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FLUID AND ELECTROLYTES PART 1

PEDIATRICS DR. LORENZANA

INTRODUCTION Children have more water compared to adults. And this also
explains why we have more water issues than young
Pediatric patients, esp infants, are predisposed to children. In other words, we are more prone to dehydration
problems.
disturbances in hydration & acid-base balance.
Larger surface area in relation to volume of his body,
COMPARTMENTS OF TOTAL BODY WATER
Thus incur more insensible loss and more renal
expenditure than adults.
% of body weight in an older child or adult
Higher metabolic rate leads to higher proportional
turnover of body fluids esp. of the ECF (2X that of
adult)
Prone to more fluid losses via multiple routes compared to
adults
Immaturity of infant’s kidneys – less capacity to concentrate
urine
infants – 800 mOsm/L
older children & adults – 1500 mOsm/L
Infants tend to concentrate urine half the capacity
of the adults. So they tend to loss more fluid and
unable to conserve it.

DISTRIBUTION OF FLUIDS

ICF – intracellular fluid – within the cells

ECF – extracellular fluid – outside cell
interstitial fluid – in between them
plasma water - intravascular
transcellular water – special fluids (CSF, synovial fluid,
pleural fluid)

Total body water, intracellular fluid, and extracellular fluid as a

percentage of body weight and a function of age.

The concentrations of the major cations and anions in the

intracellular space and the plasma, expressed in mEq/L

Graph that tells you that an infant at birth is composed of

80% water. There’s a shift between the ICF and the ECF. After
a year, the ICF doubles. And during adolescence, male has
more fluid than females and this is due to fats.

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 ICF & ECF composition very different. Na & Cl – dominant ions in So, mataas ang blood sugar mo, what happens is more fluid in the
ECF. K – Major cation in ICF. Proteins, phosphates & organic vessel… then mababa ang Na. but there is a way to correct it:
anions most abundant in ICF (do not cross the cell membrane) [Na]corrected =
[Na]measured + 1.6 × ([glucose] - 100mg/dL)/100
Na-K-ATPase pump- responsible for distribution of Na & K- uses
So if I tell you that glucose is 500, how do you go about it?
cellular energy to actively extrude Na from the cell and move the 500/100, is 4 right? X 1.6= 6.4. so this is what you add to
K into the cell. whatever you got, then you request for the blood exam. Na
Remember the table. is 130, glucose is 6, so it is 136.
What separates the ICF and ECF? Semi-permeable membrane. So what happens when a child losses fluid? So it usually comes
from the ECF compartment. Its like naghemorrhage ka, then it is
MECHANISM OF SODIUM ABSORPTION the ECF compartment that is affected. Bumabagsak. That is the
first thing that would happen.
absorbed in the GUT The other one is, electrolyte problem. You can either end up with:
Na is for the maintenance of the tonicity. So if we ingest Na, it Isotonic solution no change
enters either: Hypotonic solution cell swell
together with chloride Hypertonic solution cell shrink
alone So you remember these 3 because this is exactly what happens
in exchange with hydrogen when a child gets dehydrated. Isotonic, no net flow. Hypotonic
with glucose or amino acid dehydration, mababawasan yung ECF, the patient mihgt go to
so, when this happens, Na gets into the ICF from the luminal side shock. On the other hand, pag hypetonic, fluid in the ICF will go to
what happens if there’s this change in the electrochemical ECF.
gradient? So, it is not anymore in homeostasis, so something has Clinical Features of Sodium Osmolality Disturbance
to happen. Mas concentrated sya diba? So ano ang mangyayari?
______ water to balance it. (sorry hindi ko marinig si doc. T___T) Isotonic Hypotonic Hypertonic
Take a look at the last statement with glucose or amino acid,
familiar with oresol? Diba may glucose yun? This is the reason Warm, velvety,
bakit may glucose ang Oral rehydration solution. It aids in Cold and clammy
Cold and dry doughy
absorption. Very poor
Skin Poor elasticity Normal to slightly
physiologic reason for the addition of glucose in the elasticity and
and turgor poor elasticity and
Oresol turgor
turgor
optimal ratio of Na to glucose: 1:1 to 1.4 In fact,
we have the optimal ratio. It means to say that if your
Na is 100, your glucose is 100-144???
Clammy or moist
REGULATION OF OSMOLALITY AND VOLUME Presence of
Lips hypersalivation Parched: patient
and Dry and shedding of complains of
OSMOLALITY
Tongue tears if serum extreme thirst
What is osmolality? This are all the electrolytes found in the
sodium is
plasma
110mEq/L or less
plasma Osmolality = 285–295
mOsm/kg = 2 × [Na] + [glucose]/18 + [BUN]/2.8 way to
predict it.
sodium value X 2 = provides an approximation of the
osmolality. so if we get the normal value of Na which is Lethargic when
135-145, 140x2=280+10=290, fair enough.(bat nag plus 10 pa undisturbed,
si doc??? @____@) So we can say that if we get the Na level hyperirritable
and double it, we can more or less say that it’s the total Comatose; when aroused,
osmolality. occasionally with focal or
Cns Lethargic
effective osmolality (tonicity) generalized generalized
determines the osmotic force mediating the shift of convulsions seizures, ↑
water between the ECF and the ICF muscle tone and
for example, if tonicity is high within the vascular tendon reflexes,
space… what is going to happen? The water will flow in meningismus
(in the Intravascular space). If mababa, out!
Same goes with oncotic pressure.

