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When Necrotizing Fasciitis Is Complicated By Gout

Emphasizing the need for early diagnosis of necrotizing fasciitis, these authors offer a closer look at a case involving progressive pain and erythema in the lower extremity for a 76-year-old patient with multiple comorbidities.

Necrotizing fasciitis is a life- and limb-threatening disease characterized by rapidly progressive skin and soft tissue infection causing widespread tissue necrosis and systemic illness. The bacterial infection quickly spreads along fascial planes between the subcutaneous tissues and fascia producing toxins resulting in tissue ischemia, liquefactive necrosis and systemic illness.1 One may also use the term necrotizing soft tissue infection to encompass cases in which the extent of necrosis progresses beyond the fascia to include muscle, skin and other surrounding tissue.2 

There are four types of necrotizing fasciitis.3 The most common type is Type I polymicrobial infection, which accounts for 55 to 90 percent of the cases and often presents in patients with immunodeficiency such as those with diabetes. Type II refers to monomicrobial infections with pathogens such as group A streptococcus. The Centers for Disease Control and Prevention (CDC) tracks necrotizing fasciitis caused by group A streptococcus and estimates 700 to 1,200 cases each year in the United States although this is likely an underestimation.4 Type III necrotizing fasciitis describes cases with gram negative pathogens and includes marine associated pathogens such as the Vibrio species. Type IV necrotizing fasciitis is associated with fungal infections.3

Necrotizing fasciitis is classically a clinical diagnosis, which is confirmed with intraoperative findings.3,5 It most commonly affects the lower extremities, presenting there in approximately 50 percent of cases.5 Clinical exam findings include disproportionate pain with tenderness beyond apparent margins of infection, erythema, blistering, crepitus and warmth.1,6 A delay in cutaneous manifestations early in the course of the disease process can mask the extent of infection on initial evaluation. Necrotizing fasciitis can spread one inch per hour with little associated overlying skin change.1 Classic radiographic findings include dissecting soft tissue emphysema along fascial planes but this is only apparent in 16.9 to 55 percent of patients and may not be evident until later in the disease process.5,7 Ultrasound, computed tomography (CT) and magnetic resonance imaging (MRI) provide higher sensitivity and specificity for necrotizing fasciitis in comparison to plain film radiography.5 

Computed tomography is the primary imaging modality for evaluation of necrotizing fascitiis. Findings on CT include asymmetric thickening of fascia, soft tissue emphysema, blurring of fascial planes, inflammatory fat stranding, reactive lymphadenopathy and non-enhancement of muscular fascia.1,5 The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score may be useful in distinguishing necrotizing fasciitis from other soft tissue infections.8 Both laboratory values and imaging may have little to add diagnostically when clinical suspicion is high enough to warrant treatment.2 

The treatment of necrotizing fasciitis requires emergent aggressive surgical debridement with the goal of resecting to a margin of healthy soft tissue.3 This may and often does require multiple operative debridements. Reported mortality associated with necrotizing fasciitis ranges between 25 to 35 percent and increases directly proportional with the time to index surgical intervention.1 Multiple researchers have identified delay in surgery as an independent predictor of mortality.5,7,9 Early recognition may be difficult as the disease is often clinically similar to other diagnoses such as isolated cellulitis and gout. Failure to accurately diagnose and anticipate the severity of infection upon presentation despite clinical appearance can negatively impact mortality and limb salvage. With this in mind, we present a case of necrotizing fasciitis complicated by a comorbid diagnosis of gout requiring an extensive limb salvage effort.  

When A Patient Presents With Recalcitrant Pain and Redness In The Right Ankle 

A 74-year-old male with a history of poorly controlled type 2 diabetes mellitus and coronary artery disease transferred to our hospital with right ankle pain recalcitrant to intravenous antibiotics that were initiated at an outside hospital. Other considerations with the patient’s medical history include current use of an automatic implantable cardioverter defibrillator; stage 3 chronic kidney disease; the use of diuretic medication to help treat heart failure; hyperlipidemia; hypertension; and a history of gout.

