Gastrointestinal and Nutritional Disorders

14 Gastrointestinal and Nutritional Disorders








Essential anatomy and physiology


This section summarizes the basic anatomy and physiology of major structures composing the GI tract (Fig. 14-1). See the Chapter 14 Supplement on the Evolve Website for additional information on maturational anatomy and physiology.






Stomach


The stomach is a hollow muscular organ that serves as a temporary reservoir for ingested food, and is the site of the initial phases of protein digestion. Three smooth muscle layers of the stomach mix food with gastric secretions, creating a substance called chyme. Two muscular sphincters, the LES at the entrance to the stomach and the pyloric sphincter at the stomach outlet, contract to contain food within the stomach while the food is being churned and mixed with the gastric secretions. These muscle barriers also protect cells of the esophagus and duodenum from caustic stomach acid, which can erode and ulcerate the mucosa.


Specialized cells within the gastric mucosa (called parietal cells and chief cells) produce mucus, acid, enzymes, hormones, and intrinsic factor. Each of these products has a specific role in digestion.


Secreted mucus forms a protective barrier between the mucosa and the acid and proteolytic enzymes. Acid produced by partial cells creates a gastric pH of 1 to 2 that dissolves food fiber, acts as a bactericide against swallowed organisms, and converts pepsinogen to pepsin. Pepsinogen arises from chief cells. Under the influence of gastric acid, pepsinogen is converted into pepsin, a proteolytic enzyme that continues the breakdown of proteins that was started by gastric acids. Intrinsic factor is a glycoprotein required for vitamin B12 absorption.27


Gastric secretions consist predominantly of hydrochloric acid, potassium chloride, and sodium chloride. Stimulated parietal cells dispense these substances into the lumen of the stomach through active transport involving a proton pump. Histamine—H2 type—stimulates the H2 receptors in parietal cells, causing the cells to secrete gastric acid. H2 receptor antagonists inhibit gastric acid secretion by preventing histamine from activating the H2 receptors. Proton pump inhibitor medications inhibit hydrochloric acid directly at the cellular level.





Small Intestine


The small intestine (Fig. 14-2) begins beyond the pylorus of the stomach and is divided into the duodenum (receives enzymes important for digestion), the jejunum (principle absorbing site), and the ileum (the only site for the absorption of vitamin B12 and bile acids). Two layers of smooth muscle, an outer longitudinal layer, and an inner thicker circular layer produce peristalsis.



The inner mucosal layer has transverse folds or plicae circulares. This design increases surface area (and absorption) and slows the progression of food, allowing more time for digestion to occur. Villi, which are extensions of the mucosal layer, cover the mucosal folds as projections. These villi, composed of absorptive columnar cells and mucus-secreting goblet cells, are considered the functional units of the GI tract. Each villus is covered with tiny projections called microvilli; together these form the brush border of the intestine. This brush border contains digestive enzymes and contributes to the transfer of nutrients and electrolytes. See the Chapter 14 Supplement, Nutrition section, on the Evolve Website for additional information about the digestion of nutrients.


Epithelial cells in the small intestine have one of the most rapid turnover rates of any cells in the body. Villus cells continuously proliferate to maintain a consistent quantity within the intestinal epithelium. The loss of villi leads to decreased absorptive capacity. The capacity to renew these villi is lower during infancy and can be compromised in malnourished states and by intestinal disorders. Recovery following injury to the intestinal mucosa (e.g., from viral infection or malnutrition) may be prolonged, creating a vicious cycle of impaired intestinal function and persistent malabsorption leading to malnutrition and further compromise of intestinal function.







Liver


The liver is one of the largest organs of the body, and it performs hundreds of functions. It is divided into right and left lobes by the falciform ligament (Fig. 14-3). The right lobe is the largest lobe, composed of the right lobe proper, the caudate lobe (posterior surface), and the quadrate lobe (inferior surface).



The liver has 50,000-100,000 functional units or lobules composed of hepatic plates (i.e., plates of hepatocytes) that each radiate centrally around a central vein (Fig. 14-4). The porta hepatis is a fissure that serves as the entry point for the hepatic artery, the portal vein, and the common bile duct. The artery, vein, and duct divide into intralobular branches as they follow the septa throughout the liver.



Nearly three quarters of the blood flow to the liver is supplied by the portal venous system that carries blood from the GI tract that is rich in nutrients to the liver. The remaining 25% of hepatic blood flow is well-oxygenated blood from the hepatic artery.


The hepatobiliary system has many synthetic, metabolic, storage, and removal functions. Bile is composed of bile salts and is made by hepatocytes within the liver. Bile is secreted into the bile canaliculi or the spaces between the rows of hepatic cells. The bile is then transported to the terminal interlobular ducts, to the right or left hepatic duct, and eventually to the common bile duct. The bile is stored in the gallbladder until it is secreted into the duodenum.


The liver is responsible for a wide variety of synthetic, metabolic, and excretory functions. In addition to bile production, liver functions include the synthesis of plasma proteins and clotting factors. The liver synthesizes almost all plasma proteins, including albumin and clotting factors I, II, V, VII, IX, X, and XI. The liver metabolizes carbohydrates, proteins, and lipids. It is the major storage site for glycogen, fat, and fat-soluble vitamins (A, D, E, and K). In addition, the liver deactivates many drugs and waste products, including conversion of ammonia to urea.


Toxic metabolic waste products from medications and bilirubin are metabolized in the liver through oxidation or conjugation reactions. Metabolic products are then excreted in the bile or urine. Kupffer cells are macrophages that line the sinusoid vessels and serve as the liver’s internal immune system; they remove intestinal and foreign bacteria in addition to other toxins.





Nutrition


There is little evidence to identify the best nutritional support of the critically ill child.30,44 A recent Cochrane review that attempted to assess the impact of enteral and parenteral nutrition (PN) on clinically important outcomes in the critically ill child found only one trial that was relevant to the review question.30 Appropriate nutritional assessment, determination of energy requirements, and the timing, route, and type of nutritional delivery have yet to be established for seriously ill or injured children in the critical care unit.



Recommended Daily Nutritional Intake


Adequate energy (caloric) intake is necessary for rapid growth and development throughout childhood. During infancy the requirement for energy intake per kilogram is greater than in all other age groups. The average requirements for energy intake during infancy and childhood are shown in Table 14-1. Of note, these requirements are for healthy, active infants and children.


