SHA

A
MIK
SIE
SUBJECT:PEDIATRICS DATE:JUNE 30,2008
JAS

TOPIC: GIT 2
N
RAI
S LECTURER: DR. RUBY ANN L. PUNONGBAYAN
FAR TRANSGROUP: TAMPON NI BINDOY
HUA
JOS
RCO
MA
Y INTUSSUSCEPTION • Hydrostatic reduction vs. “air” enema
ISA
DY • Occurs when a portion of the alimentary tract is
CAN
NG telescoped into an adjacent segment
KRI
A • Most common cause of intestinal obstruction bet.3 mos-
EIS
6yrs.old; M > F
E
ANN
H • Unknown cause in most cases
KYT
ON • Correlation with adenovirus
AAR
E
LPH • Most often ileocolic & ileoileocolic
A
• Upper portion of bowel (intussusceptum) invaginates into
LA
KAR
G the lower part (intussuscipiens) dragging its mesentery
PEN along with it into the enveloping loopmesentery
KC
ADI constricts & obstructs venous returnintussusceptum
AN engorgesedema & bleeding from the mucosa leads to
MA bloody stool
AM
NA PEPTIC ULCER DISEASE
MO • Severe paroxysmal colicky pain that recurs at frequent
F intervals with straining efforts; legs & knees are flexed • Ulcers are deep lesions that breach the integrity of the
BUF
with loud crying epithelium & penetrate through the muscularis mucosa.
DIE
GOL
A • If not reduced-shocklike state • Erosions are superficial & stop short of the muscularis
EZR
propria.
•
KIX
RIZ 60% of infants pass currant jelly stool
NEY
• Both lesions occur in the presence of gastric
LAI • Palpation of abdomen: slightly tender sausage-shaped
inflammation or gastritis
mass in the RUQ which may increase in size & firmness
AN
XTI
during a paroxysm of pain
CES • Pathogenesis incompletely understood
OPS
HO • Plain abdominal X-ray: (+)density
CE • Ulceration occurs when aggressive factors (gastric acid,
digestive enzymes, H.pylori) overwhelm the natural
•
VIN
Barium enema: filling defect or cupping in the head of
E
barriers that protect the gastroduodenal lining
ESS barium; coiled-spring sign (thin rim of barium trapped
(bicarbonate-mucus barrier, gastric epithelial cells,
DEN around the invaginating part within the intussuscipiens)
ILLE mucosal blood flow, PGs)
CEC
• Ultrasound: tubular mass & a doughnut or target
JAM • May be present in either parent of an affected child
KC appearance
OY
• Gastroduodenal inflammation due to H.pylori found
• Tx: reduction of an acute intussusception is an
PIP
CH primarily in the mucus layer covering gastric epithelial
emergency procedure; if with signs of shock, peritoneal
cells
NRI
HEI irritation or intestinal perforation, reduction is not done
T
• H.pylori produces urease that catalyzes conversion of
•
BAR
Success rate of X-ray reduction is 50% if symptoms are
RYL urea in the gastric juice to NH3 & HCO3 which buffer the
SHE present >48 hrs & 70-90% if reduction is done within the gastric acid
1st 48 hrs
LH
RAP
A • Classic symptom of epigastric pain alleviated by
Page 5

TIN • Resection with end-to-end anastomosis is done if ingestion of food is present only in a minority of children
AIN manual operative reduction fails.
ALL
TTE
YVE
RY
MA
 • Majority with poorly localized pain • Antacids (AlMg salts)neutralize acid;H2 receptor blockers
suppress acid secretion; Hydrogen pump inhibitors
• After 6 yrs old, clinical features may be similar to those in
adults; dull or aching pain, GI blood loss, have
exacerbations & remissions
GASTROENTERITIS
• Typical ulcer pain with prompt relief after antacids found
2 types of acute infectious diarrhea:
in <33% of patients

