Pediatrics_Nelson

Pediatrics_Nelson. A complete blood count may provide evidence for inflammation (white blood cell [WBC] and platelet count), poornutrition or bleeding (hemoglobin, red blood cell volume, reticulocyte count), and infection (WBC number and differential, presence of toxic granulation). Serum electrolytes, bloodurea nitrogen (BUN), and creatinine help define hydration status. Tests of liver dysfunction include total and direct bilirubin, alanine aminotransferase, aspartate aminotransferase for evidence of hepatocellular injury, and γ-glutamyltransferase oralkaline phosphatase for evidence of bile duct injury. Hepatic synthetic function can be assessed by coagulation factor levels,prothrombin time, and albumin level. Pancreatic enzyme tests (amylase, lipase) provide evidence of pancreatic injury or inflammation. Urinalysis can gauge dehydration and identify a possible source of protein loss.


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Pediatrics_Nelson. Consultation with a radiologist is often advisable to discuss appropriate imaging, decide what variants of the technique to use, and learn how to prepare the patient for the study. A plain abdominal x-ray to document excessive retained stool when history is consistent with constipation and encopresis is not necessary, as examination alone can confirm the diagnosis. Endoscopy permits the direct visualization of the interior of the gut. Video endoscopes may be used even in very small infants by pediatric gastroenterologists. Wireless capsule endoscopy (Fig. 126-1) enables visualization of lesions beyond the reach of conventional endoscopes.


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Pediatrics_Nelson. Consultation with a pediatric gastroenterologist for endoscopy is recommended for further evaluation of suspectedesophageal or gastric inflammation unresponsive to medications and to confirm the diagnosis of eosinophilic esophagitisor celiac disease, evaluate gastrointestinal bleeding, evaluatesuspected inflammatory bowel disease, and screen for polypdisorders. In addition, a trained endoscopist can removeesophageal and gastric foreign bodies and place feeding tubes. Available @ StudentConsult.com Figure 126-1 Wireless capsule endoscopy: Aphthous ulcers (arrows) in jejunum diagnostic of Crohn’s disease in patient with negative find-ings on upper endoscopy and colonoscopy.


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Pediatrics_Nelson. Abdominal pain can result from injury to the intra-abdominal organs or overlying somatic structures in the abdominalwall, or from extra-abdominal diseases. Visceral pain results when autonomic nerves within the gut detect injury, transmitting sensation by nonmyelinated fibers. The pain is vague, dull,slow in onset, and poorly localized. A variety of stimuli, including normal peristalsis and various intraluminal chemical andosmotic states, activate these fibers to some degree. Regardlessof the stimulus, visceral pain is perceived when a threshold ofintensity or duration is crossed. Lower degrees of activation may result in perception of nonpainful or perhaps vaguelyuncomfortable sensations, whereas more intensive stimulation of these fibers results in pain. Overactive sensation may be thebasis of some kinds of abdominal pain, such as functional abdominal pain and irritable bowel syndrome.


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Pediatrics_Nelson. In contrast to visceral pain, somatic pain results when overlying body structures are injured. Somatic structures include the parietal peritoneum, fascia, muscles, and skin of the abdominal wall. In contrast to pain emanating from visceral injury, somatic nociceptive fibers are myelinated and are capable of rapid transmission of well-localized painful stimuli. When intra-abdominal processes cause inflammation or injury to the parietal peritoneum or abdominal wall structures, poorly localized visceral pain becomes well-localized somatic pain. For example, in acute appendicitis, the initial activation of visceral nociceptive fibers yields poorly localized discomfort in the mid-abdomen. When the inflammatory process extends to the overlying parietal peritoneum, the pain becomes severe and localizes to the right lower quadrant. This is called somatoparietal pain.


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Pediatrics_Nelson. Referred pain is a painful sensation in a body region distant from the true source of pain. The location of referred pain is predictable based on the locus of visceral injury. Stomach pain is referred to the epigastric and retrosternal regions, and liver and pancreas pain is referred to the epigastric region. Gallbladder pain often is referred to the region below the right scapula. Somatic pathways stimulated by small bowel visceral afferents affect the periumbilical area, and colonic injury results in infraumbilical referred pain.


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Pediatrics_Nelson. Acute abdominal pain can signal the presence of a dangerous intra-abdominal process (e.g., appendicitis or bowel obstruction) or may originate from extraintestinal sources (e.g., lower lobe pneumonia or urinary tract stone). Not all episodes of acute abdominal pain require emergency intervention. Appendicitis and volvulus, for example, must be ruled out as quickly as possible. Few patients presenting with acute abdominal pain actually have a surgical emergency, but they must beseparated from cases that can be managed conservatively. Table 126-1 lists a diagnostic approach to acute abdominal painin children. Events that occur with a discrete, abrupt onset, suchas passage of a stone, perforation of a viscus, or infarction, resultin a sudden onset of pain. Gradual onset of pain is common withinfectious or inflammatory causes, such as appendicitis and IBD.


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Pediatrics_Nelson. A standard group of laboratory tests usually is performed for acute abdominal pain (see Table 126-1). An abdominal x-ray series evaluates for bowel obstruction or nephrolithiasis. Ultrasound or computed tomography (CT) can visualize the appendix if appendicitis is suspected but the diagnosis remains in doubt. If the initial evaluation suggests intussusception, a barium or pneumatic (air) enema may be used to diagnose and treat this condition (see Chapter 129).


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Pediatrics_Nelson. Table 126-2 lists the differential diagnosis of acute abdominal pain in children. The urgent task of the clinician is to rule out surgical emergencies. In young children, malrotation with volvulus, incarcerated hernia, congenital anomalies, and intussusception are common concerns. In older children and teenagers, appendicitis is more common. An acute surgical abdomen is characterized by signs of peritonitis, including tenderness, abdominal wall rigidity, guarding, and absent or diminished bowel sounds. Helpful characteristics of onset, location, referral, and quality of pain are noted in Table 126-3. Available @ StudentConsult.com Recurrent abdominal pain is a common problem, affecting more than 10% of all children. The peak incidence occurs between ages 7 and 12 years. Although the differential diagnosis of recurrent abdominal pain is fairly extensive (Table 126-4),most children do not have a serious (or even identifiable) underlying illness causing the pain.


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Pediatrics_Nelson. Onset Sudden or gradual, prior episodes, association with meals, history of injury Nature Sharp versus dull, colicky or constant, burning Location Epigastric, periumbilical, generalized, right or left lower quadrant, change in location over time Associated Fever, vomiting (bilious?), diarrhea (bloody?), symptoms abdominal distention Extraintestinal Cough, dyspnea, dysuria, urinary frequency, symptoms flank pain Course of Worsening or improving, change in nature or symptoms location of pain, aggravating and alleviating factors General Growth and nutrition, general appearance, position hydration, degree of discomfort, body position Abdominal Tenderness, distention, bowel sounds, rigidity, guarding, mass Genitalia Testicular torsion, hernia, pelvic inflammatory disease, ectopic pregnancy Surrounding Breath sounds, rales, rhonchi, wheezing, flank structures tenderness, tenderness of abdominal wall structures, ribs, costochondral joints


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Pediatrics_Nelson. Surrounding Breath sounds, rales, rhonchi, wheezing, flank structures tenderness, tenderness of abdominal wall structures, ribs, costochondral joints Rectal Perianal lesions, stricture, tenderness, fecal examination impaction, blood CBC, C-reactive Evidence of infection or inflammation protein, ESR AST, ALT, GGT, Biliary or liver disease bilirubin Amylase, lipase Pancreatitis Urinalysis Urinary tract infection; bleeding due to stone, trauma, or obstruction Plain flat Bowel obstruction, appendiceal fecalith, free and upright intraperitoneal air, kidney stones abdominal films CT scan Intra-abdominal or pelvic abscess, appendicitis, Crohn’s disease, pancreatitis, gallstones, kidney stones Barium enema Intussusception, malrotation Ultrasound Gallstones, appendicitis, intussusception, pancreatitis, kidney stones


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Pediatrics_Nelson. Barium enema Intussusception, malrotation Ultrasound Gallstones, appendicitis, intussusception, pancreatitis, kidney stones ALT, Alanine aminotransferase; AST, aspartate aminotransferase; CBC, complete blood count; CT, computed tomography; ESR, erythrocyte sedimentation rate; GGT, γ-glutamyltransferase. Intussusception* Malrotation with volvulus Ileus* Incarcerated hernia Postoperative adhesion Children with functional abdominal pain characteristically have pain almost daily. The pain is not associated with meals Meconium ileus equivalent (cystic fibrosis) or relieved by defecation and is often associated with a ten-Duplication cyst dency toward anxiety and perfectionism. Symptoms often result from stress at school or in novel social situations. The *Common.


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Pediatrics_Nelson. pain often is worst in the morning and often prevents or delays children from attending school. Irritable bowel syndrome (IBS) is a subset of functional abdominal pain, characterized by onset of pain at the time of a change in stool frequency or consistency, a stool pattern fluctuating between diarrhea and constipation, and relief of pain with defecation. Symptoms in IBS are linked to gut motility. Pain is commonly accompanied in both groups of children by school avoidance, secondary gains, anxiety about imagined causes, lack of coping skills, and disordered peer relationships (Table 126-5). One needs to distinguish between functional pain/IBS andmore serious underlying disorders. Warning signs for underlying illness are listed in Table 126-6. If present, further investigation is necessary. Some laboratory evaluation is warranted


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Pediatrics_Nelson. Table 126-3 Distinguishing Features of Abdominal Pain in Children DISEASE ONSET LOCATION REFERRAL QUALITY COMMENTS Functional: irritable bowel syndrome Recurrent Periumbilical, splenic and hepatic flexures None Dull, crampy, intermittent; duration 2 h Family stress, school phobia, diarrhea and constipation; hypersensitive to pain from distention Esophageal Recurrent, after Substernal Chest Burning Sour taste in mouth; reflux meals, at bedtime Pancreatitis Acute Epigastric-hypogastric Back Constant, sharp, Nausea, emesis, marked boring tenderness Inflammatory Recurrent Depends on site of Dull cramping, Fever, weight loss, ± Lactose Recurrent with milk Lower abdomen None Cramping Distention, gaseousness, diarrhea intolerance products Urolithiasis Acute, sudden Back Groin Severe, colicky pain Hematuria Pyelonephritis Acute, sudden Back None Dull to sharp Fever, costochondral tenderness, dysuria, urinary frequency, emesis


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Pediatrics_Nelson. Urolithiasis Acute, sudden Back Groin Severe, colicky pain Hematuria Pyelonephritis Acute, sudden Back None Dull to sharp Fever, costochondral tenderness, dysuria, urinary frequency, emesis Adapted from Andreoli TE, Carpenter CJ, Plum F, et al: Cecil Essentials of Medicine, Philadelphia, 1986, WB Saunders. *Common. even in the absence of warning signs. The initial evaluationrecommended in Table 126-7 is a sensible approach, avoidingunnecessary testing and providing ample sensitivity for mostserious underlying disorders. While waiting for laboratory andultrasound results, a 3-day trial of a lactose-free diet can evaluate for lactose intolerance. If tests are normal and no warningsigns are present, testing should be stopped. If there are warning signs, progression of symptoms, or laboratory abnormalities that suggest a specific diagnosis, additional investigation may be warranted. Treatment of Recurrent Abdominal Pain