Table 14-1 Daily Energy Requirements for Infants and Children
























Age kcal/kg
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

It is useful to divide energy requirements into resting energy expenditure (REE) and requirements for growth and physical activity. REE is determined by the basal metabolic rate or the energy consumed for the normal maintenance of cellular energy. Estimates of an ill child’s REE by standard equations are unreliable, and indirect calorimetry is not always available to clinicians.44 Caloric requirements for the hospitalized child may be substantially more or less than the normal daily recommended requirements. Hypermetabolic states, excessive nutrient losses, trauma, burns, and surgery will increase energy requirements, whereas neurologic impairment, reduced activity, and ventilator support can decrease energy needs. Typically, fever increases energy requirements 12% per day for each degree Celsius elevation in temperature above 37°   C.


A dietitian should assist in the assessment of the child’s nutritional needs. These assessments will require basic anthropometric measurements (including body mass index [BMI] percentile), obtained as the child’s clinical status allows. Clinicians are challenged to determine appropriate needs for the obese child (i.e., with a BMI greater than the 85th percentile), and it may be appropriate to determine caloric requirements based on ideal body weight.


Fluid and electrolyte requirements vary as a function of age, weight, and clinical condition. Normal daily fluid and electrolyte requirements are listed in Table 14-2. Any calculation of maintenance fluid requirements should use the formulas only to estimate a baseline. The actual volume of fluid administered to the patient must be tailored to the patient’s clinical condition and fluid balance. For additional information about fluid and electrolyte balance, see Chapter 12.


Table 14-2 Formulas for Estimating Daily Maintenance Fluid and Electrolyte Requirements for Children





























































  Daily Requirements Hourly Requirements
Fluid Requirements Estimated from Weight*
Newborn (up to 72   h after birth) 60-100   mL/kg (newborns are born with excess body water)
Up to 10   kg 100   mL/kg (can increase up to 150   mL/kg to provide caloric requirements if renal and cardiac function are adequate) 4   mL/kg
11-20   kg 1000   mL for the first 10   kg + 50   mL/kg for each kg over 10   kg 40   mL for first 10   kg + 2   mL/kg for each kg over 10   kg
21-30   kg 1500   mL for the first 20   kg + 25   mL/kg for each kg over 20   kg 60   mL for first 20   kg + 1   mL/kg for each kg over 20   kg
Fluid Requirements Estimated from Body Surface Area (BSA)
Maintenance 1500   mL/m2 BSA
Insensible losses 300-400   mL/m2 BSA
Electrolytes
Sodium (Na) 2-4   mEq/kg
Potassium (K) 1-2   mEq/kg
Chloride (Cl) 2-3   mEq/kg
Calcium (Ca) 0.5-3   mEq/kg
Phosphorous (Phos) 0.5-2   mmol/kg
Magnesium (Mg) 0.4-0.9   mEq/kg

* The “maintenance” fluids calculated by these formulas must only be used as a starting point to determine the fluid requirements of an individual patient. If intravascular volume is adequate, children with cardiac, pulmonary, or renal failure or increased intracranial pressure should generally receive less than these calculated “maintenance” fluids. The formula utilizing body weight generally results in a generous “maintenance” fluid total.




Enteral Nutrition


Enteral feeding is preferable to parenteral nutrition, because enteral feedings will maintain gut structure and function and will reduce complications and cost. Specific benefits include intestinal trophism and preservation of the gut barrier to minimize bacterial translocation.38


Selection of the appropriate formula is based on the patient’s age and disease process. Because breast milk is the preferred source of nutrition for infants, nursing mothers should be provided with a breast pump if their infant is unable to breast feed but can be fed enterally. Standard infant formulas are not appropriate for the premature infant (specialty premature formulas should be used) or for children older than 1 year. Specific formulas are available for disease states such as renal failure (NovaSource Renal [Nestlé Nutrition, North America, Minneapolis, MN] or Nepro [Abbott Nutrition, Columbus, OH]) or liver insufficiency (e.g., Pregestimil [Mead Johnson Nutrition, Evansville, IN] for infants, Peptamen Jr. [Nestlé Nutrition, North America, Minneapolis, MN] and PediaSure Peptide [Abbott Nutrition, Columbus, OH] for children). The renal formulas are not designed specifically for children, so they should be used with caution.


If possible, the patient should be encouraged to take nutrition orally; however, for many critically ill children enteral nutrition is provided through a feeding tube. Enteral feedings should be tailored to each patient. When a gastric feeding tube is in place, continuous feedings are often initially provided to achieve goal calories before transitioning to physiologic bolus feedings. Children with significant reflux may benefit from venting of the gastric tube (i.e., leave the tube open to air, with the open end elevated above the level of the stomach).


Postpyloric feeding should be considered for children with delayed gastric emptying and poor intestinal motility who are intolerant to gastric feedings. To prevent dumping syndrome, feedings into the jejunum are administered at a continuous hourly rate.


The practice of aspirating residual liquid and refeeding it is controversial. Although a large volume of residual feeding that remains in the stomach may contribute to inadvertent aspiration,45 the residual volume that should be considered significant has not been clearly established. Nurses should measure and record the volume of residual feeding and notify the on-call provider according to unit policy or orders. Enteral feeding delivery devices, routes, placement methods, nursing considerations, and complications are summarized in Table 14-4.




Parenteral Nutrition (PN)


When a child is unable to absorb nutrients through the GI tract, or when the child requires a supplement to enteral nutrition, PN is indicated. PN is defined as the administration of nutrients by the intravascular route. PN was first demonstrated as a practical mode of nutritional therapy in the 1960s and is now widely accepted as beneficial for nutritionally compromised children. Some children receive PN in the home setting.


PN may be used over a long period of time to allow a poorly functioning GI tract to rest. PN can also be used for long periods in children with “short gut” and for critically ill children with multiorgan failure when enteral feeding is not possible.




Parenteral Nutrition Solutions


PN solution consists primarily of glucose (as a source of carbohydrate), amino acids (as a source of protein), and fat emulsions. Dextrose provides 3.4   Kcal/g and constitutes 60% to 70% of the total PN caloric intake. 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). Protein provides 4   Kcal/g and should constitute 14% to 20% of the total PN caloric intake. 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 adequate calories from fat (0.5   g/kg per day) prevents essential fatty acid deficiency states. Electrolytes, vitamins, minerals, and trace elements are added to these solutions to meet the child’s known nutritional requirements.


