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Complications of Ankle Fracture in Patients With Diabetes

Chaudhary, Saad B. MD, MBA; Liporace, Frank A. MD; Gandhi, Ankur PhD; Donley, Brian G. MD; Pinzur, Michael S. MD; Lin, Sheldon S. MD

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Journal of the American Academy of Orthopaedic Surgeons: March 2008 - Volume 16 - Issue 3 - p 159-170
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In the United States, more than 20 million Americans, approximately 7% of the population, have been diagnosed with diabetes.1 Advances in medical management have resulted in longer life spans and more active lifestyles for these patients. Ankle fractures are common orthopaedic injuries that, when diagnosed and treated in patients with diabetes, carry a high complication rate. A recent review of more than 160,000 patients with diabetes treated for ankle fractures from 1988 through 2000 showed that 5.71% of the patients had diabetes. The diabetic patients had a significantly higher in-hospital mortality rate, in-hospital postoperative complication rate, length of stay, and rate of nonroutine discharges (P < 0.001 for all).2 All diabetic ankle fracture patients need to be informed of potential complications, which include impaired wound healing, infection, malunion, loss of reduction, hardware failure, nonunion, and Charcot arthropathy2-9 (Table 1). Physiologic blood glucose control and an organized multidisciplinary approach are critical in avoiding complications and improving outcomes.3,10 Although the diabetic foot and ankle have been extensively studied, a standard treatment protocol for diabetic patients with ankle fractures still does not exist.

Table 1
Table 1:
Treatment Complications of Ankle Fractures in Patients With Diabetes


Understanding the basic science of the pathogenesis of diabetes-related complications provides insight into managing diabetic patients with ankle fractures. The main pathology in diabetes is microangiopathy and peripheral neuropathy.8 Diabetes impairs the patient's immune, renal, vascular, and nervous systems, leading to multisystem complications. The presence of a fracture further exacerbates the existing problem of a tenuous blood supply in a potentially insensate limb. As a result, both soft-tissue healing (eg, diabetic ulcer, postoperative incision) and fracture healing are impeded.11–13

Impaired Wound Healing

Diabetic wound healing has long been recognized as a major complication of diabetes and a formidable challenge. To understand the pathogenesis of impaired diabetic wound healing, two fundamental pathophysiologic states must be examined: hyperglycemia and hypoxia.

Hyperglycemia is the primary consequence of diabetes. Alterations in insulin levels or insulin-receptor affinity result in excess blood glucose. Structural and functional proteins exposed to prolonged periods of elevated blood glucose result in enzymatic glycosylation. In time, these proteins may undergo nonenzymatic glycosylation reactions, yielding irreversible advanced glycation end-products (AGEs). AGEs attach to collagen, basement membrane, low-density lipoproteins, and inflammatory cell receptors and disrupt and/or impair their function. Over time, these products accumulate in tissues.14 Glycosylated hemoglobin (HbA1c) levels are a timeaverage measure of blood glucose levels over the 120-day life span of red blood cells. The kidney and some other tissues (eg, nerves, blood vessels, optic lens) do not require insulin for glucose transport. Instead, hyperglycemia local to these tissues results in elevated intracellular glucose, which is shunted to the sorbitol pathway. The end result is decreased myo-inositol levels and cell damage, as evidenced by the neuropathy14 and angiopathy in patients with diabetes.

Diabetes affects small and large vessels alike, leading to tissue hypoxia, a common secondary phenomenon. Regional and local ischemia with large-vessel arteriosclerosis, particularly of the lower extremities, and localized small-vessel angiopathy are noted in the diabetic population.14 Compounding this ischemia is the increased blood viscosity and decreased compliance of red blood cells seen in patients with diabetes. HbA1c has a higher affinity for oxygen, thereby impairing oxygen delivery to various tissues, resulting in ischemia.15

Macroscopic measurements to predict wound healing in diabetic patients generally are markers of large-vessel patency and local smallvessel perfusion of the skin. A palpable pulse is considered to be a sign of good distal blood flow. The use of semiquantifiable values, such as the ankle-brachial index (ABI) measurement, may not be reliable in diabetic patients because of medial calcific sclerosis (Mönckeberg sclerosis) causing an inability to achieve adequate vessel compression. One valuable clinical marker of adequate local perfusion for healing has been transcutaneous oxygen pressure (tcpo2) measurements.16 A tcpo2 value of 30 mm of mercury (Hg) has been shown consistently to be the minimum value required for the healing of diabetic surgical wounds and also for the successful outcome of lower extremity diabetic infections. Values of <20 to 30 mm Hg may indicate the need for angiography and treatment.17,18 Another mechanism for estimating tissue healing is the use of Doppler toe pressure measurements. The threshold for toe pressure associated with adequate limb perfusion is 30 mm Hg.

