GI Bleeding
Gastrointestinal bleeding or gastrointestinal hemorrhage describes every form of blood loss in the
gastrointestinal tract, from the pharnyx to the rectum
Microscopic bleeding: amount of bledding is so small it can only be detected by lab testing
Hematochezia: upper GI bleeding vomiting of bright red blood
Melena : upper gastrointestinal bleeding black, tarry stool containing digested blood
Hematochezia: lower gastrointestinal bleeding red blood per rectum
Classification
Upper Gastrointestinal Bleeding

source is from pharynx to ligament of Treitz
Lower Gastrointestinal Bleeding

source below ligament of Treitz to anus
Management
1. ensure patient stability
2. establish adequate oxygen delivery
3. intravenous access
4. fluid and blood rescucitation
5. identification of underlying problem
6. correction of underlying problem
Diagnosis
Esophagogastroduodenoscopy
Colonoscopy
Radionuclide imaging
Arteriography
Diagnostic Laparoscopy
Intraoperative endoscopy
COMMON CAUSES OF GI BLEED IN INFANTS
Bacterial Enteritis
Milk Protein Allergy
Intussusception
Swallowed, Maternal Blood
Anal Fissure
Lymphonodular hyperplasia
Necrotizing Enterocolitis
Meckel diverticulum
Bacterial enteritis
o
o
o
Inflammation of the small intestines
Most commonly due to ingestion of improperly prepared food or contaminated water
common causes: Salmonella, Shigella, Campylobacter, Escherichia coli, Clostridium difficile
Pathophysiology
o
Inflammatory
 Invasion of mucosa
 Production of cytotoxins
Clinical Manifestation

diarrhea (bloody), abdominal cramps, Vomiting, signs of dehydration, Fever, tenesmus
Diagnosis

assess degree of dehydration, stool examination, stool culture, proctosigmoidoscopy
Treatment

fluid and electrolyte replacement, prevent spread of enteropathogen, antimicrobial treatment
Milk/food protein allergy

First form of allergy to affect infants and young children
Pathogenesis

IgE mediated, Non IgE mediated, Mixed
IgE mediated

Food allergen-specific IgE antibodies binds to mast cells, basophils, macrophages, dendritic cells
interleukins, cytokines, leukotrienes, TNF vasodilation, smooth muscle contraction, mucus
secretion
Non-IgE mediated (cell-mediated)

Food allergen-specific T cells  secrete excessive amounts of various cytokines delayed
inflammation
Clinical Presentation




Allergic eosinophilic gastritis
o intense eosinophilic infiltration
o vomiting
o hematemesis
o abdominal pain
o anorexia
o failure to thrive
Food induced enterocolitis syndrome
o Irritability
o Protracted vomiting
o Diarrhea (bloody)
o Anemia
o Failure to thrive
o Hypotension
Allergic Proctocolitis
o 1st few months of life in healthy infant
o Streaks of blood in the stool
o Mild diarrhea
Food-induced enteropathy
o Celiac disease
 6 mos- 2y/o
 Disorders where proximal SI mucosa is damaged as a result of exposure to gluten
(wheat, oat, rye, barley)
 cell mediated inflammatory response to gliadin causing villus atrophy and
damage to surface epithelium
Diagnosis


Cell mediated
o Eliminate diet
o Double blind, placebo-controlled food challenge
IgE mediated
o Prick skin test
o Radioallergosorbent test (RAST)
Treatment


Elimination of diet
Epinephrine
Prognosis

85% outgrow allergy by 3y/o
Prevention

Delay food introduction
Intussusception
Swallowed Maternal Blood


Hematemesis during first few days of life
Diagnosis APT’S TEST
o Maternal Hb- yellow
o Fetal Hb- red, pink
Anal Fissure





Small laceration of the mucocutaneous junction of the anus
Consequence of constipation
s/sx: pain on defecation, bright red blood on stool surface
diagnosis: anal inspection
treatment: parental education, stool softener
Nodular lymphoid hyperplasia




Hyperplasia of the peyers patches in the distal ileum
s/sx: bleeding, diarrhea, abdominal cramps
associated with milk-protein hypersensitivity
immunoglobulin deficiency



enterocolitis
inflammatory bowel disease
spontaneously resolves
Necrotizing enterocolitis





Most common life-threatening emergency of the GI tract in the neonatal period
Various degrees of mucosal or transmural necrosis of the intestines
etiology: multifactorial
incidence : 1-5% of NICU px
assoc with prematurity low birthweight
Pathogenesis
Risk factors
Prematurity
Enteral feedings
Pathogenic organisms
Pathology
Necrotic segment of intestines
Gas accumulation in the submucosa
Progression of necrosis
Clinical Manifestation
o
o
o
o
o
o
Insidious or sudden
Non-specific
Abdominal distention
Bloody stools
Severe illness
Bowel perforationperitonitisSIRS  shock  death
o
o
o
o
Plain abdominal film pneumatosis intestinalis, pneumoperitoneum
Hepatic UTZ: portal vein gas
Blood culture
Paracentesis: bowel perforation
Diagnosis
Treatment
o
o
o
o
o
o
o
Cessation of feeding
Gastric decompression
Airway/ventilation support
Circulation support
Fluid and electrolyte correction
Nutritional support
Surgery: brown paracentesis, erythema of abdominal wall, palpable mass, failure of medical
management
Meckel’s Diverticulum




Remnant of the embryonic yolk sac
omphalomesenteric / vitelline duct  connects yolk sac to gut for nutrition  placenta forms 
5th-7th wk: duct involutes
most frequent congenital GI anomaly
3-6cm outpouching of ileum
Clinical manifestation
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usually during 1st 2 years of life
brick-red, painless, rectal bleeding
anemia (self-limited)
sx of obstruction
Diagnosis
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



