Abdominal pain is a common complaint in pediatric population, often resulting in unscheduled office or emergency room visits. This symptom can be acute, recurrent, or chronic.

Acute abdominal pain generally refers to pain that has been present for <24 hours. When the presentation is acute, the challenge for the evaluating physician is to differentiate potentially life-threatening and serious medical conditions from benign self-limited ones. The frequency of surgical intervention in patients presenting with acute abdominal pain is around 1%,1 but the possibility of overlooking a serious organic etiology is a cause of concern to evaluating physicians and families.

Children are considered to have recurrent or chronic abdominal pain if they have experienced at least three bouts of abdominal pain, severe enough to affect activities, over a period of at least 3 months. Though this definition was initially used by Apley and Nash2 as the entry criteria for their descriptive study, it later became a term to describe all children with abdominal pain without known organic etiology. Recurrent abdominal pain (RAP) should be used as a description rather than as a diagnosis. RAP may occur in functional abdominal pain (FAP; see below), but this pattern of discomfort can also occur with organic disease.3Functional gastrointestinal disorders (FGID) include a combination of chronic and/or recurrent symptoms not explained by known biochemical or structural abnormalities. According to Rome III criteria, symptoms must occur at least once per week for at least 2 months before making a diagnosis of FGID.4 In a study of 227 patients with recurrent and chronic abdominal pain, only 76 (33%) were found to have well-defined organic etiologies.5

Abdominal pain accounts for 2–4% of all pediatric office visits.6 In a study by Hyams et al., 13% of middle-school students and 17% of high-school students experienced weekly abdominal pain. In that study, approximately 8% students saw their physician for abdominal pain evaluation in the previous year.7 In Apley and Nash original study involving 1000 children in primary and secondary schools, 10.8% of children had RAP, with a female preponderance (female to male ratio of 1.3:1).2 In that survey, the age distribution was also examined. Ten to 12% of males aged 5–10 years had RAP, followed by decline in prevalence and a later peak at age 14 years. Females showed a sharp rise in prevalence after age 8 years and by age 9 years 25% of this group experienced RAP. The long-term outcome of patients with FGID is not known, but studies indicate patients with history of chronic abdominal pain that began in childhood and treated by a subspecialist are more likely to have lifelong psychiatric problems and migraine headaches.3 Genetic factors and early life events may have a role in the pathogenesis of chronic abdominal pain.

Family History

There is a higher prevalence of alcoholism, psychiatric disorders, somatization disorders, migraine, and chronic pain symptoms among family members. Familial clustering is often seen in patients with FGID. Subjects with FGID, in a study by Locke et al., had an increased risk of reporting a first-degree relative with abdominal pain and/or bowel distrurbance.8 Possible explanations of familial clustering could include both environmental and/or genetic factors.

Early Life Events

Noxious stimuli experienced during the neonatal period, when nociceptive neuronal circuits are formed, may result in decreased pain thresholds later in life. Respiratory distress, neonatal infections, colic, neonatal surgeries, or congenital hydronephrosis is reported in approximately 20% patients with chronic abdominal pain.9

Pain originating in the gut is initiated by stimulation of receptors (nociceptors) sensitive to specific mechanical and chemical stimuli. Stretch and the contractile force are the principal mechanical stimuli. Other stimuli, even crushing, cutting, or tearing of the viscera, do not cause pain. Mechanical nociceptors are located in the muscularis layers, between the muscularis layer and submucosa of hollow viscera, in the serosa of solid organs, and in the mesentery. Various intra-abdominal processes cause pain by stimulating these mechanical nociceptors (Table 1–1). Chemical nociceptors are present within the mucosa and submucosa of the gut. Various triggers such as inflammation, tissue ischemia and necrosis, and radiation injury stimulate these receptors via injury-associated release of mediators, such as prostaglandins, leukotrienes, bradykinin, serotonin, substance P, calcitonin gene-related peptide, histamine, and H+ and K+ ions.10 These substances and mast cell proteases such as 5-HT3 receptors have the potential of elevating the sensitivity of intestinal sensory nerves. Postinfectious irritable bowel syndrome (IBS) develops in a significant percentage of individuals after an acute bout of infectious enteritis. It is unclear if this is the result of exposure of neural and glial elements of the enteric nervous system to the elevated levels of these inflammatory mediators.