Podiatry consultation took place on the second day of hospitalization at our institution. The physical exam revealed diminished sensation, intact vascular status and tenderness with palpation to the posterior right heel. Erythema was present along the Achilles tendon and posterior hindfoot/ankle but there was no break in the integument (see first photo above). Prior workup included blood cultures, unremarkable plain film radiographs, an ultrasound of the posterior ankle with retrocalcaneal bursitis described by the radiologist and a serum uric acid lab value within normal limits. 

On our consultation, we noted a Laboratory Risk Indicator for Necrotizing Fasciitis score of 1 (low risk) for elevated glucose. The patient’s C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were mildly elevated to 11.7 mg/dL (reference range 0.0 to 0.8 mg/dL) and 58 mm/hr (reference range zero to 15 mm/hr) respectively. Intravenous antibiotics were discontinued on the third day at the hospital. Gout was the suspected diagnosis with confirmation by dual-energy computed tomography (see second photo above) on the patient’s third day at the hospital. The patient’s primary medical team started colchicine for treatment.  

The patient reported a reduction in pain and the clinical appearance of the erythema improved. Discharge plans included a 15-day tapered course of oral prednisone. 

The patient returned to emergency services three days after discharge with increased pain and swelling to the right leg. His white blood cell count was elevated to 15.8 cells/μL at that time and there was an elevated D-dimer as well. A lower extremity venous duplex ultrasound revealed no evidence of deep vein thrombus. The patient again received a diagnosis of gout but the emergency room provider also prescribed a five-day course of cefadroxil. The emergency room provider recommended follow-up with his primary care provider through the local Veterans Administration (VA) facility, but there was no discharge follow-up outpatient appointment arranged with the podiatry department. 

The next evaluation took place at the local VA 23 days after initial hospitalization discharge. An ambulance transferred the patient to emergency services at an outside hospital with increased pain to the right leg and weakness. In the emergency department, providers noted erythema and open necrotic ulceration to the posterior right leg (see third photo above). The patient was tachycardic, tachypneic and hypotensive with a systolic blood pressure of 90 mmHg. The patient received an intravenous fluid bolus. After blood cultures were obtained, the patient received initial antibiotics consisting of metronidazole and levofloxacin. Labs obtained in the emergency department included an elevated white blood cell count of 14.12 cells/μL and an elevated CRP of 68.4 mg/L. 

The Laboratory Risk Indicator for Necrotizing Fasciitis score based on initial lab scores was four points, indicating low risk for necrotizing fasciitis. Radiographs of the right ankle revealed soft tissue emphysema extending from the calcaneus to the mid-shaft of the tibia and tracking along the course of the Achilles tendon (see fourth photo above). The patient was subsequently transferred to our hospital’s critical care unit via ambulance with concerns of severe sepsis and necrotizing fasciitis. 

Pertinent Aspects Of Emergent Surgical Intervention

Podiatry was consulted upon the patient’s hospital admission. Physical exam findings revealed a necrotic ulceration to the posterior aspect of the right heel with exposed Achilles tendon, purulent drainage, surrounding erythema and tenderness to palpation (see third photo above). We emergently took the patient to the operating room for incision and drainage with removal of all nonviable tissue and placement of antibiotic polymethylmethacrylate cement-impregnated beads.

After general anesthesia was administered via endotracheal intubation, we positioned the patient in a padded prone position with a thigh tourniquet applied but never inflated. We created a longitudinal linear incision from the posterior heel midline to the distal one-third of the leg and excised the existing ulceration at full thickness, sending the specimen for pathology examination. Gross purulence was evident surrounding the site of ulceration and we obtained deep tissue and swab cultures. 

The distal Achilles tendon itself was liquefied and nonviable. We accordingly excised this portion of the tendon and sent the specimen for pathology. The exposed calcaneus appeared discolored and was in close proximity to the infection so we performed a bone biopsy for histopathological analysis. The infection spread along the deep crural fascia plane and the fascia appeared gray and ecchymotic. After further excision of the affected portions of the fascia, we sent those out for histopathological exam as well. Excisional debridement included a portion of the aponeurosis and necrotic-appearing, nonviable gastrosoleus muscle. 

