7. PEDIATRIC GASTROENTEROLOGY

8/7/2019 7. PEDIATRIC GASTROENTEROLOGY

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PEDIATRICPEDIATRIC

GASTROENTEROLOGYGASTROENTEROLOGY


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GENERAL POINTS

1 month age: preference for sweet & salty foods

4 month age: Interest in solids increases6 month age: Recommended to begin solids

First few months of life: Oral & pharyngeal movements necessary for

swallowing solids develop

Meconium: Dark, viscous material that is normally passed within the first 48

hrs of life

Transition stools: Green-brown stools passed after beginning of feeding

followed by yellow brown milk stools after 4-5 days

If white grey obstructed jaundice

4 6 month age: Pancreatic amylase secretion

Length of Esophagus

At birth: 8-10 cm

2-3 years: 16-20 cm

Adult: 25 cm


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LES normally relaxes to vent swallowed air & to permit physiologic reflux

episodes

Physiologic GE reflux resolves in 80% infants by 6 months of age

Stomach volume

1-3 month: 90-150 ml

1 year: 250-300 ml

5 year: 700-850 ml

Adult: 2000 ml

Acid secretion low at birth & increases dramatically by 24 hr

Length of Small IntestineAt birth: 270 cm

4 years: 450-550 cm (adult length)

MMC occurs less often in neonates

Fat absorption is less efficient


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Liver is palpable 1-2 cm below costal margin at birth

Riedel lobe: thin projection of the right lobe

Newborn are relatively intolerant of prolonged fasting (d/t decreased

ketogenesis)Fatty acid oxidation provides a major source of energy in early life

13th week of gestation: Pancreas can be identified

16th week of gestation: Immature zymogen granules in primitive acini

20th week of gestation: Mature zymogen granules containing amylase,

trypsinogen, & lipase

8th week of gestation: Glucagon

12-16th week of gestation: Islet of langerhans appear

Although, amylase & lipase are present in pancreas early in gestation,

secretion is low in infants (adult levels reached by 1 year of life)

Low levels are partially compensated by salivary amylase & lingual lipase

This is the cause of diarrhea in infants fed on formulas high in glucose & fats

(fat & glucose intolerance)


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VOMITINGVOMITING

BiliousBilious == GIGI obstructionobstructionBloodBlood ((HemetemesisHemetemesis)) == UpperUpper GIGI bleedbleed (MCC(MCC PortalPortal

HTNHTN;; othersothers GastricGastric ulcer)ulcer)

FeverFever == GastroenteritisGastroenteritis (MCC(MCC ofof vomitingvomiting inin infancy)infancy)

EmesisEmesis onlyonly (no(no nausea)nausea) == GERDGERD

UndigestedUndigested foodfood == Achalasia Achalasia (relieved(relieved onon feedingfeeding ininproppedpropped upup position)position)

ProjectileProjectile emesisemesis == PyloricPyloric stenosisstenosis,, AntralAntral web,web, AnnularAnnular

pancreaspancreasTenseTense fontanellefontanelle == increasedincreased ICPICP

OlderOlder adolescentadolescent femalefemale == pregnancy,pregnancy, migranemigrane,, bulemiabulemia

SoonSoon afterafter birthbirth == EsophagealEsophageal atresiaatresia


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ACUTE ABDOMINAL PAINACUTE ABDOMINAL PAIN

TraumaTrauma == perforation,perforation, hemorrhage,hemorrhage, musculoskeletalmusculoskeletal injury,injury,

pancreatitispancreatitis

BiliousBilious vomitingvomiting == obstructionobstruction

PeritonitisPeritonitis == appendicitis,appendicitis, cholecystitischolecystitis,, PIDPID

AdolescentAdolescent femalefemale == PID,PID, pregnancy,pregnancy, ovulatoryovulatory painpain

CurrantCurrant jellyjelly stoolstool == intussusceptionintussusception ((11stst && MCMC symptomsymptom isis

abdominalabdominal pain)pain)

