Treatment of feeding disorders is uniquely complex, as it often bridges cutting-edge medicine with the intrica- cies of higher order personality and social dynamics, all with the worthy goal of maximizing children’s potential to feed themselves. Physicians treating feeding disorders must realize that all their medical knowledge encom- passes only one facet of the required skill-set—the remainder lies with professionals that include dietitians, speech and language pathologists, occupational thera- pists, and behavioral psychologists. A team approach, utilizing all of these professionals, is critical to achieve the desired results.
REFERENCES
1. Manikam R, Perman JA. Pediatric feeding disorders. J Clin Gastroenterol. 2000;30(1):34–46.
2. Rudolph CD. Feeding disorders in infants and children.
J Pediatr. 1994;125(6 Pt 2):S116–S124.
3. Davies WH, Satter E, Berlin KS, et al. Reconceptualizing feeding and feeding disorders in interpersonal context:
the case for a relational disorder. J Fam Psychol.
2006;20(3):409–417.
4. Lindberg L, Bohlin G, Hagekull B. Early feeding problems in a normal population. Int J Eat Disord. 1991;10(4):395–405.
5. Thommessen M, Heiberg A, Kase BF, Larsen S, Riis G.
Feeding problems, height and weight in different groups utilized for appetite stimulation in children with feed-
ing disorders.34
Generally, behavioral techniques are used in combi- nation and are fi rst employed in an outpatient setting. At times, outpatient strategies plateau or are unfeasible due to either medical complexity or a requirement for greater environmental control; in these situations inpatient treat- ment is the only opportunity. When these strategies prove insuffi cient in the outpatient setting, inpatient treatment allows a tighter control of appetite by limiting the child to three meals. Importantly, this should only be performed in an inpatient setting where weight, hydration, and glyce- mia/ketosis may be monitored. Occasionally, children may present with a primary psychiatric diagnosis that limits the effectiveness of behavioral strategies. In these cases clinicians may require psychiatric consultation to consider the use of psychotropic medications.
In both outpatient and inpatient settings, thera- peutic interventions are best conducted in specialized feeding rooms (Figure 3–5) that typically have a two- way mirror through which people may observe the ses- sion without distracting the child and feeding provider.
When a specialist is feeding, parents may be in the observation room with additional personnel receiving specialized instruction with the goal of continuing the treatment at home. When the parent is feeding, a treat- ment specialist can remotely coach the parent via a wireless earpiece.
FIGURE 3–5■ Photograph of a clinic feeding room at the Children’s Hospital of Wisconsin. The feeding room includes suitable tables and chairs for children of all ages. The room is viewed through a two-way mirror separating it from a viewing room where parents can observe a session with a psychologist or a speech and language pathologist. When the parent is feeding, he or she may also be coached remotely from this room via a wireless speaker earpiece.
and adult populations. Folia Phoniatr Logop. 1999;51 (4–5):158–171.
21. Willging JP. Endoscopic evaluation of swallowing in chil- dren. Int J Pediatr Otorhinolaryngol. 1995;32(suppl):
S107–S108.
22. Bosma JF, Hepburn LG, Josell SD, Baker K. Ultrasound demonstration of tongue motions during suckle feeding.
Dev Med Child Neurol. 1990;32(3):223–229.
23. Suiter DM, Leder SB, Karas DE. The 3-ounce (90-cc) water swallow challenge: a screening test for children with suspected oropharyngeal dysphagia. Otolaryngol Head Neck Surg. 2009;140(2):187–190.
24. Stoeckli SJ, Huisman TA, Seifert B, Martin-Harris BJ.
Interrater reliability of videofl uoroscopic swallow evalua- tion. Dysphagia. 2003;18(1):53–57.
25. Willging JP, Thompson DM. Pediatric FEESST: fi beroptic endoscopic evaluation of swallowing with sensory testing.
Curr Gastroenterol Rep. 2005;7(3):240–243.
26. Owayed AF, Campbell DM, Wang EE. Underlying causes of recurrent pneumonia in children. Arch Pediatr Adolesc Med. 2000;154(2):190–194.
27. Thurlbeck WM. Postnatal human lung growth. Thorax.
1982;37(8):564–571.