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Pediatrics_Nelson. Treatment of Recurrent Abdominal Pain A child who is repeatedly kept home from school becauseof pain receives reinforcement in the form of being excusedfrom responsibilities and withdraws from full social functioning. This tends to both increase anxiety and prolong thecourse. To break the cycle of pain and disability, the childwith functional pain must be assisted in returning to normal activities immediately. Instead of being sent home fromschool with stomachaches, a child may be allowed to take ashort break from class until symptoms abate. The child and parents should be informed that pain is likely to be worse onthe day the child returns to school as anxiety worsens dysmotility and enhances pain perception. Medications may behelpful. Fiber supplements may help to manage symptoms ofIBS. Probiotics and peppermint oil can be beneficial in treating IBS. In difficult and persistent cases, cognitive behavioral A. Diagnostic Criteria for Childhood Functional Abdominal Pain


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Pediatrics_Nelson. A. Diagnostic Criteria for Childhood Functional Abdominal Pain Must include all of the following: 1. 2. 3. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms. B. Diagnostic Criteria for Childhood Functional Abdominal Pain Syndrome Must include functional abdominal pain at least 25% of the time and 1 or more of the following: 1. Some loss of daily functioning 2. Additional somatic symptoms such as headache, limb pain, or difficulty sleeping C. Diagnostic Criteria for Irritable Bowel Syndrome Must include all of the following: 1. Abdominal discomfort (an uncomfortable sensation not described as pain) or pain associated with 2 or more of the following at least 25% of the time: a. improved with defecation b. onset associated with change in frequency of stool c.


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Pediatrics_Nelson. improved with defecation b. onset associated with change in frequency of stool c. onset associated with a change in form (appearance) of stool 2. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process that explains the subject’s symptoms. D. Diagnostic Criteria for Abdominal Migraine Must include all of the following: 1. Paroxysmal episodes of intense, acute periumbilical pain that lasts for 1 hour or more. 2. Intervening periods of usual health lasting weeks to months. 3. The pain interferes with normal activities. 4. The pain is associated with 2 or more of the following: a. b. c. d. e. f. 5. No evidence of an inflammatory, anatomic, metabolic, or neoplastic process considered that explains the subject’s symptoms. *Criteria fulfilled 2 or more times in the preceding 12 months. E. Diagnostic Criteria for Cyclic Vomiting Syndrome Must include all of the following: 1.


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Pediatrics_Nelson. *Criteria fulfilled 2 or more times in the preceding 12 months. E. Diagnostic Criteria for Cyclic Vomiting Syndrome Must include all of the following: 1. Two or more periods of intense nausea and unremitting vomiting or retching lasting hours to days. 2. Return to usual state of health lasting weeks to months. F. Functional Diarrhea Must include all of the following 1. Daily painless, recurrent passage of three or more large, unformed stools. 2. Symptoms lasting more than 4 weeks. 3. Onset of symptoms that begins between 6 and 36 months of age. 4. Passage of stools that occur during waking hours. 5. There is no failure to thrive if caloric intake is adequate. Courtesy of the Rome Foundation. Abnormal screening laboratory study (anemia, hypoalbuminemia,


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Pediatrics_Nelson. 5. There is no failure to thrive if caloric intake is adequate. Courtesy of the Rome Foundation. Abnormal screening laboratory study (anemia, hypoalbuminemia, Family history of inflammatory bowel disease, celiac disease, or therapy, amitriptyline, or a selective serotonin reuptakeinhibitor may be helpful. When significant anxiety or socialdysfunction persists, a mental health professional should beconsulted. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Vomiting is a coordinated, sequential series of events that leads to forceful oral emptying of gastric contents. It is a common problem in children and has many causes. Vomiting should be distinguished from regurgitation of stomach contents, also known as gastroesophageal reflux (GER), chalasia, or “spitting up.” Although the end result of vomiting and regurgitation is similar, they have completely different characteristics. Vomiting is usually preceded by nausea and is accompanied by forceful gagging and retching. Regurgitation, on the other hand, is effortless and not preceded by nausea.


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Pediatrics_Nelson. In neonates with true vomiting, congenital obstructive lesions should be considered. Allergic reactions to formula in the first 2 months of life may present with vomiting. Infantile GER (“spitting up”) occurs in most infants and can be large in volume, but is effortless and these infants do not appear ill. Pyloric stenosis occurs in the first months of life and is characterized by steadily worsening, forceful vomiting that occurs immediately after feedings. A visibly distended stomach, often with visible peristaltic waves, is often seen before vomiting. Pyloric stenosis is more common in male infants; the family history may be positive. Other obstructive lesions, such as intestinal duplication cysts, atresias, webs, and midgut Determine degree of functional impairment (e.g., missing school) CBC ESR Amylase, lipase Urinalysis Abdominal ultrasound—examine liver, bile ducts, gallbladder, pancreas, kidneys, ureters (move to follow up)


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Pediatrics_Nelson. Urinalysis Abdominal ultrasound—examine liver, bile ducts, gallbladder, pancreas, kidneys, ureters (move to follow up) Trial of 3-day lactose-free diet CT scan of the abdomen and pelvis with oral, rectal, and intravenous contrast Barium upper GI series with small bowel follow-through Endoscopy of the esophagus, stomach, and duodenum CBC, Complete blood count; CT, computed tomography; ESR, erythrocyte sedimentation rate; GI, gastrointestinal. *Consider using one or more of these to investigate warning signs, abnormal laboratory tests, or specific or persistent symptoms.


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Pediatrics_Nelson. malrotation, should be considered. Metabolic disorders (e.g.,organic acidemias, galactosemia, urea cycle defects, adrenogenital syndromes) may present with vomiting in infants. Inolder children with acute vomiting, viruses and food poisoning are common. Other infections, especially streptococcalpharyngitis, urinary tract infections, and otitis media, commonly result in vomiting. When vomiting is chronic, centralnervous system (CNS) causes (increased intracranial pressure,migraine) must be considered. Cyclic vomiting syndrome or migraine may be the etiology of recurrent vomiting. Whenabdominal pain or bilious emesis accompanies vomiting, evaluation for bowel obstruction, peptic disorders, and appendicitismust be immediately initiated.


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Pediatrics_Nelson. Table 126-8 lists common diagnoses that must be considered and their important historical features. Given the frequency of viral gastroenteritis as the etiology, it is important to be alert for unusual features that suggest another diagnosis. Viral gastroenteritis usually is not associated with severe abdominal pain or headache and does not recur at frequent intervals. Physical examination should include assessment of the child’s hydration status, including examination of capillary refill, moistness of mucous membranes, and skin turgor (see Chapter 38). The chest should be auscultated for evidence of rales or other signs of pulmonary involvement. The abdomen must be examined carefully for distention, organomegaly, bowel sounds, tenderness, and guarding. A rectal examination and testing stool for occult blood should be considered.


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Pediatrics_Nelson. Laboratory evaluation of vomiting should include serumelectrolytes, tests of renal function, complete blood count, amylase, lipase, and liver function tests. Additional testing may berequired immediately when history and examination suggest aspecific etiology. Ultrasound is useful to look for pyloric steno-sis, gallstones, renal stones, hydronephrosis, biliary obstruction,pancreatitis, malrotation, intussusception, and other anatomic Table 126-8 Differential Diagnosis and Historical Features of Vomiting DIFFERENTIAL DIAGNOSIS HISTORICAL CLUES Viral gastroenteritis Fever, diarrhea, sudden onset, absence of pain Gastroesophageal reflux Effortless, not preceded by nausea, chronic Hepatitis Jaundice, history of exposure Otitis media Fever, ear pain Urinary tract infection Dysuria, unusual urine odor, frequency, incontinence Pneumonia Cough, fever, chest discomfort Milk or soy protein intolerance (infants) Associated with particular formula or food, blood in stools


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Pediatrics_Nelson. Pneumonia Cough, fever, chest discomfort Milk or soy protein intolerance (infants) Associated with particular formula or food, blood in stools Peptic ulcer or gastritis Epigastric pain, blood or coffee-ground material in emesis, pain relieved by acid blockade Appendicitis Fever, abdominal pain migrating to the right lower quadrant, tenderness Intestinal atresia Neonate, usually bilious, polyhydramnios Midgut malrotation Pain, bilious vomiting, GI bleeding, shock Intussusception Colicky pain, lethargy, vomiting, currant jelly stools, mass occasionally Duplication cysts Colic, mass Pyloric stenosis Nonbilious vomiting, postprandial, <4 mo old, hunger, progressive weight loss Bacterial gastroenteritis Fever, often with bloody diarrhea Hydrocephalus Large head, altered mental status, bulging fontanelles Meningitis Fever, stiff neck Migraine syndrome Attacks scattered in time, relieved by sleep; headache Cyclic vomiting syndrome Similar to migraine, usually no headache


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Pediatrics_Nelson. Meningitis Fever, stiff neck Migraine syndrome Attacks scattered in time, relieved by sleep; headache Cyclic vomiting syndrome Similar to migraine, usually no headache Brain tumor Morning vomiting, accelerating over time, headache, diplopia Motion sickness Associated with travel in vehicle Metabolic disease Presentation early in life, worsens when catabolic or exposure to substrate Pregnancy Morning, sexually active, cessation of menses Drug reaction or side effect Associated with increased dose or new medication Cancer chemotherapy Temporarily related to administration of chemotherapeutic drugs abnormalities. CT may be indicated to rule out appendicitis or to observe structures that cannot be visualized well by ultrasound. Barium studies can show obstructive or inflammatorylesions of the gut and can be therapeutic, as in the use of contrast enemas for intussusception (see Chapter 129).


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Pediatrics_Nelson. Treatment needs to address the consequences and the causesof the vomiting. Dehydration must be treated with fluid resuscitation. This can be accomplished in most cases with oralfluid-electrolyte solutions, but intravenous (IV) fluids may berequired. Electrolyte imbalances should be corrected by appropriate choice of fluids. Underlying causes should be treatedwhen possible.


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Pediatrics_Nelson. The use of antiemetic medications is controversial. These drugs should not be prescribed until the etiology of the vomitingis known, and then only for severe symptoms. Phenothiazines, such as prochlorperazine, may be useful for reducing symptoms in food poisoning and motion sickness. Their side-effectprofile must be considered carefully, however, and the doseprescribed should be conservative. Anticholinergics (e.g., scopolamine) and antihistamines (e.g., dimenhydrinate) are usefulfor the prophylaxis and treatment of motion sickness. Drugsthat block serotonin 5-HT3 receptors, such as ondansetron andgranisetron, are frequently used for viral gastroenteritis and canimprove tolerance of oral rehydration therapy. They are helpful for chemotherapy-induced vomiting, often combined withdexamethasone. No antiemetic should be used in patients withsurgical emergencies or when a specific treatment of the underlying condition is possible. Correction of dehydration, ketosis,and acidosis is helpful


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Pediatrics_Nelson. No antiemetic should be used in patients withsurgical emergencies or when a specific treatment of the underlying condition is possible. Correction of dehydration, ketosis,and acidosis is helpful to reduce vomiting in most patients withviral gastroenteritis.


