Review – Kaplan Pediatrics: Gastrointestinal Disorders

ORAL CAVITY

 

Cleft Lip and Palate

• Most are multifactorial inheritance; also autosomal dominant in families (most with isolated cleft palate)
• Clefts are highest among Asians, lowest among African descent

•        Increase in other malformations with isolated cleft palate

• Most important early issue is feeding (special nipple needed)
• Complications—increased risk of otitis media, hearing loss, speech problems
• Treatment—surgical correction
  • Lip at 3 months of age
  • Palate at <1 year

 

 

GASTROENTERITIS

 

Acute Diarrhea

A 13-month-old child has had a 3-day history of green watery stools. She has also been vomiting for 1 day. Physical examination reveals a febrile, irritable baby with dry mucous membranes and sunken eyes.

 

• Etiology (see Table 14-1)

Table 14-1. Causes of Diarrhea (Acute and Chronic)

 

	Infant	Child	Adolescent
Acute	•    Gastroenteritis •    Systemic infection •    Antibiotic	•    Gastroenteritis/Food poisoning •    Systemic infection	•    Gastroenteritis/ food poisoning •    Systemic infection
Chronic	•    Postinfectious lactase deficiency •    Milk/soy intolerance •    Chronic diarrhea of infancy •    Celiac disease •    Cystic fibrosis	•    Postinfectious lactase deficiency •    Irritable bowel syndrome •    Celiac disease •    Lactose intolerance •    Giardiasis •    Inflammatory bowel disease	•    Irritable bowel syndrome •    Inflammatory bowel disease •    Lactose intolerance •    Giardiasis •    Laxative abuse

 

• Common organisms (see Table 14-2)

 

 

Table 14-2. Common Causes of Acute Diarrhea

Bacterial (Inflammatory)	Viral	Parasitic
Campylobacter	Norovirus	Giardia lamblia (most common)
Enteroinvasive E. coli	Rotavirus	E. histolytica
Salmonella	Enteric adenovirus	Strongyloides
Shigella	Astrovirus	Balantidium coli
Yersinia	Calicivirus	Cryptosporidium parvum
Clostridium difficile		Trichuris trichiura
E. coli 0157:H7

 Note

Antidiarrheal compounds should never be used in children.

Note

Common causes of bloody diarrhea:

Campylobacter Amoeba (E. histolytica) Shigella

1. E. Coli

Salmonella

• Major transmission is fecal/oral or by ingestion of contaminated food or water
• Clinical presentation
  • Diarrhea, vomiting, abdominal cramps, nausea, fever (suggests inflammation and dehydration)
  • Can present from an extraintestinal infection, g., urinary tract infection, pneu- monia, hepatitis
• Management

−   Assess hydration and provide fluid and electrolyte replacement

• Prevent spread
• In some cases, determine etiology and provide specific therapy (some are not treated)
• Think about daycare attendance, recent travel, use of antibiotics, exposures, intake of seafood, unwashed vegetables, unpasteurized milk, contaminated water, uncooked meats to isolate differential diagnosis of organisms

• Labs
  • Most cost-effective, noninvasive testing is stool examination

 

• Mucus, blood, leukocytes → colitis (invasive or cytotoxic organism)
• Stool cultures—with blood, leukocytes, suspected hemolytic uremic syndrome, immunosuppressed, in outbreaks
• Clostridium difficile toxin—if recent history of antibiotics
• Ova and parasites
• Enzyme immunoassays for viruses or PCR (rarely need to be diagnosed)

 

Chronic Diarrhea

 