• Dx: Endoscopy – method of choice 1. Noninflammatory – enterotoxin production by bacteria,

destruction of villus by viruses, adherence by parasites
• Test H.pylori if there is documented duodenal/gastric
2. Inflammatory – due to bacteria that invade the intestine
ulcer or MALT lymphoma (antral micronodules
directly or produce cytotoxins
representing lymphoid follicles)-biopsy (from antrum,
body & transition zone of stomach); rapid urease test **Chronic or persistent diarrhea - >14 days duration may be due
done in biopsy sample to infection or any enteropathogen infecting an
immunocompromised host or residual symptoms due to
• Ab detection of H.pylori in blood, urine, saliva & stool
damage to the intestine
(low sensitivity & specificity in low prevalence areas); Ag
detection in stool; urea breath test

• Tx: with H.pylori who have ulcers, MALT lymphoma, Etiology

atrophic gastritis with intestinal metaplasia; cost-benefit
ratio of eradicating H.pylori (at least 2 antibiotics & a • Inflammatory: C.jejuni, C.difficile, EIEC, Salmonella,
potent antacid for 1-2 wks) Shigella, Yersinia

• Noninflammatory: EPEC, ETEC, V.cholera

• Antibiotics are given to select patients with bacterial

enteritis to shorten the clinical course, to decrease
excretion of the causative organism, or to prevent
complications

• Viral: rotavirus, adenovirus, astrovirus, Norwalk, calicivirus

• Parasitic: G.lamblia, E.histolytica, B.coli, Strongyloides,

spore-forming protozoa
STRESS ULCER DISEASE
• Other causes: anatomic defects, malabsorption,
endocrinopathies, food poisoning, neoplasms,
• Underlying causes of secondary PUD not fully understood
miscellaneous (milk allergy, immunodeficiency states,
• Factors that interfere with host defense mechanisms are laxative abuse, ulcerative colitis, motility disorders)
involved (mucosal blood flow, PG synthesis, acid/mucus
production)
General Approach
• Infants: related to infection or dehydration
• Assess the degree of dehydration & provide fluid &
• Older children: related to trauma electrolyte replacement.

• Curling ulcers – associated w/ burns (>25%) • Prevent spread of the enteropathogen.

• Cushing ulcer – head trauma/surgery • Determine etiologic agent in selected cases & provide
specific therapy if indicated.
• Associated with hemorrhage or perforation

• Drug-related: due to NSAIDs

Clinical Evaluation of Dehydration
• Tx: remove inciting cause; control of gastric acidity for 6
Page 5

wks is active
> Mild (3-5%): normal or inc.pulse, dec.UO, thirsty, normal PE • Diagnosis of food borne or water borne illness is considered
when >2 persons have ingested common food/water
develop a similar acute illness.

> Moderate (7-10%): inc.HR, little or no UO, irritable/lethargic,

sunken eyes & fontanel, dec.tears, dry mucous membranes,
mild tenting of the skin, delayed capillary refill, cool and pale Average composition of diarrhea:

> Severe (10-15%): rapid and weak pulse, dec. BP, no UO, very • Sodium – 55 mEq/L
sunken eyes and fontanel, no tears, parched mucous
membranes, tenting of the skin, very delayed capillary refill, cold • Potassium – 25 mEq/L
and mottled
• Bicarbonate –15 mEq/L
• For older children, mild, moderate, and severe dehydration
represent 3%, 6%, and 9% respectively of BW lost.

• Volume of stool should be measured and an equal volume

of replacement solution should be given
General Approach
• Replace stool ml/ml every 1-6 hrs
• Ask about oral intake; frequency & volume of stool output;
general appearance & activity of the child; frequency of
urination; recent travel; use of antimicrobials; intake of
seafood, contaminated water, uncooked meat or unwashed Composition of ORS
vegetables; duration of diarrhea; presence of blood; other
symptoms (fever, tenesmus, vomiting)

• Stool culture: if HUS is suspected; bloody diarrhea; stool Solution Glucose Na K Cl Base
with fecal leukocytes; during outbreak;
immunocompromised patients
WHO solution 111 90 20 80 30
• Management of dehydration is the cornerstone.
Pedialyte 140 45 20 35 30
• Rapid rehydration with replacement of ongoing losses
during the 1st 4-6 hrs Glucolyte 165 50 20 42 28

