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CHAPTER I2 AT\?ICAL PYODERMA GANGRENOSUM of TFIE LOWER EXTREMITY a Case Presentation and Comprehensive Disease Overview

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CHAPTER I2 AT\?ICAL PYODERMA GANGRENOSUM of TFIE LOWER EXTREMITY a Case Presentation and Comprehensive Disease Overview CHAPTER I2 AT\?ICAL PYODERMA GANGRENOSUM OF TFIE LOWER EXTREMITY A Case Presentation and Comprehensive Disease Overview Gerard V Yu, DPM, FACFAS Robert M. Brarens, DPM Amanda Meszdt os, DPM Pyoderma Gangrenosum (PG) is a destructive, inflamma- Von den Drieschr''' and75o/o by Bennett er al']ro the legs. tory skin disease first reported in 1916 as "phagedenisine Other variants include Pustular PG (a.k.a. Atypical PG geometrique" by Brocq. It was subsequently characterized (A?G)) that typically presents on the extensor surfaces of as PG by Brunsting, Goeckerman and O'Leary in 1930 the upper extremiry and trunk, Superficial Bullous PG and again in 7982.'''1 These authors have implicated (SBPG) generally presenting on the hands, neck and head, streptococci and staphylococci as the causative agents and Vegetative PG (a.k.a. Pyostomatitis Vegetans (\?G)) because of the seemingly purulent nature of the disease.' Of that presents in the oral cavity and genitais (all). Additional interest is after nearly 74 years the precise etiology of this forms include Malignant PG (MPG), Superficial condition still remains unclear. Multiple authors have Granulomatous PG (SGPG) and Familial PG (FPG). The suggested a noninfectious dysregulation of the immune variant's specific associated underlying disease predilection system as the primary etiology,3 while others have will be covered later in the text. hypothesized a possible genetic component.''3 Currently it is believed that PGt infectious involvement is secondary if CASE PRESENTHTION: present at all. Belonging to the dermatologic class of neutrophilic dermatoses, this pathologic condition should A 53-year-old Caucasian female presented June 2003 with be considered in a differential diagnosis of chronic non- a chief complaint of redness, sweiling, and exquisite pain healing ulcerations recalcitrant to normal therapies.' Since on the medial portion of the left ankle and adjacent the specific pathogenesis of this clinic entiry remain pretibial area. She related redness and pain beginning undefined, its management for the most part is empirically approximately one week prior at which time she sought based on clinicopathologic findings.'-3 medical assistance at the local urgent care center. She was Pyoderma Gangrenosum (PG) is a rare clinical diagnosed with cellulitis, given a short course of entity with a reported incidence of 1 in 100,000 persons Augmentin@ (Amoxicillin/Clavulanate) which she each year.t It has been reported to both be equai in completed. The erythema increased and a central bluish- distribution between the sexes,''a't with some authors purple blister developed that erupted some time during the I suggesting a preference of women to men 2'.7.2'6 week and began to express a seropurulent yellow discharge. Predominately presenting between the ages of 25 and 50, She related a fever of 100.1F the evening prior, but denies PG has been reported in both infants'r and children.'o chills, nausea, vomiting, diarrhea or generalized malaise. The associated prevalence of underlying systemic She denied any significant trauma to the area at this time. disease ranges from 50-7\o/o of affected patients with The patient was familiar to our service having Inflammatory Bowel Disease as the leading co-morbidity at previously undergone a subtalar joint fusion in 7997 for a reported incidence of 30o/o.2)t't Systemic disease onset treatment of left posterior tibial tendon dysfunction and however may precede, coincide, or follow the presentation adult acquired flat foot syndrome healing without of a PG lesion.' Death from PG is rare, generally occurring complication (Figure 1). At the time of her original surgery from complications of the associated disease or as a result her past medical history was positive for a single episode of ofits therapy. gout, rheumatoid arthritis (diagnosed in 1995), and Lupus There are four predominant variants of PG presently (diagnosed in 1995). Her Rheumatologist was managing accepted in the literature, the most common being the her medically on Plaquenilt, Voltaren'o and Prednisone. ulcerative form (UPG). UPG has a prevalence to the lower She was also treated conservatively for a Morton's extremiq, and trunk, with a reported incidence of 80% by neuroma in the right foot with complete resolution. CHAPTER 12 6t Prior to presentation at our oflice for her current every 5-7 months since its original appearance. exacerbation, she had been managed by her primary care On her last hospitalizarion, in November 2002, she physician and had been hospitalized on multiple occasions was started on prednisone (80mg QD) for a suspected