eMedicine Specialties > Infectious Diseases > HEENT Infections

Rhinocerebral Mucormycosis: Treatment & Medication

Author: William P Baugh, MD, Assistant Clinical Professor of Dermatology, University of California Irvine School of Medicine and Western School of Medicine; Medical Director, Full Spectrum Dermatology; Consulting Staff, Department of Dermatology, St Jude Medical Center
Coauthor(s): Cynthia L Chen, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Contributor Information and Disclosures

Updated: Feb 11, 2009

Treatment

Medical Care

Rhinocerebral mucormycosis (RCM) is treated by (1) reversing underlying immunocompromised states, (2) administering systemic antifungals, and (3) performing urgent surgical debridement. No studies address the appropriate dose or formulation of antifungal therapy; therefore, a wide range of doses and formulations are used until the underlying cause of the immune suppression is under control. Antifungal therapy alone or surgical therapy alone is ineffective.

  • Aggressively control hyperglycemia and acidosis.
  • Discontinue or maximally reduce chemotherapy and immunosuppressive therapy.
  • Promptly initiate antifungal therapy. Amphotericin B is the only reliable systemic antifungal agent approved for the treatment of mucormycosis.
  • Garner and Machin (2008) reported on the use of prophylactic posaconazole (second-generation azole antifungal) during an outbreak of mucormycosis. None of 15 children considered to be at high risk who received the drug developed mucormycosis.18
  • Several studies have reported salvage therapy with posaconazole in patients with zygomycosis refractory or intolerant to other treatments. Whether posaconazole is superior to amphotericin B is still being studied.
  • Granulocyte colony-stimulating factor (GCSF) can be administered to reconstitute host defenses and to enhance leukocytosis.19
  • If disease is limited to the sinus and orbit (ie, sino-orbital), debridement and systemic antifungals combined with local amphotericin irrigation may control the process.
  • Hyperbaric oxygen (HBO) therapy has been used in an attempt to control the infection. Experts suggest that HBO may have fungistatic activity by reducing tissue hypoxia and acidosis. No studies address its efficacy.
  • Dexamethasone has been used to treat brain edema.

Surgical Care

The mainstay of therapy is extensive debridement of all infected and necrotic tissue with drainage of all sinus and abscess fluid collections.

  • Immediately obtain consultation with a surgeon. Conservative attempts to spare tissue may result in retention of the organism and subsequent treatment failure.
  • Intraoperative frozen sections help to determine involved tissues and margins.
  • Treatment may require orbital debridement and exenteration.
  • A delay in surgery may decrease the likelihood of survival in all forms of invasive mucormycosis.
  • Wide excision should ideally occur before CNS invasion.
  • The role of endoscopic sinus surgery is unclear, although it may provide an initial diagnostic role.20

Consultations

  • Infectious diseases specialist
  • Neurosurgeon
  • Ophthalmologist
  • Otolaryngologist

Medication

Although the currently approved azoles are active against the phaeohyphomycoses that cause fungal sinusitis, they have no activity against Mucor molds. Amphotericin B is fungistatic for Mucor molds but is the only reliable systemic antifungal agent. Amphotericin is a highly toxic agent that is administered intravenously in its conventional form or in 1 of 3 new lipid-complex formulations. Amphotericin has also been administered via intracavitary (ie, via catheter into the space), interstitial, and intrathecal routes.21 Reports document the use of nebulized amphotericin B for sinonasal disease. Large doses are required for cure.

Only conventional amphotericin B is approved by the US Food and Drug Administration (FDA) as initial therapy for rhinocerebral mucormycosis (RCM); thus, it is considered the standard therapy for invasive mucormycosis. Lipid formulations are approved if the creatinine level rises to greater than 2.5 mg/dL, if adverse events are severe and persistent, or if disease progresses despite a total dose greater than 500 mg. Experience with the lipid formulations is growing, but no head-to-head studies have been performed. Many experts initiate therapy with a lipid-complex formulation in patients with pre-existing renal impairment. Some experts argue that lipid-formulation amphotericin offers better penetration across the blood-brain barrier and into the sinus.

Use amphotericin at the maximum dose tolerated for this life-threatening infection. Experimental antifungal agents have demonstrated in vitro activity against the Mucor molds and may offer additional treatment options in the future.

The evidence for iron chelators (ie, deferoxamine) as a potential therapeutic intervention has been increasing in animal studies. While deferoxamine is an iron chelator from the perspective of the human host, it actually serves as a siderophore, delivering free iron to Mucor. Animal studies have shown that administration of iron chelators to mice with Rhizopus infection markedly improved survival and may be just as effective as liposomal amphotericin B.

