Residency Insight - A PRESENT Podiatry eZine
Residency Insight -- A PRESENT Podiatry eZine

Our guest editors today are Ali Abadi, DMP and Phillip I. Kauffman, DPM, FACFAS. Dr. Abadi graduated from Temple School of Podiatric Medicine in May 2009. He is currently a first year resident in Virtua West Jersey Hospital, Pm&s 36. He received his Masters Degree in Biochemistry and Molecular Biology from Georgetown University and BS in Biology form George Mason University, VA. Dr Phillip Kauffman, one of the brightest attending doctors at Virtua, or as Ali refers to him as "an amazing teacher and mentor."
 —Ryan Fitzgerald, DPM



An Unusual Presentation of Gout:
Tophaceous involvement of the Achilles tendon, a case report


by Phillip I. Kauffman, DPM, FACFAS and Ali Abadi, DPM

Chronic hyperuricemia metabolically can produce acute gout, most commonly to joints of the lower extremity. Chronic gout will produce tophaceous deposits within those joints. Infrequently reported is tophaceous development within soft tissue structures such as the body of tendons. We present a case of gouty tophi entirely within the Achilles tendon.

Gout is the most common inflammatory arthritis in men;1 an aging population, increasing obesity, and lifestyle changes will render it more common.2 In this case, we observed Gouty tophi inside the Achilles tendon.


Case Report: A 42 Years-old, Indian male initially presented with persistent recurrent posterior right heel pain, which has been intermittently symptomatic for the past 6 years. It happens, per his description, on a yearly basis.  When describing his symptoms, he admitted to prolong standing exacerbating his pain, but denies any trauma or history of acute gouty attack.

HPI: Past medical history is significant for hypothyroidism and hypercholesterolemia. Medication is daily use of Synthroid tablets and notes no known drug allergies. Social history is positive for daily alcohol consumption, 1 to 2 drinks per day. Family history is positive only for diabetic mellitus; negative for gout.

PE: Physical examination of the patient revealed pain on palpation at the distal Achilles tendon of the right foot, with focal intensity localized to the calcaneal attachment, consistent with insertional Achilles tendonitis. Percussion of the tarsal tunnel and porta pedis is negative for Tinnel’s or Valieux sign. (Fig1)

Figure 1

Labs: Recent hematological examination including CBC, WBC, Rheumatoid factor, CRP, ESR and serum uric acid were unremarkable and within normal limits.

Imaging: Radiographic evaluation of the affected foot and ankle region demonstrated spurring of the posterior superior aspect of the calcaneus. (Fig 2)

Figure 2


MRI imaging of the region revealed a calcaneal enthesophytes at the Achilles insertion. Also, within the distal Achilles, there is a well circumscribed 3x7x24 mm focus of abnormal signal intensity wholly within the body of the Achilles tendon. The remainder of the Achilles tendon appeared intact. This mass was was described as a well-defined, homogeneously bright signal on T2 weighted imaging and decreased signal intensity on Sagital T1 images. (Fig 3, a-d)

Figure3a

Figure3b

Figure3c

Figure3d

 

 

Treatment: After a period of attempted conservative care,  including immobilization with CAM walker, NSAIDS, cortisone injection and physical therapy, surgical excision was ultimately performed under a “high ankle” tourniquet inflated to 250 mmHg. A 7 cm central linear skin incision was performed allowing for adequate visualization of the distal Achilles tendon and the posterior calcaneus. (Fig4)

Figure4

Dissection of the hypertrophic Achilles tendon body allowed direct visualization of a chalky white mass entirely encapsulated within the tendon. (Fig5) This was sent to the pathology department for microscopic exam. In addition to the debridement and repair of the Achilles tendon, the hypertrophic bone and spurring of the posterior superior aspects of the calcaneus was excised as well. (Fig6).

Figure 5

Figure 6

The Pathology report revealed chalky white material consistent with the diagnosis of gouty tophi.

Discussion: Although there are many joint diseases which present as acute monoarthritis, the  most common causes are due to gout or calcium pyrophosphate dehydrate crystal deposition (CPPD) also known as pseudogout.1 Gout is the most common inflammatory arthritis in men.

The underlying metabolic disorder leading to Gout is a hyperuricemic state7 which is a consequence of either decreased renal excretion (90%) or over production of uric acid (10%).7 Literature review reveals a peak incidence of hyperuricemia between the ages of 30-50 with the prevalence increasing with age.3 Factors affecting serum urate concentration are listed in Table 1 (below). Clinically, Gout is a consequence of  the deposition of monosodium urate monohydrate crystals into synovial, bursal, and cartilaginous tissues.

