charcot arthropathy of the diabetic foot. current concepts and review of ...

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or joint dislocation in 3. MR images of two cases were not available. MRIs performed in the coalascence phase demostrated regional bone edema in conjunc-.
Scandinavian Journal of Surgery 91: 195–201, 2002

CHARCOT ARTHROPATHY OF THE DIABETIC FOOT. CURRENT CONCEPTS AND REVIEW OF 36 CASES T.-K. Pakarinen1, H.-J. Laine2, S. E. Honkonen2, J. Peltonen2, H. Oksala3, J. Lahtela1, 3 1 2 2 3

Medical School, University of Tampere, Tampere, Finland Section of Orthopaedics and Traumatology, Department of Surgery, Tampere University Hospital, Tampere, Finland Department of Internal Medicine, Tampere University Hospital, Tampere, Finland

ABSTRACT

Background and Aims: The incidence of diabetic Charcot neuroarthropathy has increased. The purpose here was to study the current diagnostics and treatment of the Charcot foot. Materials and Methods: During a time period from 1994 to 2000, a total of 36 feet were diagnosed as cases of diabetic Charcot neuroarthropathies. A retrospective analysis of patient records and radiographs was undertaken. A review of the recent literature is presented. Results: 29 cases were diagnosed in the dissolution stage, 2 in coalascence, and 5 in the resolution stage. The diagnostic delay averaged 29 weeks. Treatment with cast immobilisation ranged from 4 to 37 weeks (mean 11 weeks). A total of 14 surgical procedures were carried out on 10 patients: six exostectomies, four midfoot arthrodeses, one triple arthrodesis, one tibiocalcaneal arthrodesis and two below-knee amputations. A radiological fusion was achieved in two thirds of the attempted arthrodeses. Conclusions: A physician should always consider the Charcot neuroarthropathy when a diabetic patient has an inflamed foot. In the absence of fever, elevated CRP or ESR, infection is a highly unlikely diagnosis, and a Charcot process should primarily be considered. The initial treatment of an inflamed Charcot foot consists in sufficiently long non-weightbearing with a cast, which should start immediately after the diagnosis. The prerequisites of successful reconstructive surgery are correct timing, adequate fixation and a long postoperative non-weightbearing period. In the resolution stage most Charcot foot patients need custom-molded footwear. Key words: Diabetes; neuroarthropathy; Charcot foot INTRODUCTION Charcot arthropathy was originally described in many joints in connection with tabes dorsalis and syCorrespondence: Heikki-Jussi Laine, M.D. Department of Surgery Tampere University Hospital P.O. Box 2000 FIN - 33521 Tampere, Finland Email: [email protected]

ringomyelia. In the western world Charcot arthropathy is nowadays mainly associated with diabetic feet. The pathophysiology of this devastating joint destroying process is poorly understood, but is considered to be a multifactorial and neuropathy is regarded as mandatory (1, 2). Advances in treatment have resulted in both increased lifespan and improved quality of life for the diabetic patients, but eventual problems with their feet. The prevalence of peripheral polyneuropathy in the diabetic population is estimated to be 9–32 % (3, 4) and that of the Charcot neuroarthropathy 0.09–1.4 %. (5–10). The real in-

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T.-K. Pakarinen, H.-J. Laine, S. E. Honkonen, J. Peltonen, H. Oksala, J. Lahtela TABLE 1 Classification system of Eichenholtz (modified by Johnson 1998).

Stage

Radiographic features

Clinical findings

I- Dissolution

Demineralization of regional bone, periarticular fragmentation, dislocation of joint

Acute inflammation (easily confused with infection): erythema, warmth

II- Coalescence

Absorption of osseus debris in soft tissues, organisation and early healing of fracture fragments, periosteal new-bone formation

Less inflammation, less fluctuation in swelling, increased stability at fracture site

III- Resolution

Smoothing of edges of large fragments of bone, sclerosis, osseous or fibrous ankylosis

