Nelson Pediatric 22nd Edition 2024, Volume 2 PDF

 The Digestive System PART...

 The Digestive System PART XVI during a meal. Toddlers and young children also tend to eat only a lim- Section 1 ited variety of foods. Parents should be encouraged to view nutritional intake over several days and not be overly concerned about individ- Clinical Manifestations ual meals. Infancy and adolescence are periods of rapid growth; high nutrient requirements for growth may be associated with voracious appetites. The reduced appetite of toddlers and preschool children is of Gastrointestinal often a worry to parents who are used to the relatively greater dietary intake during infancy. Demonstration of age-­appropriate growth on a Disease growth curve is reassuring. The number, color, and consistency of stools can vary greatly in the same infant and between infants of similar age, without apparent explanation. The earliest stools after birth consist of meconium, a dark, viscous material that is normally passed within the first 48 hours of Chapter 351 life. With the onset of feeding, meconium is replaced by green-­brown transition stools, often containing curds, and, after 4-­5 days, by yellow-­ Normal Digestive Tract brown milk stools. Stool frequency is extremely variable in normal infants and can vary from none to seven per day. Breastfed infants can have frequent small, loose stools early (transition stools), and then after Phenomena 2-­3 weeks can have very infrequent soft stools. Some nursing infants might not pass any stool for 1-­2 weeks and then have a normal soft Asim Maqbool and Chris A. Liacouras bowel movement. The color of stool has little significance except for the presence of blood or absence of bilirubin products (white-­gray rather than yellow-­brown). The presence of vegetable matter, such as peas or corn, in the stool of an older infant or toddler ingesting solids is nor- Gastrointestinal function varies with maturity; what is a physiologic mal and suggests poor chewing and not malabsorption. A pattern of event in a newborn or infant might be a pathologic symptom at an intermittent loose stools, known as toddler’s diarrhea, occurs com- older age. A fetus can swallow amniotic fluid as early as 12 weeks of monly between 1 and 3 years of age. These otherwise healthy grow- gestation, but nutritive sucking in neonates first develops at about 34 ing children often drink excessive carbohydrate-­containing beverages. weeks of gestation. The coordinated oral and pharyngeal movements The stools typically occur during the day and not overnight. The vol- necessary for swallowing solids develop within the first few months ume of fluid intake is often excessive; limiting sugar and unabsorbable of life. Before this time, the tongue thrust is upward and outward to carbohydrate-­containing beverages and increasing fat in the diet often express milk from the nipple, instead of a backward motion, which lead to resolution of the pattern of loose stools. propels solids toward the esophageal inlet. By 1 month of age, infants A protuberant abdomen is often noted in infants and toddlers, espe- appear to show preferences for sweet and salty foods. Infants’ inter- cially after large feedings. This can result from the combination of weak est in solids increases at approximately 4 months of age. The recom- abdominal musculature, relatively large abdominal organs, and lordotic mendation to begin solids at 6 months of age is based on nutritional stance. In the first year of life, it is common to palpate the liver 1-­2 cm and cultural concepts rather than maturation of the swallowing process (see Chapter 61). Infants swallow air during feeding, and burping is encouraged to prevent gaseous distention of the stomach. A number of normal anatomic variations may be noted in the mouth. A short lingual frenulum (“tongue-­tie”) may be worrisome to parents but only rarely interferes with nursing, bottle feeding, eating, or speech, generally requiring no treatment. Surface furrowing of the tongue (a geographic or scrotal tongue) is usually a normal finding. A bifid uvula may be isolated or associated with a submucous cleft of the soft palate (Fig. 351.1). Regurgitation, the result of gastroesophageal reflux, occurs com- monly in the first year of life. Effortless regurgitation can dribble out of an infant’s mouth but also may be forceful. In an otherwise healthy infant with regurgitation; volumes of emesis are commonly approxi- mately 15-­30 mL but occasionally are larger. Most often, the infant remains happy, although possibly hungry, after an episode of regurgita- tion. Episodes can occur from one to several times per day. Regurgita- tion gradually resolves in 80% of infants by 6 months of age and in 90% by 12 months. If complications develop or regurgitation persists, gastroesophageal reflux is considered pathologic rather than merely developmental and deserves further evaluation and treatment. Com- Fig. 351.1 Classic submucous cleft palate with triad of bifid uvula (large arrow), furrow along the midline of the soft palate (arrowheads), plications of gastroesophageal reflux include failure to thrive, pulmo- and a notch in the posterior margin of the hard palate (small arrow). The nary disease (apnea or aspiration pneumonitis), and esophagitis with midline furrow is sometimes referred to as the zona pellucida, reflect- its sequelae (see Chapters 369 and 370). ing the translucent nature of this area in some patients. (From Hasan A, Infants and young children may be erratic eaters; this may be a worry Gardner A, Devlin M, Russell C. Submucous cleft palate with bifid uvula. to parents. A toddler might eat insatiably or refuse to consume food J Pediatr. 2014;165:872.) 2223 Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 2224 Part XVI u The Digestive System below the right costal margin. The normal liver is soft in consistency and percusses to normal size for age. A Riedel lobe is a thin projection Table 352.1  Some Nondigestive Tract Causes of of the right lobe of the liver that may be palpated low in the right lateral Gastrointestinal Symptoms in Children abdomen. A soft spleen tip might also be palpable as a normal finding. ANOREXIA In thin young children, the vertebral column is easily palpable, and an Systemic disease: inflammatory, neoplastic overlying structure may be mistaken for a mass. Pulsation of the aorta Cardiorespiratory compromise can be appreciated. Normal stool can often be palpated in the left lower Iatrogenic: drug therapy, unpalatable therapeutic diets quadrant in the descending or sigmoid colon. Depression Blood loss from the gastrointestinal tract is never normal, but Anorexia nervosa swallowed blood may be misinterpreted as gastrointestinal bleeding. VOMITING Maternal blood may be ingested at the time of birth or later by a nurs- Inborn errors of metabolism ing infant if there is bleeding near the mother’s nipple. Nasal or oropha- Medications: erythromycin, chemotherapy, nonsteroidal ryngeal bleeding is occasionally