MelanaMelana == upperupper GIGI bleedbleed

NonNon--specificspecific == gastroenteritis,gastroenteritis, UTI,UTI, pneumonia,pneumonia, functionalfunctional

abdominalabdominal painpain

MCC of abdominal pain in children = Worm colic


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TRACHEOESOPHAGEAL FISTULATRACHEOESOPHAGEAL FISTULA

AND ESOPHAGEAL ATRESIAAND ESOPHAGEAL ATRESIA

11//40004000 birthsbirths

9090%% tracheosophagealtracheosophageal abnormalitiesabnormalities presentpresent asas blindblind

upperupper esophagealesophageal pouchpouch withwith aa fistulafistula betweenbetween aa lowerlower

esophagealesophageal segmentsegment andand thethe lowerlower portionportion ofof thethetracheatrachea


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11//33 ofof patientspatients willwill havehave otherother congenitalcongenital abnormalitiesabnormalities(VACTERL(V ACTERL VVertebral,ertebral, AAnalnal atresiaatresia,, CCardiac,ardiac,TTracheoracheoEEsophegealsophegeal fistula,fistula, RRenal,enal, andand LLimbimb abnormalities)abnormalities)

EsophagealEsophageal atresiaatresia withoutwithout TEFTEF == excessiveexcessive secretionssecretions

TEFTEF withoutwithout esophagealesophageal atresiaatresia (H(H--type)type) == chokingchoking duringduring

feedingfeeding


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EsophagealEsophageal atresiaatresia withwith distaldistal TEFTEF

diagnoseddiagnosed byby placingplacing NGTNGT

(unable(unable toto advanceadvance intointo

stomach)stomach)

CXRCXR willwill showshow coiledcoiled tubetube andand nono

airair inin stomachstomach


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FOREIGN BODY INGESTIONFOREIGN BODY INGESTION

MostMost cancan bebe diagnoseddiagnosed withwith CXRCXR ((9090%% areare radiopaqueradiopaque))CoinsCoins inin thethe coronalcoronal planeplane == esophagusesophagus

CoinsCoins inin sagittalsagittal planeplane == tracheatrachea

EndoscopyEndoscopy usuallyusually neededneeded forfor removalremoval andand evaluationevaluation


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CONGENITAL PYLORIC STENOSISCONGENITAL PYLORIC STENOSIS

11//200200 -- 11//750750 livelive birthsbirths

CommonestCommonest surgicalsurgical disorderdisorder ofof thethe stomachstomach duringduring infancyinfancy

66 timestimes moremore commoncommon inin malesmales

PresentsPresents betweenbetween 33 wkswks && 22 mthsmths

NonNon--bilious,bilious, projectileprojectile vomitingvomiting

WeightWeight lossloss

O/EO/E:: VisibleVisible peristalsisperistalsis;; MassMass abdomenabdomen

HypochloremicHypochloremic hypokalemichypokalemic alkalosisalkalosis ifif notnot noticednoticed earlyearly

IxIx:: BariumBarium mealmeal:: StringString signsign ororDoubleDouble tracktrack signsign

PyloromyotomyPyloromyotomy forfor treatmenttreatment


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Age group: INFANTS (6-11 months)

Intermittent colicky pain (1st & MC symptom) + Vomiting +

Bloody mucus stools after abdominal pain (Currant jelly)

It is the MCC of intestinal obstruction in children

(MCC of acute intestinal obstruction in neonates DUODENAL

ATRESIA)

H/o URTI, change of milk formula, or vaccination

O/E: Sausage shaped mass in the RUQ

Empty right iliac fossa

INTUSSUSCEPTIONINTUSSUSCEPTION


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IxOC: Barium enema (both diagnostic & therapeutic)

CI to enemai. Symptoms > 24 hrsii. Air fluid levels on plain abdominal X ray (evidence ofobstruction)iii. USG showing intestinal ischemia

If enema not therapeutic, do laparotomy


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DUODENAL ATRESIADUODENAL ATRESIA

50% of all intestinal50% of all intestinal atresiasatresiasAssociated with multiple anomalies (GI, cardiac,Associated with multiple anomalies (GI, cardiac, anorectalanorectal, or, or

esophageal)esophageal)

40% have40% have trisomytrisomy 2121

Classic doubleClassic double--bubble signbubble sign


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MECKEL DIVERTICULUMMECKEL DIVERTICULUM

MCCMCC ofoflowerlower GIGI bleedingbleeding inin childrenchildren

EctopicEctopic tissuetissue isis commoncommon ((8080%% beingbeing gastricgastric inin originorigin andand55%% ofof pancreatic)pancreatic)

