Depends on how high the serum levels are! Although the clearance of both amylase and lipase appears to be impaired in patients with significant renal insufficiency (eg, creatinine clearance <50ml/min), serum levels greater than 2-4 times the upper limits of normal for these enzymes are still considered suggestive of pancreatitis in these patients1-3.
Interestingly, in hemodialysis patients, elevation of lipase may also be due to the lipolytic effect of heparin during this procedure. That’s why obtaining serum lipase levels before, not after, hemodialysis has been recommended4
Also fascinating is that most of the elevation of serum amylase in patients with significant renal insufficiency appears to be related to the elevation of salivary, not pancreatic, isoenzyme of amylase4.
Final fun fact: Did you know that at one time the diagnosis of pancreatitis was based on the activity of serum on starch (for amylase) and olive oil (for lipase)? 5
- Levitt MD, Rapoport M, Cooperband SR. The renal clearance of amylase in renal insufficiency, acute pancreatitis, and macroamylasemia. Ann Intern Med 1969;71:920-25. http://annals.org/aim/article/683643/renal-clearance-amylase-renal-insufficiency-acute-pancreatitis-macroamylasemia
- Collen MJ, Ansher AF, Chapman AB, et al. Serum amylase in patients with renal insufficiency and renal failure. Am J Gastroenterol 1990;85:1377-80. https://www.ncbi.nlm.nih.gov/pubmed/1699413
- Royce VL, Jensen DM, Corwin HL. Pancreatic enzymes in chronic renal failure. Arch Intern Med 1987;147:537-39. https://www.ncbi.nlm.nih.gov/pubmed/2435254
- Vaziri ND, Change D, Malekpour A, et al. Pancreatic enzymes in patients with end-stage renal disease maintained on hemodialysis. Am J Gastroenterol 1988;83:410-12. https://www.ncbi.nlm.nih.gov/pubmed/2450453
- Editorial. Pancreatic enzymes. N Engl J Med 1963;268:901-2. http://www.nejm.org/doi/pdf/10.1056/NEJM196304182681613
Cryoglobulins (CGs) are immunoglobulins that precipitate in the blood under cold conditions (<37◦ C) and redissolve upon warming1. The term “cryoglobulinemia” is commonly used to describe patients with a systemic inflammatory syndrome that is often associated with small-to-medium vessel vasculitis due to cryoglobulin-containing immune complexes. Although some patients with cryoglobulinemia may be asymptomatic, most present with a range of diseases characterized by fatigue, arthralgia, skin rashes or necrosis, purpura, neuropathy, bowel wall ischemia and/or glomerulonephritis and kidney failure.
Wintrobe and Buell are credited for first describing cryglobulinemia in 1933 when assessing a patient who ultimately was found to have multiple myeloma2. Since then the spectrum of diseases associated with CG has expanded to also include seemingly disparate conditions such as hepatitis C, autoimmune disorders and monoclonal gammopathy of undetermined significance (MGUS). A commonly cited classification scheme for CG is shown (Table)3. It should be emphasized that some CGs may not fit neatly into this scheme.
In our patient, the positive CG serum test should be interpreted in the clinical context in which it was obtained while searching for risk factors as well as signs and symptoms that may be associated with cryoglobulinemia.
Table. Classification of cryoglobulinemia
||Isolated monoclonal immunoglobulin, either IgM or IgG (less commonly IgA or free immunoglobulin light chains
||Multiple myeloma, Waldenström’s macroglobulinemia, monoclonal gammopathy of undetermined significance (MGUS)
||Mixture of monoclonal IgM and polyclonal IgG
||Hepatitis C, HIV, other viral infections
||Polyclonal mixture IgM and IgG
||Autoimmune disorders, hepatitis C
- Takada S, Shimizu T, Hadano Y, et al. Cryoglobulinemia (review). Mol Med Rep 2012;6:3-8
- Wintrobe MM, Buell MV. Hyperproteinemia associated with multiple myeloma. Bull Johns Hopkins Hosp 52: 156-165, 1933
- Brouet JC, Clauvel JP, Danon F, et al. Biological and clinical significance of cryoglobulins. Am J Med 1974; 57:775-88.
Contributed by Kirstin Scott, Medical Student, Harvard Medical School
Several case reports in the literature have stressed the association of bladder dysfunction (BD) with chronic alcohol abuse1,2. Although some cases may be associated with concurrent thiamine deficiency (with its attendant neuropathy), other cases of BD do not appear to be. The mechanism of BD in this setting may be related to the toxic effect of alcohol on peripheral, autonomic and/or central nervous systems2,3.
Binge drinking may also be associated with urinary retention, with spontaneous atraumatic urinary bladder rupture having been reported on several occasions4. Lastly, alcohol withdrawal alone may precipitate urinary retention5.
Unfortunately, many cases of abdominal pain due to urinary retention in the setting of alcohol abuse or withdrawal may be mistakenly attributed to ascites or other causes5. High index of suspicion for BD is essential to minimize its complications.
