Review Article Acute and Chronic Paronychia of the Handupload.orthobullets.com/journalclub/free_pdf/24603826... · 2016. 10. 3. · the paronychia (Figure 3). Blanching may indicate

Review Article

Acute and Chronic Paronychia ofthe Hand

Abstract

Acute and chronic infections and inflammation adjacent to thefingernail, or paronychia, are common. Paronychia typically developsfollowing a breakdown in the barrier between the nail plate and theadjacent nail fold and is often causedby bacterial or fungal pathogens;however, noninfectious etiologies, such as chemical irritants,excessivemoisture, systemic conditions, andmedications, can causenail changes. Abscesses associated with acute infections mayspontaneously decompress or may require drainage and local woundcare along with a short course of appropriate antibiotics. Chronicinfections have a multifactorial etiology and can lead to nail changes,including thickening, ridging, and discoloration. Large, prospectivestudiesareneeded to identify thebest treatment regimen for acuteandchronic paronychia.

Inflammation of the tissue immedi-ately surrounding the nail, knownasparonychia, is commonly caused byacute or chronic infection. Paronychiacan be acute (,6 weeks duration) orchronic ($6 weeks duration) andtypically develops following a break-down in the barrier between the nailplate and the adjacent nail fold that isoften caused by bacterial or fungalpathogens. However, noninfectiousetiologies such as chemical irritants,excessive moisture, systemic con-ditions, and medications also cancause paronychia. Management op-tions include activity modificationalong with medical and/or surgicalintervention based on the etiology,duration, extent of paronychialinvolvement, and the associated riskfactors present.1,2

Anatomy

The tip of the finger is composed ofosseous tissue, soft tissue, and spe-cialized tissues that produce and sup-port the nail distal to the insertions of

the flexor and extensor tendons.3

Fibrous septa located within the pulpof the finger stabilize the vascular fi-brofatty tissue and bridge the dermisto the periosteum of the distal pha-lanx.4 The nail bed, which has a con-voluted attachment to the periosteumof the distal phalanx, resists traumaticavulsion. In humans, the fingernailprotects the fingertip and enhances itsdexterity and sensation by exertingcounterpressure for the volar pulpduring touch and facilitating skilledhand function, such as the abilityto pick up and manipulate smallobjects.5

The nailbed comprises germinal andsterile matrices, with the germinalmatrix located on the palmar aspect ofthe nail fold and terminating at thedistal extent of the lunula. This matrixis more vascular than the remainder ofthe nail bed and produces nearly all ofthe nail via gradient parakeratosis.4

Near the periosteum, germinal matrixcells originate as basilar cells. Theyduplicate and are driven dorsally incolumns toward the nail. The cells

March 2014, Vol 22, No 3 165

Adam B. Shafritz, MD

Jeff M. Coppage, MD

From the Department of Orthopaedicsand Rehabilitation, University ofVermont College of Medicine,Burlington, VT.

Neither of the following authors norany immediate family member hasreceived anything of value from or hasstock or stock options held ina commercial company or institutionrelated directly or indirectly to thesubject of this article: Dr. Shafritz andDr. Coppage.

J Am Acad Orthop Surg 2014;22:165-174

http://dx.doi.org/10.5435/JAAOS-22-03-165

Copyright 2014 by the AmericanAcademy of Orthopaedic Surgeons.

Copyright � the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.

flatten and stream distally when theymeet the resistance of the nail, leadingto longitudinal nail growth.4 The nailbed and the nail plate are involved inthe continuum of nail production at allstages.The sterile matrix lies distal to the

lunula. Its contribution to nail pro-duction varies. Cells that originatefrom the sterilematrix enlarge, flatten,and elongate; large cells eventuallybreak downand are incorporated intothe nail. In most people, the nail isthicker distally than proximally, pro-viding evidence of the contribution ofthe sterile matrix to nail production.The nail plate is anchored to theunderlying linear ridges in the squa-mous epitheliumof the sterilematrix.4

The nail adheres less to the germinalmatrix than to the sterile matrix.The paronychium is defined as the

soft tissue lateral to the nail bed,whereas the term perionychium refersto the paronychium and nail bed6

(Figure 1). Primate studies suggest thatafter nail removal, the sterile matrixcontributes little to nail regenerationand the nail is primarily reformed by

the paronychium.7 The junction wherethe sterile matrix of the distal nail bedmeets the skin of the fingertip is calledthe hyponychium. A keratinous plugwith abundant neutrophils and lym-phocytes composes the hyponychium,which serves as a barrier in preventingmicrobial invasion of the subungualarea.4 The nail fold is an anatomictransition between the nail bed and theparonychium. The eponychium lies atthe most distal and dorsal portion ofthe nail fold; this is where the nail foldattaches to the surface of the nail. Atthis junction, the nail vest (a thin veil oftissue) is formed.