The combination of local ischemia and elevated blood glucose creates a poor environment for wound healing. Under hypoxic conditions, fibroblast migration is inhibited, and fibroblasts lose their ability to proliferate. Wound collagen deposition is directly proportional to wound oxygen tension and perfusion.19 In diabetic wounds, collagen production is severely impaired because of the local ischemic condition.20

Along with having impaired healing properties, the ischemic diabetic wound results in an environment that has an increased susceptibility to infection. Any local infection compromises the wound healing process even further because of a release of bacterial enzymes and metalloproteinases, which degrade fibrin and growth factors.21 Simple experiments in healthy wounds have shown that the presence of >105 bacteria per 1 gram of tissue imparts a <19% chance of successful wound healing.22

In addition to elevated HbA1c levels, risk factors for poor healing in patients with diabetes include vasculopathy, smoking, hypertension, dyslipidemia, and advanced age.23 Increased body mass index and delays >2 weeks in starting treatment also have a negative effect on healing.24,25 The most important factor in maintaining a proper milieu for wound healing in the patient with diabetes is physiologic blood glucose control (ie, HbA1c levels of <6.0%).12

Delayed Fracture Healing

In certain systemic conditions such as diabetes mellitus, the fracture healing process is significantly impaired. Three retrospective studies26–28 have evaluated complications following elective arthrodesis in diabetic patients. Although the subjects in these studies represent a subpopulation of diabetic patients with neuropathy, the noted increased incidence of delayed union, nonunion, and pseudarthrosis is marked.26,27 Perlman and Thordarson28 compared the results of ankle fusions in several nonunion risk groups and found a higher incidence of nonunion in patients with diabetes (3/8 patients [38%]) compared with patients without diabetes (14/51 [27%]). A comparative study by Loder13 demonstrated a significant delay (ie, 163% of expected time) in fracture healing in diabetic patients without neuropathy. Although the value of this study was compromised by variability in patient demographics, fracture patterns, and locations, diabetic patients in Loder's study13 experienced a significant (187%) increase in time to union. Cozen,11 in a comparative cohort study of patients with lower extremity fractures, reported more than double the healing time in nine diabetic compared with nine nondiabetic patients (8.2 months versus 3.6 months, respectively, with three of nine diabetic patients achieving partial unions).

In the 30 years since the publication of the original diabetic fracture studies, the exact pathogenesis of impaired osseous healing has not been elucidated. An increased understanding of the fracture healing process can be obtained from data regarding the effect of diabetes on collagen synthesis and cellular proliferation. Collagen synthesis (content as well as type) is abnormal during the early stages of fracture healing in untreated diabetic animals. Spanheimer et al29 reported a decreased synthesis of collagen by articular cartilage and bone cells from diabetic rats incubated in vitro. Topping et al30 further characterized the type of impaired collagen synthesis present during the diabetes mellitus fracture healing process. In this diabetic rat model, type X collagen synthesis was decreased in the fracture callus. Type X collagen is critical in endochondral ossification and vascular invasion. Therefore, its inhibition may adversely affect bone healing. Overall, the correlation of decreased mechanical strength and decreased or abnormal collagen synthesis suggests that early events play an important, persistent, and deleterious role in diabetic fracture healing.

Several mechanisms have been proposed attempting to explain the slow fracture healing process in the patient with diabetes.3 Essentially, diabetes impairs fracture healing beginning with a reduction in early cellular proliferation, continuing with a delay in endochondral ossification, and ending with decreased biomechanical strength of the fracture callus.31–33

Management of Ankle Fractures in Diabetic Patients


The initial patient encounter should entail a detailed history, including the mechanism of injury, time elapsed since injury, and medical comorbidities, especially glycemic control, peripheral neuropathy, nephropathy, and other end-organ effects. Based on patient history, a medical or an endocrine consult may be appropriate to help ensure physiologic glycemic control.

A thorough and expedient physical examination is warranted. The examination begins with a circumferential inspection for open or tenuous wounds, followed by a vascular examination. The association of vascular insufficiency with diabetes is well-documented. The posterior tibial and dorsalis pedis arteries are palpated, and the foot is checked for capillary refill. In the absence of palpable pulses, an ABI measurement may be made; however, this value is not as reliable in diabetic patients compared with other patients, secondary to vascular calcification. Noninvasive vascular studies (eg, Doppler ultrasound), as well as invasive studies (ie, arteriography), may be required. Furthermore, in the absence of palpable pulses and with an ABI measurement of <0.5, a vascular surgery consult is warranted.

