Infantile Vomiting
AUTHOR
Natan Cramer, MD, Instructor of Pediatrics, University of Arizona, Tucson
PEER REVIEWER
Catherine A. Marco, MD, Professor of Emergency Medicine, Wright State University Boonshoft School of Medicine, Kettering, OH
Every viral season, something gets missed. All vomiting is not acute gastroenteritis! The clinician needs to have a thorough understanding of the process of vomiting to formulate a complete differential accurately and in a timely manner. A complete history, physical exam, and targeted diagnostic testing are used to ensure an accurate diagnosis with effective management is instituted.
— Ann M. Dietrich, MD, FAAP, FACEP
Definition of Vomiting
One of the most common neonatal presentations to the emergency department is vomiting, particularly within the first two weeks of life.1 The American Gastroenterological Association defines vomiting as the process by which gastric material is actively and forcefully expelled backward from the stomach and out through the mouth. Regurgitation, in contrast, is a passive process. Vomiting itself is broken down into three sequential bodily actions: the pre-ejection phase, the retching phase, and the ejection phase.2,3 Although vomiting is an advantageous physiologic process, in reality it often is unsettling for caregivers and clinicians during the infant period. The amount of vomiting itself causes anxiety for parents, who, similarly to healthcare workers, generally are unable to accurately visually estimate emesis volumes.4 The natural history of infantile vomiting generally is reassuring, with surgical causes of vomiting occurring much less frequently compared to medical causes.5 However, when faced with particular red flags in the history and physical exam, the suspicion should be raised for either a surgical pathology or a morbid medical condition.
Pathophysiology of Vomiting
Emesis is the culmination of complex physiological signaling. Four main triggers lead to a common pathway resulting in expulsion of gastrointestinal contents. The various types of triggers ultimately act upon the vomiting center, which is located in the brainstem at the region of the lateral medullary reticular formation. The four types of trigger systems are the vestibular system, the chemoreceptor trigger zone, the vagal afferent system, and the high cortical center. Multiple receptor types are found in the vomiting center, including muscarinic (M1), histaminic, neurokinin 1, and serotonin receptors. The chemoreceptor zone (area postrema) is located in the bottom of the fourth ventricle and is positioned outside of the blood-brain barrier, responding effectively to chemical pro-emetic signatures in the cerebrospinal fluid and blood. The area postrema is the proposed zone in which uremia, hypercalcemia, and diabetic ketoacidosis act to induce vomiting in these states.2,3 The zone is composed chiefly of dopamine 2 (D2) receptors. The vestibular system is responsible for vomiting associated with labyrinthine disease or motion sickness. The main receptors involved in this system are the muscarinic and histaminic receptors. The vagal afferent system acts as a relay system to send gastrointestinal structural triggers, including distention and irritation, to the vomiting center. This system operates with serotonin receptors. The higher cortical centers are not well elucidated but are believed to be associated with psychological induced vomiting states.3 (See Figure 1.) The various relay systems highlight the necessity for a broad differential diagnosis in cases of vomiting, as gastrointestinal and non-gastrointestinal causes both ultimately lead to this common pathway. The pathophysiology of vomiting is clinically relevant, as evidence has elucidated the benefit of antiemetic therapy, which chiefly operates through serotonin antagonism.
Figure 1. Physiologic Relay System of Vomiting2,3 |
 |
Historical Assessment of a Vomiting Infant
When a patient presents to an acute care setting with vomiting, it is crucial to consider if the vomiting is surgical or non-surgical in nature.6 (See Figure 2.) Red flags in the history pointing to a surgical cause for the vomiting include bile- or blood-containing emesis or diarrhea and, potentially, abdominal distention noted by the parents.5 In the setting of concern for obstruction, the color or consistency of the vomit can help identify the location of the blockage. Undigested food or milk suggests emesis originating from the stomach or higher.7 Bile-stained emesis, whose color can range from light to dark green, represents a blockage distal to the ampulla of vater.3 Feculent vomit suggests an issue originating within the large bowel.7 The color of bloody vomit (hematemesis) also may help with identifying the severity of a hemorrhage within the gastrointestinal tract. Bright red vomit points to a brisk upper gastrointestinal bleed, whereas “coffee-ground” emesis points to a slow bleed exposed to gastric acid converting the blood to a darker shade.3 Characterization of apparent abdominal pain is crucial when evaluating for particular causes of obstruction. For example, paroxysmal, colicky pain points to intussusception, whereas apparent pain with any movement points to peritoneal irritation.7,8 Even the velocity of the emesis can aid in diagnosis. For example, the rapid expulsion of the vomit during the ejection phase points to etiologies in which there is gastric outlet obstruction, as in pyloric stenosis. Rapid expulsion also may be seen in cases of increased intracranial pressure.3
Figure 2. Obstructive Causes of Vomiting Likely Needing Gastrointestinal Surgical Intervention5,6,7,20,25,32 |
 |
When faced with concern for bowel obstruction, the age of the patient can help a clinician differentiate between particular surgical etiologies.7 Prenatally, polyhydramnios may be associated more specifically with proximal bowel obstruction. In neonates, a lack of meconium passage within the first 48 hours of life would be concerning for bowel obstruction. Other obstructive symptoms include vomiting and abdominal distention between the first 24-36 hours of life.7,9 In a scenario fulfilling the aforementioned criteria, the practitioner should consider a congenital gastrointestinal pathology, such as meconium ileus, Hirschsprung disease, imperforate anus, bowel atresia, and malrotation, causing the underlying obstruction.7 This is in contrast to pyloric stenosis, which is expected to manifest within the first several weeks or more of life, and intussusception, which is uncommon in the newborn period altogether.