28. Weir K, McMahon S, Chang AB. Restriction of oral intake of water for aspiration lung disease in children. Cochrane Database Syst Rev. 2005;4:CD005303.
29. Brody AS, Klein JS, Molina PL, Quan J, Bean JA, Wilmott RW. High-resolution computed tomography in young patients with cystic fi brosis: distribution of abnormalities and correlation with pulmonary function tests. J Pediatr.
2004;145(1):32–38.
30. Linscheid T, Budd K, Rasnake L. Pediatric feeding prob- lems. In: Roberts M, ed. Handbook of Pediatric Psychology.
3rd ed. New York: Guilford Press; 2003:481–498.
31. Davies WH, Ackerman LK, Davies CM, Vannatta K, Noll RB. About your child’s eating: factor structure and psy- chometric properties of a feeding relationship measure.
Eat Behav. 2007;8(4):457–463.
32. Silverman A. Feeding and vomiting problems in pediatric populations. In: Roberts M, Steele R, eds. Handbook of Pediatric Psychology. 4th ed. Guilford Publications; 2009.
33. Linscheid TR. Behavioral treatments for pediatric feeding disorders. Behav Modif. 2006;30(1):6–23.
34. Davis AM, Bruce AS, Mangiaracina C, Schulz T, Hyman P.
Moving from tube to oral feeding in medically fragile nonverbal toddlers. J Pediatr Gastroenterol Nutr.
2009;49(2):233–236.
of disabled children. Acta Paediatr Scand. 1991;80(5):
527–533.
6. Thommessen M, Kase BF, Heiberg A. Growth and nutri- tion in 10 girls with Rett syndrome. Acta Paediatr.
1992;81(9):686–690.
7. Dahl M, Thommessen M, Rasmussen M, Selberg T. Feed- ing and nutritional characteristics in children with mod- erate or severe cerebral palsy. Acta Paediatr. 1996;85(6):
697–701.
8. Field D, Garland M, Williams K. Correlates of specifi c childhood feeding problems. J Paediatr Child Health.
2003;39(4):299–304.
9. Burklow KA, Phelps AN, Schultz JR, McConnell K, Rudolph C. Classifying complex pediatric feeding disor- ders. J Pediatr Gastroenterol Nutr. 1998;27(2):143–147.
10. Arvedson JC, Brodsky L. Pediatric Swallowing and Feeding;
Assessment and Management. 2nd ed. Canada: Singular Publishing Group; 2002.
11. Beauchamp GK, Mennella JA. Early fl avor learning and its impact on later feeding behavior. J Pediatr Gastroenterol Nutr. 2009;48(suppl 1):S25–S30.
12. Jiang J, Zhu W, Shi F, et al. Thick visual cortex in the early blind. J Neurosci. 2009;29(7):2205–2211.
13. Kirby M, Noel RJ. Nutrition and gastrointestinal tract assessment and management of children with dysphagia.
Semin Speech Lang. 2007;28(3):180–189.
14. Morton RE, Wheatley R, Minford J. Respiratory tract infections due to direct and refl ux aspiration in children with severe neurodisability. Dev Med Child Neurol.
1999;41(5):329–334.
15. Pentiuk SP, Miller CK, Kaul A. Eosinophilic esophagitis in infants and toddlers. Dysphagia. 2007;22(1):44–48.
16. Noel RJ, Putnam PE, Rothenberg ME. Eosinophilic esophagitis. N Engl J Med. 2004;351(9):940–941.
17. Richards CA, Milla PJ, Andrews PL, Spitz L. Retching and vomiting in neurologically impaired children after fun- doplication: predictive preoperative factors. J Pediatr Surg.
2001;36(9):1401–1404.
18. Lasser MS, Liao JG, Burd RS. National trends in the use of antireflux procedures for children. Pediatrics.
2006;118(5):1828–1835.
19. DeMatteo C, Matovich D, Hjartarson A. Comparison of clinical and videofl uoroscopic evaluation of children with feeding and swallowing diffi culties. Dev Med Child Neurol.
2005;47(3):149–157.
20. O’Donoghue S, Bagnall A. Videofl uoroscopic evaluation in the assessment of swallowing disorders in paediatric
CHAPTER 4
Diarrhea
Dawn R. Ebach
further by pathophysiologic mechanism (Figure 4–1;
Table 4–1).1 The small bowel both secretes and absorbs water and electrolytes, as well as absorbs nutrients.
