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Chronic and Recurrent Abdominal Pain

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Chronic abdominal pain (CAP) persists for more than 3 mo either continuously or intermittently. Intermittent pain may be referred to as recurrent abdominal pain (RAP). Acute abdominal pain is discussed in Acute Abdomen and Surgical Gastroenterology: Acute Abdominal Pain. CAP occurs any time after 5 yr of age. Up to 10% of children require evaluation for RAP. About 2% of adults, predominantly women, have CAP (a much higher percentage of adults have some type of chronic GI symptoms, including non-ulcer dyspepsia and various bowel disturbances).

Nearly all patients with CAP have had prior medical evaluation that did not yield a diagnosis after history, physical, and basic testing.

Pathophysiology

Functional abdominal pain syndrome (FAPS) is pain that persists > 6 mo without evidence of physiologic disease, shows no relationship to physiologic events (eg, meals, defecation, menses), and interferes with daily functioning. FAPS is poorly understood but seems to involve altered nociception. Sensory neurons in the dorsal horn of the spinal cord may become abnormally excitable and hyperalgesic due to a combination of factors. Cognitive and psychologic factors (eg, depression, stress, culture, secondary gain, coping and support mechanisms) may cause efferent stimulation that amplifies pain signals, resulting in perception of pain with low level inputs and persistence of pain long after the stimulus has ceased. Additionally, the pain itself may function as a stressor, perpetuating a positive feedback loop.

In addition, menopause increases GI symptoms in several disorders including irritable bowel syndrome, inflammatory bowel disease, endometriosis, and nonulcer dyspepsia.

Etiology

Perhaps 10% of patients have an occult physiologic illness (see Table 1: Approach to the Patient with Upper GI Complaints: Physiologic Causes of Chronic Abdominal PainTables); the remainder have a functional process. However, determining whether a particular abnormality (eg, adhesions, ovarian cyst, endometriosis) is the cause of CAP symptoms or an incidental finding can be difficult.

Table 1

Physiologic Causes of Chronic Abdominal Pain

Cause

Suggestive Findings*

Diagnostic Approach

GU disorders

Congenital abnormalities

Recurrent UTIs

IVU

Ultrasonography

Endometriosis

Discomfort before or during menses

Laparoscopy

Ovarian cyst, ovarian cancer

Vague lower abdominal discomfort, bloating, sometimes a palpable pelvic mass

Pelvic ultrasonography

Gynecologic consultation

Renal calculi

Fever, flank pain

Urine culture

IVU

CT

Sequelae of acute PID

Pelvic discomfort, history of acute PID

Pelvic examination

Sometimes laparoscopy

GI disorders

Chronic appendicitis

Several previous discrete episodes of RLQ pain

Abdominal CT

Ultrasonography

Chronic cholecystitis

Recurrent colicky RUQ pain

Ultrasonography

Hydroxy iminodiacetic acid scan

Chronic hepatitis

Upper abdominal discomfort, malaise, anorexia

Jaundice uncommon

About 1/3 have history of acute hepatitis

Liver tests

Viral hepatitis titers

Chronic pancreatitis, pancreatic pseudocyst

Episodes of severe epigastric pain, sometimes malabsorption (eg, diarrhea, fatty stool)

Usually a history of acute pancreatitis

Serum amylase and lipase levels

CT

Colon cancer

Discomfort uncommon but colicky discomfort may occur with partial obstruction of left colon

Often with occult or visible blood in stool

Colonoscopy

Crohn's disease

Episodic severe pain with fever, anorexia, weight loss, diarrhea

Extraintestinal symptoms (joints, eyes, mouth, skin

CT enterography or upper GI series with SBFT

Colonoscopy and esophagogastroduodenoscopy with biopsies

Gastric cancer

Dyspepsia or mild pain, often occult blood in stool

Upper endoscopy

Granulomatous enterocolitis

Family history, recurrent infections in other sites (eg, lungs, lymph nodes)

ESR

Barium enema

Hiatus hernia with gastroesophageal reflux

Heartburn, sometimes regurgitation of gastric contents into mouth

Barium swallow

Endoscopy

Intestinal TB

Chronic nonspecific pain, sometimes palpable RLQ mass, fever, diarrhea, weight loss