Overall, medical nonobstructive causes of vomiting are much more common in the infantile period than bowel obstruction.7 (See Figure 3.) However, before entertaining more benign causes of vomiting in the neonate (younger than 4 weeks of age), it is important to remember that this population is relatively immunocompromised, and serious bacterial illnesses in this age group can present simply with vomiting in the absence of fever.7,10 Such infections include but are not limited to urinary tract infections, necrotizing enterocolitis, sepsis, and meningitis.7
Figure 3. Medical Causes of Vomiting in Infants5,7,59 |
|
Non-gastrointestinal causes are much more varied. |
 |
Neck stiffness characteristically is not a prominent finding in newborns with meningitis; in fact, meningeal signs typically are difficult to localize and determine in those younger than 18 months of age.7,10,11 Sixty percent of cases of neonatal meningitis will be associated with temperature instability, highlighting the significant number of cases presenting with a normal body temperature.11,10 More often, meningitis is noted by a history of vomiting and lethargy.7 Similar to meningitis in the preverbal population, the signs and symptoms of urinary tract infection can be quite subtle. A simple history of high fever, vomiting, a stark lack of typical upper respiratory tract symptoms, or other source of infection may be the only clue.12 It is important to assess for risk factors that may place a neonate or infant at increased risk for serious bacterial infections. Such risk factors include a history of prematurity, low birth weight, congenital urogenital or spinal anomalies, race, gender, circumcision status, chorioamnionitis, maternal group B streptococcus colonization, or prolonged rupture of membranes during delivery.11,12
Although rarer, inborn errors of metabolism also can cause infantile vomiting. Suspicion should be raised if an infant has an abnormal smell, lethargy, poor feeding, and growth failure. Symptoms of a metabolic disorder often worsen during concurrent illnesses, and the diagnosis may be missed if the family did not follow up with genetic screening or if the patient is an immigrant.5,13,14
Vomiting is one of the most common presenting symptoms found to be associated with pediatric brain tumors diagnosed in the emergency department. Interestingly, emesis as a leading historical clue occurs more frequently and often precedes the development of focal neurologic deficits.15,17 A common belief is that infants are well-buffered against increased intracranial pressure because of the presence of fontanelles and spacious subarachnoid cisterns. In reality, the innate properties of volume and pressure adaptation in the cephalic anatomy of the infant are somewhat offset by the low compliance of the small central nervous system.16 Thus, neurologic emergencies to consider in the vomiting infant include those that cause increased intracranial pressure, such as hydrocephalus, brain mass, cerebral edema, and trauma. It is especially important to have a high index of suspicion for an intracranial mass in infants with persistent vomiting who have undergone extensive gastrointestinal workups with no firm diagnosis.17
Another key historical piece of information important to elicit from caregivers includes whether there has been weight loss, pointing to concern for gastroesophageal reflux disease (GERD), or etiologies associated with malabsorption, such as celiac disease or inflammatory bowel disease, especially in the setting of chronic diarrhea.3,5
When a diagnosis of acute gastroenteritis is suspected (information from the history), identifying the type of symptoms can help delineate the likely underlying organism. It is important to ascertain if the patient has traveled recently, has been exposed to contaminated food or water, or has been exposed to positive sick contacts. In certain circumstances, if a particular infectious agent is identified, the health department must be notified. In addition to bilious emesis and other historical red flags pointing to a surgical issue, a presumed diagnosis of acute gastroenteritis should be questioned if there is the presence of fever > 39° C in patients 3 months of age or older or > 38° C in patients younger than 3 months of age.18 Acute gastroenteritis should be a diagnosis of exclusion once other more serious etiologies have been ruled out.
Regardless of the underlying cause of vomiting, the patient’s hydration status also always should be assessed. Historical red flags that should increase the concern for dehydration include the following: symptoms in patients ≤ 1 year of age with the most danger being in patients < 6 months, five or more episodes of diarrhea within the previous day, and two or more episodes of vomiting within the same time period.18 Dehydration often is associated with electrolyte imbalance such as hypernatremia. A clinician should investigate if there is increased muscle tone, increased reflexes, a history of seizures, tremors, and altered mental status.18 (See Figure 3.)
Finally, as an infant gets older and becomes more mobile, it is crucial to consider a toxic ingestion as well. Therefore, it is important to ask the family if medications are locked up at home and if the house is childproofed. Particular agents of concern include prescription drugs such as digoxin, over-the-counter medications such as acetaminophen or aspirin, and heavy metals such as iron and lead. Relatively more benign and common etiologies to consider include gastroenteritis and paralytic ileus. Assessing for stool output can help delineate between these two ailments.7
Physical Examination and the Assessment of a Vomiting Infant
Red flags for a surgical pathology in the physical exam may include abdominal distention and abdominal peristaltic waves visible to the clinician.5 (See Table 1.) However, it is important to recall that in the early stages of midgut volvulus, there may be bilious vomiting without much abdominal distention, with the proximal bowel being the source of obstruction. Once ischemia occurs, then distention, ileus, hematochezia, and bloody vomit occur.19 A similar scenario is true of duodenal atresia, in which abdominal distention may not be evident or simply may be present in the upper abdomen, as the rest of the intestine post-obstruction is empty.20 Bowel obstruction in neonates also should be suspected when more than 15-20 mL of bilious fluid is aspirated from the stomach.7,9 It is important to assess the bowel sounds as well, as high-pitched or absent bowel sounds may raise the concern for obstruction.7 With regard to pyloric stenosis, classic teaching dictates that a palpable “olive” likely will be present in the right hypochondrium. Older evidence has shown the “olive” to be present in more than 50% of cases of pyloric stenosis.21 Although pediatric surgeons had a palpation sensitivity of 74% in St. Louis, a recent study indicated that the physical exam finding might be less prevalent in the current age of earlier diagnosis (13.6%).21,22 It is important to note that this recent study was a retrospective chart review and that at least one other recent retrospective review mentions the presence of an “olive” still occurring a striking 48% of the time.21,23
Table 1. Common Historical Clues and Physical Exam Findings in Obstructive Cases of Infantile Emesis3,7,19,20,32,38,46,48,54,60 |
|||
Historical Findings |
Physical Clues |
Classic Imaging/
|
|
|
Duodenal Atresia |
Vomiting/non-toleration of feeds since birth, which may or may not be bilious in nature No meconium passage Often, there is a history of prematurity or Down syndrome The patients are generally well appearing |
Absence of diffuse abdominal distention |
Aerated stomach and an enlarged duodenal bulb (“double bubble”) on abdominal radiograph |
|
Pyloric Stenosis |
Progressive projectile non-bilious vomiting within the first 3-6 weeks of life |
Palpable “olive” on exam with visible peristaltic waves |
Hypochloremic , hypokalemic, metabolic alkalosis Pyloric enlargement on ultrasound (in particular a pyloric muscle thickness of > 3 mm) |
|
Intussusception |
Classic triad of vomiting (typically non-bilious), paroxysmal abdominal pain, and bloody stool in a child between 3 months to 6 years of life |
Right upper quadrant mass |
“Doughnut” and pseudokidney signs on ultrasound |
|
Malrotation with Volvulus |
Sporadic bilious or non-bilious containing emesis with colicky abdominal pain Some patients can present in shock with bloody stools |
Upper abdominal distention initially Progressive signs of peritonitis and diffuse distension as symptoms worsen |
Duodenal obstruction on upper GI with or without the duodenojejunal “corkscrew” appearance |
|
Meconium Ileus |
Associated with cystic fibrosis; 20-30% of patients have concomitant atresia |
Abdominal distention right after birth |
The meconium will have a “bubbly” appearance on the abdominal radiograph There may be absence of gas in the right iliac fossa Proximal to the obstruction, there will be dilated loops of small bowel Additionally, there may be intra-abdominal calcifications that are evident if there was prenatal intestinal perforation Microcolon will be seen on contrast enema |
|
Meconium Plug Syndrome |
Bilious emesis and signs of intestinal obstruction, which is relieved by rectal exam |
Passage of a meconium plug that is hard and with a white tip, representing thick mucus |
Lack of filling in the distal colon and rectosigmoid on contrast enema |
|
Hirschsprung Disease |
Typically there is no meconium passage within the first few days of life There is decompression with rectal exam |
Lack of rectal gas on radiograph There also will be dilated loops proximal to the defect and potentially a perforation Definitive diagnosis is made by rectal biopsy |
|
An alternate opinion is that the sensitivity for palpation has gone down with increased reliance on imaging.22 Despite the potential decrease in sensitivity, it was shown in St. Louis that even if a palpation sensitivity was only 37% among pediatric surgeons, it still would be more cost effective for the patient to be evaluated by a surgeon prior to diagnostic imaging as opposed to the opposite scenario.22 Part of the reasoning was because the positive predictive value for “olive” palpation among that group of pediatric surgeons was roughly equivalent to the radiological studies at that institution (approximately 99%). Thus, it was hypothesized that if a physician were able to feel an “olive” with accuracy, a radiological study would not be needed for confirmation.
