Gastrointestinal System

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GASTROINTESTINAL SYSTEM

Sarah A. Martin

DEVELOPMENTAL ANATOMY OF THE GASTROINTESTINAL SYSTEM

A. Embryologic Development of the Digestive Tract (Figure 7.1)

1. The digestive tract develops from the primitive gut, which differentiates into the foregut, midgut, and hindgut by the fourth week of gestation (Little, 2015).

a. Foregut. The foregut consists of the pharynx, esophagus, stomach, proximal duodenum, liver, pancreas, gallbladder, and extrahepatic bile ducts.

b. Midgut. The midgut consists of the distal duodenum, jejunum, ileum, cecum, appendix, ascending colon, and proximal part of transverse colon.

c. Hindgut. The hindgut consists of the remainder of the colon and rectum.

2. The esophagus and trachea are a single tube until the fourth week of gestation, at which time the tracheoesophageal septum begins to separate the structures.

FIGURE 7.1 Primitive gut.

Source: From Kenner, C., & Lott, J. W. (Eds.). (2014). Comprehensive neonatal nursing (5th ed., p. 18). New York, NY: Springer Publishing.

3. Development of the gut is nearly complete by week 20 of gestation.

DEVELOPMENTAL PHYSIOLOGY OF THE GASTROINTESTINAL SYSTEM

A. Gastric Activity

1. Gastric motility in infants is decreased and somewhat irregular compared with the adult due to delayed maturation of feedback control mechanisms, delayed gastric emptying, and immature coordination of contractions between the antrum of the stomach and the duodenum.

2. Gastroesophageal reflux (GER) is common during the first year because of a complex set of factors, including pressure−volume changes and anatomic relationships causing inappropriate relaxation of the lower esophageal sphincter (LES).

B. Immature Neonatal Liver

The liver matures in function during the first year of life. Toxic substances are inefficiently detoxified.

ANATOMY AND PHYSIOLOGY OF THE GASTROINTESTINAL SYSTEM

A. Structure and Function (Figure 7.2)

1. Oral Cavity. The oral cavity serves as a reservoir for chewing and mixing food with saliva. Salivary glands include the submandibular, sublingual, and parotid glands. Saliva is composed of water, small amounts of mucus, sodium bicarbonate, chloride, potassium, and amylase. Amylase begins carbohydrate digestion.

2. The esophagus propels swallowed food to the stomach. The upper esophageal sphincter prevents air from entering the esophagus during respiration. The LES closes after swallowing to prevent reflux of gastric contents into the esophagus.

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FIGURE 7.2 Gastrointestinal structures.

Source: Reprinted with permission from Jacob, S. W., & Francone, C. A. (1989). Elements of anatomy and physiology (2nd ed.). Philadelphia, PA: W. B. Saunders.

3. Stomach

a. The stomach is a hollow, muscular organ that acts as a reservoir for ingested food. It secretes digestive juices that mix with digested food (chyme). Parietal cells secrete hydrochloric acid and intrinsic factor. Intrinsic factor is a glycoprotein that is required for vitamin B₁₂absorption. The secretion is regulated by stimuli (i.e., H₂-histamine receptors). Chief cells secrete pepsinogen, which combines with hydrochloric acid to break down protein.

b. Gastric emptying is affected by the volume of food, osmotic pressure, and chemical composition of the contents. Emptying is controlled by the pyloric sphincter. Delayed emptying is caused by foods with high fat content, solid foods, sedatives, sleep, and specific hormones (i.e., secretin and cholecystokinin). Accelerated emptying is caused by foods with high carbohydrate content, liquids, increased volume, and medications (e.g., metoclopramide, erythromycin ethylsuccinate [EES], and azithromycin [zithromax]).

4. The small intestine is the primary site for digestion and absorption of fats, amino acids, proteins, carbohydrates, and vitamins. The small intestine is anatomically adapted to increase surface digestion and absorption due to folds of mucosa lined with villi and the brush-border membrane. The brush border contains digestive enzymes and contributes to the transfer of nutrients and electrolytes. The epithelial absorptive cells are called enterocytes. Glutamine (amino acid) stimulates the proliferation of enterocytes. The gastrointestinal (GI) tract continuously renews the cells lining its surface.

a. The duodenum is the primary site for the absorption of iron, trace metals, and water-soluble vitamins.

b. The jejunum is the principal absorption site for proteins and sugar carbohydrates. Ninety percent of nutrients and 50% of water and electrolytes are absorbed here.

c. The ileum is responsible for absorption of bile salts and vitamin B₁₂. The ileocecal valve controls the entry of digested material from the ileum into the large intestine and prevents reflux into the small intestine. Digestion in the ileum continues by the action of pancreatic enzymes, intestinal enzymes, and bile salts. Carbohydrates are broken down into monosaccharides and disaccharides and are absorbed by villous capillaries. Proteins are degraded to peptides and amino acids and are absorbed by villous capillaries. Fats are emulsified and reduced to fatty acids and monoglycerides.

5. Large Intestine. The anatomic segments of the colon or large intestine include the cecum, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum. Water and electrolytes are reabsorbed in the descending colon. Feces are stored 533in the rectum. The greatest growth of anaerobic and gram-negative aerobic bacteria is in the ascending colon. Bacteroides fragilis (anaerobic) and Escherichia coli (aerobic) play a role in metabolizing bile salts and synthesizing vitamins.

6. Pancreas. The pancreas’s exocrine function is to secrete bicarbonate and enzymes (e.g., amylase, lipase) for digestion and absorption of fats, carbohydrates, and proteins. The pancreas’s endocrine function involves islet cells, which function in glucose homeostasis by synthesizing and secreting insulin.

7. Liver

a. Liver functions include the following:

i. Formation of clotting (coagulation) factors I, II, V, VII, IX, X, and XI

ii. Synthesis of plasma proteins (albumin, fibrinogen, and 60%−80% of globulins)

iii. Synthesis and transportation of bile (bile salts, pigment, and cholesterol)

iv. Storage of glycogen, fat, and fat-soluble vitamins

v. Metabolism of fats, carbohydrates, and proteins

vi. Metabolism and deactivation of bilirubin, ammonia, and many toxins by oxidation or conjugation reactions

b. Three fourths of the blood supply to the liver is supplied by the portal venous system (blood rich in nutrients) and one fourth by the hepatic artery (blood rich in oxygen).

c. Nutrients are absorbed from the GI tract and transported by either the portal or lymphatic circulation. The lymphatic system plays a pivotal role in transporting lipid-soluble substances.

8. Biliary Tree and Gallbladder. The biliary tree serves as the conduit for bile flow from the liver to the duodenum. The gallbladder provides a storage and concentration site for bile.

9. Splanchnic Circulation. The splanchnic circulation supplies blood to the stomach, small intestine, and colon. It receives one fourth of the body’s cardiac output. The major arterial branches are the celiac, superior mesenteric, and inferior mesenteric. Venous drainage from the stomach, pancreas, small intestine, and colon flows to the portal vein to the liver and then to the heart through the hepatic vein and inferior vena cava.

B. Regulation of Fluid and Electrolyte Movement

1. Large volumes of water, electrolytes, proteins, and bile salts are secreted and reabsorbed throughout the GI tract, resulting in massive fluid and electrolyte shifts.

2. Fluid and electrolyte movement occur concurrently with digestion and absorption of nutrients.

CLINICAL ASSESSMENT OF THE GI SYSTEM

A. General Principles of Abdominal Assessment

Examination of the abdomen can be difficult in a child. A frightened child will not cooperate with the examination. A child suffering from multisystem trauma will be unable to localize pain. The preferred order of assessment is inspection, auscultation, palpation, and percussion.

B. Abdominal Examination Assessment Techniques

1. Inspection. Evaluate for size, contour, symmetry, integrity, visible peristalsis, umbilicus, masses, and wounds. Underdeveloped abdominal musculature in children allows easier visualization of masses and fluid waves. Abdominal distention (the abdomen is normally rounded in infants and toddlers) is the hallmark sign of obstruction.

2. Auscultation

a. Determine the absence, presence, and character of peristalsis or bowel sounds (borborygmi). Bowel sounds are absent in paralytic ileus and peritonitis. A venous hum heard over the upper area of the abdomen suggests portal obstruction. A bruit (caused by turbulent blood flow through a partially occluded artery) suggests abnormal blood flow caused by an arteriovenous malformation (AVM) or aneurysm. High-pitched or hyperactive bowel sounds suggest an obstruction.

b. Bowel sounds should be heard every 5 to 30 seconds. Listen to all four quadrants for a few minutes to confirm the presence or absence of bowel sounds.

3. Palpation. Begin with light palpation and assess for guarding and tenderness. Consider using the diaphragm of your stethoscope with a focus on the child’s face when palpating to asses for pain. With deep palpation, assess for abdominal tone, masses, 534pulsations, fluid, and organ enlargement. The liver is normally palpated at the right costal margin (RCM) or is nonpalpable. Palpation should be started by the iliac crest to ensure hepatomegaly is appreciated. The spleen is not normally palpable.

4. Percussion. Percussion is used to estimate the size of organs and aids in the diagnosis of ascites, obstruction, and peritonitis. Assess for abdominal distention, fluid, masses, or organ enlargement. Percussion of solid organs (liver and spleen) and ascites elicits dullness. Absence of dullness over the liver may be found with free air in the abdomen secondary to perforation. The stomach is tympanic when empty. Depending on contents, the intestines’ tone is hyperresonant to tympanic.

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.

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2. In younger children, the contour of the abdomen 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 abdomen remains protuberant when the child stands.

INVASIVE AND NONINVASIVE DIAGNOSTIC STUDIES

There are numerous laboratory and radiologic diagnostic studies that are obtained for children with a GI disorder. Common laboratory abnormalities for liver disease are summarized in Table 7.1. Diagnostic studies commonly used to determine GI disease are summarized in Table 7.2.

536TABLE 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.