Imbalance between secretion and absorption can lead to diarrhea. The primary function of the colon is to absorb fl uid and electrolytes as well as storage of its contents until it can be expelled. The colon absorbs fl uid and
DEFINITIONS AND EPIDEMIOLOGY
Diarrhea is defi ned as a change in bowel movement pattern resulting in an increase in stool volume and/or frequency, usually with loose to watery stool consis- tency. Acute and chronic diarrhea are defi ned based on duration of symptoms. Acute diarrhea lasts 14 days, whereas chronic diarrhea persists for longer. In general, to be considered diarrhea, three or more stools are passed per day. Patients with chronic diarrhea may have periods of loose or frequent stools with normal bowel movements in between episodes. Diarrhea can also be defi ned based on stool volume; however, measuring this accurately is often diffi cult. Normal stool volume is about 5–10 g of stool/kg body weight/day for infants and about 100–200 g of stool/day in children and adults. A 24-hour stool volume of 10 g/kg in infants and200 g in children and adults is considered diar- rhea. Acute diarrhea is common. It is most often sec- ondary to viral infections. Other causes of acute diar- rhea include toxin-induced diarrhea and antibiotic-associated diarrhea. Infectious diarrhea is most often found in children under age 5 years with a rate of about one to three episodes per year. Causes of chronic diarrhea are more diverse and range from func- tional disorders such as Toddler’s diarrhea and irritable bowel syndrome (IBS) to disorders that may impact overall health such as infl ammatory bowel disease or celiac disease.
PATHOGENESIS
Diarrhea occurs due to a derangement in small bowel, colonic, or pancreatic function. Besides the classifi ca- tion of acute and chronic, diarrhea may be divided
Osmotic Secretory
Motility Inflammatory
Direction of fluid flow Osmotic agent White blood cell
FIGURE 4–1 ■ (A) Normal intestine. Overall effect is absorption of fl uid. (B) Osmotic diarrhea—osmotic agents draw fl uid into the intestinal lumen. (C) Secretory diarrhea—increased fl uid into the intestinal lumen, usually secondary to opening of channels by toxins or hormones. (D) Motility—increased rate of transit reduces absorp- tion. (E) Infl ammatory—decreased absorption of water, electrolytes, and nutrients.
A
D
B
E
C
electrolytes. Disruption of the colon’s function leads to frequent, loose, and occasionally bloody stools. The motor function of the intestines regulates forward pro- pulsion of its contents. Abnormalities in this motility may also lead to diarrhea.
Osmotic diarrhea (Figure 4–1b; Table 4–1) occurs when increased solute load in the bowel lumen leads to decreased fl uid absorption and increased fl uid secre- tion.2 Stools are loose and often foul-smelling. Bloat- ing, abdominal distention, and gas are also characteris- tic. Carbohydrate malabsorption, such as from lactose intolerance, is an example of osmotic diarrhea. Another example occurs with ingestion of poorly absorbed sol- utes, including non-digestible sugars such as lactulose or sorbitol, or osmotic laxatives such as polyethylene glycol and milk of magnesia. Fat malabsorption from pancreatic insuffi ciency or bile acid depletion can also lead to osmotic diarrhea. When poorly absorbed fats and carbohydrates reach the colon, they are hydrolyzed by colonic bacteria, producing short-chain fatty acids that further increase the solute load. Injury to the small intestine mucosa results in decreased absorptive sur- face area and loss of brush border digestive enzymes, causing generalized malabsorption. Examples include decreased gut length from surgical excision and decreased absorptive area secondary to severe celiac or Crohn’s disease.
Osmotic diarrhea subsides with fasting, which eliminates the osmotic load. This can be a useful diag- nostic test for malabsorptive diarrhea in the hospital- ized patient receiving intravenous fl uids. Stool studies are also helpful, revealing an acidic pH due to fermenta- tion, with increased osmotic gap. The osmotic gap is
calculated after measuring stool sodium and potassium using the following formula:
290 2(Na K)
Because of the relatively free movement of water across the intestinal mucosa, all stools can be assumed to have an osmolarity equivalent to serum (290). The sum of sodium and potassium must be multiplied by 2 to account for their accompanying anions. An osmotic gap 50 is consistent with the presence of other unmea- sured solutes in the stool, indicating that the diarrhea is osmotic in nature.
