Midfoot Stress Fractures in a Patient with Recurrent Gout:
A Case Report
Marc Lucente DC, MA, DIANM1, Jeffrey P. Krabbe DC, MS, DACBN, CISSN, CSCS2
1 Associate Professor, Department of Clinical Sciences, Palmer College of Chiropractic, Florida Campus
2 Associate Professor, Department of Life Sciences & Practice Foundations, Palmer College of Chiropractic, Florida Campus
Published: December 2020
Journal of the International Academy of Neuromusculoskeletal Medicine
December 2020, Volume 17, Issue 2
The original article copyright belongs to the original publisher. This review is available from: http://ianmmedicine.org ©2020 Lucente/Krabbe and the International Academy of Neuromusculoskeletal Medicine. This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Objective: The purpose of this case report is to describe the presentation of stress fractures in a patient with recurrent acute gout attacks.
Clinical Features: A 39-year-old male with a history of acute gout attacks presented with intense pain, swelling, and redness of the right midfoot. History revealed no incidence of trauma. The patient reported that previous gout flares had resolved over several days, yet this had persisted for several weeks with greater pain, swelling, and redness. X-ray examination showed no appreciable gouty arthropathy.
Intervention and Outcome: The patient was referred for MRI examination of the right foot. MRI revealed nondisplaced stress fractures of the cuboid and lateral cuneiform.
Conclusion: Gout is a fairly common condition in which repeated attacks may compromise structural integrity of affected regions. Practitioners must be aware of the potential for further complications, including stress fractures, in the recurrent acute gout patient.
Key Words: Gout, stress fractures, chiropractic
Gout is a common form of inflammatory arthritis that occurs due to the deposition of monosodium urate crystals in synovial and other tissues.1-3 A common pathogenic factor with gout is hyperuricemia (>6.8 mg/dl), although only 10-15% of patients with hyperuricemia develop gout.1-3 Gout is further defined by four distinct stages of disease progression: asymptomatic, acute, intercritical or interval, and chronic (tophaceous).2,3 In asymptomatic hyperuricemia approximately 85-90% of patients with elevated serum uric acid do not develop gout. Acute gout can be characterized by specific signs and symptoms such as severe pain, erythema, and swelling that typically begins in the early morning or middle of the night. Acute gout is also considered monoarticular occurring most commonly in the lower extremity (e.g., first metatarsophalangeal joint, midfoot, ankle, knee) and is typically self-limiting with spontaneous resolution.2,3 Intercritical gout is defined by the intervals between the attacks which are referred to as intercritical periods. Over time, subsequent attacks may increasingly involve more joints and have a longer duration as crystals persist allowing a more definitive diagnosis.2,3 Chronic (tophaceous) gout takes several years to progress. It is associated with chronic joint pain, reduced activity, and structural damage, along with more frequent attacks that can become disabling due to erosive and destructive arthritis.2,3
Over the past 20 years, the prevalence rate of gout has increased world-wide.5,6 From an epidemiological standpoint, men are most affected by gout (2-6 times higher incidence), as well as older patients (increasing incidence until age 70), those living in developed countries (North America, Western Europe), and certain ethnicities (Taiwanese, Pacific Islanders, New Zealand Maori).1,2,4 Increased risk of gout is associated with obesity, hypertension, high consumption of alcohol and high-purine foods, and family history of gout.1-3 Low-dose aspirin and several types of antihypertensive medications including diuretics, beta-blockers, and most of the renin-angiotensin system agents also increase risk.1-3
One of the most common initial presentations of gout is a self-limiting acute attack. The classic signs and symptoms include severe pain, erythema, warmth, swelling of one or more joints, and skin desquamation, which may occur over the inflamed area.1,2 The gold standard for diagnosis of gout is demonstration of monosodium urate crystals in synovial fluid analysis or in tophus by polarized light microscopy, however gout is most commonly diagnosed based upon history and examination along with response to treatment.1-3
While most acute attacks of gout will spontaneously resolve in 7-14 days, early treatment to hasten the resolution of symptoms with allopurinol is recommended within 12 hours.7,8 In patients experiencing mild-moderate pain, monotherapy with allopurinol, nonsteroidal anti-inflammatory drugs, corticosteroids, or intra-articular corticosteroid injection is recommended.7,8,9 Non-pharmacologic treatments in addition to medication include rest, ice, and elevation of the affects joint(s).7,8
The literature is inconclusive as to the relationship between gout and the incidence of fracture. A mechanism of bone weakening due to inflammation from repeated gout flare-ups has been suggested by a Taiwanese population-based cohort study which concluded that gout increases the risk of fracture.10 Yet a recent meta-analysis came to the conclusion that gout is not associated with fracture risk.11 This case study suggests a relationship between mid-foot stress fractures and possible bone weakening due to recurrent acute gout flareups.