A neurologic analysis of the extremity and foot is also of utmost importance to rule out injury or neuropathy. In addition to motor testing, sensation must be assessed. Sensory deficits can be quantified using a 5.07 Semmes-Weinstein monofilament (SWM). Several sizes of monoilaments are commercially available, ranging from 1.65 to 6.65. The ability to feel the 4.17 Semmes-Weinstein monofilament implies normal protective sensation, whereas the inability to sense the 5.07 SWM (10 g) monofilament correlates with the presence or history of an ulcer and neuropathy.

Plain radiographs and computed tomography may be used to characterize the fracture. Plain anteroposterior, lateral, and mortise radiographs of the ankle typically are sufficient. It is also important to get both full-length tibia radiographs to rule out proximal fibular involvement. In addition, simulated weightbearing radiographs of the contralateral foot may be helpful to assess for changes resulting from Charcot disease (Figure 1).

Figure 1
Figure 1:
Treatment algorithm for diabetic patients with ankle fracture.

General Treatment Principles

Once any life- or limb-threatening injuries have been addressed, vascular flow to the extremity/foot is ensured, followed by provisional reduction of a deformity or dislocation. Care for the soft-tissue envelope cannot be overemphasized; in addition to reducing the fracture and the ankle joint, any open wound must be appropriately dressed in a sterile dressing and the extremity splinted with definitive care in a timely manner. A delay in initial diagnosis or inadequate immobilization can result in Charcot arthropathy.24 Prolonged non-weight bearing, followed by rehabilitation, are the final steps in the management process.

Nonsurgical Treatment

Ankle fractures in patients with diabetes vary widely in severity. Treatment depends on the location of the fracture and its effect on the articular surface as well as on ankle stability. Nondisplaced fractures in highrisk patients can be managed nonsurgically in a cast (although this is controversial).8,34 Treatment entails casting with non-weight-bearing restriction until fracture healing is demonstrated. Typically, the patient with diabetes is immobilized with non-weight-bearing precautions for a duration two to three times that of a nondiabetic patient in order to avoid complications of malunion and Charcot arthropathy.3 Charcot arthropathy, a delayed sequela of diabetic ankle fractures, can develop even following nondisplaced fractures. Patients with preexisting neuropathy are at an increased risk of unrecognized microtrauma that can result in Charcot changes over time.3,6

McCormack and Leith8 reported on 26 ankle fractures in diabetic patients: 19 were treated surgically and 7 immobilized in casts. In the surgical group, the authors reported one wound complication (5%), four infections (21%) leading to two amputations (11%), and two deaths (11%), for an overall complication rate of 47%. No complications were reported in the nonsurgical group. Because of these results, the authors suggested that surgical intervention in lowdemand elderly patients may be ill-advised; malunion may be an acceptable outcome. Several factors, however, such as the degree of diabetic control, as well as the presence of neuropathy or peripheral vascular disease and associated medical comorbidities, were not reported.8

Schon and Marks34 reviewed the results of 28 neuropathic ankle fractures in patients with diabetes, 15 nondisplaced and 13 displaced. Treatment of the nondisplaced fractures consisted of immediate immobilization with no weight bearing for 3 months (5 fractures), immobilization and initial non-weight bearing for 9 months (7), or delayed immobilization (3). All of the nondisplaced ankle fractures healed without evidence of Charcot arthropathy or infection.

Connolly and Csencsitz6 reported their results for five diabetic ankle fractures treated with casting in five patients with insulin-dependent diabetes mellitus (mean age, 40 years). Two patients developed an infection that resulted in amputation; two developed Charcot neuropathy. Two patients required an ankle fusion after infection or Charcot neuropathy. One patient developed a malunion (terminal treatment), and another underwent delayed surgical fixation, with a resultant functional fibrous ankylosis. The authors concluded that early surgical intervention is preferable in patients with diabetes and ankle fractures.6

Since Kristiansen's series in 198335 on ankle fractures in patients with diabetes, the increased rate of complications in this population has not been disputed. However, the debate still continues in regard to the exact and appropriate type of surgical versus nonsurgical treatment of displaced ankle fractures in diabetic patients. Much of the literature consists of case series that highlight the extremes of potentially poor outcomes. To date, no reference exists that provides a clear algorithm supporting either nonsurgical treatment or surgical intervention based on fracture displacement in this population. Plan of care must be tailored individually to each patient based on his or her diabetic control, diabetic comorbidities, and fracture type.