However, it is important to stress that this retrospective review occurred at an institution in which there was a higher cost for radiological studies (ultrasound and upper gastrointestinal series) vs. surgical consultation at that time. This cost-effective model would apply only to places with experienced surgeons and where the cost of a surgical referral would be cheaper than a radiological study.22 In addition, as it is a retrospective review, the authors noted that often they were unable to tell whether a physical exam took place before or after the imaging was performed. As such, it is possible that the physicians were “primed” to feel an “olive” if there already was image confirmation, leading to potentially falsely increased palpation sensitivity.22
Physical examination can aid in the setting of suspected increased intracranial pressure, as the sutures may be splayed, the fontanelle bulging, the head circumference increasing, and a positive “setting-sun” of the eyes (eye gaze deviation downward with upper eyelid retraction) may be noticeable.7,12,13,24 However, the strongest indicators of severely increased intracranial pressure are dilated, poorly reactive pupils and poor mentation. Infants typically do not present with papilledema or cranial nerve abducens palsy.16
Signs of dehydration, such as delayed capillary refill, a sunken fontanelle, absent tears, and diminished skin turgor, might be evident on exam.6
Case Studies
The following clinical scenarios illustrate the difference between morbid and benign causes of infantile vomiting.
Case 1
A newborn female with downslanting palpebral fissures, poor tone, single transverse palmar crease, and clinodactyly bilaterally presents with intractable bilious vomiting within the first 48 hours of life. In addition, the infant has not passed meconium thus far. On abdominal KUB (kidneys, ureters, bladder) radiograph, the infant has a paucity of distal bowel gas, and the proximal bowel and stomach appear dilated with air. What is the underlying genetic abnormality and the potential diagnosis in light of this genetic defect?
Diagnosis. In the case mentioned above, suspicion for atresia of the duodenum should come to mind in light of the patient’s physical stigmata and abdominal film finding. A typical presentation involves a lack of meconium passage or abdominal distention coupled with vomiting and feeding intolerance. The lack of abdominal distention is due to an empty bowel distal to the atretic portion of duodenum. Typically, there is bilious vomiting, as the obstruction is most often post-ampullary in location.3,20 However, it is important to note that the vomiting can be nonbilious in a third of infants who have the atretic portion proximal to the ampulla of vater.6,20 Additionally, approximately one-third of patients will have visible jaundice. By far, duodenal atresia is the most common type of small bowel atresia, followed closely by jejunal.3 Small intestinal atresia frequently is associated with multisystem congenital anomalies, and the association between duodenal atresia and Down syndrome is well-documented in the literature. However, duodenal atresia also is frequently associated with simple prematurity as well. Duodenal atresia is diagnosed prenatally by ultrasound approximately 50% of the time.20 Abdominal radiograph films typically will show the classic “double bubble sign.”3 However, a retrospective study performed over six years in Australia found abdominal plain radiographs to be a suboptimal screening tool for detecting intestinal obstruction in newborns, carrying a 50% sensitivity and a slightly better specificity of 80%. Comparatively, contrast imaging carries a sensitivity of 100% and specificity of 91% for intestinal obstruction.25
Management. Emergency medical management of intestinal atresia is restricted to bowel rest, gastric decompression, and stabilization of electrolyte abnormalities related to the persistent vomiting. Ultimate treatment requires a surgical intervention.3 Although patients with bowel atresia will show marked intolerance to feeding and can appear sick, bowel atresia generally is less life-threatening in the acute period as compared to an ischemic disease, such as midgut volvulus or necrotizing enterocolitis.19
Case 2
A 9-day-old ex-32-week gestation infant boy admitted to the NICU has progressively worsening regurgitation, and he has mild abdominal distention on physical exam. What is the diagnosis and what is the severity?
Diagnosis. Necrotizing enterocolitis is the most common cause for bowel perforation in the neonate. Necrotizing enterocolitis infrequently presents within the first three days of life; rather, the disease process typically will manifest within the first week of life in mature infants, and 1-3 weeks of life in premature infants. As more premature infants present with necrotizing enterocolitis at later corrected gestational ages and more premature infants are being discharged prior to the corrected gestational age of 40 weeks, more infants are presenting with necrotizing enterocolitis to the emergency department.19 Necrotizing enterocolitis can have a subtle presentation; however, it classically presents with acute onset of bilious vomiting, abdominal distention, decreased bowel sounds, and palpable bowel loops on exam.19,26 X-ray findings can range from a mildly obstructive bowel gas pattern to pneumatosis intestinalis to air in the biliary tree. Procalcitonin and nCD64, a mid-phase biomarker and early-phase biomarker, respectively, have been recommended as part of the initial workup along with a late-phase biomarker for the diagnosis of necrotizing enterocolitis or neonatal sepsis. However, these biomarkers cannot differentiate between these two entities in the early stages of the illness. Although it appears attractive, serial measurements of these biomarkers have not been validated to guide antibiotic stewardship in cases of necrotizing enterocolitis.27
Management. Necrotizing enterocolitis typically is divided into three levels of severity.31 (See Table 2.) As part of the severity scoring assessment, abdominal films are required for confirmation.6 Treatment is two-tiered, involving medical therapy and surgical management. Medical therapy involves bowel rest, intravenous (IV) antibiotics and fluids, and serial abdominal films to monitor for progression. A 2012 Cochrane review evaluated various empiric antibiotic regimens for patients with necrotizing enterocolitis. As aerobic and anaerobic bacteria both are implicated in necrotizing enterocolitis, empiric therapy should cover both types of organisms. However, beyond this concern, the authors were unable to recommend one regimen over another. One study included in the review indicated a trend toward stricture development in patients receiving clindamycin as part of their regimen. As such, future case-controlled studies are recommended to further evaluate this potential association.28,29 With regard to surgical management, either a peritoneal drain or exploratory laparotomy may be necessary.6 A Cochrane analysis of two randomized, controlled trials did not show a definitive benefit or harm in one surgical method over another in low birth-weight premature infants. The studies included in the analysis suffered from small sample sizes and, thus, no concrete recommendations could be derived.30
Table 2. Neonatal Necrotizing Enterocolitis Staging Scheme |
|
|
In the setting of a history of perinatal stress |
|
|
Stage 1 (suspected) |
|
|
Stage 2 (definite) |
|
|
Stage 3 (advanced) |
|
|
Adapted from: Bell MJ, Ternberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis. Ann Surg 1978;187:1-7. |
|
Case 3
A 4-week-old boy presents with progressively worsening vomiting over the past 10 days that his parents described as “shooting across the room.” He appears hungry immediately after the vomiting and clinically is dehydrated with a sunken fontanelle. What is the diagnosis and what are the next immediate steps in management?
