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Dual plating technique for comminuted second metatarsal fracture in the diabetic obese patient: A case report

Posted on December 31, 2017 | Comments Off on Dual plating technique for comminuted second metatarsal fracture in the diabetic obese patient: A case report

by Sham Persaud DPM, MS1*, Anthony Chesser DPM1, Karl Saltrick DPM1

The Foot and Ankle Online Journal 10 (4): 4

Metatarsal fractures represent a common fracture type accounting for 35% of all fractures within the foot and 5% of total skeletal fractures annually. Central metatarsal fractures are caused by excess torsional force applied to the bone or direct trauma, with most fractures being attributed to the latter. As with most fractures, minimally displaced fractures of the central metatarsals are amenable to conservative treatment including protected immobilization and RICE therapy. In general, physicians may be accepting of subtle displacement of central metatarsal fractures accepting up to 10 degrees of displacement and 3mm of translation in any direction. When displacement is too great, metatarsal fractures are treated with closed reduction with percutaneous pin fixation or ORIF with pin or single plate fixation. This case report presents a case of a gentleman who suffered from a comminuted metatarsal with a unique fracture pattern that required dual plating technique for proper reduction of the fracture. With this unique fracture type, dual plate technique optimized fixation in order to stabilize an unstable fracture of a second metatarsal in an obese patient with diabetes.

Keywords: metatarsal fracture, stress fracture, diabetes, obesity, metatarsal plate

ISSN 1941-6806
doi: 10.3827/faoj.2017.1004.0004

1 – West Penn Hospital Foot and Ankle Institute, 4800 Friendship Ave, Pittsburgh, PA 15224
* – Corresponding author: shamjoseph.persaud@ahn.org

Metatarsal fractures represent a common fracture type accounting for 35% of all fractures within the foot and 5% of total skeletal fractures annually [1]. These fractures can be isolated injuries, simultaneous fractures with other metatarsals and foot fractures with ligamentous Lisfranc injuries. They can also be either traumatic or caused by prolonged stress across the bone. Most metatarsal fractures are generally a result of low energy trauma, however high energy crush injuries may occur [2].

Metatarsal fractures occur in multiple locations and are generally divided by location into proximal metaphyseal, diaphyseal/shaft, and head/neck fractures. Proximal fractures are generally associated with Lisfranc injuries. Proximal metatarsal fractures generally remain stable and well aligned secondary to the multiple ligamentous and tendinous structures which stabilize the metatarsals [2-4]. Diaphyseal fractures are generally oblique in nature, but can present in many fracture patterns. These fractures are less stable and should be evaluated for shortening and displacement [5]. The diaphyseal region is the most common site for stress fractures of metatarsals, especially the central metatarsals. Stress fractures, if untreated, can progress to complete transverse or oblique fractures. If displacement is present with diaphyseal fractures, it typically occurs plantarly and laterally [1].

Central metatarsal fractures occur considerably more than first metatarsal fractures. These fractures can affect more than one metatarsal as metatarsal 2-4 generally act as a unit. The literature states that 63% of third metatarsal fractures occur with either a second or fourth metatarsal fracture or 28% with both. Therefore, extensive evaluation of radiographs and possibly the use of other imaging modalities should be used if an isolated metatarsal fracture is identified in metatarsals 2-4 [2].

Central metatarsal fractures are caused by excess torsional force applied to the bone or direct trauma, with most fractures being attributed to the latter [1,2]. Direct trauma includes crush injuries or penetrating injuries to the foot. Spiral or oblique fractures are produced by a twisting injury over a fixed forefoot. Secondary to central metatarsal lack of motion, soft tissue attachments, and stable articulations, these fractures are intrinsically stable. However, when displacement occurs, the central metatarsals are more likely to displace as a unit [1,2].

As with most fractures, minimally displaced fractures of the central metatarsals are amenable to conservative treatment including protected immobilization and RICE therapy. In general, physicians may be accepting of subtle displacement of central metatarsal fractures accepting up to 10 degrees of displacement and 3mm of translation in any direction [6-9]. Plantar displacement is often tolerated the least out of all planes of deformity secondary to excessive plantar pressures. Dorsally displaced fractures can cause excessive strain on adjacent metatarsals leading to transfer plantar lesions and possible adjacent stress fractures. Frontal and transverse plane deformity, generally are well tolerated. However, it has been shown that displacement in the frontal or transverse plane may cause nerve irritation in the metatarsal interspaces, as well as, digital deformity over time [6-9].

The goal of central metatarsal fractures is to achieve anatomic alignment of the metatarsal using stable fixation. This goal can be achieved using both open and closed techniques. In patients with significant comorbidities or vascular compromise achieving extra stable reduction utilizing minimally invasive techniques is idea [1].

Percutaneous Kirschner (K-wire) wire pinning can be performed with a variety of techniques for adequate fixation. The most common method includes intramedullary fixation across the fracture site with use of a large diameter k-wire. Crossing multiple k-wires may also be an acceptable technique for fixating metatarsal fractures [10]. Advantages of k-wire fixation include the ability to maintain vascularity to the fractured bone with minimal dissection and soft tissue disruption. The main disadvantage is the inability for direct visualization and manipulation of the fracture [1].

Open reduction internal fixation (ORIF) is also a viable option for treatment of metatarsal fractures, especially if the fracture is significantly displaced or comminution is present. ORIF technique has the advantage of being able to visualize the fracture site in order to achieve complete anatomic reduction with application of more stable fixation [1]. In terms of fixation, screw fixation is possible for oblique type fractures, however, use of screws for central metatarsal fractures may be challenging. If ORIF technique is used, fixation generally consists of either k-wire fixation, or the use of dorsal plate fixation using mini or small fragment plates and screws. Locking plates may also be beneficial in patients with significant comorbidities or poor bone stock [1].  

Complications are relatively uncommon with either technique. Common complications with fixation of central metatarsal fractures include delayed or non-union, malunion, metatarsalgia, or digital deformity. In general delayed union or malunion complications are secondary to poor blood supply due to dissection techniques or comorbidities, or excess stress secondary to chronic stress fracture and foot deformity [1].

Biomechanical studies have shown that biplane fixation has increased stiffness as well as a decrease chance of hardware failure resulting in a more stable construct. Dayton et al in their biomechanical study showed that biplane plating showed to have superior or equivalent stability in multiplanar orientations as compared to a single plate with interfragmentary screw. However, dual plating is not without its drawbacks; Increased soft tissue dissection, periosteal stripping, theoretical increased operating room time, increased chance of hardware irritation, and increased cost are several disadvantages to dual plating [11].

There have been numerous studies that reference orthogonal/dual plating throughout the body for fracture reduction and stabilization [11-23]. However; there have been no studies for dual plating lesser metatarsals for acute fractures. The purpose of this case study was to provide a scenario where the application of dual plating technique to an unstable lesser metatarsal fracture was warranted.

Case Report

A 52-year-old male presented with acute tenderness to the 2nd metatarsal of the right foot. The pain began approximately one week prior to presenting to us. He denied any injury to his recollection. He initially thought it was a gout flare up secondary to his history of gout flare ups and was prescribed a Medrol dose pack by his PCP which provided no relief. Therefore, the patient went to the emergency room in which radiographs were taken which demonstrated the patient had a displaced mid-diaphyseal fracture to the second metatarsal of the right foot (Figure 1). The patient also stated that within the last week he had also noticed lateral deviation of his second digit which was progressive. This was confirmed via physical exam as a flexible deformity secondary to displacement of the metatarsal fracture site. Physical exam revealed acute swelling and warmth about the midfoot and forefoot of the right foot focused about the second metatarsal. No ecchymosis was present. There was also point tenderness to the second metatarsal with reducible lateral deviation of the second digit at the level of the second metatarsophalangeal joint (MTPJ). With the radiographic displacement present and the patient’s medical history including diabetes, obesity, gout and other associated medical ailments it was decided the best course of action for the patient was to schedule the patient for ORIF of the second metatarsal with capsulotomy and extensor tendon lengthening to the second digit all right foot. Until the surgery the patient was placed in a Jones compression dressing and placed in a CAM walking boot.

Figure 1 Pre-operative radiographs AP, oblique, lateral.

One week after initial presentation, the patient underwent ORIF of the second metatarsal with capsulotomy and extensor tendon lengthening of the second MTPJ of the right foot. Incision placement was made on the dorsal aspect of the second metatarsal beginning at level of the proximal third of the metatarsal extending distally past the second MTPJ. Dissection was carried down to the level of the extensor tendons in which a Z-tenotomy of the extensor digitorum longus tendon, as well as, a complete tenotomy of the extensor digitorum brevis tendon was performed.

At this time, attention was focused to the fracture site. Using standard techniques all bone callus was debrided and the fracture was reduced by joystick technique utilizing a 0.062 K-wire in the capital fragment in order reduce the fracture and pull the metatarsal out to length. Once adequate reduction was achieved, the fracture sites were fixated provisionally with 0.045 K-wires. With further evaluation and thought, it was determined that two plate fixation would be optimal fixation with the current fracture pattern. This was achieved utilizing two 6-hole mini-fragment locking plates oriented obliquely into the bone and staggered for proper locking screw placement (Figure 2). With the two plate construct, both medial and lateral dorsal fragments were fixated to the constant plantar fragment achieving stable fixation.