RuleRule ofof 22ss 22%% ofof populationpopulation

22 feetfeet fromfrom ileocecalileocecal junctionjunction

22 inchesinches inin lengthlength

22 cmcm inin diameterdiameter

22::11 malemale::femalefemale ratioratio UsuallyUsually asymptomaticasymptomatic beforebefore 22 yearsyears ofof ageage

DiagnosisDiagnosis isis usuallyusually mademade byby MeckelMeckel scanscan (ectopic(ectopic tissue)tissue)


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LACTASE DEFICIENCYLACTASE DEFICIENCY

CommonCommon disorderdisorder afterafter ageage 22

CongenitalCongenital (rare)(rare)

AcquiredAcquired (Viral/Bacterial(Viral/Bacterial gastroenteritisgastroenteritis MCC)MCC)

AcidicAcidic stoolsstools (pH(pH > 00..55%% ofofreducingreducing substancesubstance inin freshfresh stoolsstools

BreathBreath hydrogenhydrogen testtest isis diagnosticdiagnostic testtest

EndoscopicEndoscopic biopsybiopsy withwith measurementmeasurement ofof mucosalmucosal enzymeenzyme

activityactivity isis thethe goldgold standardstandard


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ARTIDiarrheaMalariaMeaslesHIVPrenatal Disordersothers

18 %

25 %

23 %

4 % 5 %

10 %

15 %

Causes of death in children < 5yr

DIARRHEA


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MCC of under 5 mortality in INDIA

Definition: Passage of watery stools 3 in 24 hrs OR a recent

change in consistency of stools

TYPES

1. Acute watery diarrhea (diarrhea for < 14 days)

2. Dysentery (Acute bloody diarrhea)3. Persistent diarrhea (starts acutely & lasts for 2 wks-2 months)

4. Chronic diarrhea (diarrhea for > 2 months)

4. Diarrhea with severe malnutrition

Sequele of diarrhea

Dehydration (MC cause of death)

Malnutrition

Infections


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MC infective cause of diarrhea inchildren is ROTAVIRUS, followedby ETEC

CAUSES OF ACUTE DIARRHEA

Viral

Rotavirus (MC),

Adenovirus,

Astrovirus,

Coxsackie virus,

Echovirus

Bacteria

E. coli (ETEC),Salmonella,

Campylobacter,

Yersinia enterocolitica,

Clostridium difficile,

Shigella,Vibrio cholerae (Cholera)

Parasites

Giardia,

Cryptosporidium parvum,

Entamoeba histolytica


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DYSENTRY

Presence of blood and pus in the stools, abdominal cramps and

fever

Gross blood in the stools is the most reliable sign

Causes: Shigella

EHEC

EIEC


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Total Body water = 60% of body weight

20 % (1/3 rd) as ECF

40% (2/3 rd) as ICF

5% (1/4th of ECF) = Plasma volume

15% (3/4th of ECF) = Interstitial fluid (ISF)

ECF = Relatively rich in Sodium with lower potassium

Diarrheal losses come from ECF


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Loss of water from the body reduction in the volume of ECF

Sodium is a major osmotic determinant of ECF

In 50% of cases, the concentration of sodium in the ECFremains nearly normal (ISONATREMIC DEHYDRATION)

In 45-50% cases, excessive sodium may be lost in the stools

relative decline in the serum and ECF sodium level hyponatremia fall in osmolality of ECF movement of waterfrom the ECF to ICF further shrinkage of the alreadyreduced ECF volumes (HYPONATREMIC DEHYDRATION)

In about 5% of diarrhea cases (especially if the child has beengiven fluids with more salts), serum sodium levels may beelevated the osmotic pressure of ECF become higher Shiftof water from ICF to ECF (HYPERNATREMICDEHYDRATION)


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Diarrhea stools contain large amounts of potassium