A 39-year-old Caucasian male had first experienced symptomatology in the right midfoot consistent with acute gout in 2014 and was diagnosed with gout by his primary care physician in 2015. The diagnosis of gout was based on history and physical examination. Laboratory values for CBC were within normal limits and serum uric acid was measured at 8.1mg/dL (normal range 3.7 – 8.6mg/dL). The patient reported a family history of gout in both the mother and father. Other known factors that contribute to increased risk of gout were absent. The appearance of gout in this patient was consistent with the classic presentation of a self-limiting acute attack. The gout attack symptoms would typically present in the middle of the night and would cause the patient to wake from sleep. The pain was sharp and severe, with redness, heat, and swelling of the right calcaneus and right dorsal midfoot. Upon the onset of a gout attack, weight bearing and ambulation were precluded by pain. The pain intensity was rated at an 8/10 on an 11 point numeric scale with 0 being no pain and 10 being the most intense pain imaginable. The patient reported taking 800 mg of ibuprofen at the onset of a gout attack, with minimal palliative effect. This describes the self-management of gout attacks during 2014, prior to diagnosis.
After the diagnosis of gout was made, management changed to 50 mg of prednisone 1 time per day for 3 days. The prednisone allowed the patient to return to normal activities of daily living with minimal pain and discomfort within 3 days when taken at the onset of an attack. However, these therapies did not influence the long-term management of gout, as the frequency of the attacks remained static at several per year.
The patient had been provided with dietary advice regarding common dietary triggers for gout such as meat, seafood, and alcoholic beverages. He stated overall poor compliance with these dietary recommendations.
The patient experienced what appeared to be his most severe midfoot acute gout attack in 2018. Management with 50 mg of prednisone 1 time per day for 3 days did not result in resolution of the typical signs and symptoms of gout as it had in the past. The pain, swelling, and redness lingered for several weeks. (Figures 1 & 2)
Figure 1. Two weeks after onset of attack
Figure 2. Two weeks after onset of attack
Due to the nature of the presentation and concern over structural changes, radiographs of the foot were taken. Dorsoplantar, lateral, and oblique images of the right foot (Figures 3, 4, & 5 respectively) demonstrated adequate bone density, normal joint spaces, and no appreciable gouty arthropathy.
After a negative x-ray examination, advanced imaging was ordered. MRI examination revealed moderately intense marrow edema of the cuboid and lateral cuneiform as well as patchy linear sclerosis within the trabecula suggestive of nondisplaced and/or stress fractures of the cuboid and lateral cuneiform. (Figures 6, 7, & 8)
The patient was advised to avoid strenuous exercise as well as extended time on his feet for 6 weeks to allow healing of the fractures, and was referred for nutritional counseling with the goal of lessening the frequency of future gout attacks. Over the next 2 months the symptoms slowly abated and the patient was able to return to normal activities of daily living.
This case describes the presentation of midfoot stress fractures in a patient with recurrent acute gout. The cuboid and lateral cuneiform are uncommon areas for stress fracture to occur.12 Furthermore, the patient did not have a history of engagement in activities typical of an overuse injury such as high intensity repetitive force exercise.13 This suggests a relationship between the midfoot stress fractures and the recurrent acute gout attacks in that area. Inflammatory reactions causing joint deterioration and bone remodeling in the hands and feet is well evidenced in cases of rheumatoid arthritis.14 This case hypothesizes structural weakening leading to stress fractures as a result of recurrent inflammation from acute attacks of gout. Future research into the structural effects of recurrent acute gout attacks may identify a particular mechanism and address the current gap in knowledge. Also of interest is the patient’s use of prednisone. Long-term corticosteroid use is associated with reduced bone density and increased risk of fracture.15 However, the available literature is focused on ongoing daily corticosteroid therapy, as opposed to short-term as needed use over a period of several years as described in this study.16 Further research may elucidate a relationship between short-term as needed prednisone use and decreased bone mineralization that can increase fracture risk.
While gout is a common condition, this case presents an uncommon complication. The literature remains inconclusive and repeated attacks may compromise the structural integrity of affected areas. Practitioners should be aware that the potential exists for further complications, including stress fractures, in the recurrent acute gout patient.
This case report is limited in scope and stress fractures are not part of the classic presentation of gout. Current literature is inconclusive as to the relationship between gout and stress fractures.
Written consent for publication was obtained from the patient.
The authors declare that they have no competing interests.
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- Walsh LJ, Lewis SA, Wong CA, et al. The impact of oral corticosteroid use on bone mineral density and vertebral fracture. Am J Respir Crit Care Med. 2002;166(5):691-695.
- Van Staa TP, Leufkens HGM, Abenhaim L, et al. Use of oral corticosteroids and risk of fractures. J Bone Miner Res. 2000;15(6):993-1000.