Antifungal agents

Their mechanism of action may involve inhibition of fungal cell membrane formation and impairing the integrity of fungal cell membrane.


Amphotericin B (Fungizone)

Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism.

Adult

0.25-1 mg IV test dose infused over 30-60 min; observe for severe fever, chills, hypotension
1-1.5 mg/kg/d IV infusion over 4-6 h

Pediatric

0.5-1 mg/kg/d IV recommended test dose infusion over 4-6 h
Alternatively: 0.25 mg/kg IV on day 1, 0.5 mg/kg IV on day 2, then 1 mg/kg/d IV

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor renal function, serum electrolytes (eg, magnesium, potassium), liver function, CBC, and hemoglobin concentrations; resume therapy at the lowest level (eg, 0.25 mg/kg) when therapy is interrupted for more than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in neutropenic patients receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion)


Amphotericin B lipid complex (ABLC, Abelcet)

Amphotericin B in phospholipid complexed form. Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism.

Adult

5 mg/kg/d IV infusion over 2 h

Pediatric

Administer as in adults

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed


Amphotericin B (AmBisome)

A lipid preparation consisting of amphotericin B within unilamellar liposomes. Delivers higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity.
Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism.

Adult

5-7.5 mg/kg/d IV infused over 2 h

Pediatric

5 mg/kg/d IV infused over 2 h

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed


Amphotericin B colloidal dispersion (Amphocil, ABCD)

A lipid preparation consisting of amphotericin B attached to lipid discoid structures.
Polyene antibiotic with poor oral availability. Produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing leakage of intracellular components and fungal cell death. Toxicity to human cells may occur via this same mechanism.

Adult

2-7.5 mg/kg/d IV infused over 2 h

Pediatric

Administer as in adults

Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Acute infusional toxicities per conventional amphotericin B occur at a somewhat lower rate; nephrotoxicity is less frequent and less severe, but can still occur; monitoring of electrolytes, BUN, and creatinine is still required, and potassium and magnesium should be replaced as needed


Fluconazole (Diflucan)

Bis-triazole antifungal agent. Fluconazole binds to the fungal p450 enzymes and stops the cells that make ergosterol, the main component of the cell wall.

Adult

Individualize; 200 mg PO on day 1, then 100 mg/d PO for at least 2 wk

Pediatric

Individualize; 6 mg/kg on day 1, then 3 mg/kg/d for at least 3 wk; treat for at least 2 wk after symptoms resolve; max 12 mg/kg/d

Fluconazole may increase the concentration and enhance the effects of warfarin, antidiabetic sulfonylurea medication (tolbutamide, glibenclamide, gliclazide, glipizide), phenytoin, theophylline, ciclosporin, and celecoxib

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Side effects include vomiting, diarrhea, abdominal pain, and skin rashes; may cause hepatoxicity

More on Rhinocerebral Mucormycosis

Overview: Rhinocerebral Mucormycosis
Differential Diagnoses & Workup: Rhinocerebral Mucormycosis
Treatment & Medication: Rhinocerebral Mucormycosis
Follow-up: Rhinocerebral Mucormycosis
Multimedia: Rhinocerebral Mucormycosis
References
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Further Reading

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Keywords

rhinocerebral mucormycosis, RCM, phycomycosis, zygomycosis, rhinoorbital mucormycosis, rhino-orbital mucormycosis, Mucorales, Rhizopus, Absidia, Mucor, Rhizomucor, Saksenaea, Apophysomyces

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Contributor Information and Disclosures

Author

William P Baugh, MD, Assistant Clinical Professor of Dermatology, University of California Irvine School of Medicine and Western School of Medicine; Medical Director, Full Spectrum Dermatology; Consulting Staff, Department of Dermatology, St Jude Medical Center
William P Baugh, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Laser Medicine and Surgery, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia L Chen, Western University of Health Sciences College of Osteopathic Medicine of the Pacific
Disclosure: Nothing to disclose.

Medical Editor

John M Leedom, MD, Professor of Medicine, Keck School of Medicine, University of Southern California; Chief, Division of Infectious Diseases, Department of Internal Medicine, Los Angeles County, University of Southern California Medical Center
John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Thomas M Kerkering, MD, Chief of Infectious Diseases, Virginia Tech, Carilion School of Medicine, Roanoke, Virginia
Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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