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Pediatrics_Nelson. Available @ StudentConsult.com Diarrhea is a major cause of childhood morbidity and mortality worldwide. Deaths from diarrhea are rare in industrializedcountries, but are common elsewhere. Acute diarrhea is a majorproblem when it occurs with malnutrition or in the absence ofbasic medical care (see Chapter 30). In North America, mostacute diarrhea is viral and is self-limited, requiring no diagnostic testing or specific intervention. Bacterial agents tend to causemuch more severe illness and typically are seen in food-associated outbreaks or in regions with poor public sanitation. Bacterial enteritis should be suspected when there is dysentery(bloody diarrhea with fever) and whenever severe symptoms arepresent. These infections can be diagnosed by stool culture orother assays for specific pathogens. Chronic diarrhea lasts more than 2 weeks and has a wide range of possible causes, includingserious and benign conditions that are more difficult to diagnose.


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Pediatrics_Nelson. Parents use the word diarrhea to describe loose or watery stools, excessively frequent stools, or stools that are large in volume. Constipation with overflow incontinence can be mislabeled as diarrhea. A more exact definition of diarrhea is excessive daily stool liquid volume (>10 mL stool/kg body weight/day). Stool texture, volume, and frequency help to characterize the episode of diarrhea.


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Pediatrics_Nelson. Diarrhea may be classified by etiology or by physiologic mechanisms (secretory or osmotic). Etiologic agents include viruses,bacteria or their toxins, chemicals, parasites, malabsorbed substances, and inflammation. Table 126-9 lists common causes of diarrhea in childhood. Secretory diarrhea occurs when the intestinal mucosa directly secretes fluid and electrolytes intothe stool and is the result of inflammation (e.g., inflammatorybowel disease, chemical stimulus). Secretion also is stimulatedby mediators of inflammation and by various hormones, suchas vasoactive intestinal peptide secreted by a neuroendocrinetumor. Cholera is a secretory diarrhea stimulated by the enterotoxin of Vibrio cholerae, which causes increased levels of cAMP within enterocytes and leads to secretion into the small-bowellumen.


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Pediatrics_Nelson. Osmotic diarrhea occurs after malabsorption of aningested substance, which “pulls” water into the bowellumen. A classic example is the diarrhea of lactose intolerance. Osmotic diarrhea also can result from generalizedmaldigestion, such as that seen with pancreatic insufficiency or with intestinal injury. Certain nonabsorbable laxatives, such as polyethylene glycol and milk of magnesia,also cause osmotic diarrhea. Fermentation of malabsorbed substances (e.g., lactose) often occurs, resulting in gas,cramps, and acidic stools. A common cause of chronic loosestools in early childhood is functional diarrhea, commonly known as toddler’s diarrhea. This condition is defined byfrequent watery stools in the setting of normal growth and Common Gastroenteritis* Gastroenteritis* Gastroenteritis* Systemic infection Food poisoning Food poisoning Antibiotic associated (?) Systemic infection Antibiotic associated Antibiotic associated


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Pediatrics_Nelson. Common Gastroenteritis* Gastroenteritis* Gastroenteritis* Systemic infection Food poisoning Food poisoning Antibiotic associated (?) Systemic infection Antibiotic associated Antibiotic associated Common Postinfectious secondary lactase deficiency Cow’s milk/soy protein intolerance Chronic nonspecific diarrhea of infancy (toddler’s diarrhea) Celiac disease Cystic fibrosis AIDS enteropathy Postinfectious secondary lactase deficiency Irritable bowel syndrome Celiac disease Lactose intolerance Giardiasis Inflammatory bowel disease Irritable bowel syndrome Inflammatory bowel disease Lactose intolerance Giardiasis Laxative abuse (anorexia nervosa) Celiac disease


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Pediatrics_Nelson. Rare Primary immune defects Familial villous atrophy (?) Secretory tumors Congenital chloridorrhea Acrodermatitis enteropathica Lymphangiectasia Abetalipoproteinemia Eosinophilic gastroenteritis Short bowel syndrome Intractable diarrhea syndrome Autoimmune enteropathy Factitious Acquired immune defects Secretory tumors Secretory tumor Primary bowel tumor Pseudo-obstruction AIDS enteropathy Factitious AIDS enteropathy AIDS, Acquired immunodeficiency syndrome. *Gastroenteritis includes viral (rotavirus, norovirus, astrovirus) and bacterial (Salmonella, Shigella, Escherichia coli, Clostridium difficile, Yersinia, Campylobacter, other) agents. weight gain and is caused by excessive intake of sweetened liquids, overwhelming the disaccharide absorptive capacityof the intestine. Diarrhea typically improves tremendouslywhen the child’s beverage intake is reduced or changed. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Stools are isosmotic, even in osmotic diarrhea, because of the relatively free exchange of water across the intestinalmucosa. Osmoles present in the stool are a mixture of electrolytes and other osmotically active solutes. To determinewhether the diarrhea is osmotic or secretory, the osmotic gap is calculated: Assuming the stool is isosmotic (an osmolarity of 290 mOs-m/L), the measured stool sodium and potassium (and their associated anions, accounting for an equal amount) accounts for much of the osmolality. Secretory diarrhea is characterized by an osmotic gap of less than 50. A number significantly higher than 50 defines osmotic diarrhea and indicates that malabsorbed substances other than electrolytes account for fecal osmolarity.


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Pediatrics_Nelson. Another way to differentiate between osmotic and secretory diarrhea is to stop all feedings (in hospitalized patientsreceiving intravenous fluids). If the diarrhea stops completely while the child is NPO (nothing by mouth), thepatient has osmotic diarrhea. A child with a pure secretory diarrhea would continue to have massive stool output.Neither method for classifying diarrhea works perfectly,because most diarrheal illnesses are a mixture of secretoryand osmotic components. Viral enteritis damages the intestinal lining, causing malabsorption and osmotic diarrhea. Theassociated inflammation results in release of mediators that cause excessive secretion. A child with viral enteritis mayhave decreased stool volume while NPO, but the secretorycomponent of the diarrhea persists until the inflammationresolves.


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Pediatrics_Nelson. The history should include the onset of diarrhea, number and character of stools, estimates of stool volume, and presence of other symptoms, such as blood in the stool, fever, and weight loss. Recent travel and exposures should be documented, dietary factors should be investigated, and a list of medications recently used should be obtained. Factors that seem to worsen or improve the diarrhea should be determined. Physical examination should be thorough, evaluating for abdominal distention, tenderness, quality of bowel sounds, presence of blood in the stool or a large fecal mass on rectal examination, and anal sphincter tone.


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Pediatrics_Nelson. Laboratory testing should include stool culture and complete blood count if bacterial enteritis is suspected. If diarrhea occurs after a course of antibiotics, a Clostridium difficile toxin assay should be ordered; if stools are reported to be oily orfatty, fecal fat content or fecal elastase to test for pancreatic insufficiency should be measured. Tests for specific diagnosesshould be sent when appropriate (e.g., serum antibody testsfor celiac disease; colonoscopy for suspected ulcerative colitis). A trial of lactose restriction for several days or lactosebreath hydrogen testing is helpful in the evaluation of lactoseintolerance. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com Constipation is a common problem in childhood. When a child is thought to be constipated, his parents may be concerned about straining with defecation, hard stool consistency, large stool size, decreased stool frequency, fear of passing stools, or any combination of these. Physicians define constipation as two or fewer stools per week or passage of hard, pellet-like stools for at least 2 weeks. A common pattern of constipation is functional constipation, which is characterized by two or fewer stools per week, voluntary withholding of stool, and infrequent passage of large-diameter, often painful stools. Children with functional fecal retention often exhibit “retentive posturing” (standing or sitting with legs extended and stiffor crossed legs) and have associated fecal incontinence caused by leakage of retained stool (encopresis).


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Pediatrics_Nelson. The differential diagnosis is listed in Table 126-10. Functional constipation commonly occurs during toilet training, when the child is unwilling to defecate on the toilet. Retained stool becomes harder and larger over time, leading to painful defecation. This aggravates voluntary withholding of stool, with perpetuation of the constipation.


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Pediatrics_Nelson. Hirschsprung disease is characterized by delayed meconium passage in newborns, abdominal distention, vomiting, occasional fever, and foul-smelling stools. This condition is caused by failure of ganglion cells to migrate into the distal bowel, resulting in spasm and functional obstruction of the aganglionic segment. Only about 6% of infants with Hirschsprung disease pass meconium in the first 24 hours of life, compared with 95% of normal infants. Most affected babies rapidly become ill with symptoms of enterocolitis or obstruction. Affected older children do not pass large-caliber stools because of rectal spasm, and they do not have encopresis. Other causes of constipation include spinal cord abnormalities, hypothyroidism, drugs, cystic fibrosis, and anorectal malformations (see Table 126-10). A variety of systemic disorders affecting metabolism or muscle function can result in constipation. Children with developmental disabilities have a great propensity for constipation because of


Pediatrics_Nelson

Pediatrics_Nelson. A variety of systemic disorders affecting metabolism or muscle function can result in constipation. Children with developmental disabilities have a great propensity for constipation because of diminished capacity to cooperate with toileting, reduced effort or control of pelvic floor muscles during defecation, and diminished perception of the need to pass stool.


