GASTROINTESTINAL SYSTEM
C. Developmental Considerations
1. The abdominal wall is less muscular in the infant and toddler, making the abdominal organs easier
to palpate. In the infant, the liver can be palpated 1 to 2 cm below the RCM at the midclavicular line.
2. In younger children, the contour of the abdo- men is protuberant because of immature abdominal musculature. After 4 years of age, the abdomen is no longer protuberant when the child is in a supine position; but, because of lumbar lordosis, the abdo- men remains protuberant when the child stands.
INVASIVE AND NONINVASIVE DIAGNOSTIC STUDIES
There are numerous laboratory and radiologic diagnos- tic studies that are obtained for children with a GI disor- der. Common laboratory abnormalities for liver disease are summarized in Table 7.1. Diagnostic studies com- monly used to determine GI disease are summarized in Table 7.2.
TABLE 7.1 Liver Function Tests
LFT Function Pediatric Reference
Value
Changes With Liver Failure
ALT ALT catalyzes the reversible transfer of an amino group between the amino acid alanine and α-glutamic acid.
<37 IU/L ALT initially increases with cell
destruction. Following cell necrosis, enzyme level peaks and then decreases. It may be an ominous sign if the enzyme level peaks and falls rapidly. ALT is more hepatic specific as compared to AST. Isolated increases are characteristic of hepatitis.
AST AST catalyzes the reversible transfer of the amino group between the amino acid aspartate and α-ketoglutamic acid.
<34 IU/L AST initially increases with cell
destruction. Following cell necrosis, enzyme level peaks and then
decreases. It is an ominous sign if the enzyme level peaks and falls rapidly.
Isolated increases are characteristic of hepatitis.
ALP ALP cleaves phosphates from compounds with a single phosphate group. The hepatic isoenzymes are believed to be largely derived from the epithelium of the intrahepatic bile ducts, rather than from hepatocytes.
Newborn: <310 IU/L 1 mo−1 y: <360 IU/L 1−10 y: <290 IU/L 10−15 y: <400 IU/L
>15 y: <110 IU/L
ALP levels increase with inflammation or obstruction of the hepatobiliary tract.
(continued )
INVASIVE AND NONINVASIVE DIAGNOSTIC STUDIES ■ 535
LFT Function Pediatric Reference
Value
Changes With Liver Failure
GGTP GGTP is an isoenzyme of ALP. GGTP catalyzes the transfer of glutamyl groups among peptidase and amino acids.
<120 IU/L Hepatobiliary causes should be
considered with increased levels.
Significantly increased levels reflect hepatobiliary obstruction, whereas moderately elevated levels may suggest hepatocellular destruction.
Bilirubin Bilirubin is a by-product of the heme portion of the breakdown of the hemoglobin molecule. Fat-soluble bilirubin binds to albumin as indirect bilirubin for transport to the liver.
In the liver, fat-soluble bilirubin is detached from the albumin and conjugated with glucuronic acid, rendering it water soluble. Direct bilirubin is excreted into the hepatic ducts and eventually into the intestinal tract.
Total bilirubin Newborn: 1−12 mg/dL;
Child: 0.2−1.3 mg/dL Direct: 0.1−1.3 mg/dL
Indirect: 0.1−1.3 mg/dL
Increased indirect bilirubin levels occur as the liver is unable to conjugate the bilirubin with impaired synthetic function or in the presence of an excessive load of bilirubin in cases of hemolysis. Impaired excretion of direct bilirubin into the bile ducts or biliary tract results in increased levels of direct bilirubin with increased amounts absorbed into the blood.
Impaired synthetic function and obstruction increase total bilirubin levels.
PT PT is the laboratory measure of the time for a fibrin clot to form after tissue thromboplastin (factor III) and calcium are added to the sample. PT allows for clinical evaluation of the extrinsic clotting cascade.
10.5−13.5 sec A prolonged PT reflects poor utilization of vitamin K due to parenchymal disease or low levels of vitamin K due to obstructive jaundice. With clinical hepatic failure, the failure of the PT to respond after the administration of IV vitamin K reflects significant parenchymal injury.
Albumin Albumin is the major circulating plasma protein responsible for maintaining plasma oncotic pressure. Albumin levels reflect a component of liver synthetic function.
3.8−5.4 mg/dL The half-life of albumin is 21 days;
therefore, hypoalbuminemia is present with chronic hepatic failure. Interpret with caution, as protein intake and albumin administration may alter the albumin level.
Ammonia Ammonia is formed from the deamination of amino acids during protein metabolism and is a by-product of the breakdown of colonic bacteria proteins.
Newborn: 50−84 mcg/
dL
Child: 12−38 mcg/dL
Increased ammonia levels reflect decreased synthetic function. Elevated ammonia levels can occur in the presence of acute or chronic hepatic failure. Elevated ammonia levels may alter neurologic status.
ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGTP, γ-glutamyl transpeptidase;
LFT, liver function test; PT, prothrombin time.
Source: Adapted from Martin, S. A. (1992). The ABCs of pediatric LFTs. Journal of Pediatric Nursing, 18(5), 445−449.
