Gastroenterology




Delayed Passage of Meconium



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  • The delayed passage of meconium may be the result of a mechanical or functional bowel obstruction.
  • Virtually all infants, term and preterm, will have passed meconium by 48 h of age.
  • The evaluation of any infant with delayed passage of meconium should begin with a thorough physical examination and history.
  • For infants who are unstable, the infant must first be stabilized before the investigation begins as to the cause of delayed stooling.




Differential Diagnosis, Evaluation, and Management of Delayed Passage of Meconium



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Cause


Diagnosis


Management


Anorectal abnormality (imperforate anus, anal stenosis)


Imperforate anus should be evident on physical examination


Anal stenosis may be evident on physical examination


Surgical consult


Repogle to low intermittent suction


IV fluids


Remember that high anal atresias may be associated with GU abnormalities


Meconium plug


Contrast enema shows the meconium plug with a normal-caliber colon


Enema is usually therapeutic


If abnormal stooling continues, consider diagnosis of Hirschsprung’s disease and rectal biopsy


Meconium ileus


Contrast enema reveals a microcolon from ileal obstruction with stool


Enema can be therapeutic but may need surgical intervention


Hirschsprung’s disease


Contrast enema shows a distally narrowed segment (aganglionic) leading to a dilated proximal segment (normal colon)


If suspected, rectal biopsy will provide the definitive diagnosis


Surgical consult


Repogle to low intermittent suction


IV fluids


Diverting colostomy is standard; end-to-end anastomosis if affected segment is very short


Ileal atresia


Contrast enema shows no reflux of contrast into the terminal ileum


Surgical consult


Repogle to low intermittent suction


IV fluids


Malrotation


Infants usually present with bilious emesis


Upper GI or contrast enema shows a malpositioned cecum


Surgical consult


Repogle to low intermittent suction


IV fluids


Volvulus


Surgical emergency because the ischemic gut may progress to frank necrosis


Plain film of the abdomen reveals a massively dilated proximal colon


Contrast enema reveals a midtransverse colon obstruction


Emergent surgical consult


Repogle to low intermittent suction


IV fluids


Ileus


May be secondary to a number of factors:



  • Sepsis
  • NEC
  • Hypokalemia
  • Hypothyroidism
  • Hypermagnesemia
  • Narcotic analgesia therapy

Bowel rest


IV fluids


Treatment of underlying condition causing the ileus





Upper Gastrointestinal Tract Bleeding



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  • The evaluation of any infant with GI bleeding should begin with a thorough physical examination and history.
  • For infants who have massive bleeding and are unstable, the infant must first be stabilized before the investigation begins.




Differential Diagnosis, Evaluation, and Management of Upper Gastrointestinal Tract Bleeding



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Cause


Confirmatory Tests


Management


Swallowed maternal blood (bleeding on the first day)



  • Apt test on gastric contents to evaluate for maternal hemoglobin

No treatment necessary


NEC



  • Plain radiograph of abdomen with left lateral decubitus view to evaluate for pneumatosis intestinalis and pneumoperitoneum
  • Rare to have upper GI bleeding; indicates severe, late disease
  • Infants will generally be extremely ill


  • See “Necrotizing Enterocolitis” section for specific management

Coagulopathy



  • Check PT, PTT, fibrinogen, D-dimer, platelets to evaluate for the presence of DIC
  • May see bleeding from other sources as well
  • Confirm that vitamin K was given at delivery
  • Specific factor deficiencies can cause extensive GI bleeding and should be investigated if clinical suspicion is high


  • Treat underlying cause of DIC
  • Replenish platelets and coagulation factors with transfusion of FFP (see Chapter 37 for specific guidelines on transfusion)
  • Specific factor replacement indicated for deficiencies
  • Administer vitamin K if not given at birth

NG trauma



  • Can be suspected in an infant who appears well, has a benign abdominal exam, and whose bleeding clears quickly


  • No specific therapy is required
  • Use the smallest NG tube possible

GI tract anomaly such as volvulus, malrotation, Hirschsprung’s disease



  • Abdominal exam may reveal significant distension and rigidity
  • Abdominal plain film may show significant dilatation of bowel loops, the interpretation of which should be made in the context of the clinical exam
  • Infant will generally appear ill


  • Surgical intervention as soon as the diagnosis is made to halt bowel necrosis

Stress gastritis



  • May be suspected in an infant who appears well, has a benign abdominal exam, and whose bleeding clears quickly


  • No specific therapy is required
  • H2 blockers may be used in an attempt to reduce gastric acid secretion, although efficacy/safety data are limited