The PN orders are individually tailored to deliver appropriate amounts of fluid, nutrients, and electrolytes. The critically ill child’s fluid requirements often change and may differ from estimated maintenance fluid requirements. In addition, it may be necessary to alter electrolyte content based on the child’s clinical condition or changes in medications. For example, medications such as furosemide (Lasix) will increase the daily potassium requirements; if the furosemide dose is reduced, the child will require less supplementary potassium.


When PN is initiated, there is gradual titration of additives until goal calories are achieved. The goal calories should be determined by the healthcare provider in consultation with a dietitian or pharmacist.



Nursing Responsibilities


The nurse must closely monitor the child’s clinical appearance and fluid and electrolyte balance to prevent and detect complications of PN as soon as possible. This monitoring requires documentation of the quantity and content of the child’s fluid intake and output and evaluation of the child’s fluid and electrolyte status and daily weight. A sample monitoring schedule for children receiving PN is provided in Table 14-5.


Table 14-5 Sample Monitoring Schedule for Children Receiving Parenteral Nutrition: Must Be Tailored to Child’s Clinical Status



































































Monitoring Frequency
General and Anthropometric Measurements
Vital signs Every 4   hours, or more often as patient condition warrants
Weight Daily
Strict intake and output Constant
Caloric intake Daily
Height Weekly
Head circumference Weekly (for children younger than 2 years)
Blood Sampling
Glucose Initial + Daily until stable (more often in neonates)
Electrolytes Initial + Daily until stable
BUN, Creatinine Initial + Weekly
Ca2+/ionized calcium, image, Mg2+ Initial + Weekly (image, Mg2+should be checked daily if values not within reference range)
Alkaline phosphatase, AST, ALT Initial + Weekly
Total and direct bilirubin Initial + Weekly
Total protein, albumin Initial + Weekly
Prealbumin Initiation
Triglycerides, cholesterol Weekly
Zinc, copper, selenium, manganese, iron Monthly
Glucose point-of-care testing When PN is abruptly discontinued, cycled, or if signs or symptoms of hypoglycemia or hyperglycemia suspected
CBC count with differential When febrile
Blood culture When febrile

ALT, Alanine aminotransferase; AST, aspartate aminotransferase; BUN, blood urea nitrogen; Ca2+, calcium; CBC, complete blood count; Mg2+, magnesium; PN, parenteral nutrition; image phosphorous.


Whenever the child receives concentrated glucose solutions, the nurse must verify that the fluid volume and content are appropriate for the child’s estimated daily requirements. Before every new bag of PN solution is infused, the nurse should confirm that the prepared solution is accurate and consistent with the order by checking the solution content against the provider’s original order. Reduction in the PN administration rate (e.g., if the intravenous [IV] catheter malfunctions or with the initiation of enteral feedings or feeding advancement) will reduce the child’s fluid, glucose, and electrolyte intake unless enteral feedings provide the difference.


Potential complications of PN include electrolyte abnormalities, infection, cholestasis leading to hepatic dysfunction, and hyperlipidemias (with triglyceride administration). In critically ill children, there is an association between hyperglycemia and organ dysfunction.33


Because PN solution contains a high concentration of glucose, it provides an excellent medium for bacterial growth. When hanging a new bag of PN solution and tubing, the nurse must use strict aseptic technique to prevent line contamination. Many hospitals require that the entire tubing system (between PN solution and the patient, including infusion pump tubing) be changed every 24   hours to decrease the possibility of significant bacterial growth. The dressing over the catheter insertion site should be changed when it is no longer occlusive (per hospital policy), using sterile technique and an occlusive dressing. The nurse should assess the catheter insertion site for evidence of inflammation (erythema or exudate) and should report any abnormalities to the appropriate provider. Wound exudate should be cultured and sent for gram stain analysis as ordered (or per protocol). Nurses should be careful to follow the healthcare institutional policies and protocols to prevent central venous catheter-associated blood stream infections (see Chapter 22, Box 22-6 for further information).


Monitor the child’s temperature at least every 4   hours (or according to hospital PN policy). Blood cultures are typically ordered if the child’s temperature rises above 38.5°   C or if the child develops signs of infection. The child may be placed on empiric antibiotics until culture results are available. The antibiotics are then adjusted if the culture is positive and the bacterial sensitivities or susceptibilities support a change. Often the catheter is maintained during an attempt to clear an existing infection, because if the child requires long term PN it may be difficult to achieve and maintain venous access. Therefore existing access sites are salvaged if possible.


When PN is initiated, a low glucose concentration and a low rate of infusion are used, and then both are increased gradually so that the child’s insulin production can accommodate the glucose load. Once the PN infusion is established, providers should maintain the infusion at a uniform rate as ordered; it should not be decreased or increased, because hypoglycemia or hyperglycemia can result. Once goal calories are achieved, it may be appropriate to stop the PN for increasing time intervals, allowing intervals without the PN. When neonates or children are receiving high dextrose compositions, dosing may need to be decreased and increased (with a gradual decrease in rate of administration before and gradual increase after the off cycle) to prevent hypoglycemia or hyperglycemia. To discontinue PN, the glucose concentration and the rate should be weaned gradually.


When PN infusions are initiated, serum glucose measurements can be performed several times per day. Point-of-care glucose measurements may be performed every 4 to 8   hours in infants if unit or hospital policy allows such testing. The presence of either glucosuria or ketonuria should be reported to an on-call provider, and the child’s serum glucose level should be checked. Glucosuria usually indicates the presence of high serum glucose levels that exceed the renal threshold of 150 to 200   mg/dL blood.


If the PN catheter infiltrates or becomes occluded, providers should promptly insert a temporary IV catheter to continue glucose administration and avoid the development of hypoglycemia that could result from a sudden cessation of glucose infusion. Monitor the child closely for clinical evidence of hypoglycemia (e.g., lethargy, irritability, tremors, diaphoresis, tachycardia, headache, vomiting, dizziness, blurred vision) until the PN infusion is resumed. Point-of-care glucose measurements can be obtained from infants to rule out hypoglycemia. An additional source of IV glucose administration may be needed if the PN solution contains a dextrose concentration of greater than the maximum 12.5% dextrose solutions that can be infused peripherally.