Table 14-3. Organism-Specific Associations and Therapy

Organism	Association	Therapy
Rotavirus	Watery diarrhea, vomiting, ± fever	Supportive
Enteropathogenic E. coli	Nurseries, daycare	Supportive care in severe cases, neomycin or colistin
Enterotoxigenic E. coli	Traveler’s diarrhea	Supportive care trimetho prim-sulfamethoxazole in severe cases
Enterhemorrhagic E. coli	Hemorrhagic colitis, HUS	No antimicrobial therapy in suspected cases due to ↑ risk of HUS; supportive care only
Salmonella	Infected animals and contam- inated eggs, milk, poultry	Treatment indicated only for patients who are ≤3 months of age, toxic, has disseminated disease, or S. typhi
Shigella	Person-to-person spread, contaminated food	Trimethoprim/sulfamethoxazole
Campylobacter	Person-to-person spread, contaminated food	Self-limiting; erythromycin speeds recovery and reduces carrier state; recommended for severe disease
Yersinia enterocolitica	Pets, contaminated food, arthritis, rash	No antibiotic therapy; aminoglycosides plus a third-gener- ation cephalosporin for infants ≤3 months of age or with culture-proven septicemia
Clostridium difficile	History of antibiotic use	Metronidazole or vancomycin and discontinuation of other antibiotics
Staphylococcus aureus	Food poisoning (onset within 12 h of ingestion)	Supportive care, antibiotics rarely indicated
Entamoeba histolytica	Acute blood diarrhea	Metronidazole
Giardia	Anorexia, nausea, abdominal distension, watery diarrhea, weight loss Cysts ingested from infected individual or from contami- nated food or water	Metronidazole, furazolidone
Cryptosporidium	Mild diarrhea in immuno- compromised infants; severe diarrhea in AIDS patients	Raising CD4 count to normal is best treatment. No proven therapy (antimicrobial); strong supportive care; may try rifabutin

Definition of abbreviations: HUS, hemolytic uremia syndrome

 

 

Note

Schwachman-Diamond Syndrome

• Pancreatic insufficiency
• Neutropenia
• Malabsorption

Intestinal lymphangiectasia

• Lymph fluid leaks into bowel lumen
• Steatorrhea
• Protein-losing enteropathy

Disaccaridase Deficiency

• Osmotic diarrhea
• Acidic stools

Abetalipoproteinemia

• Severe fat malabsorption form birth
• Acanthocyes
• Very low to absent plasma cholesterol, triglycerides,

 

Chronic Diarrhea and Malabsorption

• Patterns
  • From birth
  • After introduction of a new food
• Clinical presentation
  • Chronic nonspecific diarrhea of infancy:

°      Weight, height, and nutritional status is normal, and no fat in stool

• Excessive intake of fruit juice, carbonated fluids, low fat intake usually present in history

• Diarrhea with carbohydrates—CHO malabsorption
• Weight loss and stool with high fat malabsorption

• Workup of chronic diarrhea (simple, noninvasive testing to be done first)
  • History and physical, nutritional assessment; stool for pH, reducing substances, fat, blood, leukocytes, culture, difficile toxin, ova, and parasites
  • Blood studies—complete blood count and differential, ESR, electrolytes, glucose, BUN, and creatinine
  • Sweat test, 72-hour fecal fat, breath hydrogen tests
• Initial evaluation
  • Fat:

°      Most useful screening test is stool for fat (Sudan red stain)

• Confirm with 72-hour stool for fecal fat (gold standard for steatorrhea)
• Steatorrhea is most prominent with pancreatic insufficiency; all require a sweat chloride
• Serum trypsinogen is also a good screen (reflects residual pancreatic function)

• Screen for CHO malabsorption—measure reducing substances in stool (Clinitest)
  • Breath hydrogen test—after a known CHO load, the collected breath hydrogen is analyzed and malabsorption of the specific CHO is identified
• Protein loss—cannot be evaluated directly (large proportion of bacterial protein and dietary protein almost completely absorbed before terminal ileum; amino acids and peptides are reabsorbed)
  • Screen—spot stool a1-antitrypsin level
• More common differential diagnosis of malabsorption

−   Giardiasis—only common primary infection causing chronic malabsorption; duodenal aspirate/biopsy/immunoassay (Giardia)