HYPERGLYCEMIA (DKA) Febrile

Normal to low Very low
temperature
Vital temperature; temperature; BP
there is a shift of water from the ICF to the ECF space causes BP normal
signs normal to low “in shock”
dilution of the sodium in the ECF space hyponatremia Normal to slightly
BP; rapid PR thready pulse
despite an elevated plasma osmolality. incraesed PR

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 Diarrhea – most common in children
HYPERNATREMIA Emesis/nasogastric suction
MECHANISMS OF BRAIN EDEMA DURING CORRECTION OF Osmotic cathartics (lactulose)
HYPERNATREMIA CUTANEOUS LOSSES
Burns
Excessive sweating
RENAL LOSSES
Osmotic diuretics (mannitol)
Diabetes mellitus
Chronic kidney disease (dysplasia and obstructive uropathy)
Polyuric phase of acute tubular necrosis
Post obstructive diuresis

HYPONATREMIA
CAUSES OF HYPONATREMIA

HYPOVOLEMIC HYPONATREMIA -
Third space losses
Extrarenal losses Gastrointestinal
(emesis, diarrhea) – most common cause
Skin (sweating or burns)
A rapid decrease of the serum concentration during treatment of Renal losses
hypernatremia causes movement of water into brain cells, leading Thiazide or loop diuretics
to cerebral edema. The presence of idiogenic osmoles in brain Osmotic diuresis
cells is responsible for the osmotic gradient. Postobstructive diuresis
Hypernatremia = cells shrink. Can you imagine your brain as cell Polyuric phase of acute tubular necrosis
Juvenile nephronophthisis (MIM
that shrinks in hypertonic dehydration. Nature is good, we have
256100/606966/602088/604387)
idiogenic osmoles that prevents/buffers theses changes. It Autosomal recessive polycystic kidney disease
prevents edema when there is rapid treatment of hypernatremia. (MIM 263200)
Tubulointerstitial nephritis
CAUSES OF HYPERNATREMIA Obstructive uropathy
Cerebral salt wasting
EXCESSIVE SODIUM Proximal (type II) renal tubular acidosis (MIM
Improperly mixed formula 604278)[*]
Excess sodium bicarbonate Lack of aldosterone effect (high serum potassium)
Ingestion of seawater or sodium chloride Absent aldosterone (e.g.,21-hydroxylase deficiency
Intentional salt poisoning (child abuse or Münchausen [MIM 201910])
syndrome by proxy) Pseudohypoaldosteronism type I (MIM 264350 and
Intravenous hypertonic saline 177735)
Hyperaldosteronism Urinary tract obstruction and/or infection
WATER DEFICIT EUVOLEMIC HYPONATREMIA
Nephrogenic diabetes insipidus Water intoxication – punishment daw?
Acquired Iatrogenic (excess hypotonic intravenous fluids)
X-linked (MIM 304800) Feeding infants excessive water products
Autosomal recessive (MIM 222000) Swimming lessons
Autosomal dominant (MIM 125800) Tap water enema
Central Diabetes Insipidus Child abuse
Acquired Psychogenic polydipsia
Autosomal recessive (MIM 125700) Diluted formula
Autosomal dominant (MIM 125700) Marathon running with excessive water intake –
Wolfram syndrome (MIM 222300) you’re not supposed to drink plain water. ORESOL
Increased insensible losses na lang daw.
Premature infants Beer potomania
HYPERVOLEMIC HYPONATREMIA
Radiant warmers
Congestive heart failure
Phototherapy
Cirrhosis
INADEQUATE INTAKE
Nephrotic syndrome
Ineffective breast-feeding
Renal failure
Child neglect or abuse
Capillary leak due to sepsis
Adipsia (lack of thirst)
Hypoalbuminemia due to gastrointestinal disease
WATER AND SODIUM DEFICITS
(protein-losing enteropathy)
Gastrointestinal losses

