Vomiting and Regurgitation

Associated Symptoms

Temporal associations of vomiting with specific time of the day, relation to meals, intake of specific foods, and other inciting events can give important diagnostic clues (see Table 15.4 ). Of all the causes of early morning emesis, the most worrisome is increased intracranial pressure. More common causes of early morning nausea and vomiting are CVS, dysautonomia, and chronic sinusitis with postnasal drip. Pregnancy should be ruled out in all sexually active females . Post-tussive emesis should direct diagnostic attention to the cause of the cough itself. Food vomited many hours after its consumption is suspicious for delayed gastric emptying or gastric outlet obstruction. Episodic vomiting associated with abdominal pain precipitated after consumption of a large quantity of fluids and resolving after diuresis can be a result of intermittent hydronephrosis caused by ureteropelvic junction (UPJ) obstruction.

Associated symptoms ( Table 15.5 ) can be crucial in differentiating serious life-threatening conditions that require urgent intervention from the more benign causes of vomiting. Vomiting with neurologic signs such as headache, altered sensorium, and seizures should alert providers to consider intracranial or metabolic disorders. Abdominal pain is a central symptom associated with vomiting and its character and location can further help narrow the diagnosis (see Chapter 13 ). Abdominal pain can be categorized as visceral, parietal, or referred pain. Visceral pain is caused by excessive contraction, distension, inflammation, or ischemia of the walls of hollow viscera (stomach, intestines, bile duct, ureter) or the capsule of solid organs (liver, spleen, kidney). Patients usually have difficulty describing visceral pain. It can be dull, intermittent, vague, or colicky and is poorly localized, often to the midline. Common examples are pain secondary to infectious gastroenteritis, functional abdominal pain disorders, toxic irritation, intestinal obstruction, etc. Parietal pain is sharp, constant, and well localized to the area of the underlying problem. It signifies inflammation of the contiguous peritoneum. It is exacerbated with movement, is associated with localized tenderness on examination, and requires immediate medical attention. Parietal pain is present in conditions such as acute cholecystitis, pancreatitis, appendicitis, and perforation of viscus. Referred pain describes pain perceived in an area remote from the site of the inciting pathologic process. Abdominal pain may therefore be a symptom of disease localized in the thorax, pelvis, or retroperitoneum.

When suspecting a psychosocial cause of vomiting, providers should inquire about anxiety, binge eating, body image, and any recent stressors. Minor head injury can also present as vomiting in children, especially toddlers. There is evidence to suggest that vomiting after a minor head injury may be related to intrinsic patient factors rather than the severity of the injury. Vomiting that is persistent or latent in onset may be more likely to signify head injury. Emesis following a recent history of blunt abdominal trauma should raise the suspicion of a duodenal hematoma.

Medical, Family, and Social History

Previous surgery, hospitalizations, and medications may provide important clues. A family history of fetal or neonatal deaths suggests a genetic or metabolic cause; similar illness in family members or other contacts may suggest infections or common toxic exposures. Psychosocial stressors may be found in adolescents with bulimia, peptic ulcer disease, chronic marijuana use, or intentional self-poisonings.

Abdominal Examination

Simple observation of operative scars may suggest the possibility of obstruction from intestinal adhesions, and visible distention may represent ascites caused by liver disease or intraluminal distention caused by intestinal obstruction or ileus. The order of the examination is important because auscultation performed after stimulation of intestinal motility by palpation may artifactually change the auscultatory findings. An important distinction in the vomiting child is whether bowel sounds are increased, as in gastroenteritis or in bowel obstructions, or absent, as in ileus caused by peritonitis or in chronic intestinal pseudo-obstruction. Increased bowel sounds resulting from luminal obstruction are often characterized by intermittent “rushes” of high-pitched sounds that are coordinated with episodes of colicky pain. Although seen infrequently, visible peristalsis in infants and a succussion splash in children are indications of a gastric outlet obstruction that is causing gastric distension and retention of fluid. Palpate the abdomen and pelvis for area of tenderness and signs of peritoneal inflammation as they often represent disorders necessitating further imaging and/or surgery. Also palpate for presence of organomegaly and abdominal masses. Hepatosplenomegaly can be found in various metabolic or inflammatory diseases. Abdominal masses can be congenital (e.g., mesenteric cyst) or acquired (e.g., neuroblastoma) and result in bowel obstruction (see Chapter 20 ). Examine genitalia and hernia sites for ambiguous genitalia, ovarian/testicular torsion, and strangulated hernias. Vague periumbilical pain is quite nonspecific, but the localized, very sharp pain signifying inflammation of the peritoneum requires immediate attention. Initial luminal obstruction may progress to ileus as peritonitis intervenes. Localization of nonperiumbilical pain or tenderness helps a great deal in determining the diseased intraabdominal organ (see Table 15.5 ).