Surgical Treatment

For displaced ankle fractures, the standard of care is open reduction and rigid internal fixation with prolonged non-weight bearing. In diabetic patients with ankle fractures, however, surgery is rife with complications. Kristiansen35 reported results of 10 diabetic ankle fractures treated by open reduction and internal fixation: 40% were neuropathic, 90% went on to fracture union, 10% developed a Charcot ankle, and 60% developed a surgical infection. Similarly, in their series of 10 diabetic ankle fractures managed surgically, Low and Tan36 reported a 40% infection rate, which resulted in two amputations (20%), and the development of Charcot ankle in a patient with preexisting neuropathy.

In the study by Schon and Marks,34 13 displaced ankle fractures were treated either by casting (4) or surgical intervention (9). Closed treatment of the displaced fractures resulted in a 100% nonunion/malunion rate, with three of the fractures ultimately requiring ankle fusion. The fourth fracture was treated by late open reduction and internal fixation at 3 months. Surgical fixation of displaced ankle fractures resulted in one infected nonunion, one wound complication requiring a free flap, one Charcot ankle requiring fusion, and one failure of fixation. No infections or amputations were reported.34 In this study, the poor clinical outcome of nonsurgical treatment of diabetic patients with displaced ankle fractures bolsters the need for surgical intervention.

Blotter et al4 reviewed 44 surgically treated ankle fractures in 21 diabetic patients and 46 control patients. A statistically higher complication rate was noted in the diabetic group (43%) compared with the nondiabetic group (15%). Patient age range was 19 to 77 years (median, 55 years). Seven of the diabetic patients (33%) had insulindependent diabetes mellitus; 14 (66%) had non-insulin-dependent diabetes mellitus. The patients with insulindependent diabetes mellitus incurred a 57% complication rate compared with a 36% complication rate for those with non-insulin-dependent diabetes mellitus. The authors reported seven infections (21%), two amputations (9.5%), two Charcot joints (9.5%), and one nonunion (4.7%) in the diabetic group. Infection developed in two of the three open diabetic fractures (67%). These investigators concluded that patients with diabetes mellitus are at a 2.76-fold increased risk for complications compared with nondiabetic patients and that strict adherence to a postoperative protocol is crucial to ensure a good outcome.4

A recent study by White et al9 specifically focused on open ankle fractures in patients with diabetes mellitus. Fourteen open ankle fractures were identified in 13 patients. The average number of surgical procedures per patient was five; mean follow-up was 19 months. Nine extremities had wound healing complications; five patients ultimately required below-knee amputations. Three of 14 fractures (21%) had uneventful healing without any complications.9

Jones et al37 retrospectively reviewed 42 patients with diabetes mellitus and acute, closed, rotational ankle fracture. Twenty-one patients had comorbidities and 21 did not. Patients were individually matched to 42 nondiabetic control patients by age, sex, fracture type, and surgical versus nonsurgical treatment. The diabetic patients without comorbidities did not differ significantly in complications compared with the nondiabetic control patients, except that the diabetic patients required long-term bracing. However, the diabetic patients with comorbidities had more complications (47%) than did the nondiabetic control patients (14%). History of Charcot neuropathy led to the highest rates of complications. Other risk factors for complications included duration of diabetes, use of insulin, and presence of nephropathy or neuropathy. Risk factors not associated with complications included age, gender, type of fracture, and method of treatment.37

Surgical Techniques

Several techniques have been developed to help minimize complications linked with diabetic ankle fractures. Some techniques address issues of osteopenia or wound necrosis, which are common problems in diabetic patients with ankle fractures.

Fractures that require surgery in the diabetic patient need rigid fixation to avoid loss of reduction. However, before discussing fixation, the importance of soft-tissue stabilization must be emphasized. Bibbo et al3 stressed the importance of a treatment protocol that involves prompt reduction and splinting to reduce soft-tissue trauma, followed by delayed surgery after resolution of edema and medical status. To maintain reduction while soft-tissue stabilization is pending, an external fixator may be necessary; the external fixator may be combined with internal fixation based on the ultimate condition of the soft-tissue envelope.3,34 External fixation may be either the first part of a staged reconstruction or definitive treatment if severe softtissue injury is present. Usually, stage one consists of preliminary stabilization (ie, transarticular external fixator and plating of the fibula); the second stage allows for definitive internal fixation once soft-tissue stabilization has been achieved (Figure 2). Typically, 10 to 14 days is required for soft-tissue stabilization. The presence of skin wrinkles at the potential surgical site indicates an appropriate period of delay for softtissue stabilization.

