Updated: Aug 5, 2009
Mesenteric lymphadenitis refers to inflammation of the mesenteric lymph nodes. This process may be acute or chronic, depending on the causative agent. It causes a clinical presentation that is often difficult to differentiate from acute appendicitis.
Microbial agents are thought to gain access to the lymph nodes via the intestinal lymphatics. Organisms subsequently multiply and, depending on the virulence of the invading pathogen, elicit varying degrees of inflammation and, occasionally, suppuration.
Grossly, the lymph nodes are enlarged and often soft. The adjourning mesentery may be edematous, with or without exudates. If a contiguous primary source of infection (eg, the appendix) is present, evidence of inflammation is often apparent.
Microscopically, the lymph nodes show nonspecific hyperplasia and, in suppurative infection, necrosis with numerous pus cells.
The true incidence of this disease is not known, because it can be easily missed or mistaken for other diagnoses. The condition is generally thought to be common. Up to 20% of patients undergoing appendectomy have been found to have nonspecific mesenteric adenitis.
Frequency is similar to that of the United States. Yersinia enterocolitica infection has a geographic variation. This infection is most common in the temperate countries of Europe, North America, and Australia; it has been particularly noted in Eastern Europe.
Mesenteric lymphadenitis generally is a benign disease, but patients with sepsis may have a fatal outcome.
The condition affects males and females equally. Yersinia infection is more common in boys than in girls.
Onset and progression may be insidious or sometimes dramatic. Clinical features of associated organ involvement, such as enterocolitis or ileitis in Yersinia infection, may be present. Clinical presentations include the following:
No set of physical findings is pathognomonic of mesenteric lymphadenitis.
| Appendicitis | Pyelonephritis, Acute |
| Benign Neoplasm of the Small Intestine | Salpingitis |
| Cholecystitis | Urinary Tract Infection, Females |
| Chronic Mesenteric Ischemia | Urinary Tract Infection, Males |
| Ectopic Pregnancy | |
| Inflammatory Bowel Disease |
Meckel diverticulitis
Intestinal duplication
Regional enteritis
Intussusception
Intestinal lymphoma
Other causes of acute abdomen (eg, porphyria, sickle cell vasoocclusive crises, cecal tumor, Familial Mediterranean Fever)
The objective of medical management is to quickly identify patients who require surgical intervention (ie, for appendicitis) and to refer appropriately. Empiric, broad-spectrum antibiotics may be used in moderately to severely ill patients and should cover Yersinia strains, commonly causative in mesenteric adenitis. General supportive care includes hydration and pain medication after excluding acute surgical abdomen. Patients with mild, uncomplicated presentations do not require antibiotics, and supportive care generally suffices.
Make early contact with a general surgeon while evaluating the patient to exclude etiologies that require urgent surgery.
No particular diet is recommended. Temporary withholding of oral intake may be necessary while nausea and vomiting resolve and initially until a definitive diagnosis is confirmed.
No restriction of activity is required.
Antibiotics are often started empirically in moderately to severely ill patients, using broad-spectrum antibiotics intended to cover the commonly associated pathogens. Antibiotic treatment should then be adjusted based on the sensitivity of the isolated pathogen. Treatment duration is variable based on the cause and severity of illness. For uncomplicated cases, antibiotic treatment is not necessary.
When indicated, empiric antimicrobial therapy must be comprehensive and should cover the likely pathogens in the context of the clinical setting. Given the predominance of Y enterocolitica, initial antibiotic selection from trimethoprim-sulfamethoxazole (TMP-SMX), third-generation cephalosporins, fluoroquinolones, aminoglycosides, and doxycycline should be considered. These agents provide broad coverage for enteric pathogens.
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Exerts a bactericidal effect by inhibiting protein synthesis. Used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis).
Loading dose: 15 mg/kg or 1 g for 70-kg adult IV over 1 h
Maintenance dose (6h later): 7.5 mg/kg or 500-mg infusion for 70-kg adult IV over 1 h q6-8h; not to exceed 4 g/d
Administer as in adults, using body weight
Toxicity may be increased by cimetidine; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
Lincosamide used for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, thus causing cessation of RNA-dependent protein synthesis.