Tuberculin test

Endoscopy for biopsy

CT with oral contrast

Lactose intolerance

Bloating and cramps after ingesting milk products

H2 breath test

Trial of elimination of lactose-containing foods

Pancreatic cancer

Severe upper abdominal pain often radiating to back

Occurs late in disease, so weight loss common

May cause obstructive jaundice

CT

Magnetic resonance cholangiopancreatography or ERCP

Parasitic infestation (particularly giardiasis)

History of travel/exposure, cramps, flatulence, diarrhea

Stool examination for ova or parasites

Peptic ulcer disease

Upper abdominal pain relieved by food and antacids

May awaken patient at night

Endoscopy and biopsy for Helicobacter pylori H. pylori breath test

Stool examination for occult blood

Postoperative adhesive bands

Previous abdominal surgery

Colicky discomfort accompanied by nausea, sometimes vomiting

Upper GI series, SBFT, or enteroclysis

Ulcerative colitis

Crampy pain with bloody diarrhea

Sigmoidoscopy

Rectal biopsy

Colonoscopy

Systemic disorders

Abdominal epilepsy

Very rare, episodic pain, no other GI symptoms

EEG

Familial angioneurotic edema

Family history, pain often with peripheral angioedema and fever

Serum complement level (C4) during attacks

Familial Mediterranean fever

Family history, fever and peritonitis often accompany bouts of pain

Starts in childhood or adolescence

Genetic testing

Food allergy

Symptoms developing only after consuming certain foods (eg, seafood)

Elimination diet

Henoch-Schönlein purpura

Palpable purpuric rash, joint pains, occult blood in stool

Biopsy of skin lesions

Lead poisoning

Cognitive/behavioral abnormalities

Blood lead level

Migraine equivalent

Rare variant with epigastric pain and vomiting

Mainly in children

Usually family history of migraine

Clinical evaluation

Porphyria

Recurrent severe abdominal pain, vomiting, benign abdomen on examination

Sometimes with neurologic symptoms (eg, muscle weakness, seizures, mental disturbance)

Some types have skin lesions

Urine porphobilinogen and delta δ-aminolevulinic acid screening

RBC deaminase assay

Sickle cell disease

Family history

Also recurrent pain in nonabdominal sites

Sickle preparation

Hb electrophoresis

* Findings are not always present and may be present in other disorders.

PID = pelvic inflammatory disease; RLQ = right lower quadrant; RUQ = right upper quadrant; SBFT = small-bowel follow through.

Modified from Barbero GJ: Recurrent abdominal pain. Pediatrics in Review 4:30, 1982 and from Greenberger NJ: Sorting through nonsurgical causes of acute abdominal pain. Journal of Critical Illness 7:1602-1609, 1992.

Evaluation

History: History of present illness should elicit pain location, quality, duration, timing and frequency of recurrence, and factors that worsen or relieve pain (particularly eating or moving bowels). A specific inquiry as to whether milk and milk products cause abdominal cramps, bloating, or distention is needed, because lactose intolerance is common, especially among blacks.

Review of systems seeks concomitant GI symptoms such as gastroesophageal reflux, anorexia, bloating or “gas,” nausea, vomiting, jaundice, melena, hematuria, hematemesis, weight loss, and mucus or blood in the stool. Bowel symptoms, such as diarrhea, constipation, and changes in stool consistency, color, or elimination pattern, are particularly important.

In adolescents, a diet history is important because ingestion of large amounts of cola beverages and fruit juices (which may contain significant quantities of fructose and sorbitol) can account for otherwise puzzling abdominal pain.

Past medical history should include nature and timing of any abdominal surgery and the results of previous tests that have been done and treatments that have been tried. A drug history should include details concerning prescription and illicit drug use as well as alcohol.

Family history of RAP, fevers, or both should be ascertained, as well as known diagnoses of sickle cell trait or disease, familial Mediterranean fever, and porphyria.

Physical examination: Review of vital signs should particularly note presence of fever or tachycardia.

General examination should seek presence of jaundice, skin rash, and peripheral edema. Abdominal examination should note areas of tenderness, presence of peritoneal findings (eg, guarding, rigidity, rebound), and any masses or organomegaly. Rectal examination and (in women) pelvic examination to locate tenderness, masses, and blood are essential.

Red flags: The following findings are of particular concern:

  • Fever
  • Anorexia, weight loss
  • Pain that awakens patient
  • Blood in stool or urine
  • Jaundice
  • Edema
  • Abdominal mass or organomegaly

Interpretation of findings: Clinical examination alone infrequently provides a firm diagnosis.