mistaken for gastrointestinal bleeding antiinflammatory drugs, marijuana (see Chapter 142). Red dyes in foods or drinks can turn the stool red Increased intracranial pressure but do not produce a positive test result for occult blood. Brain tumor Jaundice is common in neonates, especially among premature Infection of the urinary tract Labyrinthitis infants, and usually results from the inability of an immature liver to Adrenal insufficiency conjugate bilirubin, leading to an elevated indirect component (see Pregnancy Chapter 137). Persistent elevation of indirect bilirubin levels in nurs- Psychogenic ing infants may be a result of breast milk jaundice, which is usually Abdominal migraine a benign entity in full-­term infants. An elevated direct bilirubin is Poisoning/toxins not normal and suggests liver disease, although in infants it may be Renal disease a result of extrahepatic infection (urinary tract infection). The direct DIARRHEA bilirubin fraction should account for no more than 15–20% of the Infection: otitis media, urinary tract infection total serum bilirubin. Elevations in direct bilirubin levels can follow Uremia indirect hyperbilirubinemia as the liver converts excessive indirect to Medications: antibiotics, cisapride direct bilirubin and the rate-­limiting step in bilirubin excretion shifts Tumors: neuroblastoma from the glucuronidation of bilirubin to excretion of direct bilirubin Pericarditis into the bile canaliculus. Indirect hyperbilirubinemia, which occurs Adrenal insufficiency commonly in normal newborns, tends to tint the sclerae and skin CONSTIPATION golden yellow, whereas direct hyperbilirubinemia produces a greenish Hypothyroidism yellow hue. The degree of jaundice does not always directly correlate Spina bifida with serum bilirubin levels. An elevated total serum bilirubin warrants Developmental delay closer examination, fractionation of bilirubin (direct and indirect), and Dehydration: diabetes insipidus, renal tubular lesions ongoing surveillance. Atypical elevations of unconjugated bilirubin are Medications: narcotics Lead poisoning associated with risk for kernicterus (see Chapter 140). Elevations in Infant botulism conjugated bilirubin are reviewed in the chapter on cholestasis (see Chapter 404.1). ABDOMINAL PAIN Pyelonephritis, hydronephrosis, renal colic Visit Elsevier eBooks+ at eBooks.Health.Elsevier.com for Bibliography. Pneumonia (lower lobe) Pelvic inflammatory disease Porphyria Fabry disease Angioedema Endocarditis Abdominal migraine Chapter 352 Familial Mediterranean fever Sexual or physical abuse Systemic lupus erythematosus Major Symptoms and School phobia Sickle cell crisis Signs of Digestive Tract Vertebral disk inflammation Psoas abscess Pelvic osteomyelitis or myositis Disorders Medications Anterior (abdominal) cutaneous nerve entrapment syndrome (ACNES) Asim Maqbool and Chris A. Liacouras ABDOMINAL DISTENTION OR MASS Ascites: nephrotic syndrome, neoplasm, heart failure Discrete mass: Wilms tumor, hydronephrosis, neuroblastoma, mesenteric cyst, hepatoblastoma, lymphoma Disorders of organs outside the gastrointestinal (GI) tract can produce Pregnancy symptoms and signs that mimic digestive tract disorders and should be JAUNDICE considered in the differential diagnosis (Table 352.1). In children with Hemolytic disease normal growth and development, treatment may be initiated without Urinary tract infection a formal evaluation based on a presumptive diagnosis after taking a Sepsis history and performing a physical examination. Poor weight gain or Hypothyroidism weight loss is often associated with a significant pathologic process and Panhypopituitarism usually necessitates a more formal evaluation. Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  Chapter 352 u Major Symptoms and Signs of Digestive Tract Disorders 2225 DYSPHAGIA dysfunction, manifest by dysphagia with solids. The most serious com- Difficulty in swallowing is termed dysphagia. Painful swallowing is plication of oropharyngeal dysphagia is life-­threatening aspiration. termed odynophagia. Globus is the sensation of something stuck in A complex sequence of neuromuscular events is involved in the the throat without a clear etiology. Swallowing is a complex process transfer of foods to the upper esophagus. Abnormalities of the muscles that starts in the mouth with mastication and lubrication of food that involved in the ingestion process and their innervation, strength, or is formed into a bolus. The bolus is pushed into the pharynx by the coordination are associated with transfer dysphagia in infants and chil- tongue. The pharyngeal phase of swallowing is rapid and involves pro- dren. In such cases, an oropharyngeal problem is usually part of a more tective mechanisms to prevent food from entering the airway. The epi- generalized neurologic or muscular problem (botulism, diphtheria, glottis is lowered over the larynx while the soft palate is elevated against neuromuscular disease). Painful oral lesions, such as acute viral sto- the nasopharyngeal wall; respiration is temporarily arrested while the matitis or trauma, occasionally interfere with ingestion. If the nasal air upper esophageal sphincter opens to allow the bolus to enter the esoph- passage is seriously obstructed, the need for respiration causes severe agus. In the esophagus, peristaltic coordinated muscular contractions distress when suckling. Although severe structural, dental, and salivary push the food bolus toward the stomach. The lower esophageal sphinc- abnormalities would be expected to create difficulties, ingestion pro- ter relaxes shortly after the upper esophageal sphincter, so liquids that ceeds relatively well in most affected children if they are hungry. rapidly clear the esophagus enter the stomach without resistance. Esophageal dysphagia occurs when there is difficulty in transport- Dysphagia is classified as oropharyngeal dysphagia and esophageal ing the food bolus down the esophagus. Esophageal dysphagia can dysphagia. Oropharyngeal dysphagia occurs when the transfer of the result from neuromuscular disorders or mechanical obstruction (Table food bolus from the mouth to the esophagus is impaired (also termed 352.3). Primary motility disorders causing impaired peristaltic func- transfer dysphagia). The striated muscles of the mouth, pharynx, and tion and dysphagia are rare in children. Eosinophilic esophagitis can upper esophageal sphincter are affected in oropharyngeal dysphagia. present with esophageal dysphagia. Achalasia is an esophageal motility Neurologic and muscular disorders can give rise to oropharyngeal disorder with associated inability of relaxation of the lower esophageal dysphagia (Table 352.2). Chiari malformations, Russell-­ Silver syn- sphincter; it rarely occurs in children. Motility of the distal esophagus drome, and cri du chat may present with upper esophageal sphincter is disordered after surgical repair of tracheoesophageal fistula or acha- lasia. Abnormal motility can accompany collagen