Afferent nociceptive sensory neurons are either slow, unmyelinated C fibers or fast, myelinated A-δ fibers. The C fibers are located in visceral peritoneum, mesentery, and viscera. Signals transmitted by these fibers result in dull, poorly localized pain. Because pain fibers from abdominal organs communicate bilaterally with more than one adjacent spinal level, visceral pain is often felt in midline as a poorly localized sensation. The location of abdominal pain is determined by the developmental origin of the affected viscera (Table 1–2). A-δfibers are found in the somatic structure surrounding the viscera: the abdominal wall, retroperitoneal skeletal muscles, and parietal peritoneum. These fibers have small receptive fields and nociceptive signals through these fibers result in sharp, well-localized sensations.

Patterns of Pain

Understanding the types of pain fibers and their dis-tribution is important to understanding clinical phenomena. Visceral pain from most of the gut is poorly localized and difficult to characterize due to activation of unmyelinated C fibers reporting to several spinal levels at once. A good example of this is the pain associated with Crohn’s disease of the small intestine. Somatoparietal pain results from stimulation of the parietal peritoneum, and is more intense and somewhat better localized than visceral sensation. Somatic pain occurs when somatic structures, innervated by A-δ fibers, are injured or inflamed. In some cases, as in acute appendicitis, pain begins as poorly localized, dull periumbilical discomfort due to inflammation of the inner layers of the appendix, and then becomes progressively more severe and better localized with subsequent inflammation of first the parietal peritoneum and then the adjacent abdominal wall. Referred pain is felt in a body area that has its somatic innervation from the same spinal segments receiving visceral pain fibers from the diseased organ. It is usually well localized, as in left shoulder pain from myocardial infarction. Common patterns of referred pain in acute abdominal processes are shown in Figure 1–1.

Pain Perception

Afferent nerves mediating painful stimuli from abdominal viscera follow the distribution of the autonomic nervous system and have cell bodies in dorsal root ganglia. Although nociceptive fibers run together with the sympathetic fibers through sympathetic ganglia (celiac, superior mesenteric, and inferior mesenteric ganglia), they are not part of the sympathetic nervous system. The sympathetic nervous system does not convey pain, but may participate in the sensitization of peripheral nociceptors. The autonomic nervous system plays a role in pain modulation and the associated behavioral and emotional responses to pain. Secondary autonomic effects such as sweating, perspiration, and pallor often accompany visceral pain. The emotional aspects of pain are interpreted in the limbic system and frontal cortex through projection from the brain stem (reticular formation nucleus). Thus, it is important to conceptualize pain as a function of two phenomena: one providing the sensory information from afferent nociceptors and the other modulating the sensation and producing emotional, cognitive, physiological, and behavioral responses.

The functional connections between the brain and the spinal cord result in both inhibitory and excitatory modifications of afferent pain impulses. There are inhibitory mechanisms at the level of the spinal cord (inhibitory interneurons of substantia gelatinosa). Inhibitory neurons originating in mesencephalon, periventricular gray matter, and caudate nucleus participate in descending inhibition, and have dampening effect on pain.11 Pain can be defined as nociceptive when it results from stimulation of peripheral nociceptors by mechanical or chemical stimuli (stretch, local injury, or inflammation). Changes in the pain pathway can result in neuropathic pain from aberrant signaling or alteration in inhibitory central processes. Neuropathic pain can happen without stimulation of peripheral nociceptors.

