Updated: Aug 11, 2009
Paronychia is a soft tissue infection around a fingernail. Paronychia occurs in 2 forms: acute and chronic. The etiology, infectious agent, and treatment are usually different for each form, and the 2 forms are often considered separate entities.
Mechanism
Paronychia, whether acute or chronic, results from a breakdown of the protective barrier between the nail and the nail fold. The entry of organisms into the moist nail crevice results in the bacterial or fungal (yeast or mold) colonization of the area.
Anatomy
The anatomy of the nail complex is shown in Media File 1. The nail is longitudinally flanked by 2 lateral folds or perionychium. Proximally, it is covered by the eponychium. Distal to the perionychium, the region immediately beneath the free edge of the nail is the hyponychium. The hyponychium serves as a tough physical barrier that resists bacterial infection.
The nail or nail plate lies immediately on top of the nail bed, which consists of 2 portions involved in the production, migration, and maintenance of the nail. The proximal portion, called the germinal matrix, contains active cells that are responsible for generating new nail. Damage to the germinal matrix results in malformed nails. The distal portion, the sterile matrix, adds thickness, bulk, and strength to the nail. The white crescent-shaped opacity at the proximal end of the nail is the lunula, which is the visible portion of the germinal matrix. The whiteness of the lunula is due to the poor vascularity of the germinal matrix. The nail arises from a mild proximal depression called the nail fold. The nail divides the nail fold into 2 components: the dorsal roof and the ventral floor, both of which contain germinal matrices. The skin overlying the nail fold is called the nail wall.
The nail bed receives its blood supply from the 2 terminal branches of the volar digital artery. A fine network in the proximal nail bed and in the skin proximal to the nail fold of the finger provides venous drainage. Lymphatic drainage follows a course similar to that of the venous network. The lymphatic network is dense in the nail bed, especially in the hyponychium. Innervation is derived from the trifurcation of the dorsal branch of the volar digital nerve. One branch goes to the nail fold, one to the pulp, and one to the distal tip of the finger.
Paronychia is the most commonly encountered hand infection, representing approximately 35% of all infections of the hand. Susceptible people include those whose occupations require them to have their hands in prolonged contact with water; such persons include bartenders, florists, bakers, and homemakers. In addition, individuals who are immunocompromised, such as those with HIV infection or those undergoing steroid therapy, are predisposed to paronychia.
The motion of the affected finger may be limited in acute cases.
No racial predilection is reported.
Paronychia is more common in women than in men, with a female-to-male ratio of 3:1.
Paronychia may occur in patients of all ages.
The patient's history is crucial in determining the possibility of more serious underlying systemic conditions that may predispose the patient to paronychia. These underlying conditions may include diabetes, obesity, hyperhidrosis, immunologic defects, polyendocrinopathy, and drug-induced immunosuppression.
| Candidiasis, Chronic Mucocutaneous | Herpes Simplex |
| Candidiasis, Cutaneous | Nail Cosmetics |
| Candidiasis, Mucosal | Onycholysis |
| Cellulitis | Onychomycosis |
| Contact Dermatitis, Allergic | Pemphigus Vulgaris |
| Contact Dermatitis, Irritant | Squamous Cell Carcinoma |
| Cutaneous Manifestations of HIV Disease |
Herpetic whitlow is a viral infection of the pulp of the fingertip and the perionychium that can often be confused with the more common acute bacterial paronychia (see Herpetic Whitlow). Clear vesicles that are grouped on an erythematous base are characteristic of herpetic whitlow. Herpes simplex virus 1 causes approximately 60% of cases of herpetic whitlow, and herpes simplex virus 2 causes the remaining 40% of cases.
Malignancies, such as melanoma and squamous cell carcinoma, or lesions, such as chancres, granulomas, warts, or cysts, can occasionally mimic a paronychia.1
The treatment of choice depends on the extent of the infection. If diagnosed early, acute paronychia without obvious abscess can be treated nonsurgically. If an abscess has developed, incision and drainage must be performed. Surgical debridement may be required if fulminant infection is present.
Herpetic whitlow and paronychia must be distinguished because the treatments are drastically different. Misdiagnosis and mistreatment may do more harm than good. Once herpetic whitlow is ruled out, one must determine whether the paronychia is acute or chronic and then treat it accordingly.2
If paronychia does not resolve despite best medical efforts, surgical intervention may be indicated. Also, if an abscess has developed, incision and drainage must be performed. Surgical debridement may be required if fulminant infection is present.