Figure 2
Figure 2:
Anteroposterior (A) and lateral (B) radiographic views of a diabetic pedestrian struck in a traffic accident. The patient sustained a pilon fracture and a transverse fibular fracture. Anteroposterior (C) and lateral (D) radiographic views of the same patient temporized in transarticular external fixation for 12 days. Mortise (E) and lateral (F) radiographic views demonstrating definitive fixation of the pilon fracture and a percutaneous retrograde screw fixation of the lateral malleolus (to minimize lateral soft-tissue dissection).

Using this protocol, Sirkin et al38 reported on a series of 56 pilon fractures in 53 nondiabetic patients. The authors divided the fractures into two groups: closed and open injuries. They noted low wound complication rates of 5.3% in all fractures and of 2.9% in the closed pilon fractures. Patients in the closed pilon group with an isolated ankle injury were treated on an outpatient basis. Minor wound healing problems were treated successfully with local wound care and oral antibiotics, without need for hospital admission.38 Patterson and Cole39 used a similar protocol in a series of 21 patients with equally encouraging results.

Osteopenia/osteoporosis also is frequently a matter of concern when dealing with diabetic patients. Therefore, supplementation to standard ankle fixation is commonly required. To increase rigidity of fixation, longer plates, supplementary Kirschner wires (K-wires) in plated fibulas, multiple fibula-tibia syndesmotic fixation, and transcalcanealtibial Steinmann pin fixation all have been suggested as adjuncts to standard surgical options in patients both with and without diabetes.40–43 The use of locked plating may provide the added stability in situations of severe bone loss and comminution commonly seen in diabetic patients. Also, percutaneous fibula fixation may be considered in order to avoid soft-tissue dissection, thereby decreasing wound complications. In a retrospective review, Ray et al44 reported on 24 nondiabetic patients with Weber B and low Weber C displaced lateral malleolus fractures. Following closed reduction and percutaneous internal fixation with an intramedullary, fully threaded, selftapping screw, the authors reported a 95.5% union rate and no deep wound infections or painful hardware complications.

To minimize loss of reduction and malunion in nondiabetic, elderly osteoporotic bone, Koval et al42 suggested a method for improved screw purchase during fibula plate fixation. First, retrograde 1.6-mm K-wires are placed across a reduced distal fibula fracture, with penetration of the medial fibular cortex in the proximal fragment. Then a precontoured one-third tubular plate is applied to the lateral aspect of the fibula with its screws interdigitating with the intramedullary retrograde K-wires. All 19 patients who underwent treatment with this technique went on to union without loss of reduction (average follow-up, 15.4 months). In addition, 89% of these elderly, nondiabetic, osteopenic patients had no, slight, or mild pain. Furthermore, biomechanical testing proved this construct to be superior to the standard mode of fixation. The specimens augmented with K-wires had 81% greater resistance to bending and twice the resistance to motion during torsional testing42 (Figure 3).

Figure 3
Figure 3:
Anteroposterior (A), mortise (B), and lateral (C) radiographic views of a diabetic patient with a right bimalleolar ankle fracture with a syndesmotic injury. Anteroposterior (D), mortise (E), and lateral (F) radiographic views after fixation, showing placement of three retrograde 1.6-mm K-wires across the fibula fracture to enhance screw purchase. Fixation was performed 7 days after the injury.

In an effort to further improve fixation stiffness, Schon et al34 used multiple tetracortical fibula-to-tibia screw fixation through the one-third tubular plate in the proximal fibula fragment. Dunn et al40 have reported that, biomechanically, the construct using the three tetracortical syndesmotic screws was significantly stiffer in resisting axial and external rotation loads compared with intramedullary K-wire-supplemented fixation (Figure 4). Perry et al43 employed a similar technique in a series of six patients with failed neuropathic ankle fractures. The authors used a 4.5-mm dynamic compression plate and multiple 4.5-mm tetracortical syndesmotic screws. All six patients were satisfied with results at final follow-up.43

Figure 4
Figure 4:
Attempted mortise radiographic view (A) and a lateral (B) view of a 19-year-old man with brittle insulin-dependent diabetes mellitus following a motor vehicle accident. The patient sustained a right bimalleolar ankle fracture and a syndesmotic injury. Mortise (C) and lateral (D) radiographic views following fixation. The patient underwent locked-plate fixation with four tetracortical syndesmotic screws. The medial side was fixed with two standard partially threaded screws. The definitive fixation was performed 7 days after the injury.