Acute Paronychia

Etiology and Risk FactorsMost acute paronychias are the resultof minor trauma to the nail bed that isoften related to onychophagia (ie, nailbiting), finger sucking, picking ata hangnail, an ingrown nail, man-icures, dishwashing, or puncture-typetrauma with or without a retainedforeign body. Such trauma disrupts the

fingertip’s natural barrier to outsidepathogens, resulting in inoculation ofthe perionychium. In three studies witha total of 61 patients with paronychia,approximately 25% of paronychiaswere caused by anaerobic bacteria,25% by aerobic bacteria, and 50%by mixed aerobic and anaerobic bac-teria.8-10 The most common aerobicpathogens responsible for acute par-onychia include Staphylococcusaureus, gamma-hemolytic strepto-cocci, Eikenella corrodens, group Ab-hemolytic streptococci, and Klebsi-ella pneumoniae.8 Common anaerobicbacteria responsible for paronychiainclude Bacteroides species, gram-pos-itive anaerobic cocci, and Fusobacteriaspecies.8 Enterococcus faecalis, Pro-teus species, and Pseudomonas aer-uginosa are other isolated organismsthat can cause paronychia.8 In addi-tion, nonbacterial pathogens such asyeast (Candida albicans) and viruses(eg, herpes simplex) have been iden-tified as causative organisms. A spe-cific trauma or inciting event maynot be identified in all cases of acuteparonychia.

Figure 1

Nail platewith sterile matrix below

Hyponychium

ParonychiumLunula

Eponychium

Nail fold with germinal matrix below

Nail vest

A

Germinal matrixSterile matrix

Hyponychium

Nail bedNail plate

Insertion ofextensor tendon

Dorsal floorVentral floor

Nailfold

DIP joint

B

Illustrations of dorsal (A) and cross-section (B) views of the anatomy of the fingertip and nail bed. DIP = distalinterphalangeal

Acute and Chronic Paronychia of the Hand

166 Journal of the American Academy of Orthopaedic Surgeons


Clinical PresentationPatients with acute paronychias typ-ically present with localized pain,redness, inflammation, and edema ofthe paronychium that is typicallylimited to a single digit. The timing ofpresentation varies, but is often 2 to5 days after the initial trauma. Fluc-tuance of the paronychium may notbe observed with early presentation.In patientswith delayed presentation,fluctuance may extend around thenail, involving the eponychium aswell as the paronychium on both theradial and ulnar sides of the digit (ie,runaround infection). Purulence maydevelop underneath the nail plate,causing the nail plate to pull awayfrom the sterile matrix; this may bemore accurately described as a peri-onychial infection (Figure 2).

DiagnosisDiagnosis of acute paronychia isbased on the patient’s history andphysical examination. A detailedhistory is crucial for evaluation of riskfactors that may be associated withan atypical causative organism. Forexample, contact with oral secretions

may provide exposure to specificanaerobic bacteria such as Eikenellacorrodens or the herpes virus. Expo-sure to animals may result in anincreased risk of infection with gram-negative organisms such as Pasteurellamultocida.Turkmenetal11 described the use of

a digital pressure test to identify thepresence and extent of paronychialabscesses. The test is performed byapplying light pressure to the distalvolar aspect of the affected digit andobserving for blanching in the area ofthe paronychia (Figure 3). Blanchingmay indicate the presence of anabscess. Typically, radiographs andlaboratory tests are not needed fordiagnosis of acute paronychia.

Differential DiagnosisAlthough gram-positive bacterial in-fections account for most cases ofacute paronychia, a wide differentialshould be considered. Herpetic whit-low is a manifestation of herpes sim-plex infection and presents as one ormore blisters grouped on the distal

aspect of the digit12 (Figure 4). Theblisters are typically filled with serous-type fluid, but the fluid may be moreopaque and can be easily mistaken forpurulence. Herpetic whitlow is oftenseen in healthcare professionals (eg,dental professionals) who are at riskof topical exposure to the virus, butthe condition may also be seen inpersons with a primary herpes sim-plex infection.13 A definitive diagnosisis made based on Tzanck smear orviral culture results. Incision anddrainage are contraindicated.In addition, to herpetic whitlow,

other conditions such as psoriasis,Reiter syndrome, and pemphigusvulgaris can mimic acute or chronicparonychia. Medications such as ret-inoids, antiretrovirals, and chemo-therapeutics can cause paronychialinflammation, as well.

Nonsurgical ManagementManagement of paronychia dependslargely on the amount of inflamma-tion and whether an abscess is pres-ent. In patients who present witha minimal amount of inflammationand no abscess formation, frequentsoaks with warm water, aluminumacetate (Burrow solution),14 vine-gar,15 a dilute povidone-iodinesolution16 or chlorhexidine may besufficient. However, no studies have

Figure 2

A, Photograph of a fingertipdemonstrating an acute paronychiaand its sequelae. The patientpresented with acute onset of pain andswelling. The abscess spontaneouslydecompressed under the nail fold andnail plate. B, Photograph of thefingertip obtained 3 weeks later. Theinfection resolved and a new nail isgrowing to replace the one present atthe time of infection.

Figure 3

Photograph of a fingertipdemonstrating an abscess, whichis evident from the blanched areacaused by simple digital pinchpressure. (Courtesy of RobertStrauch, MD, New York, NY.)

Figure 4

Photograph of a fingertipdemonstrating herpetic whitlow.(Reproduced with permission fromUsatine RP, Tinitigan R: Nongenitalherpes simplex virus. Am FamPhysician 2010;82[9]:1075-1082.)

