Paronychia

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Practice Essentials

Paronychia is a soft tissue infection around a fingernail that begins as cellulitis but that may progress to a definite abscess.[1] The 2 types of paronychia are as follows[2] :

The image below depicts paronychia.



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Classic presentation of paronychia, with erythema and pus surrounding the nail bed. In this case, the paronychia was due to infection after a hangnail....

Signs and symptoms

Physical findings in acute paronychia include the following:

Further extension of the infection can lead to the involvement of both lateral folds as it tracks under the nail sulcus; this progression is called a runaround infection

Physical findings in chronic paronychia include the following:

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of paronychia is based primarily on patient history and physical examination. Some laboratory studies, however, can be useful. These include the following:

Management

Treatment strategies for paronychia include the following:

See Treatment and Medication for more detail.

Background

Paronychia is a soft tissue infection around a fingernail. More specifically, it is a superficial infection of epithelium lateral to the nail plate that begins as cellulitis but that may progress to a definite abscess.[1] The 2 forms of paronychia, acute and chronic, usually differ in etiology, infectious agent, and treatment and are often considered separate entities.[2]

The acute infection, which is painful and purulent, is most frequently caused by staphylococci, although it commonly has mixed aerobic and anaerobic flora.[7] The patient's condition and discomfort are markedly improved by a simple drainage procedure. Chronic paronychial infections are usually fungal, rather than bacterial, in nature (see the images below).



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Classic presentation of paronychia, with erythema and pus surrounding the nail bed. In this case, the paronychia was due to infection after a hangnail....



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In this case of paronychia, no pus or fluctuance is involved in the nail bed itself.



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Typical appearance of paronychia.

Epidemiology

Paronychia is the most common hand infection in the United States, representing 35% of these disorders.[3] The infection is more common in women than in men, with a female-to-male ratio of 3:1.

Quality of life

A study by Belyayeva et al indicated that certain nail disorders, including paronychia, can have a particularly high impact on quality of life. Using responses to a questionnaire from 1063 patients with disorders of the fingernails and/or toenails, the investigators found that the effect on quality of life was greatest in patients with nail problems resulting from trauma, infections (including onychomycosis and paronychia), structural abnormalities, and inflammatory diseases (including psoriasis). Quality of life was particularly reduced in women, patients aged 60-79 years, and persons with multiple nail involvement.[8]

According to the report, the results suggest that quality of life is influenced more by the effect of a nail disease on the appearance of the nail than it is by the actual severity of the disease.

Anatomy

The nail organ is an integral component of the digital tip. It is a highly versatile tool that protects the fingertip, contributes to tactile sensation by acting as a counterforce to the fingertip pad, and aids in peripheral thermoregulation via glomus bodies in the nail bed and matrix. Because of its form and functionality, abnormalities of the nail unit result in functional and cosmetic issues.

The anatomy of the nail complex is shown in the image below. 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.



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Depicted are the nail fold (A), dorsal roof (B), ventral floor (C), nail wall (D), perionychium (E), lunula (F), nail bed (G), germinal matrix (H), st....

Nail plate and bed

The nail, or nail plate, lies immediately on top of the nail bed, which consists of the following 2 portions, which are involved in the production, migration, and maintenance of 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.

Nail fold

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.

Vascular system

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.

Pathophysiology and Etiology

Paronychia, whether acute or chronic, results from a breakdown of the protective barrier between the nail and the nail fold. The occurrence of cracks, fissures, or trauma allowing organisms to enter the moist nail crevice leads to bacterial or fungal (yeast or mold) colonization of the area.[9] Early in the course of this disease process (< 24 h), cellulitis alone may be present. An abscess can form if the infection does not resolve quickly.

Acute paronychia

Acute paronychia usually results from a traumatic event, however minor, that breaks down the physical barrier between the nail bed and the nail; this disruption allows the infiltration of infectious organisms. (See the image below.)



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Paronychial erythema and edema with associated pustule. This suggests a bacterial etiology.

Acute paronychia can result from seemingly innocuous conditions, such as hangnails, or from activities such as nail biting, finger sucking, manicuring, or artificial nail placement. Causative organisms include the following[10] :

Chronic paronychia

Chronic paronychia is caused primarily by the yeast fungus Candida albicans.[12] Other, rare causes of chronic paronychia include the following:

Therefore, benign and malignant neoplasms should always be excluded when chronic paronychia does not respond to conventional treatment.