Diagnosis. In young infants between 3-6 weeks of age, pyloric stenosis should be considered a significant potential underlying etiology for progressive vomiting. Pyloric stenosis has an incidence of 2-3 infants per 1,000 births. Prematurity has been shown to be a significant risk factor, along with other factors such as male gender, cesarean delivery, and being a first-born child.3,33 However, premature babies are known to develop symptoms relatively later compared to full-term infants.34 Maternal smoking, formula feeding, and alcohol use during pregnancy also are thought to be risk factors.33,35,36 Other known genetic and environmental factors are involved as well, but their role in pathogenesis is not fully clear.36 However, it is known that a maternal history of pyloric stenosis carries a 20% risk for a male offspring and a 10% risk for female offspring.3
One of the more commonly studied environmental risk factors for pyloric stenosis is exposure to macrolide agents, in particular erythromycin. Infants with pyloric stenosis presumed to be secondary to erythromycin were noted to be less likely to have projectile vomiting; however, they were more likely to have electrolyte disturbances despite having a shorter duration of vomiting prior to admission. On average, they were younger on presentation compared to classic cases as well.34 Other macrolides have been implicated in the development of pyloric stenosis. A 2015 study evaluated the risk of both azithromycin and erythromycin on the development of pyloric stenosis. The results indicated that erythromycin exposure had a higher adjusted odds ratio compared to azithromycin exposure for the development of pyloric stenosis, although both agents clearly were risk factors within the newborn to 6 weeks of age time frame. For a given macrolide exposure, the risk for pyloric stenosis development was higher in infants exposed to the medication within the first two weeks of life compared to those exposed after two weeks of life. After six weeks of life, there was no statistically increased risk of pyloric stenosis with either macrolide. The number needed to harm for macrolide exposure in the first two weeks of life was 56 for the azithromycin group and 35 for the erythromycin group.37
The classic presentation of pyloric stenosis involves worsening vomiting (often projectile in nature) after feeds and the eventual development of dehydration. The projectile nature of the vomiting can be explained physiologically, as the first two phases of vomiting may be bypassed with vomiting solely being achieved by the ejection phase.2,3 A small minority of patients (1.4%) will present with bilious emesis. Conversely, “icteropyloric syndrome” is a more common phenomenon that is seen in approximately 8% of infants. This presentation is defined by the combination of indirect hyperbilirubinemia and pyloric stenosis.3
The diagnosis of pyloric stenosis typically is made by abdominal ultrasound. A muscle thickness of > 3 mm of the pylorus on ultrasound has been shown to be the most reliable and accurate predictor of true disease out of all the morphologic measurements. The diagnosis can be made confidently if the following are noted: typical history, pyloric muscle thickness of > 3 mm, and abnormal pyloric function (represented by absent muscle relaxation and gastric fluid advancement). It also is crucial to mention how timing affects making an accurate diagnosis. Given the known pathophysiology of hypertrophy, the disease has a typical natural progression. An equivocal ultrasound result simply may reflect an early presentation of a young infant. If suspicion remains high, the infant should have a repeat ultrasound a few days later.38 If the presentation is atypical or if there is a confounding history, a barium study can be performed of the upper gastrointestinal tract to rule out any type of gastrointestinal obstructive disease in addition to pyloric stenosis. The potential benefits of the study need to be weighed with the increased risk of radiation and cost as compared to abdominal ultrasound.
Management. Initial management of pyloric stenosis involves correcting any potential electrolyte or acid-base disturbance and intravascular volume resuscitation prior to surgery. The classic metabolic presentation of pyloric stenosis is hypochloremic hypokalemic metabolic alkalosis. The acid-base derangement, if not corrected prior to surgery, is associated with postoperative apnea. Multiple randomized, controlled studies have shown no significant clinical outcome difference with regard to open vs. laparoscopic pyloromyotomy.3
Case 4
A 10-month-old female presents with recurrent episodes of quick-onset fussiness, screaming, and bringing her legs to her chest, followed by visibly pain-free episodes with normal feeding. Intermittently, there is nonbilious vomiting that is not forceful in nature. On initial presentation to the emergency department, the patient appears slightly fatigued but otherwise is acting normally. However, within 10 minutes of the history and physical exam, the patient has a pain crisis in front of the provider. During this time, there is a noticeable bulge felt in the right upper quadrant of the abdominal area during exam. What is the diagnosis and what are the next steps in management?
Diagnosis. Intussusception is the most common reason for obstruction between the ages of 3 months and 6 years of life. The highest incidence of the disorder is found within the first year of life.7,39 The condition is defined by proximal bowel invagination into more distal segments, causing vascular congestion and swelling; thus, the condition is a surgical emergency.8
The typical site for intussusception is the ileocecal region, as more than 80% of cases occur at this location.40 If the obstruction persists, eventual arterial obstruction and necrosis ensue.8,41 Alternatively, bowel perforation without peritonitis has been reported as well.42 In infants younger than 4 months of age, intussusception is less common. As such, subtle presentations can occur, and a younger patient simply may present with excessive vomiting as the only symptom.43 Altered mental status with or without gastrointestinal complaints also may be a presentation for intussusception.44 The vomiting may or may not be coincident with the episodic pain, and it may even be feculent in nature if there is prolonged illness.45 Bile-stained vomit is not commonly found to be associated with this etiology; one study reported it to be present in
< 2% of cases and typically when the obstruction is advanced.32,46
The prototypical presentation is paroxysmal episodes of abdominal pain separated by periods of calm and normal behavior. “Currant jelly stool” is not an early finding of this disease, but in fact represents the prolonged congestion leading to vascular compromise with subsequent mucosal sloughing.8,47 As such, less than 25% of cases present with the classic triad of emesis, apparent abdominal pain, and bloody bowel movements.8
In light of the difficulty in diagnosing solely on clinical grounds, ultrasound has evolved as a major tool in evaluating for this condition. A 1992 study highlighted the high sensitivity and specificity of ultrasound in diagnosing intussusception.48 Using a sample population of 65 patients for whom the diagnosis of intussusception was considered, ultrasound was proven to have a sensitivity of 100% and a specificity of 93%, with confidence intervals ranging between 86-100% and 86-96%, respectively. Even more significant, the negative predictive value noted was 100%, with a confidence interval of 94-100%.48 Although plain films have poor sensitivity and specificity for intussusception, a left lateral decubitus or an upright abdominal film is warranted to rule out bowel perforation, which would be a contraindication to enema reduction.8,49
Management. Modern therapy for intussusception involves either hydrostatic or pneumatic reduction. A recent meta-analysis found that pneumatic reduction was more successful in reducing intussusception compared to hydrostatic reduction. The number-needed-to-treat for preventing one failure by hydrostatic reduction by opting to perform pneumatic reduction was nine (95% confidence interval, 8-12). Patients with obvious peritonitis or failure to reduce with an enema should receive an immediate surgical consultation.50
Case 5
A 15-month-old boy presents with acute onset of severe abdominal pain, bilious vomiting, and bloody stool. On exam, the patient is tachycardic and hypotensive. Although the patient was writhing in pain initially, the patient is now rigid and does not want to move. The abdomen is distended. What is the diagnosis?