• HIV or congenital T- or B-cell defects
• Small-bowel disease—gluten enteropathy, abetalipoproteinemia, lymphangiectasia
• Pancreatic insufficiency—fat malabsorption (cystic fibrosis is most common con- genital disorder associated with malabsorption)
• Most common anomaly causing incomplete bowel obstruction with malabsorption is malrotation
• Short bowel—congenital or postnatal loss of >50% of small bowel with or without a portion of the large intestine (presence of ileocecal valve is better)
• Celiac disease—associated with exposure to gluten (rye, wheat, barley, derivatives)

 

• Patients mostly age 6 months to 2 years

−   Permanent intolerance

• Genetic predisposition (HLA DQ2)
• Clinical presentation
• Diarrhea
• Failure to thrive
• Growth retardation
• Vomiting
• Anorexia, not interested in feeding
• Ataxia
• Evaluation
  • Blood for anti-tissue transglutaminase (IgA) and serum IgA (false if IgA deficiency) (best initial test)
  • Definitive test—small intestine biopsy
• Treatment—lifelong, strict gluten-free diet

 

 

VOMITING

 

Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF)

• Three basic types:
• Isolated EA
• Isolated (H-type) TEF
• EA and distal TEF
• Most common anatomy is upper esophagus ends in blind pouch and TEF connected to distal esophagus
• H-type—presents chronically and diagnosed later in life with chronic respiratory problems
• Half with associated anomalies—VACTERL association
• Clinical presentation in neonate (EA or EA + TEF)

−   Frothing, bubbling, cough, cyanosis, and respiratory distress

− With feedings → immediate regurgitation and aspiration

• Clinical presentation with just TEF—feeding problems and recurrent aspiration
• Diagnosis

−   Inability to pass nasogastric/orogastric tube

− Esophageal atresia: x-ray shows coiled nasogastric tube in blind pouch with no distal gas (gasless abdomen)

− Isolated TEF: esophagram with contrast media (or bronchoscopy or endoscopy with methylene blue)

– Esophageal atresia and distal fistula: coiled nasogastric tube in blind pouch the large amount of air in stomach and intestines

• Treatment—surgical ligation of TEF and resection with end-to-end anastomosis of esophageal atresia

 

 

 

Note

VACTERL Association Nonrandom association of birth defects:

Vertebral anomalies

Anal atresia

Cardiac defect TracheoEsophageal fistula Renal anamolies

Limb abnormalities

 

 

Gastroesophageal Reflux Disease (GERD)

A 4-month-old is admitted with episodes of apnea occurring 20–30 min after feeds. The mother states the baby has been spitting up since birth. She is at the fifth percentile for weight.

 

Note

Prokinetic agents (metaclopramide, bethanechal or erythromycin) have no efficacy in the treatment of GERD in children.

 

Note

Pyloric stenosis is high yield for the Step 2 CK exam.

 

• Etiology—insufficient lower esophageal sphincter tone early in life
• Symptoms during first few months of life; resolves by 12–24 months of age; in older children—chronic (more like adults); only half resolve completely
• Clinical presentation

−   Postprandial regurgitation

• Signs of esophagitis—arching, irritability, feeding aversion, failure to thrive

− Obstructive apnea, stridor, lower airway disease (cough, wheezing)

• Diagnosis
  • Most by history and physical

−   Barium esophagram and upper gastrointestinal studies

• Esophageal pH monitoring (best test)—quantitative and sensitive documentation of acid reflux (normal pH in lower esophagus is <4 only 5−8% of time)
• Endoscopy—erosive esophagitis and complications
• Radionucleotide scintigraphy (Tc)—to document aspiration
• Laryngotracheobronchoscopy—for extraesophageal GERD
  • Management
    • Conservative with lifestyle management: normalize feeding technique, appropri- ate volume, thicken feeds, positioning
    • Pharmacologic:
      • H2-receptor antagonist (ranitidine, cimetidine, famotidine)—first-line with overall best safety profile
      • Proton pump inhibitor (omeprazole, lansoprazole, pantoprazole)—most potent for severe reflux and esophagitis
    • Surgery—fundoplication for refractory esophagitis, strictures, chronic pulmonary disease, continued obstructive apnea

 

Pyloric Stenosis

A 4-week-old boy has nonbilious projectile vomiting. Physical examination is remarkable for a small mass palpated in the abdomen.