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Pediatrics_Nelson. Table 126-10 includes typical characteristics of the common causes of constipation. Congenital malformations usually cause Table 126-10 Common Causes of Constipation and Characteristic Features CAUSES OF CONSTIPATION CLINICAL FEATURES Hirschsprung disease History: Failure to pass stool in first 24 h, abdominal distention, vomiting, symptoms of enterocolitis (fever, foul-smelling diarrhea, megacolon). Not associated with large-caliber stools or encopresis Examination: Snug anal sphincter, empty, contracted rectum. May have explosive release of stool as examiner’s finger is withdrawn Laboratory: Absence of ganglion cells on rectal suction biopsy specimen, absent relaxation of the internal sphincter, “transition zone” from narrow distal bowel to dilated proximal bowel on barium enema


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Pediatrics_Nelson. Functional constipation History: No history of significant neonatal constipation, onset at potty training, large-caliber stools, retentive posturing, may have encopresis Examination: Normal or reduced sphincter tone, dilated rectal vault, fecal impaction, soiled underwear, palpable fecal mass in left lower quadrant Laboratory: No abnormalities, barium enema would show dilated distal bowel Anorectal and colonic History: Constipation from birth due to abnormal anatomy malformations Examination: Anorectal abnormalities are shown easily on physical examination Anal stenosis Anteriorly displaced anus is found chiefly in females, with a normal-appearing anus located close to the Anteriorly displaced anus posterior fourchette of the vagina Imperforate anus Laboratory: Barium enema shows the anomaly Colonic stricture


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Pediatrics_Nelson. Multisystem disease Muscular dystrophy Cystic fibrosis Diabetes mellitus Developmental delay Celiac disease History: Presence of other symptoms or prior diagnosis Examination: Specific abnormalities may be present that directly relate to the underlying diagnosis Laboratory: Tests directed at suspected disorder confirm the diagnosis Spinal cord abnormalities History: History of swelling or exposed neural tissue in the lower back, history of urinary incontinence Meningomyelocele Examination: Lax sphincter tone due to impaired innervation, visible or palpable abnormality of lower back Tethered cord usually (but not always) present Sacral teratoma or lipoma Laboratory: Bony abnormalities often present on plain x-ray. Magnetic resonance imaging (MRI) of spinal


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Pediatrics_Nelson. Drugs History: Recent use of drugs known to cause constipation Narcotics Examination: Features suggest functional constipation Psychotropics Laboratory: No specific tests available symptoms from birth. Functional constipation is overwhelmingly the most common diagnosis in older patients. Constipation in older children often begins after starting school, when free and private access to toilets may be restricted. Use of some drugs, especially opiates and some psychotropic medications, also is associated with constipation.


Pediatrics_Nelson

Pediatrics_Nelson. For a few specific causes of constipation, directed diagnostictesting can make the diagnosis. A narrowed, aganglionic distalbowel and dilated proximal bowel on barium enema suggestsHirschsprung disease. Rectal suction biopsy confirms the absenceof ganglion cells in the rectal submucosal plexus, with hypertrophy of nerve fibers. Lack of internal anal sphincter relaxation canbe shown by anorectal manometry in Hirschsprung’s disease.Hypothyroidism is diagnosed by examination and by thyroidfunction testing. Anorectal malformations are easily detected byrectal examination. Cystic fibrosis (meconium ileus) is diagnosedby sweat chloride determination or CFTR gene mutation analysis (see Chapter 137). Most children with constipation have functional constipation and do not have any laboratory abnormality. Examination reveals normal or reduced anal sphincter tone(owing to stretching by passage of large stools). Fecal impaction isusually present, but a large-caliber, empty rectum may be found ifa


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Pediatrics_Nelson. Examination reveals normal or reduced anal sphincter tone(owing to stretching by passage of large stools). Fecal impaction isusually present, but a large-caliber, empty rectum may be found ifa stool has just been passed.


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Pediatrics_Nelson. Evaluation and Treatment of Functional Constipation In most cases of constipation, the history is consistent with functional constipation—absence of neonatal constipation, active fecal retention, and infrequent, large stools with soiling. In these patients, no testing other than a good physical examination is necessary. Young children with painful defecation must have a prolonged course of stool softener therapy to alleviate fear of defecation. The child should be asked to sit on the toilet for a few minutes on awakening in the morning and immediately after meals, when the colon is most active and it is easiest to pass a stool. Use of a positive reinforcement system for taking medication and sitting on the toilet is helpful for younger children. The stool softener chosen should be non–habit forming, safe, and palatable. Polyethylene glycol and milk of magnesia are the most commonly used agents. Available @ StudentConsult.com


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Pediatrics_Nelson. Available @ StudentConsult.com GI tract bleeding can be an emergency when large-volume bleeding is present, but even the presence of small amounts of blood in stool or emesis is sufficient to cause concern. Evaluation of bleeding should include confirmation that blood truly is present, estimation of the amount of bleeding, stabilization of the patient’s intravascular blood volume, localization of the source of bleeding, and appropriate treatment of the underlying cause. When bleeding is massive, it is crucial that the Ingested maternal blood* Hematemesis or rectal, large Apt test indicates adult hemoglobin is present, cracked maternal nipples, amount Peptic disease Hematemesis, amount varies Blood found in stomach on lavage Coagulopathy Hematemesis or rectal, bruising, other sites History of home birth (no vitamin K) Allergic colitis* Streaks of bloody mucus in stool Eosinophils in feces and in rectal mucosa


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Pediatrics_Nelson. Coagulopathy Hematemesis or rectal, bruising, other sites History of home birth (no vitamin K) Allergic colitis* Streaks of bloody mucus in stool Eosinophils in feces and in rectal mucosa Necrotizing enterocolitis Rectal Sick infant with tender and distended abdomen Volvulus Hematemesis, hematochezia Acute tender distended abdomen Peptic disease Usually hematemesis, rectal possible Epigastric pain, coffee-ground emesis Esophageal varices Hematemesis History or evidence of liver disease Intussusception* Rectal bleeding Crampy pain, distention, mass Meckel diverticulum* Rectal Massive, bright red bleeding; no pain Bacterial enteritis* Rectal Bloody diarrhea, fever NSAID injury Usually hematemesis, rectal possible Epigastric pain, coffee-ground emesis >2 YEARS OLD Inflammatory bowel disease Usually rectal Crampy pain, poor weight gain, diarrhea Pseudomembranous colitis Rectal History of antibiotic use, bloody diarrhea


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Pediatrics_Nelson. Inflammatory bowel disease Usually rectal Crampy pain, poor weight gain, diarrhea Pseudomembranous colitis Rectal History of antibiotic use, bloody diarrhea Juvenile polyp Rectal Painless, bright red blood in stool; not massive Nodular lymphoid hyperplasia Rectal Streaks of blood in stool, no other symptoms Mallory-Weiss syndrome* Hematemesis Bright red or coffee-ground, follows retching Hemolytic uremic syndrome Rectal Thrombocytopenia, anemia, uremia Hemorrhoids Rectal Dilated external veins, blood with wiping NSAID, Nonsteroidal anti-inflammatory drug. *Common patient receive adequate resuscitation with fluid and blood products before moving ahead with diagnostic testing. GI bleeding has different causes at different ages (Table 126-11). Red substances in foods, beverages, or medications (such as cefdinir) occasionally can be mistaken for blood. A test for occultblood is worth performing whenever the diagnosis is in doubt.


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Pediatrics_Nelson. The GI tract may not be the source of the observed fecal blood.A history of cough and examination of the mouth, nostrils, andlungs is needed to exclude these as a source of hematemesis.Blood in the toilet or diaper may be coming from the urinarytract, vagina, or even a severe diaper rash. If the bleeding is GI, it is important to determine the source as high in the GI tract ordistal to the ligament of Treitz. Vomited blood is always proximal. Rectal bleeding may be coming from anywhere in the gut.When dark clots or melena are seen mixed with stool, a higherlocation is suspected, whereas bright red blood on the surface ofstool probably is coming from lower in the colon. When upperGI tract bleeding is suspected, a nasogastric tube may be placedand gastric contents aspirated for evidence of recent bleeding.


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Pediatrics_Nelson. The location and hemodynamic significance of the bleeding can also be assessed by history and examination. The parents should be asked to quantify the bleeding. Details of associated symptoms should be sought. Assessment of the vital signs including orthostatic changes when bleeding volume is large, pulses, capillary refill and assessment of pallor of the mucous membranes provides valuable information. Laboratory assessment and imaging studies should be ordered as indicated (Table 126-12). Coagulation tests: prothrombin time, partial thromboplastin time Tests of liver dysfunction: AST, ALT, GGT, bilirubin Occult blood test of stool or vomitus Blood type and crossmatch Evaluation of Bloody Diarrhea Stool culture, Clostridium difficile toxin Sigmoidoscopy or colonoscopy CT with contrast Evaluation of Rectal Bleeding with Formed Stools Evaluation of Hematemesis Evaluation of Bleeding with Pain and Vomiting (Bowel Obstruction)


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Pediatrics_Nelson. Evaluation of Rectal Bleeding with Formed Stools Evaluation of Hematemesis Evaluation of Bleeding with Pain and Vomiting (Bowel Obstruction) ALT, Alanine aminotransferase; AST, aspartate aminotransferase; CBC, complete blood count; CT, computed tomography; GGT, γ-glutamyltransferase; GI, gastrointestinal. Hematemesis or rectal bleeding Place NG tube Blood in stomach Yes Shock, orthostatic hypotension, poor perfusion Yes Transfer to intensive care unit Vital signs stabilized? Intravenous bolus of 20 mL/kg saline or lactated Ringer's solution Check CBC, PT, PTT, platelets Transfuse with PRBCs, FFP Platelets as required Endoscopy, imaging studies or surgery as required for diagnosis and management No Leave tube in place, monitor output Treatment of GI bleeding should begin with an initial assessment, rapid stabilization, and a logical sequence of diagnostic tests. When a treatable cause is identified, specific therapyshould be started. In many cases, the amount of blood is small,


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Pediatrics_Nelson. Figure 126-2 Initial management of gastrointestinal bleeding. CBC, Complete blood count; FFP, fresh frozen plasma; NG, nasogastric; PRBCs, packed red blood cells; PT, prothrombin time; PTT, partial thromboplastin time. and no resuscitation is required. For children with large-volume bleeds, the ABCs of resuscitation (airway, breathing, circulation) should be addressed first (see Chapters 38 and 40).Oxygen should be administered and the airway protected with an endotracheal tube if massive hematemesis is present. Fluid boluses and transfusion with packed red blood cells as required should be administered through two large-bore IVs. Frequent reassessment should continue to ensure maintenance of physiological stability (Fig. 126-2).


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Pediatrics_Nelson. Medications taken for a variety of conditions may cause oral abnormalities. Drugs with anticholinergic properties diminish saliva production and increase the risk of dental caries and parotitis. Tetracyclines taken before the eruption of the permanent teeth stain the enamel. Excessive fluoride in vitamin preparations or in drinking water can result in mottled teeth. Gingival hypertrophy may be caused by cyclosporine, phenytoin, and calcium channel blockers.


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Pediatrics_Nelson. Gastroesophageal reflux disease (GER) can lead to substantial enamel erosion and caries. Neonatal hyperbilirubinemia can result in bluish discoloration of the deciduous teeth. Renal failure is associated with mottled enamel of the permanent teeth. Congenital syphilis causes marked abnormalitiesin the shape of teeth, especially incisors and molars. Celiacdisease can result in enamel defects. Crohn’s disease is associated with oral aphthous ulcers. Abnormal pigmentation ofthe lips and buccal mucosa is seen with Peutz-Jeghers syndrome and Addison disease. Candidiasis is seen commonlywith immunodeficiency disorders and diabetes. Leukemicinfiltrates result in gum hyperplasia and bleeding; treatmentof neoplastic conditions can cause severe mucositis. Sometumors, including lymphoma, may present as mass lesions ofthe buccal cavity.


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Pediatrics_Nelson. Osteogenesis imperfecta is associated with abnormal dentin and risk of caries. Children with ectodermal dysplasiascommonly have malformed or missing teeth. Pierre Robin syndrome is associated with micrognathia and cleft palate. Disorders resulting in facial dysmorphism can have a profound effect on dental occlusion and mandibular function. Examples include mandibulofacial dysostosis, Crouzon syndrome, conditions associated with dwarfism, and others.