537PHARMACOLOGY

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) infusion. 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, bradycardia, arrhythmias, wheezing, bronchospasm, abdominal cramping, vomiting, water intoxication, 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 hemorrhage, 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 diarrhea. 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 anaphylactic 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 hypoprothrombinemia caused by malabsorption, drug- or anticoagulant-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 followed 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 adolescents: 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 warning: 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 Agents

1. Cimetidine (Tagamet; Slaughter, Stenger, Reagan, & Jadcherla, 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. A histamine-2 receptor antagonist (H₂ blocker) that decreases the secretion of acid.

b. Uses. Used for short-term treatment of active duodenal ulcers and gastric ulcers, gastroesophageal reflux disease (GERD), or for long-term prophylaxis and prevention of upper GI tract bleeding.

c. Dosage. Neonate: administer 5 to 10 mg/kg daily PO in divided doses every 6 to 12 hours. Infant: administer 10 to 20 mg/kg daily PO in divided doses every 6 to 12 hours. Child: administer 20 to 40 mg/kg daily PO in divided doses every 6 hours. Dose reductions are recommended for patients with renal impairment.

d. Side effects include bradycardia, tachycardia, hypotension, diarrhea, nausea, vomiting, dizziness, headache, agitation, gynecomastia, 538elevated serum creatinine, elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT), neutropenia, pancytopenia, and thrombocytopenia.

e. Additional warnings. The use of H₂ blockers and proton-pump inhibitors (PPIs) has been associated with increased incidence of gastroenteritis and community-acquired 539pneumonia in children (Stark & Nylund, 2016). In neonates, there is an associated increased incidence of infectious complications and necrotizing enterocolitis (NEC; Slaughter et al., 2016).

2. Ranitidine (Zantac; Slaughter et al., 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. A histamine-2 receptor antagonist that decreases the secretion of acid.

b. Uses. Used for short-term treatment of active peptic ulcer disease, GERD, or long-term prophylaxis and prevention of hypersecretory states and bleeding.

c. Dosage. GI bleed or stress ulcer prophylaxis. Infant: administer 2 to 6 mg/kg daily via IV divided every 8 hours. Child and adolescents: administer 3 to 6 mg/kg daily via IV, divided every 6 hours, for a maximum of 300 mg daily; 0.15 to 0.5 mg/kg/dose for one dose followed by 0.08 to 0.2 mg/kg/hr continuous IV infusion. GERD dosing is 5 to 10 mg kg/d divided twice daily; maximum daily dose is 300 mg daily. Dose reduction is recommended for patients with renal impairment.

d. Side effects include bradycardia (rapid IV administration), tachycardia, agitation, headache, dizziness, nausea, vomiting, elevated serum creatinine, hepatitis, arthralgia, leukopenia, and thrombocytopenia.

e. Additional warnings. The use of H₂ blockers and PPIs has been associated with increased incidence of gastroenteritis and community-acquired pneumonia in children (Stark & Nylund, 2016). In neonates, there is an associated increased incidence of infectious complications and NEC (Slaughter et al., 2016).

3. Famotidine (Pepcid; Slaughter et al., 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. A histamine-2 receptor antagonist that decreases the secretion of acid.

b. Uses. Used in therapy and treatment of peptic ulcer disease, GERD, and hypersecretory states.

c. Dosage. GERD: In infants, administer 0.5 to 1 mg/kg daily PO up to 8 weeks or 0.25 to 0.5 mg/kg daily via IV. In children and adolescent dosing is 0.25 to 0.5 mg/kg/dose every 12 hours up to 20 mg/dose. Stress ulcer prophylaxis: In infants, children, and adolescents, administer 0.5 to 1 mg/kg/dose every 12 hours, with a maximum dose of 20 mg/dose. Dose reductions are recommended for patients with renal impairment.

d. Side effects include arrhythmias, tachycardia, headache, dizziness, constipation, diarrhea, thrombocytopenia, and pancytopenia.

4. Omeprazole (Prilosec; Slaughter et al., 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. PPI; direct inhibitor of hydrochloric acid secretions at the cellular level. It demonstrates antimicrobial activity against Helicobacter pylori.

b. Uses. Used for short-term treatment (4−8 weeks) of severe erosive esophagitis and severe GERD and duodenal ulcer disease associated with H. pylori.

c. Dosage. GERD: In infants, administer 0.7 mg/kg/dose daily PO; for children greater than or equal to 1 year and adolescents 5 kg to less than 10 kg, administer 5 mg Q day PO; 10 kg to less than 20 kg, 10 mg Q day PO; greater than or equal to 20 kg, 20 mg Q day PO; Erosive esophagitis: 5 kg to less than 10 kg, administer 5 mg Q day PO; 10 kg to less than 20 kg, 10 mg Q day PO; greater than or equal to 20 kg, 20 mg Q day PO. H. pylori eradication: administer 1 to 2 mg/kg/d divided into two doses; maximum single dose of 20 mg. The capsule form of the medication is a sustained-release capsule. The capsule can be opened and the beads mixed with an acidic medium such as 1 tablespoon of applesauce. The tablets of medication should not be crushed. The manufacturer suggests using the suspension for administration in a nasogastric (NG) tube.

d. Side effects include bradycardia, tachycardia, nausea, diarrhea, abdominal cramps, headache, dizziness, skin rash, elevated liver enzymes, hypomagnesemia, proteinuria, skin rash, and thrombocytopenia.

5. Pantoprazole (Protonix; Slaughter et al., 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. In PPI, pantoprazole is a direct inhibitor of hydrochloric acid secretions at the cellular level. This PPI more directly inhibits acid secretion compared with other PPIs. It demonstrates antimicrobial activity against H. pylori.

b. Uses. Used to treat GERD (Food and Drug Administration [FDA] approved in ages ≥5 years), pathological hypersecretory conditions, and as an adjunct to duodenal ulcer treatment associated with H. pylori.

c. Dosage. GERD: Infants and children younger than 5 years, administer 1.2 mg/kg/d daily for 4 weeks; children 5 to 11 years, 20 or 40 mg PO daily; children and adolescents, 20 or 40 mg once daily. For gastric acid suppression when PO administration is not appropriate or tolerated, the dose is 0.8 or 1.6 mg IV once daily, maximum dose 80 mg.

d. Side effects include hypotension, hypertension, headache, urticaria, pruritus, hyperglycemia, hypermagnesemia, nausea, vomiting, diarrhea, constipation, urinary frequency, elevated liver enzymes, elevated triglyceride levels, cough, and dyspnea. Anaphylaxis has been reported with IV administration.

6. Lansoprazole (FIRST-Lansoprazole; Slaughter et al., 2016; Stark & Nylund, 2016; Taketomo et al., 2015)

a. Action. PPI; acts as a direct inhibitor of hydrochloric acid secretion at the cellular level.

b. Uses. For short-term treatment of symptomatic GERD (up to 8 weeks; FDA approved for ≥1 year); for duodenal ulcer treatment associated with H. pylori, erosive esophagitis, and hypersecretory conditions.

c. Dosage. GERD: Infants 1 to 2 mg/kg/d for weight-based dosing; for fixed dosing in infants older than 3 months, administer 7.5 mg twice a day or 15 mg daily; children 1 to 11 years who weigh less than or equal to 30 kg, 15 mg daily for up to 12 weeks; children greater than 30 kg, 30 mg daily for up to 12 weeks; children 12 years or older, 15 mg once daily for up to 8 weeks.

d. Side effects include hypertension, hypotension, nausea, dyspepsia, abdominal pain, diarrhea, constipation, elevated liver enzymes, dizziness, and headache.

7. Sucralfate (Carafate; Taketomo et al., 2015)

a. Action. Gastric protectant; paste formation and ulcer adhesion occur within 1 to 2 hours of administration and last up to 6 hours.

b. Uses. Used for short-term management of duodenal ulcers and gastritis; typically may be used for esophageal, gastric, and rectal erosions.

c. Dosage. Dose is not established; administer 40 to 80 mg/kg/d PO in divided doses every 6 hours. Administer 1 hour before meals or on an empty stomach.

d. Side effects include constipation and rarely, anaphylaxis, bezoar formation, and hypersensitivity. Decreased absorption of concurrently administered drugs may occur. Safety and efficacy in children have not been established.

8. Calcium Carbonate (Maalox; Taketomo et al., 2015)

a. Action. Maalox is an antacid that neutralizes gastric acid.

b. Uses. Provides symptomatic relief for peptic ulcer, gastritis, esophagitis, hiatal hernia, and treatment of hyperphosphatemia in end-stage renal failure.

c. Dosage. In children 2 to 5 years, administer one tablet (400 mg calcium carbonate) as symptoms occur (not to exceed 3 tablets/d); children older than 5 years to 11 years, two tablets (800 mg) as symptoms occur (not to exceed 6 tablets/d); children older than 11 years, two to four tablets as symptoms occur (not to exceed 15 tablets/d).

d. Side effects include headache, laxative effect, hypercalcemia, and hypophosphatemia.

540C. Prokinetics

1. Metoclopramide (Reglan; Taketomo et al., 2015)

a. Action. A potent dopamine receptor antagonist that blocks dopamine receptors in the chemoreceptor trigger zone, preventing emesis; accelerates gastric emptying and intestinal transit time.

b. Uses. For GERD, prevention of postoperative and chemotherapy-related nausea and vomiting, assist with postpyloric feeding tube placement, and diabetic gastroparesis.

c. Dosage. Postpyloric feeding tube placement: In children younger than 6 years, administer 0.1 mg/kg once; 6 to 14 years, give 2.5 to 5 mg as a single dose; and older than 14 years, administer 10 mg as a single dose. GERD: In infants, children, and adolescents, administer 0.1 to 0.2 mg/kg/dose every 6 to 8 hours with a maximum dose of 10 mg.

d. Side effects include extrapyramidal reactions, seizures, hypertension, hypotension, atrioventricular block, constipation, diarrhea, neutropenia, and leukopenia.