 

• Epidemiology—more common in whites of Northern European ancestry, firstborn males
• Clinical presentation

−   Nonbilious, projectile vomiting

− Still hungry and desire to feed more

• Usually age ≥3 weeks (1 week to 5 months)

 

• Mild-to-moderate dehydration, hypochloremic, hypokalemic metabolic alkalosis
• Palpation of a firm, movable, 2-cm, olive-shaped, hard mass in midepigastrium; left to right peristaltic wave

• Diagnosis—best test is ultrasound (a target-like appearance in cross-section)
• Treatment
  • Rehydrate, correct electrolytes (NaCl, KCl)

−   Pylorotomy

 

Duodenal Atresia

A newborn presents with bilious vomiting with every feed. Abdominal film reveals a double bubble.

 

 

• Epidemiology
  • Half are born premature

−   Down syndrome

• With other anomalies—malrotation, esophageal atresia, congenital heart defects, anorectal malformation, renal anomalies

• Clinical presentation
  • Bilious vomiting without abdominal distention on first day of life (obstruction just distal to ampulla)

− Polyhydramnios prenatally

− Many with jaundice (increased enterohepatic circulation)

• Diagnosis
  • X-ray shows classic double bubble with no distal bowel
  • X-ray spine for anomalies; ultrasound for other anomalies
• Treatment

−   Nasogastric decompression

• Intravenous fluids

− Surgery—duodenoduodenostomy

 

Note

Jejunal or Ileal Atresia Most present on the first day of life.

There is bile-stained emesis with abdominal distention. (With duodenal atresia, there is no abdominal distention.)

Plain films show air-fluid levels.

Contrast studies of the upper and lower intestine can delineate level of obstruction.

Ultrasound may also differentiate intestinal atresia from meconium ileus from malrotation.

 

Table 14-4. Congenital Bowel Obstruction

Lesion	Etiology	DDX	Clinical Background/ Presentation	Diagnosis	Management Algorithm/Definitive Treatment
Duodenal Atresia	Failed recanalization of bowel lumen 4th–7th week gestation	•     Duodenal stenosis •     Annular pancreas •     Duplication cysts •     Ladd bands from malrotation	•     Polyhydramnios •     50% premature •     Other organ system anomalies •     Half with chromosomal anomalies, especially trisomy 21 Presentation •     First day •     Bilious vomiting w/o abdominal distention •     Jaundice	•        Prenatal sonogram •        Postnatal plain X-ray: double- bubble with NO distal bowel gas •        CXR, spine films •        Echocardiogram •        Renal ultrasound for other most common anomalies	•     NG/OG decompression •     NPO + IV fluids + electrolyte balance •     Broad-spectrum antibiotics Definitive Treatment: Surgery when stable— duodenoduodenostomy
Jejunal and Ileal Atresias	Intrauterine vascular accident → segmental infarction and resorption of fetal intestine	•     Meconium ileus/ plug •     Malrotation + volvulus •     Hirschprung disease	•     Possible role with antenatal cigarette and/or cocaine use •     Very little familial inheritance (aut. rec.) •     Little extraintestinal anomalies Presentation •     Polyhydramnios •     Abdominal distention at birth or with first feeds + vomiting, may be bilious •     Few with delayed or no passage of meconium •     Jaundice	•     Less likely to be detected in utero •        Plain X-ray: multiple air-fluid levels proximal to obstruction in upright or lateral decubitus •        Ultrasound: differentiate with meconium ileus and identify malrotation •        Contrast studies to localize	•     NG/OG •     IV fluid and electrolyte balance prior to surgery •     Antibiotics Definitive Treatment: Surgery—resect dilated proximal bowel then end-to-end anastamosis

(Continued

 

Table 14-4. Congenital Bowel Obstruction (Continued)