Because serum magnesium, phosphate, and calcium levels may fall during PN therapy, providers will monitor the concentration of these elements at least weekly. Trace element deficiencies are more likely to develop with long-term PN therapy or when PN therapy is used in premature infants. The signs and symptoms of copper deficiency include anemia, neutropenia, loss of taste (obviously difficult to assess), and rash. Zinc deficiency can produce an erythematous maculopapular rash (called acrodermatitis enteropathica) over the face, trunk, and digits; poor wound healing; hair loss and loss of taste; and a functional ileus.62 A chromium deficiency can produce a diabetes-like syndrome.62


Complications of the PN catheter may also develop. Cardiac arrhythmias can occur if the central venous catheter migrates into the heart, particularly into the right ventricle. Venous thrombosis can develop if a clot is allowed to form at the catheter tip. Superior vena caval thrombosis can complicate PN therapy, particularly in infants who require prolonged PN therapy. An air embolus can be caused by careless coupling of the IV line or stopcock.


Because the central venous PN catheter is inserted into a relatively large vein, a loose or cracked tubing connection can rapidly result in significant loss of blood (i.e., hemorrhage). It is important that the nurse check all tubing and catheter connections at least every hour. Because insertion of a central venous catheter creates risk of significant complications, the nurse must ensure that the catheter is secured in place with no possibility of dislodgement. If catheter misplacement or migration is suspected, a chest radiograph may be needed to verify placement (for further information, see Chapter 10).


Fat emulsions are typically piggybacked into the PN line just before the solution enters the vein. This practice evolved during the initial years of parenteral alimentation using fat emulsions and arose from a concern that prolonged contact between the PN amino acids and the lipids would cause emulsification of the fat and result in the production of fat emboli.


Administration of fat emulsion is contraindicated in neonates with jaundice. Lipid binds with albumin and will displace bilirubin, resulting in an increased risk of hyperbilirubinemia.


Children who receive prolonged PN frequently demonstrate abnormalities in liver function studies (i.e., elevation of the liver enzymes and bilirubin values). Many of these abnormalities are transient and resolve shortly after PN nutrition is discontinued; however, if these abnormalities are noted, the child should be weaned from the PN as clinically appropriate.


Cholestatic jaundice is a serious but incompletely understood complication of PN that is associated with periportal fibrosis, bile duct proliferation, and bile stasis. This complication contributes to morbidity and mortality in younger infants and children with short gut syndrome (SGS) following intestinal resection.10 The first sign of cholestatic jaundice is elevation in concentrations of liver enzymes (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]). In addition, the bilirubin will begin to rise and the child may appear jaundiced; cholestasis is defined as a direct bilirubin greater than 2   mg/dL. Risk of cholestatic jaundice can be reduced by cycling and limiting lipid administration to 1   g/kg per day or using alternate day dosing of the fat emulsion. If cholestasis is present, treatment includes administration of ursodeoxycholic acid.



Common clinical conditions



Intestinal Failure


Intestinal failure is the loss of the absorptive function of the intestine, with resulting malabsorption and malnutrition necessitating PN support. Although the terms intestinal failure and short gut syndrome (SGS) are sometimes used interchangeably, children can have intestinal failure even when they have normal bowel length. Most children afflicted with this disease are diagnosed at less than 1 year of age and are rendered “short gut” when extensive surgical resection of the intestine is required during infancy to treat congenital anomalies or necrotizing enterocolitis (NEC).


With the availability of PN as a form of replacement therapy, many children with intestinal failure survive to adulthood. Multidisciplinary teams (including a nurse practitioner, gastroenterologist, surgeon, dietitian, social worker, and speech therapist) can provide medical and surgical care for intestinal rehabilitation and to promote optimal growth and development in this patient population. Early referrals to such teams should be made for children that are dependent on PN.




Pathophysiology


Each child with intestinal failure is unique, because there are no absolute criteria for the amount and type of bowel needed to sustain absorption of nutrients for appropriate growth. The normal estimated bowel length at birth is 250 ± 40   cm.22 After the loss of a bowel segment, the intestine undergoes a process termed intestinal adaptation. As a general rule, infants can experience acceptable intestinal function with less than 15   cm of intestine if the ileocecal valve is intact, and with 30 to 45   cm of intestine if the ileocecal valve is absent or does not function.17 It is unlikely that children with less than 20   cm of remaining bowel will be able to grow and develop with enteral nutrition alone. Intestinal transplantation may offer hope to these patients.


Many children with SGS no longer have a functioning ileocecal valve; this results in more rapid intestinal transit and decreased absorption of nutrients. Small bowel distension results in stasis and bacterial overgrowth. Small bowel bacterial overgrowth can result in bacterial translocation and sepsis that contributes to morbidity and mortality in this patient population. For these reasons, enteral antibiotics, and most recently probiotics (bacteria administered to support healthy intestinal flora), are often prescribed for children with SGS to minimize small bowel bacterial overgrowth.


Intestinal adaptation is characterized by increasing intestinal mass, lengthening of villi, and improved absorption at the epithelial level.10,22 This process allows for the remaining intestine to compensate for the loss of the bowel by increasing its surface area and functional abilities.10 Successful adaptation is described as the ability to achieve normal growth, fluid balance, and electrolyte concentration without PN.53 The time frame required for adaptation is unclear and dependent on the etiology of the SBS and the functional state of the remaining bowel, although adaptation can occur over weeks to months.10,22 Children have been transitioned to enteral feedings exclusively over periods as long as 8 years. There are a number of metabolic derangements that occur after loss of bowel that are summarized in Table 14-6.


Table 14-6 Metabolic Derangements and Consequences in Children with Short Gut Syndrome































Derangements Consequences
Early
Gastric hypersecretion Peptic ulceration
Dumping syndrome Diarrhea, hyperglycemia, reactive hypoglycemia
Rapid intestinal transit Nutrient malabsorption
High output from enterostomies Electrolyte disturbances
Late
Bile and fatty acid malabsorption Gallstones, steatorrhea
Bowel dilation and stasis Bacterial overgrowth syndrome, D-lactic acidosis
Anastomotic ulceration Gastrointestinal bleeding

From Cohran VC and Kocoshis SA: Short bowel. In Baker S, Baker R, David A, editors: Pediatric nutrition support, Sudburry, MA, 2007, Jones and Bartlett.



Management


The care of patients with intestinal failure includes complementary medical and surgical interventions with the goals of optimizing oral or enteral diet, PN prescription, treatment of bacterial overgrowth, and use of stool bulking agents. Surgical procedures include bowel lengthening procedures and intestinal transplantation.


