Recurrent Abdominal Pain: An Update

The definition of recurrent abdominal pain (RAP) derives from the seminal description by Apley of paroxysmal abdominal pain in children between the ages of 4 and 16 years that persists for more than 3 months and affects normal activity. RAP is not a diagnosis. It may be the predominant clinical manifestation of a large number of precisely defined organic disorders, but in the majority of cases, RAP is due to a functional bowel disorder. The modifier “functional” is used in gastroen-terology if no specific structural, infectious, inflammatory, or biochemical cause for the abdominal pain can be determined. It is the delicate interface between organic and functional forms of pediatric RAP that challenges the primary care pediatrician. Because the exact etiology and pathogenesis of the pain are unknown and because no specific diagnostic markers exist, a diagnosis of functional bowel disorder often is viewed as a diagnosis of exclusion. Yet, functional abdominal pain can and should be a diagnosis that meets specific criteria. The diagnosis is established by a constellation of criteria based on a careful history, physical examination, and minimum laboratory investigation. Management can be instituted if these criteria are met, and appropriate follow-up is assured.RAP has been reported to occur in 10% to 15% of children between the ages of 4 and 16 years. At least as many children experience chronic pain but maintain normal activity and rarely come to the attention of the physician.Apley observed that males and females are affected equally in early childhood up until the age of 9, at which point the incidence decreases in males. The incidence in females continues to increase until age 11 to 12 years, such that between 9 and 12 years of age the female-to-male ratio approaches 1.5 to 1. Onset of chronic pain in a child younger than 4 years old requires a more in-depth organic evaluation, particularly for structural abnormalities. Gender,intelligence, and personality traits do not distinguish patients who have functional pain from those who have organic pain. The majority of patients are of average intelligence. The generalization that patients who have functional abdominal pain are superintellects, perfectionists, overachievers,bad mixers, or constant worriers is without foundation.Children who have RAP tend to exhibit one of three clinical presentations: 1) isolated paroxysmal abdominal pain, 2) abdominal pain associated with symptoms of dyspepsia, and 3) abdominal pain associated with an altered bowel pattern. Symptoms of dyspepsia include: pain associated with eating; epigastric location of pain; and nausea, vomiting, heartburn,oral regurgitation, early satiety, excessive hiccups, and excessive belching. Symptoms of altered bowel pattern include: diarrhea, constipation, or a sense of incomplete evacuation with bowel movements. Functional abdominal pain is by far the most common cause of each presentation. The differential diagnosis, however, includes a heterogeneous group of anatomic, infectious,noninfectious inflammatory, and biochemical disorders.The etiology and pathogenesis of functional abdominal pain are unknown. It is generally agreed that the pain is genuine and not simply social modeling, imitation of parental pain, or a means to avoid an unwanted experience (eg, school phobia or malingering). It is not clear whether the different clinical presentations of functional abdominal pain result from a heterogeneous group of disorders or represent variable expressions of the same disorder. The frequent occurrence of upper and lower bowel symptoms in the same patient (particularly nonulcer dyspepsia and irritable bowel in an adolescent) suggests that the latter scenario may be the case. The prevailing viewpoint is that the pathogenesis of the pain involves disordered gastrointestinal motility or visceral hypersensitivity. There appears to be a genetic vulnerability because of the high frequency of complaints of pain in family members. A family history of irritable bowel syndrome, peptic ulcer, previous appendectomy, or migraine headaches is common. That most children “outgrow” pain symptoms also suggests neuroendocrine development as a factor in the pathophysiology. In some patients, associated symptoms, including headache, pallor, and dizziness,suggest a generalized dysfunction of the autonomic nervous system.Motility disturbances have been described in children by using manometric evaluation, measurements of intestinal transit, and surface electrophysiologic recordings. Studies to date in heterogeneous patients who have functional abdominal pain have described increased intensity of intestinal muscle contraction in both the small bowel and colon and delayed intestinal transit time. A characteristic motility disturbance has yet to be identified for any of the subgroups of functional abdominal pain. The concept of visceral hypersensitivity is derived from studies in adults who have irritable bowel syndrome and report enhanced awareness of balloon distention in all segments of the gastrointestinal (GI) tract from esophagus to rectum. Adult studies also suggest an increased awareness of normal intestinal motor activity in some patients. An altered threshold of gut-wall receptors, an altered modulation in the conduction of the sensorial input,or an altered conscious threshold in the central nervous system (CNS) could explain visceral hypersensitivity. Altered motor response or altered visceral sensation to gut distention caused by certain luminal contents such as lactose, fructose, sorbitol, fatty acids, and bile acids may explain why selected patients who have functional abdominal pain experience a qualitative improvement in pain symptoms when treated with dietary restrictions. Altered conscious threshold in the CNS may explain why concurrent stressful life events such as death or separation from a significant family member, physical illness or chronic handicap in parents or siblings, school problems, poverty or financial problems, and recent geographic moves may provoke or reinforce the pain behavior.The role of inflammation or immunomodulation in the pathogenesis of functional abdominal pain must be considered in view of the frequent finding of nonspecific inflammatory changes in intestinal biopsies at all levels of the GI tract. Inflammatory changes may be the cause or the effect of altered intestinal motility. Immune responses alter neural and endocrine function; in turn,neural and endocrine activity modify immunologic function. Activated immunocompetent cells such as monocytes, lymphocytes, and macrophages that take up residence in the intestinal tract may secrete a repertoire of cytokines and inflammatory mediators that can lead to profound changes in enteric neural function. The enteric or central nervous systems also may modulate intestinal immune responses. Activation of the sympathetic nervous system causes leukocytosis, sequestration of lymphocytes, and inhibition of natural killer cell activity. Sensory neurons also contain a variety of neurotransmitters and neuropeptides that can affect lymphocyte function,including substance P, vasoactive intestinal polypeptide, angiotensin II,calcitonin gene-related peptide, and somatostatin. Personality, behavior,coping style, and emotional state also influence immune responses and may have implications in functional abdominal pain.The morbidity associated with RAP affects psychosocial function. It interferes with normal school attendance and performance, peer relationships,participation in organizations and and and family Studies have that in children who have RAP school and that is than in in of patients. The of the pain also to the The and of RAP on which the pain and to reinforce responses such as normal activity. The pain is by social attention at the of pain, pain, at the of pain, from school on of pain, and the of normal activity on of school parents to the report of pain by that the child or to the and or or the pain than the child is all from the child or normal the pain reinforce the pain when the child when or of pain. 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