Criticism of the use of multiple fibula-to-tibia tetracortical screws includes the concern of altered ankle biomechanics as well as changes to the stiffness of the syndesmosis. Clinically, however, this concern has not been significant because ambulation progressively restores motion between the tibia and fibula in spite of fixation. This phenomenon is demonstrated by lysis around syndesmotic screws, as shown by Kaye45 in a retrospective review of 30 nondiabetic patients who underwent screw fixation for syndesmotic disruption. Moreover, fracture patterns with significant fibular comminution and existing degeneration at the tibia-fibula joint may make it difficult to acquire syndesmotic screw fixation through the tibia-fibula joint. The multiplescrew technique ensures restoration of fibular length and maintenance of the tibia-fibula relationship (Figure 5).

Figure 5
Figure 5:
Attempted mortise radiographic view (A) and a lateral view (B) of a diabetic male smoker struck in a traffic accident. The patient sustained a left bimalleolar equivalent ankle fracture. Anteroposterior (C), mortise (D), and lateral (E) radiographic views after fixation. The patient had preexisting tibiofibular joint degeneration. A long fibular plate was used with tibiofibular screws, including a screw through the tibiofibular joint to span the fracture segment. The patient also had complex foot fractures requiring fixation. The ankle fixation was performed 10 days after the injury because the patient had significant swelling resulting from his high-energy foot and ankle fractures.

The introduction of locked plating also may help attain stable fixation. Fixed-angle screws do not rely on friction between the plate and bone; therefore, failure requires “cutting out” of all points of fixation on one side of the fracture, as opposed to the loosening of individual screws, resulting in localized failure of the construct (as is seen with traditional plating). A recent biomechanical study has shown that, compared with traditional plating, locked fixation is equivalent at retaining its original stiffness in distal fibula fractures when subjected to cyclical loading. Moreover, fixation with standard plates was dependent on bone mineral density, whereas the locking plate was independent of bone mineral density. Thus, locked plating may be advantageous in fixing distal fibula fractures in osteoporotic patients46 (Figure 4). The use of locked plating in distal fibula fractures, however, is still controversial. A biomechanical study by Minihane et al47 indicates that a posterolateral antiglide plate demonstrates improved stability compared with lateral locked plate fixation for osteoporotic distal fibula fractures. Further clinical data are needed to justify the use of locked implants in distal fibular fixation.

In patients with unstable ankle fractures and loss of protective sensibility, transarticular fixation and prolonged protected weight bearing have been suggested as a viable treatment option. To improve construct rigidity in 15 diabetic patients with neuropathy, Jani et al41 used retrograde transcalcaneal-talar-tibial fixation with large Steinmann pins or screws in conjunction with standard techniques of open reduction and internal fixation. Postoperatively, patients were placed in a short leg, total-contact cast and made non-weight-bearing for 12 weeks. Removal of the intramedullary implants took place at 12 to 16 weeks, followed by use of a CAM (controlled ankle motion) walker or cast immobilization with partial weight bearing for an additional 12 weeks. Finally, patients were transitioned to a custom-molded ankle-foot orthosis or to custom total-contact inserts. The rate of major complications for all fractures was 25%; this figure is lower than historic rates of 30% and 43%, respectively, for diabetic patients with and without neuropathy. The total amputation rate was 13% (8% for closed fractures). No deaths or Charcot malunions were reported. The treatment regimen combining transarticular fixation with extended, protected weight bearing provided 13 of 15 patients with a stable ankle for weight bearing and activity.41

In an attempt to decrease complications of wound healing, percutaneous fibula fixation may be attempted in closed, low-energy, noncomminuted, length-stable fibula fractures. This may be done with either a plate or an intramedullary screw. Through a limited incision distally and by use of fluoroscopy, a precontoured small-fragment plate can be advanced in a retrograde fashion along the lateral aspect of the fibula to the appropriate level. Next, through small incisions, screw fixation can be obtained. This technique does not preclude tetracortical syndesmotic fixation. Furthermore, as reported by Ray et al44 in a retrospective review of displaced lateral malleolus fractures in patients with diabetes, percutaneous intramedullary screw fixation can be achieved in transverse fractures of the lateral malleolus by using a retrograde screw, which requires minimal softtissue dissection (Figure 2).


Diabetic patients with ankle fracture are consistently at greater risk of sustaining a complication during treatment compared with nondiabetic patients. Basic management of wounds and fractures in diabetic patients begins with optimizing the woundhealing environment by adopting a multidisciplinary approach. The primary focus should be to ensure appropriate insulin therapy and maintain optimal blood glucose levels. Appropriate tissue oxygenation and maximization of limb vascularity also are important treatment goals for patients with diabetes who have sustained an ankle fracture.