for the same problem, beginning December 99', in a vasculitis. She was referred to a dermatologist and a nationally known local tertiary care center where she second rheumatologist for further consultation. A two underwent several "complete workups" for this problem. week course of oral Levaquin@ was prescribed along with The patientt labs in December 99' were remarkable for an Iocal compressive dressings daily. At the time of her elevated platelet count of 498WuL, C-reactive protein consultation with the dermatologist her "cellulitis" had (CRP) of 4.lmgldl and erythrocyte sedimenration rate resolved completely minimizing the value of the consult. (ESR) of S3mm/hr. A CBC with differential was done and The rheumatologist questioned her previous diagnosis of within normal limits. An anti-nuclear antibody (ANA) rheumatoid arthritis (RA), and lupus, however believed panel of 0.2 and rheumatoid factor (RF) of iess than 20 there was an undefined underlying connective tissue were both considered negative. (Thble 1) She did have a disease, and continued the patient on 60 mg daily oral positive single light growth blood culture of coagulase Prednisone therapy for treatment of the connectiye tissue negative staphylococcus. An arthrocentesis ofher left ankle disorder for three and a half months. During this time her was unremarkable; cultures were negative. An MRI was leg remained symptom free, and without flare-up. She performed showing a subcutaneous effusion medial was taken off of the steroids due to a combination of and superior to the ieft medial malleolus with no bony significant weight gain and systemic side effects including involvement. She underwent rV antibiotic therapy with high blood pressure, headaches, and hirsutism from Vancomycin while hospitalized and was discharged on oral prolonged steroid use. In June of 2003 (2 months after Dicloxacillin and advised to follow up with a rheumatologist. discontinuing steroids) she presented with increased She was seen for follow-up by a rheumatologist symptoms in the same area as the previous lesions. following discharge. He felt she had a cellulitis of The patientt current medical history is positive for unknown origin and suggested it was from the retained recurrent urinary tract infections, non-inflammatory hardware with possible osteomyelitis despite the negative generalized arthritis and a continuing questionable diag- MRI study. A three phase bone scan thar was interpreted nosis of RA, SLE, and inflammatory bowel disease (IBD) as subacute inflammatory arthrids involving the left rwo weeks prior to this visit. Her medications included proximal foot without significant focal abnormaliry noted Zolpidem, Propoxyphene, Hydrocodone, ketorolac, and over the left ankle. Clinical correlation was suggested. Her hormone replacement therapy. dicloxacillin and NSAID therapies were discontinued. Our physical examination on June 16th 2003 Although she was cleared of the concern of septic revealed an area of significant erythema and inflammation arthritis; he did feel the potential for osteomyelitis which was exquisitely painful to light touch making warranted treatment. A PICC line was established and examination essentially limited to our visual observation. a 6 week course of IV antibiotics was prescribed by (Figure 2) The erythema had nonspecific borders, infectious disease. In addition, the patient received an oral encompassing primarily the medial aspect of the ankle and prednisone taper. The "cellulitis" has been recurrent with Ieg. The mild calor was disproportionate to the severiry of episodes of complete resolution followed with a reoccurrence the clinical picture. There was a mild joint effusion with Figure 1. STJ fusion completed in 1997 for the treatment ofAdult Acquired Figrrre 2. 6.16.03-Clinical presentation Nonspecific erythematous border. Flat Foor. Unevenrlul po\(operJri\e couh(. Three 0.5cm bullae without obsenable drainage and a yellow opaque crust proximally. CHAPTER 12 Thble 1 SUMMARY OF I-ABORAIORY FINDINGS IN THIS PAIIENT Date Test Result Normal Values 12.12.99 synovial fluid analysis bloody, turbid clear, yellow o/oNeut = 80 0-25o/o no organisms on GS/C&S 12.13.99 \xtsc 10.65 4.0-1 1.0 k/ul PLI 4t9 150-400 K/uL 12.t4.99 Haptoglobin 3t4 37-246 mgldL LD 159 t00-220 ulL 72.15.99 \TBC 8.74 4.0-11.0 k/ul- PLT 457 150-400K/uL %Neut 65.t 40-70o/o o/oLymph 24.5 22-44o/o Albumin 3.5 3.5-5.0 gldL CRP 5) 0-1.0mg/dl Iron 20 30-140 ug/dl TIBC 301 210-415 ug/dl IronSat 7 11-46 o/o ANA 0.2 (negative) <1.5 OD ratio RF <20 (negative) <20IUlmL C3 complement 140 76-199 mg/dl C4 complement t5 16-64 mgldL 12.78.99 CRP 2.8 0-2.0 mgldL X-ray O for osteo MRI (-) for osteo 12.27.99 CRP 4.1 0-1.0 mg/dl ESR 83 0-30 mm/hr 12.30.99 triphase Tech-99 scan (-) for osteo 3.22.00 \TBC 6.55 4-1t.]kluL o/oNeut 54.40o/o 40-70o/o CRP ) 0-1.0mg/dl ESR 57 0-3Omm/hr C3 complement 96 75-t99mgldL C4 complement 14 r6-64mgldL 11.2001 ANA
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