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A 47-year-old man with a necrotic wound after trauma
Digital Journal of Ophthalmology 2021
Volume 27, Number 2
May 17, 2021
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Donald C. Hubbard II, BS | Texas A&M College of Medicine Jacob W. Fleenor, MD | Baylor Scott and White Eye Institute and Texas A&M College of Medicine Maxwell G. Su, MD | Baylor Scott and White Eye Institute and Texas A&M College of Medicine Jonathan H. Tsai, MD | Baylor Scott and White Eye Institute and Texas A&M College of Medicine
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| Diagnosis and Discussion | Mucormycosis is an aggressive, opportunistic fungal infection that most commonly causes pulmonary, sino-orbital tract, gastrointestinal tract, and skin disease.(1)Fungi from multiple genera can be involved, most commonly, Rhizopus, Mucor, Apophysomyces, Absidia, and Cunninghamella. Data suggest that Rhizopus is most frequently isolated in cases of rhino-orbital mucormycosis.(1) Well-established risk factors for development of the disease include diabetic ketoacidosis (DKA) and immunocompromised state. Trauma has also been described in case reports as a risk factor for cutaneous mucormycosis.(2) However, iron overload is one that is less frequently recognized.(3) Experiments have examined the relationship between Rhizopus growth and serum iron–binding capacity. Studies by Artis et al showed that low levels of serum iron did not support the growth of Rhizopus oryzae; however, the addition of excess iron resulted in profuse growth.(4)
Signs of mucormycosis can appear similar to the presentation of necrotizing fasciitis as well as preseptal or orbital cellulitis. This mimicry can complicate the diagnosis and highlights the importance of surgical pathology on initial debridement. On examination, periorbital edema, proptosis, chemosis, visual acuity deficits, and ophthalmoplegia may be noted. In the initial phases of mucormycosis, infected tissue appears erythematous, eventually progressing to a violaceous color and ultimately becoming a black, necrotic eschar.(5) It is associated with a high mortality rate, even with treatment. It has been estimated that even with the combination of surgical debridement and amphotericin B, the mortality rate for mucormycosis exceeds 50%.(5)
Our patient displayed signs of a rapidly progressive, necrotizing infection as evidenced by his physical examination and imaging findings. Based on the extensive facial involvement and acute progression of his disease, we suspected etiologies with a fulminant time course. However, necrotizing fasciitis and orbital cellulitis appeared to be plausible explanations. It was difficult to make a single unifying diagnosis until pathology results returned. His only predisposing risk factors were trauma from the motor vehicle accident contaminated by soil and iron overload, which was most likely secondary to the >30 blood transfusions he received during the treatment of his motor vehicle injury.
Treatment success is dependent on early recognition of symptoms as well as early initiation of medical and surgical therapies. However, identification of early disease may prove difficult, as infected tissue may appear normal.(5) The keystone of treatment is the combination of liposomal amphotericin B and surgical debridement.(1) Additionally, there is anecdotal evidence that adjunctive intraorbital irrigation with amphotericin B may improve treatment outcomes.(6) Proof-of-concept experiments have suggested that iron chelation with deferiprone may be effective in the treatment of mucormycosis in a DKA mouse model.(7) However, the drug was associated with a narrow therapeutic window, and doses above 100 mg/kg proved to be toxic. Of note, deferoxamine, another iron chelator, has been suggested to be a siderophore for several species of fungi and is associated with increased incidence of mucormycosis.(7)
In conclusion, this 47-year-old man with no history of diabetes mellitus or immunocompromised state—both commonly understood risk factors for mucormycosis— developed a rapidly progressive, necrotic facial lesion due to mucormycosis. He received more than 30 blood transfusions, which likely led to an iron-overloaded state. Secondary hemochromatosis appears to be associated with the development of mucormycosis. It would be an inadequately supported claim to assert that iron overload was a direct causative factor for mucor infection or proliferation in this patient; nevertheless, it is plausible that iron overload played an important role in its emergence, given the patient’s many transfusions. This case illustrates the importance of recognizing iron overload as a possible risk factor to consider in mucormycosis and suggests that the differential diagnosis in patients that present with scenarios similar ours be broadened accordingly. | |
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