Following extensive debridement, only healthy-appearing viable, bleeding bone and soft tissue remained. After irrigation of the surgical site with a combination of saline and 50,000 IU of bacitracin we created antibiotic cement beads with a combination of polymethylmethacrylate bone cement and tobramycin. We added an additional 1 g of vancomycin as well as 2.4 g tobramycin to the original bone cement and tobramycin combination when creating the antibiotic beads. We implanted these antibiotic beads into the surgical site and subsequently utilized a povidone-iodine impregnated gauze roll (see fifth photo above). We then applied a bulky, well-padded Jones dressing to the operative lower extremity from the distal toes to the knee. 

The patient transferred back to the critical care unit in stable condition. 

After surgical debridement and cultures were obtained, the patient was started on postoperative, broad spectrum intravenous vancomycin and piperacillin/tazobactam. Intravenous fentanyl was available for pain control. On the second day in the hospital, the patient transferred out of the critical care unit to a bed on the general medical unit and vancomycin was discontinued based on preliminary culture results. 

The patient also returned to the operating room on the second hospital day for repeat incision and drainage. Exploration of the previous surgical site revealed no further abscess or infection. We irrigated again with a combination of saline and 50,000 IU of bacitracin. We excised the aponeurosis of the calf muscle and sent this as a specimen for histopathological analysis. To facilitate closure, we also excised the posterior aspect of the calcaneus and sent this to pathology. Employing absorbable and non-absorbable sutures, we partially closed the wound, leaving a remaining wound that measured 9.0 cm x 3.5 cm x 1.0 cm (see sixth photo above). We placed a silver reticulated foam sponge on the wound with negative pressure wound therapy (NPWT) set to continuous pressure at 125 mm Hg, and subsequently applied a bulky Jones dressing. The patient returned to the general medical floor for continued intravenous antibiotics and wound therapy. 

On the patient’s fourth day in the hospital, the Infectious Disease team switched intravenous antibiotics to ceftriaxone. Subsequent surgical culture results revealed Citrobacter freundii and Enterobacter cloacae complex that are both resistant to cefoxitin but otherwise susceptible to other antibiotics. Based on these results, the patient was switched to oral cefpodoxime on the fifth day in the hospital. Pathology results did not reveal osteomyelitis. Soft tissue samples sent to pathology returned with non-specific findings such as purulent inflammation. Pathology specimens did not show any tophaceous gout. 

On the patient’s fifth hospital day, the NPWT sponge change demonstrated no new evidence of infection and developing granulation tissue at the surgical site. The remaining wound measured 8.0 cm x 3.0 cm x 0.8 cm. The patient continued to receive NPWT set at a 125 mm Hg continuous mode. On the patient’s ninth hospital day, he was discharged to a skilled nursing facility with NPWT in place. Oral antibiotics continued for four days after hospital discharge.

Facilitating Wound Closure With Split-Thickness Skin Grafting

After the hospital discharge, the patient received twice weekly silver sponge changes through staff at the skilled nursing facility and through the attending surgeon’s wound clinic. The wound base continued to granulate and decrease in depth to a level where skin grafting became appropriate. Twenty-eight days after hospital discharge, the patient returned to the operating room with subsequent admission to the hospital floor. Debridement revealed healthy viable soft tissues and no further signs of infection. The measurements of the wound at this time were 7.5 cm x 2.5 cm. 

After harvesting of a 0.020-inch split thickness skin graft (STSG) from the posterolateral aspect of the ipsilateral thigh, we meshed and applied the graft to the recipient wound bed (see sixth photo above). After securing the graft with 3-0 chromic gut suture, we applied NPWT at 75 mm Hg continuous mode and a bulky Jones dressing. 

On the third postoperative day, there was nearly 100 percent take of the graft and no complications. On the fifth postoperative day, the patient was discharged back to the skilled nursing facility after removal of NPWT showed continued graft take. The patient continued to follow up in the attending surgeon’s wound clinic. The graft continued to mature and fully healed 24 days after application. At this point, we recommended use of a compressive stocking and daily moisturization, allowing partial weightbearing in a surgical boot. 

