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Author: Deborah Mulligan-Smith, MD, FAAP, FACEP, Director, Institute for Child Health Policy; Associate Professor of Pediatrics, Nova Southeastern University, Fort Lauderdale, FL; Attending Physician, Joe DiMaggio Children’s Hospital, Hollywood, FL.
Peer Reviewer: Ronald M. Perkin, MD, MA, FAAP, FCCM, Professor and Chairman, Department of Pediatrics, The Brody School of Medicine, East Carolina University, Greenville, NC.
Emergency department (ED) physicians often are confronted with a problem (i.e., vomiting, diarrhea, rash), not a diagnosis. The challenge to the ED physician is to develop a rational approach to the problem based on the child’s history and physical examination.
Based on the clinical information, the ED physician must formulate a cost effective diagnostic evaluation. Fortunately, the majority of children who present with vomiting will have a benign disease and clinical course. Identifying the child with an atypical history, risk factors that point to a serious disease (i.e., significant weight loss), or suspicious findings on physical examination (i.e., split sutures, murmur, etc.) are critical for the patient and rewarding to the physician. This issue provides an opportunity for ED physicians to expand their differential diagnosis and enhance their diagnostic skills for the child who presents with vomiting.
— The Editor
Nausea is a prodrome of vomiting. It is the conscious recognition of subconscious excitation in an area of the medulla that is linked to the vomiting center. Stimuli may originate from irritative impulses from the gastrointestinal tract, a portion of the brain associated with motion sickness, or from the cortex to initiate vomiting. A common cause of nausea is distention or irritation of the duodenum or lower small intestine. As a preliminary step to vomiting, the intestine contracts forcefully while the stomach relaxes. Intestinal contents reflux into the stomach. Nausea is not always experienced prior to the act of vomiting.
Vomiting is the means by which the upper gastrointestinal tract rids itself of its contents when the gut becomes excessively irritated, over-distended, or even over-excited. Distention or irritation of the stomach or duodenum provides a strong stimulus resulting in the act of vomiting. The "vomiting center" for both vagal and sympathetic afferents lies in the medulla at the level of the dorsal motor nucleus of the vagus. Motor reactions initiated to cause the vomiting act are transmitted from the vomiting center through the fifth, seventh, ninth, 10th, and 12th cranial nerves to the upper gastrointestinal tract and through the spinal nerves to the diaphragm and abdominal muscles. Once there is sufficient stimulus, the subsequent sequence of events is: a deep breath, raising of the hyoid bone and the larynx to pull the cricoesophageal sphincter open, closing of the glottis and lifting of the soft palate to close the posterior nares, and a strong downward contraction of the diaphragm with simultaneous contraction of all the abdominal muscles. This force squeezes the stomach between the abdominal muscles, building intragastric pressure. At the same time, reverse peristalsis begins in the antral region of the stomach and passes over the body of the stomach, forcing the contents toward the esophagus. The pathway ends with gastroesophageal sphincter relaxation, allowing for expulsion of the gastric contents through the esophagus.
Apart from direct stimuli of the gastrointestinal tract, vomiting may be caused by impulses arising in areas of the brain outside the vomiting center. The chemoreceptor trigger zone is located bilaterally on the floor of the fourth ventricle. Electrical stimulation and some pharmaceutical agents can stimulate the chemoreceptor trigger zone directly.
Many people experience the sensation of nausea or the act of vomiting as a result of rapid change in motion. Motion stimulates the receptors of the labyrinth, and impulses are transmitted via the vestibular nuclei into the cerebellum. Passing through the uvula and nodule of the cerebellum, signals are transmitted to the chemoreceptor trigger zone and then to the vomiting center.1,2
True vomiting can be characterized by the sequence of nausea, retching, and emesis, and can be categorized as bilious or nonbilious. Bilious vomiting occurs when bile is purged along with the gastric contents. In nonbilious vomiting, antegrade intestinal flow is preserved, and the majority of the bile drains into the distal portions of the intestine. Conditions leading to bilious vomiting involve either a disorder of motility or physical blockage. Obstruction of the gastrointestinal tract can occur at almost any point along its course. Abnormal consequences of obstruction depend on the site of the gastrointestinal tract affected. Table 1 lists the causes of bilious vs. nonbilious vomiting.