2. Erythromycin (E.E.S.; Taketomo et al., 2015)

a. Action. Works as a motilin receptor agonist and increases LES tone.

b. Uses. A macrolide antibiotic that can be used as a prokinetic agent.

c. Dosage. In children, an initial dose of 3 mg/kg QID (four times a day) PO.

d. Side effects include QTc prolongation, ventricular arrhythmias, bradycardia, skin rash, abdominal pain, nausea, vomiting, diarrhea, eosinophilia, and cholestatic jaundice.

D. Antidiarrheal Agents

1. Imodium (Loperamide; Taketomo et al., 2015)

a. Action. Acts directly on the intestinal muscles through the opioid receptor to inhibit peristalsis and transit time. The drug reduces stool volume, causes decreased fluid and electrolyte losses, and demonstrates antisecretory activity.

b. Uses. Used for treatment of acute diarrhea (FDA approved in children ≥2 years) although manufacturer recommends avoiding use in children younger than 2 years as acute enteritis often necessitates treatment of fluid and electrolyte imbalances; for chronic diarrhea associated with inflammatory bowel disease and intestinal failure, and to decrease volume of ileostomy output.

c. Dosage. Acute diarrhea: In children 2 to 5 years weighing 13 to less than 21 kg, a dose of 1 mg after each subsequent loose stool, with dose repeated for each subsequent stool for a maximum of 3 mg/d; children 6 to 8 years weighing 21 to 27 kg, administer 2 mg for first loose stool, with 1 mg/dose repeated for each subsequent stool for a maximum of 4 mg/d; children 9 to 11 years weighing 27.1 to 43 kg, administer 2 mg for first loose stool, with 1 mg/dose repeated for each subsequent stool for a maximum of 6 mg/d; children older than 12 years, 4 mg for first loose stool, with 2 mg/dose repeated for each subsequent stool for a maximum of 8 mg/d. For chronic diarrhea related to intestinal failure or other noninfectious causes, larger doses are generally needed. Dosing initial 1 to 1.5 mg/kg/d in four divided doses with final dose range up to 0.5 mg/kg BID (twice a day).

d. Side effects include dizziness, abdominal cramping, and constipation.

2. Clonidine (Catapres; Fragkos, Zárate-Lopez, & Frangos, 2016; Taketomo et al., 2015)

a. Action. Stimulates α₂-adrenoreceptors in the brainstem resulting in decreased sympathetic outflow.

b. Uses. Use to decrease GI losses in children with stomas related to the constipating side effect of the medication. Other more established uses include treatment of hypertension and use for withdrawal prophylaxis.

c. Dosage. For GI use, patches have been used in dosing of 0.1 to 0.3 mg/24 hr with patches changed weekly.

d. Side effects include hypotension, cardiac arrhythmia, agitation, constipation, diarrhea, and abnormal hepatic function tests.

E. Other Agents

1. Lactulose (Cephulac; Taketomo et al., 2015)

a. Action. Hyperosmotic laxative; ammonia detoxicant.

b. Uses. Used to prevent and treat portal-systemic encephalopathy. This treatment is controversial because the benefit of this therapy can be diminished relative to potential fluid and electrolyte disturbances.

c. Dosage. For infants, administer 2.5 to 10 mL/d PO divided three or four times per day. In children, 40 to 90 mL/d PO divided 541three to four times per day. Adjust dosage to produce two to three stools per day.

d. Side effects include abdominal discomfort, diarrhea, nausea, and vomiting.

2. Magnesium Hydroxide (Milk of Magnesia; Taketomo et al., 2015)

a. Action. An antacid that can be used as a cathartic or laxative for constipation.

b. Uses. Used for bowel evacuation and treatment of hyperacidity.

c. Dosage. When used as a laxative in children ages 2 to 5 years, administer 5 to 15 mL/d PO or in divided doses. In children ages 6 to 12 years, administer 15 to 30 mL/d PO or in divided doses. As an antacid, administer 2.5 to 5 mL PO as needed.

d. Side effects include hypotension, diarrhea, respiratory depression, and hypermagnesemia.

3. Polyethylene Glycol-Electrolyte Solution (GoLYTELY; Taketomo et al., 2015)

a. Action. Induces catharsis with strong electrolyte and osmotic effects.

b. Uses. Used as a bowel preparation for procedures and for treatment of constipation.

c. Dosage. For bowel preparation, 25 mL/kg/hr PO/NG until rectal effluent is clear.

d. Side effects include metabolic acidosis, potential for electrolyte disturbances, nausea, cramps, and abdominal distension.

4. Polyethylene Glycol 3350 (MiraLax)

a. Action. An osmotic agent, causes water retention in the stool.

b. Uses. Used to treat occasional constipation.

c. Dosage. For infants, children, and adolescents, administer 0.2 to 0.8 mg/kg/d; maximum daily dose of 17 g/d.

d. Side effects include metabolic acidosis, potential for electrolyte disturbances, nausea, cramps, and abdominal distension.

F. Immunosuppressive Therapy

1. Basic Principles. Combination therapy is used to maximize therapeutic benefit of agents while minimizing associated toxicities, including infection and malignancy. Institution of specific protocols and organ-specific therapies exist with goals of therapy to maintain sufficient drug levels to prevent rejection. Combination protocols are used to increase drug efficacy and minimize drug toxicity.

2. Tacrolimus (Prograf; Taketomo et al., 2015)

a. Action. A calcineurin inhibitor that suppresses the synthesis of interleukin-2, the cytokine needed for lymphocyte activation.

b. Dosage. Administer 0.01 to 0.06 mg/kg daily via a continuous IV infusion or 0.10 to 0.3 mg/kg daily PO in divided doses twice a day. Dosing is variable depending on the organ transplanted and may be based on drug levels. Patients with renal or hepatic impairment should receive dosing from the lower end of the dosing ranges.

c. Side effects. With IV use, greater toxicity is observed with a high anaphylaxis risk, including arrhythmias, hypertension, nephrotoxicity, central nervous system (CNS) effects (insomnia, headache, tremor, seizure, paresthesia), hyperkalemia, hypomagnesemia, hyperglycemia, GI tract symptoms, alopecia, and lymphoproliferative disease (LPD).

3. Cyclosporine (Sandimmune; Taketomo et al., 2015)

a. Action. A calcineurin inhibitor that binds to the intracellular protein cyclophilin that inhibits T-cell proliferation through inhibition of interleukin-2 synthesis.

b. Dosage. Note that there are modified and nonmodified formulations of this medication. Nonmodified: administer 2 to 10 mg/kg daily via IV in divided doses every 8 to 24 hours for maintenance; postoperatively, administer 5 to 15 mg/kg daily PO divided every 12 to 24 hours; maintenance dosing is usually 3 to 10 mg/kg/d. Dosing is variable depending on the organ transplanted and may be based on drug levels. The PO dose is approximately three times the IV dose.

c. Side effects include hypertension, nephrotoxicity, CNS toxicity (headache, tremor, seizure, paresthesia), hypomagnesemia, GI tract symptoms, gum hyperplasia, hirsutism, and LPD.

4. Corticosteroids. Methylprednisolone (Solu-Medrol) and Prednisone (Taketomo et al., 2015)

a. Action. An anti-inflammatory agent that depresses the immune system by decreasing T-lymphocytes and monocyte activation.

b. Dosage

i. Methylprednisolone. Administer 0.5 to 1.7 mg/kg daily via IV in divided doses every 6 to 12 hours.

542ii. Prednisone. Administer 0.05 to 2 mg/kg daily PO in divided doses one to four times daily.

c. Side effects include glucose intolerance, hyperglycemia, possible suppression of the hypothalamic−pituitary−axis, peptic ulcers, weight gain, hypertension, hyperlipidemia, sodium and water retention, osteoporosis, infection, abnormal hair growth and thinning, and increased risk of bruising and acne.

5. Mycophenolate Mofetil (Cellcept; Taketomo et al., 2015)

a. Action. An antimetabolite that inhibits T- and B-cell proliferation by inhibiting the inosine monophosphate dehydrogenase pathway, preventing lymphocyte proliferation.

b. Dosage. Administer 600 mg/m²/dose twice daily PO; maximum daily dose of 2,000 mg/d.

c. Side effects include hypertension, headache, rash, nausea, vomiting, dyspepsia, cough, leukopenia, neutropenia, thrombocytopenia, increased malignancy risk, and anemia. Females within child-bearing years must receive counseling on pregnancy risk and have a pregnancy test prior to starting therapy, 2 weeks after starting therapy, and at follow-up visits.

6. Azathioprine (Imuran; Taketomo et al., 2015)

a. Action. Azathioprine is an antimetabolite that inhibits DNA synthesis.

b. Dosage. Initial dose is 3 to 5 mg/kg daily administered either PO or IV. Maintenance is 1 to 3 mg/kg per day taken once daily.

c. Side effects include bone marrow suppression (anemia, leukopenia), hepatotoxicity, pancreatitis, nausea and vomiting, increased malignancy risk, and mucosal ulceration.

NUTRITIONAL CONCEPTS

A. Nutrition Assessment

1. Pediatric Critical Care Best Practices

a. Thirty-one percent of pediatric intensive care unit (PICU) patients in an international point prevalence survey of 31 PICUs were determined to be malnourished (Mehta et al., 2012).

i. Malnourished patients included both underweight and overweight children. There is greater morbidity and mortality in the underweight child as compared to the overweight child.

b. Within 48 hours of admission, children in the PICU should undergo a detailed nutrition assessment, including a detailed dietary history, identification of changes in anthropometry, functional status, and nutrition-focused physical exam (Mehta et al., 2017).

2. Anthropometrics

a. An accurate weight (kg), length (cm), and body mass index should be documented at admission. Serial weight measurement is recommended as weight loss is the best single physical exam indicator of malnutrition risk.

b. A head circumference should be obtained in children younger than 3 years old (Mehta et al., 2017).

c. The z-scores for body mass index should be used to screen for extreme values (weight for length <2 years) or weight for age (if an accurate height is not available; Mehta et al., 2017).