Diagnosis. Malrotation is a condition that presents classically during childhood, particularly in the newborn period. A 15-year review of malrotation cases indicated that 64% of cases occurred in infants younger than 1 month of age.51 However, late-onset cases have been described in the literature, with one review indicating that 14.8% of diagnosed patients were older than 1 year of age.52 Malrotation has been described as a congenital defect in which there is incomplete rotation of the intestines in utero. The incomplete rotation sets the small bowel at risk for midgut volvulus, which is defined as torsion of the small intestine around the focal point of the superior mesenteric artery axis, causing obstruction and eventually cutting off the blood supply.53 Malrotation with midgut volvulus anatomically causes obstruction at the third part of the duodenum.19 It is important to distinguish between malrotation, the inborn condition, and midgut volvulus, the acute worsening of this condition by obstruction. The defect classically is associated with colicky abdominal pain and bilious vomiting; however, the presentation may be more subtle and chronic.7 Malrotation also may present as gastrointestinal bleeding, nonbilious vomiting, diarrhea, or even a sepsis or shock-like picture if volvulus is of concern.54 In fact, after 2 months of age, nonbilious vomiting as a symptom of malrotation presents at approximately equal rates to bilious vomiting.55 If the presentation involves abdominal pain and shock, then midgut volvulus with a gangrenous bowel is likely to be found.54 Malrotation even has been described as presenting with malabsorption and failure to thrive, although this is found less frequently in the newborn period and is more consistent with an older presentation.56,57
Management. With regard to suspected midgut volvulus, an upper gastrointestinal series still is considered the fastest and most reliable way of determining obstruction at the level of the duodenum and the position of the ligament of Treitz in the suspicion of an underlying malrotation.56 Delayed films are useful, particularly in cases in which distention of the bowel or indwelling tubes make it difficult to ascertain the anatomy of the upper gastrointestinal tract. If suspicion persists for malrotation, then in these cases, delayed films will allow for assessment of malpositioning of the cecum.
Assessment of cecal anatomical positioning also may be done with a quick contrast enema if the patient’s physical presentation is not appropriate for waiting for delayed films.56 At this time, ultrasound findings remain insufficiently sensitive to be used as a screening tool.53 As death to the bowel and, thus, the patient can occur within a few hours, it is imperative that the patient undergo surgical consultation as soon as this condition is suspected.20
A 2010 retrospective review highlighted the benefits of a laparoscopic approach for a Ladd’s procedure compared to an open approach. The review noted that there was shorter hospital duration, shorter time to attaining full feeds, and less wound infection in the laparoscopic group. However, it should be noted that overall the laparoscopic group consisted of older patients and that there was a higher degree of postoperative volvulus (5.6%) compared to the open group (0.8%). This should be weighed against the significantly increased risk of postoperative obstruction in the open Ladd’s population (13.3%) compared to the laparoscopic group (0%).58
Case 6
A 4-month-old infant girl presents to the emergency department with chronic spit-up post-feeding. The resident reviewing the case glances at the growth chart and notices that the infant has been gaining weight appropriately thus far. No other concerning symptoms or signs are elicited. What is the diagnosis and what advice should be given to the parents?
Diagnosis. In the infantile period, gastroesophageal reflux (GER) and GERD are the two most prevalent causes of vomiting. As such, the patient’s history and physical exam should guide the presumptive diagnosis. GER is defined by the passive reverse flow of contents from the stomach into the esophagus.3 There are multifactorial reasons for infants to have GER. Infants have short esophagi and often lie flat. Coupled with large volumes of liquid feeds and low esophageal sphincter tone, GER can develop.61
On the other hand, GERD is a pathologic process defined as GER plus adverse complications, including chronic wheezing, apneic events, chronic otitis media, and failure to thrive.3,61 Certain conditions, such as cerebral palsy, repaired esophageal atresia, and congenital diaphragmatic hernia, increase the risk for GERD.61 Weight is an excellent surrogate marker for determining clinically if a patient is suffering from GERD or simply has benign functional reflux or GER. Patients with GERD either will not gain weight appropriately or will lose weight.3
As a common benign process in healthy term infants, the incidence of GER peaks at approximately 4 months of age, when the majority of infants (67%) will present with symptoms defined by at least one episode of regurgitation daily. Between 6-7 months of age, the prevalence decreases from 61% to 21%. By 10-12 months, GER becomes even rarer among the healthy infant population (5%).62 Certainly by 18 months of age, if the symptoms persist, then the patient requires further workup including a referral to a pediatric gastroenterologist.3,63 Further workup may include a barium study of the upper gastrointestinal tract to rule out underlying anatomic defects causing persistent feeding intolerance and vomiting. However, in most cases, GER is a clinical diagnosis that does not require extensive testing.3
Management. In cases of GER, supportive measures and reassurance often are the only management needed. Supportive measures include inhibiting overfeeding and adjusting positioning during feeds. The total daily requirement for volume of feeds in a formula-fed infant is 150-200 mL/kg.14 This volume recommendation provides the necessary amount of calories for growth. Conversely, for breastfeeding infants, adequate feeding volumes should be guided by on-demand feeding patterns.64 In reality, parental feeding practices often are guided by fussiness and nighttime waking. These factors, combined with growth percentiles in the upper ranges, may be tip-offs that the infant is being overfed.65 Crib head elevation has not been shown to significantly reduce symptoms of reflux. As protein milk intolerance commonly can be missed, a two- to four-week trial of hypoallergenic formula may be warranted in infants with poor weight gain or significant symptoms lasting longer than four weeks.3,63 Although controversial, complete exclusion of dairy products in the mother of a breastfeeding infant with milk protein intolerance may or may not provide benefit.3
A 2008 Cochrane review highlighted the controversial nature of thickening feeds. Not only were there a paucity of studies investigating the intervention noted, but some of the studies were funded by thickening manufacturers. In addition, although thickening agents were noted to statistically increase the percentage of regurgitation-free infants and to reduce subjective symptomatology assessed by caregivers/treating physicians, the clinical significance was questioned, as it was noted that regurgitation was decreased by only 0.6 episodes per day in certain studies. Not enough data were present to recommend one thickening agent over another. Pooled objective measurements from multiple studies to indicate reduced reflux in those fed with thickened formulas proved unable to show a significant decrease in the reflux index, defined by the percentage of time that the esophageal pH is < 4.66 The reflux index is not arbitrary, but rather is based on adult studies in which acid reflux was associated with an esophageal pH of < 4. Monitoring of pH in infants can be a challenge to interpret, as the high frequency of feeds can buffer the gastric acidity and produce false-negative results.63 However, it should be mentioned that infants on thickened feeds were noted to have increased weight gain.66 The authors of the review postulated that if the duration of the interventions in the studies was longer than the maximum of eight weeks, then this factor might be of clinical significance for those infants with issues with weight gain. Despite a lack of statistically evident difference in safety between thickened formulas and regular formulas among the sparse cohort of studies, significant potential safety concerns were raised. Depending on the thickening agent used, the safety concerns included decreased nutrient absorption, increased coughing, increased diarrhea, altered intestinal mucosal response, and allergic reactions.66
A 2014 Cochrane review of pharmacologic agents shed light on the lack of evidence for certain common practices.61 The review indicated that there were insufficient data comparing proton pump inhibitors (PPIs) and antihistamines. Thus, one class was not found to be more beneficial than another, and there is no evidence for using both agents at the same time. In general, PPIs were shown to have moderate evidence for clear benefit in older children with GERD, but there was weaker evidence for benefit in infants younger than 1 year of age. No distinct evidence has been found for proven benefit of PPI use in GER. One potential physiological reason for the decreased efficacy in younger children could be that the parietal cells are less prone to respond to the medication within the first 20 months of life.61 There is no current evidence indicating that omeprazole is more efficacious than any other PPI. However, pantoprazole was associated with a higher incidence of side effects compared to both omeprazole and lansoprazole. No randomized, controlled trials evaluated the use of ranitidine in GER.