vascular disorders. Mechanical obstruction can be intrinsic or extrinsic. Intrinsic struc- tural defects cause a fixed impediment to the passage of food bolus Table 352.2  Causes of Oropharyngeal Dysphagia because of a narrowing within the esophagus, as in a stricture, web, or tumor. Extrinsic obstruction is caused by compression from vas- NEUROMUSCULAR DISORDERS cular rings, mediastinal lesions, or vertebral abnormalities. Structural Cerebral palsy Brain tumors defects typically cause more problems in swallowing solids than liq- Cerebrovascular disease/stroke uids. In infants, esophageal web, tracheobronchial remnant, or vas- Chiari malformation cular ring can cause dysphagia. An esophageal stricture secondary to Polio and postpolio syndromes esophagitis (chronic gastroesophageal reflux, eosinophilic esophagitis, Multiple sclerosis chronic infections) occasionally has dysphagia as the first manifesta- Myositis tion. An esophageal foreign body or a stricture secondary to a caustic Dermatomyositis ingestion also causes dysphagia. A Schatzki ring, a thin ring of mucosal Myasthenia gravis tissue near the lower esophageal sphincter, is another mechanical cause Muscular dystrophies of recurrent dysphagia, and again is rare in children. Acquired or inherited dystonia syndrome Dysautonomia When dysphagia is associated with a delay in passage through the esophagus, the patient may be able to point to the level of the chest METABOLIC AND AUTOIMMUNE DISORDERS where the delay occurs, but esophageal symptoms are usually referred Hyperthyroidism Systemic lupus erythematosus Sarcoidosis Amyloidosis Table 352.3  Causes of Esophageal Dysphagia INFECTIOUS DISEASE Meningitis NEUROMUSCULAR Botulism Eosinophilic esophagitis Diphtheria Achalasia cardia Lyme disease Diffuse esophageal spasm Neurosyphilis Scleroderma Viral infection: polio, coxsackievirus, herpes, cytomegalovirus GERD STRUCTURAL LESIONS INTRINSIC LESIONS Inflammatory: abscess, pharyngitis Foreign bodies including pills Congenital web Esophagitis: GERD, eosinophilic esophagitis, infections Cricopharyngeal bar Stricture: corrosive injury, pill induced, peptic Dental problems Esophageal webs Bullous skin lesions Esophageal rings Plummer-­Vinson syndrome Esophageal diverticula Zenker diverticulum Neoplasm Extrinsic compression: osteophytes, lymph nodes, thyroid swelling, Chagas disease aberrant right subclavian artery (dysphagia lusoria) EXTRINSIC LESIONS OTHER Vascular compression Corrosive injury Mediastinal lesion Side effects of medications Cervical osteochondritis After surgery Vertebral abnormalities After radiation therapy GERD, Gastroesophageal reflux disease. Adapted from Gasiorowska A, Faas R. Current approach to dysphagia. Gastroenterol Adapted from Gasiorowska A, Faas R. Current approach to dysphagia. Gastroenterol Hepatol. 2009;5(4):269–279. Hepatol. 2009;5(4):269–279. Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 2226 Part XVI u The Digestive System to the suprasternal notch. When a patient points to the suprasternal (CTZ) are most often implicated by chemical stimuli with chemother- notch, the impaction can be found anywhere in the esophagus. apy a prime example. Visceral stimuli can include ingestions, gastric hyperacidity, physical stress, psychologic stressors, mechanical disten- REGURGITATION tion of the stomach, and impaired GI motility; vagal and sympathetic Regurgitation is the effortless movement of stomach contents into the nerves are involved in this process. Vestibular pathways are most often esophagus and mouth. It is not associated with distress, and infants implicated in nausea related to motion sickness. Increased intracranial with regurgitation are often hungry immediately after an episode. The pressure can also present with nausea plus or minus vomiting. lower esophageal sphincter prevents reflux of gastric contents into the Chronic nausea is more common in adolescents and may be coinci- esophagus. Regurgitation is a result of gastroesophageal reflux through dental with other functional GI disorders, including functional dyspep- an incompetent or, in infants, immature lower esophageal sphincter. sia, delayed gastric emptying/gastroparesis, and constipation. There are This is often a developmental process, and regurgitation or “spitting” gender and ethnic differences with respect to chronic nausea in adoles- resolves with maturity. Regurgitation should be differentiated from cence, with adolescent White females with anxiety more at risk than vomiting, which denotes an active reflex process with an extensive dif- other groups; there may be alterations in the brain gut axis coupled ferential diagnosis (Table 352.4). with increased visceral hypersensitivity and hyperalgesia at play in the setting (see Chapter 212). Dehydration and autonomic dysfunction NAUSEA may also present with nausea as one facet of GI manifestations. Nausea has been described as an unpleasant, subjective sensation of Nausea is often a clinical diagnosis, and while the differential diag- impending/imminent vomiting, often with epigastric sensation that nosis is extensive, negative findings do not equate to the patient not may be painless. Nausea is frequently associated with typical auto- having nausea. Nausea is often distressing, disruptive, and may be nomic signs that accompany vomiting. Not all nausea is a prodrome disabling with respect to normal function. Table 352.5 reviews com- to vomiting. There are multiple potential triggers to nausea, includ- mon medical conditions associated with nausea, as well as treatment ing environmental exposures (toxins, odors), unpleasant visual stim- strategies. Hydration is important in many of these conditions. Many uli, visceral pain, anxiety, stress, and a variety of additional etiologies of the medications used employ antihistamine, serotonergic, dopa- (Table 352.5). minergic, and potentially even opioid pathways (although these are The central nervous system (CNS) is frequently implicated for nau- still controversial). These agents are active at both the CNS and GI sea. Receptors and neural pathways at the chemoreceptor trigger zone level, with significant brain-­gut axis interplay. Complementary and Table 352.4  Differential Diagnosis of Emesis During Childhood INFANT CHILD ADOLESCENT COMMON Gastroenteritis Gastroenteritis Gastroenteritis Gastroesophageal reflux Systemic infection GERD Overfeeding Gastritis Systemic infection Anatomic obstruction* Toxic ingestion/poisoning Toxic ingestion/poisoning/marijuana Systemic infection† Pertussis syndrome Gastritis Pertussis syndrome Medication Sinusitis Otitis media Reflux (GERD) Inflammatory bowel disease Sinusitis Appendicitis Otitis media Migraine Anatomic obstruction* Pregnancy Eosinophilic esophagitis Medications Ipecac abuse, bulimia Concussion RARE Adrenogenital syndrome Reye syndrome Reye syndrome Inborn errors of metabolism Hepatitis Hepatitis Brain tumor (increased intracranial pressure) Peptic ulcer Peptic ulcer Subdural hemorrhage Pancreatitis Pancreatitis Food poisoning Brain tumor Cholecystitis Rumination Increased intracranial pressure Brain tumor Renal tubular acidosis Middle ear disease/labyrinthitis Increased intracranial pressure Ureteropelvic junction obstruction Chemotherapy Concussion Pseudoobstruction Achalasia Middle ear disease/labyrinthitis Cyclic vomiting (migraine) Chemotherapy Esophageal stricture Cyclic vomiting (migraine) Duodenal hematoma Biliary colic Inborn error of metabolism Renal colic Pseudoobstruction Porphyria Gastroparesis Diabetic ketoacidosis Adrenal insufficiency Pseudoobstruction Intestinal tumor Gastroparesis Achalasia Superior mesentery artery syndrome Distal intestinal obstruction syndrome *Includes malrotation, pyloric stenosis, intussusception, Hirschsprung disease, adhesions, and hernias. †Meningitis, sepsis. GERD, Gastroesophageal reflux disease. Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  Chapter 352 u Major Symptoms and Signs of Digestive Tract Disorders 2227 Table 352.5  Examples of Causes and Management of Nausea FUNCTIONAL GASTROINTESTINAL DISORDERS TREATMENT APPROACHES Gastroesophageal reflux Diet and lifestyle; acid reduction, refluxate management Esophagitis (reflux related, eosinophilic, etc.) Acid reduction, identifying and restricting environmental/dietary triggers Dyspepsia Dietary and lifestyle modification; acid reduction; cyproheptadine Gastroparesis Smaller, more frequent meals; dietary modification; prokinetic agents (D2 antagonists such as metoclopramide and domperidone*; low-­dose erythromycin or azithromycin) Constipation Adequate hydration, diet and lifestyle modification, stool softeners, stimulant laxatives, additional adjunct measures if/as indicated Visceral hyperalgesia Tricyclic antidepressants (e.g., amitriptyline), cognitive behavioral therapy, hypnotherapy, biofeedback, physical therapy for desensitization; biofeedback; stress reduction OTHER GASTROINTESTINAL DISORDERS Gastritis (medication/NSAID induced; Reduce/remove medications involved; treat the underlying cause Helicobacter pylori) Gastrointestinal dysmotility Adequate hydration; diet/feeding or eating modification; promotility agents Biliary dysfunction (cholelithiasis, Treat the underlying cause cholecystitis, biliary dyskinesia) Fundoplication Smaller, more frequent meals; cyproheptadine to improve gastric accommodation CENTRAL NERVOUS SYSTEM Increased intracranial pressure Treat underlying cause Migraines, headaches Migraine prophylactic agents, including cyproheptadine. Abortive medications including triptans. Motion sickness/vestibular dysfunction Antihistamines (e.g., diphenhydramine, hydroxyzine) anticholinergics (e.g., scopolamine) Autonomic dysfunction Adequate hydration, increased salt intake, diet and lifestyle modification Chemotherapy-­induced nausea and vomiting 5-­HT3 receptor antagonists; D2 antagonists; NK-­1 antagonists; butyrophenones; benzodiazepines; dexamethasone; synthetic cannabinoids Postoperative nausea and vomiting 5-­HT3 receptor antagonists NON-­GI AND NON-­CNS ETIOLOGIES OF NAUSEA Uremia Treat the underlying disorder Endocrine disorders [e.g., hypothyroidism] Treat the underlying disorder *D2 receptor antagonists such as metoclopramide and domperidone have a significant side effect profile, and have a U.S. Food and Drug Administration black box warning, and should be used with caution. NK-­1, Neurokinin 1. alternative medicine approaches including using ginger, peppermint, DIARRHEA aromatherapy, and biofeedback may be helpful. Behavior psychology Diarrhea is best defined as excessive loss of fluid and electrolyte in the and social work may be helpful in decreasing disability and enhancing stool. Acute diarrhea is defined as sudden onset of excessively loose functionality. stools of >10 mL/kg/day in infants and >200 g/24 hr in older children, which lasts 2 years: 1 to 1.5 mg/kg/dose PO Dimenhydrinate is available as q6-­8h, max: 25 mg/dose 50 mg tablets, prescribe in 12.5 mg increments Meclizine (Antivert) >2 to 12 years: 25 mg to 50 mg PO patches 1 to 4 times daily, max: Withdrawal (cholinergic 100 mg/day rebound) symptoms reported with long-­term use, limit duration or consider weaning Scopolamine (Transderm-­Scop) >15 kg: 1 transdermal patch with extended use applied behind the ear every 3 days MISCELLANEOUS Visceral Hypersensitivity, Feeding Cyproheptadine* 0.25 mg/kg/day PO in 1-­3 divided C onsider starting with bedtime Intolerance doses, usual max: 4 mg/dose dose and titrating up to prevent Antihistamine/serotonin daytime sedation antagonist Associated with tachyphylaxis Benefit reported in patients with visceral hypersensitivity Anticholinergic effects may decrease motility Pseudo-­obstruction Octreotide* 0.5 to 1 mcg/kg subQ once daily, M  ay cause bradycardia, Somatostatin analog max: 100 mcg/dose hypoglycemia Adrenal Crisis Hydrocortisone 100 mg/m2 IV/IM x1, followed by R  eported regimens vary, refer 25 mg/m2/dose IV/IM q6h, max: to individual protocols 100 mg/day Taper as clinically indicated *Limited data available Table 352.9  Supportive and Nonpharmacologic Therapies for Vomiting Episodes DISEASE THERAPY All Treat cause Obstruction: operate Allergy: change diet (±steroids) Metabolic error: Rx defect Acid peptic disease: H2Ras, PPIs, etc. COMPLICATIONS Dehydration IV fluids, electrolytes Hematemesis Transfuse, correct coagulopathy Esophagitis H2Ras, PPIs Malnutrition NG or NJ drip feeding useful for many chronic conditions Meconium ileus Gastrografin enema DIOS Gastrografin enema; balanced colonic lavage solution (e.g., GoLYTELY) Intussusception Barium enema; air reduction enema Hematemesis Endoscopic: injection sclerotherapy or banding of esophageal varices; injection therapy, fibrin sealant application, or heater probe electrocautery for selected upper GI tract lesions Sigmoid volvulus Colonoscopic decompression Reflux Positioning; dietary measures (infants: rice cereal, 1 tbs/oz of formula) Psychogenic components Psychotherapy; tricyclic antidepressants; anxiolytics (e.g., diazepam: 0.1 mg/kg PO tid-­qid) DIOS, Distal intestinal obstruction syndrome; GI, gastrointestinal; H2RA, H2-­receptor antagonist; NG, nasogastric; NJ, nasojejunal; PPIs, proton pump inhibitors; tbs, tablespoon. From Kliegman RM, Greenbaum LA, Lye PS, eds. Practical Strategies in Pediatric Diagnosis and Therapy. 2nd ed. Philadelphia: Elsevier; 2004: p. 319. Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 2232 Part XVI u The Digestive System Table 352.10  Mechanisms of Diarrhea PRIMARY MECHANISM DEFECT STOOL EXAMINATION EXAMPLES COMMENT Secretory Decreased absorption, Watery, normal Cholera, toxigenic Persists during fasting; bile increased secretion, osmolality with ion gap Escherichia coli; carcinoid, salt malabsorption can electrolyte transport 100 mOsm/kg laxative abuse carbohydrate malabsorption; no stool leukocytes Increased motility Decreased transit time Loose to normal-­appearing Irritable bowel syndrome, Infection can also contribute stool, stimulated by thyrotoxicosis, to increased motility gastrocolic reflex postvagotomy dumping syndrome Decreased motility Defect in neuromuscular Loose to Pseudoobstruction, blind Possible bacterial unit(s) stasis (bacterial normal-­appearing stool loop overgrowth overgrowth) Decreased surface area Decreased functional Watery Short bowel syndrome, Might require elemental (osmotic, motility) capacity celiac disease, rotavirus diet plus parenteral enteritis alimentation Mucosal invasion Inflammation, decreased Blood and increased Salmonella, Shigella Dysentery evident in colonic reabsorption, WBCs in stool infection; amebiasis; blood, mucus, and WBCs increased motility Yersinia, Campylobacter infection VIP, Vasoactive intestinal peptide; WBC, white blood cell. From Kliegman RM, Greenbaum LA, Lye PS. eds. Practical Strategies in Pediatric Diagnosis and Therapy. 2nd ed. Philadelphia: Elsevier; 2004: p 274. mechanism. Diarrhea not associated with an exogenous secreta- difficulty every third day should be treated as constipation. Consti- gogue can also have a secretory component (congenital microvillus pation can arise from defects either in filling or emptying the rectum inclusion disease). Secretory diarrhea is usually of large volume and (Table 352.12). persists even with fasting. The stool osmolality is predominantly A nursing infant might have very infrequent stools of normal con- indicated by the electrolytes, and the ion gap is 100 mOsm/kg or sistency, which is usually a normal pattern. True constipation in the less. The ion gap is calculated by subtracting the concentration of neonatal period is most likely secondary to Hirschsprung disease, electrolytes from total osmolality: intestinal pseudoobstruction, or hypothyroidism. Ion gap Stool osmolality  [(Stool Na  stool K) 2] Defective rectal filling occurs when colonic peristalsis is inef- fective (in cases of hypothyroidism or opiate use and when Osmotic diarrhea occurs after ingestion of a poorly absorbed bowel obstruction is caused either by a structural anomaly or by solute. The solute may be one that is normally not well absorbed Hirschsprung disease). The resultant colonic stasis leads to exces- (magnesium, phosphate, lactulose, or sorbitol) or one that is not sive drying of stool and a failure to initiate reflexes from the rectum well absorbed because of a disorder of the small bowel (lactose with that normally trigger evacuation. Emptying the rectum by sponta- lactase deficiency or glucose with rotavirus diarrhea). Malabsorbed neous evacuation depends on a defecation reflex initiated by pres- carbohydrate is fermented in the colon, and short-­chain fatty acids sure receptors in the rectal muscle. Therefore stool retention can are produced. Although short-­chain fatty acids can be absorbed in also result from lesions involving these rectal muscles, the sacral the colon and used as an energy source, the net effect is increase in spinal cord afferent and efferent fibers, or the muscles of the abdo- the osmotic solute load. This form of diarrhea is usually of lesser men and pelvic floor. Disorders of anal sphincter relaxation can also volume than a secretory diarrhea and stops with fasting. The osmo- contribute to fecal retention. lality of the stool will not be explained by the electrolyte content, Constipation tends to be self-­p erpetuating, whatever its cause. because another osmotic component is present and so the anion Hard, large stools in the rectum become difficult and even pain- gap is >100 mOsm. ful to evacuate; thus more retention occurs and a vicious circle Motility disorders can be associated with rapid or delayed transit and ensues. Distention of the rectum and colon lessens the sensitivity are not generally associated with large-­volume diarrhea. Slow motility of the defecation reflex and the effectiveness of peristalsis. Fecal can be associated with bacterial overgrowth leading to diarrhea. The impaction is common and leads to other problems. Eventually, differential diagnosis of common causes of acute and chronic diarrhea watery content from the proximal colon might percolate around is noted in Table 352.11. hard retained stool and pass per rectum unperceived by the child. This involuntary encopresis may be mistaken for diarrhea. Con- CONSTIPATION stipation itself does not have deleterious systemic organic effects, Any definition of constipation is relative and depends on stool but urinary tract stasis with increased risk of urinary tract infec- consistency, stool frequency, and difficulty in passing the stool. A tions can accompany severe long-­standing cases and constipation normal child might have a soft stool only every second or third day can generate anxiety, having a marked emotional impact on the without difficulty; this is not constipation. A hard stool passed with patient and family. Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  Table 352.11 Differential Diagnosis of Diarrhea INFANT CHILD ADOLESCENT ACUTE Common Gastroenteritis (viral > bacterial > protozoal) Gastroenteritis (viral > bacterial > protozoal) Gastroenteritis (viral > bacterial > protozoal) Systemic infection Food poisoning Food poisoning Antibiotic associated Systemic infection Antibiotic associated Overfeeding Antibiotic associated Rare Primary disaccharidase deficiency Toxic ingestion Hyperthyroidism Hirschsprung toxic colitis Hemolytic uremic syndrome Appendicitis Adrenogenital syndrome Intussusception Neonatal opiate withdrawal CHRONIC Common Postinfectious secondary lactase deficiency Postinfectious secondary lactase deficiency Irritable bowel syndrome Cow’s milk or soy protein intolerance (allergy) Irritable bowel syndrome Inflammatory bowel disease Chronic nonspecific diarrhea of infancy Celiac disease Lactose intolerance Excessive fruit juice (sorbitol) ingestion Cystic fibrosis Giardiasis Celiac disease Lactose intolerance Laxative abuse (anorexia nervosa) Cystic fibrosis Excessive fruit juice (sorbitol) ingestion Constipation with encopresis AIDS enteropathy Giardiasis Inflammatory bowel disease AIDS enteropathy Rare Primary immune defects Primary and acquired immune defects Secretory tumor Autoimmune enteropathy Secretory tumors Primary bowel tumor IPEX and IPEX-­like syndromes Pseudoobstruction Parasitic infections and venereal diseases Glucose-­galactose malabsorption Sucrase-­isomaltase deficiency Appendiceal abscess Microvillus inclusion disease (microvillus atrophy) Eosinophilic gastroenteritis Addison disease Congenital transport defects (chloride, sodium) Secretory tumors Primary bile acid malabsorption Factitious syndrome by proxy Hirschsprung disease Shwachman syndrome Secretory tumors Acrodermatitis enteropathica Lymphangiectasia Abetalipoproteinemia Eosinophilic gastroenteritis Short bowel syndrome IPEX, Immunodysregulation polyendocrinopathy enteropathy X-­linked. From Kliegman RM, Greenbaum LA, Lye PS, eds. Practical Strategies in Pediatric Diagnosis and Therapy, 2nd ed. Philadelphia: Elsevier; 2004: p. 272. Table 352.12 Causes of Constipation NONORGANIC (FUNCTIONAL): RETENTIVE