Abdominal Pain
2. EVALUATION
3.3. Chronic Pancreatitis
Treatment for patients with chronic pancreatitis focuses on minimizing future pancreatic damage (e.g., by avoiding alcohol) and symptoms of pain and abnormal exocrine and endocrine function (Table 3). Chronic pancreatitis pain tends to be severe and typically requires opioid analgesics. The use of opioids may be particularly challenging in patients with alcohol-related chronic pan-creatitis because of the risk for medication misuse and abuse (see Chapter 17).
Pancreatic enzymes and other agents may also improve pain severity. In a recent large, randomized study, investigators found an improvement rate of more than 50% in patients with chronic pancreatitis treated with the cholecys-tokinin A-receptor antagonist loxiglumide 600 mg/day (currently not available in the United States) (23). Pancreatic surgery and celiac plexus blocks or neu-rolysis are not recommended for most patients with chronic pancreatitis.
Patients with poor exocrine function, manifested by steatorrhea and weight loss, should be treated with a low-fat diet and pancreatic enzyme supplementa-tion. Patients with poor endocrine function and glucose intolerance typically require insulin therapy.
4. SUMMARY
Abdominal pain may be caused by a readily identified pathology (e.g., gastri-tis, ulcer disease, or inflammation) or present as a chronic pain complaint with-out a correctable pathology. Chronic abdominal pain is typically diagnosed in patients with a stable pain history for at least 3 months who lack symptoms and signs of other pathology (e.g., fever, significant weight loss, or anemia). Although blood tests and radiographs often fail to identify obvious abnormalities in pa-tients with chronic abdominal pain, functional abdominal pain disorders (e.g., IBS) are not psychological syndromes. Measures of psychological distress are
Steatorrhea Pancreatic enzymes
Glucose intolerance Insulin
aCurrently not available in the United States.
indeed higher in patients with functional abdominal pain disorders; however, the rate of psychological distress is not elevated in individuals with these disorders who are not seeking medical care. Therefore, psychological distress is a marker of treatment-seeking behavior rather than abdominal pain.
Historical reports of symptoms (changes in bowel habits, occurrence of bloat-ing, and pain with lifting or change in posture) and physical examination signs (e.g., Carnett’s sign of myofascial pain) can help the clinician distinguish the causes of chronic abdominal pain. In general, most types of chronic abdominal pain can be managed with a both medication- and nonmedication-based pain management strategies. Treatment strategies, however, are often specific to indi-vidual pain diagnostic categories (e.g., serotonin receptor agents or antidepres-sants for IBS, trigger-point injection for myofascial pain, and enzyme supplementation and analgesics for chronic pancreatitis).
REFERENCES
1. Gladman LM, Gorard DA. General practitioner and hospital specialist attitudes to functional gastrointestinal disorders. Aliment Pharmacol Ther 2003; 17:651–654.
2. Jones MP. Death by diagnosis. Ann Intern Med 2001; 135:307.
3. Halder SS, McBeth J, Silman AJ, Thompson DG, MacFarlane GJ. Psychosocial risk factors for the onset of abdominal pain: results from a large prospective popu-lation-based study. Int J Epidemiol 2002; 31:1219–1225.
4. Cherry DW, Woodwell DA. National Ambulatory Medical Care Survey: 2000 summary. Adv Data 2002; 5:1–32.
5. Hasselström J, Liu-Palmgren J, Rasjö-Wrååk G. Prevalence of pain in general practice. Eur J Pain 2002; 6:375–385.
5a. Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut 1999; 45(suppl 2):1143–1147.
6. Hungin AS, Whorwell PJ, Tack J, Mearin F. The prevalence, patterns and impact of irritable bowel syndrome: an international survey of 40,000 subjects. Aliment Pharmacol Ther 2003; 17:643–650.
7. McGarrity TJ, Peters DJ, Thompson C, McGarrity SJ. Outcome of patients with chronic abdominal pain referred to chronic pain clinic. Am J Gastroenterol 2000;
95:1812–1816.
8. Otsuki M. Chronic pancreatitis in Japan: epidemiology, prognosis, diagnostic cri-teria, and future problems. J Gastroenterol 2003; 38:315–326.
9. Olden KW. The challenge of diagnosing irritable bowel syndrome. Rev Gastro-enterol Dis 2003; 3(Suppl 3):S3–S11.
10. Holten KB. Irritable bowel syndrome: minimize testing, let symptoms guide treat-ment. J Fam Pract 2003; 52:942–949.
11. Sparkes V, Prevost AT, Hunter JO. Derivation and identification of questions that act as predictors of abdominal pain of musculoskeletal origin. Eur J Gastroenterol Hepatol 2003; 15:1021–1027.
12. Thomson H, Francis DM. Abdominal-wall tenderness: a useful sign in the acute abdomen. Lancet 1977; 2:1053–1054.
16. Hobbis IA, Turpin G, Read NW. A re-examination of the relationship between abuse experience and functional bowel disorders. Scand J Gastroenterol 2002; 4:
423–430.
17. Leserman J, Li Z, Drossman DA, Hu YJ. Selected symptoms associated with sexual and physical abuse history among female patients with gastrointestinal disorders:
the impact on subsequent health care visits. Psychol Med 1998; 28:417–425.
18. Drossman DA. Do psychosocial factors define symptom severity and patient sta-tus in irritable bowel syndrome? Am J Med 1999; 107(Suppl 5A):41S–50S.