Drug-induced gastritis



  • Common medications associated with bleeding include indomethacin and corticosteroids


  • Discontinue use of offending agents if clinically possible

Bleeding varices from end-stage liver disease



  • History will reveal long-standing liver disease from any cause
  • Exam may show marked jaundice, hepatomegaly, splenomegaly, caput medusae around umbilicus, prominent superficial veins on abdomen


  • Direct visualization via endoscopy may be needed to localize the cause of bleeding and possibly institute therapy





  • Serial hematocrits can be followed to track the severity of blood loss.
  • Transfuse PRBCs as indicated (see Chapter 37 chapter for further information).
  • Direct visualization with endoscopy may have to be undertaken to evaluate and possibly treat the cause of bleeding.




Lower Gastrointestinal Tract Bleeding



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  • The evaluation of any infant with GI bleeding should begin with a thorough physical exam and history.
  • For infants who have massive bleeding and are unstable, the infant must first be stabilized before the investigation begins as to the cause of GI bleeding.




Differential Diagnosis, Evaluation, and Management of Lower Gastrointestinal Tract Bleeding



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Cause


Confirmatory Tests


Management


Swallowed maternal blood (bleeding on the first day)


Same as above.


Same as above.


NEC


Same as above.


Same as above.


Coagulopathy


Same as above.


Same as above.


Nasogastric trauma


Same as above.


Same as above.


GI tract anomaly such as volvulus, malrotation, Hirschsprung’s disease, Meckel’s diverticulum


Same as above.


Same as above.


Stress gastritis


Same as above.


Same as above.


Drug-induced


Same as above.


Same as above.


Milk protein allergy



  • Can occur with cow’s milk based formulas
  • ∼50% of infants who have milk protein allergy will cross react with soy formulas


  • Change to an elemental formula will cause resolution of symptoms, and can be diagnostic

Anal fissure



  • Careful examination of the anal opening may reveal a superficial tear


  • No specific therapy
  • Topical application of petroleum jelly may aid in healing

Bleeding varices from end-stage liver disease


Same as above.


Same as above.






  • Serial hematocrits can be followed to track the severity of blood loss.
  • Transfuse PRBCs as indicated (see Chapter 37 chapter for further information).
  • Direct visualization with endoscopy may have to be undertaken to evaluate and possibly treat the cause of bleeding.




Gastroesophageal Reflux Disease (GERD)



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  • GER is defined as passage of gastric contents into the esophagus.
  • GER is very common in term and preterm neonates.
  • A very large majority of infants exhibit no signs of clinical compromise and hence do not warrant specific treatment (GER) vs. infants who experience feeding difficulties, poor weight gain, failure to thrive, etc as a direct result of reflux (GERD).
  • For infants who have persistent “spitting up,” care must be taken to ensure that there is no true underlying pathology as a cause.
  • Apnea and GER are common occurrences in premature infants, but studies have shown no temporal relationship between the two.




Risk Factors




  • Congenital diaphragmatic hernia
  • Esophageal atresia repair
  • Gastroschisis
  • Omphalocele
  • Short bowel syndrome (SBS)
  • Bronchopulmonary dysplasia
  • Neurologic deficits




Differential Diagnosis




  • Differential diagnosis for GER should include:

    • GI tract anatomic abnormalities: Esophageal webs or stenosis, duodenal web or stenosis, malrotation, gastric outlet obstruction
    • Inborn errors of metabolism
    • Renal dysfunction
    • Neurologic deficits
    • Bronchopulmonary dysplasia




Clinical Presentation




  • Dysphagia
  • Odynophagia
  • Arching of the back with feeds
  • Irritability
  • Failure to thrive
  • Hematemesis




Management




  • Initial management should be aimed at nonpharmacologic maneuvers (eg, GERD precautions):

    • Positioning of the infant with the head of the bed elevated.
    • Changing the rate of feeding (slow rate of bolus feeds to 60-90 minutes, feed less volume more frequently).
    • Consider thickening feeds with commercially available thickeners.
    • Discontinuation of caffeine for apnea of prematurity may ameliorate symptoms of GER.

  • Pharmacologic therapy can be used if the above measures fail, but data on efficacy in this patient population are very limited.

    • Use of H2 blockers or PPIs to decrease gastric acid release have been reported with mixed results
    • Use of promotility agents is not advocated because of potentially serious side effects (eg, Parkinsonian reaction and tardive dyskinesia with the use of metoclopramide, may not be reversible).
    • Infants with severe symptoms as above have GERD.
    • Infants with GERD often have true esophagitis or gastritis and have been shown to benefit from gastric acid reduction.

