When A Diabetic Foot Ulcer Is Complicated With Tophaceous Gout
In an interesting case study, this author discusses the diagnostic workup and multidisciplinary efforts to resolve a longstanding combination of a diabetic foot ulcer and tophaceous gout.
A 77-year-old male with multiple comorbidities presented with a chief complaint of a chronic wound on the right great toe. He noted that the wound had been present for “years.” The patient said that he had previously been evaluated by a vascular surgeon but denied receiving treatment by any wound specialist. The only treatment he had used was an OTC topical antibiotic cream. Additionally, the patient reported having an HgA1C below 7%.
In regard to the patient’s past medical history, he underwent coronary artery bypass surgery six months prior to his initial visit to our wound center. In addition to having coronary artery disease, the patient had diabetes mellitus, renal insufficiency, hyperlipidemia and tophaceous gout. The patient also had arthroscopic knee surgery in the past. He reported no known allergies. The patient’s current medications included glipizide (Glucotrol, Pfizer), metroprolol (Dutoprol, AstraZeneca), docusate (Colace), digoxin, warfarin, bumetanide (Bumex, Hoffmann-La Roche), rosuvastatin calcium (Crestor, Astra Zeneca), sitagliptin (Januvia, Merck) and mupirocin (Bactroban).
During the physical examination, the patient was alert and oriented. Dorsalis pedis and posterior tibial pulses were normal and equal bilaterally. He had +1 pitting edema bilaterally. The patient had several subcutaneous tophaceous deposits on the sides of both heels and elbows. The wound on the right great toe (see figure 1) was 2.6 cm x 2.7 cm x 0.4 cm. The base of the wound was covered with significant amounts of tophaceous material. There was mild erythema surrounding the wound but no drainage or odor.
The lab findings revealed a white blood cell count of 10.1 and a uric acid level of 10.2. The X-ray showed significant punched out areas of the interphalangeal joint of the right great toe (see figure 2).
Pertinent Treatment Insights
This patient presented with a very deep and complicated wound. His vascular supply was poor with ankle brachial indices of 0.9 and toe/brachial pressures of 0.4. The patient’s tophaceous gout was never properly addressed nor controlled. Prior to performing any local intervention, we referred the patient for vascular consultation and he subsequently underwent endovascular intervention, which improved perfusion to an acceptable level (TPIs of 0.75). After consultation with his primary physician and nephrologist, the patient began taking febuxostat 40 mg (Uloric, Takeda Pharmaceuticals) daily.
Figure 3 clearly shows the bed of the wound with tophi. We took the patient to the OR and debrided the wound (see figure 4). Due to the depth of the wound, we applied VAC therapy (KCI) soon after surgery and continuously monitored the wound for progress (see figures 5 and 6).
We saw the patient weekly at our wound center. At each visit, we debrided the wound of biofilm and tophi, and used 4% topical lidocaine to minimize pain. We replaced the VAC therapy after each debridement and a visiting wound care nurse performed dressing changes during the week at the patient’s home.
After two months, the wound base showed good granulation with no new tophi. We subsequently applied Apligraf (Organogenesis) four times over the following two months (see figures 7, 8 and 9).
The patient’s wound healed uneventfully (see figure 10) and he was discharged from the wound center.
What You Should Know About Tophaceous Gout
Tophaceous gout occurs when the amount of serum uric acid in the bloodstream increases and monosodium urate crystals form. These crystals then grow into tophi and appear as chalky lumps. The levels of uric acid can remain high for many years before one sees symptoms of tophaceous gout. In this case, the patient’s peripheral vascular disease as well as his toe deformity combined with the urate crystal formation to create a dorsal wound. In addition, gout and type 2 diabetes often coexist in people with common physical characteristics and conditions, the most prominent being obesity.
