Proctitis in Emergency Medicine Medication

  • Author: Lisandro Irizarry, MD, MPH, FAAEM; Chief Editor: Robert E O'Connor, MD, MPH   more...
 
Updated: Mar 30, 2012
 

Medication Summary

Drug therapy consists of antibiotics, antivirals, corticosteroids, and GI agents.

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Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Metronidazole (Flagyl)

 

Active against various anaerobic bacteria and protozoa. Appears to be absorbed into cells. Intermediate metabolized compounds are formed and bind DNA and inhibit protein synthesis, causing cell death. Antimicrobial effect may be due to production of free radicals.

Indicated for invasive E histolytic infections.

Vancomycin (Vancocin)

 

Has excellent in vitro activity against C difficile. Kills organism by inhibiting cell wall synthesis. Significant luminal levels after PO vancomycin can be obtained because it is poorly absorbed from the GI tract. Major disadvantage is cost. PO vancomycin is relatively expensive, with a wholesale cost of approximately $150 for a 10-d supply. Because of the cost and the concern over the emergence of vancomycin-resistant enterococci strains, its use should be reserved for patients who cannot tolerate metronidazole, patients who do not respond to metronidazole, pregnant patients, and patients < 10 y. Also preferred for severe cases and in patients who are high risk. Unlike IV metronidazole, IV vancomycin is not excreted into the GI lumen; therefore, delivering effective doses by this route is difficult.

Ciprofloxacin (Cipro)

 

Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Usually administered on empiric basis in patients with severe colitis in addition to steroids. Also used for the treatment of pouchitis after colectomy and ileo-anal anastomosis.

Ceftriaxone (Rocephin)

 

Used because of an increasing prevalence of penicillinase producing N gonorrhoeae. It inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, causing bacterial growth inhibition.

Doxycycline (Doryx, Bio-Tab, Vibramycin)

 

Required with ceftriaxone for the treatment of gonorrheal proctitis. Inhibits protein synthesis and, thus, bacterial growth by binding with the 30S and possibly the 50S ribosomal subunits of susceptible bacteria.

Penicillin G benzathine (Bicillin L-A)

 

A bactericidal used in the treatment of rectal syphilis. Interferes with bacterial cell wall synthesis during active multiplication, inhibiting bacterial growth.

Tetracycline (Sumycin)

 

Treats susceptible bacterial infections of both gram-positive and gram-negative organisms as well as infections caused by Mycoplasma, Chlamydia, and Rickettsia species. Inhibits bacterial protein synthesis and, thus, bacterial growth by binding with 30S and possibly 50S ribosomal subunit(s) of susceptible bacteria.

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Rectal anti-inflammatory agents

Class Summary

These agents decrease inflammation associated with proctitis, perhaps by inhibiting prostaglandin synthesis.

Sulfasalazine (Azulfidine)

 

Useful in the management of ulcerative colitis; acts locally in the colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis.

Mesalamine (Rowasa, Asacol, Canasa, Pentasa)

 

Used for treatment of mildly to moderately active ulcerative colitis. The usual course of therapy in adults is 3-6 wk. Some patients may need concurrent oral and rectal therapy.

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Antivirals

Class Summary

These agents are used for the treatment of herpes-related proctitis. They inhibit viral replication by competing with deoxyguanosine triphosphate for viral DNA polymerase.

Acyclovir (Zovirax)

 

Reduces duration of symptomatic lesions. Indicated for patients who present within 48 h of experiencing rash. Patients taking acyclovir experience less pain and faster resolution of cutaneous lesions.

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immunity to diverse stimuli.

Dexamethasone (AK-Dex, Alba-Dex, Baldex, Decadron, Dexone)

 

Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV regimen to a PO regimen in a 1:1 ratio.

Prednisolone (Articulose-50, Delta-Cortef, PediaPred)

 

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisone (Sterapred)

 

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Chemoprotective agent

Class Summary

These agents reduce the cumulative renal toxicity associated with the repeated administration of chemotherapy agents like cisplatin.

Amifostine (Ethyol)

 

Prodrug that is dephosphorylated by alkaline phosphatase in tissues to a pharmacologically-active free thiol metabolite. The free thiol is available to bind to, and detoxify, reactive metabolites of cisplatin; and can also act as a scavenger of free radicals that may be generated (by cisplatin or radiation therapy) in tissues.

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Urinary analgesics

Class Summary

Agents that serve as buffers and protect the tissues from chemotherapeutic agents can be used.

Pentosan polysulfate sodium (Elmiron)

 

Response rate is 71-100%, and recurrence rate is 23%. Protects transitional epithelium by restoring the bladder glycosaminoglycan layer.

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Contributor Information and Disclosures
Author

Lisandro Irizarry, MD, MPH, FAAEM  Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine

Lisandro Irizarry, MD, MPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Ibis Yarde, MD  Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael S Beeson, MD, MBA, FACEP  Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eugene Hardin, MD, FAAEM, FACEP  Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH  Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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