Permanent enlargement of the foot and ankle, fixed deformity, minimum daily swelling or activity-related swelling, normalization of skin temperature

cidence is estimated to be higher since many cases remain undiagnosed (1). Nonoperative treatment is considered to the gold standard for most neuroarthropathic processes, but in the presence of marked instability, severe deformity and recurrent ulcerations, reconstructive surgery must be considered (11– 16). We present a retrospective review of patients treated for the diabetic Charcot foot and a review of the recent literature on this condition. The purpose was to clarify the current treatment methods and emphasize the essential factors for successful treatment.

noses assessed. At the initial visit to our institution the rank and speciality of the treating physician – whether or not the diagnosis was correct – and initial recommended treatment were recorded. Radiological findings were classified according to Eichenholtz (11, 17) and with clinical findings the stage of the disease process was determined as dissolution, coalasence or resolution (Table 1). The involvement in hindfoot, midfoot or forefoot was classified according to Sanders and Frykberg (1, Table 2). Weightbearing radiographs and MRI were analysed if available. The treatment regimen was recorded: duration of casting and use of any kind of orthoses, duration of nonweightbearing and partial weightbearing, need for custommade insoles and possible intravenous bisphosphonate medication. All surgical procedures were noted, indication, type, timing, complications and outcome of each procedure included. Of the 32 patients, 13 (41 %) had type I diabetes (IDDM, insulin dependent diabetes mellitus) and 19 (59 %) type II (NIDDM, non-insulin dependent diabetes mellitus). Twenty-eight patients (88 %) required insulin for control of their diabetes, whereas 4 (12 %) were managed with diet or oral medication. The mean body mass index of male and female patients was 32.9 kg/m2 (SD 5.5kg/m2) and 34.3 kg/m2 (SD 8.5 kg/m2), respectively. The average duration of IDDM was 28 yrs (8–58 yrs) and NIDDM 14 yrs (1–28 yrs). Glycosylated hemoglobin averaged 9.4 %. Student’s t-test was used to compare continuous variables with Gaussian distribution and Pearson chi-square test to compare discrete variables.

MATERIAL AND METHODS

RESULTS

During the 6-year period from May 1994 to October 2000, a total of 36 feet of 32 patients were diagnosed as diabetic Charcot neuroarthropathies in the Departments of Surgery and Internal Medicine in Tampere University Hospital. There were 22 males and 10 females. The right foot was involved in 16 cases. The average follow-up time was 21 months (range 1–81 months). Study data were obtained retrospectively from patient records and radiographs. Demographic data were recorded at the time of diagnosing the neuroarthropathy. The type and duration of diabetes, presence of neuropathy, retinopathy and nephropathy and percentage of glycosylated hemoglobin value were also recorded, as well as coexistent medical diseases and medication. Disease-specific data were collected: the presence or absence of instigating trauma and temperature differences between the feet at the time of the correct diagnosis. The duration of symptoms prior to diagnosis was evaluated and diagnostic delay and possible preceding false diag-

In 8 of the 36 cases an instigating traumatic event could be identified. Of the 36 feet, 29 were diagnosed in the dissolution, two in the coalescence, and five in the resolution stage. Midfoot was involved in 31 cases, forefoot in five cases, talocrural joint in three and calcaneus in one. In four cases (11 %) more than one area was involved (midfoot together with forefoot or talocrural joint). In 22 cases (61 %), the correct diagnosis was made either by a referring physician or at the initial visit to our institution. Twenty-six cases were first seen by an internist (resident or specialist) and 10 by a surgical resident or specialist. The average delay from the first symptoms to the right diagnosis was 29 weeks (range 1–164, SD 32). Preceding false diagnoses were erysipelas (n = 10), deep venous thrombosis (n = 5), gout (n = 4), osteoarthrosis/arthritis