Adam B. Shafritz, MD, and Jeff M. Coppage, MD

March 2014, Vol 22, No 3 167


evaluated the effectiveness of soaksalone.A topical antibiotic may be added

to the treatment regimen in patientswith minimal erythema and noabscess formation. Topical and/ororal antibiotics should be used inpatients with substantial erythemaand abscess formation. Topical an-tibiotics may be used alone or incombination with a corticosteroid.Wollina17 compared the efficacyof fusidic acid and betamethasoneversus gentamycin ointment foracute paryonychia in a nonblindedstudy. Erythema, swelling, exuda-tion, and pain were graded ona scale of 0 (absent) to 3 (heavy).The author reported a 50% reduc-tion in pain in the fusidic acid andbetamethasone group after 3.5 62.0 days compared with a 50%reduction in pain after 5.1 6 3.1days in the gentamycin group. Bothregimens were effective and had noassociated complications.Oral antibiotic regimens such

as trimethoprim-sulfamethoxazole,cephalexin, amoxicillin and clav-ulanate, or clindamycin (in patients

with sensitivity to penicillins) shouldprovide coverage against gram-posi-tive organisms, including S aureusand streptococci.1 Tosti and Ilyas18

recommend the use of agents thatare effective against methicillin-resistant S aureus, such as oral tri-methoprim-sulfamethoxazole, if thisbacterium has been documentedin .10% of community-acquiredhand infections at a given institu-tion. In the setting of suspectedinfection with oral flora, broad-spectrum antibiotics such as amox-icillin/clavulanate or clindamycinshould be used to provide coverageagainst anaerobic bacteria.1

Surgical ManagementIn general, surgical management ofacute paronychia is reserved for pa-tients with a discrete abscess, failure ofnonsurgical care, and/or extensiveinvolvement of the eponychium.Numerous surgical techniques havebeen described for management ofacute paronychia, and each techniquehas a role based on the structuresaffected and the extent of involvement.To our knowledge, no studies havecompared the efficacy of adminis-tering oral antibiotics alone versusdrainage.19 Some authors recom-mend a course of oral antibioticsafter drainage,20 whereas othersrecommend drainage and localwound care alone.2 No studies havecompared the efficacy of adminis-tering oral antibiotics after drainagewith that of drainage and woundcare alone.To drain an abscess, a No. 11 or 15

scalpel blade (with sharp edgepointed away from the nail), a freerelevator, or a small hemostat is in-serted into the nail sulcus andbeneaththe nail fold until the abscess is de-compressed (Figure 5). This obviatesthe need to create a skin incision inthe lateral nail fold, which can putthe intervening tissue at risk for skinbridge necrosis.21 However, thistreatment option requires that the

abscess be immediately adjacent tothe nail sulcus. A piece of mesh gauzemay be placed beneath the nail foldto allow for continued drainage.21

Ogunlusi et al22 described a morelimited approach for draining anabscess. The tip of a 21- or 23-gaugeneedle is used to lift the nailfold, allowing egress of purulence.Drainage is followed by oral antibi-otic therapy. The authors usedthis technique in 8 patients with 10paronychias and noted resolution ofacute paronychia in all patients after2 days. The authors concluded thatneither anesthesia nor daily dressingchanges were required with thistechnique.Extensive abscesses or those not

immediately adjacent to the nail sulcusmay require the creation of skin in-cisions to promote drainage. A smallincision made in the paronychiumdirectly over the abscess can facilitatedrainage (Figure 6). The sharp edge ofthe blade should be pointed awayfrom the nail to avoid injury to thematrix, which can lead to subsequentnail deformity. Alternatively, a longi-tudinal incision can be made in linewith the lateral nail fold to decom-press the abscess.15 In the setting ofeponychia or runaround infection,longitudinal incisions can be made onboth sides of the nail. If incisions aremade in line with the nail folds, thefold can be reflected proximally, irri-gated, and returned to its originalposition (Figure 7). A piece of gauzemay be placed under the nail fold tofacilitate continued drainage. Incases in which the abscess hasspread beneath the nail plate toform a subungual abscess, partialor complete removal of the nailplate may be indicated, particularlyif the paronychia is related to aningrown nail. Complete removal ofthe nail plate is reserved for cases inwhich spreading infection has under-mined the entire plate, causing com-plete separation of the nail plate fromthe underlying sterile matrix.

Figure 5

A B

Illustrations demonstratingdecompression of an abscess usinga blade (A) or an elevator (B). Theparonychia is elevated from the nailvia the nail sulcus with care taken toavoid injury to the nail bed.




Treatment failure and recurrence areuncommon after appropriate manage-ment of acute paronychia. Failure torecognize a significant abscess orincomplete drainage or débridementmay result in persistent or recurrentinfection. Local factors such as theextent of infection or host factors (eg,diabetes mellitus, other immunocom-promised states) may play a role inimpaired clearance of infection; how-ever, no studies have demonstrated therole of host factors with respect to acuteparonychia. Several studies cite treat-ment failure as a risk factor for thedevelopment of chronic paronychia,but sparse evidence has beenreported with regard to factors thatcontribute to failed management ofacute paronychia. To our knowl-edge, no evidence exists to suggestthat improper management ofparonychial infection leads to felonsor osteomyelitis.