The patient was discharged from the skilled nursing facility two weeks later and was casted for a custom-fabricated dorsiflexion stop ankle foot orthosis (AFO). The hinges on the first AFO created a lateral ankle pressure ulceration so he subsequently switched to a solid AFO with complete resolution of the ulceration. The patient continued to feel unsteady with his gait, trialed several AFOs and ultimately switched to a noodle-type AFO with a deep heel cup. 

At the last follow-up, 27 months postoperatively, the patient had no new ulcerations and the graft site remained completely healed. The patient had 0/5 plantarflexion strength on the right operative limb and decreased muscle mass, but was able to ambulate with an eight-inch lace-up ankle boot and no gait aid. The patient subjectively reported no feelings of weakness to the operative leg.  

What The Literature Reveals About The Relationship Between Necrotizing Fasciitis And Gout

Emergent aggressive surgical debridement is the primary treatment for necrotizing soft tissue infections. Failure to identify the severity of the disease negatively impacts patient morbidity and mortality. Upward of 23 percent of lower extremity cases involving necrotizing fasciitis result in a proximal level of amputation or death.10 In a retrospective review involving 89 patients with necrotizing fasciitis admitted to a hospital over the course of five years, Wong and colleagues found that only 14.6 percent of patients had the correct diagnosis at the time of admission.7 In addition, they found that a greater than 24-hour delay in surgery increased the relative risk of mortality by 9.4 times. 

A relative lack of significant skin changes in early stages of necrotizing fasciitis in comparison to the severity of the disease is not uncommon due to primary involvement along muscle fascia. A comorbid diagnosis of gout may further delay accurate identification and treatment. 

An increasing body of literature recognizes the relationship between gout and necrotizing fasciitis. Gout is a dangerous comorbidity as providers may incorrectly attribute initial symptoms of necrotizing fasciitis to gout and the treatment of gout with non-steroidal anti-inflammatory drugs (NSAIDs) may further delay other symptoms, such as fever.11 In a 2013 retrospective review of necrotizing fasciitis cases, Lin and team reported that 45.3 percent of those studied had diabetes mellitus but gout was the second most common comorbid condition at 25.3 percent.12

Yu and coworkers published a case series in 2004 consisting of 15 cases of necrotizing fasciitis associated with gout, accounting for 4.8 percent of their hospital’s necrotizing soft tissue infection cases.13 Six of the cases included wounds associated with tophi. The mean time from the onset of symptoms to hospitalization was four days. The case series included four amputations and three patient deaths. 

In their retrospective review of 82 necrotizing fasciitis cases, Nisbet and colleagues identified gout as one of two independent predictors of mortality.14 Fewer than 50 percent of patients in this study were febrile upon hospital admission in this study and this may possibly be attributed to the treatment of gout with NSAIDs.14 When it comes to patients with recent treatment of or a history of gout, clinicians should have a higher index of suspicion for necrotizing fasciitis. 

One may calculate the Laboratory Risk Indicator for Necrotizing Fasciitis score in an effort to further support the diagnosis of necrotizing fasciitis but a recent systematic review of the scoring system indicates poor sensitivity.15 In a study evaluating the accuracy of the Laboratory Risk Indicator for Necrotizing Fasciitis score in the emergency room setting, researchers found a high false positive rate in confirmed cases of cellulitis and a high false negative rate in cases of confirmed necrotizing fasciitis.16 One can confirm the diagnosis of necrotizing fasciitis primarily based on operative findings such as the “positive finger sign,” in which a surgeon’s finger inserted along the fascial planes easily dissects the tissues without resistance, in addition to dishwater drainage, purulence and fascial necrosis.2,3 

In Summary

In this case study, the patient had a monomicrobial, gram negative necrotizing fasciitis complicated by a recent history of gout. The initial workup may seem bleak when the infection is well established at the time of diagnosis. Misleading comorbid conditions such as gout and inaccurate scoring systems may delay diagnosis. Despite a grim prognosis, this case study demonstrates how one may still attempt meticulous surgical debridement, which may reveal intact deep soft tissue compartments, preventing a more radical amputation. With the use of NPWT and subsequent split-thickness skin graft application, the patient went on to a full recovery with adjunctive need of an AFO. 

