the well nourished child give fluids quickly as in IMNCI
Diarrhoea Treatment Plan C
• Give ORS (5ml/kg/h) as soon as able to drink
• Reassess after 6 hours (infants), 3 hours (children),
• classify dehydration and choose appropriate diarrhoea
treatment plan
Cont’d
• If severe malnutrition, proceed to assessment and treatment.
• Do not give IV fluids if possible
• Give ReSoMal 5ml/kg every 30min for 2hr,
• Then 5-10ml/kg/hr for the next 4-10hr
• Assess blood glucose – give dextrose if low (<54 mg%)
Fluid administration
NO severe malnutrition WITH severe malnutrition
• Give Ringer’s Lactate • Do not give IV fluids
• Infants: • Give ReSoMal 5ml/kg every 30
– 30mls/kg over 1 hour
– 70mls/kg over next 5 hours
mins for first 2 hours
• Children ≥1 year:
• Then 5-10mls/kg for the next 4-10
– 30mls/kg over 30min then hours
– 70mls/kg over2½ hours • Give more ReSoMal if child wants
• Assess child every 1-2 h more or large stool loss or vomiting
• If not improving: • Check blood glucose and treat if
– Give fluid more rapidly <3mmol/l (<54mg/dl)
– Inform senior staff • Treat malnutrition as per guidelines
• As soon as child can drink
– Give ORS 5ml/kg/h
Others
• Plan A and B in addition
• Zinc
• Feeding
• antimicrobials
Electrolyte Disorders
Cont’d
• is one of common morbidity & mortality in critical ill children
• Infants and young children are at greater risk than adults
• Difference in body composition
• Higher metabolic rate
• Immaturity for physiologic regulation systems
• Sodium
• Potassium
• Calcium
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Sodium
Infants receive sodium from
Breast milk (approximately 7 mEq/L) and
Formula (7-13 mEq/L, for 20 calorie/oz formula)
Readily absorbed throughout the GI tract
Excretion occurs in
Stool and sweat
Kidney

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Hypernatremia
Serum Na+ >145 mEq/L
Moderate or severe hypernatremia has significant morbidity bc
Result of underlying disease
Effects of hypernatremia on the brain
Risks of overly rapid correction

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Causes Of Hypernatremia

Excessive Sodium Water Deficit


• Improperly mixed formula • Central/nephrogenic diabetes insipidus
• Excess sodium bicarbonate • Inadequate intake
• Intravenous hypertonic saline • Ineffective breastfeeding
• Child neglect or abuse
• Hyperaldosteronism
• Adipsia (lack of thirst)
• Intentional salt poisoning
• Increased insensible losses
Premature infants
Radiant warmers
Phototherapy
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Water And Sodium Deficits

• Gastrointestinal losses • Renal losses


Diarrhea Osmotic diuretics (mannitol)
Emesis/nasogastric suction Diabetes mellitus
Chronic kidney disease (dysplasia&
Osmotic cathartics (lactulose) obstructive uropathy)
• Cutaneous losses Polyuric phase of acute tubular
Burns necrosis
Excessive sweating Post-obstructive diuresis

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Cont’d
Based on degree of hypernatremia
Mild - Na 146-149 mmol/L
 Manage cause , Rarely requires treatment
Moderate -150-169 mmol/L
 After initial resuscitation, replace deficit and maintainance over 48hrs
Severe > 170 mmol/L
 Medical emergency
 After initial resuscitation, replace deficit and maintainance over 48 hrs
 Based on presentation
 Acute
 Chronic-
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Clinical Manifestations
Acute hypernatremia
• Neurological symptoms-  irritability, restlessness, weakness
• Acute rise of Na > 160 mEq/L- altered mental status, coma, and
seizures
• From cerebral & subarachnoid hemorrhage, demyelination,
• In cases of excessive fluid losses; signs & symp of DHN

Chronic hypernatremia- usually asymptomatic


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Complications

Brain hemorrhage

Thrombotic complications

Central pontine myelinolysis

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Diagnosis
• Serum Na+ level
• History
• Fractional excretion of Na+
• Gastric sodium concentrations
• Aldosterone level (mild hypernatremia, edema, hypertension, hypokalemia, and
metabolic alkalosis)
• Urine osmolality---- low in DI and high in extra renal loses

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Treatment
• Chronic hypernatremia should not be corrected rapidly to avoid brain swelling
• Goal is to decrease serum [Na+ ] by <10 mEq/L every 24 hr
• If child has seizures 20 to rapid correction, admin of hypotonic fluid should
be stopped
• Infuse with 3% saline to reverse edema

• Acute, severe hypernatremia


• Can be corrected more rapidly with 5%

dextrose
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in water (D5W) Fluid and electrolyte Y12HMC 31
Cont’d
• Dialysis; when hypernatremia is severe and is caused by Na
intoxication excess of 200 mEq/L
• Loop diuretics
• And treat the causative agent
• Eg; Desmopressin acetate; central DI