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Pediatrics_Nelson. Most infants are born without teeth. Natal teeth are present at birth, are usually supernumerary, and may be poorly attached. Usually, no treatment is necessary, but removal by a dentist may be needed if they are causing difficulties with feeding or injuries to the tongue. Table 127-1 presents the ages when normal deciduous teeth are acquired. The lower central incisors are typically the first to erupt, followed by the upper central incisors, lateral incisors, first molars, and bicuspids. Delayed eruption may occur in association with hypopituitarism, hypothyroidism, osteopetrosis, Gaucher disease, Down syndrome, cleidocranial dysplasia, and rickets. Deciduous teeth begin to be replaced by the permanent teeth at around age 6 PRIMARY, AGE (mo) PERMANENT, AGE (yr) years. The sequence of replacement is similar to that of the appearance of deciduous teeth.


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Pediatrics_Nelson. PRIMARY, AGE (mo) PERMANENT, AGE (yr) years. The sequence of replacement is similar to that of the appearance of deciduous teeth. Dental caries, commonly referred to as “cavities,” occurs as a result of interactions between the tooth enamel, dietary carbohydrates, and oral flora. There is increased susceptibility if the enamel is abnormal or hypoplastic. Bacteria (Streptococcus mutans) that can adhere to and colonize the teeth, survive at low pH, and produce acids during fermentation of carbohydrates cause dental caries. The diet has a significant role. A classic example is “bottle mouth,” or baby bottle caries. This condition results when infants are allowed to have a bottle in the mouth for prolonged periods, especially during sleep, and with sweet beverages or milk in the bottle. Bacteria then have continuous substrate for acid production and can destroy multiple teeth, especially the upper incisors. Sticky sweet foods, such as candy, have the same effect.


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Pediatrics_Nelson. Risk of caries is associated with lack of dental care and poorsocioeconomic status and, predictably, is greatest in developingcountries. Baby bottle caries is seen in 50% to 70% of low-incomeinfants. Treatment of caries is with dental restorative surgery. Thecarious portion is removed and filled with silver amalgam or plastic. If the damage is severe, a protective crown may be required;extraction of the tooth may be necessary when not salvageable.If not properly treated, dental decay results in inflammation andinfection of the dental pulp and surrounding alveolar bone, whichcan lead to abscess and facial space infections.


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Pediatrics_Nelson. Avoiding inappropriate use of bottles and excessive sweets isa commonsense remedy for baby bottle caries. Oral hygiene offers some protection, but young children (<8 years old)do not have the ability to brush their own teeth adequately;brushing should be done by the parents. Fluoride supplementation of community water supplies to a concentration of 1 ppm is highly effective in reducing dental caries.Home water supplies, such as from a well, should have thefluoride content tested before supplements are prescribed.If the child spends part of the day at another location, thetotal fluoride concentration from all sources must be considered before prescribing any oral supplements. Excessivefluoride supplementation causes fluorosis, a largely cosmetic defect of chalky white marks and brown staining ofthe teeth.


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Pediatrics_Nelson. Cleft lip and palate occur separately or together and affect approximately 1 in 700 infants. It is more common in Asians (1:500) and least common in Africans (1:2500). Clefting occurs with two possible patterns: isolated soft tissue cleft palate or cleft lip with or without associated clefts of the hard palate. Isolated cleft palate is associated with a higher risk of other congenital malformations. The combined cleft lip/palate type has a male predominance.


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Pediatrics_Nelson. Cleft lip is due to hypoplasia of the mesenchymal tissues withsubsequent failure of fusion. There is a strong genetic component; the risk is highest in children with affected first-degreerelatives. Monozygotic twins are affected with only 60%concordance, suggesting other nongenomic factors. Environmental factors during gestation also increase risk, including drugs (phenytoin, valproic acid, thalidomide), maternalalcohol and tobacco use, dioxins and other herbicides, and possibly high altitude. Chromosomal and nonchromosomal syndromes are associated with clefting, as are specific genesin some families.


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Pediatrics_Nelson. Cleft lip can be unilateral or bilateral and associated with cleftpalate and defects of the alveolar ridge and dentition. When present, palatal defects allow direct communication between the nasal and oral cavities, creating problems with speech and feeding. Management includes squeeze-bottle feedings, special nipples, nipples with attached shields to seal the palate, and gastrostomy in severe cases. Surgical closure of the cleftlip is usually done by 3 months of age. Closure of the palate follows, usually before 1 year of age. Missing teeth are replaced by prostheses. Cosmetic results are often good, but depend on the severity of the defect. Speech is nasal as a result of the cleft palate. Surgical treatment is effective, but sometimes does not restore palatal function completely. Speech therapy or, occasionally, the use of a speech-assisting appliance may help. Frequent episodes of otitis media are common, as are defects of teeth and the alveolar ridge.


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Pediatrics_Nelson. Oropharyngeal Candida albicans infection, or thrush, is common in healthy neonates. The organism may be acquiredin the birth canal or from the environment. Persistent infection is common in breastfed infants as a result of colonization or infection of the mother’s nipples. Thrush in healthyolder patients can occur, but should suggest the possibilityof an immunodeficiency, broad-spectrum antibiotic use, ordiabetes. Thrush is easily visible as white plaques, often with a “fuzzy” appearance, on oral mucous membranes. When scraped with a tongue depressor, the plaques are difficult to remove, and the underlying mucosa is inflamed and friable. Clinical diagnosis is usually adequate, but may be confirmed by fungal culture or potassium hydroxide smear. Oropharyngeal candidiasis is sometimes painful (especially if associated with esophagitis) and can interfere with feeding.


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Pediatrics_Nelson. Thrush is treated with topical nystatin or an azole antifungal agent such as fluconazole. When the mother’s breasts are infected and painful, consideration should be given to treating her at the same time. Because thrush is commonly self-limited in newborns, withholding therapy in asymptomatic infants and treating only persistent or severe cases is a reasonable approach. Available @ StudentConsult.com


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Pediatrics_Nelson. Gastroesophageal reflux (GER) is defined as the effortless retrograde movement of gastric contents upward into the esophagusor oropharynx. In infancy, GER is not always an abnormality.Physiologic GER (“spitting up”) is normal in infants youngerthan 8 to 12 months old. Nearly half of all infants are reportedto spit up at 2 months of age. Infants who regurgitate meet thecriteria for physiologic GER so long as they maintain adequate nutrition and have no signs of respiratory complications oresophagitis. Factors involved in causing infantile GER includeliquid diet; horizontal body position; short, narrow esophagus;small, noncompliant stomach; frequent, relatively large-volumefeedings; and an immature lower esophageal sphincter (LES).As infants grow, they spend more time upright, eat more solidfoods, develop a longer and larger diameter esophagus, have a larger and more compliant stomach, and experience lower caloric needs per unit of body weight. As a result, most infantsstop spitting up


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Pediatrics_Nelson. develop a longer and larger diameter esophagus, have a larger and more compliant stomach, and experience lower caloric needs per unit of body weight. As a result, most infantsstop spitting up by 9 to 12 months of age.


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Pediatrics_Nelson. Gastroesophageal reflux disease (GERD) occurs when GERleads to troublesome symptoms or complications such as poorgrowth, pain, or breathing difficulties. GERD occurs in a minorityof infants but is often implicated as the cause of fussiness. GERDis seen in fewer than 5% of older children. In older children, normal protective mechanisms against GER include antegradeesophageal motility, tonic contraction of the LES, and the geometry of the gastroesophageal junction. Abnormalities that causeGER in older children and adults include reduced tone of the LES, transient relaxations of the LES, esophagitis (which impairsesophageal motility), increased intra-abdominal pressure, cough,respiratory difficulty (asthma or cystic fibrosis), and hiatal hernia. Available @ StudentConsult.com Cough Hoarseness Wheezing Abdominal Pain Failure to Thrive


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Pediatrics_Nelson. Available @ StudentConsult.com Cough Hoarseness Wheezing Abdominal Pain Failure to Thrive The presence of GER is easy to observe in an infant who spits up. In older children, the refluxate is usually kept down by reswallowing, but GER may be suspected by associated symptoms, such as heartburn, cough, epigastric abdominal pain, dysphagia, wheezing, aspiration pneumonia, hoarse voice, failure to thrive, and recurrent otitis media or sinusitis. In severe cases of esophagitis, there may be laboratory evidence of anemia and hypoalbuminemia secondary to esophageal bleeding and inflammation. When esophagitis develops as a result of acid reflux, esophageal motility and LES function are impaired further, creating a cycle of reflux and esophageal injury.


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Pediatrics_Nelson. A clinical diagnosis is often sufficient in children with classic effortless regurgitation and no complications. Diagnostic studies are indicated if there are persistent symptoms or complications or if other symptoms suggest the possibility of GER in the absence of regurgitation. A child with recurrent pneumonia, chronic cough, or apneic spells without overt emesis may have occult GER. A barium upper GI series helps to rule out gastric outlet obstruction, malrotation, or other anatomic contributors to GER. Because of the brief nature of the examination, a negative barium study does not rule out GER. Another study, 24-hour esophageal pH probe monitoring, uses a pH electrode placed transnasally into the distal esophagus, with continuous recording of esophageal pH. Data typically are gathered for 24 hours and analyzed for the number and temporal pattern of acid reflux events. Esophageal impedance monitoring records the migration of electrolyte-rich gastric fluid in the esophagus.


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Pediatrics_Nelson. gathered for 24 hours and analyzed for the number and temporal pattern of acid reflux events. Esophageal impedance monitoring records the migration of electrolyte-rich gastric fluid in the esophagus. Endoscopy is useful to evaluate for esophagitis, esophageal stricture, and anatomic abnormalities.


Pediatrics_Nelson

Pediatrics_Nelson. In otherwise healthy young infants, no treatment is necessary. For infants with complications of GER, an H2 blocker or pro-ton-pump inhibitor may be offered (Table 128-1), but these have shown little benefit in infants with uncomplicated GER and/or fussiness. Prokinetic drugs, such as metoclopramide, occasionally are helpful by enhancing gastric emptying and increasing LES tone, but they are seldom very effective and may lead to complications. When severe symptoms persist despite medication, or if life-threatening aspiration is present, surgical intervention may be required. Fundoplication procedures, such as the Nissen operation, are designed to enhance the antireflux anatomy of the LES. In children with a severe neurologic defect who cannot tolerate oral or gastric tube feedings, placement of a feeding jejunostomy may be considered as an alternative to fundoplication. In older children, lifestyle changes should be discussed, including cessation of smoking, weight loss, not eating


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Pediatrics_Nelson. of a feeding jejunostomy may be considered as an alternative to fundoplication. In older children, lifestyle changes should be discussed, including cessation of smoking, weight loss, not eating before bed or exercise, and limiting intake of caffeine, carbonation, and high-fat foods. However, proton pump inhibitor therapy is more effective in reducing symptoms and healing.