Lesion	Etiology	DDX	Clinical Background/ Presentation	Diagnosis	Management Algorithm/ Definitive Treatment
Meconium Ileus	Abnormal viscous secretions → distal 20-30 cm of ileum collapsed and proximal bowel dilated and filled with thick meconium impacted in ileum	•     Meconium plug •     Atresias •     Hirschprung disease •     Malrotation + volvulus	•     80-90% will be diagnosed with CF •     May perforate in utero → meconium peritonitis (calcifications) Presentation: •     Vomiting becomes persistent with prominent abdominal distention •     No passage of meconium •     May present as bowel perforation and peritonitis •     Palpation of “doughy” or cordlike masses	•        Plain films: dilated loops of bowel proximal to obstruction that vary with width and not evenly filled with gas •     Presence of bubbly or granular appearance in RLQ (meconium with gas bubbles) •     No air-fluid levels as secretions are too viscid to layer •        Ultrasound to verify if questionable •        Water-soluble enema (Gastrografin or Hypaque) will localize •        Test for CF	•     NPO •     NG/OG decompression •     IV fluid and electrolyte balance •     Antibiotics Definitive Treatment: First: hypertonic water- soluble contrast enema to attempt wash-out If fails—laparotomy
Meconium Plugs	Decreased water content for many possible reasons leads to lower colonic or anorectal meconium plug	•     Meconium ileus •     Hirschprung disease	•     Majority not associated with CF, unless in small bowel •     Infants with polycythemia, dehydration and small left colon as may be seen with IODM •     Maternal opiate use or treatment with MgSO4 Presentation: Failure of meconium passage and abdominal distention	•        Plain films: low obstruction with proximal bowel dilatation and multiple air-fluid levels	•     NG/OG + NPO •     IV fluid and electrolyte balance •     Antibiotics Definitive Treatment: •     Evacuation with glycerin suppository if very low or saline enema or hypertonic water-soluble contrast if higher •     Observe for possible Hirschprung disease •     Consider sweat test if contrast shows small bowel plug.

(Continued)

 

Table 14-4. Congenital Bowel Obstruction (Continued)

Lesion	Etiology	DDX	Clinical Background/ Presentation	Diagnosis	Management Algorithm/ Definitive Treatment
Malrotation	•     As developing bowel rotates in and out of abdominal cavity (weeks 5-12), superior mesenteric artery acts as the axis •     With nonrotation, 1st and 2nd part of duodenum are in normal position, but because of inadequate mesenteric attachment to posterior wall, rest of small bowel occupies RLQ and colon the left •     Failure of cecum to move to the RLQ → failure to form broad-based adhesions to posterior wall → superior mesenteric artery is tethered by a narrow stalk (causes volvulus) and Ladd bands can extend from cecum to RUQ and obstruct at duodenum.	•     Intestinal atresias •     Meconium ileus •     Hirschprung disease	•     Other anomalies of abdominal wall – Diaphragmatic hernia – Gastroschisis – Omphalocele – Heterotaxy syndrome (CHD, malrotation, asplenia/ polysplenia) Presentation: •     1st year of life with > 50% in first month with symptoms due to intermittent volvulus and/ or Ladd band obstruction -acute and chronic obstruction (recurrent pain and vomiting) •     Can present in first week with bilious emesis and acute obstruction •     May have malabsorption due to bacterial overgrowth •     Any age with acute obstruction due to volvulus	•        Plain film: may show double- bubble with evidence of small amount of distal gas (prior to the volvulus) or a gasless abdomen •        Ultrasound: inversion of superior mesenteric artery and vein •        Upper GI: malposition of ligament of Treitz and small bowel obstruction with corkscrew appearance or duodenal obstruction with “bird’s beak” appearance	•        If volvulus: emergency surgery after IV and fluids •     Otherwise NPO, NG/ OG •     Correct fluid and electrolyte imbalance. Definitive Treatment: •        Surgery: any patient of any age with any significant rotational abnormality •        Volvulus: acute surgical emergency

(Continued)

 

 

Table 14-4. Congenital Bowel Obstruction (Continued)