Rectal Examination

A rectal examination may be helpful in the vomiting child as the presence and consistency of rectal stool may be determined. A large fecal impaction may possibly contribute to vomiting in some young children. Pelvic masses and tenderness identified by rectal exam may represent appendicitis, ovarian torsion, or pelvic inflammatory disease. The stool should always be tested for blood and should be considered for testing for pH, reducing substances, fat, leukocytes, and infectious organisms, depending on the presentation.

General Approach

Cardinal symptoms or signs accompanying the vomiting direct the differential diagnosis. When vomiting is a result of intraabdominal disease, it is useful to define whether obstruction, dysmotility, inflammation, or ischemia is the mechanism. Abdominal pain, which frequently accompanies vomiting, can suggest both the type of disorder and the organ involved (see Table 15.5 ). Symptoms referable to non-GI organ systems direct attention to those systems. For example, accompanying neurologic symptoms may direct attention to central nervous system disorders, metabolic disease, poisonings, or psychobehavioral disease.

Esophageal Obstruction

Esophageal strictures or obstruction produces dysphagia with welling up or drooling of oropharyngeal secretions or esophageal contents rather than actual vomiting; the material is undigested. Respiratory symptoms from aspiration may be prominent.

Esophageal Atresia

Esophageal atresia is a congenital malformation defined by the discontinuity of the esophagus. Infants present at birth with a prenatal history of polyhydramnios and intolerance of initial feeding. The esophageal atresia is accompanied by a distal tracheoesophageal fistula (TEF) in 85% of cases, by a proximal fistula in a small percentage, and by no fistula in the remainder ( Fig. 15.2 ). Esophageal atresia is associated with other anomalies in 15–50% of patients; cardiac, anorectal, and genitourinary defects are most common. Ten percent of all esophageal atresia patients and 25% of those without a fistula have the VATER or VACTERL (vertebral, anorectal, cardiac, tracheoesophageal, renal, radial, limb) association. As many as 33% of affected infants are premature. Diagnosis can usually be made by plain films after passage of an opaque rubber catheter, which coils in the upper pouch ( Fig. 15.3 ). Treatment is surgical.

Congenital Esophageal Stenosis

Congenital esophageal stenosis is defined as an intrinsic narrowing of the esophagus present at birth. Infants usually tolerate breast-feeding and start to present with vomiting and regurgitation with the introduction of semisolid or solid food. A milder degree of stenosis may not present until later in childhood. Stenoses are categorized into three histopathologic types: tracheobronchial remnants that often contain cartilage, fibromuscular stenoses, and membranous webs. Contrast radiography can diagnose the first two, while endoscopy is needed to diagnose webs. Tracheobronchial rings generally necessitate surgery, membranous webs can be treated with endoscopic dilation, and muscular stenoses may respond to dilation or may necessitate surgery.

Esophageal Strictures

Esophageal strictures ( Fig. 15.4 ) are acquired lesions that can be categorized as inflammatory (secondary to gastroesophageal reflux disease [GERD] and eosinophilic esophagitis), anastomotic (post-TEF repair), or related to corrosive injury (acid, alkali, pills, battery ingestions). The clinical presentation is the same for all these conditions: patients primarily present with dysphagia, recurrent vomiting, or food impaction. The strictures are best demonstrated with contrast radiography; endoscopic biopsies may be important for diagnosis of the etiology. GERD may be treated pharmacologically but may also require an antireflux surgery (fundoplication). Endoscopic dilation of the stricture is performed repeatedly with balloons or semirigid bougies until the strictured site remains patent.

Miscellaneous Causes

Foreign body ingestion is a common pediatric problem with up to 75% of cases in children age 4 years or younger. Coins are the most commonly ingested foreign body. The esophagus, in particular the upper one third, is a common site for obstruction. Patients may present with drooling, vomiting, cough, and stridor, and if lodged in the esophagus, urgent endoscopic removal is required.

Extrinsic esophageal compression may result from an aberrant subclavian artery, vascular ring, and mediastinal masses (lymphoma, germ cell tumors). Vascular rings occur when the esophagus and trachea are encircled, displaced, or compressed by the aorta or its aberrant branches and can present with stridor, dysphagia, and emesis. It is often an incidental finding on chest x-ray. In symptomatic cases, even after a vascular ring has been detected by plain radiography or esophagography, advanced cross-sectional imaging is recommended for more detailed evaluation.