Figure 2 Intraoperative radiographs AP, oblique, lateral.

After fixating the fracture site, soft tissue balancing for the lateral deviation of the second digit was performed. With reduction of the fracture, the digit deviation had decreased dramatically. The remaining deformity was addressed by performing a lateral capsulotomy at the level of the MTPJ and repairing the extensor longus tendon in an elongated state providing no tension to the digit at the level of the second MTPJ.

Post-operatively the patient remained non-weight bearing in a CAM walking boot for 4 weeks. After 4 weeks, the patient began to progressively bear weight on his right foot in a CAM boot only. After 2 weeks of weight bearing in a CAM boot the patient was transitioned into a tennis shoe comfortably. At that time, serial radiographs were obtained showing adequate consolidation of the fracture site with maintained reduction and position (Figure 3). The patient was able to return to work in full capacity at 8 weeks with no restrictions.  

Figure 3 Post-op clinical pictures and radiographs AP, oblique and lateral.

Discussion

Comminuted fractures of any long bone can be challenging to treat surgically. Though there are many techniques which have been shown to be viable options for such fracture types, dual plating has been shown to provide adequate stability and maintain correction of complex fractures of long bones.

As stated, Dayton et al were able to show that a dual locking plate technique with single cortex locking screws, when compared to single locking plate with interfragmentary screw fixation, showed superior or equivalent stability in multiplanar orientations of force application in both static and fatigue testing. Though this study was used primarily to show stability at fusion sites such as the first tarsometatarsal joint, the results are very applicable to complex fractures of long bones [11].

Dual plating has also been documented as a viable option for fracture fixation within the literature. There have been many studies within orthopedic literature showing the successful use of dual plating technique for fracture ORIF of fractures not within the foot and ankle [18-23]. However, there is also extensive literature is the use of dual plating for complex ankle fractures [12-17].

Kwaadu et al. evaluated the use of dual plate technique for the repair of complex fibular fractures on 25 patients. All 25 patients underwent benign postoperative courses with eight patients having complications all of which were wound complications. No additional operations were performed as a result of this technique. No patient undergoing this technique complained of any hardware irritation, and no hardware removal was required. The average time to radiological healing confirmed via radiograph was 7.5 weeks [12]. Vance et al. reviewed 12 consecutive patients who underwent ORIF of fibular fractures utilizing two 1/3 tubular plates for fixation. All fractures healed both clinically and radiographically. Only one patient required hardware removal. FAOS scores were obtained at a mean of 25.6 months after surgery and showed results of pain (87.6, SD = 9.5), activities of daily living (90.4, SD = 14.5), symptoms (93.3, SD = 9.5), sports (89.5, SD = 18.1), and quality of life (57.4, SD = 21.3) [13].

Our case report demonstrated successful use of dual plating technique for ORIF of a comminuted metatarsal fracture. It is our belief that this technique provides added support which was needed secondary to the fracture pattern presented. Dual plating is warranted in cases when traditional fixation techniques (i.e. K-wire fixation, screw, single plate) will not allow for appropriate reduction or stabilization of the fracture segment. This fixation technique can be another tool in the surgeon’s armamentarium.  While this case study was not the first to incorporate dual plating in fracture cases, it is the first to document dual plate technique for lesser metatarsal fractures.

References

  1. Buddecke D, Polk M, Barp E. Metatarsal fractures. Clin Podiatr Med Surg. 2010 Oct;27(4):601-24.
  2. Petrisor B, Ekrol I, Court-Brown C. The epidemiology of metatarsal fractures. Foot Ankle Int 2006;27:172–5.
  3. Maskill J, Bohay D, Anderson J. First ray injuries. Foot Ankle Clin N Am 2006;11: 143–63.
  4. Pearson J. Fractures of the base of the metatarsals. BMJ 1962;1:1052–4.
  5. Maxwell J. Open or closed treatment of metatarsal fractures: indications and techniques. J Am Podiatry Assoc 1983;73:100–6.
  6. Hansen ST. Foot injuries. In: Browner BD, Jupiter JB, Levine AM, et al, editors. Skeletal trauma. Philadelphia: WB Saunders Company; 1998. p. 2405–38.
  7. Early J. Metatarsal fractures. In: Bucholz R, Heckman J, Rockwood C, et al, editors. Rockwood and green’s fractures in adults. Lippincott, Williams, & Wilkins; 2001. p. 2215.
  8. Shereff M. Complex fractures of the metatarsals. Orthopedics 1990;13(8):875–82.
  9. Armagan O, Shereff M. Injuries to the toes and metatarsals. Orthop Clin North Am 2001;32(1):1–10.
  10. Donahue M, Manoli A. Technical tip: transverse percutaneous pinning of metatarsal neck fractures. Foot Ankle Int 2004;25(6):438–9.
  11. Dayton P, Ferguson J, Hatch D, Santrock R, Scanlan S, Smith B. Comparison of the mechanical characteristics of a universal small biplane plating technique without compression screw and single anatomic plate with compression screw. J Foot Ankle Surg. 2016 May-Jun;55(3):567-71.
  12. Kwaadu KY, Fleming JJ, Lin D. Management of complex fibular fractures: double plating of fibular fractures. J Foot Ankle Surg. 2015 May-Jun;54(3):288-94.
  13. Vance DD, Vosseller JT. Double Plating of Distal Fibula Fractures. Foot Ankle Spec. 2017 Feb 1:1938640017692416.
  14. Singh SK, Wilson MG. A Double Plate Technique for the Management of Difficult Fibula Fractures. Techniques in Foot & Ankle Surgery. 2005:4(4); 235-239.
  15. Savage TJ, Stone PA, McGarry JJ. Internal fixation of distal fibula fractures: a case presentation demonstrating a unique technique for a severely comminuted fibula. J Foot Ankle Surg. 1995 Nov-Dec;34(6):587-92; discussion 596.
  16. Lowe JA, Tejwani N, Yoo BJ, Wolinsky PR. Surgical techniques for complex proximal tibial fractures. J Bone Joint Surg Am. 2011 Aug 17;93(16):1548-59.
  17. Wykes PR, Eccles K, Thennavan B, Barrie JL. Improvement in the treatment of stable ankle fractures: an audit based approach. Injury. 2004 Aug;35(8):799-804.
  18. Helfet DL1, Hotchkiss RN. Internal fixation of the distal humerus: a biomechanical comparison of methods. J Orthop Trauma. 1990;4(3):260-4.
  19. Shin SJ, Sohn HS, Do NH. A clinical comparison of two different double plating methods for intraarticular distal humerus fractures. J Shoulder Elbow Surg. 2010 Jan;19(1):2-9.
  20. Nauth A, McKee MD, Ristevski B, Hall J, Schemitsch EH. Distal humeral fractures in adults. J Bone Joint Surg Am. 2011 Apr 6;93(7):686-700.
  21. Kaipel M, Majewski M, Regazzoni P. Double-plate fixation in lateral clavicle fractures-a new strategy. J Trauma. 2010 Oct;69(4):896-900.
  22. Prasarn ML, Meyers KN, Wilkin G, Wellman DS, Chan DB, Ahn J, Lorich DG, Helfet DL. Dual mini-fragment plating for midshaft clavicle fractures: a clinical and biomechanical investigation. Arch Orthop Trauma Surg. 2015 Dec;135(12):1655-62.
  23. Hirvensalo E, Lindahl J, Kiljunen V. Modified and new approaches for pelvic and acetabular surgery. Injury. 2007 Apr;38(4):431-41.

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Neuropathic Ankle Arthrodesis with Intramedullary Nail Fixation

Posted on July 1, 2012 | Comments Off on Neuropathic Ankle Arthrodesis with Intramedullary Nail Fixation

by Brent Bernstein, DPM FACFAS1, Zachary Ritter, DPM2, Robert Diamond, DPM FACFAS3

The Foot and Ankle Online Journal 5 (7): 1

Tibiotalocalcaneal/Tibiocalcaneal arthrodesis with intramedullary nail fixation is a useful and stable means through which to address complex rearfoot deformities. In this manuscript, we have critically analyzed the modalities and surgical outcomes within existing literature comparing each to our institutional results and have found a critical void in information. In tracking and addressing variables such as smoking cessation, glucose control, weight management, vascular stability, extremity ulcerations and postoperative pedorthics we have observed improved operative outcomes and fusion rates. In reviewing the literature, we have found bone union rates of 79.6%, non-union rates of 7.6%, fracture rates of 1.4% and amputation rates of 4.7%. Those results were then compared to our rates of 88.88%, 11.12%, 0% and 0% respectively. Yet, while our institution noted improved results, a meaningful meta-analysis was difficult to achieve considering that most literature failed to make note of the aforementioned variables. Accordingly, we offer that a strict preoperative regimen of glycemic control, vascular patency, weight management and smoking cessation, in conjunction with strict postoperative non-weight bearing and aggressive wound management will improve overall results. Furthermore, it is our suggestion that future research address these topics.

Key Words: Neuropathic Ankle Arthrodesis, Intramedullary Nail Fixation, Charcot, Ankle Fusion, Diabetes

Accepted: June, 2012

Published: July, 2012

ISSN 1941-6806
doi: 10.3827/faoj.2012.0507.0001

Charcot neuropathic osteoarthropathy is a destructive disease of neurologic origin that contributes to both bone and joint abnormalities.