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Case study 2
• A 9-month-old infant is admitted with persistent vomiting and
diarrhea. HR 160 beats/min, RR 28 breaths/min, BP 78/54
mm Hg, weight 8 kg
• Despite initial fluid resuscitation with 40 mL/kg normal saline,
patient remains tachycardic.
• Has this patient received adequate fluid resuscitation?
• What risk factors does this patient have for electrolyte
disturbances?
Case study cont’d
• Initiate additional fluid bolus with 20 mL/kg normal
saline and reassess.
• Choice of maintenance fluid:
• 5% dextrose 1/2 normal saline, or
• 5% dextrose normal saline.
• No potassium chloride (KCl) until patient has had urine
output.
• How do you target fluid management?
Case study 3
• A 6-month-old, 10-kg infant was admitted 2 days ago with
bacterial meningitis and now has generalized tonic-clonic
seizures.
• After ensuring ABCs are adequate, the infant is given 0.1
mg/kg IV lorazepam with no response. Dose is repeated,
but seizures persist
• What is your next step for this child's management?
Case cont’d
• Continue close monitoring of ABCs.
• Consider loading with phenobarbital or fosphenytoin.
• Obtain serum electrolytes.
• Consider CT to rule out other causes of seizures (ischemic stroke
or intracranial bleed).
• Patient is still having seizures and airway is adequate.
• Serum sodium is 115 mEq/L
• What is your intervention?
Management of hyponatremia
• Symptomatic hyponatremia: Treat with IV 3% saline.
• Goal: increase sodium level rapidly only to point where seizures stop (aim >
120 mEq/L).
• Sodium deficit calculation: 0.6 x (weight in kg) x (target-measured sodium).
• In this example, to bring sodium up by 5 mEq, administer 0.6 x 10 x 5 = 30
mEq (60 mL 3% saline).
• 3-5 ml/kg 3 % saline
• Deliver IV over 15-20 min (3% saline is 500 mEq/L of sodium [0.5 mEq/ml]).
• Once seizures are controlled, remainder of sodium deficit is corrected
by an increase of not more than 0.5-1.0 mEq/L/h.
Diagnosis of SIADH, CSW, and DI
Hyponatremia
Case study 5
• An 8-month-old infant with complex congenital heart disease
and significant postoperative anasarca transferred out of ICU 24
hours ago
• He is on intermittent IV furosemide with good urine output
• You are called to evaluate him for frequent PVCs and PACs. He
is clinically and hemodynamically stable.

What are the next steps in management?


Case study 6
• 2-year-old child with short
bowel and dependent on total
parenteral nutrition with few
episodes of emesis. TPN rate
was doubled 4 h ago in
effort to provide additional fluid.
• Now the patient is pale and diaphoretic with weak pulses.
• What do you see on the ECG?
• What are other potential causes of hyperkalemia ?
Potassium
• Factors which affects potassium distribution
Insulin(Na+,K+-ATPase)
Acid–base status
ß-Adrenergic agonists(Na+,K+-ATPase)
Alpha-Adrenergic agonists

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Hyperkalemia
• When serum K+ > 5.5 mg/dl

• False Laboratory Transcellular Shifts


Hemolysis Acidosis
Tissue Ischemia During Rhabdomyolysis
Blood Drawing Tumor Lysis Syndrome
Thrombocytosis Tissue Necrosis
Hemolysis/Hematomas/GI Bleeding
Leukocytosis
Exercise
• Increased Intake Hyperosmolality
Intravenous Or Oral Insulin Deficiency
Blood Transfusions
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Cont’d

Decreased Excretion Medications

• Renal failure • Angiotensin-converting enzyme


• Primary adrenal disease (CAH) inhibitors
• Angiotensin II blockers
• Hyporeninemic
hypoaldosteronism • Potassium-sparing diuretics
• Renal tubular disease(Aquired, • NSAIDS
congenital) • Digoxin
• ß-blockers
• Cotrimoxazole
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Clinical Manifestations

• Ventricular fibrillation and asystole

• Paresthesias, fasciculations, weakness

• Cardiac toxicity usually precedes these clinical symptoms.

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Treatment
• 3 basic goals

(1) Stabilize the heart to prevent life-threatening arrhythmias

(2) Decrease serum potassium level

(3) Remove potassium from the body

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Cont’d
• Stabilize the heart
• 10% Ca+2 gluconate; 0.5 mL/kg by IV slow infusion over 5-10 min with
cardiac monitoring

• Decrease serum K level(trancellular shift)


• RI; 0.1U/kg, max. dose of 10 IU with D10% at a dose of 5 mL/kg over 30
mins with RBS monitoring
• Inhaled beta-adrenergic agonists ; repeat three times
• Sodium
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bicarbonate 1-2 mEq/L over 1 hour
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Remove potassium from the body
• Loop diuretic

• Sodium polystyrene sulfonate (Kayexalate) is an exchange resin that is


given either rectally or orally

• Dialysis-if the patient has either severe renal failure or high rate of
endogenous potassium release (TLS or rhabdomyolysis).