• Reintroduce food once rehydration is complete! Hydrite 55 45 10 40 15

• Antidiarrheals generally not recommended! Glucost 55 45 10 40 5

Cholyte 111 45 20 42 28

Clinical Syndromes Servidrat 140 56 20 46 30

• General rule: occurring in <1 hr – chemical poisoning, Gatorade 58 14.6 3.5

toxins from fish or shellfish
Approximate Electrolyte Composition of Commonly
Consumed Fluids
• Vomiting & diarrhea 1-6 hrs – S.aureus

• Watery diarrhea, abdominal cramps 8-72 hrs – Salmonella

Na K Cl HCO3 CHO g/dl
• Bloody diarrhea >15 hrs – Shigella, Salmonella
Apple juice 0.4 26 --- --- 11.9
• Neurologic symptoms 0-6 hrs- fish, shellfish, MSG; 0-24 hrs
– mushroom; 18-24 hrs – C.botulinum Coca-cola 4.3 0.1 --- 13.4 10.9

• Severity of disease depends on the amount inoculated into Gatorade 21 2.5 17 --- 5.9
the food or water
Ginger ale 3.5 0.1 --- 3.6 9
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Milk 22 36 28 30 4.9
Orange juice 0.2 49 --- 50 10.4

PLAN C

* Not recommended for oral rehydration therapy Age First give 30 Then give 70 ml/kg in:
ml/kg in:
< 1 year old 1 hour 5 hours
> 1 year old 30 minutes 2 ½ hours
ASSESSMENT OF DIARRHEA PATIENTS FOR
DEHYDRATION (WHO)

PLAN A

3 rules for treating diarrhea at home:

CHRONIC DIARRHEA
1. Give the child more fluids than usual to prevent dehydration
(give these fluids until the diarrhea stops). • Increased total daily stool output with increased stool water
content
2. Give the child plenty of food to prevent malnutrition (give an
extra meal daily for 2 weeks). • Diarrhea that lasts more than 2 weeks

3. Take the child to the health worker if the child does not get
• Results from altered intestinal water and electrolyte
better in 3 days or develops any of the following:
transport
Many watery stools
• GI tract of an infant handles 285 ml/kg/day of fluid (intake
Repeated vomiting plus intestinal secretion) with a stool output of 5-10 g/kg/day

Marked thirst • Stool output in infants & children contains approximately

per liter, 20-25 mEq of Na, 50-70 mEq of K, 20-25 mEq of
Eating or drinking poorly Cl

Fever • Mechanisms responsible for the absorptive capacity are

caused by the function of several transport proteins located
Blood in the stool at the brush border membrane of the small and large
intestine

If the child will be given ORS solution at home:

Pathophysiologic mechanisms:
Age Amount of ORS Amount of ORS to
to give after provide for use at • Osmotic diarrhea
each loose stool home
< 24 months 50-100 ml 500 ml/day
• Secretory diarrhea
2-10 years old 100-200 ml 1000 ml/day
> 10 years old As much as 2000 ml/day • Mutations in apical membrane transport proteins
wanted
• Reduction in anatomic surface area

PLAN B • Alteration in intestinal motility

• Approximate amount of ORS required (in ml) can also be

calculated by multiplying the patient’s weight (in kg) times
 Osmotic diarrhea – due to the presence of nonabsorbable
75
solutes in the GIT; classic ex: lactose intolerance due to
lactase enzyme deficiency
• Reassess after 4 hours.
causes: malabsorption of water-soluble nutrients,
• If the child vomits, wait 10 minutes and then continue giving
excessive intake of carbonated fluids & nonabsorbable
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ORS but more slowly (a spoonful every 2-3 mins).

solutes
 Stops with fasting, has a low pH, (+) reducing substances

 Secretory diarrhea – activation of intracellular mediators • Phase IV: hormonal studies (VIP, gastrin, secretin)
like cAMP, cGMP that stimulate active Cl secretion from the
crypt cells & inhibit the neutral coupled NaCl absorption;
toxin-mediated injury to the tight junctions
Treatment
Classic ex: cholera, E.coli enterotoxins, Clostridium
difficile, vasoactive peptides • Maintain adequate nutritional intake to permit normal
growth & development
Continues with fasting, extremely watery stool, high
volume • If diarrhea is due to CHO intolerance, have a trial period of
decreased lactose or sucrose.