TABLE 2 Classification system of Sanders and Frykberg (1). Type

Affected area

1

Interphalangeal, metatarsophalangeal joints and metatarsal bones

2

Tarsometatarsal joints

3

Naviculocuneiform, talonavicular, and calcaneocuboid joints

4

Talocrural and subtalar joint

5

Calcaneus

Charcot arthropathy of the diabetic foot

(n = 5), fracture (n = 2) and unspecific inflammation/ osteomyelitis/tumor (n = 4). A diagnostic or followup MRI was carried out in 22 cases, 20 of them in the dissolution and two in the coalescence stage. In the dissolution phase the MRI findings constituted regional bone edema in 9 cases, regional bone edema with bony destruction in 6 and bony destruction or joint dislocation in 3. MR images of two cases were not available. MRIs performed in the coalascence phase demostrated regional bone edema in conjunction with midfoot destruction. At the initial visit to our institution 18 cases were not assigned treatment, total non-weightbearing and casting were prescribed in 13 cases, total non-weightbearing and fixed ankle boot- orthosis in 3, and total non-weightbearing only in 2 cases (Table 3.). At some stage in the treatment process 21 cases received plaster cast treatment, casting time averaged 11 weeks (range 4–37, SD 7). Half of the cases had orthosis in some phase of their treatment, average duration 10 weeks (range 3–19, SD 7). Skin temperatures and temperature differences between the affected and non-affected foot were measured in 17 patients during the immobilisation period. Eighteen patients (50 %) received bisphosphonate treatment (pamidronate 30–60 mg infusions once a week for six weeks): no complications were registered. There was no difference in casting time between patients who received (11 weeks) and patients who did not receive (13 weeks) pamidronate. In 10 patients temperature differences between the feet at the outset and after immobilisation could be reliably determined. At the beginning of immobilisation the temperature differ-

197 TABLE 3

Treatment prescribed at initial visit to our institution according to stage of disease process. Stage

No treatment

Cast + total non-weightbearing

Total non-weightbearing

15 00 03

11 02 00

3 0 2

I (n = 29) II (n = 2) III (n = 5)

ence between feet was 2.5 °C and after immobilisation 0.9 °C (p = 0.04). A total of 14 surgical procedures were performed to 10 patients with an average follow-up time of 21 months (range 1.5–72, SD 19). Eleven operations were carried out in the resolution, one in the coalescence and two in the dissolution stage of the disease process (Table 4.). After six exostectomies two postoperative wound infections were noted and successfully treated with oral antibiotics. A single exostectomy was successful in four patients and no subsequent ulcerations were observed during follow-up. One patient (patient 6, Table 4.) required two separate exostectomies after failed triple arthrodesis and recurrent ulcerations. All the exostectomies were performed on feet with ulcers healed. A total of six arthrodeses (4 midfoot, one tibiocalcaneal and one triple arthrodesis) were attempted and radiological fusion was achieved in four cases (patients 3, 7, 9 (1. operation) and 10). Three procedures (patients 3, 6 and

TABLE 4 Data on 10 surgically treated patients. Patient Sex, age Indication, stage

Procedure

Fixation method

Postoperative treatment

01

M, 50

Recurrent ulcerations, stage III

Exostectomy

None

3 weeks plaster cast and assisted weightbearing

02

M, 70

Recurrent ulcerations, stage III

Exostectomy

None

2,5 weeks plaster cast and assisted weightbearing

03

M, 57

Talonavicular destruction, stage II

Arthrodesis

Kirschner wires, a staple

plaster cast 5 months

04

F, 58

Recurrent ulcerations, stage III

Exostectomy

None

4 weeks plaster cast treatment + orthosis

05

M, 63

Talocrural destruction and gross instability, stage III

Below-knee amputation

None

Conventional

06

F, 44

1. Gross instability, stage I 2.–3. Recur. ulcers, stage III

1. Triple arthrodesis 2.–3 Exostectomy × 2

1. Rush pin and a staple 1. 12 weeks plaster cast 2.–3. None 2.–3. Not recorded

07

M, 50

Talocrural destruction, stage III

Tibiocalcaneal arthrodesis External fixation

3 months partial weightbearing

08

M, 41

Recurrent ulcerations, stage III

Exostectomy

None

Unrestricted weightbearing

09

F, 51

1. 2. 2. 3.

1. 2. 2. 3. 2.

