Morning Report July 9, 2012
Symptoms
Acute (or subacute)
Chronic
Localized
Diffuse
Single (ie. Monoarticular)
Multiple
Static
Progressive
Constant
Intermittent
Single Episode
Recurrent
Abrupt
Gradual
Severe
Mild
Painful
Nonpainful
Bilious
Nonbilious
Sharp/Stabbing
Dull/Vague
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Predisposing Conditions
 Age, gender, preceding events (trauma, viral illness,
etc), medication use, past medical history (diagnoses,
surgeries, etc)
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Pathophysiological Insult
 What is physically happening in the body
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Clinical Manifestations
 Signs and symptoms that result from the
pathophysiological insult
 Use semantic qualifiers
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GER/GERD
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Protein intolerance
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Gastroenteritis
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Pyloric stenosis
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UTI
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Malrotation with
midgut volvulus
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Intestinal
atresia/stenosis
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Intussusception
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Predisposing conditions
 Presentation in the first few months of life, peaks at 4
months
 Resolves in up to ~90% by 12 months and nearly all by
24 months
 Likely combination of genetic predisposition and
environmental factors (liquid diet
/overfeeding/horizontal body positioning)
 Immature lower esophageal sphincter

Pathophysiological insult
 Passage of stomach contents into the esophagus, can
be physiologic
 Disease state caused by frequent or persistent
episodes of esophageal exposure to caustic gastric
contents that produce esophagitis/esophageal
symptoms or respiratory sequelae or failure to thrive

Clinical manifestations
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Postprandial regurgitation, nonbillious
Irritability, arching, choking, gagging, feeding aversion
Failure to thrive
Respiratory symptoms of obstructive apnea, stridor, or
lower airway disease
 Sandifer syndrome

Predisposing conditions
 Manifests in the first several months of life
 First form of allergy to affect infants and children
 About 2.5% of children experience this allergy within
the first 3 yrs of life
 Most children “outgrow” this allergy, ~50% resolve
within 3-5 years

Pathophysiological insult
 Cell-mediated hypersensitivities
 Lymphocytes, primarily food allergen-specific T cells,
secrete cytokines that lead to chronic inflammatory
process in skin, GI tract, or respiratory tract
 Most commonly provoked by cow’s milk or soy-based
formulas

Clinical manifestations
 Irritability
 Protracted vomiting and diarrhea that may result in
dehydration
 Vomiting generally occurs 1-3hrs after feeds
 Prolonged exposure leads to abdominal distention,
bloody diarrhea, anemia, and failure to thrive

Predisposing conditions
 Risks include environmental contamination , increased
exposure to enteropathogens
 Young age, immunodeficiency, malnutrition, lack of
exclusive or predominant breast-feeding
 2nd leading cause of child mortality worldwide

Pathophysiologic insult
 Numerous pathogens: viral, bacterial, and parasitic
 Noninflammatory diarrhea caused by enterotoxin
production by some bacteria, destruction of villus cells
by viruses, adherence by parasites, and adherence
and/or translocation by bacteria
 Inflammatory diarrhea caused by bacteria that directly
invade the intestine or produce cytotoxins that cause
fluid, protein and cells to enter the intestinal lumen

Clinical manifestations
 Acute onset of vomiting followed by diarrhea,
abdominal cramps, and possible fever
 Vomiting is a self-protective process that may reduce
the load of infectious organisms or associated
toxins/irritants
 Watery versus bloody diarrhea related to etiology
 Timing of symptoms related to whether preformed
toxins are present and to the enteropathogen involved

Predisposing conditions
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Males affected 4 to 6 times more frequently
1/3 of cases in first-born infants
Genetic predisposition
Use of erythromycin
Increased incidence with B and O blood types

Pathophysiological insult
 Hypertrophy and spasm of the pyloric muscle resulting
in gastric outlet obstruction
 Abnormal muscle innervation, elevated serum levels
of prostaglandins, and infant hypergastrinemia have
been implicated
 Also, reduced neuronal nitric oxide might contribute
to the pathogenesis

Clinical manifestations
 Typically a 3- to 6-week-old infant with progressive or
intermittent vomiting after feeding
 Nonbilious emesis, often projectile in nature
 Infant is often hungry after vomiting
 Hypochloremic hypokalemic metabolic alkalosis and
dehydration
 Palpable small “olive-shaped mass” in right midepigastric area, visible gastric peristaltic wave after
feeding

Predisposing conditions
 Female, uncircumcised males
 Primary or secondary urinary tract obstructions
 Indwelling catheters

Pathophysiological insult
 Cystitis – infection localized to the bladder
 Pyelonephritis – infection of the renal parenchyma,
calyces, and renal pelvis
 Renal abscess – intrarenal or perinephric
 Most common organism: E. coli; other organisms:
Enterococcus, Pseudomonas, Klebsiella, Proteus, S.
saprophyticus