Likewise, with regard to prokinetic agents like erythromycin, no randomized, controlled trials were performed for either GER or GERD. In addition, there is no evidence to support empiric domperidone use in infants. The clearest benefit for GER was from alginate agents that impede reflux by increasing the viscosity of gastric fluid.61 Occasionally, a surgical procedure is chosen to ameliorate GERD. The principal strategy used is a Nissen fundoplication. This procedure attempts to reduce factors associated with GERD, such as hiatal hernias and other anatomic considerations. However, if dysmotility is present, then retching will persist despite this procedure.61
Case 7
A 10-month-old presents to the emergency department with three days of nonbilious vomiting, followed most recently by profuse amounts of watery diarrhea. On physical exam, the patient is noted to be approximately 10% dehydrated. What is the diagnosis and what is most appropriate management?
Diagnosis. Acute gastroenteritis (AGE), as defined by the American Academy of Pediatrics, is the rapid onset of diarrheal illness with or without fever, vomiting, nausea, or abdominal pain.67 Diarrhea itself is defined by passing at least three formless, watery stools in a 24-hour time frame.68 Although mortality from AGE has decreased in the developed world, significant morbidity and public health concerns remain with this illness.18 The classic symptoms of vomiting and diarrhea quickly can lead to significant dehydration if not managed properly. There are many different infectious causes of AGE, including viruses, bacteria, and parasites. Considering that the majority of cases are viral and self-limiting, microbial workup should be restricted only to those patients who have persistent, unimproved diarrhea past the typical seven days’ duration or in select cases of recent travel.18,67,69 A hunt for an infectious agent also should be done for patients with severe illness portending sepsis or an immunocompromised state. Likewise, laboratory investigation should be performed if there is bloody diarrhea or significant mucus in the stools.18
Management. Antidiarrheal agents are not indicated, and antibiotics are warranted only in certain circumstances. The cornerstone of management rests principally on rehydration therapy. In general, oral rehydration is preferred over IV rehydration in cases of mild to moderate dehydration. Oral rehydration therapy (ORT) is comprised of two phases of treatment. The first phase is rehydration (over 3-4 hours) with an oral rehydration solution (ORS).70 The second phase is maintenance, which involves replacement of persistent fluid and electrolyte losses after the patient has returned to a normal volume status.69
Historically, physicians in developed countries have been reluctant to use the standard World Health Organization (WHO) oral rehydration solution for fear that it may cause hypernatremia. The formulation’s sodium concentration of 90 mmol/L represented the balanced needs of a diverse population, including those affected by cholera (known to have high sodium stool losses) and noncholera diarrhea. Thus, in the past, physicians instead have recommended various nonphysiologic “clear liquids,” which are detrimental, causing osmotic diarrhea and electrolyte abnormalities.69,71 Based on further evidence, the new standard WHO-ORS recommended in infants and children with noncholera diarrhea has a lower sodium concentration (75 mEq/L), lower glucose concentration (75 mmol/L), and lower osmolarity (245 mOsm/L) compared to the original solution developed.72
ORT is effective because it facilitates rehydration by using native gut physiology without compromising the need for an invasive measure. Because of co-transporters in the bowel, glucose in the solution promotes sodium and water absorption from the gut lumen into the bloodstream. Potentiated cotransport of electrolytes and water due to the presence of various organic molecules occurs even in cases of infectious diarrhea, despite the known morphologic changes that occur in the gut as a result of the illness.69,73-79 Evidence for this conclusion revolves around the fact that although diarrhea has been shown to have a negative effect on intestinal absorption, fasting does not appear to help and, in fact, is harmful in its own right.77,78 Conversely, although stool output may worsen with feeding, enteral nutrition is known to promote intestinal cell replenishment.69
There is evidence that the introduction of full-strength lactose-free formula after rehydration can decrease stooling and provide a better nutritional result.69 Most patients with AGE do not require a lactose-free formula unless they are malnourished or in cases of marked enteropathy.70 For breastfeeding infants, this method of nutrition should continue during and after the rehydration phase.70 Even in cases of intractable vomiting, more than 90% of patients can be treated successfully with ORS as long as it is provided in small volumes (5-10 mL) by syringe or spoon every 1-2 minutes, with a gradual increase as tolerated.69
Another particularly useful alternative if a patient will not tolerate drinking is to place a nasogastric tube to provide rehydration therapy.18,70 In fact, there is evidence to show that nasogastric administration of ORS is associated with better rehydration as defined by a quicker renormalization of the urinary specific gravity and greater clearance of ketonuria compared to IV rehydration.80
For minimally dehydrated patients for whom output is not measured easily, a typical ORS dosage is 10 mL/kg for every watery stool and 2 mL/kg for every episode of vomiting.70 For patients who have mild to moderate dehydration, 50-100 mL/kg of ORS should be given over a 2-4 hour period for fluid deficit, and additional ORS should be given for any ongoing losses.70 It should be noted that a 2013 article found no proven differences regarding duration of hospital stay between pediatric patients with mild to moderate dehydration receiving either ORT or IV rehydration therapy.68 Patients with severe dehydration generally were excluded from the studies reviewed. Additionally, there are no proven differences between ORT and IV rehydration therapy in the development of hyponatremia or hypernatremia. Since ORT it is less costly and less invasive, the current recommendation is to give ORT in cases of mild to moderate AGE, thus eliminating the chance of iatrogenic phlebitis.68,76 A 2006 Cochrane review noted that for every 25 pediatric patients receiving ORT, one would fail therapy and subsequently require IV rehydration therapy.73
There are a few clinical scenarios in which ORT is not recommended.69,73 ORT is associated with a higher incidence of paralytic ileus compared to IV rehydration therapy; thus, if there are inaudible bowel sounds prior to the initiation of ORT, then initial rehydration with IV therapy should be reconsidered.68,69 Additionally, ORT is absorbed less if there is glucose malabsorption, causing a decreased ability to correct the dehydration. In fact, the diarrhea may worsen and a diagnosis of glucose malabsorption will be made once the diarrhea improves with parenteral therapy.69 It should be noted that carbohydrate malabsorption is rare, as it presents in less than 1% of infants with acute diarrhea.70
ORT, in particular, also is contraindicated in cases of shock and severe dehydration, in which IV therapy is preferred.69 In cases of severe dehydration, IV therapy of lactated Ringer’s solution or normal saline should be provided in increments of 20 mL/kg until deficits in perfusion and mental status are resolved. It generally is safe to start IV rehydration prior to the return of basic metabolic panel results, as either of these solutions is appropriate for resuscitation in hyponatremic or hypernatremic dehydration.70 Severe dehydration is an indication for inpatient admission.70
Antiemetics are a potentially beneficial adjunct to ORT, as they have been linked to improved cessation of vomiting and, thus, improved oral toleration.81 A 2011 Cochrane review evaluated the efficacy of different antiemetics and their effect on public healthcare in children with AGE. Oral ondansetron, in particular, had a favorable side effect profile. Additionally, it was associated with decreased IV rehydration rates and a reduced chance of initial hospital admission from the emergency department in cases of mild or moderate dehydration. However, the medication was not seen to decrease readmission or re-visit rates 72 hours after discharge from the initial emergency department visit.81 IV ondansetron was found to reduce vomiting and hospital admission rates well. As such, a single dose of oral ondansetron was recommend as an adjunctive therapy to ORT in cases of mild to moderate dehydration secondary to AGE.81 Granisetron, a longer-acting serotonin receptor antagonist, was evaluated for any benefit in altering the course of illness after discharge from the emergency department. However, in this single study, the therapy was not found to be effective at controlling vomiting post-discharge.82
Children should not return to daycare until 48 hours after the last episode of diarrhea or vomiting. In addition, children should not swim in a public setting within two weeks of the last episode of diarrhea.18
Conclusion
Vomiting in the infant is a multidisciplinary concern that likely will be encountered sometime during practice. From an acute care perspective, the key is to differentiate between surgical causes and medical causes, as this differentiation affects patient care and disposition. It is crucial to interrogate for red flags in the history and physical exam so as to not miss a devastating disease process. Once red flags are either elicited or ruled out through a systematic thought process using the patient’s age and risk factors, a robust differential diagnosis can be formulated and appropriate and timely interventions instituted.