Chronic Paronychia

Etiology and Risk FactorsChronic paronychia is inflamma-tion of the perionychium that hasbeen present for .6 weeks. Thisinflammation can have many causes

and often is related to repeatedexposure to environmental irri-tants, with colonization by fungalor bacterial pathogens that occursafter disruption of the barrierformed by the eponychium and nailvest. Exposure to irritants can takemany forms and persons witha higher risk of chronic paronychiainclude those with frequent exposureto moisture and/or chemical irri-tants.23 Homemakers, bartenders,barbers, dishwashers, cooks, food

handlers, swimmers, and nurses arecommonly identified as having anincreased risk of chronic paronychia.21

Conditions such as diabetes melli-tus and immunosuppression alsopredispose patients to developmentof chronic paronychia.15

C albicans is a pathogen commonlyassociated with chronic paronychia;this fungus has been found in culturesin 40% to 95% of cases.2,15,23,24 Theexact role that it plays in the devel-opment and maintenance of chronic

Figure 6

Photographs demonstrating decompression of an abscess adjacent to the paronychium of the thumb. The thumb isanesthetized using a digital block. A, The area of fluctuance is incised. B, The abscess is decompressed. C, A probe is usedto break up any loculations. (Courtesy of Jeffrey Yao, MD, Redwood City, CA.)

Figure 7

A B C

Illustrations demonstrating management of acute paryonchia with eponychialinvolvement via reflection of the proximal nail fold. A, Two parallel incisions aremade in line with the nail fold. The nail fold is elevated (B) and gauze packing isplaced underneath it (C).


March 2014, Vol 22, No 3 169


paronychia is unclear. The presenceof Candida may represent a second-ary colonization of the nail fold thatcan contribute to the developmentof chronic paronychia by inducingan additional persistent inflamma-tory response. In a study of chronicparonychia, Stone and Mullins25

soaked fingers in water until theywere macerated and then inoculatedthe perionychium with either viableor nonviable Candida. Inflamma-tory conditions similar to chronicparonychia developed in bothgroups, demonstrating the inflam-matory effect caused by the patho-gen. Tosti et al24 compared the useof topical steroids versus systemicantifungals formanagement of chronicparonychia and found that the patientstreated with topical corticosteroidalone showed more clinical improve-ment than those treated with anti-fungal agents alone. Eradication ofCandida was associated with cure inonly 2 of 18 patients who testedpositive for infection at the outsetof the study. The authors concludedthat, in patients with chronic par-onychia, Candida is a secondarycolonizer of the nail fold, and chronicparonychia is an inflammatory dis-order rather than a primary mycoticinfection.

Clinical Presentation andDiagnosisTypically, a thorough history andphysical examination is sufficientto diagnose chronic paronychia. Thepatient’s history typically revealsexposure to one or more risk factors.Chronic paronychia presents witherythema, swelling, and pain,although the degree of erythema andswelling is often less than that asso-ciated with acute paronychia.15 Ingeneral, symptoms are present for.6weeks at the time of diagnosis. Epi-sodic exacerbation of symptomscan occur, and such episodes mayfollow exposure to moist environ-ments.15 The proximal nail foldmay become raised and separatedfrom the underlying nail. Chronicparonychia may have associatednail changes including ridging,grooving, discoloration, and/orrounding of the nail plate (Figure8). Further diagnostic testing maybe warranted in atypical cases inwhich malignancy or systemic eti-ologies are suspected.

Differential DiagnosisCertain antiretroviral and chemother-apeutic medications have been impli-cated in the development of acute

and chronic paronychia.26-31 Anti-retroviral medications (eg, indinavir,lamivudine), have been associatedwith the development of paronychiaand periungual pyogenic granulo-mas.32-34 The toes are often involvedbut finger involvement has beendescribed, as well.32,34 The similaritybetween the cutaneous side effectsassociated with protease inhibitorsand those associated with retinoid-based therapies have led to the the-ory that protease inhibitors alterretinoid metabolism, resulting inthe aforementioned cutaneous sideeffects. Toma et al34 found thatindinavir and several other proteaseinhibitors can significantly increaseplasma retinoic acid concentrations.Some of the proposed mechanismsinclude enhanced conversion of retinolto retinoic acid caused by an in-dinavir-mediated increase in theactivity and/or expression of retinaldehydrogenase, inhibition of cyto-chrome P450-mediated catabolismof retinoic acid, and/or increasedactivity of retinoid-responsive geneproducts.34 Anti-epidermal growthfactor receptor (EGFR) chemothera-peutic agents (eg, cetuximab, gefitinib,lapatinib) have been associated withthe development of paronychia, aswell.28,31,35 The inhibition of EGFRby anti-EGFR agents has been impli-cated in the development of chronicparonychia.28

Malignancies of the periungualregion and paraneoplastic conditionsmay mimic acute or chronic par-onychia. Several conditions causea paronychia-like presentation,including squamous cell carci-noma,36,37 melanoma,38 Kaposisarcoma,39 digital papillary adeno-carcinoma,40 myeloma-associatedsystemic amyloidosis,41 bronchogeniccarcinoma,42 renal cell carcinoma,43

subungual keratoacanthoma, andleukemia cutis.44 These diagnosesshould be considered in patients whopresent with signs and symptoms ofparonychia, particularly in those with

Figure 8

Lateral (A) and dorsal (B) photographs of the thumb demonstrating chronicparonychia. Note that the nail is thickened, yellowed, ridged, and rounded.




recalcitrant paronychia or those witha history of cancer.