Obesity as a causative factor in gout is well documented.1 Diet may raise the serum uric acid by up to 2 mg per 100 ml, an amount sufficient to produce clinical gout in a previously mildly hyperuricemic person. Moreover, the incidence of both the “maturity onset” form of diabetes mellitus and gout rises sharply in late middle age.2
Uric acid has a chemical similarity to alloxan, which can induce diabetes by necrosis of the w-cells of the islets of Langerhans.3 It is known that ketoacidosis will produce hyperuricemia by reducing the renal clearance of urate.
Researchers have noted that the development of diabetes improves clinical gout.2 Conversely, hyperuricemia may diminish the clinical expression of diabetes. It would seem clear that the association of gout and diabetes mellitus is not uncommon.
In this case study, treatment was successful and involved multiple specialists including vascular surgery, nephrology, primary care and wound care. The wound care consisted of multiple modalities including debridement, negative pressure and bioengineered skin (Apligraf) over several months.
Dr. Davidson is Chief of the Podiatry Section of the Department of Orthopedics with the Kaleida Health System in Western New York. he is on medical staff of the Center for Wound Care & Hyperbabric Medicine at The Erie County Medical Center. He is an Assistant Clinical Professor in the Department of Orthopedics at the State University of New York at Bffalo School of Medicine and Biomedical Sciences. Dr. Davidson is a past President of the American Board of Podiatric Orthopedics. He is a past President and Fellow of the American Academy of Podiatric Sports Medicine. Dr. Davidson is a Diplomate of the American Board of Podiatric Surgery and the American Board of Podiatric Orthopedics and Primary Podiatric Medicine. He is in private practice with multiple office locations in Western New York.
1. Whitehouse FW, Cleary WJ Jr. Diabetes mellitus in patients with gout. JAMA. 1966;197(2):73-6.
2. Bartels EC, Balodimos MC, Corn LR. The association of gout and diabetes mellitus. Med Clin North Amer. 1960;44:433-438.
3. Dunn JS, Sheehan HL, McLetchie NGB. Necrosis of islets of Langerhand produced experimentally. Lancet. 1993:1:484-7.
4. Liu Q, Gamble G, Pickering K, Morton D, Dalbeth N. Prevalence and clinical factors associated with gout in patients with diabetes and prediabetes. Rheumatology (Oxford). 2012;51(4):757-759.
5. Zhu Y, Zhang Y, Choi HK. The serum urate-lowering impact of weight loss among men with a high cardiovascular risk profile: the Multiple Risk Factor Intervention Trial. Rheumatology (Oxford). 2010;49(12): 2391-2399
6. Rodriguez G, Soriano LC, Choi HK. Impact of diabetes against the future risk of developing gout. Ann Rheum Dis. 2010;69(12):2090-2094.
7. Dao HH, Harun-Or-Rashid M, Sakamoto J. Body composition and metabolic syndrome in patients with primary gout in Vietnam. Rheumatology (Oxford). 2010;49(12):2400-2407.
8. Rider TG, Jordan KM. The modern management of gout. Rheumatology (Oxford). 2010;49(1): 5-14.
9. Roddy E, Mallen CD, Hider SL, Jordan KP. Prescription and comorbidity screening following consultation for acute gout in primary care. Rheumatology (Oxford). 2010;49(1):105-111.
10. Kim SY, Choi HK. Gout and quality of life. J Rheumatology. 2009;36(5): 865-868.
11. Doherty M. New insights into the epidemiology of gout. Rheumatology (Oxford). 2009;48 Suppl 2:ii2-ii8.
12. Samaras N, Rossi C. Images in clinical medicine. Tophaceous gout. N Engl J Med. 2012;366(3):e6.
13. Dobson M, Alwahab Y, Fazal MA. Interphalangeal joint involvement of the big toe. J Am Podiatr Med Assoc. 2012;102(3):256-258.
14. Winnard D, Wright C, Taylor WJ, et al. National prevalence of gout derived from administrative health data in Aotearoa, New Zealand. Rheumatology (Oxford). . 2012;51(5): 901-909.