The author would like to thank Aaron Leetch, MD, Assistant Professor of Emergency Medicine & Pediatrics; Residency Director, Combined Emergency Medicine & Pediatrics Residency, University of Arizona College of Medicine, Tucson, for his valuable guidance and help with editing and reviewing this article.
REFERENCES
- Flanagan CF, Stewart M. Factors associated with early neonatal attendance to a paediatric emergency department. Arch Dis Child 2014;99:239-243.
- Quigley EM, Hasler WL, Parkman HP. AGA technical review on nausea and vomiting. Gastroenterology 2001;120:263-286.
- Parashette KR, Croffie J. Vomiting. Pediatr Rev 2013;34:307-319; quiz 320-321.
- Pitre DG, Acker A. Accuracy of parents and health care professionals at estimating infant emesis volume. Paediatr Child Health 2013;18:21-24.
- Paul SP, Whinney J, Fernando AM. Red flag causes of vomiting in infants. J Fam Health Care 2014;24:19-23.
- Ratnayake K, Kim TY. Evidence-based management of neonatal vomiting in the emergency department. Pediatr Emerg Med Pract 2014;11:1-20; quiz 20.
- Fuchs S, Jaffe D. Vomiting. Pediatr Emerg Care 1990;6:164-170.
- Waseem M, Rosenberg HK. Intussusception. Pediatr Emerg Care 2008;24:793-800.
- Talbert JL, Felman AH, DeBusk FL. Gastrointestinal surgical emergencies in the newborn infant. J Pediatr 1970;76:783-797.
- Pong A, Bradley JS. Bacterial meningitis and the newborn infant. Infect Dis Clin North Am 1999;13:711-733.
- Swanson D. Meningitis. Pediatr Rev 2015;36:514-524; quiz 525-526.
- Jackson EC. Urinary tract infections in children: Knowledge updates and a salute to the future. Pediatr Rev 2015;36:153-166.
- Green M. Green and Richmond Pediatric Diagnosis: Interpretation of Symptoms and Signs in Different Age Periods. Philadelphia: WB Saunders; 1986.
- Whinney J, Paul SP, Candy DCA. Clinical update: Vomiting in infants. Community Pract 2013;86:44-47.
- Lanphear J, Sarnaik S. Presenting symptoms of pediatric brain tumors diagnosed in the emergency department. Pediatr Emerg Care 2014;30:77-80.
- Larsen GY, Goldstein B. Increased intracranial pressure. Pediatr Rev 1999;20:234-239.
- Teo W-Y, Myseros JS. The gut or the brain? Gastrointestinal misdiagnoses of infantile brain tumors. Childs Nerv Syst 2014;30:1449-1453.
- Khanna R, Lakhanpaul M, Burman-Roy S, Murphy MS, Guideline Development Group and the technical team. Diarrhoea and vomiting caused by gastroenteritis in children under 5 years: Summary of NICE guidance. BMJ 2009;338:b1350.
- Hostetler MA, Schulman M. Necrotizing enterocolitis presenting in the emergency department: Case report and review of differential considerations for vomiting in the neonate. J Emerg Med 2001;21:165-170.
- Burge DM. The management of bilious vomiting in the neonate. Early Hum Dev 2016;102:41-45.
- Glatstein M, Carbell G, Boddu SK, et al. The changing clinical presentation of hypertrophic pyloric stenosis: The experience of a large, tertiary care pediatric hospital. Clin Pediatr 2011;50:192-195.
- White MC, Langer JC, Don S, DeBaun MR. Sensitivity and cost minimization analysis of radiology versus olive palpation for the diagnosis of hypertrophic pyloric stenosis. J Pediatr Surg 1998;33:913-917.
- Taylor ND, Cass DT, Holland AJA. Infantile hypertrophic pyloric stenosis: Has anything changed? J Paediatr Child Health 2012;49:33-37.
- Chattha AS, Delong GR. Sylvian aqueduct syndrome as a sign of acute obstructive hydrocephalus in children. J Neurol Neurosurg Psychiatry 1975;38:288-296.
- Malhotra A, Lakkundi A, Carse E. Bilious vomiting in the newborn: 6 years data from a Level III Centre. J Paediatr Child Health 2010;46:259-261.
- Neu J, Weiss MD. Necrotizing enterocolitis: Pathophysiology and prevention. JPEN J Parenter Enteral Nutr 1999;23(5 Suppl):S13-S17.
- Gilfillan M, Bhandari V. Biomarkers for the diagnosis of neonatal sepsis and necrotizing enterocolitis: Clinical practice guidelines. Early Hum Dev 2017;105:25-33.
- Shah D, Sinn JKH. Antibiotic regimens for the empirical treatment of newborn infants with necrotising enterocolitis. Cochrane Database Syst Rev 2012;(8):CD007448.
- Faix RG, Polley TZ, Grasela TH. A randomized, controlled trial of parenteral clindamycin in neonatal necrotizing enterocolitis. J Pediatr 1988;112:271-277.
- Rao SC, Basani L, Simmer K, et al. Peritoneal drainage versus laparotomy as initial surgical treatment for perforated necrotizing enterocolitis or spontaneous intestinal perforation in preterm low birth weight infants. Cochrane Database Syst Rev 2011;(6):CD006182.
- Bell MJ, Ternberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis. Ann Surg 1978;187:1-7.
- Brennan DF. Bilious vomiting in a 9-month-old Infant. Acad Emerg Med 1997;4:706-710.
- Svenningsson A, Svensson T, Akre O, Nordenskjöld A. Maternal and pregnancy characteristics and risk of infantile hypertrophic pyloric stenosis. J Pediatr Surg 2014;49:1226-1231.
- Honein MA, Paulozzi LJ, Himelright IM, et al. Infantile hypertrophic pyloric stenosis after pertussis prophylaxis with erythromycin: A case review and cohort study. Lancet 1999;354:2101-2105.
- Wayne C, Hung J-HC, Chan E, et al. Formula-feeding and hypertrophic pyloric stenosis: Is there an association? A case–control study. J Pediatr Surg 2016;51:779-782.
- Peters B, Oomen MWN, Bakx R, Benninga MA. Advances in infantile hypertrophic pyloric stenosis. Expert Rev Gastroenterol Hepatol 2014;8:533-541.
- Eberly MD, Eide MB, Thompson JL, Nylund CM. Azithromycin in early infancy and pyloric stenosis. Pediatrics 2015;135:483-488.
- Rohrschneider WK, Mittnacht H, Darge K, Tröger J. Pyloric muscle in asymptomatic infants: Sonographic evaluation and discrimination from idiopathic hypertrophic pyloric stenosis. Pediatr Radiol 1998;28:429-434.