Nonsurgical ManagementThe first step in management ofchronic paronychia is avoiding irri-tants and moisture. Topical and sys-temic therapies can be used, aswell.21,23,24,45,46 Tosti et al24 per-formed a double-blind randomizedcontrolled trial to compare theeffectiveness of systemic antifungalmedications (250 mg of terbinafinedaily or 200 mg of itraconazoledaily) with that of a topical cortico-steroid (0.1% 5 mg of methylpred-nisolone aceponate daily). A placebowas provided for each group. Thetreatment period lasted 3 weeks. At 3weeks, the authors noted a signifi-cant increase in the clinical cure rateof the topical corticosteroid groupcompared with that of the antifungalgroup (P , 0.01). The authorsreported improved or cured par-onychia in 42 of 48 nails (87.5%) inthe corticosteroid group comparedwith 22 of 64 nails (34.4%) inthe itraconazole group and 19 of57 nails (33.3%) in the terbinafinegroup. Tosti et al24 concluded thattopical corticosteroid therapy shouldbe used as a first-line treatment forchronic paronychia. They also rec-ommended that chronic paronychialinfection should be regarded as aninflammatory disorder of the nailfold rather than an onychomycosis.In a study of 17 patients with

chronic paronychia, Daniel et al45 re-ported good results with a combinedirritant avoidance regimen and topi-cal application of a 0.77% ciclopiroxsuspension, a broad-spectrum anti-fungal with anti-inflammatory prop-erties,47 for 6 to 12 weeks. Chronicparonychia resolved in all 17 pa-tients. The authors recommendedmanagement of primary factors (eg,exposure, irritants, inflammation)and secondary fungal colonization toreduce recurrence and avoid treat-ment failure caused by the inflam-

matory effects of secondary fungalcolonization. The addition of a topi-cal antifungal agent to topical corti-costeroid therapy has been described;however, the use of a topical anti-fungal and corticosteroid has notbeen shown to be superior to the useof a topical corticosteroid alone.In a study of 45 patients with

chronic paronychia, Rigopouloset al46 compared the safety and effi-cacy of twice-daily application of0.1% betamethasone 17-valerateointment with application of 0.1%tacrolimus ointment or an unmedi-cated emollient over a 3-weekperiod. Both the betamethasone andtacrolimus groups demonstratedstatistically significant improvement(P , 0.001) in cure or improvementrate versus the emollient group, withtacrolimus therapy demonstratingthe highest efficacy. Thus, a 1- to 2-week course of 0.05% betametha-sone cream or 0.1% betamethasonesolution or lotion has been recom-mended for management of chronicparonychia.1 For refractory cases ofchronic paronychia, some authorshave recommend a trial of a systemicantifungal before proceeding with aninvasive procedure.1 In an earlierstudy on paronychia, Rigopouloset al1 described the use of a shortcourse of systemic corticosteroids forpatients with severe involvement ofmultiple fingers.

Surgical ManagementSurgical management of chronic par-onychia is typically reserved forrefractory cases. Several surgicaltechniques have been described andinvolve excision or elevation of theinvolved tissue of the eponychium.Chronic inflammation of the epo-nychium leads to progressive fibrosis,edema, induration, and rounding ofthe cuticle border, which act togetherto compromise the natural barrierfunction and impair blood flow to theaffected tissues, making spontaneoushealing difficult.48,49

In 1976, Keyser and Eaton48

described the use of eponychialmarsupialization for management ofchronic paronychia. The originaltechnique involved excision ofa crescent-shaped area of the dorsalaspect of the proximal nail foldwithout concomitant nail removal.The excision area begins 1 mm fromthe distal border of the eponychiumand extends approximately 6 mmproximally and from one lateral nailfold to the other to include all in-flamed tissue. Excision is followedby hydrogen peroxide soaks anddressing changes until reepitheliali-zation occurs (typically within 2weeks). The authors noted excellentresults with this technique, withchronic paronychia cured in 28 of31 digits. The exact mechanism bywhich marsupialization promoteshealing is not well understood.In 1981, Baran and Bureau50

described a technique that involved enbloc excision of the proximal nail foldwithout nail plate removal. A 5- to6-mm–wide section of involved epo-nychial tissue spanning from one lat-eral nail fold to the other was excisedand, in contrast to marsupialization,a distal rim of tissue was not spared.After en bloc excision, postoperativecare consisted of dressing changes andapplication of a topical antibioticpreparation. The proposed benefit isa simpler andmore effective techniquethan marsupialization with concomi-tant nail plate removal that providessatisfactory functional and cosmeticresults. However, objective outcomedata were not provided in the study.In a long-term study of 25 patients