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Pediatrics_Nelson. This chronic immune-mediated disorder is characterized byinfiltration of eosinophils into mucosa of the esophagus. It isthought to be triggered by non–IgE-mediated allergic reactions toingested foods or aeroallergens. EoE may have a familial connection; no specific gene has yet been identified. Incidence appears to be increasing with estimated prevalence of more than 4 per10,000 children. It may be more common in males than females. The presentation of EoE often varies with age. In young children, it may present with oral aversion, vomiting, and failure to thrive. In school-age children, it may present with vague abdominal pain or vomiting. In adolescents and adults, it presents with dysphagia and food impactions. These symptoms are attributed to the inflammatory response in the esophagus leading to edema and poor esophageal motility.


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Pediatrics_Nelson. Diagnosis requires multilevel esophageal biopsies via flexible endoscopy with the finding of more than 15 eosinophils per high-power field (Fig. 128-1). Treatment with high-dose proton pump inhibitor therapy is recommended to exclude the possibility that findings are secondary to severe acidic esophageal injury. Gross findings at endoscopy include normal appearance, esophageal furrowing, trachealization, and eosinophilic abscesses (Fig. 128-2). A barium study may reveal Table 128-1 Treatment of Gastroesophageal Reflux THERAPIES COMMENTS CONSERVATIVE THERAPIES Towel on caregiver’s shoulder Cheap, effective. Useful only for physiologic reflux Thickened feedings Reduces number of episodes, enhances nutrition Smaller, more frequent feedings Can help some. Be careful not to underfeed child Avoidance of tobacco smoke and alcohol Always a good idea. May help reflux symptoms Abstaining from caffeine Inexpensive, offers some benefit


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Pediatrics_Nelson. Avoidance of tobacco smoke and alcohol Always a good idea. May help reflux symptoms Abstaining from caffeine Inexpensive, offers some benefit Positional therapy—upright in seat, elevate Prone positioning with head of crib or bed up is helpful, but not for young infants because of risk of SIDS Weight loss when indicated Increased weight (especially abdominal) increases intra-abdominal pressure, leading to reflux H2 receptor antagonist Reduces heartburn, less effective for healing esophagitis Metoclopramide Enhances stomach emptying and LES tone. Real benefit is often minimal Feeding jejunostomy Useful in child requiring tube feeds. Delivering feeds downstream eliminates GERD GERD, Gastroesophageal reflux disease; LES, lower esophageal sphincter; SIDS, sudden infant death syndrome. Figure 128-1 Histologic image of eosinophilic esophagitis. Note the large number of eosinophils within the lamina propria.


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Pediatrics_Nelson. Figure 128-1 Histologic image of eosinophilic esophagitis. Note the large number of eosinophils within the lamina propria. a food impaction in an acutely symptomatic patient or esophageal stricture in someone with chronic disease. Exposure to identified causative antigens needs to be eliminated. Identification can be difficult, as typical allergy testing (skin prick, RAST, and immunocap assays) only identifies IgE-mediated antigens. Atopic patch testing may be more reliable but is not standardized and can be difficult to perform. One approach is to eliminate cow’s milk, soy, wheat, eggs, peanuts, and fish/shellfish from the diet, as these are the most Figure 128-2 Endoscopic picture of eosinophilic esophagi-tis. White plaques on the surface are collections of eosinophils (eosinophilic abscesses). Linear furrowing is also seen.


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Pediatrics_Nelson. Figure 128-2 Endoscopic picture of eosinophilic esophagi-tis. White plaques on the surface are collections of eosinophils (eosinophilic abscesses). Linear furrowing is also seen. common causative dietary antigens. Repeat endoscopies are often necessary to document efficacy of these eliminations. An elemental diet can also be used and is very effective, but often requires either nasogastric or gastrotomy administration because of its poor palatability. Systemic glucocorticoids can decrease symptoms, but longterm use is discouraged secondary to complications. Swallowed “topical” glucocorticoids administered via a metered dose inhaler (fluticasone) or mixed as a slurry (budesonide) Esophageal atresia Esophageal atresia H-type TEF with distal TEF with no TEF (4%) (85%) (8%)


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Pediatrics_Nelson. Esophageal atresia Esophageal atresia H-type TEF with distal TEF with no TEF (4%) (85%) (8%) Esophageal atresia Esophageal atresia with with proximal TEF proximal and distal TEF Figure 128-3 Various types of tracheoesophageal fis have shown benefit. Candida esophagitis or oral thrush are the most common side effects. Endoscopy can be used to relieve food impactions and to dilate esophageal strictures secondary to EoE. The prognosis for EoE is largely unknown. Symptoms tend to wax and wane over time. Failure to thrive or weight loss may be seen due to difficulty in eating. Food impactions are a common complication in the older child and may require endoscopic removal. Chronic inflammation of the esophagus can predispose to esophageal strictures and possibly dysplasia.


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Pediatrics_Nelson. The esophagus and trachea develop in close proximity to each other during weeks 4 to 6 of fetal life. Defects in the mesenchyme separating these two structures result in a tracheoesophageal fistula (TEF), often in association with other anomalies (renal, heart, spine, limbs). This defect occurs in about 1 in 3000 live births. TEF is not thought to be a genetic defect. The most common forms of TEF occur with esophageal atresia; the “H-type” TEF without atresia is uncommon, as is esophageal atresia without TEF (Fig. 128-3). Associated defects include the VACTERL association—vertebral anomalies (70%), anal atresia (imperforate anus) (50%), cardiac anomalies (30%), TEF (70%), renal anomalies (50%), and limb anomalies (polydactyly, forearm defects, absent thumbs, tulas (TEF) with relative frequency (%).


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Pediatrics_Nelson. syndactyly) (70%). A single-artery umbilical cord is often present. Infants with esophageal atresia have a history of polyhydramnios, exhibit drooling, and have mucus and saliva bubbling from the nose and mouth. Patients with a TEF are vulnerable to aspiration pneumonia. When TEF is suspected, the first feeding should be delayed until a diagnostic study is performed. The simplest test for TEF is to gently attempt to place a 10For larger tube via the mouth into the stomach. The passageof the tube is blocked at the level of the atresia. A chest x-rayreveals the tube coiled in the esophageal pouch. Air can beinjected through the tube to outline the atretic pouch. Barium should not be used because of extreme risk of aspiration,but a tiny amount of dilute water-soluble contrast agent canbe given carefully, then aspirated when the defect is clearlyshown.


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Pediatrics_Nelson. The treatment of TEF is surgical. The fistula is divided and ligated. The esophageal ends are approximated and anastomosed. In some cases, primary anastomosis cannot be performed because of a long gap between the proximal and distal esophagus. Various techniques have been described to treat this problem, including pulling up the stomach, elongating the esophagus by myotomy, and simply delaying esophageal anastomosis and providing continuous suction to the upper pouch while allowing for growth. The surgically reconstructed esophagus is not normal and is proneto poor motility, GER, anastomotic stricture, recurrent fistula, and leakage. The trachea also is malformed; tracheomalacia and wheezing are common.


Pediatrics_Nelson

Pediatrics_Nelson. Young children often place nonfood items in their mouths. When these items are swallowed, they may become lodged in the esophagus at the thoracic inlet or at the LES. The most common objects are coins. Smaller coins may pass harmlessly into the stomach, where they rarely cause symptoms. Other common esophageal foreign bodies include food items, small toys or toy parts, disk batteries, and other small household items. Children with a prior history of esophageal atresia or with poor motility secondary to GER or eosinophilic esophagitis are more prone to food impactions, which seldom occur in the normal esophagus.


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Pediatrics_Nelson. Some children are asymptomatic, but most exhibit some degree of drooling, food refusal, or chest discomfort. Olderchildren usually can point to the region of the chest wherethey feel the object to be lodged. Respiratory symptomstend to be minimal, but cough or wheezing may be present,especially when the esophagus is completely blocked by alarge object, such as a piece of meat, which presses on thetrachea. Plain chest and abdominal radiographs should be taken when foreign body ingestion is suspected. Metallic objectsare easily visualized. A plastic object often can be seen if thechild is given a small amount of dilute x-ray contrast material to drink, although endoscopy is probably safer and moredefinitive.


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Pediatrics_Nelson. Endoscopy is ultimately necessary in most cases to remove an esophageal foreign body. Various devices can be used to remove the object, depending on its size, shape, and location.Coins usually are grasped with special-purpose forceps andremoved. Nets, baskets, and snares also are available. Whenever objects that may threaten the airway are being recovered, endoscopy should be performed with endotrachealintubation and under general anesthesia. Removal is usually not necessary if the object is small and in the stomachas it will most likely pass without complication. Endoscopyis emergent for removal of any esophageal foreign body ifsymptomatic or if the ingested foreign body is a suspecteddisc battery in the esophagus or multiple magnets located inthe upper tract.


Pediatrics_Nelson

Pediatrics_Nelson. Sharp objects may lacerate or perforate the esophagus; smooth objects present for a long time also may result in perforation due to ulceration. Corrosive objects, such as zinc-containing pennies and disc batteries, can cause considerable local tissue injury and esophageal perforation. Magnets can lead to perforation and fistula formation when they connect between adjacent loops of bowel.


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Pediatrics_Nelson. In adolescents, caustic ingestion injuries are usually the result of suicide attempts. In toddlers, ingestion of household cleaning products typically is accidental. Injurious agents include drain cleaners, toilet bowl cleaners, dishwasher detergents, and powerful bleaching agents. Childproof lids for commercial products offer some protection, but have not eliminated the problem. Lye-based drain cleaners, especially liquid products, cause the worst injuries because they are swallowed easily and liquefy tissue rapidly. Full-thickness burns can occur in seconds. Granular products are less likely to cause esophageal injury during accidental exposures because they burn the tongue and lips and often are expelled before swallowing. Less caustic agents, such as bleach and detergents, cause less serious injury. Pill ulcers occur when certain medications (tetracyclines and nonsteroidal anti-inflammatory drugs [NSAIDs]) are swallowed without sufficient liquids, allowing prolonged direct contact


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Pediatrics_Nelson. injury. Pill ulcers occur when certain medications (tetracyclines and nonsteroidal anti-inflammatory drugs [NSAIDs]) are swallowed without sufficient liquids, allowing prolonged direct contact of the pill with the esophageal mucosa.


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Pediatrics_Nelson. Caustic burns cause immediate and severe mouth pain. The childcries out, drools, spits, and usually drops the container immediately. Burns of the lips and tongue are visible almost immediately.These burns clearly indicate the possibility of esophageal involvement, although esophageal injury can occur in the absence oforal burns. Symptoms may not be present; further evaluationby endoscopy usually is indicated with any significant history ofcaustic ingestion. Pill injury causes severe chest pain and oftenprominent odynophagia (painful swallowing) and dysphagia.