19. Drossman DA, McKee DC, Sandler RS, et al. Psychosocial factors in the irritable bowel syndrome: a multivariate study of patients and nonpatients with irritable bowel syndrome. Gastroenterology 1998; 95:701–708.
20. Aaron LA, Bradley LA, Alarcon GS, et al. Psychiatric diagnoses in patients with fibromyalgia are related to health care-seeking behavior rather than to illness.
Arthritis Rheum 1996; 39:436–445.
21. Drossman DA, Toner BB, Whitehead WE, et al. Cognitive-behavioral therapy versus education and desipramine versus placebo for moderate to severe func-tional bowel disorders. Gastroenterology 2003; 125:19–31.
22. Spanier JA, Howden CW, Jones MP. A systematic review of alternative therapies in the irritable bowel syndrome. Arch Intern Med 2003; 163:265–274.
23. Shiratori K, Takeuchi T, Satake K, Matsuno S. Clinical evaluation of oral admin-istration of a cholecystokinin: a receptor antagonist (loxiglumide) to patients with acute, painful attacks of chronic pancreatitis: a multicenter dose-response study in Japan. Pancreas 2002; 25:E1–E5.
CME QUESTIONS—CHAPTER 6
1. Which of the following symptoms are common in patients with musculoskeletal abdomi-nal pain?
a. Pain aggravated by lifting b. Pain aggravated by eating c. Pain coughing or deep breaths d. A and C
e. All of the above
2. Rome II diagnostic criteria for irritable bowel syndrome include:
a. Pain occurring in 12 or more weeks during the preceding year b. Pain relieved by bowel movements
c. Change in bowel frequency when pain began d. Change in stool appearance when pain began e. All of the above
3. Medications used to treat diarrhea in patients with irritable bowel syndrome include:
a. Alosetron b. Loperamide
c. Oral cromolyn sodium d. All of the above
4. Which of the following is not a routine therapy for chronic pancreatitis?
a. Abstinence from alcohol b. Pancreatic enzymes c. Opioid analgesics d. Celiac plexus neurolysis
91
From: Chronic Pain: A Primary Care Guide to Practical Management Edited by: D. A. Marcus © Humana Press, Totowa, NJ
life, playing football through high school and college and continuing to play in amateur leagues during his early work years. He comes to his doctor with a chief complaint of right knee pain, which has been increasing progressively over the last 8 years. An earlier evaluation revealed positive rheumatoid factor (RF), and he was diagnosed with rheumatoid arthritis (RA). This was managed with nonste-roidal anti-inflammatory drugs (NSAIDs) and steroids. Although he experienced pain reduction with the anti-inflammatory analgesics, he developed severe gastri-tis and needed to discontinue therapy. He was referred to a rheumatologist for more aggressive therapy, but was fearful of the side effects of methotrexate, which he had read about on the Internet. He decided to discontinue all exercise programs and began sedentary activities. During this time, he sprained his ankle twice after stepping off curbs and had recurrent attacks of low back sprain after carrying small loads, such as groceries or laundry. Mr. Harris subsequently tried to resume his previous jogging program without success. At this new consulta-tion, Mr. Harris reports that his knee is most bothersome after prolonged sitting or after jogging for about 15 minutes. He also reports stiffness in both hands and in his left hip, and right knee when he first gets up in the morning, although this goes away after he “works it out” with range-of-motion exercises and a few minutes of walking. On examination, Mr. Harris is slow to get out of his chair and reports feeling “stiff” after sitting in the waiting room for 1 hour. Examina-tion of the knee shows slight bony deformity with no inflammaExamina-tion of the joint.
Passive range of motion is slightly reduced with joint crepitus. No joint instabil-ity is identified. Radiographs of the knee show narrowing of the joint space and the presence of osteophytes. His primary care physician (PCP) makes a diagno-sis of osteoarthritis and treats him with acetaminophen. He also enrolls Mr. Har-ris in an arthritis pool therapy program at the local YMCA and recommends a bicycling program as well. Two months later, Mr. Harris reports improvement in both pain and activity tolerance.
* * *
Mr. Harris shows characteristic features of osteoarthritis (OA), the most common form of arthritis in adults. OA typically affects the large, weight-bearing joints in a nonsymmetrical fashion, with the knee frequently affected.
Interestingly, RF is not specific for RA; in fact, it may be positive in patients with OA and negative in RA, particularly during the early stages of the disease.
Mr. Harris’ PCP treated him appropriately with a well-tolerated analgesic.
Anti-inflammatory medications are not the first choice for patients with OA because it is not an inflammatory condition.
Distinguishing between degenerative and inflammatory arthritis is essential in patients with chronic joint complaints. Disease pathology, pattern of joint involvement, and recommended treatments are dissimilar for degenerative and inflammatory arthritis. In addition, maintaining good condition of supportive tissues around joints is essential for minimizing new pain complaints and main-taining good function. Although the OA identified in Mr. Harris is likely the result of years of joint overuse, too much rest for the joints will not improve symptoms. As he discovered, too much rest increases the risk for injury from minor trauma because of a lack of the normal protection of the joint that is provided by strong and flexible muscles, tendons, and ligaments.
KEY CHAPTER POINTS
• Arthritis is a common cause of chronic joint pain, with the prevalence increas-ing with age.
• The most common type of chronic arthritis is degenerative OA.
• Patients with OA are treated with symptomatic therapy and rehabilitation.
• RA therapy requires specific disease-modifying drugs that are often prescribed after consultation with a rheumatologist.
• Aerobic exercise is important for reducing pain and maintaining function in both OA and RA.