In order for the bowel to adapt it must be fed; therefore initiation of early enteral feeding is paramount. Enteral feeding can start with a continuous infusion of nutrition administered through a nasogastric, gastrostomy, or transpyloric feeding tube. Appropriate fluid administration is as important as caloric intake. Many of these children will require 150% to 160% of maintenance fluid to remain hydrated. Once a continuous rate of feeding is tolerated, the time interval can be shortened and feedings can be consolidated if larger volumes are tolerated. Once a consolidated hourly feeding schedule is tolerated, the child can be advanced to bolus feeding.


Often 20   Kcal/ounce feedings are initiated and can be advanced to higher caloric density (to as high as 30   Kcal/ounce [1   Kcal/mL]) as tolerated. Usually these children are fed with casein hydrolysate formulas and elementary amino acid-based formulas such as Pregestimil (Mead Johnson, Evansville, IN), EleCare (Abbott Nutrition, Columbus, OH), and Neocate (Nutricia North America, Gaithersburg, MD) in infants and Peptamen Jr (Nestle Nutrition, North America, Minneapolis, MN) and Neocate Jr.(Nutricia North America, Gaithersburg, MD) in older children. These formula types are easier to digest and are less likely to trigger an immune response, so they will enhance bowel adaptation.10


The eventual goal of medical and surgical therapy is appropriate growth with enteral intake alone, without the need for PN. Promotion of oral food intake should be encouraged; many of these children will have an oral aversion.


When children are unable to achieve appropriate growth with enteral feedings, they may be considered surgical candidates for procedures to restore normal bowel diameter, lengthen the bowel, or both. The goals of surgical intervention include reducing stasis, improving motility, and increasing the effective mucosal surface area.29 The most common short bowel procedures are the Bianchi, Kimura, and the serial transverse enteroplasty procedure.


The Bianchi procedure is the oldest procedure and involves a longitudinal incision to create two tubes to lengthen the bowel (Fig. 14-5). The Kimura procedure (Fig. 14-6) is an alternative procedure for patients with SGS and inadequate mesentery who are not candidates for the Bianchi procedure. The serial transverse enteroplasty (STEP) procedure augments bowel length by stapling dilated bowel in a zigzag fashion to achieve more effective bowel surface area (Fig. 14-7).





With advances in surgical techniques and immunosuppressive therapy, intestine transplantation is successful as an isolated procedure and when combined with transplantation of other organs.54 A major reason for the increased success of intestinal transplantation is the availability of more potent immunosuppressants such as tacrolimus (Prograf). The major limiting factor that prevents widespread use of transplantation is the lack of available organs for transplantation. Because children with less than 15   cm of bowel are not likely to tolerate enteral feeding and thrive, they should be referred to an intestinal rehabilitation and transplant program as soon as possible.


The ideal intestine donor has the same blood type, weighs within 10% of the recipient’s body weight, and is close in age to the recipient. All intestine recipients have a stoma to allow for bowel surveillance and access for endoscopy and biopsy. Figure 14-8 shows the technical details of isolated intestine transplant procedure and intestine transplant in combination with other organs.54



The priorities of care for patients with liver-intestine failure (so-called “ABCs” of care) in the pediatric critical care unit include aeration, bowel integrity, and caloric or hydration requirements. As with any critical care patient, the nurse will assess and support the child’s airway, breathing, and circulation. Bowel integrity is initially assessed by evaluating the physical appearance of the stoma (normal stoma appears pink and moist) and enteric output. Initially caloric requirements are met with PN. Enteral feedings are initiated as soon as possible after the transplant.


Critical care goals are to support the patient to be hemodynamically stable, with adequate oxygenation and ventilation, free of requirement for mechanical ventilation support. Airway clearance and spontaneous ventilation may be ineffective as a result of the lengthy abdominal surgical procedure (and resultant need for anesthetic administration during the long procedure), visceral edema, and pain. With the postoperative resolution of coagulopathies, aggressive chest physiotherapy is initiated. Intestine recipients generally require mechanical ventilation longer than isolated liver recipients (see Liver Transplantation in Chapter 17), because intestine recipients typically are in poor health before the transplant and often have a precarious fluid balance. Additional challenges include open abdominal wounds and potential need for surgical reexploration for complications such as perforation or bleeding.


Complications of intestine transplant procedures include rejection, infection, and posttransplant lymphoproliferative disease (PTLD). Signs and symptoms of intestinal graft rejection include a pale or dusky stoma, an increase or decrease in enteric output, abdominal pain, and guaiac positive output. Postoperative endoscopic biopsies of the transplanted bowel are made through the child’s stoma on a routine and as needed basis. Rejection is not usually a visual finding during endoscopy, and there are no known confirmatory laboratory tests. Endoscopy with biopsy is the gold standard.


Infection is a common complication following intestine transplant. Viral infection is the most threatening infection for the intestine recipient. Primary infections are typically more serious and occur when the recipient has had no previous exposure to a virus and becomes infected in the posttransplant period. A secondary infection represents reactivation of a previous latent virus.


The most common infecting organisms are cytomegalovirus and Epstein-Barr virus. For the isolated intestine recipient efforts are made to match the recipient and donor cytomegalovirus status. The donor-recipient serology relationship is important because prophylactic therapy is initiated based on viral titers.


Post-transplant lymphoproliferative disorder (PTLD) is one of the most underrated complications of immunosuppression. PTLD is the development of continually proliferating B-lymphocytes, presumably under the influence of Epstein-Barr virus. Diagnosis is made by clinical examination and histologic review. Clinical signs and symptoms include fever, lymphadenopathy, GI symptoms, and weight loss. If the biopsy specimen is diagnostic for PTLD, treatment includes holding or reducing immunosuppression and initiating IV antiviral therapy and immunoglobulin therapy (see Chapter 17 for additional information).


PTLD is a difficult complication to treat following intestine transplantation, because rejection can develop following withdrawal of immunosuppression. Therefore careful titration of immunosuppression is imperative to promote recovery, although the graft may be lost to preserve the child’s life.



Gastrointestinal Bleeding



Etiology and Pathophysiology


GI bleeding in children can result from inflammation of the intestine, congenital or acquired visceral or vascular anomalies, trauma, esophageal varices, ulcers, or coagulopathies. The incidence of acquired GI bleeding in critically ill children receiving mechanical ventilation has been reported to be as high as 51.8% in some series.14,47 Identified risk factors include a pediatric risk of mortality 2 score of 10 or higher, operating room procedures longer than 3   hours, hepatic insufficiency, coagulopathy, respiratory failure, and high-pressure ventilator settings of greater than or equal to 25   cm H2O.14,47


Upper GI bleeding originates proximal to the ligament of Treitz. Causes include gastritis, peptic ulcer disease (from nonsteroidal antiinflammatory use and from Helicobacter pylori infection), esophageal or gastric varices, and vascular malformations.