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YOUNG and CHESKA
 Insulin
HYPERKALEMIA β-Adrenergic agonists
CAUSES OF HYPERKALEMIA Drugs/toxins (theophylline, barium, toluene, cesium
chloride)
SPURIOUS LABORATORY VALUE Hypokalemic periodic paralysis (MIM 170400)
Hemolytic Thyrotoxic period paralysis
Tissue ischemia during blood drawing EXTRARENAL LOSSES
Thrombocytosis Diarrhea
Leukocytosis Laxative abuse
INCREASED INTAKE Sweating
Intravenous or oral Sodium polystyrene sulfonate (Kayexalate) or clay ingestion
Blood transfusions RENAL LOSSES
Potassium should be incorporated to With metabolic acidosis
intravenous fluid to avoid hyperkalemia. Distal rental tubular acidosis (MIM
DECREASED EXCRETION 179800/602722/267300)
Renal failure Proximal renal tubular acidosis (MIM 604278)[*]
Primary adrenal disease Ureterosigmoidostomy
Acquired Addison disease Diabetic ketoacidosis
21-hydroxylase deficiency (MIM 201910) Without specific acid-base disturbance
3β-hydroxysteroid dehydrogenase Tubular toxins: amphotericin, cisplatin,
deficiency (MIM 201810) aminoglycosides
Lipoid congenital adrenal hyperplasia Interstitial nephritis
(MIM 201710) Diuretic phase of acute tubular necrosis
Adrenal hypoplasia congenital (MIM Postobstructive diuresis
300200) Hypomagnesemia
Aldosterone synthase deficiency (MIM High urine anions (e.g., penicillin or penicillin
203400) derivatives)
Adrenoleukodystrophy (MIM 300100)
DECREASED EXCRETION ACID BASE BALANCE
Medications BICARBONATE BUFFER SYSTEM
Angiotensin-converting enzyme
inhibitors Based on relationship between carbon dioxide(CO2) and
Angiotensin II blockers bicarbonate (HCO3)
Potassium-sparing diuretics CO2 + H20 H+ HCO3 – it only means that pagtumaas ang H
Calcineurin inhibitors ion ng patient mo, the patient will move to the left… he’ll end up
Nonsteroidal anti-inflammatory drugs having C02 and water, and what happen to C02? ilalabas sya sa
Trimethoprim respiratory SYSTEM mo.
Heparin Henderson-Hasselbach equation for bicarbonate and carbon
Drug-induced potassium channel dioxide remember this equation:
syndrome pH = 6.1 + log[HCO3] / [CO2]
Renal tubular disease H = 24 x PCO2 / HCO3
Pseudohypoaldosteronism type I (MIM 264350 pH is directly related to HCO3 over CO2 level while
and 177735) your H is directly related to CO2 over HC03.
Pseudohypoaldosteronism type (MIM 145260) Therefore, ibig sabihin lang nun, pag mataas ang
Urinary tract obstruction CO2, then tataas ang HCO3 to lower, basic.
Sickle cell disease So why are we so concern about the pH? Bakit
Kidney transplant ayaw natin ng mataas at mababa? Ayaw ba natin?
Why is it important to know this? What are the causes of Baka gusto nyo LOL why? What is special?
ARF? May Pre-renal, renal, and post renal right? You should Because we need an optimal pH to protect us and
watch for K level if your patient has ARF. Syempre hindi na for optimal function of vital organs, like sa stomach
nya kaya ilabas eh. Your K is very toxic to the heart. And your natin.
K level has a very narrow range, that’s why it is very Normal Values of Arterial Blood Gas
important to note this. pH - 7.35–7.45
[HCO3-] - 20–28 mEq/L
HYPOKALEMIA Pco2 - 35–45 mm Hg
CAUSES OF HYPOKALEMIA Three-step process for interpreting acid-base disturbances
step 1, determine whether the pH is low (acidemia) or high
SPURIOUS (alkalemia).
High white blood cell count step 2. establish an explanation for the acidemia or
DECREASED INTAKE alkalemia.
Anorexia nervosa step 3, calculate the expected compensation and determine
TRANSCELLULAR SHIFTS whether a mixed disturbance is present. Met. alk., metabolic
Alkalemia

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YOUNG and CHESKA
 alkalosis; met. acid, metabolic acidosis; resp. alk., respiratory Comparison of Previous and Current Classification of Dehydration
alkalosis; resp. acid., respiratory acidosis. (DHN) Caused by Diarrhea
Previous
METABOLIC ACIDOSIS No DHN
Mild DHN
so we have metabolic alkalosis, metabolic acidosis, Moderate DHN
respiratory acidosis and respiratory alkalosis. The most Severe DHN
common problem encountered in pediatrics is metabolic Current
acidosis. No symptoms of DHN
3 basic mechanisms: Some DHN
Loss of bicarbonate from the body Severe DHN
Impaired ability to excrete acid by the kidney
Addition of acid to the body (exogenous or ASSESS FOR DEHYDRATION
endogenous) A B C
*Lethargic
DIARRHEA Look at *Restless, (weak) or
Well, alert
condition irritable unconscious;
Most common cause of metabolic acidosis in children floppy
Bicarbonate loss from the body Very dry
Eyes Normal Sunken
Kidneys attempt to balance the losses by increasing acid and sunken
secretion, but metabolic acidosis occurs when this Tears Present Absent Absent
compensation is inadequate it can lead to metabolic Mouth and
Wet Dry Very dry
acidosis. tongue
Volume depletion (losses of sodium and water) Drinks
Drinks
potentially exacerbates the acidosis by causing shock and Thirst Drinks poorly or is
lactic acidosis normally;
(major) eagerly not able to
Renal failure secondary to dehydration also limits acid not thirsty
drink
excretion and contributes to the acidosis. Feel: Skin *Goes back *Goes back
Goes back
pinch slowly (<2 very slowly
quickly
(major) sec) (>2 sec)
>2 signs inc
>2 signs inc
No signs of 1 *sign* -
Decide 1 *sign*
DHN SEVERE
SOME DHN
DHN
Treat Plan A Plan B Plan C