Meckel radionuclide scan
ultrasound
angiography
CT scan
exploratory laparoscopy
Treatment

Excision
COMMON CAUSES OF GI BLEED (CHILD)
Bacterial Enteritis
Intussusception
Anal Fissure
Colonic Polyps
Peptic Ulcer/ Gastritis
Colonic Polyps
Familial polyposis syndromes



associated with colonic polyps
important bec of malignant potential
clinical manifestations: bright red, painless, rectal bleeding, usually during or after defecation, irondeficiency anemia, abdominal pain, prolapse of polyps, symptoms of malabsorption
Type:
1. Juvenile colonic polyps
a. most present between 2-10 y/o
b. most common childhood bowel tumor
c. solitary, few mm – 3 cm in size
d. erythematous, friable, pedunculated
e. majority has no malignant potential
2. Multiple juvenile colonic polyps
a. more than 3 to 5
b. identical to solitary polyp in character
c. increased risk for GI cancerDiagnosis:
diagnosis: colonoscopy every 3 years for multiple polyps and strong family history of juvenile polyposis
treatment : removal by snare cautery, transabdominal polypectomy
prognosis : recurrence
Peptic Ulcer Disease
Rare in children
More often secondary to a systemic disease
Pathology: gastroduodenal inflammation or gastritis
ulcers are deep lesions, erosions are superficial
2 classification: primary & secondary
Primary Inflammation:


Most commonly caused by Helicobacter pylori
Gram (-) spiral, flagellated organism in the mucus layer




urease-producing
acquired early in life ( before 5 y)
mode of transmission unknown
tends to be permanent unless treated
Secondary Inflammation
o
o
o
o
Sepsis
Burns
Medication
Eosinophilic gastritis
Pathogenesis
Aggressive factors overwhelm natural barriers
1. bicarbonate-mucus barrier
2. prostaglandins
3. gastric epithelial cells
4. mucosal blood flow
Clinical Manifestations
Neonates: GI bleed
Neonates- 2y/o: vomiting, GI hemorrhage, slow growth
Preschool: periumbilical post-prandoal pain, vomiting, GI bleed
>6y/o: epigastric pain (dull, aching),
Diagnosis


endoscopy : localization, biopsy , therapeutic
for H. pylori : rapid urease test, tissue culture, stool antigen test, antibody detection in blood,
serum, saliva, urine
Treatment

H. Pylori
o 2 antibiotics= 1 potent antacid x 1-2 weeks
o Indications to treat:
 documented ulcer
 (+) hx of ulcers

 atrophic gastritis
 intestinal metaplasia
Secondary inflammation
o Inciting cause should be removed
o Antacids: 1ml/kg/dose
o H2 receptor blockers
o Hydrogen pump inhibitors
COMMON CAUSES OF FI BLEED IN ADOLESCENTS
Bacterial Enteritis
Colonic Polyps
Peptic Ulcer/ Gastritis
Inflammatory Bowel Disease
Inflammatory Bowel Disease



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onset commonly during adolescence or young adulthood
idiopathic chronic intestinal inflammation
2 disorders : ulcerative colitis, Chron’s disease
risk factors: genetic, environmental
Pathogenesis


Abnormality in the intestinal mucosal immune regulation
mediators of inflammation cause tissue destruction
ULCERATIVE COLITIS
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


Localized the colon, spares the upper GI
Mucosal involvement
Asians have low risk
chronicity (beyond 2 wks)
- S/sx : bloody stool/diarrhea
 abdominal pain
 tenesmus
 extraintestinal manifestations
Diagnosis
Typical presentation
Chronicity
Endoscopic/histologic exam of colon
-microulcers
- acute or chronic inflammation
- crypt abscesses
Treatment



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Aminoglycoside (sulfasalazine)
Hydrocortisone enema
oral corticosteroid (Prednisone)
immunomodulators
o Azathioprine
o Cyclosporine
Infliximab
colectomy
Prognosis



20-30% spontaneousimprovement
child responds initially to medical mgt
>10 years : increase risk for cancer
CROHNS DISEASE
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

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involves any region of GI tract
transmural inflammation; skip areas
involves ileum and colon
chronicity (beyond 2 wks)
S/sx : bloody stool/diarrhea
o abdominal pain
o tender mass on RLQ
o tenesmus
o extraintestinal manifestations
Diagnosis





typical presentation
chronicity
upper GI series: aphthuous ulcers, cobblestone appearance
CT / MRI
colonoscopy
Treatment





5-aminosalicylate
 Mesalamine
 Sulfasalazine
corticosteroid
immunomodulators
Infliximab
Surgical for localized disease of ileum or colon
Prognosis



high morbidity, low mortality
children maintained longer on steroid
>10 years : increase risk for cancer
COMPARISON
Rectal bleeding
Diarrhea
Abdominal pain
Abdominal mass
Growth failure
Perianal disease
Rectal disease
Pyoderma gangrenosum
Mouth ulceration
Thrombosis
Colonic disease
Ileal disease
Strictures
Fissures
Fistulas
Toxic Megacolon
Risk for cancer
Skip lesions
Transmural involvement
Crypt abscesses
Granulomas
Linear Ulcerations
pANCA
anti-Saccharomyces cerevisciae Ab
CROHN DISEASE
sometimes
variable
common
common
common
common
Occasional
rare
common
less common
50-75%
common
common
common
common
none
increased
common
common
Less common
common
uncommon
uncommon
common
ULCERATIVE COLITIS
common
common
variable
Not present
Variable
Unusual
Universal
present
rare
present
100%
none
unusual
none
unusual
present
greatly increased
not present
unusual
common
unusual
common
common
uncommon