HYPOKALEMIA, if diarrhea persists

Hypokalemia is more pronounced in children with severe

malnutrition

Intestinal secretions are alkaline bicarbonate is lost in diarrheal

stools METABOLIC ACIDOSIS


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SIGNS OF DEHYDRATION

1. LOSS OF SKIN TURGOR

Impaired skin elsticity (On pinching, it takes a few seconds forthe skin fold to return to normal)

Lost in Iso- & Hyponatremic dehydration

May be masked in Hypernatremic dehydration


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2. HYPOTENSION

Results from a decline in the blood volume

- Cold extremities

- Thin, thready pulse

- Reflex tachycardia

- Decreased Urine output (good indicator of the severity of

illness)

- Depressed fontanel

- Sunken eyes,

- Dry tongue

Functional ability of the kidney of infants is not fully developed

as compared to older children cannot regulate the metabolic

derangements

Chronic decreased perfusion of the kidneys may lead to Renal

failure


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3. SIGNS OF HYPOKALEMIA

Abdominal distension

Paralytic ileus and

Hypotonia of muscles

ECG: U waves, ST depression and flat T waves

4. KUSSUMAULS BREATHING

OTHER CLINICAL FEATURES

Child becomes IRRITABLE, POOR FEEDING

NAUSEA/VOMITING + FEVER (Infective diarrhea)WEIGHT LOSS

ASSOCIATED INFECTIONS (Pneumonia, OM)


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INVESTIGATIONS & NUTRITIONAL ASSESSMENT

Weight for Age: BEST PARAMETER to assess nutritional status(acute malnutrition)

Stool microscopy & culture

Serum electrolytes


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MANAGEMENT

ORAL REHYDRATION THERAPY1. Home made solution

2. WHO-ORS

3. Food based solutions (Rice water with Salt)

4. Lassi, Kanji, Coconut water, Dal soup

WHO-ORS is ordinarily used for all types of diarrhea at all ages

ORS should be given with a teaspoon or in small sips from a cup

A child with profuse vomiting is more likely to retain the fluid if it

is consumed in small sips rather than large gulps

Large gulps often induces gastrocolic reflex


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WHO ORS

Ingredients in grams/liter

(Old WHO-ORS)

(New low osmolarity ORS)

Concentration in mmol/L

(Old WHO-ORS)

(New low osmolarity ORS)

Sodium chloride: 3.5 (2.9) Sodium: 90 (75)

Trisodium citrate dehydrate:2.9 (2.9)

Potassium: 20 (20)

Potassium chloride: 1.5 (1.2) Chloride: 80 (65)

Glucose, anhydrous: 20 (13.5) Citrate*: 10 (10)

Water:- 1 L (1 L) Glucose: 111 (75)

New ORS was designed to prevent hypernatremia seen with the

use of old ORS in neonates & very young infants with immature

kidney functions


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ASSESSMENT OF SEVERITY OF DEHYDRATION

Severe dehydration

Child is Lethargic, unconscious

Very dry tongue (palpation)Drinks poorly (or not able to drink)

Very sunken eyes with absent tears

(Dry eyes)

Signs of dehydration

Skin goes back very slowly after

pinchingTreatment: Use Plan C urgently

No dehydration

Child is alertMoist tongue

Drinks normally (not thirsty)

Normal eyes with tears

No signs of dehydration

Skin goes back quickly after

pinchingTreatment: Plan A

Some dehydration

Child is Irritable

Dry tongue

Drinks eagerly (thirsty)

Sunken eyes with absent tears

Signs of dehydration

Skin goes back slowly after

pinching

Treatment: Plan B


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PLAN A

Give ORS & food based solution at home

Mother asked to visit health center

i. If the child does not get better in 3 days, or

ii. If the child develops any of the following danger signs:

a. many watery stools

b. repeated vomiting

c. marked thirst

d. eating or drinking poorlye. fever, and

f. blood in stool


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PLAN B

All cases to be treated in Health center or Hospital

Rehydration therapy: Correction of the existing water &electrolyte deficit Give 75 ml/kg of ORS in the first 4 hours

Maintenance therapy: Replacement of ongoing losses due tocontinuing diarrhea to prevent recurrence of dehydration

Begins when signs of dehydration disappear (usually within 4hrs)

ORS should be administered in volume equal to diarrhea losses(10-20mL/Kg for each liquid stool)