Secretory diarrhea (Figure 4–1c; Table 4–1) is caused by derangements in mechanisms regulating fl uid and electrolyte movement in the small bowel mucosa, leading to active secretion of electrolytes, with passive loss of water.3 This is characterized by chloride and bicarbonate secretion and inhibition of sodium and chloride absorption. Disorders caused by bacterial toxins, such as cholera (Vibrio cholerae) and traveler’s diarrhea (enterotoxigenic Escherichia coli), are classic examples. Secretory diarrhea can also result from secretagogues produced by tumors; Zollinger–Ellison syndrome (gastrin) and vasoactive intestinal peptide (VIP)-secreting tumors, or VIPomas, are rare examples of this in children. Regardless of cause, secretory diar- rhea is characterized by high-volume, frequent watery stools, which persist despite fasting. Stool osmolality is similar to plasma osmolality, with no osmotic gap present.2
Infl ammatory diarrhea, typically seen with bac- terial infection and inflammatory bowel disease ( Figure 4–1e; Table 4–1), is caused by disruptions in Table 6–1.
Categories of Diarrhea
Osmotic Secretory Motility Infl ammatory
Problem Maldigestion ↑ Secretion with ↓ absorption Watery
Normal osmolality (2(Na K)) Persists with fasting
↓ Transit time
Loose to normal, often worse after eating
Infl ammation leading to
↓ colonic absorption and
↑ motility Stool characteristics Watery
↓ pH
↑ osmolality (2(Na K)) Improves with fasting
Blood and/or white blood cells present
Examples Lactose intolerance Lactulose, sorbitol, or magnesium ingestion
Cholera
Congenital Cl diarrhea Enterotoxigenic E. coli
Irritable bowel syndrome Hyperthyroidism
Salmonella Shigella Ulcerative colitis Table 4–1.
ing factors such as association with diet or stress should also be elicited. Nocturnal defecation is concerning for colonic infl ammation and makes functional diarrhea (IBS or toddler’s diarrhea) less likely. The presence of abdominal pain including timing, severity, and location can be an important clue to diagnosis. Extraintestinal manifestations such as a skin rash or joint pain that can be associated with celiac disease or infl ammatory bowel disease should be inquired about. The past med- ical history may reveal a history of bowel surgery that may raise suspicion for malabsorption due to short bowel syndrome. Surgery may also lead to intestinal strictures, adhesions, or loss of the ileocecal valve, any of which may predispose to small bowel bacterial over- growth. Medication and supplement history should be obtained. Some medications (orlistat) cause malab- sorptive diarrhea, and laxative use must be ruled out.
Ingestion of non-absorbable sugars such as “sugar- free” candy or gum or excessive juice intake can pre- cipitate abdominal cramping, gas, and diarrhea. Fam- ily history can also be helpful, particularly history of infl ammatory bowel disease or celiac disease in a fi rst- or second-degree relative. Social history should include recent travel and exposures such as animal or sick con- tacts. Attendance at daycare increases the risk for infec- tious diarrhea.
Physical exam should begin with evaluation of growth parameters. Patients with lactose intolerance and IBS usually do not have weight loss or decrease in growth percentiles. However, patients with celiac dis- ease, Crohn’s disease, or pancreatic insuffi ciency may experience growth failure. Decreased subcutaneous tissue and loose skin are also signs of weight loss and possible malabsorptive disorders. Thyroid mass or fullness with or without proptosis, along with brisk refl exes and tachycardia, is suggestive of hyperthyroid- ism. Evaluate for abdominal distention, location of tenderness, and fullness. Tenderness and fullness in the right lower quadrant is concerning for Crohn’s disease.
Digital clubbing may be a sign of chronic disease such as Crohn’s disease, celiac disease, or cystic fi brosis.
Edema is suggestive of a protein losing enteropathy that may be secondary to infl ammatory bowel disease or lymphangiectasia. Perianal exam may reveal skin tags, fi ssures, or fi stulas that are suggestive of Crohn’s disease. Skin exam may reveal dermatitis herpetiformis (celiac disease), erythema nodosum (IBD), or pyo- derma gangrenosum (IBD). Perianal rash may be pres- ent secondary to prolonged diarrhea, but also may be suggestive of carbohydrate malabsorption as stool often is acidic. A combination of perianal and perioral rash may be a sign of acrodermatitis enteropathica.
