Treating Undiagnosed Charcot Neuroarthropathy Following Traumatic Hallux Varus Repair
These authors present the treatment of a non-adherent 53-year-old patient with diabetes who received treatment for previously undiagnosed Charcot following hallux varus surgery.
Hallux varus is a condition in which the great toe deviates medially away from the lesser toes. The condition is often uncomfortable or even painful for the patient to the extent that surgery is necessary to correct the underlying problem.
Hallux varus deformity generally has three possible components: medial deviation of the hallux at the first metatarsophalangeal joint (MPJ); supination of the phalanx; and interphalangeal flexion or claw toe deformity.1 Any combination of these factors can make it difficult for a patient to wear shoes or even walk in a stable manner. Hallux varus can be congenital or acquired. The incidence is relatively rare with reports ranging between 2 and 15.4 percent in the literature. The etiologies of acquired hallux varus include trauma, severe burn injury with contracture, systemic inflammatory disorders such as rheumatoid or psoriatic arthritis, Charcot-Marie-Tooth disease, avascular necrosis of the first metatarsal head, and paralysis or poliomyelitis.
Hallux varus most commonly arises as an iatrogenic complication of bunion surgery, resulting from overcorrection of hallux valgus.1 This includes staking of the first metatarsal head, overcorrection of the intermetatarsal angle, overzealous medial capsulorrhaphy, fibular sesamoidectomy, over-extensive lateral release, overcorrection of the proximal articular set angle and even overzealous post-op bandaging. Iatrogenic hallux varus is often poorly tolerated.
Due to the inevitable pain, instability and discomfort, effective treatment is crucial. Conservative treatments for mild hallux varus include taping of the hallux to adjacent toes to prevent further deviation and/or a shoe with a wider toe box to accommodate widening of the digits. Prior to surgical treatment, one should consider several factors, including hallux flexibility and mobility, along with pain. It is also crucial to consider the patient’s expectations, adherence, ability to undergo complex revision surgery, and potential acceptance of joint-sacrificing options such as arthrodesis. Appropriate treatment requires careful clinical and radiographic assessment to identify the involved factors. One would address all of these to correct all elements of the deformity.1
On another note, Charcot neuroarthropathy is a disease that typically occurs in patients with diabetes, tabes dorsalis, syringomyelia, chronic alcoholism, leprosy, trauma or infection after fractures and dislocations.2 There has even been evidence of Charcot-like joints in the presence of tophaceous gout.3
The cause of the acute Charcot foot is not known although the current thinking is that the process is mediated through a cycle of uncontrolled inflammation. In a patient with diabetes, this can develop as a result of distal symmetrical neuropathy. Any number of events that may cause local inflammation may subsequently trigger the disease. These events include minor or major trauma, infection and, in rare cases, surgery. The resultant cycle of uncontrolled inflammation causes increasing bone breakdown with weakness of the pedal bones and joints. Continued weightbearing will result in fractures, dislocations and progressive deformities of the foot, which in turn will exacerbate the inflammatory process.4
One of the most devastating complications of diabetes is Charcot osteoarthropathy. It can lead to gross structural deformities of the foot and ankle as well as subsequent skin ulceration and lower limb amputation from soft tissue or bony infection.
Studies have noted limited cases of Charcot osteoarthropathy after nerve injury, ankle fractures, femoral fractures, acetabular fractures and humerus fractures.2,5-8 However, the literature has noted fewer cases of surgically induced Charcot osteoarthropathy. Authors have reported Charcot osteoarthropathy arising after hallux limitus repair, open reduction internal fixation of the Lisfranc joint, dorsiflexory wedge osteotomies to prevent a chronic mal perforans ulcer, Keller arthroplasty for a recalcitrant hallux ulcer, partial ray resections due to bone infection, sesamoidectomies, joint arthrodesis procedures, and even after an Austin bunionectomy.9-12
However, Charcot osteoarthropathy is often unrecognized with deleterious consequences.13 We report the case of a patient who developed Charcot neuroarthropathy after surgical correction of traumatic hallux varus.
A Closer Look At The Initial Patient Presentation
A 53-year-old obese patient presented to the Temple University School of Podiatric Medicine’s Foot and Ankle Institute with a painful right first MPJ secondary to stubbing her foot against a curb in an open-toed shoe two weeks prior to her office visit. She stated that the big toe went in the opposite direction of the second toe at that time. She presented fully weightbearing in an open-toed sandal. The patient related going to the emergency room the day of the injury and having radiographs taken. Her diagnosis was a ligamentous strain. She wore a splint and got a referral to the Foot and Ankle Institute the following day.
The patient’s past medical history was positive for insulin-dependent diabetes, heart murmur, hypertension, degenerative joint disease, spinal stenosis, diabetic cardiomyopathy, gastroesophageal reflux disease (GERD) and renal failure. Her current medications at the time included rosiglitazone (Avandia, GlaxoSmithKline), insulin, metoprolol (Lopressor, Novartis), omeprazole (Prilosec, AstraZeneca), hydrochlorothiazide (Microzide, Watson Pharmaceuticals), lisinopril (Prinivil, Merck), oxycodone (Oxycontin, Purdue Pharma) and acetaminophen/oxycodone (Roxicet) as needed.