First to look at the child is the condition; the eyes(if sunken);

mouth and tongue should be wet; next is being thirst-usually
if not dehydrated not thirsty; skin pinch, if it goes back
quickly after releasing-no dehydration. On severe thirst,
sometimes kala nyo di na thirsty ang patient kasi ayaw n nya
uminom yun pala super weak n ksi sya kaya hindi na
Diarrhea is, in reality, as much a nutritional disease as makainom.
one of fluid and electrolyte imbalance, and therapy is Classify if no, some and severe DHN.
not adequate unless both aspects of the disease are Major criteria are: thirst and skin pinch.
On assessment 1 of the 2 should be a major.
treated. However, in contrast to fluid replacement,
Eg: 2, 2, 1 - some
nutritional management of diarrhea requires good 3,2,1 – some
feeding practices both during illness and between 2,2,2 – severe
episodes of diarrhea, when the child is not sick. When 1,2,3 – severe
this is done, and undernutrition is either prevented or Dapat mga 5sec. lang maassess mo na daw ang patient. Why
corrected, the risk of death from a future episode of is it important to asses patient? So that you rule out severe
diarrhea is decreased. DHN. Bec if diagnosis falls under severe this is medical
emergency na. bka in shock na ang px. So manage right
Diarrhea is one of the leading cause of morbidity and
away.
mortality in developing countries. ESTIMATE FLUID DEFICIT
Fluid Deficit as Fluid Deficit in
PATHOPHYSIOLOGY OF WATERY DIARRHEA Assessment
% of BW ml/kg BW
<5 % <50 ml/kg
Normal Intestinal Fluid Balance No Dehydration
Intestinal Absorption of Water and Electrolytes Some DHN 5-10 % 50-100 ml/kg
Intestinal Secretion of Water and Electrolytes Severe DHN >10 % >100 ml/kg

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YOUNG and CHESKA

OBJECTIVES OF TREATMENT OF DIARRHEA
Prevent DHN – even if there’s no DHN
Treat DHN
Prevent Nutritional Damage – very important bec there’s a
relation between nutrition and diarrhea.
Reduce the Duration of Severity of Diarrhea and Prevent
Future Episodes
Plan A: Treat Diarrhea at Home
Plan B: Treat Some Dehydration with ORS
Plan C: Give Extra Fluid for Diarrhea and Continue Feeding
PLAN A (PATIENT WITH NO DHN)
Can be manage at home
4 KEY ELEMENTS IN THE MANAGEMENT OF DIARRHEA
(Counsel the mother on the 4 rules of home treatment)
FLUIDS AND ELECTROLYTES
bec it is being lost.
In cholera, you lose more, than in non-cholera. Patient lose
more fluid and lose more electrolytes. So that is the basis for
the components of oresol (oral rehydrating solution). It has
all the electrolyte that px lose. Glucose- optimize the
absorption of Na+.
*Fresh Buko juice – good source of K+ and maybe some
sugars.
*Lucky me noodles – its not good, very salty. A lot of Na+,
fluoride.
FOOD
you can give anything except some food that have laxative
effective(ripe papaya and prunes – bec it is given for
constipated, so need to avoid it in px with diarrhea).
*Oil can also be given, it is a good source of concentrated
energy. Used for fat absorbable vitamins.
*BRAT diet – T-tea is a diuretics so stop giving it.
*WHO recommend to give ZINC, good for immune system.
But doc, prefer to give supplements w/ zinc than giving
supplement that has zinc only.
FOLLOW-UP
when the child is sent home. What do we need to watch for:
*if child refuses oresol intake at home, check for vomit or
voluminous.
if childs develop fever.
oresol is usually 2 packs is given. Don’t give more.
Give it For 24 hrs.
FREVENTION
PLAN B (SOME DHN)

Child with some signs of DHN.