3. Assessment of Energy Needs (kcal/kg/d)

a. Energy requirements are highly individual and vary widely (Verger, 2014).

i. Energy needs are dynamic, changing from a hypermetabolic to hypometabolic state through the trajectory of the PICU stay, largely related to changes in energy consumption and limited energy reserves.

b. The Society of Critical Care Medicine and A.S.P.E.N. recommend assessment of measured energy expenditure (MEE) by indirect calorimetry (IC; Mehta et al., 2017).

c. If IC is not feasible, the Schofield or Food Agriculture Organization/World Health Organization (WHO)/United Nations University equations may be used without the addition of stress factors.

d. Often, the requirement is determined by reference standards based on age for healthy children (Table 7.3), which should not be used for critically ill children.

B. Macronutrient, Micronutrient, and Fluid Requirements

1. Carbohydrate, protein, and fat are the macronutrients.

a. Recommended caloric distribution varies and for carbohydrates is 40% to 70%, protein is 7% to 21%, and for fat is 30% to 55%.

543TABLE 7.3 Daily Estimated Energy Needs for Healthy Infants and Children

Age	kcal/kg/d
Up to 6 months	90−110
6−12 months	80−100
12−36 months	75−90
4−6 years	65−75
7−10 years	55−75
11−18 years	40−55

i. A minimum protein intake of 1.5 mg/kg/d is recommended (Mehta et al., 2017).

ii. For obese patients, this guideline should be based on ideal body weight (Mehta et al., 2017).

b. Diets high in carbohydrates can increase carbon dioxide product and hamper ventilator weaning.

2. Micronutrients include vitamins, minerals, and electrolytes.

3. Fluid requirements vary as a function of age, weight, and clinical condition.

a. Calculation of maintenance fluids is used as a starting requirement for most children.

i. First 10 kg (1−10 kg): 100 mL/kg

ii. Next 10 kg (11−20 kg): 50 mL/kg

iii. Over 20 kg (>20 kg): 20 to 25 mL/kg

iv. For a 10-kg child, the fluid requirement is a 1,000 mL a day, or 40 mL/hr.

C. Enteral Nutrition

1. Enteral route is preferred and should be used if at all possible and determined within 24 to 48 hours of admission (Mehta et al., 2017).

a. Promotes intestinal mucosal structure and gut absorptive and barrier functions (e.g., villi).

b. Is associated with fewer infectious and metabolic complications.

2. Estimated energy needs are greater for enteral feeds as all parenteral nutrition (PN) calories are directly absorbed. Most infants require 100 to 120 kcal/kg/d.

3. Formula Selection

a. Breast milk (BM) is the preferred source of nutrition for infants, nursing mothers should be provided with a breast pump if their infant is on NPO (nothing by mouth) status or cannot breastfeed. Selection of the appropriate formula is based on the patient’s age and disease process (e.g., less protein may be needed in children with liver or renal disease). Premature infants require specialty formulas that are higher in calories per ounce and have additional vitamins and minerals.

4. Formulas have varying caloric density kcal/ounce.

a. Infants require 19 to 20 kcal/ounce, may increase to 24 kcal/ounce, 27 kcal/ounce, or 30 kcal/ounce for fluid restriction or to promote weight gain.

b. Children older than 12 months require 30 kcal/ounce formula.

c. For children younger than 12 months with poor weight gain, consider 45 kcal/ounce.

5. Enteral feeds can be administered orally, through an orogastric (OG)/NG tube, gastrostomy tube, or postpylorically through a gastrojejunostomy or jejunostomy tube.

6. Enteral nutrition is needed if the child has delayed gastric motility, intestinal dysmotility, or inability to tolerate gastric feeds or is at high risk for aspiration.

D. Parenteral Nutrition

1. An IV mixture of macronutrients (carbohydrates [dextrose or glucose], protein, and fat), and micronutrients (electrolytes, minerals, vitamins, and trace elements) for children that are unable to absorb nutrients through the GI tract.

544a. Dextrose provides 3.4 kcal/g and constitutes 60% to 70% of the total PN caloric composition.

b. Protein can be administered as trophamine (recommended for infants younger than 1 year and for children with liver failure), or as clinisol or travasol (for children older than 1 year of age). Protein provides 4 kcal/g and should constitute up to 14% to 20% of the total PN caloric composition.

c. Fat emulsions (intralipid) may be administered as a separate solution to provide a major source of calories (20% solution provides 2 kcal/mL) and should constitute 30% to 50% of the total PN caloric intake. Providing 0.5 g/kg/d prevents essential fatty acid deficiency states.

d. Electrolytes, vitamins, minerals, and trace elements are added to these solutions to meet the child’s known nutritional requirements.

2. PN can be administered through a peripheral or central line.

a. Formulations with a dextrose concentration greater than 12.5% should be administered centrally.

3. Common additives to the PN formulation include heparin, if central access is being used, and Ranitidine, if GI prophylaxis is indicated.

4. PN formulations can be commercial standard solutions or compounded individualized admixtures.

5. With PN, caloric needs are decreased by 10% to 15%, as compared to the enteral route.

6. PN “goals” are generally not achieved for 5 days, as macronutrients should gradually be advanced.

a. Possible alternatives to prescribing PN are to augment the child’s nutrition by using dextrose 10% in water (D10W) and intralipids.

7. The Society of Critical Care Medicine and A.S.P.E.N. recommend not starting PN within the first 24 hours of PICU admission (Mehta et al., 2017). When PN should be initiated is not known and should be individualized and started within the first week of admission if unable to receive enteral nutrition (EN) or for severely malnourished patients or those at risk for nutritional deterioration (Mehta et al., 2017).

8. Complications of PN administration include bacteremia if central line is present, catheter-associated central line infection (central line-associated bloodstream infection [CLABSI]), metabolic derangement, and cholestatic jaundice.

NURSING MANAGEMENT OF TUBES AND DRAINS

A. NG Tube

1. An NG tube can be used for gastric decompression, feeds, fluids administration, and medication administration or for lavage in case of poisonings or GI hemorrhage.

2. The child’s size and indication for NG placement will determine the size and type of tube that should be inserted.

a. Generally, smaller bore nonvented tubes are used for feeding.

b. Tubes used for decompression should not be used for feeds or medication administration as the necessary decompression ports may be too distal in the esophagus to safety administer feeds or medication. Do not tie off or obstruct the vent to prevent the backflow of gastric contents as this will block the vent and negate the function of the sump port.

3. See Table 7.4 for suggested steps for placing an NG tube.

4. Abdominal radiography is the most reliable method of confirming placement of an enteral tube; however, its use to verify enteral tube placement is not widespread in clinical practice due to the necessary radiation exposure (Lyman et al., 2016; Taylor, 2013). Evidence suggests that pH testing of GI secretions is the most accurate nonradiographic means of determining placement of an NG tube, although results are not 100% reliable (Gilbertson, Rogers, & Ukoumunne, 2011). Gastric aspirate has a pH of 5 or less and is usually grassy green or clear and colorless, with off-white to tan shreds of mucus (Irving et al., 2014; Taylor, 2013).

5. Nursing care involves adequately securing the tube to prevent inadvertent dislodgement, verifying position prior to use (if placement is in question radiologic verification is needed), flushing the tube after instilling medications or formula; if the tube is to be placed to suction, low intermittent suction should be used to minimize trauma to the gastric mucosa, recording input and output every 4 hours, and performing oral care every 4 hours.

545TABLE 7.4 Nasogastric Tube Placement

1. Elevate the child’s head of bed as tolerated.

2. To determine the length for nasal placement, measure from the child’s nare, to the tip of the earlobe to midway between the xiphoid process and the umbilicus. For oral placement, the measurement should be started at the mouth.

3. Mark the correct length with an indelible marker or place a piece of tape around the tube.

4. Lubricate the end of the tube with water-soluble lubricant.

5. Insert the tube into the mouth or a patent nare and gently advance the tube. Encourage the child to swallow while inserting the tube.

6. Verify the tube placement by checking gastric pH or obtaining radiologic confirmation if placement is in question.

7. Secure the tube to the child’s face.

Sources: Ellett, M. L. C., Cohen, M. D., Perkins, S. M., Croffie, J. M. B., Lane, K. A., & Austin, J. K. (2012). Comparing methods of determining insertion length for placing gastric tubes in children 1 month to 17 years of age. Journal for Specialists in Pediatric Nursing, 17(1), 19−32. doi:10.1111/j.1744-6155.2011.00302.x; Ellett, M. L. C., Cohen, M. D., Perkins, S. M., Smith, C. E., Lane, K. A., & Austin, J. K. (2011). Predicting the insertion length for gastric tube placement in neonates. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 40(4), 412−421. doi:10.1111/j.1552-6909.2011.01255.x

B. Gastrostomy Tube

1. A gastrostomy tube is used for fluid, feeds, and medication administration for children unable to tolerate oral intake. Only liquid medications should be administered through the gastrostomy tube. The tube may also be placed to gravity to allow for gastric decompression, although may not be as effective as decompression from an NG tube.

2. Gastrostomy tubes can be inserted via endoscope or percutaneous endoscopic gastrostomy (PEG) technique or surgically using an open or laparoscopic technique.

3. There are several types of tubes available, including low-profile skin-level devices (balloon and mushroom types) and balloon-ended tubes. The devices have a French size that indicates the diameter and a stem length, which is measured in centimeters.

4. Nursing care includes preventing inadvertent dislodgement (e.g., cover the tube with clothing, flex-net, bandage wrap, and disconnect tube extension sets when not in use), rotating the tube on a daily basis, and flushing the tube after instilling formula or medications to maintain patency. The tube site should be cleaned with soap and water. Care considerations for a newly placed gastrostomy tube (GT) include placing the tube to gravity in the immediate postoperative periods, “racking” or venting the tube to ensure the child can tolerate his or her own gastric secretions, and finally initiating feeds. If there is inadvertent dislodgement of the tube, it should be replaced within 3 to 4 hours with a GT study after replacement to confirm the tube is intragastric. If the child has undergone a Nissen fundoplication at the same time as GT placement, tube feeds should be vented with a Farrell bag to allow the wrap to heal (the fundus of the stomach is wrapped and sutured around the distal esophagus and LES to prevent reflux) and allow for gastric decompression as needed.