The pathophysiology of chronic, recurrent abdominal pain is not completely understood. There is a complex interplay of psychosocial and physiological factors that leads to disturbed gastrointestinal function. Physiological alterations can happen at the level of gut nociceptors, spinal afferents, central autonomic relay system, or pain centers in the brain. Failure of central down-regulation and pain amplification by psychosocial factors lead to visceral hypersensitivity. Key mediators of gut function, such as serotonin (5-HT) and corticotropin-releasing factor (CRF), may modulate input from central nervous system along the brain gut axis, and cause altered intestinal motility and visceral hypersensitivity.11,12 Important psychosocial factors contributing to pain are lack of a social support system, anxiety-provoking events, a dysfunctional or abusive relationship, family attitude toward illness, and lack of coping skills. Pathophysiological mechanisms implicated in chronic, recurrent abdominal pain are summarized in Figure 1–2.

General Approach to Pain

The evaluating physician’s role is to establish an accurate diagnosis in an expeditious manner. The immediate goal is to identify life-threatening emergencies that require urgent interventions. The most important component of the evaluation process is a carefully taken history and a detailed physical examination. Selective use of appropriate radiological and laboratory investigations may be required to establish a specific diagnosis. Both the evaluating physician and the caregivers, however, must realize that the diagnosis may remain uncertain despite a thorough initial evaluation. In the absence of an obvious indication for surgery, patients with concerning acute symptoms should be observed in the hospital or emergency department with serial abdominal examinations to clarify any diagnostic uncertainty. Infants and younger pediatric patients are especially challenging, as they are unable to describe or localize pain. Pain is often inferred based on inconsolability or crying with abdominal palpation. A school-age child can usually characterize the location, intensity, and temporal progression of pain with reasonable accuracy.

Acute Abdominal Pain

History

Important details of the history include pattern of onset, progression, location, intensity and character, aggravating and alleviating factors of abdominal pain, and associated symptoms. Key historical variables include age and gender of the patient, history of abdominal trauma or prior abdominal surgery, and a thorough review of system. Common causes of acute abdominal pain have characteristic presentations and knowledge of these characteristics is essential for an expeditious diagnosis (Table 1–3).

Physical Examination

Careful systemic and abdominal examinations are essential for accurate diagnosis. Physical examination findings must be interpreted by taking the patient’s history and age into account. Examination of external genitalia, anus, and rectum is recommended as part of evaluation for abdominal pain. Pelvic examination is important in sexually active female patients. Key elements of the physical examination are as follows:

• Appearance: Appearance, hydration status, facial expression, breathing pattern, position in bed, and degree of discomfort should be carefully assessed. A child reluctant to move or in a fetal position is likely to have peritonitis. Patients with pure visceral pain, as in biliary colic or bowel obstruction, change position frequently, often writhing in pain.
  
• Vital signs: Vital signs are useful in assessing hypovolemia and provide useful clues for diagnosis. Patients with fever and acute abdominal pain may have acute gastroenteritis, pneumonia, pyelonephritis, pharyngitis, acute cholecystitis, appendicitis, or an intra-abdominal abscess. Tachypnea may indicate pneumonia. An acidotic breathing pattern is seen when there is metabolic acidosis as in diabetic ketoacidosis, gastroenteritis with dehydration, peritonitis, and intestinal obstruction. Hypotension suggests intravascular volume loss (acute gastroenteritis and abdominal trauma with intra-abdominal hemorrhage), or third-space loss (volvulus, intussusception, and peritonitis).
  
• Abdominal examination: Abdominal examination is often difficult to perform in a crying, uncooperative sick infant or child. Young patients are best examined in their position of comfort, usually in the lap of a parent. The abdomen should be examined before other anxiety-provoking examinations (e.g., examination of throat and ear). The examining physician must make efforts to determine the degree of abdominal tenderness and its location. Severe, diffuse tenderness with abdominal wall rigidity is indicative of peritonitis. Reproducible focal tenderness is indicative of intra-abdominal inflammatory process, as with McBurney’s point tenderness in appendicitis, epigastric tenderness in acute pancreatitis, and right upper quadrant tenderness with acute cholecystitis. Abdominal distension is seen with intestinal obstruction or abdominal mass. Other inspection findings may include ecchymoses (abdominal trauma), scars (prior abdominal surgery and associated adhesions), hernias, and visible intestinal peristalsis (intestinal obstruction or gastroenteritis).
  