Reduced (Low) Osmolality ORS Solution WHO recommend that there should be a diarrhea treatment
unit on the hospital, ER. Because in SOME DHN you must
Grams/L Mmol/L
inform the px to stay and don’t go home. Bec. Konti nalang
Sodium 2.6 Sodium 75 magiging severe na ang category n to. So ask them to stay
Chloride muna Usually for 4 HOURS.
Glucose 13.5 Chloride 65
anhydrous FLUIDS
Potassium 1.5 Glucose, 75
Chloride anhydrous 50-100 fluid deficits. Give 75cc per Kg BW to be consume for
Trisodium 2.9 Potassium 20 the next 24 hrs.
citrate
Citrate 10 FOLLOW-UP

If you add this all up. The total osmolality is 245.
Make your oresol at home: NaCl – ½ tsp
Table sugar – 5-6 tsp
Baking soda – ½ tsp.
(potassium)
Pag wala kang baking soda, kumaen k nlng ng banana..
hahaha.
Pag di marunong mag timpla, ano pwede p ibigay? Juice,
when you give orange juice then squeeze it, you will get K+
and fructose(bec. its fruit.. nyahahha). But it doesn’t have
salt. So just give a chips, 1-2pcs will do.
*Soda/cola is not allowed esp to a child with DHN. Its not
true na pwede ibigay ang flat coke. Walang silbi yun. Inform
parent na ang oresol ay sa 1 liter na water ititimpla hindi s 1L
n coke. Haha.
must see patient, check often. Since nasa hospital nanaman
sya e. inform parent to watch out for ongoing fluid losses.
Take note any event of fluid losses, vomiting and diarrhea.
Also take note how much. Better na tawagin ka if mgvomit
para mkita mo un type of vomit. (eg, 10kg patient, 75 cc =
ans.750. If approx. 1 cup ang vomit. Approx. 240 un(8oz). So
just add it. 240 + 750=990.
*At the end of the 4 hr period, you assess no, some, severe.
If you successfully hydrate the px, it will be NO HDN na.
If SOME DHN, still same condition as he came in. do
admission, stay for another 4 hrs. but if want to go home give
instruction if what to do and explain the reason you want
them to stay. Be nice to patient!

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YOUNG and CHESKA
 PLAN C (SEVERE DHN)

FOOD

Breast milk is considered food, if your child is

breastfeeding, don’t discontinue. Bec if stop, mother’s
will automatically stop flowing.

FOLLOW UP

We recommend oresol, but sometimes we can’t give it or it

fails. Due to:
Purging- when fluid loss is voluminous, stool is
frequent and voluminous the oral rehydration
cannot cope up well. So just shift to other fluid
replacement.
Persistent vomiting-sign of dehydration, often
associated with diarrhea. It is when we attempt to
give oresol 3x but still vomit. e.g. we give now,
child vomits, then give again after 10 mins, child
vomits and another attempt and child vomits. So
again shift.
Inability to drink- baka ayaw nya lang ng lasa. So
again shift.
Abdominal distension – can happen on child with
diarrhea.

Black – from power point

Blue – trans from lecturer
Red – from book

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wealthy we may be, we still need to be guided and corrected
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YOUNG and CHESKA
 Quid Refert, Dummodo non Desinas, Tardius Ire

FLUIDS AND ELECTROLYTES (Part 2)

PEDIATRICS DRA. LORENZANA

REASSESSMENT IONIC COMPOSITION OF IV INFUSION

No dehydration Na+ K+ Cl- Lactate Glucose

Some dehydration Preferred
Severe dehydration Ringer’s 130 4 109 28 0
Lactate
Ringer’s 130 4 109 28 278
Lactate w/
5%
dextrose
Dhaka 133 13 98 48 140
solution
Half 61 17 51 27 278
strength
darrow w/
5%
dextrose
Accepted
Normal 154 0 154 0 0
Saline
(0.9%
NaCl)
Not acceptable
Glucose 0 0 0 0 278
(dextrose)
solution
Preferred without glucose
Maintenance solution for Potassium is 20mEq
Hyperkalemia may occur is given excess potassium
Renal Failure may ensue.
- This is in relation to patient who is in impending shock or already in shock.
If IV therapy not available:
Send to nearest facility (w/in 30 min)- give ORS to drink along the
way.
NGT- ORS can be given 20 ml/kg/hr for 6 hrs
Reassess every hour, if not improved after 3hrs, send to nearest
facility.