5. All devices with balloons will require periodic replacement as the balloons will break down. If the tube falls out and was in place for less than 4 months, notify a practitioner from the service that placed the tube as a GT study may be ordered to verify correct position.

C. Nasojejunal Tube

1. A nasojejunal (NJ) tube (also referred to as a postpyloric or postpyloric tube) can be used for continuous feed, fluids, or medication administration for children at risk for aspiration or who do not tolerate gastric feeds. Feeds should be administered at a continuous rate as a bolus feed into the intestine may result in dumping, causing increased stool output and feeding intolerance.

2. The size of the tube is based on the size of the child. NJ tubes have either a guide wire or tungsten-weighted tip to facilitate placement.

3. The approximate length of the tube to be inserted is determined by measuring from the exit port of the tube from the child’s nare to ear lobe, then from the ear lobe to the midway point between the xiphoid and umbilicus (Ellett et al., 2011, 2012).

4. At some organizations, prokinetic agents are administered to aid in successful passage of the postpyloric tube. The child should be placed right side 546lying as tolerated so the pylorus is in the lowest position, which will aid in placement. If this is not tolerated, the child should be placed supine with the head of bed elevated. Once gastric placement is achieved, the tube should be passed through the pylorus, instilling air or water, and advance until resistance is met.

5. Tube placement should be confirmed with an abdominal x-ray.

6. Nursing care involves adequately securing the tube to prevent inadvertent dislodgement, and may be secured with a bridling device, flushing the tube after instilling medications or formula, and performing oral care every 4 hours.

D. Surgical Drains

1. Surgical drains may be placed in or near the surgical wound to prevent the buildup of fluid and maintained until the amounts taper. Drains may be maintained to allow for the evaluation of the type of drainage after resuming a regular diet (e.g., Jackson-Pratt^® drain positioned by a biliary anastomosis for bile).

2. There are two types of surgical drains, active drains (closed or closed suction drains) that use negative pressure to remove fluid, and passive drains (open) that depend on the high pressure in the wound and gravity to drain the surgical site (Durai & Ng, 2010). Active drains, such as a Jackson-Pratt or Hemovac drains, have an expandable chamber that creates suction to remove fluid from the wound. In order for the drain to work, the suction bulb must be depressed and emptied at a scheduled interval or when full in order for suction to be maintained. A passive drain, such as a Penrose drain, relies on gravity to remove fluid from the wound and is usually sutured in place.

3. Document the intake and output every 4 hours. Notify the provider of a significant increase or decrease in the amount or character of the drainage. The drain should be secured to prevent inadvertent dislodgement. The surrounding skin should be assessed for irritation or breakdown.

NURSING MANAGEMENT OF WOUND AND STOMA CARE

A. Wound Care

1. Abdominal wound care is variable and can be as simple as assessment for a wound infection (e.g., redness, warmth, pain, edema, foul-smelling drainage, or wound separation) to complex dressing changes involving negative pressure therapy. For complex wound care, consultation with a wound ostomy continence (WOC) nurse is appropriate.

2. Open-wound care should employ moist wound strategies. Wet to dry dressings will provide for gentle wound debridement and allow for wound granulation. Hydrocolloid and hydrofiber dressings (e.g., Aquacel) will allow for wicking of wound drainage, promoting an environment for wound healing.

3. Wounds with excessive drainage should have frequent changes with absorptive dressings that will aid in wound healing (e.g., Mepilex, thick foam).

B. Ostomy Care

1. An ostomy is a stoma that is surgically created from either the small intestine (ileostomy) or large intestine (colostomy) with the purpose of diverting waste outside the body. An ostomy appliance is placed to allow for the collection of stool.

2. Stoma Assessment. The bowel is highly vascularized and a stoma should be pink and moist. There are no nerves in a stoma. If a stoma becomes pale or dusky that should be reported to the provider as perfusion to that intestinal segment may be impaired. Stoma output varies related to what segment of the bowel is used for stoma creation; the more proximal the bowel the more acidic and liquid the output will appear. The more distal in the colon the stoma is placed, the thicker and more formed the stool, which will be thickest in the descending colon.

3. The ostomy appliance should be changed every 3 days or sooner if it leaks. The wafer should not be in place for longer than 3 days unless the patient is in the immediate postop period and output is minimal. A warm wet washcloth can be used to remove the old pouch. The skin should be pushed down versus pulling off the wafer as this is generally less painful. Clean the skin with water and allow the skin to dry. The new wafer can be cut according to the pattern. If there is not a pattern, placing a paper towel on top of the stoma will give an approximate measure of the size (dark and wet area on the paper towel can be used as a pattern) and the size to cut on the wafer for the stoma opening. After removing the paper on the wafer, place the wafer on the skin surrounding the stoma. Hold the wafer in place for 5 minutes to allow the plastic to melt and best adhere to the skin. Apply the bag to the appliance if not a one piece or already attached.

5474. Nursing care includes emptying the bag when it is one-third full to extend the wafer adhering for a longer time to the skin. Pouches that become filled with air should be relieved to prevent wafer dislodgement. Measure and document the stoma effluence every 4 hours. Placing two to three cotton balls in the bag if the output is liquid will help absorb the effluence and prolong adherence of the appliance. If available, a WOC nurse should be consulted to optimize stoma care and educate the child and parents.

GASTROESOPHAGEAL REFLUX DISEASE

A. Definition and Etiology

1. GER is the involuntary movement of gastric contents from the stomach to the esophagus with or without regurgitation or vomiting. In the majority of infants, GER resolves by 1 year of age. GERD occurs with persistent GER that results in complications and impacts the child’s quality of life.

2. Etiology

a. At-risk children include those with prematurity, congenital esophageal abnormalities, congenital diaphragmatic hernia, neurologic impairment, cystic fibrosis, history of lung transplant, respiratory disorders, obesity, and family history of GERD.

B. Pathophysiology

1. Normally, the LES rests when there is a peristaltic wave and this relaxation is transient.

2. The LES rests (5−30 seconds) are of longer duration when the pressure in the esophagus is the same as the stomach (Barnhart, 2016) and is the physiological cause of GER.

C. Clinical Presentation

1. History

a. Evaluate symptoms and what alleviates or aggravates them, dietary history, and comorbidities.

b. GERD varies with age. Symptoms can range from persistent vomiting to intermittent spitting to apparent life-altering events with a significant decline at 1 year of age.

2. Physical Examination

a. No specific examination findings are diagnostic of GER/GERD

i. Review anthropometric measurements and growth charts.

ii. Spitting and nonbloody and nonbilious vomiting are the most common symptom in infants. Other symptoms include feeding refusal, poor weight gain, respiratory symptoms, arching, choking, and coughing (Papachrisanthou & Davis, 2015).

iii. In children, the most common symptoms are vomiting, heartburn, abdominal pain, and anorexia (Papachrisanthou & Davis, 2016).

3. Diagnostic Tests

a. There is no single diagnostic test confirmatory of GER/GERD.

b. According to the joint recommendations from the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition (Vandenplas et al., 2009):

i. Esophageal pH monitoring. This is a valid quantitative test of acid exposure; however, severity does not correlate with symptoms or complications.

ii. Combined multiluminal impedance and pH monitoring. Detects acid and nonacid reflux episodes and is superior to pH monitoring for determining the relationship between the symptoms and disease.

iii. Motility studies. Esophageal manometry studies may be abnormal but lack sensitivity and specificity for GERD diagnosis confirmation.

iv. Endoscopy and biopsy. Endoscopically visible breaks in esophageal mucosa are the most reliable to diagnose reflux esophagitis and, although it is not diagnostic of GERD, it may be helpful for the diagnosis of other disorders.

v. Upper GI. Not recommended for GERD diagnosis, may be helpful in determining alternate diagnoses.

vi. Empiric trial of aid suppression. For the older child, a 4-week trial of a PPI is used for symptom improvement; however, this is not recommended in infants and younger children. Improvement in the child’s heartburn does not confirm the GERD diagnosis as clinical improvement may be related to spontaneous improvement or placebo effect.

5484. Clinical Course

a. Persistent GER symptoms that progress to GERD with complications, including esophagitis and respiratory complications are expected.

D. Patient Care Management

1. Preventive Care or “Lifestyle Changes”

a. Infants

i. Elevate head of bed to 30 degrees, minimize overfeeding, and consider a 1- to 2-week trial of hypoallergenic formula (Garth, 2016).

b. Children

i. Elevate head of bed, encourage left side-lying positioning, weight reduction if indicated; there is no evidence to support dietary modification (e.g., minimize caffeine, fatty or spicy foods, carbonation, eat small frequent meals; Garth 2016; Vandenplas et al., 2009).

2. Direct Care

a. Pharmacology

i. Administer a PPI (up to 8 weeks)—not FDA approved in infants younger than 1 year.

ii. Administer a histamine-2 receptor antagonist—generally first-line treatment.

iii. Prokinetic agent—The adverse side effects outweigh potential benefit for GERD treatment and these agents are not recommended.

b. Surgical intervention

i. Indications for surgery include dependence on long-term medication therapy, nonadherence to medical therapy, repeated episodes of aspiration or related pneumonia episodes, and an apparent life-threatening event.

ii. Nissen fundoplication may be performed open or laparoscopically and is a 360-degree circumferential wrap of the fundus of the stomach around the intra-abdominal esophagus.

3. The child may be unable to “burp” or vomit, which can lead to gastric distension and, in rare cases, gastric rupture. The child may require placement of an NG tube or, if a gastrostomy tube is present, it is placed to gravity drainage. Feeds, if administered through an enteric tube, should be administered continuously and vented (with a Farrell bag or syringe) during the immediate postoperative period.

E. Outcomes

Symptoms that begin after 3 years of age are less likely to resolve without intervention.