150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d or 600-1200 mg/d IV/IM divided q6-8h, depending on degree of infection
8-20 mg/kg/d PO as hydrochloride and 8-25 mg/kg/d as palmitate divided tid/qid or 20-40 mg/kg/d IV/IM divided tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity, regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis
B - Usually safe but benefits must outweigh the risks.
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis
Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.
250-500 mg PO q6h
500 mg to 1.5 g IM q4-6h
500 mg to 3 g IV q4-6h; not to exceed 12 g/d
50-100 mg/kg/d PO divided q4-6h or 100-400 mg/kg/d IV/IM divided q4-6h
Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
500 mg PO q8h; not to exceed 3 g/d
20-50 mg/kg/d PO divided q8h
Reduces the efficacy of oral contraceptives; aspirin and probenecid increase concentration
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Caution advised in patients with renal disease and seizure disorders
Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Trovafloxacin (Trovan) overcomes many of these limitations. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.
250-500 mg PO bid or 200-400 mg IV q12h
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Safety for use during pregnancy has not been established.
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity.
Base initial dose on severity of infection and administer in equally divided doses; dose may range from 250-500 mg IV q6h; not to exceed 3-4 g/d; alternatively, 500-750 mg IM (or intra-abdominally) q12h
<12 years: Not established; 15-25 mg/kg/dose IV q6h suggested for > 3 mo
Fully susceptible organisms: 15-25 mg/kg/dose IV q6h suggested for > 3 mo; not to exceed 2 g/d
Moderately susceptible organisms: 15-25 mg/kg/dose IV q6h suggested for > 3 mo; not to exceed 4 g/d
Coadministration with cyclosporine may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal insufficiency; avoid use in children <12 years
Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.
1-2 g IV q6-8h; in severe infections 1-2 g IV q4h
Infants and children: 80-160 mg/kg/d IV divided q4-6h; higher doses for severe or serious infections; not to exceed 12 g/d
Probenecid may increase effects of; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis
Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive bacteria, most gram-negative bacteria, and most anaerobes.
3.1 g IV q4-6h; infuse over 30 min
75 mg/kg IV q6h
Tetracyclines may decrease effects of ticarcillin; high concentrations of ticarcillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels
Documented hypersensitivity; do not treat severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis with oral penicillin during acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT during therapy; exercise caution in patients diagnosed with hepatic insufficiencies; perform urinalysis and BUN/creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
Drug combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
<3 months: Not established
3 months to 12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adult; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
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mesenteric lymphadenitis, mesenteric adenitis, mesenteric lymph nodes, intestinal lymphatics, Yersinia enterocolitica infection, peripheral lymphadenopathy, infectious Epstein-Barr virus, EBV, acute human immunodeficiency virus, HIV, catscratch disease, CSD, acute appendicitis
Jennifer Lynn Bonheur, MD, Attending Physician, Division of Gastroenterology, Lenox Hill Hospital
Jennifer Lynn Bonheur, MD is a member of the following medical societies: American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, New York Academy of Sciences, New York Society for Gastrointestinal Endoscopy, and Sigma Xi
Disclosure: Nothing to disclose.
Mukul Arya, MD, Associate Professor of Internal Medicine, Assistant Director of Therapeutic Endoscopy, Department of Gastroenterology and Internal Medicine, Wyckoff Heights Medical Center/Weill Medical College
Mukul Arya, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Oluyinka S Adediji, MD, Consulting Staff, Department of Adult and General Medicine, Health Services Incorporated, Montgomery, Alabama
Oluyinka S Adediji, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.
Norvin Perez, MD, Clinical Assistant Professor of Emergency Medicine, Albert Einstein College of Medicine; Consulting Staff, Department of Emergency Medicine, Montefiore Medical Center
Norvin Perez, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association
Disclosure: Nothing to disclose.
Vivek V Gumaste, MD, Associate Professor of Medicine, Mt Sinai School of Medicine; Adjunct Clinical Assistant, Mt Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center
Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology and American Gastroenterological Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Douglas M Heuman, MD, FACP, FACG, AGAF, Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
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