essential informations about dehydration in children ,its causes, types, degrees and treatment in paediatric group.

1. Dr. Mona Mohammed Ali

2.  Though often considered a benign disease,
acute gastroenteritis remains a leading
cause of pediatric morbidity and mortality
around the world, accounting for 520,000
deaths annually in children younger than 5
years

3.  Because the disease severity depends on the degree
of fluid loss, accurately assessing dehydration
status remains a crucial step in preventing
mortality.
 Luckily, most cases of dehydration in children can
be accurately diagnosed by a careful clinical
examination and treated with simple, cost-effective
measures.

4.  Annually, children under five experience
an estimated 1.7 billion diarrheal
episodes worldwide, leading to 124
million outpatient visits, 9 million
hospitalizations, and 520,000 deaths

5. 1/ Viruses (70%) :
 Rotavirus
 noroviruses (Norwalk-like viruses)
 Caliciviruses.
 Astroviruses.
 EntericAdenoviruses.
 Others
 Viral gastroenteritis typicallypresents withlow-grade fever and vomiting
followedby copious waterydiarrhea (up to 10-20 bowel movements per
day), withsymptoms persisting for 3-8 days.

6. 2/ Bacteria (10-20%) :
 Campylobacter.
 Salmonella.
 Shigella.
 enterohemorrhagicEscherichiacoli(EHEC)species.
 Clostridiumdifficile cause of antibiotic-associateddiarrhea in children.
 Others
 Relative to viral gastroenteritis, bacterial disease is more likely to be
associatedwith highfevers, shaking chills, bloody bowel movements
(dysentery), abdominal cramping, and fecal leukocytes.

7. 3/Parasites :
 Giardia.
 Cryptosporidium.
 Entamoeba Histolitica .
 Others .
 Parasitic gastroenteritis generally present with watery
stools .
4/ Non-infective Diarrhea .

8.  The 2 primary mechanisms responsible for acute
gastroenteritis are as follows:
1/ Damage to the villous brush border of the
intestine, causing malabsorption of intestinal
contents and leading to osmotic diarrhea
2/ Release of toxins that bind to specific enterocyte
receptors and cause the release of chloride ions into
the intestinal lumen, leading to secretory diarrhea.

9. These include the following:
1. Diarrhea:
 3 or more loose stool per day .
 Acute Diarrhea persist less than 14 days.
 Chronic Diarrhea persist 14 days or more .
2. Vomiting.
3. Increase or decrease in urinary frequency.
4. Abdominal pain.

10. 5. Signs and symptoms of infection - Presence of fever, chills,
myalgia, rash, rhinorrhea, sore throat, cough; these may be evidence
of systemic infection or sepsis
6. Changes in appearance and behavior - Including weight loss and
increasedmalaise, lethargy, or irritability, as well as changes in the
amount and frequency of feedingand in the child’s level of thirst
7. History of recent antibiotic use - Increases the likelihoodof
Costridiumdifficile
8. History of travel to endemic areas

11.  Diabetic Ketoacidosis .
 Emergent Management of Pancreatitis
 Inflammatory Bowel Disease
 Intussusception
 Pediatric Appendicitis
 Pediatric Foreign BodyIngestion
 Pediatric PyloricStenosis
 Pediatric Urinary Tract Infection
 Peptic Ulcer Disease
 SepticShock
 Viral Hepatitis

12.  General: Weight, ill appearance, level of alertness,
lethargy, irritability .
 Head, ears, eyes, nose, andthroat (HEENT): Presence
or absence of tears, dry or moist mucous membranes,
andwhether the eyes appear sunken .
 Cardiovascular: Heart rate andquality of pulses.
 Respiratory: Rate andquality of respirations (The
presence of deep, acidoticbreathing suggests severe
dehydration )

13.  Abdomen: Abdominal tenderness, guarding, and
rebound, bowel sounds. Abdominal tenderness on
examination, with or without guarding, should prompt
consideration of diseases other than gastroenteritis.
 Back: Flank/costovertebral angle (CVA) tenderness
increases the likelihoodof pyelonephritis.
 Rectal: Quality andcolor of stool, presence of gross blood
or mucus

14.  Extremities: Capillary refill time, warmor cool
extremities
 Skin: Abdominal rash may indicate typhoidfever
(infection with Salmonellatyphi), whereas jaundice
might make viral or toxic hepatitis more likely. The
slowreturn of abdominal skin pinch suggests
decreasedskin turgor anddehydration (see the video
below), while a doughy feel to the skin may indicate
hypernatremia .