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Pediatrics_Nelson. A chest x-ray should be obtained to rule out aspiration and toinspect for mediastinal air. The child should be admitted to the hospital and given intravenous (IV) fluids until endoscopy. Thetrue extent of burns may not be endoscopically apparent immediately, but delayed endoscopy can increase the risk of perforation. Most endoscopists perform the initial endoscopy soonafter injury, when the patient has been stabilized. The extent ofinjury and severity of the burn should be carefully determined.Risk of subsequent esophageal strictures is related to the degreeof burn and whether the injury is circumferential. A nasogastric tube can be placed over a guidewire at the timeof the initial endoscopy to provide a route for feeding and to stent the esophagus. Systemic steroid use has not beenfound to be beneficial in reducing stricture formation. Broad-spectrum antibiotics should be prescribed if infection is suspected.


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Pediatrics_Nelson. Esophageal strictures, if they occur, usually develop within 1 to 2 months and can be treated with endoscopic dilation. There is a risk of perforation during dilation. Whenesophageal destruction is severe, surgical reconstructionof the esophagus using stomach or intestine may be necessary. Available @ StudentConsult.com Pyloric stenosis is an acquired condition caused by hypertrophy and spasm of the pyloric muscle, resulting in gastric outlet obstruction. It occurs in 6 to 8 per 1000 live births, has a 5-to-1 male predominance, and is more common in first-born children. Its cause is unknown.


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Pediatrics_Nelson. Infants with pyloric stenosis typically begin vomitingduring the first weeks of life, but onset may be delayed.The emesis becomes increasingly frequent and forceful astime passes. Vomiting differs from spitting up because ofits extremely forceful and often projectile nature. The vomited material never contains bile, because the gastric outlet obstruction is proximal to the duodenum. This featuredifferentiates pyloric stenosis from most other obstructivelesions of early childhood. Affected infants are ravenouslyhungry early in the course of the illness, but become morelethargic with increasing malnutrition and dehydration.The stomach becomes massively enlarged with retainedfood and secretions, and gastric peristaltic waves are often visible in the left upper quadrant. A hypertrophied pylorus (the “olive”) may be palpated. As the illness progresses,very little of each feeding is able to pass through the pylorus, and the child becomes progressively thinner and moredehydrated.


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Pediatrics_Nelson. Available @ StudentConsult.com Repetitive vomiting of purely gastric contents results inloss of hydrochloric acid; the classic laboratory finding is a hypochloremic, hypokalemic metabolic alkalosis with elevated blood urea nitrogen (BUN) secondary to dehydration. Jaundice with unconjugated hyperbilirubinemia may also occur. Plain abdominal x-rays typically show a huge stomach and diminished or absent gas in the intestine(Fig. 128-4). Ultrasound examination shows marked elongation and thickening of the pylorus (Fig. 128-5). A bariumupper GI series also may be obtained whenever doubt aboutthe diagnosis exists; this shows a “string sign” caused bybarium moving through an elongated, constricted pyloricchannel. Figure 128-4 Pyloric stenosis. Note the huge, gas-filled stomach extending across the midline, with minimal air in the intestine down-stream. (Courtesy Warren Bishop, MD.)


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Pediatrics_Nelson. Figure 128-4 Pyloric stenosis. Note the huge, gas-filled stomach extending across the midline, with minimal air in the intestine down-stream. (Courtesy Warren Bishop, MD.) Figure 128-5 Ultrasound image of infant with pyloric steno-sis. Large, fluid-filled stomach (S) is seen at right, with an elongated, thickened pylorus. The length of the pylorus is marked by the red arrows; the wall thickness is marked by the yellow arrows. Drugs NSAIDs, including aspirin Tobacco use Bisphosphonates Potassium supplements NSAIDs, Nonsteroidal anti-inflammatory drugs.


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Pediatrics_Nelson. Drugs NSAIDs, including aspirin Tobacco use Bisphosphonates Potassium supplements NSAIDs, Nonsteroidal anti-inflammatory drugs. Treatment of pyloric stenosis includes IV fluid and electrolyte resuscitation followed by surgical pyloromyotomy.Before surgery, dehydration and hypochloremic alkalosismust be corrected, generally with an initial normal salinefluid bolus followed by infusions of half-normal salinecontaining 5% dextrose and potassium chloride whenurine output is observed. In pyloromyotomy (often by laparoscope), the pyloric muscle is incised longitudinally torelease the constriction. Care is taken not to cut into the mucosa itself.


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Pediatrics_Nelson. Acid-related injury can occur in the esophagus, stomach, or duodenum. Table 128-2 lists risk factors for peptic ulcer disease in children. Helicobacter pylori is responsible for more thanhalf of ulcers in the stomach and duodenum in adults. H. pyloriplays a significant but lesser role in childhood ulcer disease. Riskfactors for acquisition of H. pylori are low socioeconomic status and poor sanitation, with the highest incidence in developing countries. Nonulcer dyspepsia includes upper abdominalsymptoms (pain, bloating, nausea, early satiety) in the absenceof gastric or duodenal ulceration. Nonulcer dyspepsia is not associated with H. pylori infection. GER (see Chapter 128) allows acidic gastric contents to injure the esophagus, resultingin esophagitis. Esophagitis is characterized by retrosternal andepigastric burning pain and is best diagnosed by endoscopy. Itcan range from minimal, with only erythema and microscopicinflammation on biopsy, to superficial erosions and finally tofrank


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Pediatrics_Nelson. andepigastric burning pain and is best diagnosed by endoscopy. Itcan range from minimal, with only erythema and microscopicinflammation on biopsy, to superficial erosions and finally tofrank ulceration.


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Pediatrics_Nelson. Typical symptoms are listed in Table 128-3. The presenceof recurrent burning epigastric and retrosternal pain is arisk factor for esophagitis. With duodenal ulcers, pain typically occurs several hours after meals and often awakenspatients at night. Eating tends to relieve the pain. Gastriculcers differ in that pain is commonly aggravated by eating, Table 128-3 Peptic Disorders, Symptoms, and Clinical Investigation SYNDROME AND ASSOCIATED SYMPTOMS CLINICAL INVESTIGATION ESOPHAGITIS Retrosternal and epigastric Endoscopy location Therapeutic trial of acid-blocker Burning pain therapy Sensation of regurgitation pH probe study Dysphagia, odynophagia Upper abdominal location Endoscopy Fullness Therapeutic trial of acid-blocker Bloating therapy Nausea Upper GI series to ligament of


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Pediatrics_Nelson. Upper abdominal location Endoscopy Fullness Therapeutic trial of acid-blocker Bloating therapy Nausea Upper GI series to ligament of Treitz—rule out malrotation CBC, ESR, amylase, lipase, abdominal ultrasound “Alarm” symptoms Weight loss Hematemesis Melena, heme-positive stools Chronic vomiting Microcytic anemia Nocturnal pain Other symptoms—same as for esophagitis and nonulcer dyspepsia Endoscopy—mandatory with alarm symptoms Test for Helicobacter pylori CBC, ESR, amylase, lipase, abdominal ultrasound CBC, Complete blood count; ESR, erythrocyte sedimentation rate; GI, gastrointestinal. resulting in weight loss. GI bleeding from either can occur.Many patients report symptom relief with antacids or acidblockers.


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Pediatrics_Nelson. resulting in weight loss. GI bleeding from either can occur.Many patients report symptom relief with antacids or acidblockers. Endoscopy can be used to diagnose the underlying condition.Empiric therapy with H2 blockers or proton pump inhibitorscan be used but may delay diagnosis of conditions such as H. pylori. For patients with chronic epigastric pain, the possibilities of inflammatory bowel disease, anatomic abnormalitysuch as malrotation, pancreatitis, and biliary disease should beruled out by appropriate testing when suspected (see Chapter126 and Table 128-3 for recommended studies). Testing for H. pylori can be performed by biopsy during endoscopy with useof a urease test or presence histologically on tissue. If endoscopyis not done, noninvasive tests for infection can be done with reasonable accuracy with H. pylori fecal antigen and 13C urea breath tests (urea is metabolized into 13CO2 by the organism).


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Pediatrics_Nelson. If H. pylori is present in association with ulcers, it should be treated with a multidrug regimen, such as omeprazole-clarithromycin-metronidazole, omeprazole-amoxicillin-clarithromycin, or omeprazole-amoxicillin-metronidazole, given twice daily for 1 to 2 weeks. Other proton-pump inhibitors may be substituted when necessary. Bismuth compounds are effective against H. pylori and can be considered. In North America, only the subsalicylate salt is available, the use of which raises some concerns about Reye syndrome and potential salicylate toxicity. Tetracycline is useful in adults, but should be avoided in children less than 8 years of age. In the absence of H. pylori, esophagitis and peptic ulcer disease are treated with a pro-ton-pump inhibitor, which yields higher rates of healing than H2 receptor antagonists. Gastric and duodenal ulcers heal in 4 to 8 weeks in at least 80% of patients. Esophagitis requires 4 to 5 months of proton-pump inhibitor treatment for optimal healing.


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Pediatrics_Nelson. Available @ StudentConsult.com Cyclic vomiting syndrome (CVS) presents with intermittentepisodes of prolonged nausea and vomiting with periods ofhealth in between. It can occur at any age but is diagnosedmost frequently in preschool to school-age children. It isthought to be a migraine variant; many patients have a positive family history of migraines, and some with CVS willeventually develop migraine headaches. Triggers to an episode often include viral illnesses, stressful or exciting events(holidays, birthdays, vacations), physical exhaustion, and menses. Episodes can start at any time, but will often start in theearly morning hours. Episodes are similar to each other in timing and duration. Repetitive vomiting can last hours todays. Patients can also have abdominal pain, diarrhea, andheadaches. Those affected are typically pale, listless, andprefer to be left alone. They may have photoor phonophobia.


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Pediatrics_Nelson. There are no specific tests for CVS, which is diagnosedbased on the history and the exclusion of other disorders.Diagnoses that should be considered include malrotationwith intermittent volvulus, UPJ obstruction, eosinophilicesophagitis, and intracranial mass lesions, and metabolic disorders. Rome III criteria for diagnosis are outlined inTable 126-5. For the acute episode, supportive treatment includes hydration; dark, quiet environment; and antiemetics such as ondansetron. In addition, abortive therapy using antimigraine medications such as NSAIDs and triptans can be used. For those with frequent or prolonged episodes, prophylactic therapy can be used, such as cyproheptadine, tricyclic antidepressants, beta blockers, or topiramate.


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Pediatrics_Nelson. During early fetal life, the midgut is attached to the yolk sacand loops outward into the umbilical cord. Beginning ataround 10 weeks’ gestation, the bowel reenters the abdomenand rotates counterclockwise around the superior mesentericartery until the cecum arrives in the right lower quadrant.The duodenum rotates behind the artery and terminates atthe ligament of Treitz in the left upper quadrant. The baseof the mesentery becomes fixed along a broad attachmentposteriorly, running from the cecum to the ligament of Treitz (Fig. 129-1A). When rotation is incomplete or otherwiseabnormal, “malrotation” is present. Incomplete rotationoccurs when the cecum stops near the right upper quadrant, and the duodenum fails to move behind the mesenteric artery; this results in an extremely narrow mesenteric root (see Fig. 129-1B) that makes the child susceptible to mid-gut volvulus, causing intestinal obstruction or mesentericartery occlusion and intestinal infarction (Fig. 129-2). It is also common


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Pediatrics_Nelson. root (see Fig. 129-1B) that makes the child susceptible to mid-gut volvulus, causing intestinal obstruction or mesentericartery occlusion and intestinal infarction (Fig. 129-2). It is also common for abnormal mesenteric attachments (Laddbands) to extend from the cecum across the duodenum,causing partial obstruction.