TABLE 7.1 Liver Function Tests (continued)
TABLE 7.2 Common Diagnostic Studies for GI Disorders
Procedure Purpose Disorder
Abdominal x-ray Flat plate
Cross table lateral Lateral decubitus
Evaluate organ size, position, gas patterns, air−fluid levels, presence of free air, position of NG or NJ tube
Bowel obstruction, perforation, ileus, NEC
Fluoroscopy
Barium swallow Examine the integrity of the esophagus,
diagnoses structural abnormalities Esophageal or strictures, GE reflux
Upper GI series Examine the esophagus, stomach,
and duodenum; diagnose structural abnormalities; delayed gastric emptying
Upper GI with small bowel
follow-through Same as upper GI with follow-up films of
esophagus to small intestine Small bowel disorders, malrotation, small bowel structure
Endoscopy
Flexible upper endoscopy Directly visualize upper GI mucosa, diagnose lesions, determine source of bleeding
Esophageal varices, severe gastritis
Endoscopic retrograde
cholangiopancreatography Directly visualize the biliary and pancreatic
ducts Pseudocyst, gallstones,
pancreatitis Flexible colonoscopy Directly visualize mucosa of large intestine,
diagnose mucosal injury, bleeding source Polyp, inflammatory bowel disease
Biopsy
Percutaneous liver biopsy Obtain liver specimens Biliary atresia, hepatitis Nuclear scans
HIDA scan Determine liver excretory function Biliary atresia
Meckel scan Evaluate location of bleeding (radioactive
isotope is taken up by parietal cells) Meckel’s diverticulum Other scans
Abdominal ultrasound Visualize organ structure, suspected appendicitis, intussusception, pyloric stenosis
Liver disease, trauma in unstable child (FAST scan), pancreatitis
Abdominal CT scan with contrast Evaluate for vascular disorders; definitive imaging of solid organs; evaluate for infection, abscess, traumatic injury, appendicitis
Organ trauma, liver disease, pancreatitis, pseudocyst
MRI Definitively image abdominal organs in
stable child Hepatic hemangioma, hepatic
AVM, appendicitis
AVM, arteriovenous malformation; FAST, focused abdominal sonography for trauma; GE, gastroesophageal; GI, gastrointestinal;
HIDA, hepatobilliary iminodiacetic acid; NEC, necrotizing enterocolitis; NG, nasogastric; NJ, nasojejunal.
Source: Modified from Simone, S. (2001). Gastrointestinal critical care problems. In M. A. Q. Curley & P. A. Moloney-Harmon (Eds.), Critical care nursing of infants and children (2nd ed., pp. 765–804). Philadelphia, PA: WB Saunders.
PHARMACOLOGY ■ 537
PHARMACOLOGY A. Antibleeding Agents
1. Vasopressin (Pitressin; Taketomo, Hodding, &
Kraus, 2015)
a. Action. Vasopressin is a nonselective, short- acting vasoconstrictor. It decreases splanchnic blood flow and portal hypertension.
b. Uses. Used to treat acute massive GI hemorrhage.
c. Dosage. Continuous intravenous (IV) infu- sion. Initial 0.002 to 0.005 units/kg/min; double as needed every 30 minutes to a maximum of 0.01 units/kg/min. If bleeding stops for 12 hours, taper the infusion off over 24 to 48 hours.
d. Side effects include hypertension, brady- cardia, arrhythmias, wheezing, bronchospasm, abdominal cramping, vomiting, water intoxi- cation, decreased urine output, hyponatremia, decreased platelet count, and hemorrhage.
2. Octreotide Acetate (Sandostatin; Taketomo et al., 2015) a. Action. Decreases splanchnic blood flow;
inhibits gastrin synthesis and gastric acid output.
b. Uses. Used to treat GI hemorrhage and intractable diarrhea. This agent has been used for the treatment of chylothorax. Sandostatin is used when conservative treatment fails.
c. Dosage. Administer 1 to 2 mcg/kg IV bolus;
infusion rate 1 to 2 mcg/kg/hr IV for GI hemor- rhage, titrating the rate to response. Continuous IV infusion following a bolus dose of 1 mcg/
kg followed by 1 mcg/kg/hr. Dosage of 1 to 10 mcg/kg every 12 hours (IV, subcutaneous [SC] administration) is used for intractable diar- rhea. Dose reductions are recommended for patients with renal failure.
d. Side effects include bradycardia, chest pain, hypertension, abdominal pain, nausea, diarrhea, headache, fat malabsorption, hypoglycemia or hyperglycemia, hypothyroidism, and possible ana- phylactic shock. The incidence of gallstones and biliary sludge is approximately 33% in children receiving the medication for more than 12 months.
3. Vitamin K1, Phytonadione (AquaMEPHYTON, mephyton; Taketomo et al., 2015)
a. Action. Provides vitamin K activity and can be used as a cofactor in the liver synthesis of clotting factors II, VII, IX, and X; however, the mechanism of stimulation is unknown.
b. Uses. Prevents and treats hypoprothrombin- emia caused by malabsorption, drug- or antico- agulant-induced vitamin K deficiency.
c. Dosage. Note: Dosing presented is for GI- specific diseases for which supplementation is needed and is based on international normalized ratio (INR).
i. Biliary atresia. Infants 1 to 6 months old: INR more than 1.2 to 1.5: 2.5 mg PO QD (orally every day). INR more than 1.5 to 1.8 initial 2 to 5 mg intramuscular (IM) once fol- lowed by 2.5 mg PO once daily. INR more than 1.8 initial 2 to 5 mg IM followed by 5 mg PO once daily.
ii. Cholestasis. Infants, child, and adoles- cents: administer 2.4 to 15 mg/d PO.
iii. Liver disease. Infants, child and adolescents: administer 2.5 to 5 mg/d PO.
d. Side effects include a transient flushing reaction, rare hypotension, hypertension, rare dizziness, rash, and urticaria. U.S. boxed warn- ing: Severe reactions resembling anaphylaxis have occurred during and immediately after IV administration. IV administration should be used when other routes of administration are not feasible and the benefits outweigh the risks.
B. Antiulcer/Gastroesophageal Reflux Disease