1. 3 staples 2. 2 staples

1. 16 weeks plaster cast 2. 12 weeks plaster cast

3. –

3. Conventional

1 staple

12 weeks plaster casting (partial WB allowed at weeks)

10

F, 53

TMT disloc., stage I Naviculocuneiform disloc., stage III Gross instability, stage III

TMT I–II dislocation, stage III

TMT I–V arthrodesis Naviculocuneiforme arthrodesis Below-knee amputation

TMT II–IV and naviculocuneifrome arthrodesis

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T.-K. Pakarinen, H.-J. Laine, S. E. Honkonen, J. Peltonen, H. Oksala, J. Lahtela

9) were not undertaken in the resolution stage but in dissolution (patients 6 and 9) and coalescence (patient 3) stages (Table 4.). Patient 9 was incorrectly diagnosed as having gout arthritis and a tarsometatarsal arthrodesis was attempted, with poor results. The dissolution stage in the patient 3 was initially treated with serial casting and talonavicular arthrodesis with Kirschner wire fixation was attempted in the coalescence stage. A postoperative Kirschner wire failure and a collapse of adjacent nacivulocuneiform joints were noted and treated with serial casting. During the follow-up period a plantigrade foot alignment was restored in only two cases (patients 7 and 10). Two postoperative superficial infections were recorded at the sites of percutaneous wires. The cast treatment after arthrodesis was 12 weeks in five and 16 weeks in one case. Two below-knee amputations were performed after a failed arthrodesis and gross instability. One patient (patient 7) with unstable ankle joint was successfully treated with ankle fusion (Table 4.). Eight of the 18 patients who were not appropriately treated with a cast and total non-weightbearing at the initial presentation at our institution underwent surgical treatment, compared to 2 of 18 patients appropriately treated (p = 0.03). There was no difference in diagnostic delay between the operated (37 weeks) and non-operated (25 weeks) patients. DISCUSSION The number of diagnosed Charcot neuroarthropathies has increased considerably in our institution during the last decade. In previous decades a few Charcot neuroarthropathies were possibly misdiagnosed as resistant infections, and below-knee amputations might have been performed on a false basis. Probably the incidence of diabetic neuroarthropathy has truly increased. Recommendations for the diagnostics and treatment of Charcot feet can be made on the basis of experiences and a review of the recent literature. The pathophysiology of this neuroarthropathy is not well understood, but it is assumed to be multifactorial (1, 2). The loss of protective sensation allows repetitive micro- and macrotrauma to produce joint and periarticular soft tissue destruction; continued weightbearing often leads to the gross deformities seen in Charcot feet (1, 7, 8, 18, 19). The abnormal vasomotor regulation resulting from autonomic denervation may also constitute a main pathological change leading to Charcot neuroarthropathy (1, 8, 19, 20). Neuroarthropathic patients have increased lower limb blood flow and arteriovenous shunting, possibly in association with increased osteoclastic activity and bone resorption (20–22). Impairment of the motoneurons innervating the intrinsic muscles of the foot may alter the loading characteristics, promoting joint instability and thus also playing a role in diabetic Charcot foot process (2, 19, 23). The duration of IDDM at the time of the first Charcot event has been reported to average 22 years and NIDDM for 8 years, but this varies considerably