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Pediatrics_Nelson. Available @ StudentConsult.com About 60% of children with malrotation present withsymptoms of bilious vomiting during the first month of life.The remaining 40% present later in infancy or childhood.The emesis initially may be due to obstruction by Ladd bandswithout volvulus. When midgut volvulus occurs, the venousdrainage of the gut is impaired; congestion results in ischemia, pain, tenderness, and often bloody emesis and stools.The bowel undergoes ischemic necrosis, and the child mayappear septic. Physicians must be alert to the possibility ofvolvulus in patients with vomiting and fussiness or abdominal pain.


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Pediatrics_Nelson. Plain abdominal x-rays generally show evidence of obstruction. Abdominal ultrasound may show evidence of malrotation. An upper gastrointestinal (GI) series shows the absence of a typical duodenal “C-loop,” with the duodenum instead remaining on the right side of the abdomen. Abnormal placement of the cecum on follow-through (or by contrast enema) confirms the diagnosis. Laboratory studies are nonspecific, showing evidence of dehydration, electrolyte loss, or evidence Figure 129-1 A, Normal rotation of the midgut. Note the long axis of mesenteric attachment (line). B, Midgut malrotation. Note the narrow mesentery, which predisposes to volvulus, and the presence of Ladd bands extending across the duodenum from the abnormally elevated cecum. (From Donellan WJ, editor: Abdominal Surgery of Infancy and Childhood, Luxembourg, 1996, Harwood Academic, pp 43/6, 43/8.)


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Pediatrics_Nelson. Figure 129-2 Malrotation with volvulus. Midgut is twisted around the mesentery, with an area of darker, ischemic intestine visible. (Courtesy Robert Soper, MD.) of sepsis. A decreasing platelet count is a common indicator of bowel ischemia. in position, but postoperative adhesions tend to hold the mesentery in place, resulting in a broad attachment and eliminating the risk of recurrent volvulus. Necrotic bowel is resected and, at times, results in short gut syndrome. Available @ StudentConsult.com Congenital partial or complete blockage of the intestine is a developmental defect that occurs in about 1 in 1500 live births. Atresia occurs in several forms (Fig. 129-3). One ormore segments of bowel may be missing completely, theremay be varying degrees of obstruction caused by webs orstenosis, or there may be obliteration of the lumen in cord-like bowel remnants. The end result is obstruction with


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Pediatrics_Nelson. Treatment is surgical. The bowel is untwisted, and Ladd bands and other abnormal membranous attachments are divided. The mesentery is spread out and flattened against the posterior wall of the abdomen by moving the cecum to the leftside of the abdomen. Sutures may be used to hold the bowel upstream dilation of the bowel and small, disused intestinedistally. When obstruction is complete or high grade, bilious vomiting and abdominal distention are present in thenewborn period. In lesser cases, as in “windsock” types of intestinal webs, the obstruction is partial, and symptoms aremore subtle. Intestinal atresia presents with a history of polyhydramnios, abdominal distention and bilious vomiting in the neonatal period. If intestinal perforation is present, peritonitis and sepsis may develop.


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Pediatrics_Nelson. Plain abdominal x-rays may localize the area of atresia andidentify evidence of perforation, such as free air or calcifications typical of meconium peritonitis. Duodenal atresiaappears as a double-bubble sign (gas in the stomach andenlarged proximal duodenum), with no gas distally. Atresiasof the distal intestine are characterized by longer segments ofdilated, air-filled bowel. Contrast studies are helpful if plainfilms are not sufficient. Atresia may be a complication ofmeconium ileus associated with cystic fibrosis. Laboratory evaluation for cystic fibrosis (see Chapter 137) is indicatedin cases of small bowel atresia. A complete blood count, serum electrolytes, liver functions, and amylase should bemeasured to identify dehydration, pancreatitis, and othercomplications.


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Pediatrics_Nelson. The treatment of intestinal atresia is surgical, but surgery must be preceded by adequate hemodynamic stabilization of the patient. Intravenous (IV) fluids, nasogastric suction, and broad-spectrum antibiotics should be given. Figure 129-3 Types of intestinal atresia. A, Internal web; B, Cordlike remnant connecting proximal and distal bowel; C, Interrupted bowel with V-shaped mesenteric defect; D, “Apple peel” atresia with surviving bowel spiraling around a marginal artery; E, Multiple atresias. (From Grosfeld JL, Ballantine TVN, Shoemaker R: Operative management of intestinal atresia based on pathologic findings, J Pediatr Surg 14:368–375, 1979.)


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Pediatrics_Nelson. Gastroschisis is an abdominal wall defect, not involving the umbilicus, through which intestinal contents have herniated. In contrast to omphalocele, the bowel is not covered by peritoneum or amniotic membrane. As a result, prolonged contact with the amniotic fluid typically causes a thick, exudative covering (a “peel”) on the exposed bowel. Gastroschisis is not associated with extraintestinal anomalies, but segments of intestinal atresia are common. After surgical reduction of the defect, return of normal bowel function may be slow and requires prolonged parenteral nutrition for infants with long atretic segments (short bowel syndrome) and infants with a thick peel.


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Pediatrics_Nelson. Omphalocele is an abdominal wall defect through the umbilicus caused by failure of the intestine to return to the abdomen during fetal life. The bowel remains within the umbilicalcord and is covered by peritoneum and amniotic membranes. This defect is associated with other congenital anomalies, especially cardiac defects, Beckwith-Wiedemann syndrome, and intestinal complications. Treatment is surgical closure, whichsometimes must be performed in stages to fit the bowel into acongenitally small abdominal cavity.


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Pediatrics_Nelson. Anorectal malformations, including imperforate anus and its variants, are embryologic defects recognized at birthby the absence of a normal anal opening. Evaluation of theseinfants should include observation for emergence of meconium from the urethra or fistulas on the perineum. A urinarycatheter should be placed if urinary distention is present.In low lesions, a fistulous opening that drains meconium is present on the perineum. Low lesions commonly are associated with fistulization between the bowel and bladder, vagina,or urethra. Lateral plain x-rays show the level of the defectand show gas in the bladder caused by a fistula. Initial treatment is a colostomy to divert the fecal flow, with subsequentanogenital reconstruction. The internal sphincter muscleis functionally absent in high lesions, and continence afterrepair is difficult to achieve. All children with imperforateanus require magnetic resonance imaging (MRI) of the lumbosacral spinal cord because of high incidence of


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Pediatrics_Nelson. lesions, and continence afterrepair is difficult to achieve. All children with imperforateanus require magnetic resonance imaging (MRI) of the lumbosacral spinal cord because of high incidence of tetheredspinal cord. Urologic dysfunction is common and should beevaluated.


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Pediatrics_Nelson. Hirschsprung disease is a motility defect caused by failure of ganglion cell precursors to migrate into the distal bowel during fetal life. The aganglionic distal segment doesnot exhibit normal motility and is functionally obstructedsecondary to spasm. In 75% of cases, the involved segmentis limited to the rectosigmoid; total colonic involvement is seen in 8%. Rarely, long segments of small bowel also are aganglionic. “Ultrashort” segment involves only a few centimeters of distal rectum. About 95% of normal infants pass stool spontaneously by 24 hours of age; 95% of infantswith Hirschsprung disease do not. Symptoms of distalbowel obstruction occur with distention and bilious vomiting. If the diagnosis is not made quickly, enterocolitis can result, associated with a high rate of mortality. Diagnosis isbased on examination and one or more diagnostic studies. Abdominal distention is present in most cases. Digital rectalexamination reveals an empty rectum that clenches aroundthe


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Pediatrics_Nelson. Diagnosis isbased on examination and one or more diagnostic studies. Abdominal distention is present in most cases. Digital rectalexamination reveals an empty rectum that clenches aroundthe examiner’s finger, giving the impression of an elongatedsphincter. When the finger is withdrawn, a powerful gush ofretained stool is often expelled. A deep rectal biopsy specimen obtained surgically or by using a suction biopsy instrument is required for diagnosis. When no ganglion cells areshown in the submucosal plexus, accompanied by nerve trunk hyperplasia, the diagnosis is certain. Barium enema and anorectal manometry may be used before biopsy, butfalse-negative and false-positive results can occur. Therapy is surgical. When the bowel is markedly distended orinflamed, an initial colostomy usually is performed abovethe aganglionic segment, followed weeks later by one of several definitive repair procedures. The transanal pull-throughexcises the aganglionic bowel and creates a primary colorectal


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Pediatrics_Nelson. performed abovethe aganglionic segment, followed weeks later by one of several definitive repair procedures. The transanal pull-throughexcises the aganglionic bowel and creates a primary colorectal anastomosis without laparotomy. This procedure can beconsidered in patients with uncomplicated involvement limited to the rectosigmoid region.


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Pediatrics_Nelson. Meckel diverticulum is a remnant of the fetal omphalomesenteric duct and is an outpouching of the distal ileumpresent in 1% to 2% of the population. Although most diverticula are asymptomatic throughout life, some cause massive, painless GI bleeding. Ectopic gastric tissue within thediverticulum causes ulceration of mucosa in the adjacentileum. Meckel diverticulum may be a lead point for intussusception or may enable twisting (volvulus) of neighboring bowel around its vascular supply. Diverticulitis mimicsappendicitis. Diagnosis may be made in most cases by technetium scan (Meckel scan), which labels the acid-producingmucosa. Because not all diverticula are seen, ultrasound, barium enteroclysis, or video capsule endoscopy may beuseful. When the level of suspicion is high, surgical or laparoscopic investigation is warranted. The treatment is surgical excision. Available @ StudentConsult.com


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Pediatrics_Nelson. The peak incidence of IBD in children is in the second decadeof life. IBD includes Crohn’s disease (CD), which can involve any part of the gut, and ulcerative colitis (UC), which affects only the colon. The incidence of IBD is increasing, especiallyin industrialized countries, for reasons that are unclear. IBD is uncommon in tropical and Third World countries. It is more common in Jewish than in other ethnic populations. Geneticfactors play a role in susceptibility, with significantly higher riskif there is a family history of IBD. Having a first-degree relative with IBD increases the risk about 30-fold. Susceptibilityhas been linked to some HLA subtypes, and linkage analysishas identified multiple other susceptibility loci on several chromosomes. Environmental factors (not yet identified) also seemto play a role because there is often nonconcordance amongmonozygotic twins. It is possible that viral infections can initiate the inflammatory process. Dietary triggers are