Metronidazole;

My patient has painful pustules and nodules in her axillae.  How can I distinguish hidradenitis suppurativa (HS) from folliculitis or recurrent skin abscesses?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

A key differentiating factor between hidradenitis suppurativa (HS) and more common conditions such as folliculitis or recurrent abscesses is the location and recurrence pattern of the lesions. HS is clinically diagnosed based on the following typical lesion characteristics:

  • Morphology: open comedones, pustules, painful nodules, abscesses, sinus tracks and scarring; 
  • Distribution: intertriginous or apocrine gland-rich areas, such as the axillae, inframammary folds, lower abdomen/waist, gluteal cleft, groin and inner thighs; and
  • Frequency: recurrent lesions in the same locations, with at least two or more episodes in six months1,2

In contrast, folliculitis involves inflammation of the hair follicle and may present with pustules or boils; however, lesions are superficial, occur anywhere hair is present, and are not complicated by deep nodules, sinus tracks or scarring.2

Although recurrent abscesses may mimic HS, they are typically unilateral or asymmetric, fluctuant and caused by bacterial infection with positive wound cultures. In contrast, HS is frequently a symmetric, sterile inflammatory condition unless secondarily infected. Additionally, abscesses generally respond to incision and drainage and antibiotics and do not result in sinus tracks or scarring.2

Once you suspect HS, your management may be guided by its severity using the following disease stages (Hurley staging).

  • Mild disease (Hurley stage I): localized lesions without sinus tracks or scarring. Treat with antimicrobial washes (chlorhexidine) and topical antibiotics (clindamycin).3
  • Moderate disease (Hurley stage II): typical lesions in multiple locations with or without sinus tracks and scarring. Treat with antimicrobial washes, topical antibiotics, and systemic antibiotics (tetracyclines or clindamycin). Consider adding rifampin, metronidazole, or moxifloxacin in refractory cases.3
  • Severe disease (Hurley stage III): diffuse painful lesions with extensive sinus tracks and scarring. Requires dermatology referral for consideration of biologics (eg, adalimumab), laser, parenteral antibiotics and/or surgical interventions.3

Across all stages of severity, patients should be counseled on smoking cessation, weight loss, diet modification and appropriate pain management.4 Acute flares may be treated with warm compresses, tetracyclines, and intralesional steroids.3 Incision and drainage is reserved for severe, painful lesions as routine drainage could worsen tunneling.5

Bonus Pearl: Did you know the average diagnosis delay for HS is up to 10 years?2 Primary care physicians have a unique position in early recognition and treatment of this debilitating disease.

Contributed by Taylor Lynch, MD, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Wieczorek M, and Walecka I. Hidradenitis suppurativa – known and unknown disease. Reumatologia 2016: 56: 337-339. doi:10.5114/reum.2018.80709. https://pubmed.ncbi.nlm.nih.gov/30647478/.
  2. Snyder, CL, Chen XL, Porter ML. Obstacles to early diagnosis and treatment of hidradenitis suppurativa: Current Perspectives on Improving Clinical Management. Clin Cosm Invest Derm 2023;16:1833-1841. doi:10.2147/CCID.S301794. https://pmc.ncbi.nlm.nih.gov/articles/PMC10361090/.
  3. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations: Part II: Topical, intralesional, and systemic medical management. J Am Acad Derm 2019;81:91-101. doi:10.1016/j.jaad.2019.02.068. https://pubmed.ncbi.nlm.nih.gov/30872149/.
  4. Hermak S, and Lev-Tov H. Integrative approaches in the management of hidradenitis suppurativa. J Am Acad Derm 2024;91: S42-S45. doi:10.1016/j.jaad.2024.09.016. https://pubmed.ncbi.nlm.nih.gov/39626999/.
  5. Chawla S, Toale C, Morris M, et al. Surgical management of hidradenitis suppurativa: A narrative review. J Clin Aesth Derm 2022;15: 35-41. https://pubmed.ncbi.nlm.nih.gov/35309275/.

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient has painful pustules and nodules in her axillae.  How can I distinguish hidradenitis suppurativa (HS) from folliculitis or recurrent skin abscesses?