Lower GI bleeding is the result of mucosal disruption distal to the ligament of Treitz and can be caused by Crohn’s disease, intussusception, or ischemic injury. Common causes of GI bleeding in children are listed in Table 14-7.


Table 14-7 Causes of Gastrointestinal Bleeding in Infants and Children



























Age Group and Status Upper GI Bleeding Lower GI Bleeding
Healthy neonate Swallowed maternal blood, hemorrhagic disease of the newborn, esophagitis, gastric duplication Swallowed maternal blood, infectious colitis, milk allergy, hemorrhagic disease of the newborn, duplication of the bowel, Meckel’s diverticulum, anal fissure
Sick neonate Stress ulcer, gastritis, vascular malformations Necrotizing enterocolitis, infectious colitis, disseminated coagulopathy, midgut volvulus, intussusception
Infancy Stress ulcer, esophagitis, gastritis, gastric duplication Anal fissure, infectious colitis, milk allergy, nonspecific colitis, juvenile polyps, intestinal duplication, intussusception, Meckel’s diverticulum
Preschool age Esophagitis, gastritis, stress ulcer, peptic ulcer disease, foreign body, caustic ingestion, vascular disease (Rendu-Osler-Weber disease, hemophilia), trauma, portal hypertension Infectious colitis, juvenile polyps, anal fissure, intussusception, Meckel’s diverticulum, angio-dysplasia, Henoch-Schönlein purpura, hemolytic-uremic syndrome, inflammatory bowel disease
School age and adolescence Esophagitis, gastritis, stress ulcer, peptic ulcer disease, portal hypertension, trauma Infectious colitis, inflammatory bowel disease, polyps, angiodysplasia, Henoch-Schönlein purpura, hemolytic-uremic syndrome, hemorrhoids, rectal trauma

GI, Gastrointestinal.


Data from Arensman RM, Browne M, Madonna MB: Gastrointestinal bleeding. In Grosfeld JL et al, editors: Pediatric surgery, ed 6, Philadelphia, 2006, Mosby; Martin SA, Simone S: Gastrointestinal system: In Slota MC, editor: Core curriculum for pediatric critical care nursing, ed 2, St Louis, 2006, Mosby-Elsevier.


Microscopic bleeding may cause no symptoms and may be detectable only through analysis of GI secretions or feces. Significant GI bleeding may result in hypovolemia and low cardiac output, shock, and death (see also Shock, in Chapter 6). See the section on Gastrointestinal Bleeding in the Chapter 14 Supplement on the Evolve Website for additional information about the pathophysiology of GI hemorrhage.



Clinical Signs and Symptoms


The appearance of the child with GI bleeding varies considerably, and it is affected by the amount and rapidity of blood loss. Usually the child is brought to the provider’s office or emergency department for treatment after vomiting blood, passing black, tarry stools (melena), or passing bright red blood per rectum (hematochezia). Bright red vomitus indicates recent or ongoing upper GI hemorrhage, whereas coffee-ground vomitus indicates partial digestion of the blood.


The color and the source of the bleeding often help to identify the location of the bleeding. Bright red vomitus usually results from esophageal or gastric bleeding, and bright red blood in the stool results almost exclusively from rectal bleeding. Maroon, black, or tarry stool often indicates the presence of upper GI bleeding; the color derives from blood that is partially digested during passage through the bowel.


The patient with sudden, significant bleeding is more likely to demonstrate faintness, pallor, tachycardia, thready pulses, diaphoresis, thirst, apprehension, and other signs of acute blood loss. The child with gradual bleeding, however, may experience only weakness and faintness; the child may be aware of passing black stools, but may not know that significant blood loss has occurred.


The child with GI bleeding may have a normal systolic blood pressure, particularly in the recumbent position, despite significant intravascular volume loss and shock. Signs of decreased peripheral perfusion are usually the earliest signs of severe hemorrhage and include tachycardia; cool, pale, mottled skin; decreased peripheral pulses; and oliguria (urine output averaging less than 0.5-1.0   mL/kg per hour despite adequate fluid intake) or anuria.


Arterial constriction makes blood pressure measurement by cuff difficult or inaccurate, because automated oscillometric blood pressure cuffs may provide falsely high readings in the presence of shock with or without hypotension. The arterial waveform displayed from an indwelling arterial line usually is dampened in appearance, with a narrow pulse pressure.


Metabolic acidosis and a rise in serum lactate may be noted. Oxyhemoglobin desaturation may not be present or detected by pulse oximetry, because existing hemoglobin may be saturated with oxygen. The oximeter device may have difficulty detecting a signal if the child’s pulses are weak. The nurse should notify an on-call provider immediately of these findings, because the patient’s status is critical (see Chapter 6 for more information about recognition and treatment of shock).


Digested blood has a specific odor that may be noted on the patient’s breath even before the onset of melena or the first expulsion of hematemesis. This odor is qualitatively the same as that of melena, but it is usually fainter. To detect early evidence of GI bleeding, all GI fluids and stools of patients at risk should be tested for the presence of blood (hemoprotein). The presence of occult blood in gastric fluid may be determined with point-of-care (bedside) testing such as the use of Gastroccult (Beckman Coulter, Brea, CA).


During the first days of life, the Apt test (named for Leonard Apt) may be performed to distinguish between swallowed maternal blood and GI bleeding as a cause of blood in the newborn’s stool.4 The Apt test is performed by placing blood from the neonate on filter paper with 1% sodium hydroxide (a reagent that reacts with fetal hemoglobin).4 Maternal blood will appear rusty brown, whereas the neonate’s blood that contains fetal hemoglobin will remain pink or red.4 The pink or red color is a positive result, indicative of presence of blood from the neonate.



Management


The three phases of management of the child with GI bleeding are resuscitation, specific diagnosis, and specific treatment. A diagnostic algorithm for upper GI bleeding is presented in Fig. 14-9.



During resuscitation and replacement of intravascular volume, nursing observations may help to determine the source of the child’s bleeding. If saline lavage through a nasogastric tube reveals grossly bloody or red-tinged aspirate, ongoing upper intestinal bleeding is present. Nursing interventions during resuscitation of the child with GI bleeding are summarized in Box 14-1.