While its pathogenesis is not completely understood, the Charcot process is thought to be a product of neurovascular and neurotraumatic etiologies with effects reaching far beyond the diabetic community.

In examining the Charcot limb it is important to understand that this deformity will typically present in three anatomic planes–the sagittal, transverse and frontal. The effects of that triplanar deformity are most notable in the Charcot ankle, with severe valgus or varus fixed deformities or occasionally “flail” ankles with the foot being stabilized on the lower extremity by soft tissue alone [1,2].

Figure 1 3-D computed tomography reconstruction of patient 1.

Often, patients also experience postural changes and a grossly unstable bony architecture presenting the need for aggressive surgical correction [3-6].  With that, one mainstay of therapy remains rearfoot fusion with intramedullary nail fixation [2,7]. It is expected that anywhere from 0.1 to 5% of all diabetic patients will develop neuropathic osteoarthropathy during the course of their disease; these odds are increased substantially in patients with end-stage neuropathy [3,4,8-10].  Moreover, diabetic patients with ulcerations are significantly more likely to undergo extremity amputation. With these odds, it is extremely important for the foot and ankle specialist to judiciously approach the Charcot joint.

Our study evaluates the results of bone fusion rates and outcomes with tibiotalocalcaneal/tibiocalcaneal arthrodesis. In order to accomplish this, we have explored our institutions outcomes alongside those of existing literature to demonstrate commonalities and techniques for successful treatment and/or interventional modalities. To this end, it is our hypothesis that meticulous preoperative planning, intraoperative techniques, and post-operative care significantly affect the success of the fusion rates.

Figure 2 Post-operative radiograph of patient 1.

Methods and Materials

An extensive literature review of selected electronic databases including PubMed, the Cochrane Database and OVID was conducted for articles using the key words “Charcot ankle”, “intramedullary nail”, and varied combinations of each. No specific time parameters were set; accordingly, articles were reviewed from inception to present. Studies were excluded if they were not available in English, did not address the use of intramedullary nail fixation for the diabetic Charcot ankle deformity or did not note postoperative weight-bearing, obesity, wound care or union type.  With that, only thirteen articles were found to meet our inclusion criteria. (It should be noted that our original inclusion criteria included monitoring of blood glucose levels, nutritional status, vascular stability and nicotine use, however literature that followed these variables was extremely limited).

Secondarily, a review of our senior authors (B.B.) patient database was conducted.  Nine consecutive patients who had undergone tibiotalocalcaneal/tibiocalcaneal arthrodesis using an intramedullary nail between January of 2005 and 2009 were selected for review. Perioperative data was obtained from our institutions electronic medical record system and wound care facility records.

Figure 3 Pre-reduction radiograph of patient 2.

Of the nine patients followed within our institution, eight were diagnosed with a Sanders IV Charcot deformity, seven had a medical history significant for diabetes mellitus, and seven weighed over 102kg. The average patient age was fifty-five years with eight males and one female.  All diabetics demonstrated a hemoglobin A1c of less than 7.5%. Stable lower extremity arterial studies as per our institutions vascular surgeons were noted along with dopplerable pedal pulses.

All patients had also transitioned from the active phase of neuroarthropathy to the chronic phase as demonstrated by cutaneous infrared thermistor readings being equalized to within 2 degree Celsius of the contralateral unaffected limb [11,12].

Figure 4 Post-operative radiograph of patient 2.

Patients who demonstrated active “hot” joints were managed pre-operatively with protected weightbearing in total contact casts with adjunctive therapy of oral or parenteral bisphosphonates or miacalcin nasal spray and/or non-invasive bone stimulation therapy until temperature readings equalized and edema had resolved.

Patients from our senior author’s practice were refused surgical intervention if at the time of surgery they 1- had an open wound, 2-had not accomplished pre-operative glycemic control, 3- had not undergone tobacco cessation, 4-had not attempted weight management or 5- did not have adequate vascular runoff/perfusion as determined by our facilities vascular testing (ABI/PVR) (Table 1).

Table 1 Preoperative requirements

Post-operatively, our patients were kept strict non-weight bearing until clinical stability was noted. At that time they were transitioned into a total contact cast and finally, as consolidation completed, to accommodative shoe gear or custom-fabricated ankle-foot orthosis. All patients were followed postoperatively at our facility’s wound care center for weekly appointments until that time when independence and function had been restored. Additionally, all post operative wounds were treated at that same facility by certified wound care specialists until the time of their resolution.

Surgical Technique

A hockey stick type incision was made over the fibula and curved distally to the level of the sinus tarsi at the base of the fourth metatarsal. The fibula was then exposed and the distal aspect of the fibula was resected. Typically, the fibula was morselized to be incorporated as bone graft material to fill osseous deficits. An accessory medial ankle incision allowed adequate debridement of devitalized talus and preparation of the joint surfaces. Standard technique included a talectomy and insertion of a wedged portion of bone (autograft from the talectomy or fresh frozen femur) to allow the tibia to seat at 90 degrees to the weightbearing surface in contact with the posterior facet of the calcaneus.  All opposing surfaces of tibia, calcaneus and navicular were denuded of cartilage and multiple subchondral drill holes were created through their articulating surfaces. Additionally, the anterior tibia and bone graft wedge were similarly fenestrated to facilitate bony fusion.

All deficits were back-filled with the morselized fibula graft. Frequently, the Achilles tendon was released at this time. The foot was then assessed for proper positioning and placement of the IM nail. At that time, the guidewire for the nail was placed within the anterior aspect of the plantar heel through the talus–centered into the medullary canal of the tibia. That was then confirmed by intraoperative C-arm guidance in AP, and lateral positions. The bone was drilled, reamed, and placement of the nail was performed utilizing the systems jig. Depending on the system utilized, compression was achieved across the arthrodesis site either externally with tightening of the jig/”top hat” against the external heel pad or plantar calcaneus, via manual compression of the heel, internally through the compression bolts, or externally via external fixation bolts incorporated on the jig. Following insertion of compression screws to fix the nail to the osseous structures, the jig was removed and the IM nail was visualized by C-arm for positioning. Subcutaneous structures were closed with 3.0 vicryl and the skin with staples (Table 2). The incisions were covered with Xeroform™ and a Robert Jones compression dressing. Postoperatively the patient was placed on bedrest with ice, elevation and subcutaneous low molecular weight heparin (Table 3).

Table 2 Intraoperative Techniques

Table 3 Postoperative Management

Results

Osseous fusion, defined as trabecular bridging at the fusion site with disappearance of appositional gapping, was noted in 88.8% of all patients within our institution. Categorically, fusion was seen in 85.7% of diabetics, 87.5% of Charcot limbs, 85.7% of those weighing over 102kg and 88.8% of those placed in a postoperative TCC.

Figure 5 Pre-reduction clinical image of patient 3.

Comparatively, literature has demonstrated fusion rates of 73%, 70.4%, 92.4% and 46.2% respectively [2-4,7,8,13-20].

Moreover, our institution demonstrated significantly fewer post-operative complications when compared to published literature 11.12% non-unions, no amputations and no osseous fractures. Somewhat skewed, however, is the above average number of post-operative wounds encountered within our institution 44.4% as opposed to 18% in literature. Although that statistic could certainly be secondary to the extent of deformity or aggressive tracking, it is hard to draw any correlations due to the lack of detailed information with those articles reviewed.

Figure 6 Post-reduction clinical image of patient 3.

Discussion

In recent years indications for tibiotalocalcaneal/tibiocalcaneal fusion have expanded, likely because of improved fixation methods [2]. Intramedullary fixation is biomechanically more rigid than crossed lag screws when examining flexion and torsional forces [13]. Accordingly, retrograde intramedullary nailing is a good option for complex tibiotalocalcaneal/tibiocalcaneal fusions, especially in patients with Charcot arthropathy [21-24]. The construct does allow for weightbearing six to eight weeks after surgery while demonstrating fusion rates that approach ninety percent.

As with any surgical patient, a thorough preoperative assessment should be performed. It is essential to consider the entire patient and not simply the deformity. Therefore, a complete physical examination and adequate overall health evaluation is essential to choose an appropriate surgical candidate.

In this small retrospective analysis, we propose that the following reasons could account for our improved fusion rate. First, critical preoperative planning, including thorough evaluation of the osseous deformity with a 3-D 64 slice CT scan and long-leg axial radiographs. Second, all patients were followed-up at our institutions wound management center to facilitate aggressive management of pre-operative and post-operative wound complications. Third, evaluation of the patient’s vascular status with non-invasive arterial testing such as toe pressures, ankle/brachial indices and arterial Doppler examination during preoperative evaluation proved to be invaluable when determining inclusion criteria. Fourth, patients were offered enrollment in weight loss and smoking cessation programs preoperatively, deferring surgery until this occurred. Fifth, physical therapy training preoperatively and strict non-weight-bearing postoperatively was maintained for eight weeks after which total contact casting and finally bracing was applied. Sixth, nutritional factors were medically evaluated and patients were under firm metabolic control.