|Table 1. Bilious vs. Nonbilious Causes of Vomiting|
|Distal obstructive lesion
• Compressing or obstructing mass lesion
• Ileus from any cause
• Incarcerated inguinal hernia
• Intestinal atresia and stenosis
• Intestinal duplication
• Malrotation with or without volvulus
• Peritoneal adhesions
• Superior mesenteric artery syndrome
|• General considerations
• Infectious disease
• Inflammation and irritation
• Metabolic/endocrine abnormalities
• Neurologic disorder
• Obstructive lesion
• Psychological disorder
Vomiting is a common symptom in childhood. Vomiting may be the chief complaint, or it may be a symptom associated with a multitude of diagnostic entities.3,4 (See Table 2.) In most cases it is merely a manifestation of a benign, self-limited illness. Chronic vomiting always should be considered abnormal. In general, the most important aspect of caring for the child is to exclude a surgical emergency.
Though often self-limited, the act of vomiting is anxiety-provoking for the parent who seeks medical attention for a child. Vomiting is a prominent feature of many disorders of infancy and childhood. The act of vomiting may be a defense mechanism to expel ingested toxins, an abnormality of the vomiting center related to increased intracranial pressure, a result of intestinal obstruction or anatomic/mucosal abnormalities, or the result of generalized metabolic disease. Regurgitation is the passive movement of gastric contents into the esophagus and out through the mouth. It is important to ascertain that the symptom complaint is true vomiting and not regurgitation. Spitting or regurgitation in the small infant usually is caused by gastroesophageal reflux, a self-limited problem that typically resolves around age 1. In the healthy, thriving child there is no need for a complex evaluation. Vomiting may be a sign of formula protein intolerance or allergy, especially in association with irritability, loose stools, or blood in the stool. Nearly 7% of infants suffer from cow milk protein intolerance; of these infants, approximately 20% are sensitive to soy protein as well.3,5 However, the child who has other symptoms or fails to thrive should receive an extensive evaluation. Infectious, endocrine, neurologic, and urinary disorders, as well as inborn errors of metabolism should be considered in the evaluation of an infant who fails to thrive. Inborn errors of metabolism generally present in early infancy, and the vomiting is associated with symptoms of lethargy, hypo- or hypertonia, seizures, and/or coma. As the same symptom complex may be associated with sepsis, it is important to maintain a high index of suspicion in the patient evaluation process. Forceful vomiting indicates a potential anatomic disorder such as pyloric stenosis. Hematemesis implies the likelihood of a proximal gastrointestinal inflammatory process. A syndrome of cyclic vomiting in children may be precipitated by psychological disorders. Acute onset of vomiting suggests infectious enteritis, ingestion, or neurologic disorder. The rapid onset differentiates these disorders from those associated with chronic or recurrent vomiting. Clues discovered while taking the patient’s history and performing a physical examination should narrow the diagnostic impression.6-8
Characteristics surrounding the act of vomiting become important clues to diagnosis. The history distinguishes true vomiting from regurgitation. For example, post-tussive emesis is common in conditions such as pneumonia or reactive airway disease. Post-prandial emesis may indicate a bowel obstruction or acute gastroenteritis. The presence of bile in the emesis is never normal. Upon completion of the history (See Table 3)9 and physical examination (See Table 4), the patient’s hydration status should be assessed and treated accordingly.
|Table 3. Evaluating the Child with Vomiting: Important Physical Exam Considerations|
|Abnormal pelvic exam
Auscultation for bowel signs
Discoloration of skin and sclera
Enlarged parotid glands and hypersalivation
Neurologic dysfunction (nystagmus, head tilt, weakness)
Palpation for a mass effect and tenderness
Tense anterior fontanelle
Visible bowel loops
|Table 4. Evaluating the Child with Vomiting: Important Historical Considerations|
Psychological or behavioral disorders
|Contacts (i.e., day care, home, school)
Pets, wildlife, insects
|Characteristics of vomiting|
Progression (increase or decrease in frequency, associated triggers)
Alleviated by meals
Alternating vomiting and lethargy
|Associated symptoms (acute, subacute, or chronic)|
Abdominal pain and frequent, forceful, or bilious emesis
Chronic headaches, fatigue, weakness, weight loss, or early morning vomiting
Nausea and epigastric pain related to meals
Right- or left-sided abdominal pain
The physical examination of the patient with vomiting is similar to that of the patient with abdominal pain.10 Non-gastrointestinal causes of vomiting are excluded, with particular attention paid to the central nervous system. An enlarged or full anterior fontanelle, lethargy, or splitting of the sutures indicates increased intracranial pressure in the infant.11,12 Associated physical findings, such as discoloration of skin and sclera, may provide clues to diagnosis of hepatotoxins or metabolic disorders. Assess the abdomen for presence and character of bowel sounds, tenderness, guarding, or rebound. Differential considerations vary according to age. For example, sexually transmitted diseases or pregnancy must be considered when evaluating the adolescent female. A thorough pelvic examination and testing also are indicated.