Is oral metronidazole (Flagyl®) effective in reducing the risk of recurrent Clostridium difficile infection (CDI)?

FA Manian MD, MPH, , Leave a comment

To date only 1 study has attempted to evaluate metronidazole’s role in preventing CDI1. This work, however,  has significant shortcomings including its retrospective nature, definition of metronidazole prophylaxis as any dose for reasons other than CDI starting 1-3 days before initiation of the primary antibiotic, undefined duration, less comorbidities in the metronidazole group, and surveillance period for CDI limited to only 7 days following initiation of the primary antibiotic. For these reasons, it is difficult to interpret the results of this study whose conclusion was that metronidazole may protective against CDI2.

In fact, there are several reasons why metronidazole prophylaxis may not be effective in CDI.   First, due to its very high bioavailability, concentrations of metronidazole in formed stool are often undetectable2,3 . Consequently, “preventive” metronidazole in patients at risk of CDI but with formed stools would not be expected to achieve high enough concentrations in the colon to be effective.  In additions, metronidazole itself may be associated with CDI4 and  vancomycin-resistant enterococci5,  and has several potential drug-interactions and adverse effects6 .

References

  1. Rodriguez S, Hernandez MB, Tarchini G, et al. Risk of Clostridium difficile infection in hospitalized patients receiving metronidazole for a non-C difficile infection. Clin Gastroenterol Hepatol 2014;12:1856-61. https://www.ncbi.nlm.nih.gov/pubmed/24681079
  2. Dupont HL. Chemoprophylaxis of Clostridium difficile infections in high-risk hospitalized patients. Clin Gastroenterol Hepatol 2014;12: 1862-63. https://www.ncbi.nlm.nih.gov/labs/articles/24768812/
  3. Bolton RP, Culshaw MA. Faecal metronidazole concentrations during oral and intravenous therapy for antibiotic associated colitis due to Clostridium difficile. Gut 1986;27:1169-1172. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433873/pdf/gut00370-0065.pdf
  4. Daly JJ, Chowdary KV. Pseudomembranous colitis secondary to metronidazole. Dig Dis Sci 1983;28:573-4.
  5.  Carmeli Y, Eliopoulos GM, Samore MH. Antecedent treatment with different antibiotic agents as a risk factor for vancomycin-resistant enterococcus. Emerg Infect Dis 2002;8:802-807. https://wwwnc.cdc.gov/eid/article/8/8/pdfs/01-0418.pdf
  6. Salvatore M, Meyers BR. Metronidazole. In Mandel, Douglas, Bennett’s Principles and Practice of Infectious Diseases-7th Ed. p. 419-426. 2010, Churchill Livingstone, Philadelphia.

 

 

Is oral metronidazole (Flagyl®) effective in reducing the risk of recurrent Clostridium difficile infection (CDI)?

Is there anyway to predict a significant rise in INR from antibiotic use in patients who are also on warfarin?

FA Manian MD, MPH, , , , , , , , , , , , , , 1 Comment

Not really!  Many of the commonly used antibiotics have the potential for increasing the risk of major bleeding through disruption of intestinal flora that synthesize vitamin K-2 with or without interference with the metabolism of warfarin through cytochrome p450 isozymes inhibition.

Although there may be some inconsistencies in the reports, generally quinolones (e.g. ciprofloxacin, levofloxacin), sulonamides (e.g. trimethoprim-sulfamethoxazole), macrolides  (e.g. azithromycin), and azole antifungals (e.g. fluconazole) are thought to carry the highest risk of warfarin toxicity, while amoxacillin and cephalexin may be associated with a more modest risk (1,2).  Metronidazole can also be a culprit (2).

References

1. Baillargeon J, Holmes HM, Lin Y, et al. Concurrent use of warfarin and antibiotics and the risk of bleeding in older adults. Am J Med. 2012 February ; 125(2): 183–189. https://www.ncbi.nlm.nih.gov/pubmed/22269622

2. Juurlink DN. Drug interactions with warfarin: what every physician should know. CMAJ, 2007;177: 369-371. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1942100/pdf/20070814s00018p369.pdf

Is there anyway to predict a significant rise in INR from antibiotic use in patients who are also on warfarin?