Determining whether CAP is physiologic or functional can be difficult. Although the presence of red flag findings indicates a high likelihood of a physiologic cause, their absence does not rule it out. Other hints are that physiologic causes usually cause pain that is well localized, especially to areas other than the periumbilical region. Pain that wakes the patient is usually physiologic. Some findings suggestive of specific disorders are listed in Table 1: Approach to the Patient with Upper GI Complaints: Physiologic Causes of Chronic Abdominal PainTables.

Functional CAP may result in pain similar to that of physiologic origin. However, there are no associated red flag findings, and psychosocial features are often prominent. A history of physical or sexual abuse or an unresolved loss (eg, divorce, miscarriage, or death of a family member) may be a clue.

The Rome criteria for diagnosis of irritable bowel syndrome are the presence of abdominal pain or discomfort for at least 3 days/mo in the last 3 mo along with at least 2 of the following: (1) improvement with defecation; (2) onset (of each episode of discomfort) associated with a change in frequency of defecation; and (3) change in consistency of stool.

Testing: In general, simple tests (including urinalysis, CBC, liver tests, ESR, amylase, and lipase) should be done. Abnormalities in these tests, the presence of red flag findings, or specific clinical findings mandate further testing, even if previous assessments have been negative. Specific tests depend on the findings (see Table 1: Approach to the Patient with Upper GI Complaints: Physiologic Causes of Chronic Abdominal PainTables) but typically include CT of the abdomen and pelvis with contrast, upper GI endoscopy or colonoscopy, and perhaps small-bowel x-rays or stool testing.

The benefits of testing patients with no red flag findings are unclear. Those > 50 should probably have a colonoscopy; those 50 can be observed or have CT of the abdomen and pelvis with contrast if an imaging study is desired. Magnetic resonance cholangiopancreatography (MRCP), ERCP, and laparoscopy are rarely helpful in the absence of specific indications.

Between the initial evaluation and the follow-up visit, the patient (or family, if the patient is a child) should record any pain, including its nature, intensity, duration, and precipitating factors. Diet, defecation pattern, and any remedies tried (and the results obtained) should also be recorded. This record may reveal inappropriate behavior patterns and exaggerated responses to pain or otherwise suggest a diagnosis.

Treatment

Physiologic conditions are treated.

If the diagnosis of functional CAP is made, frequent examinations and tests should be avoided because they may focus on or magnify the physical complaints or imply that the physician lacks confidence in the diagnosis.

There are no modalities to cure functional CAP; however, many helpful measures are available. These measures rest on a foundation of a trusting, empathic relationship among the physician, patient, and family. Patients should be reassured that they are not in danger; specific concerns should be sought and addressed. The physician should explain the laboratory findings and the nature of the problem and describe how the pain is generated and how the patient perceives it (ie, that there is a constitutional tendency to feel pain at times of stress). It is important to avoid perpetuating the negative psychosocial consequences of chronic pain (eg, prolonged absences from school or work, withdrawal from social activities) and to promote independence, social participation, and self-reliance. These strategies help the patient control or tolerate the symptoms while participating fully in everyday activities.

Drugs such as aspirin Some Trade Names
BUFFERIN
ECOTRIN
GENACOTE
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, NSAIDs, H2 receptor blockers, proton pump inhibitors, and tricyclic antidepressants can be effective. Opioids should be avoided because they invariably lead to dependency.

Cognitive methods (eg, relaxation training, biofeedback, hypnosis) may help by contributing to the patient's sense of well-being and control. Regular follow-up visits should be scheduled weekly, monthly, or bimonthly, depending on the patient's needs, and should continue until well after the problem has resolved. Psychiatric referral may be required if symptoms persist, especially if the patient is depressed or there are significant psychologic difficulties in the family.

School personnel should become involved for children who have CAP. Children can rest briefly in the nurse's office during the school day, with the expectation that they return to class after 15 to 30 min. The school nurse can be authorized to dispense a mild analgesic (eg, acetaminophen Some Trade Names
GENAPAP
TYLENOL
VALORIN
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). The nurse can sometimes allow the child to call a parent, who should encourage the child to stay in school. However, once parents stop treating their child as special or ill, the symptoms may worsen before they abate.

Key Points

  • Most cases represent a functional process.
  • Red flag findings indicate a physiologic cause and need for further assessment.
  • Testing is guided by clinical features.
  • Repeated testing after physiologic causes are ruled out is usually counterproductive.

Last full review/revision March 2008 by Norton J. Greenberger, MD

Content last modified March 2008

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