Overall, in reviewing the data offered in our literature review and that of institutional review, it is difficult to do a successful and meaningful meta-analysis given the overall lack of detailed patient information and differentiation. Most publications made little mention of preoperative variables that our authors found exceedingly important to track ABI/PVR, weight management, extent of diabetic control, preoperative wound/deformity, tobacco use, etc. In that void, as previously noted, the authors of this study were required to exclude a majority of papers found. Within the grouping of useful studies (Table 1), patient results were taken individually for correlation accounting for the varying cohort numbers (n=). Meaning, each variable along the x-axis consists of a compilation of data collected from different publications. Accordingly, it is an imperative that future studies more closely follow and account for those variables.

This study demonstrates that, while great strides are being made in the world of reconstructive surgery for neuropathic osteoarthropathy, there remains a void in critical information. Information that will not only lead to better standards in surgical management, but also to a more detailed understanding of the Charcot limb and improved techniques in limb salvage.

References

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17. Stuart MJ, Morrey BF. Arthrodesis of the diabetic neuropathic ankle joint. Clin Orthop 1990 253: 209-211. [PubMed]
18. Shibata T, Tada K, Kagawa, Chohzo H. The results of ankle arthrodesis of the ankle for leprotic neuroarthropathy. JBJS 1990 72A: 749-756. [PubMed]
19. Stone KH, Helal B. A method of ankle stabilization. Clin Orthop 1991 268:102-106. [PubMed]
20. Pelton K, Hofer JK, Thordarson DB. Tibiotalocalcaneal arthrodesis using a dynamically locked retrograde intramedullary nail. Foot Ankle Int 2006 27: 759-763. [PubMed]
21. Baravarian B, VanGils CC: Arthrodesis of the Charcot foot and ankle. Clin Pod Med Surg 2004 21: 271-289. [PubMed]
22. Fox IM, Shapero C, Kennedy A. Tibiotalocalcaneal arthrodesis with intramedullary interlocking nail fixation. Clin Pod Med Surg 2000 17:19-31. [PubMed]
23. Millett PJ, O’Malley MJ, Tolo ET. Tibiotalocalcaneal fusion with retrograde intramedullary nailing, clinical and functional outcomes. Am J Orthop 2002 31:531-536. [PubMed]
24. Wagner A, Fuhrmann R. Charcot foot treated by correction and arthrodesis of the hindfoot. Oper Orthop Traumatol 2005 17: 554-562. [PubMed]

Address correspondence to: Brent Bernstein, DPM, 303 W. Broad St, Bethlehem, PA 18018

1Director of the Charcot Reconstructive Foot Program and Attending Surgeon, Podiatric Surgical Residency, St. Luke’s University Health Network, Bethlehem, PA
2Chief Resident, Podiatric Surgical Residency, St. Luke’s University Health Network, Bethlehem, PA
3Chief of Podiatric Surgery and Residency Director, Podiatric Surgical Residency, St. Luke’s University Health Network, Bethlehem, PA

© The Foot and Ankle Online Journal, 2012

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Protected Weight Bearing During Treatment of Acute Charcot Neuroarthropathy: A case series

Posted on July 1, 2011 | Comments Off on Protected Weight Bearing During Treatment of Acute Charcot Neuroarthropathy: A case series

by Jeremy J. Cook, DPM,MPH,CPH1 , Emily A. Cook, DPM,MPH,CPH2 

The Foot and Ankle Online Journal 4 (7): 1

Standard of care in the treatment of acute Eichenholtz stage I Charcot neuroarthropathy includes complete non-weight bearing immobilized with total contact casting. This small case series of three patients focuses on patients with acute phase midfoot Charcot neuroarthropathy treated with non-casting immobilization therapy. All patients were male with a mean age of 48.7 (range 46-53) years. Patients were instructed to assume complete non-weight bearing during treatment. Due to financial restrictions, all patients reported fully weight bearing in the non-removable immobilization boot because of work related obligations. Immobilization therapy lasted a mean duration of 90.3 days (range 76 – 133 days) and was discontinued once there was clinical resolution of inflammation and osseous stability. Serial radiographs revealed absence of deformity progression and eventual consolidation in all cases. All patients remained ulcer and callus free during immobilization therapy, without progression of a rocker-bottom deformity, while fully weight bearing and maintaining full-time manual labor employment. This preliminary case series adds to the evidence base that it may be possible to allow protected weight bearing during acute phase Charcot neuroarthropathy with adequate immobilization of the foot at all times.

Key words: Diabetes, Charcot neuroarthropathy, Foot Deformity, Casting, Foot fractures, Diabetic Foot.

Accepted: June, 2011
Published: July, 2011

ISSN 1941-6806
doi: 10.3827/faoj.2011.0407.0001

Charcot neuroarthropathy is an increasingly common clinical entity encountered by foot and ankle professionals. In the early decades of the last century syphilis was the most commonly associated etiology. That has changed with the advent of insulin and the resulting extended survival of patients suffering from diabetes mellitus.

Delay in diagnosis and patient non-compliance can result in severe destruction of the foot and ankle with permanent disability from ulceration, infection, and eventual amputation. [1-14]

The standard of care for treatment of Eichenholtz stage 115 Charcot neuroarthropathy has been immobilization in a total contact cast and complete non-weight bearing. [16-20] The period of non-weight bearing immobilization should last until erythema, edema, and warmth subside and the foot becomes stable and consolidated enough to prevent anatomic destruction while ambulating. This process has been reported to last anywhere from a few months to over two years. [20-26]

Total contact casts (TCC) have been shown in numerous studies to be an effective immobilization device in the treatment of acute Charcot neuroarthropathy. [5,7-14,16-20]

It is recommended that TCCs be changed frequently in order to prevent cast irritation, ulceration and to maintain immobilization as edema subsides. Minor complications such as skin irritation are anticipated with TCC. The risk of major complications such as ulceration and infection can be minimized with proper application techniques, as well as frequent casts changes, which permit careful monitoring, and adequate patient education. [27] Many centers have specially-trained orthotists who apply TCCs on a routine basis. Most studies support changing TCCs for the treatment of Stage I Charcot neuroarthropathy every 1-2 weeks. [11,13,17,19,22,27-31] Some institutions have allowed weight bearing in the TCC due to its inherent stability with success in preliminary reports. [9,27-31]

Although weight bearing during stage I of Charcot neuroarthropathy is controversial, many patients tend to be non-compliant. This is because this period of prolonged non-weight bearing may be detrimental in quality of life and may pose to be an unacceptable disability. [32,33] While the alternative may be amputation, advances in immobilization technology may allow protected weight bearing during the early stages of Charcot without the development of severe deformity. [34,35] The purpose of this study was to report results of acute Stage 1 Charcot neuroarthropathy in individuals immobilized in a vacuum stabilization boot that maintained full weight bearing.

Case Series

Three consecutive patients presented with acute Stage I Charcot neuroarthropathy over a three month period (November 2009 to January 2010). All three patients had Brodsky type I deformity involving the tarsometatarsal and naviculocuneiform joints. [18] Patients were referred for examination and treated within two weeks of symptom onset. Clinical examination revealed erythema, warmth, and edema involving the midfoot with gross instability, crepitation with midfoot range of motion, and bounding pedal pulses. One patient had diabetic neuropathy while the other two were diagnosed with alcoholic neuropathy. Peripheral neuropathy was confirmed by the absence to detect the Semmes-Weinstein 10gm monofilament.

Two of the three patients reported a minor injury preceding the Charcot event. The third patient had had previous amputations of digits two and three for localized osteomyelitis secondary to contiguous digital ulcerations. All three patients were male with a mean age of 48.7 (range 46-53) years. All patients presented within two weeks of first symptoms and were ulcer free at the time of initial presentation with this being their first occurrence of Charcot neuroarthropathy. Radiographs were obtained with findings consistent with early signs of Charcot neuroarthropathy. (Fig. 1A and 1B) Magnetic resonance (MR) imaging further confirmed the diagnosis with diffuse bone marrow edema adjacent to the Lisfranc joint.

 

Figure 1A and 1B  Initial anterior posterior (AP) (A) and lateral (B) radiographs demonstrating soft tissue edema with early signs of osteolysis, cortical thickening, fragmentation, and osseous destruction within the tarsometatarsal and naviculocuneiform joints.

All three patients were treated with immobilization in a vacuum stabilization boot (VACOcast®, OPED Inc, Framingham, MA) with instructions to remain strictly non-weight bearing. (Fig. 2) Despite these recommendations, all three patients reported bearing weight on the affected limb in order to prevent loss of their job. All three patients were sole providers in their household with jobs that required extensive manual labor. The patients were compliant in wearing the boot at all times as this was verified through inspecting the undamaged compliance locks on the boot.

Figure 2   In this boot, by removing air from a vacuum cushion, small beads contour around the lower limb and create vacuum stabilization.

Serial monitoring was conducted by clinical examinations and plain radiographs. Patients were kept immobilized in the vacuum stabilization boot until resolution of edema, warmth (examined by palpation with back of hand and fingers and comparing to contra-lateral limb), and clinical stability was achieved. Successive radiographs were taken to ensure the absence of deformity progression every 3-4 weeks. (Fig. 3A, 3B and 3C) Throughout the treatment period each patient maintained normal full weight bearing in the conduct of their full-time jobs.

  

Figure 3A, 3B and 3C  Progression of acute phase of Charcot neuroarthropathy.  AP (A), Oblique (B) and lateral (C) views demonstrate increased osseous destruction and osteolysis.