Hypertrophic Pyloric Stenosis

Hypertrophic pyloric stenosis (HPS) is the most common cause of gastric outlet obstruction in infancy with an incidence rate of 1:400 infants. It manifests with nonbilious projectile vomiting beginning at 2–3 weeks of age and increasing during the next month or so, usually in a first-born male child. The vomitus may rarely contain some blood, and propulsive gastric waves can be seen across the abdominal wall. Dehydration, poor weight gain, hypochloremic hypokalemic metabolic alkalosis, and mild jaundice are sometimes evident. A palpable “olive” in the epigastrium (felt best during or after feeding) represents the hypertrophied pyloric muscle. Gastric distention is seen on the plain film, and a contrast study shows the “string sign” of contrast passing through the narrowed pyloric channel. Ultrasound diagnosis is less invasive and demonstrates increase of the pyloric channel length and muscle thickness ( Fig. 15.5 ). Laparoscopic pyloromyotomy is the treatment of choice. Preoperative correction of dehydration and electrolyte imbalance reduces perioperative morbidity. Junctional epidermolysis bullosum is associated with pyloric stenosis.

Other Causes of Gastric Outlet Obstruction

Eosinophilic gastroenteritis can mimic clinical signs and ultrasound appearance of HPS. Clues to diagnosis are eosinophilic infiltrate of endoscopic antral biopsies, peripheral eosinophilia, and an excellent response to treatment with a casein hydrolysate or elemental “hypoallergenic” formula. Prolonged use of prostaglandin infusion in neonates with congenital heart disease may cause transient HPS. The clinical and radiologic features of HPS are relieved after stopping prostaglandin E infusion.

In older children, gastric outlet obstruction may result from chronic peptic ulcer disease, chronic granulomatous disease, gastroduodenal Crohn disease, anatomic abnormalities such as gastric antral web, foreign bodies, and bezoars. Bezoars may be caused by hair, vegetable matter, milk curds, or medications. Contrast radiography, endoscopy, and, in some cases, histopathology is needed to make the diagnosis.

Duodenal Atresia, Stenosis, and Web; Annular Pancreas

The juxta-ampullary duodenum is susceptible to a cluster of obstructing congenital anomalies. Infants with complete duodenal obstruction, most commonly atresia, present with bilious vomiting and a radiographic “double-bubble” sign ( Fig. 15.6 ). Associated prematurity (and polyhydramnios) or anomalies, including renal, cardiac, and vertebral defects, occur in approximately 75% of infants; trisomy 21 is seen in about 50%. Double atresias, duplications, and malrotations are frequently seen. Infants with a partial duodenal obstruction caused by a stenosis or web may have such mild symptoms that they do not come to medical attention until regurgitation produces esophagitis or until a foreign body or bezoar is trapped at the obstruction. Treatment is surgical.

Duodenal Hematoma

Blunt abdominal trauma (seatbelt, steering wheel, bicycle handlebar injury; child abuse), or even endoscopic biopsies in the context of a coagulopathy, can produce an obstructing duodenal hematoma. Endoscopy in the setting of stem cell transplantation or other hematopoietic disease may place a patient at greater risk of such hematoma, requiring special consideration of the need for duodenal biopsies in these individuals. Therapy is symptomatic; jejunal feeding that bypasses the obstruction or parenteral nutrition may be required as the problem resolves.

Jejunal Atresia, Ileal Atresia, and Ileal Stenosis

Patients with these congenital lesions present with bilious vomiting and more abdominal distention than those with duodenal lesions. The atresias are readily suspected and diagnosed in the neonatal period. Stenotic lesions may require radiography for diagnosis. Treatment is surgical.

Intestinal Strictures

Strictures produce partial obstruction of the GI tract and may be located anywhere from the esophagus to the anus. They may occur postsurgically (anastomotic), may follow necrotizing enterocolitis, may be caused by penetrating Crohn disease or intestinal graft versus host disease, or may be sequalae of drug-induced ulcers (nonsteroidal antiinflammatory medications or high-dose pancreatic enzymes). Some patients may be treated with endoscopic dilatation, but many require surgical stricturoplasty (opening the bowel longitudinally and closing it transversely) or resection.

Adhesions

Obstructive symptoms in the child with a history of prior abdominal surgery may be caused by adhesive bands.

Duplications

GI tract duplication cysts are rare congenital anomalies and can occur in any portion of the GI tract but are more commonly encountered in the small intestine. These uncommon lesions may cause vomiting by extrinsic obstruction of the intestine or by intussusception. On examination, an abdominal mass may be palpable. Treatment is surgical resection.

Meconium Ileus and Distal Intestinal Obstruction Syndrome

Approximately 20% of infants with cystic fibrosis present in the newborn period with failure to pass meconium, caused by meconium ileus (MI). The sticky, poorly hydrated intestinal mucus plays a role. It can present in two forms: simple or complex MI. In simple MI, viscid meconium physically obstructs the terminal ileum and results in the dilation of the proximal small intestine. In complex MI, the meconium-distended segments of ileum can give rise to complications like prenatal volvulus, ischemic necrosis, or perforation and extrusion of the meconium into the peritoneum. The classic “soap bubble” sign may be seen on abdominal x-ray when meconium mixes with swallowed air ( Fig. 15.7 ).