• Use predigested formula (Pregestimil or Alimentum) for

• Mutational defects in ion transport protein – congenital
postgastroenteritis malabsorption syndrome
defect in Na-H exchange, Cl-HCO3 exchange
• Secretory type: consider nutritional support (most likely due
• Reduction in anatomic surface area – short bowel
to congenital defect in transport proteins)
syndrome, celiac disease

• Altered intestinal motility – due to malnutrition, intestinal

pseudo-obstruction syndrome, DM ACUTE PANCREATITIS

• Most common pancreatic disorder in children

2 major etiologic factors: • Common causes: blunt abdominal injury, mumps & other
viral illnesses, multisystem disease, congenital anomalies,
1. Intraluminal factors – involved in the digestion process; biliary microlithiasis, drugs & toxins
pancreatic, liver & brush border membrane disorders
• Pancreas
2. Mucosal factors – involved in the digestion & transport of
nutrients across the mucosa; bacterial, viral, parasitic,
fungal agents
Pathogenesis

• Theory: following an insult, lysosomal hydrolase co-

localizes with pancreatic proenzymes within the acinar cell--
 pancreastasis with continued synthesis of enzymes
occur--proenzymes are activated by cathepsin leading to
autodigestion, further activation & release of active
proteases-- lecithin is activated by phospholipase A2 into
the toxic lysolecithin

Evaluation of Chronic Diarrhea

• Phase I: history, PE, stool exam (pH, reducing Clinical Manifestations

substances), stool culture, stool for C. difficile toxin, CBC,
ESR, electrolytes, serum creatinine • Severe, steady abdominal pain (epigastric or in either
upper quadrant, appears acutely ill), persistent vomiting,
fever

• Phase II: sweat chloride, 72-hr stool collection for fat, stool • Pain increases in intensity for 24-48 hrs with vomiting
electrolytes & osmolality, stool for phenolphthalein, Mg
• Severe acute type: rare in children; severe nausea,
sulfate, PO4
vomiting, shock, jaundice, high fever, Cullen sign, Grey
Turner sign, necrotic pancreas; mortality rate of 25%
related to the systemic inflammatory response syndrome
• with multiple organ dysfunction
Page 5

Phase III: endoscopy, small bowel biopsy, sigmoisdoscopy

or colonoscopy, barium
 • Uncomplicated cases: recover over 4-5 days

Diagnosis • If associated with trauma or systemic disease: prognosis is

related to the associated medical conditions
• Acute cases: serum amylase and lipase
• ERCP or magnetic resonance cholangiopancreatography:
• Amylase elevated for up to 4 days recurrent pancreatitis

• Serum lipase is more specific for acute inflammatory

pancreatitis; rises by 4-8 hrs, peaks at 24-48 hrs & remains
elevated 8-14 days longer than serum amylase LIVER DISEASE

• Ultrasound & CT scan of the abdomen show pancreatic

enlargement, a hypoechoic, sonolucent edematous
pancreas, mass, fluid collection, abscess Metabolic Functions of the liver:

• At least 20% of children with acute pancreatitis have • Carbohydrate metabolism

normal imaging
• Protein metabolism
• Cullen’s sign
• Lipid metabolism

• Biotransformation

• Hepatic excretory function

Manifestations of Liver Disease

• Alteration in liver structure & function

• Pathologic manifestations:
Treatment
• Inflammation or necrosis – viruses, drus, toxins,
• Medical mgt: to relieve pain and to restore metabolic hypoxia, IEM, immunologic disorders
homeostasis
• Cholestasis – response to injury due to extra- or
• Analgesia intrahepatic obstruction to bile flow; accumulation in
serum of substances normally excreted in bile
• Fluid electrolyte & mineral balance restored & maintained
• Cirrhosis
• Prophylactic antibiotics useful in severe cases to prevent
infected pancreatic necrosis • Tumors

• Treatment • Clinical manifestations:

• Refeed when vomiting has resolved, serum amylase is

1. Hepatomegaly – increase in the number or size of the
falling, and clinical symptoms are resolving
cells in the liver, inflammation, infiltration, increased size or
vascular space, increased size of biliary space
• Endoscopic therapy – if due to anatomic abnormalities
(strictures or stones)
2. Jaundice – unconjugated type may indicate increased
• Severe acute type: enteral alimentation is superior to TPN production, hemolysis, reduced hepatic removal or altered
metabolism; conjugated type reflects decreased excretion
within 2-3 days of onset, antibiotics, gastric acid
by damaged hepatic parenchymal cells or disease of biliary
suppression, peritoneal lavage (to reduce risk of secondary
tract due to sepsis, endocrine or metabolic disease,
infection)
inflammation of the liver or obstruction
• Prognosis
3. Pruritus – multifactorial; retained bile components
Page 5
4. Spider angioma – due to altered estrogen metabolism in Sexual rare com rare rare rare rare
the presence of liver dysfunction trans- mon
mission
5. Palmar erythema – due to vasodilation & increased blood HAV HBV HCV HDV HEV HGV
flow Trans- no com rare no prob rare
placent mon ably
6. Xanthoma – elevated cholesterol may cause deposition of al no
lipid in the dermis & subcutaneous tissue trans-
mission
Chronic no yes yes yes no yes
7. Portal hypertension – >10mmHg difference between the infectio
portal vein & systemic veins n
Fulmina rare yes rare yes rare prob
8. Ascites – portal hypertension & hepatic insufficiency are nt ably
also present disease no
IDENTIFIED ANTIBODIES:
9. Variceal hemorrhage – results from increased pressure
within the varix which leads to changes in the diameter of • anti-HAV, IgM anti-HAV
the varix & increased wall tension
• Anti-HBsAg, IgM anti-HBsAg, anti-HBcAg, anti-HBeAg
10. Encephalopathy – prominent or subtle neurologic
• Anti-HCV
dysfunctions; may be due to altered ammonium
metabolism, synergistic neurotoxins, or “false
• Anti-HDV
neurotransmitters” with plasma amino acid imbalance
• Anti-HEV, IgM anti-HEV
11. Endocrine abnormalities – adults>children
• Anti-HGV
12. Renal dysfunction – systemic disease or toxins may affect
both organs simultaneously; altered water & sodium
activity, impaired concentrating ability; hepatorenal
syndrome – functional renal failure in patients with end- Hepatitis B Antigens & Antibodies
stage liver disease
• First clinical evidence of HBV infection is elevation of ALT
13. Pulmonary involvement – hepatopulmonary syndrome – levels which occurs about 6-7 wks after exposure
triad of hypoxemia, intrapulmonary vascular dilations & liver
disease • Anti-HBcAg – most valuable single serologic marker of
acute HBV infection because it is present as early as
14. Recurrent cholangitis – ascending infection of the biliary HbsAg and continues to be present later in the course of
system due to gram (-) enteric organisms the disease when HBsAg has disappeared

• HBcAg – inner portion of the virion that encodes the viral

DNA

VIRAL HEPATITIS • HBeAg – serves as a marker of active viral replication;

identification of infected people at increased risk of
HAV HBV HCV HDV HEV HGV transmitting HBV
Nucleic RNA DNA RNA RNA RNA RNA
acid • HBsAg – first serologic marker to appear & its rise
Incubati 30 100- 7-9 2-4 40 Un coincides with the onset of symptoms; detection of acutely
on days 120 wks mos days k or chronically infected people; antigen used in hepatitis B
(mean) days now
vaccine
n
Percuta- rare com com com no com
neous mon mon mon mon • Anti-HBs – identification of people who have resolved
trans- infections with HBV; determination of immunity after
mission immunization
Fecal- com no no no com no
oral mon mon • Anti-HBe – identification of infected people with lower risk
trans-
Page 5

mission of transmitting HBV

• Anti-HBc – identification of people with acute, resolved, or
chronic HBV infection

• IgM anti-HBc – identification of people with acute or recent

HBV infections (including HBsAg-negative people during
the “window” phase of infection)

Page 5