It's 11 p.m. on a typical call night in Rochester, Minn. My computer screen glows dully as I stare out the window watching the snow fall, dreading the thought of digging my car out of the parking lot in the morning. I again wonder at my choice to attend medical school in the North Star State.
The fateful beep of the pager goes off next to me and my resident relays that we have a patient coming up from the emergency department—left foot cellulitis. A clinic number provides me with the key to our patient's past medical history and I start to compose my admission note. I pick up the basics of his story from the ED note. Treated for cellulitis by an outside hospital; continues to have pain, swelling, erythema and inability to ambulate. Cultures and basic labs drawn in our ED and vancomycin started. Vital signs stable and the patient is afebrile. It looks like a simple admit. I'll tuck this guy in and be in my cozy call room bed by 1 a.m.
The patient hits the floor just as I'm putting the final touches on my preemptive admission note. Why wait? We head to the room. The resident gives the patient a cursory glance and, satisfied that the man is not acutely trying to expire, leaves me to my history and exam. I ask the patient to again recount the story of his acute foot issues, eliciting pesky details like changes in symptoms, history of trauma, and dates and duration of various antibiotic courses. Finally satisfied with the history, I pull up the sheets to take a look at the mischievous limb. It appears to be as described by the ED—2+ edema in the dorsum of the foot and continuing into the ankle with mild erythema. The swelling of the foot concerns me and I wonder why the ED didn't get an ultrasound to rule out deep venous thrombosis before sending the patient to the floor.
However, the patient has strong pulses and there is no pain to palpation in the calf, ankle, or even the dorsum of the foot. I start to spread apart the toes, looking for some missed wound that could be responsible for all this trouble. As I move to the great toe, my patient lets out a howl. I look up, suspicious that he is just trying to pull one over on a naïve medical student. I am surprised to find out that the pain is real. I then start the sadistic practice of localizing pain. “Does it hurt more here? Or here?” A couple more pokes and a few howls later, I have localized the pain to the left first metatarsophalangeal joint. Why wasn't this point tenderness noted in the ED? As I leave the room, I help the patient tent the bed sheets over his foot, as even the touch of the fabric causes him pain.
I head back to my resident, a differential diagnosis brewing in my brain. Cellulitis seems less likely; could this be a DVT? We must also rule out septic arthritis and osteomyelitis. Is it possible our patient was admitted just for gout? We obtain an X-ray and tap the joint. Urate crystals are seen on the microscopic synovial exam. Diagnosis: gout.
I begin to formulate a treatment plan, starting with a late- night medical history consult. I am intrigued to learn that gout was first described by the Egyptians in 2640 B.C. and has been reliably described in medical literature since that time. Even the medical greats such as Hippocrates, Galen and Sydenham put their minds to work on the “disease of kings.” Hippocrates was the first to note the disease's association with rich food and excessive alcohol consumption, as well as gout's tendency to occur in older men. Since the condition tended to afflict the wealthy, it was consistently studied throughout history.
The physician who was able to rid the royals of their rheumatic plight would have been richly rewarded. Various treatments have been popular, including moxibustion, bleeding, clay massages, herbal ointments, ox spleen, spider web and henna. Sydenham found that the only antidote for gout was “opium and more opium,” and was forced to believe that gout was a form of divine justice as it “kills more rich men than poor, more wise men than simple.”
The first use of colchicine as a treatment for gout occurred in the sixth century A.D. by the Byzantine Christian physician Alexander of Tralles. Colchicine use eventually went out of favor until its rediscovery in 1763 by Baron Von Stoerk. In the late 19th century, high dose salicylates (4-6 grams/day) became a popular treatment. However, their toxic effects made it natural for other uricosuric agents such as probenecid, benzbromarone and sulfinpyrazone to become mainstays of treatment. In 1988, George Hitchings and Gertrude Elion were awarded the Nobel Prize for the development of allopurinol, one of the greatest advancements in the treatment of gout.
For the patient at hand, we decide to stop the thiazide diuretic and give him 500 mg of naproxen. We follow that by an intra-articular injection of corticosteroid, an idea brought to us courtesy of Drs. Kendell, Hench and Reichstein, 1950 Nobel Prize recipients. The patient and I discuss dietary modifications, follow-up, and the possibility of starting allopurinol in a couple of weeks. The patient looks at the door that less than 12 hours ago he had been wheeled through. He stands up and walks out of the hospital into the blistery winter day, pain-free but still cold.