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Reply: Primary Intranasal Lining Injury Cause, Deformities, and Treatment Plan

Menick, Frederick J. M.D.

Plastic and Reconstructive Surgery: May 2015 - Volume 135 - Issue 5 - p 925e
doi: 10.1097/PRS.0000000000001178
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St. Joseph’s Hospital, Tucson, Ariz.

Correspondence to Dr. Menick, 1102 North El Dorado Place, Tucson, Ariz. 85715, drmenick@drmenick.com

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Sir:

Leishmaniasis is a parasitic disease transferred by the bite of a sandfly. Multiple species of Leishmania exist in the tropics and subtropics worldwide. Leishmaniasis presents as a cutaneous, mucocutaneous, or visceral infection of the reticuloendothelial system. Parasites spread from skin lesions to the naso-oropharyngeal mucosa, often months or years after the cutaneous lesions appear, causing bleeding and ulceration and, ultimately, destruction of the nasopharyngeal mucosa.

The disease and the specific parasite species are diagnosed by culture and molecular or biochemical testing. Serologic assays cannot differentiate between active and quiescent infection. The diagnosis and treatment are individualized and require expert consultation. Treatment depends on the health of the host, the geographic location where the infection was acquired, the specific Leishmania species, and the type of infection. As emphasized by Joob and Wiwanitkit, medical control of this parasitic disease can be difficult. It has been classified as a neglected tropical disease by the Centers for Disease Control and Prevention. Multiple research studies are underway.

The article entitled “Primary Intranasal Lining Injury: Cause, Deformities, and Treatment Plan” clarifies the process of destruction caused by primary lining injury and identifies the characteristic, progressive deformities. The injury is determined by the site, depth, and extent of injury, and the consequence of scar contraction, regardless of cause. Obviously, the primary disease must be controlled, by means of avoidance of cocaine use, cure of intranasal cancer, modulation of immune disease, and elimination of infection. Although cause may vary, the pathophysiologic injury is similar. The deformity is attributable to progressive lining loss, which leads to the destruction of cartilaginous support and, later, may progress to the covering skin. Although most often conceived of as a loss of septal support with a secondary saddle collapse, secondary healing and scar contracture are the primary causes of deformity. The lining injury must be addressed by excision of scar and recreation of the defect. Then, the missing lining, according to the site and dimensions of the defect, must be replaced to correct the specific deformity. Only then can support or external skin deficiencies be addressed.

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DISCLOSURE

The author has no financial interest to declare in relation to the content of this communication.

Frederick J. Menick, M.D.

St. Joseph’s Hospital

Tucson, Ariz.

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