Box 14-1 Nursing Interventions During Resuscitation of the Child with GI Bleeding




1. Assess and support airway, breathing, and oxygenation. Optimize oxygenation and provide supplementary oxygen as indicated. If the child’s level of consciousness is decreased, the child will likely require insertion of an advanced airway and support of ventilation.


2. Restore adequate intravascular volume. Establish vascular (intravascular or intraosseous) access. Because the rate of intravenous fluid replacement will be limited by the size of the vascular catheter, insert the largest catheter possible. It is preferable to establish two vascular catheters to allow one catheter to be used for rapid volume expansion while the other is used for administering medication and measuring the child’s CVP.


3. Assess systemic perfusion. Monitor arterial and central venous pressures and systemic perfusion.





4. Insert a urinary catheter to monitor urine output.


5. Obtain blood samples for frequent (at least every 4   h) measurement of hematocrit or complete blood count; notify an on-call provider if either falls.


6. Administer blood volume expanders or packed red blood cells as ordered. Children with active gastrointestinal bleeding should have an active type and cross match with blood available at all times.






7. Assess for signs of further hemorrhage, including signs of poor systemic perfusion, abdominal pain or tenderness, changes in bowel sounds, hematemesis, or hematochezia.


8. Administer antibleeding pharmacologic agents as prescribed. See Table 14-8 for specific drug information.


Proton pump inhibitors and histamine-2 receptor antagonists are the most commonly used pharmacologic agents to prevent the development of GI bleeding (Table 14-8). Although only a small number of critically ill children will develop gastric bleeding, the associated morbidity justifies the common practice of prophylaxis.



Upper GI endoscopy is indicated when bleeding is significant. It can be performed in the critical care unit and is the diagnostic procedure of choice. Push endoscopy is one method, and newer diagnostic tools include video capsule endoscopy. For diagnosis of small bowel bleeding, video capsule endoscopy can be a valuable diagnostic tool. A minute endoscope is embedded in a capsule that is swallowed. The capsule is propelled by peristalsis and captures images that are recorded on a hard drive attached to the patient’s belt.


Indications for urgent surgical intervention include the development of intestinal perforation (identified by the presence of free air on an abdominal radiograph) or severe hemorrhage unresponsive to blood replacement therapy. If GI bleeding is stopped effectively with medical management and after resuscitation is complete, further studies will be performed to determine the origin of the bleeding and whether the patient is stable. Surgical intervention may be required at that time.



Hyperbilirubinemia



Etiology


Bilirubin is the major byproduct of hemoglobin breakdown. Hyperbilirubinemia is an elevation in the level of total serum bilirubin (TSB); it results from an imbalance between bilirubin production and excretion. An increase in bilirubin production can result from increased red blood cell (RBC) breakdown (such as hemolysis or decreased RBC life span in the neonate), or impaired bilirubin excretion (such as decreased capacity for elimination in the neonate or cholestatic liver disease). This section addresses hyperbilirubinemia in the neonate; hyperbilirubinemia in the older child is included in the liver failure section.


When the neonate’s TSB is elevated, the bilirubin can cross the blood-brain barrier, causing acute bilirubin encephalopathy or the chronic form of bilirubin encephalopathy, kernicterus. Kernicterus is a yellow staining and brain tissue damage with degenerative lesions, resulting from central nervous system exposure to high concentrations of unconjugated bilirubin. Hyperbilirubinemia is commonly associated with prematurity, breast feeding, and other factors summarized in Box 14-2.



In the first week of life, it is estimated that approximately 60% of normal newborns will become clinically jaundiced.42 Newborns are now discharged from the hospital at approximately 24 to 48 hours after birth, before the typical TSB peak at 48 to 96 hours. As a result, hyperbilirubinemia is the most common reason for hospital readmission of the neonate. A sentinel event alert was issued by the Joint Commission in 2001, because an increased number of cases of kernicterus were being diagnosed in otherwise healthy newborns.



Pathophysiology


When RBCs reach the end of their 120-day life span, they normally are sequestered in the spleen. The cells are destroyed, and the heme portion of the hemoglobin molecule is oxidized, and bilirubin is formed. Bilirubin is bound to albumin in the plasma and taken up in the liver, where it is combined with a sugar through the action of the enzyme, bilirubin uridine diphosphate glucuronosyltransferase, making conjugated bilirubin.11 Conjugated bilirubin is water soluble, it cannot cross the blood-brain barrier, and it is normally excreted in bile (Fig. 14-10). Free bilirubin, called unconjugated (indirect) bilirubin, is lipid soluble and not water soluble. Because unconjugated bilirubin is thought to diffuse freely into the brain, high concentrations of this form of bilirubin may be neurotoxic and cause kernicterus.



Increased TSB concentrations can result from an elevation in conjugated or unconjugated bilirubin. An elevation in the level of conjugated bilirubin is known as direct hyperbilirubinemia. It most commonly results from biliary tree obstruction or liver disease, although it also may occur with metabolic disorders, sepsis, meningitis, or drug reactions.


Elevation of unconjugated bilirubin levels is known as indirect hyperbilirubinemia. It most commonly occurs as a result of excessive bilirubin production in the neonatal period. Premature and critically ill neonates bind bilirubin less effectively than do healthy infants, so indirect hyperbilirubinemia is common among premature neonates. In addition, it can result from impaired transport of bilirubin caused by hypoxia, acidosis or the administration of albumin-binding drugs that displace bilirubin from the albumin. Impaired hepatic uptake of bilirubin also may cause indirect hyperbilirubinemia.


Kernicterus is yellow (bilirubin) staining of the basal ganglia in the brain of neonates with severe jaundice. Although the precise mechanisms responsible for the entry of bilirubin into the brain are not known, disruption of the blood brain barrier from increased permeability (e.g., caused by hyperosmolarity or severe asphyxia), prolonged transit time (e.g., caused by increased central venous pressure [CVP]), or increased blood flow (e.g., caused by hypercarbia and acidosis) are thought to be contributory.63


Jaundice (icterus) can usually be detected when the child’s TSB level exceeds 3.0 to 5.0   mg/dL (normally it is less than 1.5   mg/dL). Jaundice is characterized by the accumulation of yellow pigment in the skin and other tissues. In the skin, the jaundice is apparent with digital blanching. Jaundice is usually evident first in the sclera and then progresses in a cephalocaudal distribution. The urine color may become brown as the result of the urinary excretion of conjugated bilirubin. In addition, the stools may become gray or acholic, indicating the absence of normal fecal elimination of bilirubin. Clinical signs that the jaundice is pathologic include persistently elevated direct bilirubin level, dark urine, and acholic stools. Infants with these signs should be evaluated for liver disease.