15. Accordingto the WorldHealthOrganization(WHO), a patient exhibiting 2 of the
followingsignscan be considered to have some amount of dehydration:
1. Restless, irritable
2. Sunkeneyes
3. Thirsty, drinks eagerly
4. Skinpinch goes back slowly
Accordingto the WHO, a patient exhibiting2 of the followingsigns can be considered
to havesevere dehydration:
1. Lethargic or unconscious
2. Sunkeneyes
3. Not ableto drinkor drinking poorly
4. Skinpinchgoes back veryslowly

17. • Baseline electrolytes, bicarbonate, and urea/creatinine - In any
childbeingtreated withintravenous fluids for severe dehydration.
• According to serumsodiumlevel, dehydration can be classifiedto:
-Isotonic Dehydration
-Hypernatremic Dehydration
-Hyponatremic Dehydration
• Fecal leukocytes and stool culture - May be helpful in children
presenting with dysentery

18. • Stool analysis for C difficiletoxins - In children older
than 12 months with a recent history of antibiotic use
• Stool analysis for ova andparasites - In patients with a
history of prolongedwatery diarrhea (>14 days) .
• Complete bloodcount (CBC) andbloodcultures - Any
childwith evidence of systemic infection
• If indicated, urine cultures, chest radiography, and/or
lumbar puncture should be performed

20. 1/ Rehydration :
 For severe dehydration : Plan C
 For mderate dehydration : Plan B
 For mild dehydration : Plan A
2/Probiotics
3/Zinc
4/antibiotics
5/ vaccine

21. Age First 30 ml/kg in : Then give 70 ml/kg in:
Infant
(under 12 months)
1 hour* 5 hours
Child
(12 month up to 5
years)
30 minutes* 2 ½ hours
• *Repeat once if pulse is still very weak or not detectable.
• Remember each ml contains 15 drops

22.  Reassess the patient every 1-2 hours andbehave
accordingly.
 Also give ORS per mouth 7-10ml/kg/motion to replace
the ongoing loss.
 Reassess an infant after 6 hours anda childafter 3
hours . Classify dehydration. Then choose the
appropriate plan ( A, B, or C ) to continue treatment.
 If possible observe the patient 6 hours after
rehydration.

24. • Remember eachml contains 15 drops .
• Reassess the patient every 1-2 hours and behave accordingly.
 Also give ORS per mouth7-10ml/kg/motion to replace the
ongoing loss
Reassess the patient after 4 hours . Classifydehydration. Then
choose the appropriate plan( A, B, or C ) to continue treatment.
 If possibleobserve the patient 6 hours afterrehydration.

25.  The AmericanAcademy of Pediatrics, the European Society
of Pediatric Gastroenterology and Nutrition(ESPGAN),
and the World Health Organization (WHO) all recommend
oral rehydrationsolution (ORS) as the treatment of choice
for children with mild to moderate dehydration including
those in both high-resource and low-resource settings,
basedon the results of dozens of randomized, controlled
trials and several large meta-analyses.

32.  Hypernatremia is defined as a serum
sodium concentration of more than 145
mEq/L.
 It is characterized by a deficit of total
body water (TBW) relative to total body
sodium levels .

33.  The following three mechanisms may lead to
hypernatremia, alone or in concert:
 Pure water depletion (e.g. diabetes insipidus)
 Water depletion exceeding sodiumdepletion
(e.g. diarrhea)
 Sodiumexcess (e.g. salt poisoning)

34.  Infants have a large surface area in relation to
their height or weight compared with adults and
have relatively large evaporative water losses.
 In infants, hypernatremia usually results from
diarrhea and sometimes from improperly
prepared infant formula or inadequate mother-
infant interaction during breastfeeding.

35.  As a result of increased extracellular
sodium concentration, plasma tonicity
increases. This increase in tonicity
induces the movement of water across
cell membranes, causing cellular
dehydration

36.  Hypernatremia causes decreasedcellular volume as a
result of water efflux fromthe cells to maintainequal
osmolality inside and outside the cell.
 Brain cells are especially vulnerable to complications
resulting fromcell contraction.
 Severe hypernatremic dehydration induces brain
shrinkage, which can tear cerebral bloodvessels, leading
to cerebral hemorrhage, seizures, paralysis, and
encephalopathy.

37.  In patients with prolonged
hypernatremia, rapid rehydration
with hypotonic fluids may cause
cerebral edema, which can lead to
coma, convulsions, and death.

38.  In children with acute hypernatremia, mortality rates
are as highas 20%.
 Neurologic complications relatedto hypernatremia
occur in 15%of patients.
 The neurologicsequelae consist of intellectual deficits,
seizure disorders, andspastic plegias.
 In cases of chronic hypernatremia in children, the
mortality rateis 10%.

39.  Althoughseizures can occur because of hypernatremiaper se, this is rare.
They usually occur during the treatment of hypernatremia becauseof a
rapiddecline in serumsodiumlevels. Therefore, slowly correcting
hypernatremiais important.
 Other complications include the following:
 Mental retardation
 Intracranial hemorrhage
 Intracerebral calcification
 Cerebral infarction
 Cerebral edema, especially during treatment
 Hypocalcemia
 Hyperglycemia

40.  Irritability , High-pitchedcry or wail .
 Periods of lethargy interspersed with period of irritability.
 Seizures.
 Increased muscle tone .
 Rabdomyolysis
 Oliguria
 Excessive diuresis.
 Characteristic doughy appearance of the skin.