Patients with diabetes are at significant risk for soft-tissue complications, including Charcot neuroarthropathy and peripheral vascular disease. Diabetic ankle fractures heal, but significant delays in bone healing exist. Charcot ankle arthropathy occurs more commonly in patients who were initially undiagnosed and had a delay in immobilization, or in patients treated nonsurgically for displaced ankle fractures. Although several options for nonsurgical and surgical treatment exist, respect for softtissue management is of paramount concern, as is attention to stable, rigid fixation with prolonged immobilization and prolonged restricted weight bearing, in trying to minimize problems and yield good functional results.


Evidence-based Medicine: Level I/II prospective, randomized studies include references 10, 17, and 18. The remaining references are retrospective studies, case reports, casecontrol cohort studies, reviews, and basic science studies.

Citation numbers printed in bold type indicate references published within the past 5 years.

1. Centers for Disease Control and Prevention: Available at Diabetes/ Accessed January 29, 2008.
2. Ganesh SP, Pietrobon R, Cecilio WA, Pan D, Lightdale N, Nunley JA: The impact of diabetes on patient outcomes after ankle fracture. J Bone Joint Surg Am 2005;87:1712-1718.
3. Bibbo C, Lin SS, Beam HA, Behrens FF: Complications of ankle fractures in diabetic patients. Orthop Clin North Am 2001;32:113-133.
4. Blotter RH, Connolly E, Wasan A, Chapman MW: Acute complications in the operative treatment of isolated ankle fractures in patients with diabetes mellitus. Foot Ankle Int 1999;20:687-694.
5. Boddenberg U: Healing time of foot and ankle fractures in patients with diabetes mellitus: Literature review and report on own cases [German]. Zentralbl Chir 2004;129:453-459.
6. Connolly JF, Csencsitz TA: Limb threatening neuropathic complications from ankle fractures in patients with diabetes. Clin Orthop Relat Res 1998;348:212-219.
7. Flynn JM, Rodriguez-del Rio F, Piza PA: Closed ankle fractures in the diabetic patient. Foot Ankle Int 2000;21:311-319.
8. McCormack RG, Leith JM: Ankle fractures in diabetics: Complications of surgical management. J Bone Joint Surg Br 1998;80:689-692.
9. White CB, Turner NS, Lee GC, Haidukewych GJ: Open ankle fractures in patients with diabetes mellitus. Clin Orthop Relat Res 2003;414:37-44.
10. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. NEngl J Med 1993;329:977-986.
11. Cozen L: Does diabetes delay fracture healing? Clin Orthop Relat Res 1972;82:134-140.
12. Goodson WH III, Hung TK: Studies of wound healing in experimental diabetes mellitus. J Surg Res 1977;22:221-227.
13. Loder RT: The influence of diabetes mellitus on the healing of closed fractures. Clin Orthop Relat Res 1988;232:210-216.
14. Cotran R, Kumar V, Robbins S (eds): Robbins Pathologic Basis of Disease, ed 6. Philadelphia, PA, WB Saunders, 1999.
15. Harrelson J: The diabetic foot: Charcot arthropathy. Instr Course Lect 1993;42:141-146.
16. Ubbink DT, Kitslaar PJ, Tordoir JH, Reneman RS, Jacobs MJ: Skin microcirculation in diabetic and nondiabetic patients at different stages of lower limb ischaemia. Eur J Vasc Surg 1993;7:659-6.
17. Ballard JL, Eke CC, Bunt TJ, Killeen JD: A prospective evaluation of transcutaneous oxygen measurements in the management of diabetic foot problems. J Vasc Surg 1995;22:485-490.
18. Kalani M, Brismar K, Fagrell B, Ostergren J, Jörneskog G: Transcutaneous oxygen tension and toe blood pressure as predictors for outcome of diabetic foot ulcers. Diabetes Care 1999;22:147-151.
19. Jonsson K, Jensen JA, Goodson WH 3rd, et al: Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients. Ann Surg 1991;214:605-613.
20. Hunt TK, Linsey M, Sonne M, Jawetz E: Oxygen tension and wound infection. Surg Forum 1972;23:47-49.
21. Stadelmann WK, Digenis AG, Tobin GR: Impediments to wound healing. Am J Surg 1998;176:39S-47S.
22. Krizek T, Robson M, Kho E: Bacterial growth and skin graft survival. Surg Forum 1967;18:518-519.