The laboratory evaluation depends upon the clinical presentation, and may include determination of the complete blood count (CBC), serum electrolytes, appropriate liver enzymes, blood ammonia level, metabolic studies, urinalysis, or other test suggested by the clinical presentation. Anemia and iron deficiency can occur with intestinal duplication and obstruction, gastritis or esophagitis, and ulcer disease. Electrolyte abnormalities are found in pyloric stenosis and metabolic abnormalities, while an elevated alanine aminotransferase, total bilirubin, and glutamyl transpeptidase can indicate liver, gallbladder, or metabolic disease. In the vast majority of pediatric patients with vomiting, radiographs are not helpful. Abdominal ultrasound is the test of choice for pyloric stenosis. It also is useful when considering abdominal abscess; appendicitis; pyloric stenosis; or liver, gallbladder, renal, pancreatic, ovarian, or uterine disease. Contrast radiography is useful for the evaluation and diagnosis of intestinal anatomic abnormalities such as malrotation, intussusception, or volvulus. Not generally indicated for evaluation of vomiting, computed tomography (CT) is an effective tool when anatomic abdominal detail is required (i.e., for appendicitis or appendiceal abscess).13-15
Treatment is disease-specific. Associated signs and symptoms that should lead to a pediatric subspecialist referral include weight loss, severe abdominal pain or irritability, gastrointestinal bleeding, evidence of intestinal obstruction, serum electrolyte abnormalities, an abnormal neurologic examination, dehydration, signs of an acute abdomen, or lethargy.16-21
In conclusion, because a wide variety of stimuli may produce vomiting, there are many diagnoses to consider. Differential considerations vary by age, and the spectrum of etiologies are more prevalent in specific age groups. (See Table 5.)
A 4-week-old female arrives in the emergency department (ED) with a one-day history of lethargy and vomiting. The mother reports no prenatal care but that the baby was delivered vaginally without complication. The baby and mother were discharged from the hospital two days after delivery. The baby is breastfed and has no difficulty nursing. The baby’s frequent vomiting is what brings her to the ED. Mother states the last few episodes of vomiting were green in color.
Examination. The baby is lethargic, pale, and grunting.
Vital signs are: Pulse = 190/minute, respiration rate (RR) = 60/minute, blood pressure (BP) = 90/60 mmHg, rectal temperature = 36°C.
Breath sounds are clear. Extremities are mottled. Skin turgor is poor. There are decreased bowel sounds and the distended abdomen is firm to palpation.
What is the most likely diagnosis is this case: pyloric stenosis, malrotation, duodenal atresia, sepsis, or inguinal hernia?
Discussion. The history, physical examination and a cross-reference of Tables 1 and 5 support anatomic obstruction as the presumed cause of bilious vomiting in the neonate. The first step is application of supplemental oxygen and correction of the hypovolemia in this child. Although anatomic obstruction is the major concern, this child also should receive metabolic and septic evaluations.
Malrotation results from failure of normal rotation of the midgut leading to abnormal fixation of the mesentery. The majority of patients present in the neonatal period with bilious vomiting, abdominal distension, and pain. Older patients may present with a history of feeding problems and formula intolerance with vomiting or with poor growth. Abdominal radiograph findings are variable. An upper gastrointestinal study is the study of choice to make the diagnosis. The duodenal loop may appear dilated with obstruction at the third portion, or there may be narrowing of the small bowel at the site of the obstruction and spiraling of the small bowel about the mesenteric artery. In cases of malrotation and midgut volvulus, the normal mesenteric attachments are replaced by fibrous bands called Ladd bands; surgical repair involves release of the Ladd bands (Ladd procedure) and resection of necrotic bowel as needed. Surgery should not be delayed to prevent further necrosis of the bowel.
The correct diagnosis in this case is malrotation.