Chronic paronychia most often occurs in persons whose hands are repeatedly exposed to moist environments or in those who have prolonged and repeated contact with irritants such as mild acids, mild alkalis, or other chemicals. People who are most susceptible include housekeepers, dishwashers, bartenders, florists, bakers, and swimmers. In addition, individuals who are immunocompromised, such as those with human immunodeficiency virus (HIV) infection or those undergoing steroid therapy, are predisposed to paronychia.

Other conditions associated with abnormalities of the nail fold that predispose individuals to chronic paronychia include psoriasis, mucocutaneous candidiasis, and drug toxicity from medications such as retinoids, epidermal growth factor receptor inhibitors (cetuximab) (tyrosine kinase inhibitors [neratinib, afatinib]),[13, 14] and protease inhibitors.[15, 16] Of particular interest is the antiretroviral drug indinavir, which induces retinoidlike effects and remains the most frequent cause of chronic paronychia in patients with HIV disease.

Pemphigus vulgaris

Acute or chronic paronychia may also occur as a manifestation of other diseases, such as pemphigus vulgaris. Although nail involvement in pemphigus vulgaris is rare, it can be severe, involving multiple digits and hemorrhage.[17]

Prognosis

If treated promptly, paronychia usually has a good prognosis, but it potentially can result in a more serious infection, such as septic tenosynovitis, osteomyelitis,[18] or, by spreading to the pulp space of the finger, a felon. Such infections develop more readily in patients who are immunosuppressed or in those whose condition has been mistreated or neglected. Secondary ridging, thickening, and discoloration of the nail can also occur, as may nail loss. Occasionally, patients suffer systemic infection from hematogenous extension.[19]

Patient Education

Instruct individuals to avoid any trauma to the fingernails and to avoid nail biting and finger sucking. Educate patients who work with their hands in a moist environment that such exposure predisposes them to infections. Inform patients that treatment is unlikely to be successful if their exposure to a moist or wet environment is not changed. Explain to patients who are immunocompromised that they must remain vigilant against any minor trauma to the fingertips and nails.

For patient education information, see the Skin Conditions and Beauty Center, as well as Paronychia (Nail Infection) and Nail Psoriasis.

History

The patient's history is crucial in determining the possibility of systemic conditions and risk factors that may predispose an individual to paronychia.[15, 20, 21, 22, 23, 24] These may include the following:

Patients may give a history of the following[9, 28] :

Also query patients about the duration of symptoms and a history of nail infections and previous treatment.

Because paronychia has been known to initiate from malignant lesions, any history of prior malignancy or a pigmented, irregular appearance of surrounding tissue should result in appropriate suspicion and referral for biopsy.

Painless swelling or severe swelling that radiates requires an expanded differential diagnosis.[29] Painless swelling lateral to the nail plate in a patient with osteoarthritis should prompt investigation for a mucous cyst.

Acute paronychia

The patient is usually otherwise healthy but complains of pain, tenderness, and swelling in one of the lateral folds of the nail.

Chronic paronychia

Generally, patients report symptoms lasting 6 weeks or longer. Inflammation, pain, and swelling may occur episodically, often after an exposure to water or a moist environment.

Chronic and recurrent paronychial infections should be scrutinized to rule out malignancy or fungal infection.[30, 31, 32]

Physical Examination

Acute paronychia

Physical findings in acute paronychia include the following:

In severe cases, the infection may track proximally under the skin of the finger and volarly to produce a concomitant felon. The fulminant purulence of the nail bed may generate enough pressure to lift the nail off the nail bed.

Chronic paronychia

Physical findings in chronic paronychia include the following:

Additional considerations

Other signs to look for in a physical examination include the following:

The digital pressure test can be used to detect the presence of an abscess. Pressure is applied to the palmar surface of the distal finger; if an abscess is present, the area of the abscess will blanch with palmar pressure.[33]

Approach Considerations

The diagnosis of paronychia is based primarily on patient history and physical examination. Some laboratory studies, however, can be useful.

Fluctuant paronychia usually results from bacterial infection; therefore, routine Gram staining and culture can help in identifying the causative organism.