Additionally, signs of malnutrition should be noted such as sparse, brittle hair, cheilosis, or smooth tongue.
the epithelial function of the bowel.3 Bacterial toxins can alter ion transport, leading to increased secretion.
In addition, some bacteria can invade the mucosa, directly disrupting function. Injury to the epithelial barrier, including the tight junctions, alters electro- chemical gradients. Activated macrophages secrete cytokines such as tumor necrosis factor and interleu- kins such as IL-2 that increase intestinal permeability.
Infl ammation-associated diarrhea is aggravated by the release of various secretagogues, including cytokines, prostaglandins, histamine, and leukotrienes. Brush border and enterocyte injury (or death) from infl am- mation also contributes to diarrhea. In infl ammatory diarrhea, the intestinal mucosa is thickened, hypere- mic, and edematous. Stools may contain red or white blood cells. There is frequently loss of serum proteins into the stool. A component of osmotic diarrhea may also be present in infl ammatory diarrhea secondary to malabsorption.
Motility disorders can cause diarrhea ( Figure 4–1d;
Table 4–1). Increased transit time decreases the ability of the colon to absorb fl uid.4 Increased motility may be secondary to increased secretion of serotonin, hista- mine, or other mediators. IBS and hyperthyroidism are examples of diarrhea secondary to increased motility.
Decreased motility causes stasis, which leads to small bowel bacterial overgrowth and infl ammatory diar- rhea.
The above categorizations of diarrhea are helpful in narrowing down cause. However, it is important to keep in mind that many causes of diarrhea will have one or more characteristics. For example, patients with Crohn’s disease often have osmotic diarrhea secondary to malabsorption, but will also have a secretory compo- nent secondary to infl ammation. In this situation, fast- ing results in diminished stool output without complete resolution of diarrhea.
CLINICAL PRESENTATION
Children with acute diarrhea may present to their health care provider because of frequent passage of stool, abdominal pain, poor oral intake, fever, irritability, or dehydration. The clinical history should include the onset, duration, nature, and severity of symptoms.
Assessment of hydration status is the most important aspect of the physical exam.
Patients with chronic diarrhea will present to their provider for concerns of ongoing frequent stools, abdominal pain, blood in stool, bloating and gassiness, or growth failure. History should include onset and duration of symptoms including if symptoms are intermittent. Stool frequency, consistency, and visual presence of blood should be determined. Any modify-
fever and abdominal pain. Abdominal pain can be quite severe and may be mistaken for appendicitis. Salmonella andCampylobacter are the most frequently isolated bac- terial causes of diarrhea.
Campylobacter species can be found in contami- nated poultry or other farm animals. It can precipitate immunoreactive complications such as Guillain–Barre’
syndrome, reactive arthritis, or Reiter’s syndrome.9 Salmonella species can be contracted from ani- mals such as poultry and reptiles who are carriers. It is also associated with the ingestion of poultry, eggs, and dairy; however, outbreaks from other contaminated foods such as peanuts and produce have occurred. It is most commonly seen during the summer and fall.9 Pro- longed excretion of Salmonella in the stool can occur.
Invasive infections such as osteomyelitis and meningitis can occur in young infants or immunocompromised patients.8
Patients infected with Shigella often have high fevers in addition to abdominal pain and diarrhea that may or may not be bloody. Only a small number of organisms are required to initiate infection that is most often spread from person to person but may also be contracted from contaminated food or water.8 Infection with Shigella can be complicated by hemolytic uremic syndrome, Reiter’s syndrome, or toxic megacolon.9
Yersinia enterocolitica infectious diarrhea is less common than other bacterial causes of diarrhea. It is transmitted by contaminated food, especially pork products such as chitterlings (pork intestines).8 It mim- ics appendicitis in about 40% of patients. Yersinia can lead to a migratory arthritis, Reiter’s syndrome, and ery- thema nodosum.9
Contaminated food or water is the source of E.
coli. There are fi ve subtypes of E. coli. Shiga toxin- producing E. coli is the most common cause of bloody