A 6-year-old boy fell 5 feet from the top of a playground slide. He rode his bike home and complained to his mother of a bad headache. Within an hour he vomited twice. The mother became concerned and brought him to the ED for evaluation.
Physical Exam.The boy is agitated and cannot be calmed by his mother. Vital Signs: heart rate (HR) = 110/minute; RR = 22/minute; BP = 98/70 mmHg; oral temperature = 38°C; weight = 22 kg.
The child exhibits spontaneous, unlabored respirations. His extremities are warm, with a capillary refill time of 2 seconds.
Is the management priority in this case radiologic imaging; early consultation and transfer; assessment for associated injuries; administration of dexamethasone; or stabilization of airway, breathing, and circulation?
The priority in this case is stabilization of the patient’s airway, breathing, and circulation.
Discussion. Agitation and uncooperativeness may be normal behavior in a frightened toddler; this is not appropriate for a school-age child. His cardiopulmonary status is normal. The combination of history and physical examination findings are consistent with closed head trauma. The management goal of head injury in children is to prevent secondary injury to the brain. Prevention of hypoxia, ischemia, and increased intracranial pressure is essential. Relative dehydration will decrease intracellular water and thus reduce intravascular pressure and fluid leakage from blood vessels in the brain. Therefore, supplemental oxygen by facemask and establishment of vascular access are appropriate initial interventions. This child is able to maintain his airway and is ventilating normally. Though the child walked into the ED, he remains at risk for associated injuries, including spinal cord injury. Prompt consultation with a neurosurgeon will determine the need for transport and focus neuroimaging studies. Osmolar therapy may provide some benefit in acutely decreasing intracranial pressure; however, it should not precede the aforementioned management priorities. Dexamethasone is not recommended acutely for the treatment of increased intracranial pressure.
A previously healthy 2-year-old girl has a history of upper respiratory infection for six days. Her primary care provider diagnosed an acute otitis media two days ago, for which he prescribed oral antibiotic therapy. The child is unable to take her medicine because of frequent vomiting. Dad brings his daughter back to the physician’s office complaining of persistent fever, increase in vomiting, and because she is not behaving normally.
Physical Exam. The child is listless. She moans when her body is moved. As her neck is flexed, she grimaces and brings her shoulders and knees involuntarily up off the stretcher, demonstrating nuchal rigidity. Petechiae are noted on her extremities.
Vital Signs: HR = 140/minute; RR = 40/minute; BP = 80/40 mmHg; oral temperature = 40° C; weight = 14 kg.
What is the most likely diagnosis in this case: encephalitis, Reye syndrome, meningitis, intussusception, or septic shock?
Most likely, the patient is suffering from meningitis.
Discussion. The early phases of meningitis may be confused with illnesses such as upper respiratory infection, otitis media, or simple gastroenteritis, confounding the practitioner. The younger the child, the fewer the signs and symptoms evident for the diagnosis of meningitis. The physical finding of nuchal rigidity in a febrile child suggests meningitis, but is not conclusive. The differential diagnosis for nuchal rigidity includes cervical spine trauma, myositis, retropharyngeal abscess, adenitis, pneumonia, and infection of congenital anomalies such as branchial cleft or thyroglossal duct cysts. While it is important to determine nuchal rigidity, this is difficult in infants and young children. It is reported that fewer than 15% of children younger than 18 months of age exhibit resistance to flexion of the neck. When meningitis is suspected, the diagnostic test of choice is the lumbar puncture. Common childhood bacterial pathogens include Haemophilus influenzae type b, Streptococcus pneumoniae, and Neisseria meningitidis. The availability of conjugated vaccines against H. influenzae has reduced dramatically the incidence of meningitis in childhood. In the near future, we may witness a similar reduction in cases with the widespread use of pneumococcal vaccine. Following the widespread use of H. influenzae type b vaccines, S. pneumoniae has become the most common cause of invasive bacterial infection in children in the United States. Pneumococci are the most common cause of bacteremia in young children ages 2-36 months who have fever without an identifiable source, accounting for more than 84% of recovered bacterial pathogens. Children younger than 12 months have the highest rates of pneumococcal infections. Among children younger than age 5, pneumococcal infections cause an estimated minimum of 1400 cases of meningitis, 17,000 cases of bacteremia, 71,000 cases of pneumonia, and 5 million to 7 million cases of otitis media annually. The new American Academy of Pediatrics guidelines state that the heptavalent pneumococcal conjugate vaccine (PCV7) is recommended for use in all children 23 months of age and younger. Although other pneumococcal vaccines are available, PCV7 represents the first pneumococcal vaccine approved for use in children younger than age 2. The policy recommends that PCV7 be given concurrently with other recommended childhood vaccines at 2, 4, 6, and 12-15 months. The number of PCV7 doses required depends upon the age at which vaccination is initiated. The vaccine also is recommended for all children 24-59 months of age who are at especially high risk of invasive pneumococcal infection. This includes children with sickle cell disease, human immunodeficiency virus (HIV) infection, and other children who are immunocompromised.