Lesion	Etiology	DDX	Clinical Background/ Presentation	Diagnosis	Management Algorithm/ Definitive Treatment
Hirschprung Disease	•     Developmental disorder of the enteric nervous system such that there are absence of ganglion cells in the submucosal and myenteric plexus •     Arrest of neuroblast migration from proximal to distal bowel → inadequate relaxation and hypertonicity	•     Long segment disease vs., intestinal atresia •     Meconium plug •     Meconium ileus	•     Most common cause of intestinal obstruction in neonate •     Usual short segment is male preponderance but equalizes with long segment disease •     Increased familial incidence with long segment but must (short segment) are sporadic •     May be associated with cardiovascular and urological defects and with Down syndrome	•        Plain film: distended loops of bowel •        Contrast enema may not show classic line of demarcation form small aganglionic bowel to proximal dilatation (better >1 month of age) but 24 hr films usually show retained contrast and suggests the diagnosis •        Barium enema also useful prior to surgery to define extent of aganglionic segment	•     NG/OG •     NPO •     Fluid and electrolyte management •     Evaluate for other defects Definitive Treatment: Laparoscopic single- stage endorectal pull- through is procedure of choice.
			•     80% are short (rectosigmoid) •     10-15% long (more than that)	•        Gold standard confirmation is the suction rectal biopsy
			•     5% total bowel aganglionosis
			Presentation:
			•     Most diagnosed in neonates
			•     Suspect with any delayed meconium passage in full- term infant (99% within first 48 hours) or no passage with progressive abdominal distension and vomiting
			•     Later with chronic constipation and empty rectum on digital exam with subsequent explosive release of small stool and gas
			•     Main concern is meconium enterocolitis

 

 

 

Note

A delay in treating volvulus can result in short bowel syndrome.

Note

Meckel diverticulum: “Disease of 2s”

• 2 years of age
• 2 of population
• 2 types of tissue
• 2 inches in size
• 2 ft from ileocecal valve

 

Malrotation and Volvulus

• Etiology

−   Incomplete rotation of intestine during fetal development

− Superior mesenteric artery acts as axis for rotation

− Ladd bands may extend from cecum to right upper quadrant (RUQ) to produce duodenal obstruction

• Clinical presentation
  • Most present in first year of life with acute or chronic incomplete obstruction

−   Bilious emesis, recurrent abdominal pain with vomiting

• An acute small-bowel obstruction in a patient without previous bowel surgery is suspicious for volvulus (acute surgical abdomen)

• Diagnosis

− Plain film is nonspecific—may show double bubble if there is duodenal obstruction

− Barium enema shows malposition of cecum (mobile cecum is not situated in the right lower quadrant); upper gastrointestinal will show malposition of ligament of Treitz

− Ultrasound will show inversion of superior mesenteric artery and vein (superior mesenteric vein to the left of the artery is suggestive) and duodenal obstruction with thickened bowel loops to the right of the spine; advantage is no need for contrast; start with this study

• Treatment—surgery

 

 

HEMATOCHEZIA

 

Meckel Diverticulum

A 2-year-old boy presents with a 1-week history of painless rectal bleeding. Physical examination is unremarkable. The abdomen is soft and nontender. Rectal examination is unremarkable.

 

• Etiology
  • Remnant of embryonic yolk sac (omphalomesenteric or vitelline duct), lining similar to stomach

−   Most frequent congenital gastrointestinal anomaly

• Clinical presentation
  • Acid-secreting mucosa causes intermittent painless rectal bleeding
  • May get anemia, but blood loss is self-limited
  • May have partial or complete bowel obstruction (lead point for an intussusception) or develop diverticulitis and look like acute appendicitis (much less common presentation)
• Diagnosis—Meckel radionuclide scan (Tc-99m pertechnetate)
• Treatment—surgical excision

 

Intussusception

A 15-month-old child is seen for cramping, colicky abdominal pain of 12 h duration. He has had two episodes of vomiting and a fever. Physical examination is remarkable for a lethargic child; abdomen is tender to palpation. Leukocytosis is present. During examination, the patient passes a bloody stool with mucus.