The neurotoxic sequelae of hyperbilirubinemia are the most worrisome, and a grading for acute bilirubin encephalopathy has been proposed. The earliest signs may include alteration in the tone of extensor muscles (hypotonia or hypertonia), retrocollis (backward arching of the neck), opisthotonus (backward arching of the trunk), and a poor suck.3 The early symptoms may intensify and be accompanied by a shrill cry and unexplained irritability alternating with lethargy.3 Therapy at this stage may prevent advancement of symptoms. Cessation of feeding, irritability, seizures, and altered mental status are later symptoms of acute bilirubin encephalopathy. The final stage is kernicterus and may be irreversible with the development of cerebral palsy, deafness or hearing loss, and impairment of upward gaze. Kernicterus has a significant mortality (at least 10%) and long-term morbidity (at least 70%), and most cases are reported in infants with TSB greater than 20   mg/dL.28


Noninvasive (transcutaneous) bilirubin measurements can be obtained with newer instruments. Published data suggest that in most infants the measurements are within 2 to 3   mg/dL of serum measurements and can replace TSB measurements in most cases.2 In infants undergoing phototherapy, this measurement is not reliable and should not be used.


It is possible to measure serum levels of total bilirubin and direct (or conjugated) bilirubin. Current recommendations caution against inferring the indirect (unconjugated) bilirubin from the TSB, because the difference between the total and direct bilirubin is not constant. Current guidelines recommend that providers evaluate the TSB level63; the higher the TSB, the greater the risk of bilirubin encephalopathy. Treatment is indicated for infants with bilirubin levels in excess of 20   mg/dL.



Management


If direct hyperbilirubinemia is present, the nurse should be alert for the appearance of additional signs of liver disease or decreased hepatic function. Additional diagnostic tests are indicated (these tests are reviewed in greater detail in the section, Liver Failure, later in this chapter).


Indirect hyperbilirubinemia is observed most commonly during the neonatal period, and it often complicates the care of premature infants. Neonatal indirect hyperbilirubinemia is treated with phototherapy, pharmacologic agents, or exchange transfusions to avoid kernicterus.


The current American Academy of Pediatrics (AAP) recommendations for phototherapy are based on age and TSB levels (see Evolve Fig. 14-1 in the Chapter 14 Supplement on the Evolve Website to view a graphic representation of recommended therapies based on infant age and total serum bilirubin concentration). Prophylactic phototherapy is often instituted for neonates weighing less than 1500   g. Although exclusive breast feeding can contribute to high TSB levels, the AAP recommends that breast feeding be continued with 10 to 12 feedings recommended per day, plus administration of supplementary intravenous fluid to treat dehydration.2


Phototherapy converts bilirubin to a water-soluble form that can be excreted without glucuronidation. Phototherapy units contain day lights, fluorescent tubes, fiberoptic light, and halogen bulbs. The effectiveness of phototherapy is determined by the type of light, the infant’s distance to the light, and the amount of exposed body surface area. Light emitted at a wavelength in the blue-green spectrum of 425 to 495   nm is thought to be most effective because of the optical qualities of bilirubin and the skin. The AAP recommends the use of special blue fluorescent lamps or light-emitting diodes.41,42


The infant is unclothed while receiving phototherapy to expose maximum surface area. Remove the diaper if the TSB levels are approaching exchange transfusion level. Place protective eye shields over the infant’s closed eyes, because the light can injure the retina. Exposure of body surface area may be enhanced in low-birth weight infants by placing a fiberoptic pad under the infant. Unless serum bilirubin levels are critically elevated, phototherapy should be interrupted briefly several times each day. During these interruptions the eye patches should be removed, and the infant (if condition allows) should be wrapped and held to provide comforting tactile and visual stimulation.


The infant’s insensible water loss may be increased during phototherapy, so accurate measurement of fluid intake and output is required and weights should be recorded daily. Discuss evidence of excessive fluid loss or inadequate fluid intake with the responsible provider immediately. Neonates receiving phototherapy often develop diarrhea, which can contribute to fluid loss and nutritional compromise.


The infant receiving phototherapy should be turned frequently, and pressure points should be gently massaged. The phototherapy light must be turned off while blood specimens are obtained. If the blood specimens are exposed to light (especially phototherapy), then the bilirubin may be oxidized, thus altering the measured serum bilirubin levels in the blood samples and rendering them inaccurate.


Long-term sequelae of phototherapy are not known. Known complications include potential disruption of maternal infant bonding and possible eye injuries. Transient skin bronzing can occur in infants with cholestasis, although the cause of this bronzing is not clear.


The duration of phototherapy required is affected by the TSB level, the cause of the hyperbilirubinemia, and the infant’s age. For infants readmitted for phototherapy during the first days of life, the treatment is usually discontinued when TSB levels reach 13 to 14   mg/dL. It is not uncommon for infants to experience a rebound increase in TSB level of 1 to 2   mg/dL when the therapy is discontinued.41


With the aggressive and early use of phototherapy and pharmacologic intervention, exchange transfusions are not often required. Exchange transfusions are most often used for infants with a hemolytic cause of hyperbilirubinemia. Exchange transfusion should be performed only in a pediatric or neonatal critical care unit with appropriate hemodynamic monitoring and resuscitation capabilities.


Pharmacologic options for treatment of hyperbilirubinemia include the administration of gamma globulin for hemolytic disease, possible use of tin-mesoporphyrin, and reduction of medications that bind albumin, if possible. For infants with isoimmune hemolytic disease, IV gamma globulin should be administered at a dose of 0.5 to 1   g/kg over 2   hours if TSB levels continue to rise despite phototherapy or if the TSB level is within 2 to 3   mg/dL of exchange transfusion levels.


There is some evidence to support administration of a drug that inhibits the production of heme oxygenase (the precursor to bilirubin development) to prevent hyperbilirubinemia. This drug is not yet approved by the U.S. Food and Drug Administration. Drugs that bind with serum albumin (ceftriaxone, sulfonamides, oxacillin, gentamicin, diazepam, furosemide, hydrocortisone, and digoxin) are avoided if possible, because they may displace serum bilirubin from albumin, thereby increasing the concentration of free bilirubin and the risk of bilirubin diffusion across the blood brain barrier.

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Dec 3, 2016 | Posted by in NURSING | Comments Off on Gastrointestinal and Nutritional Disorders

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