When the ED physician is confronted with a child with a chief complaint of vomiting, a broad differential should be considered. The history (acute vs chronic, weight loss, febrile vs afebrile) and physical examination (fontanelle, nuchal rigidity, abdominal examination) should guide the diagnostic evaluation. Early recognition and appropriate subspecialty referral for a child who has a disease that requires subspecialty expertise will improve the outcome for a child who presents with vomiting.
1. Boles RG, Williams JC. Mitochondrial disease and cyclic vomiting syndrome. Dig Dis Sci 1999;44:103S-107S.
2. Rashed H, Abell TL, Familoni BO, et al. Autonomic function in cyclic vomiting syndrome and classic migraine. Dig Dis Sci 1999;44:74S -78S.
3. Gremse DA, Sacks AI. Symptoms of gastritis due to Helicobacter pylori in children. South Med J 1996;89:278-281.
4. Keller VE. Management of nausea and vomiting in children. J Pediatr Nurs 1995;10:280-286.
5. Moir CR. Abdominal pain in infants and children. Mayo Clin Proc 1996;71:984-989.
6. Gudeta B. Intussusception in children: A ten-year review. East Afr Med J 1993;70:730-731.
7. Strange GR, Ahrens W, Lelyveld S, et al. Pediatric Emergency Medicine. New York: McGraw-Hill; 1996.
8. Ravelli AM, Milla PJ. Vomiting and gastroesophageal motor activity in children’s disorders of the central nervous system. J Pediatr Gastroenterol Nutr 1998;26:56-63.
9. Weinberger E, Winters WD. Abdominal pain and vomiting in infants and children: Imaging evaluation. Compr Ther 1997;23: 679-686.
10. Uhari M, Nuutinen M, Turtinen J. Adverse reactions in children during long-term antimicrobial therapy. Pediatr Infect Dis J 1996;15: 404-408.
11. Gherpelli JL, Nagae Poetscher LM, Souza AM, et al. Migraine in childhood and adolescence. A critical study of the diagnostic criteria and of the influence of age on clinical findings. Cephalalgia 1998;18:333-341.
12. Barkin RM. Pediatric Emergency Medicine Concepts and Clinical Practice 2nd ed. St. Louis, MO: Mosby-Year Book, Inc.;1997.
13. Lake AM. Gatrointestinal Manifestations of Allergic Bowel Disease in Infancy and Early Childhood. Focus Upon Food Allergy in Childhood. SHS International. August 1999.
14. Dutta P, Mitra U, Saha DR, et al. Mucoid presentation of acute entercolitis in children: Hospital-based case-control study. Acta Paediatr 1999;88:822-826.
15. Myers NA. Esophageal disorders associated with emesis in infants and children. Semin Pediatr Surg 1995;4:166-175.
16. Li BU, Murray RD, Hietlinger LA, et al. Heterogeneity of diagnoses presenting as cyclic vomiting. Pediatrics 1998;102:583-587.
17. Tsakayannis DE, Kozakewich HP, Lillehei CW. Acalculous cholecystitis in children. J Pediatri Surg 1996;31:127-130.
18. Allen ED, Byrd SE, Darling CF, et al. The clinical and radiological evaluation of primary brain neoplasms in children, Part I: Clinical evaluation. J Natl Med Assoc 1993;85:445-451.
19. Kocaman S, Ersahin Y, Mutluer S. Cerebral hydatid cysts in children. J Neurosci Nurs 1999;31:270-277.
20. Tunnessen WW. Signs and Symptoms in Pediatrics. 2nd ed. Philadelphia, PA: JB Lippincott Co; 1988.
21. Pfau BT, Li BU, Murray RD, et al. Differentiating cyclic from chronic vomiting patterns in children: Quantitative criteria and diagnostic implications. Pediatrics 1996;97:364-368.