In our patient, given the low prevalence of benign prostatic hypertrophy in men less than 40 years of age, urinary retention due to alcohol-related BD is more likely.
- Yuan R, Carcciolo VJ, Kulaga M. Chronic abdominal distension secondary to urinary retention in a patient with alcoholism. JAMA 2002;287;318-19.
- Sheremata WA, Sherwin I. Alcoholic myelopathy with spastic urinary bladder. Dis Nerv Syst 1972;33:136-139.
- Mellion M, Gilchrist JM, De La Monte S. Alcohol-related peripheral neuropathy: nutritional, toxic or both? Muscle Nerve 2011;43:309-16.
- Muneer M, Abdelrahman H, El-Menyar A, et al. Spontaneous atraumatic urinary bladder rupture secondary to alcohol intoxication: a case report and review of literature. Am J Case Rep 2015;16:778-81.
- Iga J-I, Taniguchi T, Ohmori T. Acute abdominal distension secondary to urinary retention in a patient after alcohol withdrawal. Alcohol Alcoholism 2005;40:86-87.
Most doctors have received the following page at some point in their career: “Patient having abdominal pain, please come assess.” Carnett’s sign (described by British surgeon J.B. Carnett in 1926) is a physical exam finding that helps differentiate abdominal wall from intra-abdominal sources of pain. Once the tender spot is located, the test is considered positive when the patient’s pain increases upon tensing of the abdominal wall muscles– such as by raising both legs with straight knees or lifting the head and shoulders from the bed. Conversely, if the pain decreases with this maneuver, an intra-abdominal source is more likely1,2.
A positive Carnett’s sign should broaden the differential of abdominal pain to include: hernias, irritation of intercostal nerve roots, rectus sheath hematomas, myofascial pain, anterior cutaneous nerve entrapment (latter discussed in another pearl). In the appropriate clinical setting, local corticosteroids or anesthetic injections, or the application of hot or cold packs may be therapeutic2,3.
- Carnett JB. Intercostal neuralgia as a cause of abdominal pain and tenderness. J Surg Gynecol Obstet 1926; 42:625-632.
- Bundrick JB, Litin SC. Clinical pearls in general internal medicine. Mayo Clin Proceedings 2011;86: 70–74.
- Suleiman S , Johnston DE. The abdominal wall: an overlooked source of pain. Am Fam Physician 2001; 64: 431-8.
Contributed by Brad Lander MD, Mass General Hospital, Boston, MA.
Typically, GI symptoms are more prominent in children with influenza than adults but during the H1N1 epidemic in 2009 (which has subsequently become endemic), up to 26% of hospitalized adults with H1N1 infection had abdominal pain or vomiting and up to 25% had diarrhea (1). In fact, H1N1 virus has been isolated from stool of adult hospitalized patients (2).
Interestingly, the mechanism involved in influenza-mediated intestinal injury may have less to do with direct invasion of the intestinal mucosa by the virus and more to do with immune mediated changes related to alterations in the intestinal microbiota induced by influenza virus infection itself (3)! Who would have thought?
- Writing Committee of the WHO Consultation on Clinical Aspects of Pandemic (H1N1) 2009 influenza. Clinical aspects of pandemic 2009 influenza A (H1N1) virus infection. N Engl J Med 2010;362:1708-19.
- Yoo SJ, Moon SJ, Kuak E-Y, et al. Frequent detection of pandemic (H1N1) 2009 virus in stools of hospitalized patients. J Clin Microbiol 2010; 48:2314-2315.
- Wang J, Li F, Wei H, et al. Respiratory influenza virus infection induces intestinal immune injury via microbiota mediated Th17 cell-dependent inflammation. J Exp Med 2014;211:2397-2410.
In up to 30 percent of patients with chronic abdominal pain, the source of pain appears to be the abdominal wall, not the viscera (1). As the name implies this is a pain syndrome thought to be due to the entrapment of cutaneous branches of an intercostal nerve at the level of the rectus abdominis muscle (1). A third of patients experience pain for >1 year and about 10% for > 5 years before diagnosis of ACNES is made. In about one-half of cases, ACNES begins spontaneously, with the remainder developing after abdominal surgery or pregnancy, or is associated with “sports”, “job “ or “unusual activity” (2). Identification of abdominal wall trigger points and their infiltration with lidocaine may relieve the pain instantaneously and can serve as a diagnostic test (1). Surgical neurectomy may be effective in those with only temporary or partial response to repeated lidocaine injections (1).
1. Boelens OBA, Scheltinga MR, Houterman S, et al. Randomized clinical trial of trigger point infiltration with lidocaine to diagnose anterior cutaneous nerve entrapment syndrome. Br J Surg 2013;100:217-221.
2. Boelens OB, Scheltinga MR, Houterman S, et al. Management of anterior cutaneous nerve entrapment syndrome in a cohort of 139 patients. Management of anterior cutaneous nerve entrapment syndrome in a cohort of 129 patients. Ann Surg 2011;254:1054-1058.