ORS is administered in this manner till diarrhea stops

Breast feeding continued during rehydration

If the child continues to have some dehydration after 4 hours,repeat another 4 hours treatment with ORS solution (as inrehydration therapy) and start to offer feeds, milk and

breastfeed frequently


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PLAN C

All cases to be treated in Health center or Hospital

Start IV fluids immediately (Best: Ringers lactate with 5% D)If RL not available, use 0.9% Normal saline

Give 100 mL/kg

< 1 yr: First give 30 ml/kg in 1 hr# followed by 70 ml/kg in 5 hrs

1-5 yr: First give 30 ml/kg in hr# followed by 70 ml/kg in 2 hr# Repeat if pulse is weak or not detectable

All children should be started on some ORS solution (about 5

mL/kg/hr) when they can drink without difficulty during the time

they are getting IV fluids

If unable to give IVF immediately start rehydration with ORS

using NGT at 20 mL/kg/hr (total of 120 mL/kg)

If the child is improving but still shows signs of some dehydration,

discontinue IV treatment and shift to Plan B


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DRUG THERAPY

Antibiotics (Cotrimoxazole or Ampicillin X 5 days) should be

used only for infectious agents such as Shigella, Vibrio

cholerae, Entamoeba histolytica and Giardia

Zinc supplements

Anti-motility agents may cause distension of abdomen and other

undesirable side effects of opiates

They can be dangerous (even fatal) . So dont use them !


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CAUSES OF CHRONIC PERSISTENT DIARRHEA

Giardia lamblia

Cryptosporidium parvum

EPEC

Any enteropathogen in an immunocompromised host

Damage to the intestine by an enteropathogenMilk allergy

Malabsorption syndromes


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VIRAL HEPATITIS


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VIRAL infections that can involve the liver include

Hepatitis viruses

IMN

CMV

YELLOW FEVER

RUBELLA (In children & immuno-suppressed patients)


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HEPATITIS A

MC type of viral hepatitis

Agent: Single stranded RNA, non-enveloped, PicornavirusIt is also called as RELAPSING HEPATITIS

HAV does NOT cause chronic hepatitis or a carrier state

Fulminant hepatitis is RARE

Incubation period 15-45 days

Spread by feco-oral route (ingestion of contaminated waterand foods)

Virus is shed in the faeces for 2-3 weeks before & 1 weekafter the onset of jaundice

Disease is MAXIMALLY INFECTIOUS just before the onset of

jaundiceHAV viremia is transient thus, blood borne transmission of

HAV occurs only rarely (donated blood is not specificallyscreened for HAV)

Prognosis Excellent


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Diagnosis

Anti-HAV IgM antibodies (appears at the onset of symptoms)

(persists for 6-12 months)(Diagnosis of acute illness)

Anti-HAV IgG antibodies (confers immunity life long

protective antibody)

(can be detected for years)


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HEPATITIS B

Agent:HBV - Hepadnaviridae family

It has a double stranded circular DNA having 3200nucleotidesIt is spherical & double layered (DANE PARTICLE)

Enveloped

Incubation period 30-190 days

Can produceAcute hepatitis with resolution

Non-progressive chronic hepatitis (no cirrhosis)

Progressive hepatitis (with cirrhosis)

Fulminant hepatitis

An asymptomatic carrier stateHepatocellular carcinoma

Patients with chronic hepatitis represent carriers

HBV remains in the blood up to & during active episodes ofacute & chronic hepatitis (unlike HAV)


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Types of proteins (antigens) synthesized from genome

HBsAg Envelop glycoprotein (Australian antigen)

HBeAg Protein associated with active viral replication

HBcAg Nucleocapsid core protein; it remains in the

hepatocyte for the assembly of complete virions

HBxAg Modulates gene transcription of viral as well as host

genes (viral replication, hepatocyte cell cycle check points);

plays a key role in the development of HCC in HBV infected

patients

DNA polymerase


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SEROLOGICAL DIAGNOSIS

Sequence of appearance of serum markers

HBsAg > HBeAg > IgM-AntiHBc > AntiHBe > IgG-AntiHBc >AntiHBs


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HBsAg Appears before the onset of symptoms