ACUTE ABDOMINAL TRAUMA

Acute abdominal trauma is more often blunt versus penetrating, which is considered blunt abdominal trauma. The organs most commonly injured are the spleen and liver.

A. Definition and Etiology

Anatomic differences in children compared with adults include a body size that allows greater distribution of injury, a larger body surface area that allows for greater heat loss, abdominal organs that are more anterior with less SC fat protection, and a smaller blood volume resulting in hypovolemia with relatively smaller volume losses.

B. Pathophysiology

1. Blunt injuries are caused by compression of solid or hollow viscous organs against the spine; rapid acceleration and deceleration with subsequent tearing of structures; or increased abdominal pressure resulting in contusion, laceration, or rupture of organs with subsequent hemorrhage. Solid organs are injured more often than hollow organs, and the most commonly injured organ is the spleen. Blunt trauma can result in lethal injury without visible signs of trauma.

2. Penetrating injuries are most often caused by gunshot or stab wounds. The most common injury is to the hollow viscera. The onset of peritonitis may be immediate. Wounds that penetrate the abdomen usually require surgical exploration.

C. Clinical Presentation

1. History. History is given by a parent or emergency responder report. If age appropriate, speak with the child and attempt to get a history. As with all trauma, if the history does not explain the injuries, providers should be suspicious of child maltreatment.

2. Physical Examination

a. Significant injuries to the head and extremities may overshadow abdominal injuries.

b. Signs of injury are often subtle and include rebound tenderness, pain, rigidity, pallor, grunting 549respirations, hypotension, failure to respond to fluid resuscitation, and increasing abdominal girth. Acute abdominal distention occurs even with minor trauma, especially in infants and often in children as a result of crying and swallowing air. Distention may lead to vomiting and aspiration.

c. Signs of retroperitoneal bleeding include Cullen’s sign (ecchymosis around the umbilicus) and Turner’s sign (ecchymosis over the flank).

3. Diagnostic Tests

a. Abdominal x-rays, supine and lateral, are useful for determining intraperitoneal free air, ground-glass appearance (suggests intraperitoneal blood or urine), associated lower rib fractures (indicates severe force), and signs of an ileus.

b. Ultrasound (US), or FAST (focused abdominal sonography for trauma), is a rapid diagnostic tool used to identify intraperitoneal fluid in the hemodynamically unstable child with blunt trauma. However, FAST is poor at identifying organ-specific injury and therefore does not replace the abdominal CT as a tool for definitive diagnosis of abdominal injury. The sensitivity of the FAST exam is highly variable; however, use of FAST scans has reduced the number of CT scans in some institutions (Notrica, 2015).

c. Abdominal CT scan is the standard of care for evaluation of the peritoneal cavity and retroperitoneum in the hemodynamically stable child. The use of IV contrast is recommended to evaluate organ perfusion, bowel integrity, and the presence of intraperitoneal fluid (Ellison et al., 2015).

d. Diagnostic peritoneal lavage (DPL) is a technique that is rarely performed with the advent of newer imaging techniques (e.g., FAST exam) and involves the insertion of a catheter into the peritoneal cavity. Aspiration of blood is a positive tap. If no blood is obtained, then 10 mL/kg of normal saline (NS) or Ringer’s lactate solution (RL) is infused through the catheter and the effluent is drained by gravity. Cell count and chemistries are obtained. White cell counts greater than 500 cells/mL, red cells counts greater than 100,000 cells/mL, amylase greater than 175 mg/dL, and aspirating stool or blood is a positive tap. A tap positive for blood indicates hemoperitoneum but provides no information on the bleeding source.

e. Complete blood count (CBC) and coagulation studies may help to evaluate bleeding.

f. The utility of other laboratory tests in the diagnosis of intra-abdominal injury is controversial. Elevated AST and ALT suggest liver injury (see Table 7.1). Elevated amylase and lipase suggest pancreatic injury.

g. Urinalysis should be obtained to evaluate for the presence of blood, which indicates kidney or bladder injury.

D. Patient Care Management

1. Preventive Care. Safety measures include appropriate child-restraint devices in automobiles and wearing appropriate protective gear when participating in contact sports.

2. Direct Care

a. Early management of airway, breathing, and circulation (ABC) has the most direct impact on survival. The critically ill child may require intubation and mechanical ventilation for stabilization of the airway and breathing. Circulatory stabilization requires the placement of large-bore IV lines and fluid resuscitation. Inadequate airway and fluid resuscitation are the leading causes of preventable death. Central venous pressure (CVP) and arterial blood pressure (BP) lines are placed to allow close monitoring of the child’s intravascular volume and BP.

b. Current management of blunt abdominal trauma is based on the child’s hemodynamic status (e.g., hemoglobin [Hgb] >7 mg/dL) as compared to injury severity grading scales. The mainstay of treatment remains nonoperative management for blunt solid abdominal organ injury (McVay, Kokoska, Jackson, & Smith, 2008).

c. Insertion of an NG or OG tube allows for gastric decompression, minimizes aspiration risk, and maximizes respiratory effort.

d. Serial laboratory studies are necessary for evaluation of injury, especially following the hematocrit, which is imperative to assess for ongoing bleeding. For blunt injuries for which serial values are being monitored, phlebotomy may be discontinued after two to three stable values (McVay et al., 2008).

e. Most solid-organ abdominal injuries are managed nonoperatively. The blood volume of a child is approximately 80 mL/kg. Fluid resuscitation guidelines include administering up to 40 mL/kg of saline or RL solution. If the child remains hemodynamically unstable, a blood transfusion should then be given. Indications for surgical exploration include massive fluid resuscitation 550(>40 mL/kg of blood transfusions or more than 50% of blood volume), penetrating trauma, signs of peritonitis, radiographic evidence of pneumoperitoneum, and certain blunt injuries (e.g., diaphragmatic injury or bladder rupture).

3. Organ-Specific Care

a. The spleen is the most commonly injured abdominal organ in blunt abdominal trauma.

i. Signs and symptoms include left upper quadrant (LUQ) tenderness, bruising, or abrasion, positive Kehr’s sign (LUQ pain radiating to the left shoulder), signs of decreased perfusion (pallor, tachycardia, delayed capillary refill, and hypotension), and nausea and vomiting. Other signs may include Cullen’s or Turner’s sign.

ii. Diagnostic studies. Abdominal x-ray examinations are rarely helpful but may demonstrate an elevated left hemidiaphragm or a medially displaced lateral stomach border suggesting splenic laceration. The hematocrit may be decreased related to bleeding, or leukocytosis may be noted. Definitive diagnosis is made by abdominal CT scan with contrast.

TABLE 7.5 Splenic Injury Scale

Grade	Injury Description
I
Hematoma	Subcapsular, nonexpanding, <10% of surface area
Laceration	Capsular tear, nonbleeding, <1 cm of parenchymal depth
II
Hematoma	Subcapsular, nonexpanding, 10%−50% of surface area, intraparenchymal, nonexpanding, <5 cm in diameter
Laceration	Capsular tear, 1−3 cm of parenchymal depth that does not involve a trabecular vessel
III
Hematoma	Subcapsular, >50% of surface area or expanding, ruptured subcapsular or parenchymal hematoma, intraparenchymal hematoma, >5 cm or expanding
Laceration	>3 cm of parenchymal depth or involving trabecular vessels
IV
Hematoma	Ruptured intraparenchymal hematoma with active bleeding
Laceration	Laceration involving segmental or hilar vessel producing major devascularization (>25% of spleen)
V
Laceration	Completely shattered spleen
Vascular	Hilar vascular injury that devascularizes spleen

Source: Adapted from Lynch, J. M., Meza, M. P., Newman, B., Gardner, M. J., & Albanese, C. T. (1997). Computed tomography grade of splenic injury is predictive of the time required for radiographic healing. Journal of Pediatric Surgery, 32, 1093−1096. doi:10.1016/S0022-3468(97)90406-1

iii. Classification is based on location and extent of injury (Table 7.5).

iv. Management. The standard of care is nonoperative treatment in hemodynamically stable patients. See Table 7.6 for current activity restrictions, hospital length of stay, and imaging recommendations. Patients are NPO until stable. Surgery may include a splenectomy or splenorrhaphy. In most instances, suturing the injury or splenorrhaphy results in salvage of the spleen. The ultimate goal is preservation of the immune function of the spleen. Massive splenic injury requires a splenectomy. Postoperative care includes monitoring for potential complications such as atelectasis, bleeding, ileus, pain, and infection.

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v. Complications include rebleeding or splenic laceration 3 to 5 days after the initial injury. Splenectomized children are at risk for overwhelming postsplenectomy infection (OSI). Streptococcus pneumoniae is the most common causative agent. Vaccination against encapsulated bacteria, including S. pneumoniae, Haemophilus influenzae type b, and Neisseria meningitides, is recommended after splenectomy. Daily penicillin prophylaxis is recommended in children younger than 5 years and for 2 years following splenectomy and longer if there are other immunosuppression factors or a history of OSI (Buzelé, Barbier, Sauvanet, & Fantin, 2016). Parents should be taught signs and symptoms of infection and when to seek medical attention. Children who sustain an isolated splenic injury are restricted from contact sports and strenuous physical activity for a period consisting of the grade of injury plus 2 weeks.

b. The liver is second only to the spleen as a major source of hemorrhage and is the most common source of lethal hemorrhage. Bleeding stops spontaneously with most injuries.

i. Signs and symptoms include right upper quadrant (RUQ) tenderness, ecchymosis, abrasion, enlarging abdominal girth, signs of shock, and associated injuries such as lower rib fractures, pelvic fracture, or head injury.

ii. Diagnostic studies. Definitive diagnosis is made with abdominal CT scan with contrast. Elevated transaminases are highly suggestive of liver injury, especially AST greater than 200 IU/L and ALT greater than 100 IU/L (Puranik, Hayes, Long, & Mata, 2002). A rapidly falling hematocrit suggests severe liver injury. See Table 7.6 for suggested radiologic monitoring to assess healing or continued bleeding based on the grade of injury.