(28 fingers) with chronic paronychiatreated with eponychial marsupializa-tion with or without nail removal,Bednar and Lane51 reported better re-sults in the group that underwentsimultaneous removal of the nail plate(Figure 9). Of the 23 patients with nailirregularities, the first seven weretreated with eponychial marsupializa-tion without nail removal. Two of


March 2014, Vol 22, No 3 171


these patients had a recurrence. Theremaining 16 patients underwentmarsupialization with nail removal,with no recurrence reported (P ,0.05). This technique differed slightlyfrom the technique described by Key-ser and Eaton48 in that a 3-mm cres-cent of tissue was excised and the

underlying fat and subcutaneous tissuewere left in place. In addition tomarsupialization, all patients weretreated with hydrogen peroxide soaksfollowed by cleansing with chlorhex-idine gluconate and, in patients withpositive cultures, oral antibiotics for14 days or until cultures were negative.

Grover et al49 examined the effec-tiveness of en bloc excision of theproximal nail fold with and withoutnail removal for management ofchronic paronychia. En bloc excisionof the proximal nail fold was per-formed followed by a 5- to 7-daycourse of oral antibiotics as wellas daily cleansing with antibioticsolution and application of topicalantibacterial, antifungal, and corti-costeroid creams. Of 30 patients, 12in group I (en bloc excision withoutnail removal) and 13 in group II (enbloc excision with nail removal)completed the treatment protocol.The authors reported that 70% ofpatients in group II were cured ver-sus only 41% in group I.Pabari et al52 described the use of

the Swiss roll technique for manage-ment of both acute and chronic par-onychias with runaround infection ofboth nail folds. The eponychium iselevated by making an incision onboth sides of the nail fold and then theeponychium is reflected proximally.The wound is irrigated and the fold isrolled back over a roll of nonadherentgauze dressing and then anchoredin place with nonabsorbable sutures(Figure 10). Postoperative application

Figure 9

Photographs of a finger before (A) and after (B) eponychial marsupializationwith nail removal. A, A small, crescent-shaped area proximal to theeponychium is marked for excision. B, The crescent of inflamed tissue isexcised and the nail plate is removed. (Courtesy of Daniel Zlotolow, MD,Philadelphia, PA.)

Figure 10

Intraoperative photograph (A) and illustration (B) demonstrating the Swiss roll technique for management of an acuteparonychia. A, The nail fold is incised, reflected, and rolled over nonadherent gauze. B, The edge of the nail fold isanchored with nonabsorbable sutures. (Panel A reproduced with permission from Pabari A, Iyer S, Khoo CT: Swiss rolltechnique for treatment of paronychia. Tech Hand Up Extrem Surg 2011;15[2]:75-77.)




of topical medications, either anti-biotics or steroids, was not described.The dressing and anchoring sutureswere removed 2 to 7 days post-operatively. The nail fold was allowedto return to its original position andheal by secondary intention. Proposedbenefits of this technique include theability to retain the nail and to avoidcreating a skin defect. The authorsachieved “excellent cure rates” withthis technique.With regard to treatment failure or

recurrence of symptoms after treat-ment, a paucity of data are available.This is partly due to variability inreporting outcomes as improvedversus cured. In a study of patientstreated with marsupialization withor without nail removal, Bednar andLane51 reported two recurrences inthe group that did not undergo nailremoval. Both recurrences weretreated with marsupialization withnail removal. One went on to cureand the other had persistent naildeformity and tenderness. No re-currences or treatment failures werereported in the group treated withmarsupialization with nail removal.Daniel et al45 treated simple chronicparonychia with a combined regi-men of ciclopirox and irritantavoidance and reported a cure rateof 100%. Although the authorsfound that the use of a topicalantifungal was effective for pre-venting recurrence of chronic par-onychia, no control group wasavailable for comparison.Studies have emphasized irritant

avoidance as a key factor in achievingsatisfactory results in managementof chronic paronychia.1,2,14,15,21,45

When patients are unable orunwilling to comply with this rec-ommendation, treatment failure islikely. However, a thorough evalu-ation should be performed in recal-citrant cases of chronic paronychiato rule out atypical etiologies such asthe use of specific medications (eg,antiretrovirals) or malignancies.

Summary

Acute and chronic paronychias of thehand caused by infections are com-mon. Acute paronychia typicallyindicates an acute bacterial infection.Cases without an associated abscessoften can be treated successfully withan oral antibiotic regimen and soaks.The presence of an abscess is an indi-cation for surgical drainage, which canbe accomplished through varioustechniques based on the extent ofinfection, presence of an ingrown nailor subungual abscess, and surgeonpreference. Further research is neededto determine whether oral antibiotictherapy is needed in addition to surgi-cal drainage. Therefore, the decision toprescribe antibiotic therapy afterdrainage is based on clinical judgmentand the extent of infection.Chronic paronychias represent per-

sistent inflammationof thenail fold thatis multifactorial in origin. Exposure toenvironmental and occupational irri-tants appears to be the primary cause ofthis clinical entity, with secondary fun-gal colonization common and a likelycontributor to ongoing inflammation.Management of chronic paronychiabegins with avoidance of irritants andtopical anti-inflammatory medication.The addition of topical antifungalagents has been recommended; how-ever, this is controversial.Surgical management is reserved

for refractory cases of paronychia.Several surgical procedures have beendescribed, with good to excellent re-sults reported. Nail removal in con-junction with tissue excision seems toportend better results. Larger, pro-spective studies are needed to identifya treatment regimen that is clearlysuperior for management of acute andchronic paronychias.