TYPES OF SHOCK

Hypovolemic Shock
Cardiogenic Shock
Neurogenic Shock
Distributive
Septic Shock

PATHOPHYSIOLOGY

The initial insult triggers shock, leading to inadequate oxygen delivery to

organs and tissues
- Reassess 15-30 mins, until strong rapid pulse is present. Compensatory mechanisms attempt to maintain blood pressure by
- Check every 4 hours. increasing cardiac output and systemic vascular resistance
- Reassess again after the end of the 6th hour. The body also attempts to optimize oxygen delivery to the tissues by
increasing oxygen extraction and redistributing blood flow to the brain,
In cases of collapsed vein, the ORS can be given via: heart and kidneys (at the expense of the skin and gastrointestinal tract).
- Small incision (Cut down) These responses lead to the initial state of compensated shock in which
- Intraosseous approach blood pressure is maintained.
o Tibia is usually used for pediatrics If treatment is not initiated or is inadequate, decompensated shock
o 3cm from medial flat surface develops, with hypotension and tissue damage that may lead to
o Hit the bone perpendicularly multisystem organ dysfunction and ultimately death.
o Complications include infection (osteomyelitis, embolism, and
fracture.)
- NGT can also be an alternative

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 HYPOVOLEMIC SHOCK HEMODYNAMIC RESPONSE TO HEMORRHAGE

Most common cause of shock in children worldwide, is most frequently

caused by diarrhea, vomiting or hemorrhage.
Decreased preload
Secondary to internal or external losses
Loss of components of intravascular volume
Blood: hemorrhage
Plasma: burns,
Nephritic syndrome
Water and electrolytes: Diarrhea, vomiting, Diabetes
Tachycardia and an increase in systemic vascular resistance are the initial
compensatory responses to maintain cardiac output and systemic blood
pressure;
Without adequate volume replacement, hypotention develops followed
by ischemia and further clinical deterioration
When there is pre-existing low plasma oncotic pressure (neprotic
syndrome, malnutrition, hepatic dysfunction, acute severe burns etc.)
even further volume loss and exacerbation of shock may occur because of
endothelial breakdown and worsening capillary leak.
Blood pressure is maintained when VR ↑ while CO ↓.
CARDIOGENIC SHOCK Until at certain point (in this case, yung BP nagstart bumaba around
25%)
Cardiac pump failure secondary to poor myocardial function So regardless na nag ↑ ang VR, BP will eventually start to go down.
Congenital heart disease Normal blood volume in pedia is measured by cc/kg.
Cardiomyopathies: Infectious or acquired, dilated or restrictive lschemia o NORMAL VALUE: 80cc/kg
Dysrhythmias So ano ang 25% ng 80cc
Myocardial contractility is affected leading to systolic and diastolic o 20cc/kg loss
dysfunction. o Change in BP is seen
The later phases of all forms of shock frequently have an negative effect o Narrow pulse pressure is a sign of impending shock.
on the myocardium, leading to development of a cardiogenic component
to shock state. MANAGEMENT OF SHOCK

DISTRIBUTIVE SHOCK Initial fluid volume to give is 20cc since yun yung nawala. Pero according
to WHO, 30cc/kg.
Caused by an inadequate vasomotor tone, which leads to capillary leak “kay dra, yung 20cc daw sinusunod nya”
and maldistribution of fluid into the interstitium Early recognition and prompt intervention are extremely important in the
Abnormalities of vasomotor tone management of all forms of shock
Loss of venous capacitance decreases preload The initial assessment and treatment of pediatricshock patient should
Loss of arterial capacitance decreases afterload or systematic blood include stabilization of airway, breathing and circulation.
pressure Neonates and infants in particular may have profound glucose
Anaphylaxis dysregulation in association with shock
Neurologic: loss of sympathetic vascular tone secondary to spinal cord or Glucose levels should be checked routinely and treated appropriately.
brainstem injury Rapid IV administration of 20ml/kg isotonic saline or, less often, colloid
Drugs should be initiated in an attempt to reverse shock state.
Distributive shock is a state of abnormal vasodilation o This bolus should be repeated quickly up to 60-80 ml/kg
Sepsis, hypoxia, poisonings, anaphylaxis, spinal cord injury, or o It is not unusual for severely affected patients to require this
mitochondrial dysfunction can cause vasodilatory shock. volume within the first hour
The lowering of systemic vascular resistance is accompanied initially by a If shock remains refractory following 60-80 ml/kg of volume resuscitation,
maldistribution of blood flow away from vital organs and a compensatory inotropic therapy (dopamine, norepinephrine or epinephrine) should be
increase in cardiac output. This process leads to a significant decreases in instituted while additional fluids are administered
both preload and afterload. Rapid fluid resuscitation using 60-80ml/kg is more associated with
improved survival without an increased incidence of pulmonary edema.
SEPTIC SHOCK
SIGNS OF DECREASED PERFUSION
Includes multiple forms of shock; involves a more complex interaction of
distributive, hypovolemic and cardiogenic shock. PERFUSION PERFUSION PERFUSION
↓ ↓↓ ↓↓↓
Hypovolemic: third spacing from intravascular fluid losses occurs
through capillary leak. Organ system
CNS - Restlessness Agitated/
Distributive: early shock with decreased systemic vascular resistance
Apathetic Confused
decreased afterload Anxious Stuporous
Cardiogenic: depression of myocardial function by endotoxins C Coma
Bacterial Respiration - ↑ Ventilation ↑↑ Ventilation
Viral Metabolism - Compensated Uncompensated
Fungal(immunocompromised patients are at increased risk) metabolic Metabolic
Acidemia Acidemia
GUT - ↓ motility Ileus
Kidney ↓ Urine Volume Oliguria (<0.5 Oliguria/ anuria
↑ Urine Specific mL/kg/hr) (0.5cc/kg)
gravity

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 Skin Delayed capillary Cool extremities Mottled,
refill cyanotic cold
extremities
CVS ↑ HR ↑↑ HR ↑↑ HR
Peripheral pulses ↓ Blood
pressure
Central pulses

In children, to check for the capillary refill, use the heel of the palm, make sure
it is at the level of the heart.