iii. Classification. Injuries are graded according to increasing severity (Table 7.7).

iv. Management is similar to the treatment of splenic injury and involves supportive care with a nonoperative approach (see Table 7.6). Nonoperative management requires close monitoring of vital signs and physical examinations. Fever, leukocytosis, and abdominal tenderness remote from the liver injury may indicate an occult injury. Serial hematocrits, coagulation studies, chemistries, and transaminase levels should be monitored for significant liver dysfunction and monitored until stable. Close monitoring for ongoing bleeding is necessary, and patients should remain on strict bed rest until they are stable. Surgery is indicated for the hemodynamically unstable child, signs of peritonitis, or transfusion requirements exceeding 50% of the estimated blood volume during the first 24 hours (Garcia & Brown, 2003). Children with isolated hepatic injury are restricted from contact sports and strenuous physical activity for a period consisting of the grade of injury plus 2 weeks.

v. Complications of operative management include delayed bleeding, abscess formation, abdominal compartment syndrome, biliary obstruction, and biloma.

c. The pancreas is located deep in the upper abdomen and is infrequently injured unless a significant sustained force compresses it against the spine. The classic injury is compression by bicycle handlebars in which the child flips over the bike and is impaled in the epigastrium by the handlebars. Other mechanisms include motor vehicle collisions and child maltreatment.

i. Signs and symptoms include diffuse abdominal tenderness, deep epigastric pain radiating to the back, and bilious vomiting. Pain may diminish within the first 2 hours of injury and worsen with the release of enzymes over the next 6 to 8 hours (Intravia & DeBeradino, 2013).

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ii. Diagnostic studies

1) Amylase is elevated (reference range 0−88 IU/L). The extent of amylase increase alone does not correlate with the severity of injury and may be a nonspecific finding occurring with blunt injury in the absence of pancreatic injury.

2) Lipase (reference range, 20−180 IU/L). Elevation of amylase to greater than 200 IU/L and lipase greater than 1,800 IU/L correlates with significant pancreatic injury (Nadler, Gardner, Schall, Lynch, & Ford, 1999).

3) Diagnosis is usually made by abdominal CT scan with IV contrast.

4) US is useful for diagnosis of pseudocyst.

5) Magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP) may be necessary to visualize ductal disruption or posttraumatic stricture.

6) Classification: Injury is graded based on the extent of parenchymal injury and the degree of disruption of the duct (Table 7.8).

553TABLE 7.8 Pancreatic Injury Severity Scale

Class	Injury Description
I	Contusion or laceration without duct injury
II	Ductal transection or parenchymal injury with probable duct injury
III	Proximal transection or parenchymal injury with probable duct injury
IV	Combined pancreatic and duodenal injury

Source: Adapted from Jobst, M. A., Canty, T. G., & Lynch, F. P. (1999). Management of pancreatic injury in pediatric blunt abdominal trauma. Journal of Pediatric Surgery, 34(5), 818−823.

7) Management is nonoperative if there is no ductal disruption; although operative intervention with ductal disruption is controversial (Englum, Gulack, Rice, Scarborough, & Adibe, 2016). Supportive care interventions include NPO, NG tube for gastric decompression, IV fluids, and pain management. Parenteral nutrition should be considered if NPO longer than 3 days. Children are monitored for signs of infection. If a pancreatic pseudocyst (a loculated collection of pancreatic juices) develops, patients require 6 to 8 weeks of bowel rest with PN. Surgery is usually indicated for the treatment of distal transection of the pancreas. Surgery involves drainage, partial resection, or repair of lacerated ducts.

8) Complications include the development of pancreatic fistula or pseudocyst formation. Large cysts that have not resolved after 4 to 6 weeks require drainage. Surgical drainage, percutaneous by interventional radiology, and endoscopic drainage may be performed. Because the pancreas is stimulated with oral intake, feeding tolerance must be evaluated before pulling surgical drains.

d. Stomach

i. Signs and symptoms of injury include abrasion or contusion in the upper abdomen and bloody gastric drainage. A rigid abdomen with severe pain suggests perforation. Perforation leads to signs and symptoms of peritonitis within hours of injury.

ii. Diagnostic studies. Abdominal x-ray detects free air or abnormal NG tube position.

iii. Management includes surgical repair.

e. Small and large intestine. Small bowel injuries are the third most common site of abdominal organ injury in blunt trauma (Wise, Mudd, & Wilson, 2002). Common mechanisms include the lap-belt syndrome and abuse. The colon and rectum are rarely injured in children, and injuries to these organs usually occur in the presence of maltreatment.

i. Signs and symptoms include bloody gastric drainage, absent bowel sounds, tympanic sounds on percussion, midabdominal ecchymosis, seat-belt sign, and pain that increases as peritonitis develops. Signs and symptoms of peritonitis include severe abdominal pain, tenderness, guarding, distension or rigidity, redness, absent bowel sounds, fever, leukocytosis, and respiratory distress. Evaluation of a rectal injury requires rectal examination and is often done with the patient under anesthesia.

ii. Diagnostic studies. Abdominal x-rays with supine and lateral decubitus views may reveal air−fluid levels, dilated loops of bowel, bowel-wall thickening, or a chance fracture (lumbar spine fracture). CT scan with IV contrast may have greater sensitivity and specificity.

iii. Management requires surgical repair and generally involves segmental resection with primary anastomosis and possible ostomy placement. Supportive care includes frequent monitoring, NG decompression, replacement of excessive gastric output, stress ulcer prophylaxis, antibiotic therapy, fluid and electrolyte management, PN, and pain management.

iv. Complications. Delayed perforation, stricture formation, adhesions, and short bowel syndrome may occur.

E. Outcomes

See specific organ for complications.

ACUTE GI TRACT HEMORRHAGE

A. Definition and Etiology

1. Acute bleeding from the GI tract is usually classified as either upper or lower tract bleeding.

2. Etiology is based on age. Tables 7.9 and 7.10 outline the causes of upper and lower GI bleeding.

B. Pathophysiology

The child presenting with sudden massive blood loss is at risk for hemodynamic instability. The first priority is to determine the extent of the blood loss and establish whether perfusion is compromised. Greater than 15% circulating blood volume (CBV) loss results in stimulation of autonomic cardiovascular responses to maintain BP and perfusion. Greater than 20% CBV loss results in decreased systolic BP and metabolic acidosis. Rapid fluid resuscitation is required, or cardiovascular collapse and death may occur. Upper GI bleeding is defined as bleeding that originates proximal to the ligament of Treitz. Lower GI bleed occurs distally to ligament of Treitz.

554TABLE 7.9 Causes of Upper GI Bleeding in Infants and Children

Neonates	Infants−Adolescents
Swallowed maternal blood, esophagitis	Esophagitis
Gastritis	Gastritis
Gastroduodenal ulcer	Gastroduodenal ulcer
Coagulopathy associated with infection, liver failure	Esophageal varices
Vascular anomaly	Gastrointestinal duplication
Hematologic (vitamin K deficiency)	Mallory−Weiss tear Vascular anomaly Coagulopathy Caustic ingestion

GI, gastrointestinal.

TABLE 7.10 Causes of Lower GI Bleeding in Infants and Children

Age	Causes
Neonates	Milk protein allergy Necrotizing enterocolitis Hirschsprung’s enterocolitis Midgut volvulus Hematologic (vitamin K deficiency) Coagulopathy
Infant	Milk protein allergy Anal fissure Intussusception Infectious enterocolitis Meckel’s diverticulum Vascular anomaly
Child	Anal fissure Juvenile polyps Infectious enterocolitis Inflammatory bowel disease Henoch−Schonlein purpura Hemolytic-uremic syndrome Vascular anomaly
Adolescent	Anal fissure Infectious enterocolitis Inflammatory bowel disease Vasculitis Hemorrhoids NSAID enteropathy

GI, gastrointestinal; NSAID, nonsteroidal anti-inflammatory drug.

Sources: Adapted from Lirio, R. A. (2016). Management of upper gastrointestinal bleeding in children: Variceal and nonvariceal. Gastrointestinal Endoscopy Clinics of North America, 26(1), 63−73. doi:10.1016/j.giec.2015.09.003; Sahn, B., & Bitton, S. (2016). Lower gastrointestinal bleeding in children. Gastrointestinal Endoscopy Clinics of North America, 26(1), 75−98. doi:10.1016/j.giec.2015.08.007

C. Clinical Presentation

1. History

a. Presentation of GI bleeding is shown in Table 7.11.

b. Comorbidities (liver disease), medications (e.g., steroids, nonsteroidal anti-inflammatory drugs [NSAIDs]), and possible exposures should be assessed.

2. Physical Examination

a. The location of bleeding can be identified by the color and source of the bleeding. Hematemesis is the result of acute blood loss from the upper GI tract and presents as coffee grounds emesis or frank blood. Hematochezia is bright- or dark-red blood per rectum. Melena is caused by the digestion of blood in the GI tract and presents as black, tarry stools and indicates an upper GI source of bleeding. Occult bleeding is the result of chronic blood loss.

b. Signs and symptoms of hypovolemic shock occur with acute bleeding and include tachycardia, weak peripheral pulses, pallor and mottled color, cool skin, and oliguria. BP may be normal despite significant blood loss; hypotension is a late sign of shock.

3. Diagnostic Tests

a. Laboratory studies. CBC needed to evaluate for anemia and thrombocytopenia; prothrombin time (PT) and partial thromboplastin time (PTT) to evaluate for coagulopathies; serum fibrinogen and fibrin split products to evaluate for disseminated intravascular coagulation (DIC); type and crossmatch for potential blood transfusion; guaiac test to evaluate for blood in stool or gastric fluid; chemistries, ammonia, and liver function tests (LFTs) to screen for liver dysfunction; and arterial blood gas (ABG) is measured to monitor for metabolic acidosis. If bloody diarrhea is present, send for stool culture and fecal leukocytes. A CBC, urinalysis, blood urea nitrogen (BUN), and creatinine should be obtained in patients with suspected hemolytic-uremic syndrome.