Potassium hydroxide (KOH) 5% smears may be helpful in diagnosing paronychia if Gram staining results are negative or if candidal infection is suspected, as in chronic paronychia. If Gram staining results are negative, the KOH preparation may demonstrate pseudomycelia and clusters of grapelike yeast cells. KOH wet mounts from scrapings or discharge may show hyphae.

Tzanck smears may be performed if herpetic whitlow is suspected. Smears should be performed by using base scrapings of an unroofed vesicle. The presence of multinucleated giant cells, often with visible viral inclusions, indicates a positive result.

Imaging studies

Although imaging studies are not routinely necessary with paronychia, obtain a plain film radiograph of the fingertip if osteomyelitis is suspected because of recurrent infection, elevated erythrocyte sedimentation rate (ESR), or presence of risk factors for osteomyelitis.

A radiograph can also be obtained if a foreign body is suspected or the patient has a history of recent finger trauma.

Approach Considerations

The treatment of choice depends on the extent of the infection. If diagnosed early, acute paronychia without obvious abscess can be treated nonsurgically. If soft tissue swelling is present without fluctuance, the infection may resolve with warm soaks 3-4 times daily.[1, 3, 4]

Patients with extensive surrounding cellulitis or with a history of diabetes, peripheral vascular disease, or an immunocompromised state may benefit from a short course of antibiotics. An antistaphylococcal penicillin or first-generation cephalosporin is generally effective; clindamycin and amoxicillin-clavulanate are also appropriate.[5, 6]

If an abscess has developed, however, incision and drainage must be performed. Surgical debridement may be required if fulminant infection is present.[39, 40]

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.[41]

Inpatient care

Admission for paronychia is rarely required unless associated with a significant cellulitis, tendonitis, or deep space infection of the hand requiring intravenous antibiotics.

Consultations

It is necessary to consult a hand surgeon if cellulitis, deep space infection, glomus tumor, mucous cyst, or osteomyelitis is suspected.

Long-term monitoring

Patients with recurring or chronic paronychia require frequent follow-up monitoring to prevent possible superinfections or deep-seated infections.

Pharmacologic and Other Noninvasive Treatment

Acute paronychia

Warm water soaks of the affected finger 3-4 times per day until symptoms resolve are helpful.

Oral antibiotics with gram-positive coverage against S aureus, such as amoxicillin and clavulanic acid (Augmentin), clindamycin (Cleocin), or or cephalexin, are usually administered concomitantly with warm water soaks. (Although antibiotics are commonly prescribed,[1] most patients do not require antibiotics for a simple paronychia.)

Cleocin and Augmentin also have anaerobic activity; therefore, they are useful in treating patients with paronychia due to oral anaerobes contracted through nail biting or finger sucking. Cleocin should be used instead of Augmentin in patients who are allergic to penicillin.

If the paronychia does not resolve or if it progresses to an abscess, it should be drained promptly.

Chronic paronychia

The initial treatment of chronic paronychia consists of the avoidance of inciting factors such as exposure to moist environments or skin irritants. Keeping the affected lesion dry is essential for proper recovery. Choice of footgear may also be considered.

Any manipulation of the nail, such as manicuring, finger sucking, or attempting to incise and drain the lesion, should be avoided; these manipulations may lead to secondary bacterial infections.

Mild cases of chronic paronychia may be treated with warm soaks, followed by completely drying the digit. The initial medical treatment consists of the application of topical antifungal agents. Topical miconazole may be used as the initial agent. Oral ketoconazole or fluconazole may be added in more severe cases.

Patients with diabetes and those who are immunocompromised need more aggressive treatment because the response to therapy is slower in these patients than in others.

In cases induced by retinoids or protease inhibitors, the paronychia usually resolves if the medication is discontinued.

Drainage

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 (see the image below). Surgical debridement may be required if fulminant infection is present.



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Paronychia incision and drainage.

Acute paronychia

No-incision technique

Less-advanced paronychial abscesses can be drained simply by gently elevating the eponychial fold from the nail by using a small blunt instrument such as a metal probe or an elevator (see the image below). This separation is performed at the junction of the perionychium and the eponychium and extends proximally enough to permit visualization of the proximal nail edge. Then, the proximal third of the nail can be excised with scissors and the pus evacuated.