Drugs Anatomic Anticholinergics Anal stenosis, atresia with fistula Narcotics Imperforate anus Methylphenidate Anteriorly displaced anus Phenytoin Intestinal stricture (postnecrotizing enterocolitis) Antidepressants Anal stricture Chemotherapeutic agents (vincristine) Pancreatic enzymes (fibrosing colonopathy) Abnormal Musculature Lead, arsenic, mercury Prune-­belly syndrome Vitamin D intoxication Gastroschisis Calcium channel blocking agents Down syndrome Muscular dystrophy Metabolic Disorders Hypokalemia Intestinal Nerve or Muscle Abnormalities Hypercalcemia Hirschsprung disease Hypothyroidism Pseudoobstruction (visceral myopathy or neuropathy) Diabetes mellitus, diabetes insipidus Intestinal neuronal dysplasia Porphyria Spinal cord lesions Tethered cord Intestinal Disorders Autonomic neuropathy Celiac disease Spinal cord trauma Cow’s milk protein intolerance Spina bifida Cystic fibrosis (meconium ileus equivalent) Chagas disease Inflammatory bowel disease (stricture) Tumor Connective tissue disorders Systemic lupus erythematosus Scleroderma Psychiatric Diagnosis Anorexia nervosa Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 2234 Part XVI u The Digestive System ANOREXIA ganglia, and some axons cross the midline and ascend to the medulla, Anorexia means prolonged lack of appetite. Hunger and satiety centers midbrain, and thalamus. Pain is perceived in the cortex of the post- are located in the hypothalamus; it seems likely that afferent nerves central gyrus, which can receive impulses arising from both sides of from the GI tract to these brain centers are important determinants the body. In the gut, the usual stimulus provoking pain is tension or of the anorexia that characterizes many diseases of the stomach and stretching. Inflammatory lesions can lower the pain threshold, but intestine. Satiety is stimulated by distention of the stomach or upper the mechanisms producing pain or inflammation are not clear. Tissue small bowel, the signal being transmitted by sensory afferents, which metabolites released near nerve endings probably account for the pain are especially dense in the upper gut. Chemoreceptors in the intestine, caused by ischemia. Perception of these painful stimuli can be modu- influenced by the assimilation of nutrients, also affect afferent flow to lated by input from both cerebral and peripheral sources. Psychologic the appetite centers. Impulses reach the hypothalamus from higher factors are particularly important. Tables 352.14 and 352.15 list features centers, possibly influenced by pain or the emotional disturbance of abdominal pain. Pain that suggests a potentially serious organic eti- of an intestinal disease. Other regulatory factors include hormones, ology is associated with age younger than 5 years; fever; weight loss; ghrelin, leptin, and plasma glucose, which, in turn, reflect intestinal bile-­or blood-­stained emesis; jaundice; hepatosplenomegaly; back or function. flank pain or pain in a location other than the umbilicus; awakening from sleep in pain; referred pain to shoulder, groin, or back; elevated ABDOMINAL PAIN erythrocyte sedimentation rate, white blood cell count, or CRP; ane- There is considerable variation among children in their perception mia; edema; hematochezia; or a strong family history of inflammatory and tolerance for abdominal pain. This is one reason the evaluation of bowel disease or celiac disease (see Table 352.13). chronic abdominal pain is difficult. A child with functional abdomi- Visceral pain tends to be dull and aching and is experienced in nal pain (also known as centrally mediated abdominal pain syndrome the dermatome from which the affected organ receives innervations. or brain-­gut axis dysfunction) may be as uncomfortable as one with So, most often, the pain and tenderness are not felt over the site of an organic cause. It is very important to distinguish between organic the disease process. Painful stimuli originating in the liver, pancreas, and nonorganic (functional) abdominal pain because the approach for biliary tree, stomach, or upper bowel are felt in the epigastrium; the management is based on this (Table 352.13). Normal growth and pain from the distal small bowel, cecum, appendix, or proximal physical examination (including a rectal examination) and the absence colon is felt at the umbilicus; and pain from the distal large bowel, of anemia or hematochezia are reassuring in a child who is suspected urinary tract, or pelvic organs is usually suprapubic. The pain from of having functional pain. the cecum, ascending colon, and descending colon sometimes is felt A specific cause may be difficult to find, but the nature and location at the site of the lesion because of the short mesocecum and cor- of a pain-­provoking lesion can usually be determined from the clinical responding mesocolon. The pain caused by appendicitis is initially description. Two types of nerve fibers transmit painful stimuli in the felt in the periumbilical region, and pain from the transverse colon abdomen. In skin and muscle, A fibers mediate sharp localized pain; is usually felt in the suprapubic region. The shifting (localization) of C fibers from viscera, peritoneum, and muscle transmit poorly local- pain is a pointer toward diagnosis; for example, periumbilical pain ized, dull pain. These afferent fibers have cell bodies in the dorsal root of a few hours localizing to the right lower quadrant suggests appen- dicitis. Radiation of pain can be helpful in diagnosis; in biliary colic the radiation of pain is toward the inferior angle of the right scapula, Table 352.13  Red Flags and Clues to an Organic Cause pancreatic pain is radiated to the back, and the renal colic pain is of Abdominal Pain radiated to the inguinal region on the same side. Differentiating abdominal wall pain from visceral pain is impor- Age 39.4°C suggests pneumonia, pyelonephritis, rib syndrome can follow overuse or even minor trauma to the ribs dysentery, cholangitis, more than perforation or abscess) on either side. The name originates from a popping/slipping sensa- Jaundice tion that is often reported. Slipped rib syndrome may be mistaken Distention* for hepatobiliary, splenic, pancreatic, esophageal, or gastric etiolo- Dysphagia Dysuria gies, among others. Rib fractures, costochondritis, perichondritis Emesis (especially bilious) [Tietze syndrome], and pleuritic pain may also present as an etiol- Anorexia ogy. Anterior (abdominal) cutaneous nerve entrapment syndrome Weight loss, failure to thrive (ACNES) may produce acute, recurrent, or chronic unilateral local- Positive family history (metabolic disorders, peptic ulcer disease)† ized abdominal pain. Nerve entrapment is most common at the lat- Change in urine or stool color (blood, acholic) or frequency eral border of the rectus muscle. Vaginal discharge Somatic pain is intense and usually well localized. When the Menstrual abnormalities (amenorrhea) inflamed viscus comes in contact with a somatic organ such as the pari- Sexual activity