Acknowledgment

The authors would like to thankRobert Strauch,MD, JeffreyYao,MD,

and Daniel Zlotolow, MD, for pro-viding photographs from their per-sonal collections for this article.

References

Evidence-based Medicine: Levels ofevidence are described in the table ofcontents. In this article, references 17,24, 45, 46, and 51 are level II studies.References 23 and 25 are level IIIstudies. References 48 and 49 arelevel IV studies. References 1, 8, 11,14, 15, 18-22, 50, and 52 are level Vexpert opinion.

References printed in bold typeare those published within the past5 years.

1. Rigopoulos D, Larios G, Gregoriou S,Alevizos A: Acute and chronic paronychia.Am Fam Physician 2008;77(3):339-346.

2. Rockwell PG: Acute and chronicparonychia.Am Fam Physician 2001;63(6):1113-1116.

3. Fassler PR: Fingertip injuries: Evaluationand treatment. J Am Acad Orthop Surg1996;4(1):84-92.

4. Zook EG: Anatomy and physiology of theperionychium. Hand Clin 1990;6(1):1-7.

5. Zook EG, Van Beek AL, Russell RC,Beatty ME: Anatomy and physiology of theperionychium: A review of the literatureand anatomic study. J Hand Surg Am 1980;5(6):528-536.

6. Zaias N: The Nail in Health and Disease.Lancaster, England, SP Medical andScientific Books, 1980, pp 31-34.

7. Zaias N: The regeneration of the primatenail studies of the Squirrel Monkey,SSaimiri. J Invest Dermatol 1965;44:107-113.

8. Brook I: Paronychia: A mixed infection.Microbiology and management. J HandSurg Br 1993;18(3):358-359.

9. Brook I: Bacteriologic study of paronychiain children.Am J Surg 1981;141(6):703-705.

10. Brook I: Aerobic and anaerobicmicrobiology of paronychia. Ann EmergMed 1990;19(9):994-996.

11. Turkmen A, Warner RM, Page RE: Digitalpressure test for paronychia. Br J Plast Surg2004;57(1):93-94.

12. Rubright JH, Shafritz AB: The herpeticwhitlow. J Hand Surg Am 2011;36(2):340-342.


March 2014, Vol 22, No 3 173


13. Clark DC: Common acute hand infections.Am Fam Physician 2003;68(11):2167-2176.

14. Daniel CR III: Paronychia. Dermatol Clin1985;3(3):461-464.

15. Jebson PJ: Infections of the fingertip:Paronychias and felons.Hand Clin 1998;14(4):547-555, viii.

16. StevanovicMV:Acute infections, inWolfe SW,Pederson WC, Hotchkiss RN, Kozin SH, eds:Green’s Operative Hand Surgery.Philadelphia, PA, Elsevier, 2011, pp 41-84.

17. Wollina U: Acute paronychia: Comparativetreatment with topical antibiotic alone or incombination with corticosteroid. J EurAcad Dermatol Venereol 2001;15(1):82-84.

18. Tosti R, Ilyas AM: Empiric antibiotics foracute infections of the hand. J Hand SurgAm 2010;35(1):125-128.

19. Carley SD: Best evidence topic report:Towards evidence based emergency medicine.Best BETs from the Manchester RoyalInfirmary. Emerg Med J 2005;22(1):43.

20. Ritting AW, O’Malley MP, Rodner CM:Acute paronychia. J Hand Surg Am 2012;37(5):1068-1070.

21. Canales FL, Newmeyer WL III, Kilgore ESJr: The treatment of felons andparonychias. Hand Clin 1989;5(4):515-523.

22. Ogunlusi JD, Oginni LM, Ogunlusi OO:DAREJD simple technique of drainingacute paronychia. Tech Hand Up ExtremSurg 2005;9(2):120-121.

23. Daniel CR III, Daniel MP, Daniel CM,Sullivan S, Ellis G: Chronic paronychia andonycholysis: A thirteen-year experience.Cutis 1996;58(6):397-401.

24. Tosti A, Piraccini BM, Ghetti E,Colombo MD: Topical steroids versussystemic antifungals in the treatment ofchronic paronychia: An open, randomizeddouble-blind and double dummy study.J Am Acad Dermatol 2002;47(1):73-76.

25. Stone OJ, Mullins JF: Experimental studieson chronic paronychia. Arch Dermatol1964;89:455-460.

26. Zerboni R, Angius AG, Cusini M,Tarantini G, Carminati G: Lamivudine-induced paronychia. Lancet 1998;351(9111):1256.

27. Tosti A, Piraccini BM, D’Antuono A,Marzaduri S, Bettoli V: Paronychiaassociated with antiretroviral therapy. Br JDermatol 1999;140(6):1165-1168.

28. Rigopoulos D, Gregoriou S, Belyayeva Y,Larios G, Gkouvi A, Katsambas A: Acuteparonychia caused by lapatinib therapy.Clin Exp Dermatol 2009;34(1):94-95.

