Article, Hematology

Definition of cyanosis

Correspondence

Definition of cyanosis

To the Editor,

I read with interest the article by Weng et al [1]. The authors cite that cyanosis occurs because of more than 5 g of reduced hemoglobin or methomoglobin in the arterial blood. Such a statement is incorrect. Cyanosis presents when reduced Hemoglobin levels are greater than 5 g/dL of capillary blood. This is equal to 3 g of deoxyhemoglobin per deciliter of arterial blood [2,3].

Weekitt Kittisupamongkol MD

Hua Chiew Hospital Bangkok 10100, Thailand

E-mail address: [email protected]

doi:10.1016/j.ajem.2008.12.012

References

  1. Weng YM, Chang YC, Chiu TF, Weng CS. Tet spell in an adult. Am J Emerg Med 2009;27:130.e3-e5.
  2. Lam AM. A perfect storm. N Engl J Med 2006;354:977-8 [author reply

977-8].

  1. Martin L, Khalil H. How much reduced hemoglobin is necessary to generate Central cyanosis? Chest 1990;97:182-5.

Rifampin-containing regimens for community-associated skin infection: a hazard without known benefit

To the Editor,

Skin infections are a common reason for physician and emergency department (ED) visits. Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is now the most common known etiology of skin and soft tissue infections in most places in the United States [1]. The rise of CA-MRSA infections has resulted in an increase of non-?- lactam antibiotic therapy for skin infection. Commonly, these

non-?-lactam therapies are combined with rifampin [2,3], based on the assumption that synergistic therapy with rifampin results in improved clinical efficacy. In our experience, rifampin is commonly prescribed as adjunctive therapy for documented or presumed CA-MRSA skin infections. Herein, we described a case of skin infection treated with oral rifampin in combination an oral non-?- lactam antibiotic active against MRSA who had an adverse event to rifampin-containing therapy.

A previously healthy 41-year-old woman with a history of furuncles but no history of MRSA infection presented with sudden-onset left axillary tenderness, a marble-sized mass, and low-grade fever. She was seen at a community hospital and treated with dicloxacillin. She had no response to therapy and the cellulitis increased in size over 6 hours, prompting her to go to another local ED where an emergency department (ED) physician attempted to aspirate the lesion unsuccessfully. She was given a dose of intravenous piperacillin-tazobactam and discharged on oral amoxicillin- clavulanate.

Her symptoms continued to worsen, and she presented to a third hospital the following evening (day 2). The left axillary lesion was now 5 cm in diameter, painful, and fluctuant with 2 cm surrounding erythema, warmth, and induration; and the patient had chills. On examination, she was ill-appearing and febrile to 102?F. Fine Needle aspiration was performed and Gram stain demonstrated gram-positive cocci in clusters; blood cultures were obtained. She was treated with vancomycin 1 g intravenously and given a prescription for oral trimethoprim-sulfamethoxazole (TMP- SMX) and rifampin. The following morning she developed hives and headache promptly after taking the TMP-SMX and rifampin. She returned to the hospital ED where she was diagnosed with urticaria, received another dose of vanco- mycin, and was discharged on oral clindamycin, diphenhy- dramine, and acetaminophen. Cultures of the wound returned positive for MRSA that was susceptible to clindamycin (D-test negative), TMP-SMX, rifampin, and vancomycin. Over the next 5 days, she required 2 additional incision and drainage procedures but clinically improved. The rash resolved slowly over 5 days. The patient was unable to return to her full work schedule for more than 1 week. She completed a 2-week course of oral

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