A diagnosis is often difficult when we cannot identify underlying metabolic condition. This month’s blog highlights such a case.
A 41-year-old male presented to the office with the chief complaint of pain, swelling and redness on the dorsal aspect of his left foot for a three-week duration. He denied any injury but related that he had been on his feet a lot for work.
His medical history showed diabetes, gout, hypercholesterolemia and hypertension. His daily medications included metformin, potassium citrate, allopurinol, sitagliptin (Januvia, Merck) pioglitazone (Actos, Takeda Pharmaceuticals), atorvastatin calcium (Lipitor, Pfizer) and enalapril (Vasotec, Merck). His past surgical history included arthroplasty of the left knee, arthroscopy of the left ring finger and right hand, a hernia and a colonoscopy. His social history was remarkable for mild alcohol drinking and no current smoking.
The physical exam revealed an overweight male in no acute distress who was alert and oriented. The vascular exam revealed strong pedal pulses and capillary refill immediate to the level of the toes. The neurologic exam revealed symmetric deep tendon reflexes and no evidence of loss of protective sensation (LOPS). The dermatologic exam revealed no break in the integument. I noted mild edema and erythema at the base of the second and third toes on the left foot. It is critical to perform a bilateral examination to detect subtle swelling (see Figures 1 and 2).
The orthopedic exam was remarkable for pain with palpation of the dorsal aspect of the second and third metatarsophalangeal joints (MPJ). The patient also noted pain with range of motion of the second and third MPJ. There was no pain to palpation of the plantar metatarsal heads. I noted no evidence of an intermetatarsal neuroma. Upon reviewing three X-ray views of the left foot, I did not note any acute fracture (see Figure 3).
At this point, my working diagnosis was stress fracture versus stress syndrome (periostitis) of the second and/or third metatarsal. For treatment, I had him use a fracture boot and asked him come back to the office in three to four weeks. I instructed him to ice the foot three times a day for 15 minutes.
He returned to the office three weeks later and initially improved to the point of returning to a regular shoe. Unfortunately, his pain came back. His physical exam findings were the same as his prior visit. We repeated X-rays and again found no obvious sign of a stress fracture. Knowing that it can take time for a stress fracture to be visible on X-rays, I made the same diagnosis of stress fracture. I had him resume wearing the fracture boot and prescribed dextropropoxyphene (Darvocet N-100) to take as directed and as needed. He was to follow up in three weeks.
On his three-week follow up, he stated he did well in the boot and tried to wear his regular shoe but the pain immediately returned. I ordered another X-ray and found it negative for a stress fracture. At this time, I ordered a magnetic resonance image (MRI), knowing that if it were a stress fracture, he would be better by then. Moreover, enough time had passed to detect the stress fracture.
The patient returned to the office four weeks later. The MRI showed avascular necrosis of the second metatarsal. We took X-rays again and they showed a visible defect of the second metatarsal head (see Figure 4). He ultimately had surgery to clean up the joint. I removed damaged cartilage and bone debris, and drilled any areas of cartilage defect. The patient went on to a full recovery with an asymptomatic left second toe joint.
The interesting aspect of this case is that the patient came back to see me three years later for plantar fasciitis. When I saw him, I did not even recognize him as he had lost 40 pounds. He told me he had been diagnosed with a pituitary tumor and had Cushing’s disease. Now that he had his cortisol levels in check, he no longer had diabetes, high cholesterol or hypertension.
Cushing’s disease is a metabolic condition where the body produces excess cortisol. Common symptoms include weight gain, hypertension, a round face, fatigue, irritability and excess hair growth.
It has been well reported in the literature that there is an association of avascular necrosis as a manifestation of Cushing’s disease.1 It is purported that avascular necrosis is caused by interosseous hypertension followed by intramedullary venous stasis, edema, necrosis, fibrosis and subsequent infarction. This ultimately leads to the flattening of the metatarsal head with fragmentation.
Often, it is serendipity that helps us find the answers in an unusual case such as this one.
1. Phillips KA, Nance EP Jr, Rodriguez RM, Kaye JJ. Avascular necrosis of bone: a manifestation of Cushing's disease. South Med J. 1986; 79(7):825-9.