Simple MI may be treated with hyperosmolar contrast (Gastrografin) enema performed under fluoroscopic guidance. Surgery is required for complex MI or those simple cases resistant to enema. Virtually all infants with MI have cystic fibrosis; the diagnosis should be confirmed by sweat test or DNA analysis.

Older children with cystic fibrosis who stop defecating and have abdominal pain and occasional vomiting are said to have distal intestinal obstruction syndrome (DIOS) , formerly termed meconium ileus equivalent. Initial treatment consists of rehydration, stool softening laxatives, or intestinal lavage and enemas. If not successful, then Gastrografin, administered orally or as enema often at times mixed with N-acetylcysteine (mucolytic), is nearly always successful. Surgery is rarely required. Close attention to fluid and electrolyte balance is vital in all infants and children treated with a hyperosmolar contrast medium. Avoiding dehydration and optimizing pancreatic enzyme dosage may reduce the chance of further episodes.

Incarcerated Hernia

Whenever vomiting is accompanied by signs of obstruction, sites of potential herniation should be examined for incarceration of a loop of bowel ( Fig. 15.8 ). Inguinal incarceration is most common, but other types of hernias are femoral, obturator, spigelian, umbilical (1 in 1,500 incarcerate), epigastric, mesenteric, and postoperative incisional hernias.

Inguinal hernias are often reduced by gentle, firm, constant pressure that is directed through the scrotum toward the inguinal canal. Sedation and the Trendelenburg position may facilitate reduction.

Malrotation and Volvulus

Volvulus is the twisting of a loop of bowel on the mesentery. Midgut volvulus occurs most often in the context of congenital intestinal malrotation, in which the small intestine is not normally fastened in place. This may only be clinically apparent on upper GI fluoroscopy when the duodenum and distal small bowel are seen to fill with contrast right of midline without crossing to the left upper quadrant ( Fig. 15.9 ). More than half of patients found to have malrotation present symptomatically (the rest of such cases are discovered incidentally), and about half of the symptomatic patients present in the neonatal period with bilious vomiting caused by volvulus. Those presenting later often do not have bilious vomiting; the vomiting may be intermittent for years.

Volvulus is an extremely hazardous obstructing lesion. The luminal obstruction is closed at both ends, which leads to sepsis from rapidly proliferating and translocating bacteria. There is also vascular obstruction caused by the root of the mesentery getting twisted, which quickly produces ischemia of the small intestine. Even if volvulus is diagnosed and repaired promptly, massive intestinal resection may be necessary secondary to underlying necrosis; this produces short bowel syndrome. Because volvulus may be intermittent, it may produce episodic or chronic intermittent vomiting or nonspecific abdominal pain before a lethal event. Therefore, upper intestinal contrast radiographs should be considered in all patients with intermittent vomiting, and surgery must be performed if a malrotation is found (i.e., if the ligament of Treitz is not to the left of the spine), even if volvulus is not present at the time of the examination. In an infant in whom an ongoing volvulus is suspected, a contrast study may show a “volvulus/corkscrew” pattern ( Fig. 15.10 ). In the sick infant or child in whom volvulus seems likely, surgery without contrast studies may be preferred. Surgery involves correction of any present volvulus, functional positioning of malrotation, and lysis of potentially obstructing peritoneal (Ladd) bands that cross the abdomen.

Other types of volvulus not associated with malrotation include cecal, sigmoid, and transverse colonic volvulus. They are less common in children and less apt to produce short bowel syndrome, but they too may manifest with vomiting and result in death if untreated. Sigmoid volvulus is sometimes treated nonoperatively via endoscopic release.

Meckel Diverticulum

Meckel diverticulum is a small intestinal diverticulum that represents the fibrous remnant of the omphalomesenteric duct. Although painless GI bleed is the most common presentation, it can present as intestinal obstruction or inflammation (diverticulitis). It may lead to obstructive vomiting by causing intussusception ( Fig. 15.11 ) or intestinal volvulus around the diverticular axis. It can get inflamed, leading to peritonitis (mimics appendicitis or peptic ulcer disease) and sometimes perforation, which can induce vomiting. The “rule of 2s” identifies characteristic findings: diverticula are present in 2% of the population; only 2% are symptomatic; the male:female ratio is 2:1; the diverticula occur within 2 feet of the ileocecal valve and are 2 inches long; there are 2 major types of heterotopic mucosa (gastric and pancreatic); and the condition is confused with 2 diseases (appendicitis and peptic ulcer). Treatment is surgical resection.