Figure 7


Both the incident and prevalence of gout has been on the rise in recent years4  theorized to be related to several factors, including increased age, alcohol consumption, obesity, as well as widespread diuretic use for hypertension treatment4.5 and hypothyroidism.6c

Numerous studies have associated a higher incidence of newly diagnosed gout in patients with a past medical history of hypothyroidism. It has been theorized that hypothyroidism may contribute to hyperuricemia; therefore subclinical hypothyroidism may predispose patients to gouty arthritis.6

Gout may occur in any joint of the body  including the ankle, knee, hand, wrist, elbow, and the sacroiliac joint. However, joints affected most commonly occur in the lower extremity.

Diagnosis should ultimately be performed via aspiration of the urate crystals from  an affected joint. However, in clinical practice, this test is performed only on a minority of patients. Guidelines exist for diagnosis which is frequently limited to clinical examination consisting of sudden unset, redness, swelling of a joint and acute incidence of pain.8

Figure 8

Unusual is tophi within soft tissues; specifically gouty tophi occurred inside the Achilles tendon.

Traditionally, radiology has not been of primary importance in diagnosis of gout. Rather, X-rays usually provide only verification of gout via a late stage finding of peri-articular erosion. Computed tomography (CT) scan is a more complete evaluation for observing gouty tophi.9 Gerster, et al.10 first described the characteristic appearances of gouty tophi visualized by CT.

In comparison, the appearance of articular gout in MR imaging is highly variable. Tophaceous deposits will appear low to intermediate signal intensity on T1-weighted image and range from low to high signal intensity on T2-weighted images depending on the degree of hydration of the tophi. 3

Treatment for acute gout includes: NSAIDs, (such as indomethacin), steroids and adrenocorticotrophic hormone (oral, parenteral) and colchicine are the most popular treatment. Long term treatment includes Allopurinol or Probenicid based on the results of a 24 hour urine uric acid study.

In conclusion, patient education is essential for proper long-term management of Gout. Patients who have had a previous attack should be made aware of common signs and symptoms. Patients also should be made aware that regular diet; trauma, surgery, starvation, alcohol consumption, and dosage changes of certain drugs may precipitate a gouty attack. We presented a case of Gouty tophi inside the Achilles tendon in a patient with hypothyroidism.

Figure 14


Table 1:  Factors affecting serum urate concentration 11

Factors that decrease serum urate concentration

  • Diet: low fat dairy products
  • Drugs: xanthine oxidase inhibitors (allopurinol), uricosuric drugs (sulfinpyrozone), uricase drugs (rasburicase), coumarin ant coagulants, and estrogen.

Factors that increase serum urate concentration

  • Diet: meat, fish, alcohol, obesity, and weight gain.
  • Drugs: including diuretics, low dose salicylates, pyrazinamide, ethambutol, cytotoxics and lead poisoning
  • Disease: increased purine turnover-myeloproliferative and lymphoproliferative disorders, chronic hemolytic anemia, hemoglobinopathies, thalassaemia, increased purin synthesis-glucose-6-phosphate dehydrogenase, hypertension, hypothyroidism, sickle cell anemia, 7hyperparathyroidisim, chronic renal disease.

References:

  1. Choi HK, Gout, epidemiology and life style choices, Curr opin Rheumatol 2005;17:341-5
  2. Bellamy N,Downie WW, Observation on spontaneous improvement in patients with podagra,Br J clin pharmacol 1987;24:33-6
  3. Monu JUV,pope TL: Gout: a clinical and radiologic review.Radiologic Clinics of North America 2004, 42 :169-184
  4. Hunter DJ, York M, Chaisson CE, Woods R, Niu J : Recent diuretic use and the risk of recurrent gout attacks: the online case-crossover gout study. Journal of Rheumatology 2006, 33 :1341-5
  5. Ene-Stroescu D,Gorbien MJ: Gouty arthritis: A primer on later onset gout. Geriatrics 2005, 60:24-31
  6. Erickson A, Enzenauer RJ, Nordstrom DM, Merenich  JA. The prevalence of hypothyroidism in Gout, The American Journal of medicine, September 1994,volume 97, 231-234.
  7. Terkeltaub RA : Gout. The New England Journal of medicine ,2003,349:1647-55.
  8. Li EK: Gout: a review of its etiology and treatment. Hong Kong medical Journal 2004, 10:261-70
  9. Dalbeth N, Clark B, Gregory K, Gamble GD, Doyle A, McQueen FM: Computed tomography measurement of tophus volume : comparison with physical measurement. Arthritis Rheum 2007,57:461-465
  10. Gerster JC, Landry M, Duvoisin B : Computed tomography of the knee joint as an indicator of intraarticular tophi in gout. Arthritis Rheum 1996, 39:1406-1409
  11. Underwood M. : Diagnosis and management of gout. BMJ, 2006 332:1315-9

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