(7, 18). In our material the duration of IDDM before the appearance of Charcot neuroarthropathy ranged from 8 to 58 years. The average age of the patients in our series was 51 years, which accords with observations in previous studies (7, 12). In our material the proportion of IDDM (type 1) patients (42 %) was smaller than the 82 % in a series presented by Fabrin and associates (7), but considerably greater than the 2 % reported by Armstrong and colleagues (18). It seems to be difficult to make the correct diagnosis early enough. The long delay from the first symptoms to the right diagnosis is partly a consequence of patients underrating their swollen and red but often fairly painless feet. Still, the physicians often incorrectly presume infection or venous thrombosis. The possibility of Charcot foot should always be borne in mind when examining a diabetic patient with a swollen foot. In the dissolution stage inflammatory erythema and increased warmth of the affected foot are markedly present (18). In the absence of fever, elevated C-reactive protein or erythrocyte sedimentation rate, infection is highly unlikely, and a Charcot process should be considered. According to Schon et al (16) and Armstrong et al (18) in as many as 46–73 % of Charcot foot patients an instigating event has triggered the destructive process. In our series a preceding trauma could be identified in only 22 % of the cases. The skeletal changes involved vary between regional bone edema seen only in MRI and gross instability and destruction of the whole ankle-foot complex (24, 25). Sometimes non-weightbearing radiographs of the foot do not reveal the mid-foot instability; thus the weightbearing radiographs are indispensable. MRI has made it possible to detect bone changes before they can be seen in radiographs (25). Clinically, a patient may have an inflamed foot without radiographic bone destruction. Schon and Marks (26) classified this as a “pre-Charcot” state or stage 0 neuroarthropathy. If the Charcot process is allowed to progress to bone destruction, the foot collapses and results in a “rocker-bottom“ deformation with difficult exostoses predisposing to ulcerations (27–29). The goal of conservative treatment is to interrupt the destruction process and maintain adequate foot and ankle alignment, even though most patients with midfoot involvement will permanently need custom-molded shoes regardless of properly addressed treatment (7, 12, 18). However, if immobilisation and non-weightbearing are already initiated in the “pre-Charcot” stage, further progression and long-term problems will probably be prevented and normal foot alignment restored (1, 18, 26). Total non-weightbearing is regarded as a crucial part of the successful treatment of the Charcot foot in the dissolution stage (acute inflammation) (1, 8, 18). This is usually accomplished with a below-theknee plaster cast for at least 8–12 weeks (1, 12, 26). Plaster casts must be properly and carefully completed and be changed at one to two weeks’ intervals, as they loosen due to the resolution of edema, and inspection of the skin is mandatory. When the acute inflammation has subsided and coalescence safely

Charcot arthropathy of the diabetic foot

achieved, assisted weightbearing can be gradually started (Figure 1.). This is often best accomplished using boot orthosis (fixed ankle and rocker-bottom). At the beginning of weightbearing not only the weight must be limited but also the amount of exercise. Successful treatment requires a gradual wean from non-weightbearing to partial weightbearing and eventually to full weightbearing with the use of assistive devices and continuous monitoring for reactivation of the process. It is essential to clarify the characteristics of the Charcot process to the patients in order to motivate them to go through the strenuous treatment. Also the availability of the treating team to the patients must be made as easy as possible. There are no controlled studies concerning the sufficient duration of restricted weightbearing, but it is estimated that 8 to 16 weeks would be adequate if the activity of the process has clinically diminished. Armstrong et al. (18) suggest that casting is necessary for approximately 18 weeks to return to protective footwear with protective bracing. Prolonged (12– 18 months) immobilisation may be necessary if ankle or subtalar joints are affected (30). Bisphosphonate medication has been experimented on Charcot foot (31, 32), but no randomized trials have been performed. In our series pamidronate infusions were used on selected cases without any striking benefits or disadvantages. Besides clinical signs of the subsidence of inflammation, reduction in the activity of the Charcot process can be estimated by measuring skin temperature differences between the affected and the non-affected foot during treatment (21). In our series foot temperatures had been measured in about half of the cases. The skin temperatures are now followed regularly every time a cast is replaced. The measuring conditions (preceding rest or exercise, time between cast removal and measuring etc.) certainly affect results, and these should be properly standardised. If the difference between the feet is less than 1 °C, partialweightbearing and boot orthosis are usually considered. Current knowledge of the surgical treatment of the Charcot neuroarthropathy is based mainly on the personal experiences of foot and ankle surgeons (11, 16). No prospective and well-controlled studies comparing various treatment methods have been published. It has been estimated that at some point in the disease process 5–51 % of neuroarthropathic patients will be treated surgically (7, 16, 18, 33). In the present series 31 % were operated on during the follow-up. Our experiences demonstrate that if midfoot arthrodeses are performed on an inflamed foot in the dissolution stage results are likely to be disastrous. Despite proper timing, the results of midfoot arthrodeses may be compromised in consequence of inadequate fixation or insufficient postoperative casting and non-weighbearing. The essential issues in surgery on the Charcot foot are correct timing, adequate fixation and a sufficiently long postoperative immobilisation and non-weightbearing period. If a patient with peripheral neuropathy has an acute fracture or dislocation in the foot, it can be

199

Fig. 1. Weightbearing principles during progression of Charcot neuroarthropathy.