No change in diet is required.
Patients with either acute or chronic paronychia should keep affected areas clean and dry, and they should avoid any further trauma or manipulation of the nail.
The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.
Therapy must cover all likely pathogens in the context of this clinical setting.
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d
600-1200 mg/d IV/IM divided q6-8h depending on degree of infection
8-20 mg/kg/d PO as hydrochloride or 8-25 mg/kg/d as palmitate divided tid/qid
20-40 mg/kg/d IV/IM divided tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis (allows overgrowth of Clostridium difficile)
Drug combination used against bacteria resistant to beta-lactam antibiotics. In children > 3 mo, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.
500-875 mg PO q12h or 250-500 mg PO q8h
<40 kg: 20-40 mg/kg/d PO divided bid
>40 kg: Administer as in adults
Coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity; concomitant use of disulfiram
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Give for a minimum of 10 d to eliminate organism and prevent sequelae (eg, endocarditis, rheumatic fever); after treatment, perform cultures to confirm eradication of streptococci
Mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.
Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Increases membrane permeability, causing nutrients to leak out and resulting in fungal cell death. Lotion preferred in intertriginous areas. If cream used, apply sparingly to avoid maceration effects.
Cream and lotion: Cover affected areas bid for 2-6 wk
Powder: Liberally spray or sprinkle over affected area bid
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes
Fungistatic activity. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.
200 mg PO qd; increase to 400 mg PO qd if clinically indicated
<2 years: Not established
>2 years: 3.3-6.6 mg/kg/d PO once
Isoniazid may decrease bioavailability; coadministration decreases rifampin and ketoconazole effects; may increase effect of anticoagulants; may increase toxicity of corticosteroids and cyclosporine (cyclosporine dose can be adjusted); may decrease theophylline levels
Documented hypersensitivity; fungal meningitis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hepatotoxicity may occur; may reversibly decrease corticosteroid serum levels (adverse effects avoided with dose of 200-400 mg/d); administer antacid, anticholinergics, or H2 blockers at least 2 h after administration
Patients with recurring or chronic paronychia require frequent follow-up monitoring to prevent possible superinfections or deep-seated infections.
Paronychia can result in more serious infections, such as felon, septic tenosynovitis, or osteomyelitis. Such infections occur more readily in patients who are immunosuppressed or whose condition has been mistreated or neglected.
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paronychia, eponychia, felon, finger infection, hand infection, runaround abscess, fingernail infection, runaround infection, acute paronychia, chronic paronychia, nail fold, nail wall, eponychium, lunula, nail bed, nail plate, hyponychium, Staphylococcus aureus, S aureus, Candida albicans, C albicans, eponychial marsupialization, herpetic whitlow, perionychium, perionychia, eponychia, eponychium
Steve Lee, MD, Physician in Plastic, Reconstructive, and Hand Surgery, Plastic Surgery, PLLC
Steve Lee, MD is a member of the following medical societies: American College of Surgeons and American Society of Plastic Surgeons
Disclosure: Nothing to disclose.
Allison Vidimos, R PH, MD, Consulting Staff, Section of Micrographic Surgery (Mohs) and Oncology, Department of Dermatology, Cleveland Clinic Foundation
Allison Vidimos, R PH, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Medical Association, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, and International Society for Dermatologic Surgery
Disclosure: Nothing to disclose.
Yelena Bogdan, Stony Brook University Health Sciences Center School of Medicine (SUNY)
Yelena Bogdan is a member of the following medical societies: Phi Beta Kappa
Disclosure: Nothing to disclose.
Richard K Scher, MD, Professor of Dermatology, University of North Carolina
Richard K Scher, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Cryosurgery, American College of Physicians, American Dermatological Association, American Geriatrics Society, American Medical Association, Association of Military Surgeons of the US, International Society for Dermatologic Surgery, New York Academy of Sciences, Noah Worcester Dermatological Society, Rhode Island Medical Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Julia R Nunley, MD, Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center
Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, and Women's Dermatologic Society
Disclosure: Johnson and Johnson stock holder dividends; Amgen stock holder dividends; Forest Lab, Inc stock holder dividends; Galaxo Smith Klein stock holder dividends; Covidien stock holder dividends; Novartis Grant/research funds Consulting; Biolex sub-investigator
Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.