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Simple acute paronychia can be drained by elevating the eponychial fold from the nail with a small blunt instrument such as a metal probe or elevator.....

This technique does not require an incision into the matrix. Often, no excision of any tissues is made, because only blunt dissection and separation are needed to evacuate the pus from the paronychia.

The wound should be well irrigated with isotonic sodium chloride solution, and plain gauze packing should be inserted under the fold to keep the cavity open and allow drainage.

The patient should receive oral antibiotics for 5-7 days. The packing is removed after 2 days, and warm sodium chloride solution soaks are begun.

Simple incision technique

The most simple and, often, least painful incision can be made without anesthesia, using only an 18-gauge needle. The technique is performed as follows:

Single- and double-incision techniques

If the paronychia is more advanced, it may need to be incised and drained. A digital anesthetic block is usually necessary. If an anesthetic agent is used, it should consist of 1% lidocaine (Xylocaine).[4, 42] The local injection of the anesthetic agent into the paronychia or the wound is often inadequate and more painful than the administration of drugs of a digital block.

If the paronychia involves only 1 lateral fold of the finger, a single longitudinal incision should be placed with either a number-11 or number-15 blade directed away from the nail fold to prevent proximal injury and a subsequent nail growth abnormality. If both lateral folds of the finger are involved, incisions may be made on both sides of the nail, extending proximally to the base of the nail.

The next steps are as follows (see the images below):

Chronic paronychia

The most common surgical technique used to treat chronic paronychia is called eponychial marsupialization.

In this technique, the affected digit is first anesthetized with 1% lidocaine (Xylocaine), with no epinephrine, using the digital ring block method.

Tourniquet control of the proximal digit may be accomplished by using a finger of a latex glove with the distal end cut off or by using a sterile Penrose drain at the base of the digit firmly secured using a hemostat. The surgery proceeds as follows:

Epithelialization of the excised defect occurs over the next 2-3 weeks. Nail improvement occurs over the next 6-9 months but may require as long as 12 months to become apparent.

Prevention

Patients should also avoid any further trauma to or manipulation of the nail. Hangnails should be trimmed to a semilunar smooth edge with a clean, sharp nail plate trimmer. Toenails should be trimmed flush with the toe tip. Patients should not bite the nail plate or lateral nail folds.

Patients should also avoid prolonged hand exposure to moisture. (Rubber or latex-free gloves can be worn.) If hand washing must be frequent, patients should use antibacterial soap, thoroughly dry their hands with a clean towel, and apply an antibacterial moisturizer.

Medication Summary

Most paronychia infections can be managed without antibiotics; over-the-counter analgesics are usually sufficient. If cellulitis is present, however, then antibiotics are indicated. Although penicillin covers oral flora, it does not cover methicillin-resistant Staphylococcus aureus (MRSA). Trimethoprim and sulfamethoxazole (TMP/SMZ), doxycycline, or clindamycin may be considered to cover community-acquired MRSA and anaerobic organisms. Cephalexin may also be effective. Combination therapy with an intravenous agent that provides antimicrobial activity against staphylococci is used for inpatient therapy.

Chronic paronychial infections are usually managed with oral antifungals such as ketoconazole, itraconazole, or fluconazole.[43] Many of these agents require a prolonged course with monitoring of laboratory tests to avoid complications.

Clindamycin (Cleocin)

Clinical Context:  This agent is a lincosamide used in the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). Clindamycin inhibits bacterial growth, possibly by blocking the dissociation of peptidyl transfer ribonucleic acid (t-RNA) from ribosomes, causing RNA-dependent protein synthesis to arrest.

Clindamycin widely distributes in the body without penetration of the central nervous system (CNS). It is protein bound and excreted by the liver and kidneys.

Amoxicillin and clavulanic acid (Augmentin, Augmentin XR, Amoclan)

Clinical Context:  This drug combination is used against bacteria resistant to beta-lactam antibiotics. In children over age 3 months, base dosing protocol on amoxicillin content. Because the amoxicillin/clavulanic acid ratio in 250-mg tablets (250/125) is different than in 250-mg chewable tablets (250/62.5), do not use 250-mg tablets until the child weighs more than 40 kg.