Patients wore the vacuum stabilization boot for a mean of 90.3 days (range 76 – 133 days). One patient developed a superficial abrasion on the dorsal proximal interphalangeal joint of the second digit. This healed after two weeks of wound care and the additional of padding to the boot in this area. There were no other complications experienced. During the treatment of acute Stage I Charcot neuroarthropathy, all three patients remained ulcer and callus free while ambulating in the immobilization boot. Once the Charcot events had progressed to the consolidation phase, patients were transitioned to accommodative shoes or boots with supportive inserts.

Two of the three patients were compliant with accommodative shoes and molded insoles. After 16 months from the initial presentation, both patients have not developed ulcers, callus, or progression of deformity. (Fig. 4A, 4B and 4C) During the 12 weeks that the third patient was wearing the immobilization boot, the deformity did not progress and the patient remained ulcer and callus free.

  

Figure 4A, 4B and 4C  AP (A), Oblique (B) and lateral (C) views showing progression into chronic Charcot neuroarthropathy with maintenance of anatomic alignment with consolidation of osseous destruction.

However, the third patient did not obtain prescribed accommodative shoes or inserts citing financial limitations. He was subsequently lost to follow-up for five months after completing 12 weeks of immobilization therapy. His Charcot neuroarthropathy had developed a rocker bottom foot deformity and plantar midfoot ulcer after five months of interrupting care.

Discussion

Management of Charcot neuroarthropathy is a complex process which requires flexibility and constant attention. This small case series demonstrates that despite the overt disregard for non-weight bearing management instructions, all patients were able to maintain employment and prevent progression of rocker bottom midfoot deformities during acute Eichenholtz stage I Charcot neuroarthropathy as there was continuous utilization of the vacuum immobilization boot.

Patients were continuously immobilized in a vacuum stabilizing below-knee boot with compliance confirmed by boot locks. There were minimal complications during the acute phase treatment with one patient developing a superficial digital abrasion from the boot. This was identified immediately and rectified by adjusting the boot. Despite fully weight-bearing, a rocker bottom deformity was prevented with adequate and constant immobilization.

Standard of care for acute Eichenholtz stage I traditionally includes total contact casting and complete non-weight bearing to prevent progression of deformity. This has been recently challenged by allowing weight bearing in the total contact cast in combination with frequent cast changes and close monitoring. Two prospective case series have reported successfully preventing deterioration of osseous alignment from acute phase Charcot deformity with weight-bearing total contact casts. [28,29]

The amount of non-restrained cumulative load forces across acute Charcot joints is also believed to increase the amount of deformity progression. By immobilizing the foot with a walking total-contact cast, the acute phase resolved and further progression towards a rocker bottom foot was prevented. [30]

The immobilization boot reported in this study was chosen for several reasons. Total contact casts require frequent changes and proper construction to prevent complications related to this casting technique. This immobilization boot had the advantage of clinical efficiency as no time was necessary beyond properly sizing and fitting the patient and providing instructions on its use. The vacuum boot can be adjusted to accommodate changes in edema. The removable sole allows patients to sleep with the boot without dirtying the linens. It also has a radiolucent frame that permits radiographic evaluation without removal. Finally, the compliance locking straps prevent unknown patient removal. Although none of the affected limbs had an open ulcer necessitating daily care, had local wound care been necessary by a visiting nurse an additional key would have been provided.

Limitations of this study include its retrospective nature. The initial treatment plan did not permit patients to weight bear during acute phase Charcot neuroarthropathy, however, weight bearing did not adversely impact the treatment outcome. Both mechanical and comparative studies are needed to further investigate the ability of nontraditional immobilization devices to effectively prevent osseous deformity in a disease which can cause permanent disability and eventual amputation. Future prospective studies with a larger sample size are needed to assess the long-term outcomes of this immobilization technique. Comparison studies of different immobilization techniques would also be very useful. Finally, the definition of adequate immobilization needs further investigation in order to achieve a balance of prevention of serious Charcot-related complications and quality of life.

Conclusion

Patients with acute Eichenholtz stage I midfoot Charcot neuroarthropathy were able to fully weight bear and maintain manual labor employment without development of a rocker bottom foot deformity while wearing a vacuum stabilization below-knee boot. Advances in immobilization therapy may allow improvement in the quality of life in acute phase Charcot neuroarthropathy.

References

1. Holewski, J, Moss KM, Stess RM, Graf PM, Grunfeld C. Prevalence of foot pathology and lower extremity complications in a diabetic outpatient clinic. J Rehab Res and Devel 1989 26: 35-44.
2. Sohn MW, Stuck RM, Pinzur M, Lee TA, Budiman-Mak E. Lower-extremity amputation risk after charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010 33: 98-100.
3. van der Ven A, Chapman CB, Bowker JH. Charcot neuroarthropathy of the foot and ankle. J Am Acad Orthop Surg 2009 17: 562-571.
4. Sohn MW, Lee TA, Stuck RM, Frykberg RG, Budiman-Mak E. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009 32: 816-821.
5. Boulton AJ, Jeffcoate WJ, Jones TL, Ulbrecht JS. International collaborative research on Charcot’s disease. Lancet 2009 J373 (9658): 105-106.
6. Shibuya N, La Fontaine J, Frania SJ. Alcohol-induced neuroarthropathy in the foot: a case series and review of literature. J Foot Ankle Surg 2008 47: 118-124.
7. Nielson DL, Armstrong DG. The natural history of Charcot’s neuroarthropathy. Clin Podiatr Med Surg 2008 1: 53-62.
8. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg 2008 1:17-28.
9. Pinzur MS. Current concepts review: Charcot arthropathy of the foot and ankle. Foot Ankle Int 2007 8: 952-959.
10. Sanders LJ. What lessons can history teach us about the Charcot foot? Clin Podiatr Med Surg 2008 1: 1-15.
11. Wukich DK, Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009 23: 409-426.
12. Jeffcoate WJ. Charcot neuro-osteoarthropathy. Diabetes Metab Res Rev 2008 24 (Suppl 1): S62-65.
13. Petrova NL, Edmonds ME. Charcot neuro-osteoarthropathy-current standards. Diabetes Metab Res Rev 2008 24 (Suppl 1): S58-61.
14. Chantelau E. The perils of procrastination: effects of early vs. delayed and treatment of incipient Charcot fracture. Diabet Med 2005 22: 1707–1712.
15. Eichenholtz SN. Charcot Joints. Springfield, Illinois: Charles C. Thomas, 1966.
16. Shaw JE, His WL, Ulbrecht JS. The mechanism of plantar unloading in total contact casts: implications for design and clinical use. Foot Ankle Int 1997 18: 809-817.
17. Pinzur MS, Shields N, Trepman E, Dawson P, Evans A. Current practice patterns in the treatment of Charcot foot. Foot Ankle Int 2000 21: 916–920.
18. Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, editors. Surgery of the Foot and Ankle. Vol 2. 7th ed. St. Louis, Mosby. 1999, 895-969.
19. Pinzur MS, Shields N, Trepman E, Dawson P, Evans A. Current practice Patterns in the treatment of Charcot foot. Foot Ankle Int 2000 21: 916-920.
20. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot’s arthropathy in a diabetic foot specialty clinic. Diabetic Med 1997 14: 357-363.
21. Molines L, Darmon P, Raccah D. Charcot’s foot: newest findings on its pathophysiology, diagnosis and treatment. Diabetes Metab 2010 36: 251-255.
22. Pinzur, MS. Surgical vs. accommodative treatment for Charcot arthropathy of the midfoot. Foot Ankle Int 2005 25: 545-549.
23. Myerson MS, Henderson MR, Saxby T, Short KW. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int. 1994 15: 233-241.
24. Alpert SW, Koval KJ, Zuckerman JD. Neuropathic arthropathy: review of current knowledge. J Am Acad Orthop Surg. 1996 4: 100-108.
25. Fabrin J, Larsen K, Holstein PE. Long-term follow-up in diabetic Charcot feet with spontaneous onset. Diabetes Care 2000 23: 796-800.
26. Schon LC, Easley ME, Weinfeld SB. Charcot neuropathy of the foot and ankle. Clin Orthop Relat Res 1998 349: 116-131.
27. Wukich DK, Motko J. Safety of total contact casting in high-risk patients with neuropathic foot ulcers. Foot Ankle Int 2004 25: 556-560.
28. Pinzur MS, Lio T, Posner M. Treatment of Eichenholtz stage I Charcot foot arthropathy with a weightbearing total contact cast. Foot Ankle Int 2006 27: 324-329.
29. de Souza LJ. Charcot arthropathy and immobilization in a weight-bearing total contact cast. JBJS 2008 90A:754-759.
30. Kimmerle R, Chantelau E. Weight-bearing intensity produces charcot deformity in injured neuropathic feet in diabetes. Exp Clin Endocrinol Diabetes 2007 115: 360-364.
31. Chantelau E, Kimmerle R, Poll LW. Nonoperative treatment of neuro-osteoarthropathy of the foot: do we need new criteria? Clin Podiatr Med Surg 2007 24: 483-503.
32. Pakarinen TK, Laine HJ, Mäenpää H, Mattila P, Lahtela J. Long-term outcome and quality of life in patients with Charcot foot. Foot Ankle Surg 2009 15: 187-191.
33. Sochocki MP, Verity S, Atherton PJ, Huntington JL, Sloan JA, Embil JM, Trepman E. Health related quality of life in patients with Charcot arthropathy of the foot and ankle. Foot Ankle Surg 2008 14: 11-15.
34. Verity S, Sochocki M, Embil JM, Trepman E. Treatment of Charcot foot and ankle with a prefabricated removable walker brace and custom insole. Foot Ankle Surg 2008 14: 26-31.
35. Stöckle U, König B, Tempka A, Südkamp NP. Cast immobilization or vacuum stabilizing system? Early functional results after osteosynthesis of ankle fractures. Unfallchirurg 2000 103: 215-219.