• Extra-abdominal findings: Important diagnostic clues are often obtained from extra-abdominal findings. A characteristic rash is seen in Henoch–Schönlein purpura or scarlet fever. Jaundice is observed in hepatitis, gallbladder disease, or hemolytic anemia. Evidence of trauma elsewhere may be associated with occult visceral injury.

Chronic or Recurrent Abdominal Pain

History

• If possible, interrogate the patient directly, using developmentally appropriate techniques.
  
• Ask the patient to localize the pain area with his or her own hand. Poorly localized pain suggests visceral or functional etiology.
  
• Obtain information about the quality, intensity, duration, and timing of the pain. Ask about other associated symptoms, including vomiting, diarrhea, constipation, fever, rectal bleeding, weight loss, joint symptoms, oral ulcers, dysuria, hematuria, or perianal discharge. These symptoms often indicate an organic disease.
  
• Enquire about aggravating and relieving factors of the pain, relationship to diet, activity, posture, or psychosocial stressors.
  
• Assess the impact of chronic pain on daily functioning. Is the pain debilitating? Has it become the central focus of the patient’s life? What is the impact of pain on school attendance or sports participation?
  
• Enquire about the possibility of sexual or physical abuse, unresolved grief or losses, or depression.
  
• Ask about therapeutic attempts made to relieve abdominal symptoms and their efficacy. Specifically, enquire about the use of nonsteroidal anti-inflammatory drugs, narcotics, or laxatives.

There is no literature showing that pain frequency, location, timing (postprandial and nocturnal awakening), severity, and impact on quality of life are able to distinguish between patients with organic and functional disorders. There are also insufficient data to determine whether the presence of associated symptoms such as headache, anorexia, joint pain, vomiting, nausea, flatulence, and altered bowel pattern helps in distinguishing between organic and functional disorders. The presence of alarm symptoms such as involuntary weight loss, slowing of linear growth, severe vomiting, gastrointestinal blood loss, chronic severe diarrhea, unexplained fever, localized right upper or lower quadrant pain, and family history of inflammatory bowel disease suggests a higher probability of organic disease.

Physical Examination

• Carefully note facial expression, body posture, breathing pattern, and interaction of the patient with the accompanying family members.
  
• Presence of pallor, growth retardation, acute weight loss, clubbing, jaundice, peripheral edema, or significant lymphadenopathy may indicate organic etiology.
  
• It is uncommon to find signs of autonomic arousal—diaphoresis, tachycardia, or elevated blood pressure—in absence of acute organic causes of abdominal pain.
  
• Carnett’s test distinguishes abdominal wall pain from visceral pain. The pain from palpation at the site of maximal tenderness increases in abdominal wall pain with raising the head and contracting the rectus abdominis muscle, whereas in visceral pain it decreases.
  
• The “closed-eyes” sign is often seen in patients with FAP. These patients will wince with their eyes closed when the abdomen is palpated, whereas those with organic etiology keep their eyes open, fearfully anticipating pain with abdominal palpation.
  
• Inspect the abdomen for scars (indicative of prior surgery), distension, visible peristalsis, dilated vessels, or striae. It is important to examine the perianal area and hernial orifices, and perform digital rectal examination.
  
• Reexamination of the patient during acute exacerbation of abdominal pain will often provide important clinical information.

Acute Abdominal Pain

Acute abdominal pain generally refers to pain that has been present for <24 hours. The most common causes of the acute abdomen are listed in Tables 1–4 and 1–5. A detailed description of these disorders is beyond the scope of this chapter. A brief discussion of the common causes follows.