Penicillin VK

Clinical Context:  Penicillin VK inhibits the biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached. It is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Cephalexin (Keflex)

Clinical Context:  This is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms, with primary activity against skin flora. It is used for skin infections or for prophylaxis in minor procedures.

Class Summary

Therapy must cover all likely pathogens in the context of this clinical setting.

Miconazole topical (Desenex Spray, Lotrimin AF, Baza Antifungal, Carrington Antifungal, Micaderm, Micatin)

Clinical Context:  This agent damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. By increasing membrane permeability, it causes nutrients to leak out of the cell, resulting in fungal cell death. Lotion is preferred in intertriginous areas. If cream is used, it should be applied sparingly to avoid maceration effects.

Ketoconazole (Nizoral, Extina, Xologel)

Clinical Context:  Ketoconazole has fungistatic activity. An imidazole with broad-spectrum antifungal action, it inhibits the synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Itraconazole (Sporanox, Onmel)

Clinical Context:  This is a synthetic fungistatic triazole that inhibits cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Class Summary

The mechanism of action of antifungal agents usually involves the alteration of the permeability of the cell membrane (polyenes) of the fungal cell or the inhibition of pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis.

What is paronychia?Which physical findings are characteristic of acute paronychia?Which physical findings are characteristic of chronic paronychia?How is paronychia diagnosed?What are the treatment strategies for paronychia?What is paronychia and how is it characterized?What is the prevalence of paronychia?How does paronychia affect quality of life?What is the anatomy involved in paronychia?What anatomy of the nail plate and bed are relevant to paronychia?What anatomy of the nail fold is relevant to paronychia?What anatomy of the vascular system is relevant to paronychia?What is the pathogenesis of paronychia?What causes acute paronychia?What causes chronic paronychia?Which factors increase the risk of chronic paronychia?In what condition might paronychia be a manifestation?What is the prognosis of paronychia?What information about paronychia should patients receive?What risk factors may predispose an individual to paronychia?What history suggests paronychia?What are the signs and symptoms of acute paronychia?What are the signs and symptoms of chronic paronychia?Which physical findings are characteristic of acute paronychia?Which physical findings are characteristic of severe acute paronychia?Which physical findings are characteristic of chronic paronychia?What are the signs to look for in a physical exam for paronychia?What conditions should be included in the differential diagnosis of paronychia?What are the differential diagnoses for Paronychia?What is the role of lab testing in the diagnosis of paronychia?What is the role of imaging studies in the diagnosis of paronychia?What are the treatment options for paronychia?When is inpatient treatment indicated for paronychia?Which specialists should be consulted for the management of paronychia?When is frequent monitoring indicated in the management of paronychia?What are noninvasive treatment options for acute paronychia?Which drugs are used in the treatment of acute paronychia?What is the initial treatment for chronic paronychia?What are the nonsurgical treatment options for chronic paronychia?When is surgery indicated in the treatment of paronychia?How is the no-incision technique performed for acute paronychia?How is the simple incision technique performed for acute paronychia?How is the single- and double-incision technique performed for acute paronychia?What is the role of eponychial marsupialization in the treatment of chronic paronychia?How is paronychia prevented?Which medications are used in the treatment of paronychia?Which medications in the drug class Antifungals are used in the treatment of Paronychia?Which medications in the drug class Antibiotics are used in the treatment of Paronychia?

Author

Elizabeth M Billingsley, MD, Professor of Dermatology, Pennsylvania State University College of Medicine; Director, Mohs Micrographic Surgery, Penn State Hershey Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Allison T Vidimos, MD, RPh, Chair, Department of Dermatology, Vice Chair, Dermatology and Plastic Surgery Institute, Staff Physician, Department of Dermatology and Dermatologic Surgery and Cutaneous Oncology, Cleveland Clinic; Professor of Dermatology, Department of Medicine, Case Western Reserve University School of Medicine

Disclosure: Partner received grant/research funds from Genentech for none.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.

Acknowledgements

Yelena Bogdan Stony Brook University Health Sciences Center School of Medicine (SUNY)

Disclosure: Nothing to disclose.

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White 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.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Noah Elise Gudel, DO Resident in Internal Medicine, University of Tennessee Medical Center at Knoxville

Disclosure: Nothing to disclose.