Peaks during overt disease

Declines to undetectable levels by 3-6 months

(Persistence for more than 6 months indicateschronic infection)

HBcAg It is sequestered within HBsAg coat, thus, it isnot detectable in the serum

HBeAg It is a qualitative marker for HBV replication &infectivity

It appears in the serum transiently

Subsides with the disappearance of jaundice

Persistence of this in serum beyond first 3months indicates chronic infection

HBV DNA is the quantitative marker of HBVreplication & infectivity


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AntiHBs It is the protective antibody

Appears after the disappearance of HBsAg

Occasionally, a gap may separate the

disappearance of HBsAg & the appearance of

AntiHBs Gap or window period

AntiHBc It implies that the acute infection has peaked &

the disease is on the wane


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HEPATITIS CAgent:Enveloped, Single stranded RNA Flavivirus

Incubation period: 15-190 days

Responsible for 70-90% of post transfusion hepatitis

Has a high rate of progression to chronic disease or eventualCIRRHOSIS as compared with HBV

It has a high predisposition to HCC

Elevated titers of IgG anti HCV antibodies occurring after anacute infection DOES NOT confer immunity (in contrast toHAV & HBV) Thus no immunity is produced after acuteHCV infection

Serum markers are HCV RNA, IgM-AntiHCV, IgG-AntiHCV

In chronic infection, a characteristic clinical feature isEPISODIC elevations in serum transaminases withintervening normal periods

So, PERSISTENT INFECTION & CHRONIC HEPATITIS arehallmarks of HCV infection


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HEPATITIS DIt is caused by HDV (DELTA agent or virus)

It is an incomplete RNA particle enclosed in a shell of HBsAg

Unable to replicate on its own, thus, activated by the presenceof HBV (dependent on genetic information provided byHBV)

Co-infection Infection of HDV & HBV occurring together

Leads to RECOVERY 90%

FULMINANT HEPATITIS 5%CIRRHOSIS (Rarely)

Super-infection Infection of an already HBV infected person

Leads to CHRONIC HEPATITIS (CIRRHOSIS) 80%

FULMINANT HEPATITIS 10%

ACUTE SEVERE HEPATITIS 15%HDV is absolutely dependent on HBsAg & thus, during

infection is determined by duration of HBV infection

Most commonly associated with IV drug abusers

Diagnosis HDV RNA, IgM & IgG AntiHDV antibodies


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HEPATITIS E

Most common cause of hepatitis EPIDEMICS in india

Agent: Unenveloped single stranded RNA calcivirus

A characteristic feature of the infection is the high mortality

rate among PREGNANT WOMEN (~ 20%)

NOT associated with chronic disease or persistent viremia

Diagnosis HEV RNA & HEV particles in stool


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CLINICO-PATHOLOGIC SYNDROMES

1. CARRIER STATE

Best seen for HBV

Also seen with HCV

Normal Liver

2. ASYMPTOMATIC INFECTION

No symptoms at all

Detected accidentally by the presence of elevated serum

transaminasesSee with HBV


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3. ACUTE HEPATITIS

Can be caused by all types of hepatitis virus

Has 4 phases

i. An incubation period

ii. Symptomatic pre-icteric phase (non-specific symptoms)

Seen in about 10% cases with HBV

Serum sickness like syndrome (fever, arthralgia)

iii. Icteric phase

MC with HAV

Seen 50% cases with HBV

Never seen in cases with HCV

iv. Convalescence


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4. CHRONIC HEPATITIS

It is either continuing or relapsing hepatic disease for> 6

months

5. FULMINANT HEPATITIS

When hepatic insufficiency progresses from onset of

symptoms to hepatic encephalopathy WITHIN 2-3

WEEKSCan be induced by all viral types


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TREATMENT

HBV

- Lamuvidine

- IFN

Chronic HBV IFN OR Lamivudine

Acute HBV IFN only

Detection of HBeAg warrants the use of IFN (But is given

only after confirming the replication by doing HBV DNAbecause one has to be absolutely sure before starting asit is very expensive)

IFN given in acute hepatitis reduces the progression tochronic hepatitis

HCV

Acute IFN

Chronic IFN + Ribavirin

Documents

7. PEDIATRIC GASTROENTEROLOGY