Hemorrhagic Cystitis Medication

Updated: Dec 18, 2018
  • Author: Joseph Basler, MD, PhD; Chief Editor: Edward David Kim, MD, FACS  more...
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Medication

Medication Summary

Persistent hematuria can be treated with bladder irrigation, using carboprost, 1-2% alum, or silver nitrate. If hemorrhagic cystitis does not resolve despite clot evacuation and irrigation, a variety of agents may be instilled into the bladder to promote local hemostasis. Systemic agents may also prove useful. In patients undergoing chemotherapy with cyclophosphamide, which is known to cause hemorrhagic cystitis, use of antidotes may have prophylactic benefit. Mesna binds to the urotoxic cyclophosphamide metabolite acrolein, creating stable thioester compounds with no bladder toxicity.

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Astringents

Class Summary

Various intravesical agents are used to treat hemorrhagic cystitis. Ongoing assessment of treatment effectiveness is essential for a successful patient outcome. Changing to a different irrigation agent may be necessary.

Silver nitrate

Silver nitrate is administered intravesically because of its caustic, antiseptic, and astringent qualities. Mixed results have been observed.

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Prostaglandins, Endocrine

Class Summary

Prostaglandins are useful for their cytoprotective properties.

Carboprost (Hemabate)

Carboprost is a prostaglandin that elicits cytoprotective, anti-inflammatory, and vasoconstrictive properties and produces no coagulum.

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Urologics, Other

Class Summary

Antidotes are used to manage poisoning and overdose, prevent toxic effects, and treat metabolic disorders in which toxic substances accrue. Mechanisms of action vary and include antagonism, toxin transformation, altered metabolism, chelation, and interactions with directed antibodies.

Mesna (Mesnex)

Mesna is also known as 2-mercaptoethane sulfonate. In the kidney, mesna disulfide is reduced to free mesna, which has thiol groups that react with acrolein, the metabolite of ifosfamide and cyclophosphamide considered responsible for urotoxicity. Mesna inactivates acrolein and prevents urothelial toxicity without affecting cytostatic activity. It also directly reacts with 4-hydroxy metabolites, inhibiting breakdown and release of acrolein.

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