Micelle J Haydel, MD Associate Clinical Professor of Medicine, Residency Director, Section of Emergency Medicine, Louisiana State University Health Science Center

Micelle J Haydel, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Association, Sigma Theta Tau International, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

Mark F Hendrickson, MD Chief, Section of Hand Surgery, Department of Plastic and Reconstructive Surgery, Cleveland Clinic Foundation

Disclosure: Nothing to disclose.

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.

Mohamad Marouf, MD Consulting Staff, Department of Emergency Medicine, University Hospitals Health System, Richmond Heights Medical Center

Disclosure: Nothing to disclose.

Heather Murphy-Lavoie, MD, FAAEM Assistant Professor, Assistant Residency Director, Emergency Medicine Residency, Associate Program Director, Hyperbaric Medicine Fellowship, Section of Emergency Medicine and Hyperbaric Medicine, Louisiana State University School of Medicine in New Orleans; Clinical Instructor, Department of Surgery, Tulane University School of Medicine

Heather Murphy-Lavoie, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Jerome FX Naradzay, MD, FACEP Medical Director, Consulting Staff, Department of Emergency Medicine, Maria Parham Hospital; Medical Examiner, Vance County, North Carolina

Jerome FX Naradzay, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

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: Nothing to disclose.

Richard K Scher, MD Adjunct Professor of Dermatology, University of North Carolina; Professor Emeritus of Dermatology, Columbia University

Richard K Scher, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American Dermatological Association, American Medical Association, Association of Military Surgeons of the US, International Society for Dermatologic Surgery, Noah Worcester Dermatological Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist

Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Classic presentation of paronychia, with erythema and pus surrounding the nail bed. In this case, the paronychia was due to infection after a hangnail was removed.

Classic presentation of paronychia, with erythema and pus surrounding the nail bed. In this case, the paronychia was due to infection after a hangnail was removed.

In this case of paronychia, no pus or fluctuance is involved in the nail bed itself.

Typical appearance of paronychia.

Depicted are the nail fold (A), dorsal roof (B), ventral floor (C), nail wall (D), perionychium (E), lunula (F), nail bed (G), germinal matrix (H), sterile matrix (I), nail plate (J), hyponychium (K), distal groove (L), fascial septa (M), fat pad (N), distal interphalangeal joint (O), and extensor tendon insertion (P).

Paronychial erythema and edema with associated pustule. This suggests a bacterial etiology.

Paronychia incision and drainage.

Simple acute paronychia can be drained by elevating the eponychial fold from the nail with a small blunt instrument such as a metal probe or elevator.

Wound opened with a small incision using a number-11 blade scalpel.

The wound can be explored with a blunt probe, clamps, or the blunt end of a cotton swab.

Ensure that all loculations are broken up and that as much pus as possible is evacuated.

Prior to packing or dressing the wound, irrigate the wound with normal saline under pressure, using a splash guard, eye protection, or both.

The wound can be covered with antibiotic ointment or petroleum jelly to prevent bandage adhesion.

Classic presentation of paronychia, with erythema and pus surrounding the nail bed. In this case, the paronychia was due to infection after a hangnail was removed.

In this case of paronychia, no pus or fluctuance is involved in the nail bed itself.

Typical appearance of paronychia.

Depicted are the nail fold (A), dorsal roof (B), ventral floor (C), nail wall (D), perionychium (E), lunula (F), nail bed (G), germinal matrix (H), sterile matrix (I), nail plate (J), hyponychium (K), distal groove (L), fascial septa (M), fat pad (N), distal interphalangeal joint (O), and extensor tendon insertion (P).

Simple acute paronychia can be drained by elevating the eponychial fold from the nail with a small blunt instrument such as a metal probe or elevator.

Paronychia incision and drainage.

Paronychial erythema and edema with associated pustule. This suggests a bacterial etiology.

Paronychia, side view.

After simple drainage, there is purulent return.

Wound opened with a small incision using a number-11 blade scalpel.

The wound can be explored with a blunt probe, clamps, or the blunt end of a cotton swab.

Ensure that all loculations are broken up and that as much pus as possible is evacuated.

Prior to packing or dressing the wound, irrigate the wound with normal saline under pressure, using a splash guard, eye protection, or both.

The wound can be covered with antibiotic ointment or petroleum jelly to prevent bandage adhesion.