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• Long-term management of hyperkalemia includes
• Reducing intake via dietary changes
• Eliminating or reducing medications that cause hyperkalemia
• Sodium polystyrene sulfonate & loop or thiazide diuretics
• Dialysis– in infants with chronic renal failure

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HYPOKALEMIA

• Most cases related to gastroenteritis

• Defined as serum K+<3.5mEq/L

• Severe hypokalemia <2.5mEq/L

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Causes
1) Spurious hypokalemia-occurs in 4) Extrarenal Losses
leukemia & very elevated WBC counts Diarrhea &Laxative abuse
2) Transcellular Shifts Sweating
Alkalemia Kayexalate
5) Renal Losses
Insulin
RTA
alpha-Adrenergic agonists
DKA
Drugs (Aminophyline)
Interstitial nephritis
Refeeding syndrome Diuretic phase of ATN
3.Decreased Intake Postobstructive diuresis
Anorexia nervosa Hypomagnesemia
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Clinical Manifestations

• Ventricular fibrillation and torsades depointes may occur

• ECG changes; flattened T wave, depressed ST segm, & appearance of U wave

• Muscle weakness ,cramps and ascending paralysis(if K+ level is <2.5meq/l)

• Respiratory paralysis may require mechanical ventilation

• Slowed GI motility(conistipation,ileus)

• Polyuria and polydipsia

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Treatment
• Severe or symptomatic hypokalemia requires aggressive, but cautious IV
rx,0.5-1.0 mEq/kg, given over 1 hr).

• Oral potassium is safer to treat (2-4 mEq/kg/day).

• Potassium-sparing diuretics-for excessive urinary losses

• Correction of concurrent hypomagnesemia

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Calcium

• 99% is in bone

• Normal serum calcium concentrations range from 9.0 to 10.5 mg/dL,

Regulation

• PTH gland plays central role in control of Ca2+ metabolism

• Vitamin D and Calcitonin

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• Causes
Hypocalcemia • Hypoparathyroidism
• PTH resistance
• is relatively common disorder
Causes of Neonatal Hypocalcemia
especially in the neonate
• Prematurity
• Acute hypocalcemia can cause
life-threatening events • Perinatal distress/asphyxia
• Infants of diabetic mothers
• Intrauterine growth restriction
• Maternal vitamin D deficiency

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Clinical Features
• Tetany is uncommon unless serum ionized [Ca 2+] falls below
4.3 mg/dl
• Cardiac = prolonged qt interval on ekg, hypotension, heart failure
• Neuromuscular = tetany , laryngospasm, trousseau’s & chvostek’s
sign , seizures
• Psychiatric manifestations
• Chronic; ocular disease, extrapyramidal disorders, dental
abnormalities, ectodermal , renal abnormalities
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Investigation and management

• Lab = calcium( serum, total) electrolytes, magnesium, BUN,


creatinine, and phosphorus, PTH and 25(OH)D levels

• Diagnosis = direct measurement of ionized calcium in any patient


who is acutely or chronically ill

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Treatment

• Calcium gluconate

• Magnesium sulphate

• Oral calcium supplementation

• Ergocalciferol (vitamin D2) or cholecalciferol

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Hypercalcemia
• Relatively uncommon

• Diagnosis is commonly incidental

• Total serum calcium level in a child greater than 10.3 mg/dL

• Causes
• Primary hyperparathyroidism and malignancy
• Excessive gastrointestinal absorption
• Decreased renal excretion of calcium
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Clinical Features
• Cardiovascular; shortened qt interval on ekg, hypertension, bradycardia

• Gastrointestinal; nausea and vomiting, constipation, peptic ulcer, pancreatitis

• Neuromuscular; lethargy, depression, stupor, confusion, muscle weakness

• Renal; polyuria & polydipsia, hypercalciuria, nephrocalcinosis, nephrolithiasis

• General ; weakness, metastatic calcifications, failure to thrive

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Treatment
• Mild hypercalcemia (total serum Ca2+ < 12 mg/dL, ionized < 1.5 mM
• don’t require treatment = avoiding dehydration & reducing Ca2+ in diet
• Moderate hypercalcemia (total serum Ca2+ 12–14 mg/dL)
• aggressive rehydration with normal saline
• treat primary etiology
• Bisphosphonates
• Severe hypercalcemia (total serum Ca2+ > 14 mg/dL or who are symptomatic)
• Aggressive rehydration with NS, furosemide at dose of 0.25–0.5 mg/kg
• Calcitonin , bisphosphonates

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References
1. Nelson text book of pediatrics 21st edition (Larry A Greenbaum)
2. Up-todate 2018
3. McNab 5, et al. Cochrane database syst rev 2014.
4. https://www.tandfonline.com

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