29. Nakano J, Nakamura M: Paronychiainduced by gefitinib, an epidermal growthfactor receptor tyrosine kinase inhibitor.J Dermatol 2003;30(3):261-262.

30. Dominguez MV, Ceballos VC, Costa RV,Lara TE, Florencio VD: Paronychia in anHIV-infected patient under nelfinavirtherapy. J Eur Acad Dermatol Venereol2007;21(5):710-711.

31. Konheim A, Brebach E, Samuel J,Mellott A, Gandhi M, Lacouture ME:Magnetic resonance imaging of paronychiainduced by cetuximab. Clin Exp Dermatol2009;34(7):e258-259.

32. Daudén E, Pascual-López M,Martinez-García C, García-Díez A:Paronychia and excess granulation tissue ofthe toes and finger in a patient treated withindinavir. Br J Dermatol 2000;142(5):1063-1064.

33. Sass JO, Jakob-Sölder B, Heitger A,Tzimas G, Sarcletti M: Paronychia withpyogenic granuloma in a child treated withindinavir: The retinoid-mediated side effecttheory revisited. Dermatology 2000;200(1):40-42.

34. Toma E, Devost D, Chow Lan N,Bhat PV: HIV-protease inhibitors alterretinoic acid synthesis. AIDS 2001;15(15):1979-1984.

35. Dianichi T, Tanaka M, Tsuruta N,FurueM, Noda K: Development of multipleparonychia and periungual granulation inpatients treated with gefitinib, an inhibitorof epidermal growth factor receptor.Dermatology 2003;207(3):324-325.

36. Bowles F, Wells H: Paronychia: Not alwayswhat it seems. Emerg Med J 2011;28(4):342.

37. Fung V, Sainsbury DC, Seukeran DC,Allison KP: Squamous cell carcinoma of thefinger masquerading as paronychia. J PlastReconstr Aesthet Surg 2010;63(2):e191-e192.

38. Ware JW: Sub-ungual malignant melanomapresenting as sub-acute paronychiafollowing trauma. Hand 1977;9(1):49-51.

39. Keith JE Jr, Wilgis EF: Kaposi’s sarcoma inthe hand of an AIDS patient. J Hand SurgAm 1986;11(3):410-413.

40. Gorva AD, Mohil R, Srinivasan MS:Aggressive digital papillaryadenocarcinoma presenting as

a paronychia of the finger. J Hand Surg Br2005;30(5):534.

41. Ahmed I, Cronk JS, Crutchfield CE III,Dahl MV: Myeloma-associated systemicamyloidosis presenting as chronicparonychia and palmodigital erythematousswelling and induration of the hands. J AmAcad Dermatol 2000;42(2 pt 2):339-342.

42. Khokhar N, Lee JD: Phalangeal metastasis:First clinical sign of bronchogeniccarcinoma. South Med J 1983;76(7):927.

43. Troncoso A, Ro JY, Grignon DJ, et al:Renal cell carcinoma with acrometastasis:Report of two cases and review of theliterature. Mod Pathol 1991;4(1):66-69.

44. Patel MR, Malaviya GN: Chronicinfections, in Wolfe SW, Pederson WC,Hotchkiss RN, Kozin SH, eds: Green’sOperative Hand Surgery. Philadelphia, PA,Elsevier, 2011, pp 97-98.

45. Daniel CR III, Daniel MP, Daniel J,Sullivan S, Bell FE: Managing simplechronic paronychia and onycholysis withciclopirox 0.77% and an irritant-avoidanceregimen. Cutis 2004;73(1):81-85.

46. Rigopoulos D, Gregoriou S, Belyayeva E,Larios G, Kontochristopoulos G,Katsambas A: Efficacy and safety oftacrolimus ointment 0.1% vs.betamethasone 17-valerate 0.1% in thetreatment of chronic paronychia: Anunblinded randomized study. Br JDermatol 2009;160(4):858-860.

47. Rosen T, Schell BJ, Orengo I: Anti-inflammatory activity of antifungalpreparations. Int J Dermatol 1997;36(10):788-792.

48. Keyser JJ, Eaton RG: Surgical cure ofchronic paronychia by eponychialmarsupialization. Plast Reconstr Surg1976;58(1):66-70.

49. Grover C, Bansal S, Nanda S, Reddy BS,Kumar V: En bloc excision of proximal nailfold for treatment of chronic paronychia.Dermatol Surg 2006;32(3):393-399.

50. Baran R, Bureau H: Surgical treatment ofrecalcitrant chronic paronychias of thefingers. J Dermatol Surg Oncol 1981;7(2):106-107.

51. Bednar MS, Lane LB: Eponychialmarsupialization and nail removal forsurgical treatment of chronic paronychia.J Hand Surg Am 1991;16(2):314-317.

52. Pabari A, Iyer S, Khoo CT: Swiss rolltechnique for treatment of paronychia.Tech Hand Up Extrem Surg 2011;15(2):75-77.




Documents

Review Article Acute and Chronic Paronychia of the Handupload.orthobullets.com/journalclub/free_pdf/24603826... · 2016. 10. 3. · the paronychia (Figure 3). Blanching may indicate