Address correspondence to: Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA.
Email: jeremycook@post.harvard.edu

1,2  Clinical Instructors in Surgery at Harvard Medical School, Division of Podiatric Surgery, Department of Surgery.
185 Pilgrim Road, PB Span 3, Beth Israel Deaconess Medical Center, Boston, MA. 617-632-7098

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Open Dislocated Bi-Malleolar Ankle Fracture in a Diabetic Treated with the Illizorov Apparatus: A case report in early ambulation and stabilization

Posted on February 1, 2010 | Comments Off on Open Dislocated Bi-Malleolar Ankle Fracture in a Diabetic Treated with the Illizorov Apparatus: A case report in early ambulation and stabilization

by Sutpal Singh, DPM. FACFAS1 , Chih-Hui (Jimmy) Tsai, DPM2, Albert Kim, DPM3,
Timothy Dailey, DPM4

The Foot and Ankle Online Journal 3 (2): 2

The authors describe a case report of a diabetic patient with an open bi-malleolar ankle fracture sustained after a motor vehicle accident that was treated immediately after injury. Treatment included extensive pulse lavage with antibiotic impregnated saline solution and reduction of the fractures using external fixation. Recovery lasted several months, followed by usage of a Pneumatic CAM walker. The external fixator allowed the patient to ambulate throughout the healing process. No internal fixation was utilized. After months of follow-up, there was good healing of the fractures with no infection of the tibia, fibula, and talus. The authors recommend reduction of tibial and/or fibular fracture(s) using the Ilizarov methodology especially in diabetic patients with open fractures and/or contaminated wound.

Key words: Open Ankle Fracture, Gustilo System, Bi-Malleolar ankle fracture, Ilizarov method.

Accepted: January, 2010
Published: February, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0302.0002

Historically, an open ankle fracture commonly equated with much morbidity and mortality. However with more modern therapy, the expected outcome has improved significantly. [1] The purpose of this article will be to describe a report of a diabetic patient with an open dislocated ankle fracture and the significance of treatment with the use of an Illizarov apparatus. In this article, discussion will focus on the classification, complications, and treatment protocols of open fractures to the ankle joint.

The Illizarov apparatus in our case allowed the patient ambulate during the recovery period in attempt to decrease other risks such as infection and osteomyelitis by use of open internal fixation and morbidity associated with prolonged immobility of a limb.

A fracture is considered to be open when there is a disruption of the skin and underlying soft tissues resulting in a communication between the fracture and the outside environment. Open fractures are most commonly classified according to the system developed by Gustilo and Anderson. [1,2]

The classification of open fractures is based on the size of the wound, the amount of soft tissue injury, fracture pattern and correlates with both infection and amputation rates. Type I open fractures are characterized by a clean wound smaller than 1 cm in diameter, appears clean with a simple fracture pattern and no skin crushing. The fracture can be short, oblique, or transverse. Type II presents with a laceration larger than 1 cm without significant soft tissue crushing or skin flaps, with minimal periosteal stripping; however, a more complex fracture pattern may result. Type III features a large crush component with comminution. It is larger than 5 cm, highly contaminated with extensive soft tissue injury. These injuries may also be older than six hours. Type III injuries are subdivided into three types: type IIIA which presents with adequate soft tissue coverage of the fracture despite high energy trauma or extensive laceration or skin flaps; type IIIB featuring inadequate soft tissue coverage with extensive periosteal stripping, and finally type IIIC which displays with any open fracture that is associated with vascular injury that requires repair. [2,3]

Patients with open fractures are at risk of complications of acute wound infection and osteomyelitis. The risk of a clinical infection depends on the severity of the injury and ranges from 0% to 2% for type-I open fractures, 2% to 10% for type-II, and 10% to 50% for type-III. [4] The rate of infection of open fractures is associated with the fracture characteristics, antibiotic therapy variables, and host parameters.

Another variable is the location of the open fracture with tibial open fractures resulting in twice the rates of infection than other areas of the body. [4] Other possible complications include inadequate soft tissue coverage or extensive soft tissue damage resulting in the failure to heal or even close. This may be exasperated by a compromised neurovascular status of the injured extremity or the development of a compartment syndrome. [5] Open fractures may also succumb to osseous mal-union or non-union, the loss of function, and even amputation.

Management of the open fracture is dependent upon the following principles: careful and thorough assessment of the patient; initial stabilization; classification of the injury; tetanus prophylaxis; antibiotic therapy; prompt surgical debridement and wound management; fracture stabilization through internal fixation, external fixation, or casting; early bone grafting; timely wound closure; supplemental procedures to achieve healing; and adequate follow-up. [6] In any given situation, the best option for fixation depends on a number of factors, including the bone involved, the fracture site, the wound location, and the condition of the patient. The available evidence supports the current trend toward earlier coverage and closure of open fracture wounds. [7] The ultimate goal of a surgeon when dealing with open fractures is to prevent infection, promote fracture healing, and restore alignment and function.

Case Report

A 33 year-old female who had a motor vehicle accident presents with an acute, open, dislocated, bi-malleolar fracture of the right ankle. She was immediately transferred to the emergency room. Her past medical history was significant for Type II Diabetes, diagnosed over 10 years ago. She has peripheral neuropathy, with numbness up to the mid-leg. The rest of the history and review of systems was unremarkable. The right ankle fracture presents to our service wrapped in gauze which is soaked in blood. She did not have a splint on, and the foot is severely dislocated. There is tremendous swelling, but no fracture blisters. Despite the extent of this high impact open fracture, a hand-held Doppler showed that she has good vascular status to the dorsalis pedis and posterior tibial arteries. Her capillary refill is immediate. The open ankle fracture is on the lateral side with the wound measuring approximately 9 cm x 5 cm. Even though the fibula, talus and distal tibia were exposed, there is enough skin to close the wound. Uniquely, there is no dirt or any gross contamination noted despite the nature of this accident. X-rays of the ankle indicated that she has a severely dislocated bi-malleolar ankle fracture. (Figs. 1A, B and C).

  

Figure 1A, B and C Variable views of the open ankle fracture.

The medial malleolus is comminuted. Since the open fracture is less than 6 hours old, she is taken to the operating room immediately in order to reduce the fracture using the Ilizarov frame. The patient is then allowed to ambulate directly after surgery when indicated.

Surgical Technique

Under general anesthesia, the open wound is cultured for bacterial organism. Afterwards, nine liters of bacitracin and Ancef impregnated saline is used to irrigate the wound. Two tibial rings are applied to the distal tibia and a foot plate is then applied. Both are tensioned appropriately. The foot plate is then manipulated so the fibular fracture and medial malleolar fracture are reduced in anatomical alignment. The foot plate and the tibial rings are then joined together with appropriate rods. Distraction of the foot plate is performed in order to pull the fibula and medial malleolus fractures into better alignment. The fibula is then stabilized using two K-wires while the comminuted medial malleolus is reduced using an olive wire at the largest fragment. The olive wire is inserted from distal-inferior-posterior-medial to proximal-superior-anterior-lateral, attached to the proximal tibial ring and tensioned for compression (Figs. 2A and B). The open wound is then very loosely approximated and packed with iodoform. Several days later, the culture results revealed no bacterial growth. The wound is again irrigated with normal saline and Bacitracin® and then completely closed using 3-0 prolene (Figs. 3A,3B,4,5A and 5B).

 

Figure 2  External fixation at the ankle.  Note the olive wire reducing the comminuted medial malleolar fracture. (A)  Lateral view of the ankle with an External Fixator in place. (B)

 

Figure 3  Ilizaorov Frame medial view (A) and lateral view. (B)

Figure 4  Loose approximation of the open fracture.  The iodoform packing has been removed from the open wound.

 

Figure 5  Medial View of the Ilizarov frame several months later. (A)  The Ilizarov frame several months later. (B)

Discussion

The complexity of open ankle fractures pose a challenge to many foot and ankle surgeons. By definition, an open fracture is considered contaminated or infected after six hours of no treatment. Very often in a high speed motor vehicular accident, there can be fracture of the tibia, fibula, and/or other part of the foot are present along with an open wound. In this report, we have a patient with a large open wound, bi-malleolar ankle fracture, and exposed tibial, fibular, and talus. The case is further complicated by the patient’s diabetes mellitus. However because surgery is performed immediately and the wound is clean with no gross contamination during examination, we were able to utilize the Illizarov apparatus immediately after the accident to fixate and stabilize the open ankle fracture.

An external fixator is recommended when a patient has poor bone stock, poor healing potential, open fractures, or fractures with contaminated wounds. [8] With a high level of morbidity and risk of osteomyelitis, application of internal fixation by itself followed by primary closure of the wound is not indicated. In addition, a larger wound would require a split-thickness skin graft or benefit from healing by secondary intention. Using an external fixator is not only minimally invasive, but it also allows the surgeon to stage the treatment appropriately. The patient can also benefit from being able to bear weight. Any wounds after surgery can easily be viewed and treated with an external fixator. This is of course, contraindicated when using a cast.