• Etiology

− Telescoping of bowel; most ileal-colic

• Most present at age 3 months to 6 years (80% <2 years)
• Commonly following adenovirus or rotavirus infection, upper respiratory infec- tion, otitis media

– Associated with HSP (Henoch-Schönlein purpura)

• Can also occur with a leading point—Meckel diverticulum, polyp, neurofibroma, hemangioma, malignancy
• Pathophysiology—bowel drags mesentery with it and produces arterial and venous obstruction and mucosal necrosis → classic “black currant jelly” stool
• Clinical presentation

−   Sudden onset of severe paroxysmal colicky abdominal pain; straining, legs flexed

• Progressive weakness

− Lethargy, shock with fever

• Vomiting in most (early on, it is bile-stained)
• Decreased stooling
• Blood in most patients in first 12 hours, but may be delayed or not at all
• Physical examination—slightly tender, sausage-shaped mass on right in cephalocau- dal axis
• Diagnosis
  • Ultrasound to first screen for the diagnosis (non-invasive and cost-effective; “doughnut appearance”) and look for free-air (if intussusception has caused per- foration)
  • Air enema is the next study of choice as it is far safer than the previously-used barium enema (0.1 2.5% risk of perforation); air enema may be therapeutic and prevent the need for immediate surgery
• Treatment
  • If prolonged, shock, peritoneal irritation, or perforation → surgery
  • Radiographic reduction under fluoroscopy—most will reduce if done within 48 hours of presentation (goes down to half after that time)

−   If surgical—if manual operative reduction is not possible or bowel is not viable, then resection and end-to-end anastomosis

 

CONSTIPATION

 

Functional Constipation

A 6-year-old boy complains of hard bowel movements every fifth day. Physical examination reveals normal weight and height. Abdomen is soft, and hard stool is palpable on rectal examination.

 

• Delay or difficulty in stooling for at least 2 weeks; typically after age 2 years
• Passage of painful bowel movements with voluntary withholding to avoid pain
• May have blood in stool

•        Physical examination—large volume of stool palpated in suprapubic area; rectal exam shows vault filled with stool

• Treatment
  • Patient education (bowel training program)
  • Relief of impaction—enema, then stool softeners (mineral oil, lactulose, polyeth- ylene glycol; no prolonged use of stimulants)
  • Behavioral modification
  • Deal with any psychosocial issues

 

Hirschsprung Disease

• Etiology—absence of a ganglion cells in bowel wall beginning at internal anal sphinc- ter and extending variably proximally

•        Most common reason for bowel obstruction in neonates

• Clinical presentation
  • Symptoms usually present at birth

−   Suspect in any full-term infant with a delay in passage of meconium (>24 hours)

• May have subsequent history of chronic constipation (if short aganglionic segment)

• Diagnosis
  • Rectal manometry

– Rectal suction biopsy is definitive

• Presence of transition zone on barium enema (not necessary to perform)

• Treatment—surgery (most with temporary colostomy) and wait 6−12 months for definitive correction (most achieve continence)
• Complications—enterocolitis

 

 

Note

Other causes of gastrointestinal bleeding to consider are:

1. Anal fissure (most common cause of lower gastrointestinal bleeding in infancy).
2. Accidental swallowing of maternal blood (do Apt test)
3. Peptic ulcer disease

 

Table 14-5. Functional Constipation Versus Hirschsprung Disease

 

	Functional Constipation	Hirschsprung Disease
Onset constipation	After 2 years of age	At birth
Failure to thrive	Uncommon	Possible
Enterocolitis	No	Possible
Abdominal distention	Usually not	Yes
Poor weight gain	Usually not	Common
Anal tone	Normal	Normal
Rectal	Stool in ampulla	No stool
Anorectal manometry	Distention of rectum → relaxation of internal sphincter	No sphincter relaxation
Barium enema	Large amount of stool; no transition zone	Transition zone with delayed evacuation