The change in BP is a late sign of severe dehydration.

CLINICAL TYPES OF DIARRHEA

Acute Watery diarrhea – last several hours or day. Main danger is

dehydration, (including cholera).

Acute Bloody Diarrhea (dysentery) – main dangers are damage of the

intestinal mucosa, sepsis and malnutrition and dehydration

Persistent Diarrhea – last 14cdays or longer, main danger is malnutrition

and serious non-intestinal infection. Dehydration may also occur.

Diarrhea with Severe Malnutrition – (Marasmus of Kwashiorkor): Main

dangers are severe systemic infection, dehydration, heart failure and
vitamin and mineral deficiency.

Make sure you know how to differentiate severe diarrhea with severe
malnutrition because the management is different for diarrhea and for
malnutrition.

MICROBIAL CAUSES OF ACUTE DIARRHEA

Virus
Bacteria
Parasites

VIRUS

Rotavirus
o worldwide; cold, dry season >15-25%
o 5 serotypes epidemiologically impt
o patchy damage -> blunting of the vili >absorptive capacity
return in 2-3 weeks

BACTERIA

Escherichia coli
Shigella
Campylobacter jejuni
Vibrio cholera o1 & 0139
Salmonella (non-typhoidal)

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 WHO RECOMMENDATION

Antimicrobial therapy should not be given routinely to children with

diarrhea.

ANTIDIARRHEALS

These agents, though commonly used, have no practical benefit and are
never indicated for the treatment of acute diarrhea in children.
Adsorbents (e.g. kaolin, attapulgite, smectite, activated charcoal,
cholestyramine)
o ability to bind and inactivate bacterial toxins
o None has proven practical value
o Induce slight change only in the consistency of stool.
o Does not reduce fluid and salt losses.
Antimotility drugs (e.g. loperamide hydrochloride, diphenoxylate with
atropine, tincture of opium, camphorated tincture of opium, paregoric,
codeine)
o inhibitors of intestinal motility
o can cause severe paralytic ileus, which can be fatal, and they may
prolong infection by delaying elimination of the causative
organisms.
o Sedation may occur
o Fatal central nervous system toxicity has been reported for some
agents.
o Contraindicated in children with dysentery and probably have no
role in the management of acute watery diarrhea in otherwise
healthy children.

Bismuth subsalicylate
o decreases the number of diarrhea stools and subjective
complaints
o Combinations of drugs. Combine with adsorbents, antimicrobials,
antimotility drugs or other agents.

Antibiotics – are not effective against most diarrhea – causing

organisms.
o rarely help and can make some people sicker in the long term.
o indiscriminate use may increase resistance of some disease-
causing organisms to antibiotics.
o are costly, so money is wasted
o should not be used routinely.

OTHER DRUGS

Anti-emetics
o may cause sedation.
o Vomiting usually stops when pt has been hydrated
o Ex. (prochlorperazine, chlorpromazine)
o Are of little value and are associated with potentially serious side
effects (lethargy, dystonia, malignant hyperpyrexia)

Cardiac stimulants – never indicated.

o Correct Tx of Hypovolemia and subsequent shock is IV fluids of
MANAGEMENT OF SUSPECTED DIARRHEA balance of electrolyte solution.
Why cholera is diff compared to acute diarrhea: o Ex. (adrenaline, nicotinamide)
1. Occurs usually in large epidemics
2. Voluminous watery diarrhea →severe dehydration →hypovolemic Purgative (Cathartics)
shock o makes diarrhea and dehydration worse.
3. Appropriate antibiotic may shorten course o never used.

Treatment of dehydration in Cholera Steroids – no benefit, never used.

1. Follow guidelines for fluid mngt of some and severe dehydration
2. For severe dehydration and shock, initial IV infusion should be
given rapidly to restore adequate blood volume-guided by N BP
and strong radial pulse
Usually large ORS may be needed to replace large continuing fluid
losses after dehydration corrected.
Additional therapies
o The use of probiotic nonpathogenic bacteria for prevention and
therapy of diarrhea has been successful in developing countries.
o In addition to restoring beneficial intestinal flora, probiotics can
enhance host protective immunity such as down regulation of
proinflammatory cytokines and upregulation of anti-inflammatory
cytokines.
o A variety of organisms such as Lactobacillus and Bifidobacterium
have a good safety record.