treated as in nondiabetic patients with open reduction and internal fixation if needed, but with longer immobilisation (11, 16, 26). It has been suggested that after surgery total non-weightbearing for 10–18 weeks and assisted weightbearing for 3–6 months in a cast (until warmth and edema have subsided) should be prescribed (12, 16, 34). Typically, in a neuropathic patient a subtle or repeated energy may insidiously induce fracture or dislocation with severe deformity. Most frequently there is a marked delay from symptoms to correct diagnosis and the dissolution stage has continued for weeks before the dislocated joint and bony destruction is detected. Reconstructive surgery is considered to be contraindicated in this inflammatory phase, but can be reconsidered after this phase has been succesfully treated by casting and non-weightbearing (11, 12, 15, 26). However, Simon et al. (34) have recently presented a series of 14 patients who underwent an operation in the acute phase. Their results of midfoot arthrodeses with good debridement, autogenous bone grafting, rigid plate fixation and proper immobilisation were successful without postoperative complications and the mean time to return to the use of regular shoes was 27 weeks. Sometimes the dissolution stage progresses rapidly to major bone destruction and gross instability and, if infectious ulceration with septic concurrence is present, a below-knee amputation is needed. The indications for reconstructive surgery in the resolution stage of Charcot neuroarthropathy are marked instability, severe deformity and recurrent ulcerations (11–16). The peripheral vascular status must be evaluated preoperatively and ulcerations preferably treated before any reconstructive procedures (11). The most common operative procedure in treating a neuropathic deformity causing recurrent ulceration is removal of the osseous prominence on the medial or plantar aspect of the foot. Such a decompressing exostectomy usually allows the foot to fit in a custom-molded shoe and the need for further surgical intervention can be avoided (11, 16). Catanzariti et al. (35) reported a 74 % healing rate of recurrent ulcerations treated with exostectomy. Patients with rocker-bottom deformity often have a contracted Achilles tendon, and percutaneous lenghtening of the tendon is recommended in conjunction with exosectomy (12). Casting for a few weeks is advisable pri-

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marily in order to reduce swelling and promote wound healing. Postoperative complications are usually centered on soft-tissue healing and are managed with oral antibiotics and local wound care (28). Theoretically, production of additional instability due to extensive bone resections is possible, but in our opinion not presumable. The major goal of reconstructive arthrodesis is to restore the stability and alignment of the foot and ankle so that custom molded shoes can be worn without formation of ulcerations. The recent literature has concluded that arthrodesis of an unstable Charcot joint should be performed with resection of all nonviable bone and with a sufficiently strong fixation using screws and plate and bone graft to maintain the alignment of the reduced foot (11, 12, 15, 34). Kirschner wires and staples do not provide a strong enough fixation, as also shown in our series. Obviously, a plate on the plantar surface of the medial column of the midfoot would be the most preferable fixation (34, 36). Postoperative treatment consists in casting and total non-weightbearing for at least 12– 18 weeks and further partial-weightbearing for 3 to 6 months until reliable consolidation has been achieved (11, 12, 34). In different series consolidation has been obtained in 54–100 % of cases (13, 15, 16, 34, 37, 38). A retrograde locked intramedullary nail can be used in tibiotalocalcaneal arthrodesis (11, 14, 39) External fixation is a treatment of choice in cases in which gross instability of the ankle joint has caused ulceration and fistulae (11). The revision must be sufficient and transfixation pins must be used in order to achieve durable fixation. Sometimes the deformity is so severe that only a below-knee amputation will provide a safe and reliable result (11, 15, 28). The objective would be to diagnose “pre-Charcot” stage 0 neuroarthropathies. It may be assumed that a diabetic patient with neuropathy and inflamed foot has a Charcot neuroarthropathy until proven otherwise. The correct treatment of inflammed Charcot foot – non-weightbearing – will be fulfilled when the patient is appropriately informed about the disease and motivated. In possible reconstructive surgery the essentials are correct timing, adequate fixation and a sufficiently long postoperative immobilisation and non-weightbearing period. In the resolution stage the majority of Charcot foot patients need custom-molded footwear, which must be replaced at reasonable intervals.

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Received: November 5, 2001 Accepted: June 7, 2002