Most patients with chronic abdominal pain have functional GI disorders such as functional dyspepsia or irritable bowel syndrome.
Chronic abdominal pain syndromes can be subdivided into 2 categories: intra-abdominal and abdominal wall origin.
Chronic abdominal pain may coexist with other medical and psychological syndromes such as obesity, depression, and anxiety.
Abdominal pain is the second most common recurrent pain condition in children after headaches.
DEFINITION
Abdominal pain disorders are common and can be particularly challenging given the myriad of possible underlying etiologies: ranging from the life-threatening to chronic functional disorders. The International Association for the Study of Pain (IASP) defines chronic pain as “pain which has persisted beyond normal tissue healing time”.1 Both can be seen within the office-based primary care setting, each presenting with its own set of challenges.
The continuum of abdominal pain also includes somatic complaints relating to chronic functional abdominal pain, which may be difficult to manage. The challenge in the diagnosis and management of abdominal pain syndromes results in higher usage of health care resources primarily due to investigative workup, producing higher health care costs.
A structured approach to the evaluation, assessment, and investigation of abdominal pain allows for appropriate triaging and management. Although the focus of this section will be primarily on chronic abdominal pain, an overview of acute abdominal pain syndromes pertinent to primary care practices will also be reviewed.
MECHANISMS AND PAIN PATHWAYS
Anatomical abdominal pain pathways are complex owing to the presence of and possible coexistence of different types of nociceptive pain: visceral, somatic, and referred pain.
Somatic pain is defined as “pain arising from tissues such as the skin, muscle, joint capsules, and bone.” Stimuli from somatic pain are primarily mediated by the C and A-delta afferent fibers, which also innervate the mesentery. Direct damage to the gastrointestinal tissue, such as ischemia, triggers firing of C and A-delta afferents that are present within the serosal layer of the gastrointestinal (GI) tract.
Visceral pain is defined as “pain arising from visceral organs.” Visceral pain can often be diffuse, vague, and difficult to localize in some cases. Abdominal pain is mediated by the dual supply of visceral sensory information received by the splanchnic nerves and somatic information from cerebrospinal innervations. The splanchnic pathway innervates the visceral organs, where pain signals are transmitted by free afferent nerve endings through the spinal cord to the thalamus via the paleospinal and archispinal thalamic tracts. These afferent receptors are primarily located within the mucosal epithelium of the gastrointestinal tract and are mechanosensitive, receiving information from physical alterations in the tissue due to stretch and spasms2 (Figure 18-1). Caustic agents and extreme changes in intraluminal pH can also cause firing of these visceral afferents (Table 18-1).
CLINICAL PRESENTATIONS OF ABDOMINAL PAIN
According to the CDC report, acute abdominal pain was the most common presenting complaint to emergency departments in the United States between 1998 and 2008.3 Although less common in the office-based setting, abdominal pain remains a common reason for primary care visits.4 Appropriate triaging and timely referrals by the primary physician could be potentially life-saving, especially in a practice far removed from a major facility with the capacity to intervene on major vascular emergencies.
In the primary care setting, the presentation of acute abdominal pain is most likely to be acutely atraumatic in nature (Figure 18-2).
The first immediate step in evaluating acute abdominal pain in an office-based practice should be a focused and general assessment of the patient’s appearance and vital signs, with an emphasis on any objective evidence of possible hemodynamic instability. The goal of this very first step is to determine whether emergent interventions and resuscitative measures are required before transport to the higher level-of-care and to reduce overall morbidity and mortality.
Chronic abdominal pain syndromes can be subdivided into two categories: intra-abdominal and abdominal wall origin. Evaluation of chronic abdominal pain can be complex given the myriad of possible causes, some possibly overlapping in presentation. It is also important to keep in mind that pain syndromes, regardless of their etiologies, often coexist with other medical and psychological syndromes such as obesity, depression, and anxiety.
Malabsorptive Conditions
Inflammatory Bowel Disease
Postsurgery
Crohn disease
Gastrectomy
Ulcerative colitis
Intestinal disease
Other microscopic colitis
Sprue
Pancreatic insufficiency
Collagenous colitis
Mast cell disease
Dietary Factors
Psychiatric Conditions
Lactose intolerance
Panic disorder
Caffiene
Depression
Alcohol
Somatization disorders
Fat-containing, gas-producing foods
Cruciferous vegetables
Infections
Miscellaneous Conditions
Bacteria
Endometriosis
Campylobacter, Salmonella, Yersinia
Endocrine tumors
Cacinoid
Zollinger-Ellison syndrome
Parasites
Giardia lamblia
VIPoma
HIV disease
TABLE 18-1 General Characteristics of Pain due to Visceral Pathology
1. Is poorly localized with referral to somatic structures
2. Produces nonspecific regional or whole-body motor responses
3. Produces strong autonomic responses
4. Leads to sensitization of somatic tissues
5. Produces strong affective responses
Reprinted with permission from Sikandar S, Dickenson AH. Visceral pain: the ins and outs, the ups and downs. Curr Opin Support Palliat Care. 2012;6(1):17-26.
Careful attention to reported or presenting signs and symptoms during a thorough history-taking should be of utmost importance, as physical findings may not be reproducible. Additionally, clues within the patient’s presenting complaints may lead an astute clinician to a diagnosis without ordering otherwise unnecessary or costly radiologic imaging and laboratory tests.
The initial assessment of any abdominal pain during history-taking should the 6 following features:
3. Intensity: The severity of the pain perceived by the patient.
4. Evolution: Increasing, decreasing, or unchanged in intensity.
5. Migration: Radiation of the pain from a primary site, to another.
6. Localization: Involvement of the epigastrium, mid-abdominal, or lower abdominal areas.
Diagnostic modalities can be considered if the outcomes were to be affected, significantly altering your clinical decision-making (Figure 18-3).
Abdominal wall pain, being somatic in origin, is distinct from visceral pain syndromes also with different anatomical considerations. In distinguishing abdominal wall pain from intra-abdominal sources, the abdominal examination could assess for Carnett sign: unchanged or an increase in abdominal pain with the abdomen tensed (Table 18-2).
Although opioids may be useful for acute intolerable pain including abdominal pain, it is often not the best first-line solution for chronic nonmalignant abdominal pain because of opioid-induced side effects including nausea/vomiting and constipation, which all may exacerbate the pain state. In patients with chronic abdominal pain, a multidisciplinary approach that includes cognitive behavioral therapy would be most ideal. Unless a recent intra-abdominal surgical history is present in the review of systems or history, surgical interventions are less likely to be of benefit as the first initial step. In these patients, diagnostic laparoscopies for chronic abdominal pain of unknown etiology have only been shown to result in symptomatic improvement in 50% of patients.5 In this subset of patients, symptoms may be due to postsurgical development of adhesions, cholecystitis, internal hernias, or a defect in the mesentery. Although uncommon, abdominal wall abscess formation should also be considered in the differential diagnosis.
In female patients with recent pelvic or abdominal wall surgeries, most commonly low-transverse cesarean sections, presenting with chronic abdominal wall pain of unclear etiology can be challenging. After ruling out postsurgical and incision pain, one consideration can include the diagnosis of abdominal wall endometriosis with implantation of lesions within the wall, diagnosable using ultrasound. If patient habitus prevents appropriate visualization of suspected lesions, abdominal magnetic resonance imaging can be considered. Surgical excision of such isolated lesions has been reported to be successful, without very low recurrence rates.6