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 o Saccharomyces boulardii has been shown to be effective in
antibiotic associated and in C. difficile diarrhea
o Lactobacillus rhamnosus GG was associated with reduced
diarrheal duration and severity , more evident in case of
childhood rotavirus diarrhea
Zinc Supplementation
o There is strong evidence that zinc supplementation in children
with diarrhea in developing countries leads to reduced duration
and severity of diarrhea and could potentially prevent a large
proportion of cases from recurring.
o Administration of zinc in community settings leads to increased
use of ORS and reduction in the inappropriate use of
antimicrobials.
o WHO and UNICEF recommend that all children with acute
diarrhea in at risk areas should receive oral zincin some form for
10-14 days during and after diarrhea (10 mg/day for infants <6
months of age and 20 mg/day for those >6 months.)

IMPROVED WEANING PRACTICES

Proper food preparations are advised to the mother before leaving the
hospital.

USE OF SAFE WATER

larger amounts of water facilitate improved hygiene

HANDWASHING

All family members should wash their hands thoroughly after defecation,
after cleaning a child who has defecated, after disposing of a child's stool,
before preparing food, and before eating.
An estimated 88% of all diarrheal deaths worldwide can be attributed to
unsafe water, inadequate sanitation and poor hygiene.
Improved sanitation has been shown to reduce the incidence of diarrhea
by 36%
Routine handwashing has been shown to reduce the incidence of diarrhea
be 36%
Routine handwashing with plain soap in the home can reduce the
incidence of diarrhea in all environments.
PREVENTION OF DIARRHEA

FOOD SAFETY
1. Breastfeeding
2. Improved weaning practices
3. Use of safe water Food can be contaminated by diarrheal agents at all stages of production
4. Handwashing and preparation, including:
5. Food safety o during the growing period (by use of human fertilizers)
6. Use of latrine and safe disposal of stools o in public places such as markets
7. Measles immunization o during preparation at home or in
restaurants
o when kept without refrigeration after being prepared.
BREASTFEEDING
Individual food safety practices should also be emphasized. Health
education for the general population should stress the following key
For the first 6 months of life, infants should be exclusively breastfed messages concerning the preparation and consumption of food :
protects against the risk of allergy early in life, aids in child spacing and o Do not eat raw food, except undamaged fruits and vegetables that
provides protection against infections are peeled and eaten immediately
Exclusive breast feeding protects very young infants from diarrheal o Wash hands thoroughly with soap after defecation and before
disease through the promotion of passive immunity and through preparing or eating food
reduction in the intake of potentially contaminated food and water. o Cook food until it is hot throughout
Breast milk contains all the nutrients needed in early infancy and when o Eat food while it is still hot, or reheat it thoroughly before eating
continued during diarrhea, it also diminishes the adverse impact on o Wash and thoroughly dry all cooking and serving utensils after use
nutritional status. Exclusive breast feeding for the first 6 months of life is o Keep cooked food and clean utensils separately from uncooked food
widely regarded as one of the most effective interventions to reduce the and potentially contaminated utensils
risk of premature childhood mortality and the potential to prevent 13% of o Protect food from flies by means of fly screens
all deaths of children <5 years of age.
Feeding bottles and teats should not be used because they are very
difficult to clean and easily carry the organisms that cause diarrhea.

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 USE OF LATRINE AND SAFE DISPOSAL OF STOOLS

unsanitary environment contributes to the spread of diarrhea

pathogens that cause diarrhea are excreted in the stools of an infected
person or animal
proper disposal of feces can help to interrupt
the spread of infection.
Fecal matter can contaminate water.

MEASLES IMMUNIZATION

Substantially reduce the incidence and severity of diarrhoeal disease

Rotavirus immunization
o Most infants acquire rotavirus diarrhea early in life; an effective
rotavirus vaccine would have major effect on reducing diarrhea
mortality in developing countries.
o The institution of large scale rotavirus vaccination programs has led
to a major reduction in burden of the disease and associated
mortality
o However, vaccine (live virus) associated rotavirus infection has been
reported in children with severe combined immunodeficiency
disease
o Other vaccines that could potentially reduce the burden of severe
diarrhea and mortality in young children are vaccines against Shigella
and ETEC

IMPROVED CASE MANAGEMENT OF DIARRHEA

Improved case management of diarrhea through prompt identification

and appropriate therapy significantly reduces diarrhea duration, its
nutritional penalty, and risk of death in childhood.
Improved management of acute diarrhea is a key factor in reducing the
burden of prolonged episodes of persistent diarrhea
The WHO/UNICEF recommendations to use low osmolality ORS and zinc
supplementation for the management of diarrhea coupled with selective
and appropriate use of antibiotics have a potential to reduce the number
of diarrheal deaths among children.

END

Black – from power point

Blue – trans from lecturer
Red – from book

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