Clinical manifestations
 Neonates: failure to thrive, feeding problems, direct
hyperbilirubinemia
 Infants: feeding problems, failure to thrive, vomiting,
diarrhea, unexplained fever
 >2yrs: urgency, dysuria, frequency, abdominal pain

Predisposing conditions
 Majority present in first year of life, >50% present
within first month of life
 Often associated with other abnormalities of the
abdominal wall – such as diaphragmatic hernia,
gastroschisis, and omphalocele
 Also associated with heterotaxy syndrome – complex
of congenital anomalies including congenital heart
disease, malrotation, and either asplenia or
polysplenia

Pathophysiological insult
 Nonrotation occurs when, in utero, the bowel fails to
rotate after it returns to the abdominal cavity; leaving
the cecum near the right upper quadrant
 This results in an extremely narrow mesenteric root
susceptible to volvulus
 Abnormal mesenteric attachments (Ladd bands)
extend from the cecum across the duodenum, causing
partial obstruction

Clinical manifestations
 About ~60% of children with malrotation present with
bilious vomiting during the first month of life – Could
be due to duodenal obstruction by Ladd bands or
volvulus
 If bilious emesis due to volvulus, then venous drainage
of the gut is impaired, leading to ischemia, pain,
tenderness, and possibly bloody stools
 If the bowel undergoes ischemic necrosis, the child
may appear septic

Predisposing conditions
 Congenital partial or complete blockage of the
intestine (1:1500 live births)
 Small intestine is the most common site of intestinal
atresia/stenosis (~90%)
 Possible prenatal history of polyhydraminos

Pathophysiological insult
 Intrinsic causes include inherent abnormalities of
intestinal innervation, mucus production, or tubular
anatomy
 Extrinsic causes involve compression of the bowel by
vessels, organs (annular pancreas), and cysts

Clinical manifestations
 Classic symptoms: bilious vomiting and abdominal
distention
 Findings more subtle if the obstruction is partial
 Obstruction high in the intestinal tract results in highvolume, frequent, bilious emesis with little or no
distention. Pain is intermittent and usually relieved by
vomiting.
 Obstruction in the distal small bowel leads to moderate or
marked abdominal distention with emesis that is
progressively feculent.

Predisposing conditions
 Most common between 3 months – 6 years of age,
Rare in neonates
 Most common abdominal emergency in children
<2years
 Male:female ratio of 3:1
 90% idiopathic; 2-8% with recognizable lead points
 Seasonal peaks in spring and autumn
 Risk factors: Lymphoid nodular hyperplasia, HSP, CF

Pathophysiological insult
 Proximal intestine is telescoped into a distal portion of
intestine
 Most often ileocolic, less common cecocolic and rarely
ileo-ileal
 Constriction of the associated mesentery leads to
venous congestion, edema and intestine ischemia,
then mucosal bleeding

Clinical manifestations
 Sudden onset of severe paroxysmal colicky pain that recurs
 Painful episodes associated with legs and knees flexed
 Lethargy can be associated and out of proportion to the
abdominal symptoms
 Vomiting occurs in most cases, nonbilious in the early
phase and can be bilious in the later phase
 “Currant jelly stool”
 “Sausage-shaped mass” may be palpable
Predisposing Conditions
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Age 6-24 months
 Very rare before 3 months and after 6 years
Male: Female 3:1
90% - no etiology, healthy child
Sometimes associated with viral Illness or gastroenteritis
Rare cases: HSP, CF, Celiac dz, Crohn disease, leukemia
Pathophysiologic Insult

Telescoping of the intestine into an area distal to it
 95% involve the ileocecal valve
Age < 2 years: typically no etiology for lead point

Older children: 5-10% have lead point

 Meckel’s, polyp, appendiceal stumps, enteric duplication,
ectopic pancreas, foreign body, mass
Compressed mesentery venous obstruction intestinal
mucosal ischemia  leakage of blood and mucus into
lumen

 Bowel ischemia can lead to release of endogenous opiods
Clinical Manifestations
 Intermittent, colicky episodes of abdominal pain
 Normal between episodes
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Vomiting (starts non-bilious, may progress to
bilious)
Bloody stool
Abdominal exam often normal
 Pain over site of intussusception; “sausage mass”

Lethargy
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Abdominal x-rays
 25% show normal gas
pattern
 Crescent sign

Ultrasound
 Target sign
 Very accurate
 Test of choice

Contrast or air enema
 Diagnostic and therapeutic
 Surgery aware and present
 More successful when symptoms present for <24hrs
 10% recur
 Most within 24hours of reduction – observation

Surgical reduction warranted when contrast enema
unsuccessful
 15% of patients require surgical intervention