555TABLE 7.11 Presentation of GI Tract Bleeding

Presentation	Definitions
Acute bleeding
Hematemesis	Bloody vomitus; either fresh, bright-red blood or dark, digested blood with “coffee ground” appearance
Melena	Black, sticky, tarry, foul-smelling stools caused by digestion of blood in the GI tract (seen in both upper GI and lower GI tract bleeding)
Hematochezia	Fresh, bright-red blood passed from the rectum
Chronic bleeding
Occult	Trace amounts of blood in normal-appearing stools or gastric secretions; detectable only with a guaiac test

GI, gastrointestinal.

Source: Modified from Huether, S. E., McCance, K. L., & Tarmina, M. S. (1994). Alterations of digestive function. In K. L. McCance & S. E. Huether (Eds.), Pathophysiology: The biological basis for diseases in adults and children (2nd ed.). St Louis, MO: Mosby-Year Book.

b. Abdominal x-ray examination involves a supine and lateral decubitus view to evaluate for bowel gas pattern suggesting bowel obstruction, air−fluid levels, or pneumoperitoneum. Bowel-wall thickening suggests colitis.

c. Endoscopy provides direct visualization of the GI tract to determine injury, structural defects, or source of bleeding. An upper endoscopy is the preferred diagnostic procedure to evaluate bleeding of the upper GI tract and for therapeutic treatment (injection, cautery and mechanical therapy for nonvariceal bleeding, and variceal ligation or banding for variceal bleeding; Lirio, 2016). Colonoscopy is performed for lower GI bleeding.

d. Radionuclide studies are indicated for midintestinal bleeding and are effective tests for locating subacute or intermittent bleeding. Two types are used: technetium-labeled sulfur colloid (more sensitive) and technetium-pertechnetate-labeled red blood cells (RBCs). Demonstration of IV Tc-99m pertechnetate uptake by ectopic gastric mucosa in a Meckel’s scan is helpful in diagnosing Meckel’s diverticulum.

4. Clinical Course

a. Course is variable depending on the source and etiology. Upper GI variceal bleeding can result in sudden, massive blood loss and hypovolemic shock.

D. Patient Care Management

1. Preventive Care

a. Assess for signs of respiratory distress and hemodynamic instability.

2. Direct Care

a. Secure two large-bore IVs for fluid resuscitation as needed. Administer fluid (20 mL/kg of NS or RL) or blood transfusion (20 mL/kg or more as indicated) until peripheral circulation is adequate. After central line and arterial line placement, continuously monitor CVP and BP for response to fluid resuscitation and the need for continued therapy. The initial hematocrit may be misleading; if so, serial measurements are needed.

b. Place an NG tube and administer room temperature saline lavage until bleeding stops.

c. Administer H₂-histamine receptor antagonists, PPIs, and sucralfate to minimize bleeding and prevent rebleeding.

d. Endoscopic modalities, including injection, cautery, and mechanical therapy, may be used for nonvariceal and variceal ligation or banding for variceal bleeding (Lirio, 2016).

3. Supportive Care

a. Continuously monitor vital signs.

b. Monitor PT, PTT, and fibrinogen for coagulopathies. Administer vitamin K (AquaMEPHYTON), platelets, or fresh frozen plasma (FFP) as necessary.

c. Monitor electrolytes, BUN, and creatinine for potential renal dysfunction. Monitor urine output via a urinary catheter.

d. Monitor serum ionized calcium following transfusion for potential hypocalcemia.

e. Monitor for signs of further bleeding, including poor perfusion, abdominal pain, increased abdominal girth, decreased bowel sounds, hematemesis, and hematochezia.

556f. Assess for signs and symptoms of abdominal perforation, including fever, severe or persistent abdominal pain, and abdominal rigidity.

4. Esophageal Varices

a. Acute treatment involves the administration of vasopressin (Pitressin), or octreotide (Sandostatin; see “Pharmacology” section earlier in this chapter). Insertion of a Sengstaken−Blakemore tube may be performed if endoscopy is not available. The tube has three separate lumens for gastric suction, inflation of gastric balloon, and inflation of esophageal balloon. Balloons must be deflated every 12 to 24 hours. Ensure patency of the gastric suction lumen by irrigating frequently. Frequent serious complications, including perforation or erosion of the esophagus or stomach (from hyperinflation or prolonged inflation of the balloons), limit its usefulness.

b. Endoscopic variceal ligation or banding is the treatment of choice.

c. Surgery is considered if other therapies are ineffective. Shunting procedures divert blood flow from the liver and allow decompression of the portal system with portal hypertension. Specific entities that may require surgery include Meckel’s diverticulum, duplication cyst, midgut volvulus, NEC, and intussusception (if radiologic enema reduction not effective), and a refractory bleeding ulcer.

E. Outcomes

Complications include rebleeding, shock, sepsis, and DIC.

GI TRACT ABNORMALITIES

GI tract abnormalities are often detected in the prenatal period. Congenital anomalies are summarized in Table 7.12.

ACUTE SURGICAL ABDOMEN

A. Definition and Etiology

Acute surgical abdomen refers to the sudden onset of abdominal pain and tenderness that warrants evaluation for surgical intervention that is usually caused by a bowel infarction, obstruction, or perforation. Causes in neonates include NEC, intussusception, and midgut volvulus. Causes in children and adolescents include appendicitis (a perforated appendix is a common cause of peritonitis), Meckel’s diverticulum, inflammatory bowel disease, omental torsion, ovarian torsion, intussusception (not reduced radiologically), incarcerated inguinal hernia, and trauma. Intraluminal bowel obstructions in children can be caused by foreign bodies, bezoars, with extramural causes from bowel adhesions, hernias, and internal volvulus.

B. Pathophysiology

1. Peritoneal inflammation (peritonitis) occurs as a result of injury or contamination. Primary peritonitis occurs with no obvious cause of contamination, but infection is indirectly introduced into the peritoneal cavity from the bloodstream or lymphatics. Secondary peritonitis occurs as a result of direct GI tract injury, such as with trauma. The inflammatory response causes exudation of fluid into the peritoneal cavity. Hypovolemia may occur as fluid shifts into the peritoneal cavity.

2. Upper GI tract perforations result in leakage of hydrochloric acid, digestive enzymes, or bile causing chemical peritonitis.

3. Lower GI tract perforation results in the leakage of fecal material, which releases aerobic and anaerobic bacteria into the peritoneum. Endotoxins may be released and cause bacterial peritonitis and sepsis.

4. Injury to the peritoneum causes decreased bowel motility and usually results in an ileus.

5. Obstruction can be complete, partial, or intermittent. Bowel proximal to the obstruction becomes distended due to a collection of air and GI tract contents. Distal bowel collapses from a lack of intraluminal content; therefore, proximal obstructions create more bowel collapse. With a distal obstruction, there is greater bowel distension and resultant abdominal distension.

C. Clinical Presentation

1. History. Variable depending on the location of the obstruction, the type of obstruction, and whether the obstruction is complete or partial. The onset, progression, location, and presence of other symptoms should be evaluated (e.g., stooling pattern, pain, NG output [bilious output indicative of an obstruction]). Presentation can be acute with signs of peritonitis (e.g., volvulus, traumatic visceral perforation, postsurgical bowel obstruction) or subtle and chronic with incomplete or recurring bouts of obstruction (e.g., intussusception).

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5622. Physical Examination

a. Obstruction results in abdominal distention, tenderness, bilious vomiting, possible fever, and absent or hyperactive bowel sounds. With a proximal obstruction, the abdomen may be scaphoid and with a distal obstruction, there is abdominal distension.

b. Perforation causes fever, pain, and possibly signs of respiratory distress, including tachypnea, retractions, flaring, grunting, and acidosis.

c. Signs of third spacing include increased abdominal girth and hypovolemia (tachycardia, decreased peripheral perfusion, decreased urine output, and hypotension [late sign]).

d. Symptoms of peritonitis include fever, nausea, marked abdominal distention or rigidity, erythema over the abdomen, absent or hypoactive bowel sounds, diffuse abdominal pain, guarding of the abdomen, diarrhea, and rebound tenderness.

3. Diagnostic Tests

a. Abdominal x-ray examination may reveal a paucity of gas, dilated loops of bowel, or air−fluid levels with a bowel obstruction and is usually the first radiologic study done. A lateral view reveals the presence of free air with bowel perforation.

b. Abdominal US or MRI are often done to evaluate for appendicitis as nonionizing radiation is employed. A recent systematic review reported MRI had comparable sensitivity (92%−100%) and specificity (89%−100%) for the diagnosis of appendicitis as compared to CT scan (Ogunmefun, Hardy, & Boynes, 2016).

c. Abdominal CT scan with IV and PO contrast is used to evaluate suspected abscess or mass.

d. Air enema is often done instead of a contrast enema and is a diagnostic and therapeutic treatment for intussusception. Typically, air enema results in successful reduction of the obstructed bowel with reported success rates of 50% to 80% (Makin & Davenport, 2016). Generally, water-soluble contrast is used if attempting reduction.

e. Upper GI series is the gold standard for making the diagnosis of a midgut volvulus, although this abnormality is often appreciated from an abdominal CT scan.

4. Clinical Course

a. Varies depending on the surgical pathology. Generally, symptoms are progressive. A child with significant intra-abdominal pathology may eventually develop mental status changes and become somnolent.

D. Patient Care Management

1. Direct Care

a. Provide frequent vital-sign monitoring with assessment for respiratory distress. Elevate the head of the bed 30 to 45 degrees to enhance respiratory effort.

b. Place an NG tube for gastric decompression and drainage and maintain low intermittent suction if a complete or proximal obstruction is suspected.

c. Monitor intake and output, as oliguria commonly requires fluid boluses. Placement of a urinary catheter may be indicated.

d. Surgical intervention may be indicated for persistent abdominal pain, evidence of localized peritonitis (erythema over a portion of the abdomen), and the presence of free air on abdominal x-ray examination.

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