41.  Serumsodium .
 BUN ,and creatinine.
 Urinary sodium .
 Other serumelectrolytes may be indicated.
 measuring aldosterone , renin ,cortisol ,ADH ,
and ACTH levels may be indicated
 Brain CT or MRI may be indicated .

42.  Medical care involves the correction of
hypernatremia. However, avoid rapid correction
of sodiumlevels in patients with chronic
hypernatremia, because a rapid decline in the
serumsodium concentration can cause cerebral
edema.

43.  The recommended rate of sodium correction is 0.5
mEq/h or as much as 10-12 mEq/L in 24 hours.
 Dehydration should be corrected over 48-72 hours.
 If the serumsodium concentration is more than
200 mEq/L, peritoneal dialysis should be
performed using a high-glucose, low-sodium
dialysate.

45.  Calculate the body water deficit usingone of the
following equations :
 Water deficit (in L) = [(current Na level in mEq/L ÷ 145
mEq/L) - 1] X 0.6 × weight (in kg)
 Water deficit (in L) = [(current Na level in mEq/L - 145
mEq/L)/145 mEq/L)] × 0.6X weight (in kg)
 Water deficit (in L) = [1- (145 mEq/L÷ current Na level
in mEq/L)] × 0.6 × weight (in kg)

46.  An example calculation is: A child weighs 10 kg
and has a plasma sodium concentration of 160
mEq/L.
 By using the first equation, water deficit (in L)
= [(160 mEq/L ÷ 145 mEq/L) - 1] X 0.6 × 10 =
0.62 L.

47.  The volume of replacement fluidneededto correct the
water deficit is determinedby using the concentration
of sodiumin the replacement fluid. The replacement
volume can be determinedas follows:
 Replacement volume (in L) = TBWdeficit × 1 ÷ [1 - (Na
concentration in replacement fluidin mEq/L ÷ 154
mEq/L)]

48.  If the patient from the example calculation
above has a TBW of 0.62, and if the replacement
fluid contains 0.2%NaCl (Na concentration of
34 mEq/L), the replacement volume (in L) = 0.62
L × 1 ÷ [1 - (34 mEq/L ÷ 154 mEq/L)] = 0.79 L.
This volume has to be replaced slowly over 48-72
hours.

49.  This depends on the cause and the patient's
condition .
 In hypernatremic dehydration, 0.45%or 0.2%
NaCl should be used as a replacement fluid to
prevent excessive delivery of free water and a too-
rapid decrease in the serumsodium
concentration.

50.  Serumsodiumlevels:
-Serumsodiumlevels should be monitored every 4 hours.
-Return serumsodiumlevels toward the reference range by not more
than 10 mEq/L/24h.
 Inpatient management also includes the following:
-Record daily body weights in patientswithhypernatremia.
-Frequently monitor electrolyte concentrations.
-Restrict sodiumand protein intake.
-Treat the underlyingdisease.

52.  Hyponatremia is definedas a serumor plasma
sodiumless than 135 mEq/L. Hyponatremia is among
the most common electrolyte abnormalities in
children. Drops in sodium level can lead to neurologic
findings andin severe cases significant morbidity and
mortality, especially in those withacute andrapid
changes in plasma or serumsodium.

53.  Management of hyponatremic dehydration is identical
to that of isonatremic dehydration.
 The additional sodium deficit must be calculatedand
addedto the rehydration fluids. The deficit may be
calculatedto restore the sodium to 130 mEq/L and
administeredover 48 hours, as follows:
 Sodium deficit = (sodiumdesired- sodium actual) X
volume of distribution X weight (kg)

54.  Example: Sodium = 123, weight = 10 kg, assumed volume
of distribution of 0.6; Sodiumdeficit = (130-123) X 0.6X
10 kg = 42 mEq sodium
 A simplified approach is to use 5%dextrose in 0.9%
sodiumchloride as the replacement fluid. The sodiumis
closely monitored, and the amount of sodiumin the fluid
is adjusted to maintain a slow correction (about < 0.5
mEq/L/h, with a correction goal of 8 mEq/L over 24
hours).

55.  Frequently reassessing the serumsodiumlevel during
correction is imperative. Rapid correction of chronic
hyponatremia (>2 mEq/L/h) hasbeen associatedwithcentral
pontine myelinolysis.
 Rapid partial correction of symptomatic hyponatremia has
not been associatedwithadverse effects. Therefore, if the
childis symptomatic (seizures), a more rapidpartial
correction is indicated. Hypertonic (3%) sodiumchloride
solution (0.5 mEq/mL) may be usedfor rapid partial
correction of symptomatic hyponatremia. A bolus dose of 4
mL/kgraises the serumsodiumby 3-4 mEq/L.

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