- Schnaufer L MS. Abdominal Emergencies. In: Fleisher G LS, ed. Textbook of Pediatric Emergency Medicine. Philadelphia: Williams and Wilkins; 1988:936-965.
- Stringer MD, Pablot SM, Brereton RJ. Paediatric intussusception. Br J Surg 1992;79:867-876.
- Huang H-Y, Huang X-Z, Han Y-J, et al. Risk factors associated with intestinal necrosis in children with failed non-surgical reduction for intussusception. Pediatr Surg Int 2017;33:575-580.
- Mitra SK, Rao PLNG, Bhattacharyya NC, Pathak IC. Rupture of intussuscipiens. J Pediatr Surg 1982;17:300-301.
- Newman J, Schuh S. Intussusception in babies under 4 months of age. CMAJ 1987;136:266-269.
- Singer J. Altered consciousness as an early manifestation of intussusception. Pediatrics 1979;64:93-95.
- Hess JH. Intussusception in infancy and childhood, with collection of 1,028 cases, with statistics. Arch Pediatr 1905;22(655).
- Wang G, Liu XG, Zitsman JL. Nonfluoroscopic reduction of intussusception by air enema. World J Surg 1995;19:435-438.
- Nelson MJ, Paterson T, Raio C. Case report: Transient small bowel intussusception presenting as right lower quadrant pain in a 6-year-old male. Crit Ultrasound J 2014;6:7.
- Bhisitkul DM, Listernick R, Shkolnik A, et al. Clinical application of ultrasonography in the diagnosis of intussusception. J Pediatr 1992;121:182-186.
- Hernandez JA, Swischuk LE, Angel CA. Validity of plain films in intussusception. Emerg Radiol 2004;10:323-326.
- Beres AL, Baird R. An institutional analysis and systematic review with meta-analysis of pneumatic versus hydrostatic reduction for pediatric intussusception. Surgery 2013;154:328-334.
- Stewart DR, Colodny AL, Daggett WC. Malrotation of the bowel in infants and children: A 15 year review. Surgery 1976;79:716-720.
- Andrassy RJ, Mahour GH. Malrotation of the midgut in infants and children: A 25-year review. Arch Surg 1981;116:158-160.
- Esposito F, Vitale V, Noviello D, et al. Ultrasonographic diagnosis of midgut volvulus with malrotation in children. J Pediatr Gastroenterol Nutr 2014;59:786-788.
- Raffensperger JG. Anomalies of the gastrointestinal tract. In: Raffensperger JG, ed. Swenson’s Pediatric Surgery. Norwalk: Appleton and Lange; 1990:501-522.
- Powell DM, Othersen HB, Smith CD. Malrotation of the intestines in children: The effect of age on presentation and therapy. J Pediatr Surg 1989;24:777-780.
- Lampl B, Levin TL, Berdon WE, Cowles RA. Malrotation and midgut volvulus: A historical review and current controversies in diagnosis and management. Pediatr Radiol 2009;39:359-366.
- Millar AJW, Rode H, Cywes S. Malrotation and volvulus in infancy and childhood. Semin Pediatr Surg 2003;12:229-236.
- Stanfill AB, Pearl RH, Kalvakuri K, et al. Laparoscopic Ladd’s procedure: Treatment of choice for midgut malrotation in infants and children. J Laparoendosc Adv Surg Tech A 2010;20:369-372.
- Rice GM, Steiner RD. Inborn errors of metabolism (metabolic disorders). Pediatr Rev 2016;37:3-15; quiz 16-17, 47.
- Maclennan AC. Investigation in vomiting children. Semin Pediatr Surg 2003;12:220-228.
- Tighe M, Afzal NA, Bevan A, et al. Pharmacological treatment of children with gastro-oesophageal reflux. Cochrane Database Syst Rev 2014;(11):CD008550.
- Nelson SP, Chen EH, Syniar GM, Christoffel KK. Prevalence of symptoms of gastroesophageal reflux during infancy. A pediatric practice-based survey. Pediatric Practice Research Group. Arch Pediatr Adolesc Med 1997;151:569-572.
- Sullivan JS, Sundaram SS. Gastroesophageal reflux. Pediatr Rev 2012;33:243-253; quiz 254.
- Kent JC, Mitoulas LR, Cregan MD, et al. Volume and frequency of breastfeedings and fat content of breast milk throughout the day. Pediatrics 2006;117:e387-e395.
- Heinig MJ, Follett JR, Ishii KD, et al. Barriers to compliance with infant-feeding recommendations among low-income women. J Hum Lact 2006;22:27-38.
- Horvath A, Dziechciarz P, Szajewska H. The effect of thickened-feed interventions on gastroesophageal reflux in infants: Systematic review and meta-analysis of randomized, controlled trials. Pediatrics 2008;122:e1268-e1277.
- Practice parameter: The management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996;97:424-435.
- Freedman SB, Ali S, Oleszczuk M, et al. Treatment of acute gastroenteritis in children: An overview of systematic reviews of interventions commonly used in developed countries. Evid Based Child Health 2013;8:1123-1137.
- Duggan C, Santosham M, Glass RI. The management of acute diarrhea in children: Oral rehydration, maintenance, and nutritional therapy. Centers for Disease Control and Prevention. MMWR Recomm Rep 1992;41(RR-16):1-20.
- King CK, Glass R, Bresee JS, Duggan C, Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: Oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003;52(RR-16):1-16.
- Snyder JD. Use and misuse of oral therapy for diarrhea: Comparison of US practices with American Academy of Pediatrics recommendations. Pediatrics 1991;87:28-33.
- World Health Organization. WHO Drug Information 2002;16:121-122.
- Hartling L, Bellemare S, Wiebe N, et al. Oral versus intravenous rehydration for treating dehydration due to gastroenteritis in children. Cochrane Database Syst Rev 2006;(3):CD004390.
- Schultz SG, Zalusky R. Ion transport in isolated rabbit ileum. II. The interaction between active sodium and active sugar transport. J Gen Physiol 1964;47:1043-1059.
- Fisher RB. The absorption of water and of some small solute molecules from the isolated small intestine of the rat. J Physiol 1955;130:655-664.
- Listernick R. Outpatient oral rehydration in the United States. Arch Pediatr Adolesc Med 1986;140:211.
- Hirschhorn N. The treatment of acute diarrhea in children. An historical and physiological perspective. Am J Clin Nutr 1980;33:637-663.
- Kent TH, Lindenbaum J. Correlation of jejunal function and morphology in patients with acute and chronic diarrhea in East Pakistan. Gastroenterology 1967;52:972-984.
- Schultz SG. Sodium-coupled solute transport of small intestine: A status report. Am J Physiol 1977;233:E249-E254.
- Nager AL, Wang VJ. Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration. Pediatrics 2002;109:566-572.
- Fedorowicz Z, Jagannath VA, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database System Rev 2011;(9):CD005506.
- Qazi K, BinSalleeh HM, Shah UH, et al. Effectiveness of granisetron in controlling pediatric gastroenteritis-related vomiting after discharge from the ED. Am J Emerg Med 2014;32:1046-1050.
Every viral season, something gets missed. All vomiting is not acute gastroenteritis! The clinician needs to have a thorough understanding of the process of vomiting to formulate a complete differential accurately and in a timely manner. A complete history, physical exam, and targeted diagnostic testing are used to ensure an accurate diagnosis with effective management is instituted.
Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.