etal peritoneum or the abdominal wall, pain is localized to that site. Delayed sexual development (chronic pain) Anemia Peritonitis gives rise to generalized abdominal pain with rigidity, invol- Elevated erythrocyte sedimentation rate untary guarding, rebound tenderness, and cutaneous hyperesthesia on Elevated stool calprotectin physical examination. Specific physical findings (hepatomegaly, splenomegaly, absent Referred pain from extraintestinal locations, from shared central bowel sounds, adnexal tenderness, palpable mass, involuntary projections with the sensory pathway from the abdominal wall, can guarding, focal or diffuse tenderness, positive rectal examination give rise to abdominal pain, as in pneumonia when the parietal pleural results, perianal disease, joint swelling, rashes) pain is referred to the abdomen (Fig. 352.1). *Consider 5 Fs: fat, feces, flatus (aerophagia, obstruction), fluid (ascites, hydronephrosis, cysts), and fetus (pregnancy or fetal-­like abnormal growth [e.g., tumors]). GASTROINTESTINAL HEMORRHAGE †Family history is also positive for chronic pain syndromes (constipation, irritable bowel, Bleeding can occur anywhere along the GI tract, and identification of dysmenorrhea, and lactase or sucrase deficiency). the site may be challenging (Table 352.16). Bleeding that originates Modified from Miranda A. Abdominal pain. In: Kliegman RM, Toth H, Bordini BJ, Basel D, eds. Nelson Pediatric Symptom-­Based Diagnosis. 2nd ed. Philadelphia: Elsevier; in the esophagus, stomach, or duodenum can cause hematemesis. 2023: Table 13.8, p. 229. When exposed to gastric or intestinal juices, blood quickly darkens to Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  Chapter 352 u Major Symptoms and Signs of Digestive Tract Disorders 2235 Table 352.14 Chronic Abdominal Pain in Children DISORDER CHARACTERISTICS KEY EVALUATIONS NONORGANIC Functional abdominal pain Nonspecific pain, often periumbilical Hx and PE; tests as indicated Irritable bowel syndrome Intermittent cramps, diarrhea, and constipation Hx and PE Nonulcer dyspepsia Peptic ulcer–like symptoms without abnormalities on Hx; esophagogastroduodenoscopy evaluation of the upper GI tract GASTROINTESTINAL TRACT Chronic constipation Hx of stool retention, evidence of constipation on Hx and PE; plain x-­ray of abdomen examination Lactose intolerance Symptoms may be associated with lactose ingestion; Trial of lactose-­free diet; lactose breath bloating, gas, cramps, and diarrhea hydrogen test Parasite infection (especially Giardia) Bloating, gas, cramps, and diarrhea Stool evaluation for O&P; specific immunoassays for Giardia Excess fructose or sorbitol ingestion Nonspecific abdominal pain, bloating, gas, and Large intake of apples, fruit juice, or candy diarrhea or chewing gum sweetened with sorbitol Crohn disease See Chapter 382.2 Peptic ulcer Burning or gnawing epigastric pain; worse on Esophagogastroduodenoscopy, upper GI awakening or before meals; relieved with antacids contrast x-­rays, or MRI enteroscopy Esophagitis Epigastric pain with substernal burning Esophagogastroduodenoscopy Meckel diverticulum Periumbilical or lower abdominal pain; may have Meckel scan or enteroclysis blood in stool (usually painless) Recurrent intussusception Paroxysmal severe cramping abdominal pain; blood Identify intussusception during episode or may be present in stool with episode lead point in intestine between episodes with contrast studies of GI tract Internal, inguinal, or abdominal wall hernia Dull abdomen or abdominal wall pain PE, CT of abdominal wall Chronic appendicitis or appendiceal Recurrent RLQ pain; often incorrectly diagnosed, Barium enema, CT mucocele may be rare cause of abdominal pain GALLBLADDER AND PANCREAS Cholelithiasis RUQ pain, might worsen with meals Ultrasound of gallbladder Choledochal cyst RUQ pain, mass ± elevated bilirubin Ultrasound or CT of RUQ Recurrent pancreatitis Persistent boring pain, might radiate to back, Serum amylase and lipase ± serum vomiting trypsinogen; ultrasound, CT, or MRI-­ERCP of pancreas GENITOURINARY TRACT Urinary tract infection Dull suprapubic pain, flank pain Urinalysis and urine culture; renal scan Hydronephrosis Unilateral abdominal or flank pain Ultrasound of kidneys Urolithiasis Progressive, severe pain; flank to inguinal region to Urinalysis, ultrasound, IVP, CT testicle Other genitourinary disorders Suprapubic or lower abdominal pain; genitourinary Ultrasound of kidneys and pelvis; symptoms gynecologic evaluation MISCELLANEOUS CAUSES Abdominal migraine See text; nausea, family Hx migraine Hx Abdominal epilepsy Might have seizure prodrome EEG (can require >1 study, including sleep-­deprived EEG) Gilbert syndrome Mild abdominal pain (causal or coincidental?); Serum bilirubin slightly elevated unconjugated bilirubin Familial Mediterranean fever Paroxysmal episodes of fever, severe abdominal Hx and PE during an episode, DNA pain, and tenderness with other evidence of diagnosis polyserositis Sickle cell crisis Anemia Hematologic evaluation Lead poisoning Vague abdominal pain ± constipation Serum lead level IgA vasculitis (Henoch-Schönlein purpura) Recurrent, severe crampy abdominal pain, occult Hx, PE, urinalysis blood in stool, characteristic rash, arthritis Angioneurotic edema Swelling of face or airway, crampy pain Hx, PE, upper GI contrast x-­rays, serum C1 esterase inhibitor Acute intermittent porphyria Severe pain precipitated by drugs, fasting, or Spot urine for porphyrins infections Anterior cutaneous nerve entrapment Exquisite localized (∼2 × 2 cm) tenderness that is Pain relief within 15 min of abdominal wall syndrome (ACNES) replicable, most often RLQ injection of local anesthetic; may need surgery ERCP, Endoscopic retrograde cholangiopancreatography; EEG, electroencephalogram; GI, gastrointestinal; Hx, history; IVP, intravenous pyelography; O&P, ova and parasites; PE, physical exam; RLQ, right lower quadrant; RUQ, right upper quadrant. 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All rights reserved. 