She was allergic to Medipore fabric tape (3M), metformin (Glucophage, Bristol-Myers Squibb), intravenous dye and glipizide (Glucotrol, Pfizer). She smoked briefly in college but did not currently use tobacco or alcohol. Her family history was positive for diabetes and coronary heart disease. During the patient’s initial presentation, her review of systems was unremarkable.
The patient’s initial clinical examination revealed non-palpable pedal pulses secondary to severe edema and a dried blood blister on the medial aspect of her right hallux. The hallux was significantly deviated to the midline of her body and it was more pronounced when she was weightbearing. The hallux position was non-reducible and there was pain on range of motion of the first ray. Neurologic status revealed normal reflexes, diminished vibratory sensation, intact proprioception and intact protective sensation via a 5.01 Semmes Weinstein monofilament.
Radiographs of her right foot indicated severe hallux varus deformity with injury to the lateral proximal phalanx base at the insertion of the adductor hallucis muscle. There were also two small bony fragments at the medial aspect of the first MPJ. There was significant amount of soft tissue edema. There was also a gap at the base of the first and second metatarsals. Fractures of the third and fourth toes were present.
Treatment at the initial presentation included immobilization by a posterior splint. The patient received crutches in an attempt to reduce the significant amount of edema. We discussed surgical repair due to the severity of the injury and the unlikelihood of a satisfactory conservative treatment. The senior author also ordered a non-invasive arterial vascular study to ascertain the patient’s preoperative arterial status. We discussed the risks and complications of surgery. She got specific instructions to stay off her right foot. We scheduled close re-evaluation after the necessary tests were complete.
What Transpired At The Follow-Up Appointments
The patient missed several appointments and presented for re-evaluation eight weeks after the injury. At this time, she was fully weightbearing in a sandal. No positive progression of her hallux varus deformity had occurred. Her radiographic evaluation was unchanged with the exception of healing fractures of the third and fourth toes.
Her pulse volume recording/ankle brachial index (PVR/ABI) results showed no evidence of significant peripheral vascular occlusive disease in her legs at rest. The right and left ABIs were 1.19 and 1.07 respectively.
At three months post-injury, the patient had surgery, which included an arthrodesis of the first MPJ with cross screw fixation along with pin fixation of her third proximal phalanx fracture. She wore a below knee cast, was non-weightbearing and the senior author advised her to use the crutches she received at an earlier visit.
After missing her first postoperative visit, the patient had an exam approximately two weeks post-op. The cast had broken down on the plantar aspect due to weightbearing. Her clinical exam revealed mild amounts of maceration at the incision site around the first MPJ and edema of the right foot. Her X-ray evaluation revealed significant bending of the third digit pin. She wore another below-knee cast and the senior author advised her again to keep weight completely off the right foot. The patient received a prescription for a wheelchair.
At post-op visit two, the patient continued to bear weight. Clinically, moderate to severe edema was present and the senior author felt this to be due to her non-adherence and severe increased weight gain. Radiographs taken at the two-month post-op period revealed abduction of her hallux. The screws were intact. A medial shift at the first metatarsocuneiform at the Lisfranc joint was present. Her diagnosis was a missed Lisfranc injury.
Although the patient was non-adherent and at high risk for surgery, due to the extensive deformity present, the senior author performed a metatarsocuneiform fusion after carefully discussing all alternatives, risks and complications. The patient again wore a below-knee cast at that time.
At three months post-op, the patient presented for evaluation. Her foot was edematous and the deformity had worsened clinically. Radiographs revealed continued adductus deformity of the first ray with diffuse osteoarthritic changes at the tarsometatarsal and calcaneocuboid joints. Charcot neuroarthropathy, osteomyelitis and/or septic arthritis were all part of the differential diagnosis at that time.
At this time, a bone biopsy was negative for osteomyelitis and we diagnosed Charcot neuroarthropathy. The patient received a controlled ankle motion (CAM) walker after refusing a cast and the senior author advised her to be non-weightbearing until the swelling had reduced. The patient eventually transitioned into custom-molded diabetic shoes.
A year and a half later, the Charcot changes had resolved and the senior author removed the loose hardware. No attempts at further reconstruction occurred due to her non-adherence.
Undiagnosed Charcot neuroarthropathy often leads to devastating results. Our patient developed Charcot following surgical repair of the hallux varus deformity, which initially went undiagnosed. The senior author thought the severe edema was due to a missed first metatarsocuneiform injury, her non-adherence and obesity. The patient subsequently underwent a metatarsocuneiform fusion. The undiagnosed Charcot neuroarthropathy continued and degenerative changes progressed. Once diagnosed, the patient had conservative treatment and eventually, even with the continued non-adherence, the Charcot neuroarthropathy ceased.
Dr. Pontious is a Professor and the Chair of the Department of Podiatric Surgery at the Temple University School of Podiatric Medicine in Philadelphia. She is a Fellow of the American College of Foot and Ankle Surgeons.
Mr. Ahsan is a fourth-year student at the Temple University School of Podiatric Medicine.
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