Clinicians should be aware of the dangerous and misleading comorbid diagnosis of gout and maintain a high suspicion for necrotizing fasciitis that would permit emergent aggressive surgical debridement to provide a better chance of successful treatment of this limb- and life-threatening infection. 

Dr. Barton is the Chief Podiatric Medicine and Surgery Resident at Gundersen Health System in La Crosse, Wis. 

Dr. Abicht is the Section Chair of the Podiatric Medicine and Surgery Department at Gundersen Health System in La Crosse, Wis. He is a Fellow of the American College of Foot and Ankle Surgeons.

Dr. Fuerbringer is an Attending Physician Podiatric Medicine and Surgery Department at Gundersen Health System in La Crosse, Wis. He is an Associate of the American College of Foot and Ankle Surgeons.

Online Exclusives
By Ellen C. Barton, DPM, Bradley P. Abicht, DPM, FACFAS and Brent A. Fuerbringer, DPM, AACFAS

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2. Bonne S, Kadri SS. Evaluation and management of necrotizing soft tissue infections. Infect Dis Clin North Am. 2017;31(3):497-511. 

3. Leiblein M, Marzi I, Sander AL, Barker JH, Ebert F, Frank J. Necrotizing fasciitis: treatment concepts and clinical results. Eur J Trauma Emerg Surg. 2018;44(2):279-290.

4. Centers for Disease Control and Prevention. Necrotizing Fasciitis. Available at: Published November 2018. Accessed February 23, 2021. 

5. Tso DK, Singh AK. Necrotizing fasciitis of the lower extremity: imaging pearls and pitfalls. Br J Radiol. 2018;91(1088):20180093.

6. Wang YS, Wong CH, Tay YK. Staging of necrotizing fasciitis based on evolving cutaneous features. Int J Dermatol. 2007;46(10):1036-1041.

7. Wong CH, Chang HC, Pasupathy S, Khin LW, Tan JL, Low CO. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg. 2003;85(8):1454-1460. 

8. Wong CH, Khin LW, Heng KS, tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7):1535-1541.

9. Mok MY, Wong SY, Chan TM, Tang WM, Wong WS, Lau CS. Necrotizing fasciitis in rheumatic diseases. Lupus. 2006;15(6):380-383. 

10. Angoules AG, Kontakis G, Drakoulakis E, Vrentzos G, Granick MS, Giannoudis PV. Necrotising fasciitis of upper and lower limb: A systematic review. International Journal of the Care of the Injured. 2007;38(Suppl 5):S18-S25. 

11. Veenstra RP, Manson WE, van der Werf TS, et al. Fulminant necrotizing fasciitis and nonsteroidal anti-inflammatory drugs. Intensive Care Med. 2001;27(11):1831. 

12. Lin JN, Chang LI, Lai CH, Lin HH, Chen YH. Group A streptococcal necrotizing fasciitis in the emergency department. J Emerg Med. 2013;45:781-788.

13. Yu KH, Ho HH, Chen JY, Luo SF. Gout complicated with necrotizing fasciitis - report of 15 cases. Rheumatology. 2004;43(4):518-521.

14. Nisbet M, Ansell G, Lang S, Taylor S, Dzendrowskyj P, Holland D. Necrotizing fasciitis: review of 82 cases in South Auckland. Int Med Journal. 2011;41(7):543-548.  

15. Fernando SM, Tran A, Chen W, et al. Necrotizing soft tissue infection: diagnostic accuracy of physical examination, imaging, and LRINEC Score: a systematic review and meta-anlaysis. Ann Surg. 2019;269(1):58-65.

16. Neeki MM, Dong F, Au C, et al. Evaluating the laboratory risk indicator to differentiate cellulitis from necrotizing fasciitis in the emergency department. West J Emerg Med. 2017;18(4):684-689. 





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