The complications associated with the use of an external fixator include pin tract infection and wire failure. These can be mitigated and appropriately treated with antibiotics and pin care to help prevent infection at these sites. The above patient is classified as having a Gustillo type IIIA. She has a large open wound with adequate soft tissue for coverage. She also has a severe ankle dislocation, bi-malleolar ankle fracture, and exposed tibia, fibula and talus. The external fixator was removed after 3 months. She then had a pneumatic cam walker applied. A two year follow-up showed that her ankle healed in an anatomical position with good range of motion (Figs. 6A and B).

 

Figure 6  Anteroposterior (A) and lateral view (B) two years after injury.

Conclusion

This case report shows the advantages to using external fixation for an open ankle fracture secondary to a motor vehicle accident. Use of external fixation has many advantages, as explained previously. The goals of open fracture surgery are to prevent infection, promote fracture healing, and restore function. A detailed history and physical is essential in these type of complicated cases. The surgeon must decide which surgical option is going to meet specific goals.

References

1.Patrick JH, Smelt GJ: Surgical progress-100 years ago. An assessment of Listerism at St. Thomas’s Hospital, London. Ann R Coll Surg Engl 59: 456 – 462, 1977.
2. Gustilo RB, Anderson JT: Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg 58A: 453 – 458, 1976.
3. Gustilo RB, Mendoza RM, Williams DN: Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 24: 742 -746, 1984.
4. Patzakis MJ, Wilkins J: Factors influencing infection rate in open fracture wounds. Clin Orthop Relat Res 243: 36 – 40, 1989.
5. Blick SS, Brumback RJ, Poka A, Burgess AR, Ebraheim NA: Compartment syndrome in open tibial fractures. J Bone Joint Surg 68A: 1348 – 1353, 1986.
6. Zalavras CG, Marcus RE, Levin S, Patzakis MJ: Management of Open fractures and subsequent complications. J Bone Joint Surg Am 89A: 883 – 895, 2007.
7. Okike K, Bhattacharyya T: Current concepts review: Trends in the management of open fractures. J Bone Joint Surg 88A: 2739 – 2747, 2006.
8. Molloy A, Roche A, Narayan B: Treatment of nonunion and malunion of trauma of the foot and ankle using external fixation. Foot and Ankle Clinics Sept: 563 – 587, 2009.

Address correspondence to: Sutpal Singh, DPM. FACFAS. Private practice in Southern California. Email: spsingh@aol.com

1  Chief Ilizarov Surgical Instructor at Doctors Hospital West Covina. Fellow of the American College of Foot and Ankle Surgeons, Private practice in Southern California.
2  Chih-Hui (Jimmy) Tsai, DPM, Doctor of Podiatric Medicine (R3). Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina , (PM&S-36).
3  Albert Kim, DPM, Doctor of Podiatric Medicine (R2), Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina (PM&S-36).
4  Timothy Dailey, DPM, Doctor of Podiatric Medicine (R1), Foot and Ankle Medicine and Surgery, Doctors Hospital of West Covina (PM&S-36).

© The Foot and Ankle Online Journal, 2010

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Collagen in Wound Healing: Are We Onto Something New or Just Repeating the Past?

Posted on September 1, 2009 | Comments Off on Collagen in Wound Healing: Are We Onto Something New or Just Repeating the Past?

by Ryan H. Fitzgerald, DPM1 , John S. Steinberg, DPM2

The Foot and Ankle Online Journal 2 (9): 3

Lower extremity amputations in patients living with diabetes have significant morbidity and mortality. Given the obvious link between lower extremity amputations and the ulcerations that precede them, it is incumbent upon the wound care provider to become familiar with advanced wound care products. The importance of re-establishing a functional extracellular matrix (ECM) in chronic wounds has led to a renewed interest in collagen-based wound healing products. These products can be applied either in the surgical or clinical setting. An intact functional ECM will seek to promote normal progression through the stages of wound healing. This article presents several representative collagen-based advanced wound care products utilized in wound healing, discusses their mechanism of action, and the appropriate indication for each product’s usage.

Key Words: Collagen, wound, diabetes, matrix metalloproteases, bioengineering, alternative tissue.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: July, 2009
Published: September, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0209.0003

Chronic lower extremity wounds demonstrate a considerable health care dilemma and substantial health care cost in the United States. [1,2] Chronic wounds and diabetic ulcerations represent a large component of this cost, with nearly one million new lesions diagnosed each year. [3,4,5] Furthermore, greater than 60% of non-traumatic amputations in the western world are performed on persons with diabetes [6] and the majority of these amputations are preceded by some form of infected ulceration. Therefore we can surmise that aggressive efforts at ulcer healing will have a direct influence on amputation rates. The risk is obvious; the relationship between diabetic foot ulcerations and subsequent amputation has been well documented and is well understood. [7]

There is significant morbidity and mortality at five years following amputation in this patient population. [8] This staggering data has prompted further research into the science of wound healing in an attempt to reduce diabetic foot ulcerations and their life changing sequelae.

Many of today’s wound care concepts have developed from research associated with burn therapies. [9] More recent research has focused on the wound environment, and on both the cellular and extracellular components necessary to promote wound healing. A better understanding of vasculopathy, infection, and poor nutritional status have enabled industry to target the failing biology of wounds with new products including many new collagen derivatives.

The Science

Throughout the four phases of wound healing, the extracellular matrix (ECM) provides a significant role in regulating and providing a framework for the many processes of healing. The ECM is the largest component of the dermal skin layer and is composed of a variety of polysaccharides, water and collagen proteins. [10] Collagens make up the largest fibrous components of the ECM; in the dermal matrix, the majority of collagen is type I and type III. These collagens demonstrate a fibrillar or rod shape and are composed of three triple-helix protein chains arranged in a linear fashion. This linear orientation provides much of the tensile strength of skin. In addition to longitudinal strength, bundles of collagen molecules in the ECM cross link with adjacent collagen molecules to provide additional strength and stability against shearing forces. [11]

Acute wounds create a provisional wound matrix which contains fibrin and fibronectin, which act as chemical mediators to direct cells to the site of injury and to motivate cells to proliferate and to differentiate into new, provisional matrix structures. [4,6] However, in chronic wounds, increased levels of inflammatory cells and proteases degrade the ECM components which are essential for healing. [8,12] Among these proteases, matrix metalloproteases (MMPs) play an important role in damaging the ECM and the extracellular growth factors present in a chronic wound. These MMPs are synthesized by multiple cell types, including neutrophils, fibroblasts and macrophages at the direction of chemical mediators such as inflammatory cytokines. [6] In normal healing, the MMPs function to debride away denatured elements of the ECM, thus exposing areas of intact functional matrix that are needed for wound healing. This process is highly regulated and controlled via tissue inhibitors of metalloproteases (TIMPs). [12] In chronic wounds, however, in addition to an excess number of MMPs, there is a failure in the regulation of protease activity between the MMPs and TIMPs which can result in further degradation of the ECM. This is followed by the destruction of growth factors, inhibition of angiogenesis, and breakdown of granulation tissue. [13]

For wound healing to occur, a balance is needed between the protein degrading activities of MMPs and other cellular activity that synthesizes and deposits protein components of granulation tissue. Many new collagen based wound care products aim to reduce excessive protease levels and reestablish balance in the wound environment. In addition, these products serve to contribute functional ECM proteins to stimulate the healing process. [1] Research has demonstrated that topically placed collagen can initiate wound healing by activating inflammatory cells and promoting increased vascularization of the healing tissue. [14] Other research has demonstrated that the physical three-dimensional structure of collagen has the ability to induce fibroblastic growth, which is essential in the formation of granulation tissue. [1]

The Products

There are an abundance of collagen-based products on the market today. These products can be loosely divided into groups based upon the setting in which they are applied (either in the clinic setting or in the operating room). In addition to differences in the application process, these collagen-based products can be combined with other treatment modalities, such as the addition of an alginate to manage exudate or the addition of silver to provide antimicrobial effects (See attached table).

Attached Table:  Collagen based products and their properties.

Below is a detailed discussion of several representative topical collagen products that are intended for use in the outpatient dressing setting:

FIBRACOL PLUS® (Systagenix Wound Management) combines the structural support of collagen with the exudate management of an alginate. In this way, the alginate component maintains a moist wound environment while the collagen component allows for cellular and vascular in-growth, which promotes formation of granulation tissue and neo-epithelialization at the wound site.

Promogran® (Systagenix Wound Management) combines oxidized regenerated cellulose (ORC) and collagen. This bioactive collagen product binds to and neutralizes destructive proteases in chronic wound fluid. [14]

Once bound, MMPs are rendered inactive due to alteration of their protein structure. Reduction of MMP burden in the chronic wound allows endogenous ECM protein cells to proceed to the formation of granulation tissue and normal wound healing.

PRISMA® (Systagenix Wound Management) is the next generation in the Promogran® line. This product provides the MMP binding function of Promogran® in the form of ORC and collagen with the addition of silver to provide antibiosis, thus lowering the bioburden in chronically colonized wounds. [14] PRISMA® provides a biodegradable cellular matrix that promotes cellular migration and neo-vascularization while helping to maintain bacterial balance at the wound site and to create an optimal wound healing environment.