  • Surgical intervention with fundoplication may be considered for infants who fail to respond to pharmacologic therapy and continue to display signs of GERD.




Indirect (Unconjugated) Hyperbilirubinemia



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  • 25%–50% of term neonates and a larger percentage of preterm neonates will develop clinical jaundice.
  • Clinical exam is not a reliable tool to estimate serum bilirubin level.
  • The major source of bilirubin is from the breakdown of hemoglobin in the RES.
  • Bilirubin is also produced from other heme-containing proteins in the peripheral tissues (eg, cytochromes, myoglobin)
  • Bilirubin, a nonpolar, water-insoluble molecule, is transported to the liver cells bound to serum albumin.

    • The bound form of bilirubin is unable to cross into the CNS.
    • Any factors that increase the free fraction (unbound form) of bilirubin potentially increase the amount of bilirubin that is able to cross into the CNS (ie, hypoalbuminemia, drugs, acidosis).

  • On arrival to the hepatocyte, bilirubin crosses the plasma membrane bound to the cytoplasmic protein ligandin → transported to the endoplasmic reticulum for conjugation by the enzyme UDPG-T. Inherited deficiencies or polymorphisms of the conjugation enzymes can predispose an infant to developing severe hyperbilirubinemia.
  • Conjugated bilirubin is excreted via the biliary tree into the GI tract, and eventually passed in the stools. A small fraction of conjugated bilirubin is converted back to unconjugated bilirubin via the action of β-glucuronidase, reabsorbed, and sent to the liver for re-conjugation (process of enterohepatic recirculation)
  • The majority of fetal unconjugated bilirubin is cleared via the placenta to the maternal circulation.





eFigure 35-1



Metabolism of bilirubin: (1) catalyzed by heme oxygenase, (2) catalyzed by biliverdin reductase.





Risk Factors for Indirect (Unconjugated) Hyperbilirubinemia



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Major Risk Factors


Minor Risk Factors


Factors that Decrease Risk



  • Predischarge TSB or TcB in high-risk zone
  • Jaundice in the first 24 h
  • Known hemolytic disease
  • GA 35–36 wk
  • Older sibling received phototherapy
  • Cephalhematoma or significant bruising
  • Exclusive breastfeeding (especially with poor feeding or excessive weight loss)
  • East Asian race


  • Predischarge TSB or TcB in high-intermediate-risk zone
  • GA 37–38 wk
  • Jaundice observed before discharge
  • Older sibling with h/o jaundice
  • Macrosomic IDM
  • Maternal age <25 yr
  • Male gender


  • Predischarge TSB or TcB in the low-risk zone
  • GA ≥41 wk
  • Exclusive bottle feeding
  • African American race
  • Hospital discharge >72 h





eFigure 35-2



Bhutani Nomogram: Nomogram for designation of risk (likelihood) of a subsequent bilirubin level exceeding the 95th percentile, based on the hour-specifi c serum bilirubin value, for well newborns at least 36 wk gestation and 2000 g at birth, or 35 wk gestation and 2500 g at birth. Note: These values are NOT to be used to represent the natural history of unconjugated neonatal hyperbilirubinemia. (Reproduced with permission from Hay WW JR, Levin MJ, Sodheimer JM, Deterding RR: Current Diagnosis & Treatment: Pediatrics, 19th ed. New York: McGraw-Hill. Available at www.accessmedicine.com.easyaccess2.lib.cuhk.edu.hk. Copyright © The McGraw- Hill Companies, Inc. All rights reserved.) For more information: Pediatrics 2004;114(1):297 and Pediatrics 1999;103:6.





Physiologic Unconjugated Hyperbilirubinemia




  • Generally, whereas bilirubin peaks in term neonates at 3–4 d, it peaks at 4–5 d in preterm neonates.
  • Physiologic hyperbilirubinemia occurs for several reasons:

    • Increased bilirubin production caused by decreased RBC survival in the neonate compared with adults
    • Increased enterohepatic recirculation caused by ↑ levels of β-glucuronidase and decreased gut motility
    • Decreased hepatic ligandin leading to decreased bilirubin uptake in the liver
    • Decreased UDPG-T activity leading to decreased conjugation of bilirubin
    • Decreased hepatic excretion




Nonphysiologic (Pathologic) Unconjugated Hyperbilirubinemia



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Jan 9, 2019 | Posted by in PEDIATRICS | Comments Off on Gastroenterology
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