2236 Part XVI u The Digestive System Table 352.15  Distinguishing Features of Acute Abdominal Pain in Children DISEASE ONSET LOCATION REFERRAL QUALITY COMMENTS Pancreatitis Acute Epigastric, left upper quadrant Back Constant, sharp, boring Nausea, emesis, tenderness Intestinal obstruction Acute or Periumbilical-­lower abdomen Back Alternating cramping Distention, obstipation, gradual (colic) and painless emesis, increased periods bowel sounds Appendicitis Acute (1-­3 days) Periumbilical, then localized Back or pelvis if Sharp, steady Anorexia, nausea, emesis, to lower right quadrant; retrocecal local tenderness, fever generalized with peritonitis with peritonitis Intussusception Acute Periumbilical-­lower abdomen None Cramping, with Hematochezia, knees in painless periods pulled-­up position Urolithiasis Acute, sudden Back (unilateral) Groin Sharp, intermittent, Hematuria cramping Urinary tract infection Acute Back Bladder Dull to sharp Fever, costovertebral angle tenderness, dysuria, urinary frequency Pelvic inflammatory Acute Pelvis, lower quadrant Upper thigh Aching, peritoneal Vaginal discharge, fever disease signs Small bowel Acute to Periumbilical None Cramping diffuse Emesis and obstipation obstruction subacute Ruptured ectopic Acute sudden Pelvis, lower quadrant None Sharp, intense, Vaginal bleeding, shock pregnancy localized Pancreatitis Perforated Heart Liver duodenal ulcer GERD Peptic Penetrating Biliary colic duodenal ulcer ulcer Cholecystitis, pancreatitis, Cholecystitis duodenal ulcer Small intestine Pancreatitis, pain, appendicitis renal colic Appendicitis Renal colic Rectal Colon pain lesions Ureteral colic Fig. 352.1 Common sites of referred pain from the abdominal viscera. When a patient gives a history of referred pain from the viscera, the pain’s location may not be directly over the impaired organ. Visceral embryologic development is the mechanism of the referred pain pattern. Pain is referred to the site where the organ was located in fetal development. resemble coffee grounds; massive bleeding is likely to be red. Red or lesions secondary to mucosal tears associated with emesis are causes maroon blood in stools, hematochezia, signifies either a distal bleed- of upper intestinal bleeds. Vascular malformations are a rare cause in ing site or massive hemorrhage above the distal ileum. Moderate to children; they are difficult to identify (Figs. 352.2 and 352.3). Upper mild bleeding from sites above the distal ileum tends to cause black- intestinal bleeding is evaluated with esophagogastroduodenoscopy. ened stools of tarry consistency (melena); major hemorrhages in the Evaluation of the small intestine is facilitated by capsule endoscopy. duodenum or above can also cause melena. The capsule-­sized imaging device is swallowed in older children or Erosive damage to the mucosa of the GI tract is the most common placed endoscopically in younger children. Lower GI bleeding is inves- cause of bleeding, although variceal bleeding secondary to portal tigated with a colonoscopy. In brisk intestinal bleeding of unknown hypertension occurs often enough to require consideration. Prolapse location, a tagged red blood cell scan is helpful in locating the site of the gastropathy producing subepithelial hemorrhage and Mallory-­Weiss bleeding, although CT angiography is usually diagnostic. Occult blood Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved.  Chapter 352 u Major Symptoms and Signs of Digestive Tract Disorders 2237 Table 352.16  Differential Diagnosis of Gastrointestinal Bleeding in Childhood INFANT CHILD ADOLESCENT COMMON Bacterial enteritis Bacterial enteritis Bacterial enteritis Milk protein allergy intolerance Anal fissure Inflammatory bowel disease Intussusception Colonic polyps Peptic ulcer/gastritis Swallowed maternal blood Intussusception Prolapse (traumatic) gastropathy secondary Anal fissure Peptic ulcer/gastritis to emesis Lymphonodular hyperplasia Swallowed epistaxis Mallory-­Weiss syndrome Prolapse (traumatic) gastropathy secondary to emesis Colonic polyps Mallory-­Weiss syndrome Anal fissure RARE Volvulus Esophageal varices Hemorrhoids Necrotizing enterocolitis Esophagitis Esophageal varices Meckel diverticulum Meckel diverticulum Esophagitis Stress ulcer, gastritis Lymphonodular hyperplasia Pill ulcer Coagulation disorder (hemorrhagic IgA vasculitis (Henoch-Schönlein purpura) Telangiectasia-­angiodysplasia disease of newborn) Foreign body Graft versus host disease Esophagitis Hemangioma, arteriovenous malformation Duplication cyst Sexual abuse Angiodysplasia Hemolytic-­uremic syndrome Angiodysplasia with von Willebrand disease Inflammatory bowel disease Blue rubber bleb nevus syndrome Coagulopathy Duplication cyst Angiodysplasia Angiodysplasia with von Willebrand disease Blue rubber bleb nevus syndrome Fig. 352.3 Operative features of blue rubber bleb nevus syndrome. These lesions are similar to cutaneous lesions. (From Hasosah MY, Abdul-­Wahab AA, Bin-­Yahab SA, et al. Blue rubber bled nevus syn- drome: extensive small bowel vascular lesions responsible for gastroin- Fig. 352.2 Intestinal angiodysplasia. A 7-­year-­old boy had tarry stool testinal bleeding. J Pediatr Child Health. 2010;46:63–65. Fig. 3.) for days. Panendoscopy showed multiple cherry red flat spots in the gastric mucosa, compatible with the findings of angiodysplasia in CT angiography. (From Chuang F, Lin JS, Yeung C, et al. Intestinal angiod- ysplasia: an uncommon cause of gastrointestinal bleeding in children. ABDOMINAL DISTENTION AND ABDOMINAL Pediatr Neonatol. 2011;52:214–218, Fig. 2.) MASSES Enlargement of the abdomen can result from diminished tone of the wall musculature or from increased content: fluid, gas, or solid. Ascites, the accumulation of fluid in the peritoneal cavity, distends the abdo- in stool is usually detected by using commercially available fecal occult men both in the flanks and anteriorly when it is large in volume. This blood testing cards, which are based on a chemical reaction between fluid shifts with movement of the patient and conducts a percussion the chemical guaiac and oxidizing action of a substrate (hemoglobin), wave. Ascitic fluid is usually a transudate with a low protein concentra- giving a blue color. The guaiac test is very sensitive, but random testing tion resulting from reduced plasma colloid osmotic pressure of hypo- can miss chronic blood loss, which can lead to iron-­deficiency anemia. albuminemia and/or from raised portal venous pressure. In cases of GI hemorrhage can produce hypotension and tachycardia but rarely portal hypertension, the fluid leak probably occurs from lymphatics causes GI symptoms; brisk duodenal or gastric bleeding can lead to on the liver surface and from visceral peritoneal capillaries, but ascites nausea, vomiting, or diarrhea. The breakdown products of intralu- does not usually develop until the serum albumin level falls. Sodium minal blood might tip patients into hepatic coma if liver function is excretion in the urine decreases greatly as the ascitic fluid accumu- already compromised and can lead to elevation of serum bilirubin. lates, and thus additional dietary sodium goes directly to the peritoneal Downloaded for mohamed ahmed ([email protected]) at University of Southern California from ClinicalKey.com by Elsevier on April 21, 2024. For personal use only. No other uses without permission. Copyright ©2024. Elsevier Inc. All rights reserved. 2238 Part XVI u The Digestive System Benign hepatic tumors Liver abscess Hepatoblastoma Hepatocellular carcinoma Metastatic cancer Bezoar Choledochal cyst Splenomegaly Splenic cyst Intestinal obstruction Appendiceal abscess Lymphoma Intestinal duplication Ovarian cyst/neoplasm, Mesenteric cyst abscess Tuboovarian abscess Hydrometrocolpos Fig. 352.4 Location of select intrabdominal tumors and masses. (From Densmore JC, Densmore EM. Abdominal masses. In Kliegman RM, Toth H, Bordini BJ, Basel D, eds. Nelson Pediatric Symptom-­Based Diagnosis, 2nd ed. Philadelphia: Elsevier