23. Mancini L, Ruotolo V: The diabetic foot: Epidemiology. Rays 1997;22:511-523.
24. Holmes GB Jr, Hill N: Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes. Foot Ankle Int 1994;15:182-185.
25. Sinacore DR: Acute Charcot arthropathy in patients with diabetes mellitus: Healing times by foot location. J Diabetes Complications 1998;12:287-293.
26. Papa J, Myerson M, Girard P: Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint Surg Am 1993;75:1056-1066.
27. Stuart MJ, Morrey BF: Arthrodesis of the diabetic neuropathic ankle joint. Clin Orthop Relat Res 1990;253:209-211.
28. Perlman MH, Thordarson DB: Ankle fusion in a high risk population: An assessment of nonunion risk factors. Foot Ankle Int 1999;20:491-496.
29. Spanheimer RG, Umpierrez GE, Stumpf V: Decreased collagen production in diabetic rats. Diabetes 1988;37:371-376.
30. Topping RE, Bolander ME, Balian G: Type X collagen in fracture callus and the effects of experimental diabetes. Clin Orthop Relat Res 1994;308:220-228.
31. Macey LR, Kana SM, Jingushi S, Terek RM, Borretos J, Bolander ME: Defects of early fracture-healing in experimental diabetes. J Bone Joint Surg Am 1989;71:722-733.
32. Shimoaka T, Kamekura S, Chikuda H, et al: Impairment of bone healing by insulin receptor substrate-1 deficiency. J Biol Chem 2004;279:15314-15322.
33. Lu H, Kraut D, Gerstenfeld LC, Graves DT: Diabetes interferes with the bone formation by affecting the expression of transcription factors that regulates osteoblast differentiation. Endocrinology 2003;144:346-352.
34. Schon LC, Marks RM: The management of neuroarthropathic fracturedislocations in the diabetic patient. Orthop Clin North Am 1995;26:375-392.
35. Kristiansen B: Results of surgical treatment of malleolar fractures in patients with diabetes mellitus. Dan Med Bull 1983;30:272-274.
36. Low CK, Tan SK: Infection in diabetic patients with ankle fractures. Ann Acad Med Singapore 1995;24:353-355.
37. Jones KB, Maiers-Yelden KA, Marsh JL, Zimmerman MB, Estin M, Saltzman CL: Ankle fractures in patients with diabetes mellitus. J Bone Joint Surg Br 2005;87:489-495.
38. Sirkin M, Sanders R, DiPasquale T, Herscovici D Jr: A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma 1999;13:78-84.
39. Patterson MJ, Cole JD: Two-staged delayed open reduction and internal fixation of severe pilon fractures. J Orthop Trauma 1999;13:85-91.
40. Dunn WR, Easley ME, Parks BG, Truka HJ, Schon LC: An augmented fixation method for distal fibular fractures in elderly patients: A biomechanical evaluation. Foot Ankle Int 2004;25:128-131.
41. Jani MM, Ricci WM, Borrelli J Jr, Barrett SE, Johnson JE: A protocol for treatment of unstable ankle fractures using transarticular fixation in patients with diabetes mellitus and loss of protective sensibility. Foot Ankle Int 2003;24:838-844.
42. Koval KJ, Petraco DM, Kummer FJ, Bharam S: A new technique for complex fibula fracture fixation in the elderly: A clinical and biomechanical evaluation. J Orthop Trauma 1997;11:28-33.
43. Perry MD, Taranow WS, Manoli A II, Carr JB: Salvage of failed neuropathic ankle fractures: Use of large-fragment fibular plating and multiple syndesmotic screws. J Surg Orthop Adv 2005;14:85-91.
44. Ray TD, Nimityongskul P, Anderson LD: Percutaneous intramedullary fixation of lateral malleolus fractures: Technique and report of early results. J Trauma 1994;36:669-675.
45. Kaye RA: Stabilization of ankle syndesmosis injuries with a syndesmosis screw. Foot Ankle 1989;9:290-293.
46. Kim T, Ayturk UM, Haskell A, Miclau T, Puttlitz CM: Fixation of osteoporotic distal fibula fractures: A biomechanical comparison of locking versus conventional plates. J Foot Ankle Surg 2007;46:2-6.
47. Minihane KP, Lee C, Ahn C, Zhang LQ, Merk BR: Comparison of lateral locking plate and antiglide plate for fixation of distal fibular fractures in osteoporotic bone: A biomechanical study. J Orthop Trauma 2006;20:562-566.
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