PURACOL PLUS® (Medline Industries, Inc) is a bovine derived collagen matrix, which utilizes a native, triple-helical structure to stimulates fibroblastic activity in the wound bed to promote ECM formation and thus stimulate local wound healing. Additionally, this product controls moisture in the wound environment by converting to soft, gel-like sheet that maintains intimate contact with wound bed as it absorbs exudate. PURACOL PLUS® is most commonly utilized in chronic, partial thickness wounds which demonstrate light to heavy exudate and are non-infected and non-ischemic.

Biostep® and Biostep Ag® (Smith & Nephew) are two new collagen products which are demonstrating a great deal of success in the treatment of chronic wounds. The semi-denatured porcine collagen in Biostep® attracts and bind excess MMPs present in the chronic wound environment, and the EDTA component in the product irreversibly deactivates MMPs by binding to their zinc ions. In this way the collagen in Biostep®, coupled with EDTA, functions as a competitive substrate for the MMPs and thus allows endogenous collagen matrix formation to progress undeterred as granulation tissue forms. In addition, the product contains carboxy methyl cellulose and alginate which helps to provide moisture management in an actively draining wound environment.

Biostep Ag® provides similar anti-MMP activity, while the addition of silver ions helps to maintain bacterial balance in the wound site.

OASIS® Wound Matrix (HealthPoint) is a biologically derived extracellular matrix-based wound product which is derived from porcine small intestine submucosa. Indicated in the management of partial and full thickness wounds, this product provides intact acellular collagen scaffold that allows promotes a favorable host tissue response and stimulates cellular migration, leading to restoration of tissue structure and promotion of wound healing.

Integra® Matrix (Integra Life Sciences) consists of a cross-linked bovine tendon collagen and glycosaminoglycan matrix which is available with and without a semi-permeable polysiloxane layer. [2] Glycosaminoglycans are large saccharide polymers that are important elements of the ECM; these proteins aid in cellular adhesion to the matrix, as well as playing a role in cell and tissue differentiation necessary for wound healing. [9] The semi-permeable polysiloxane membrane of the bilayer matrix functions as a temporary epidermis by protecting the deeper collagen graft tissue and wound while also controlling water vapor loss. Below the silicone layer, the collagen-glycosaminoglycan biodegradable matrix provides a scaffold for cellular invasion and capillary growth. As the graft is incorporated, the silicone layer peels away to expose new granulation tissue formation and neo-epithelialization. Additionally, this product is available in a “flowable” or injectable form that can be utilized to provide collagen and glycosaminoglycan matrix to difficult to manage wounds with tunneling or tracking components. Often this modality can be used in conjunction with the conventional graft to provide three dimensional reconstruction at complex wound sites.

GraftJacket® Regenerative Tissue Matrix (Wright Medical), which is a collagen based graft processed from donated cadaveric skin. As an allograft, this product contains components of normal skin including collagen, elastin, hyaluronan, fibronectin, and blood vessel channels. [8]

In this way, GRAFTJACKET® provides soft tissue coverage over deep structures, functions as a scaffold for new cellular in-growth. It preserves the vascular channels in the donor graft and allows for rapid revascularization necessary for wound healing.

In the operating room setting, collagen-containing products are often applied to provide coverage over a soft tissue deficit following surgical debridement or serve as a scaffold initiate the filling of a void. As with the clinically applied products described above, these collagen grafts were originally designed to be used in the treatment of partial and full thickness burns. These surgically applied collagen products, such as Integra® Matrix and GraftJacket® Regenerative Tissue Matrix, are not specifically designed to neutralize proteases as several of the previously described products. Instead, they provide a functional cellular scaffold that promotes cellular in-growth and formation of granular tissue while also providing soft tissue coverage over bone, tendons, and other deep structures. As a result, it reduces the risk of contamination and subsequent infection.

To reduce MMP burden in a wound site prior to application of these surgically applied collagen grafts, it is recommended that the wounds be debrided sharply to promote local bleeding and to remove any nonviable and necrotic soft tissue and bone that will further stagnate a wound site. Localized bleeding following debridement stimulates influx of alpha-2-macroglobin (A2M), which is a chemical agent that acts as a protease inhibitor, thus reducing proteolytic destruction of the graft. [1,11]

Conclusion

In discussion of collagen products in wound healing, it is important to understand the underlying etiologies of wound chronicity. Vascular and nutritional status, the presence of an infection or colonization, and the microenvironment present in the wound bed all combine to affect healing. Each barrier must be addressed to ensure that the wound progresses through the normal stages of healing. [1]

Research has demonstrated the importance of re-establishing a functional ECM in chronic wounds and this has led to a renewed interest in collagen based wound healing products. [8] These products seek to provide a functional ECM as well as to reduce MMP levels present in the wound bed and seek to promote normal progression through the stages of wound healing. In addition, these products can be combined with other modalities, such as alginates or heavy metals to provide additional effects to the wound environment such as management of exudate or bacterial load.

The collagen-based surgical grafting materials, such as Integra Matrix® and GraftJacket® have filled a niche that have allowed for significant increases in salvage options due to the ability to provide collagen ECM to the wound site, following sharp debridement. These surgically applied collagen wound fillers can provide soft tissue coverage over deeper structures to reduce the risk of infection. Pioneered in the burn community, much of these techniques are now being utilized to preserve limb length in partial foot amputations, which is important as the costs of health care spiral and the annual incidence of foot ulcerations continue to climb. [2]

Considering the significant morbidity and mortality associated with lower extremity amputations, and the obvious link between lower extremity amputations and the ulcerations that precede them, it is incumbent upon the clinician involved in wound care to become familiar with these advanced wound care products in order to provide patients with the greatest possibility for successful outcomes in the treatment of chronic wounds.

References

1. Schultz GS, Sibbald RG, Falanga V, Ayello EA, Dowsett C, Harding K et al: Wound bed preparation: a systematic approach to wound management. Wound Repair Regen, 2003. 11 (suppl 1): S1 – 28, 2003.
2. Voigt DPC, Edwards P: Economic study of collagen-
glycosaminoglycan biodegradable matrix for chronic wounds. Wounds 18 (1): p. 1 – 7, 2006.
3. Physicians AAoF: Clinical guidelines on diabetic foot disorders. J Foot Ankle Surgery 63 (5): 290 – 295, 2001.
4. Greiling DCR: Fibronectin provides a conduit for fibroblast transmigration from collagenous stroma into fibrin clot provisional matrix. J cell science 110 (7): 861 – 870, 1997.
5. Gordois A, Scuffham P, Shearer A, Oglesby A: The health care costs of diabetic nephropathy in the United States and the United Kingdom. J Diabetes Complications 18 (1): 18 – 26, 2004.
6. Ovington L: Overview of matrix metalloprotease modulation and growth factor protection in wound healing. Wounds 14(5): 3 – 7, 2002.
7. Moulik PK, Mtonga R, Gill GV: Amputation and mortality in new-onset diabetic foot ulcers stratified by etiology. Diabetes Care 26 (2): 491 – 494, 2003.
8. Loots MA, Lamme EN, Zeegelaar J, Mekkes JR, Bos JD, Middelkoop E: Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Dermatol 111 (5): 850 – 857, 1998.
9. Ehrenreich RZ, Ruszczak Z: Update on tissue-engineered biological dressings. Tissue Engineering 12 (9): 2407 – 2424, 2006.
10. Dalla Paola L, Faglia E: Treatment of diabetic foot ulcer: an
overview strategies for clinical approach. Curr Diabetes Rev 2 (4): 431 – 447, 2006.
11. Kainulainen V, Wang H, Schick C, Bernfield M: Syndecans, heparan sulfate proteoglycans, maintain the proteolytic balance of acute wound fluids. J Biol Chem 273 (19): 11563 -11569, 1998.
12. Trengove NJ, Stacey MC, MacAuley S, Bennett N, Gibson J, Burslem F, Murphy G, Schultz G: Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Repair Regen 7 (6): p. 442 – 452, 1999.
13. Ladwig GP, Robson MC, Liu R, Kuhn MA, Muir DF, Schultz GS: Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated with healing of pressure ulcers. Wound Repair Regen 10 (1): 26 – 37, 2002.
14. Cullen B, Watt PW, Lundqvist C, Silcock D, Schmidt RJ, Bogan D, Light ND: The role of oxidised regenerated cellulose/collagen in chronic wound repair and its potential mechanism of action. Int J Biochem Cell Biol 34 (12): 1544 – 1556, 2002.

Address correspondence to: Ryan H. Fitzgerald, DPM, AACFAS. Hess Orthopaedics & Sports Medicine, PLC
4165 Quarles Court, Harrisonburg, Virginia 22801.

1  Attending physician, Hess Orthopaedics & Sports Medicine, Harrisonburg Virginia.
2  Assistant Professor, Department of Plastic Surgery, Georgetown University School of Medicine.

© The Foot and Ankle Online Journal, 2009

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The BRAIN Principle: Managing Wounds After Application of Bioengineered Alternative Tissues to Maximize Incorporation and Wound Healing

Posted on May 1, 2008 | Comments Off on The BRAIN Principle: Managing Wounds After Application of Bioengineered Alternative Tissues to Maximize Incorporation and Wound Healing

by Jonathan Moore, DPM, MS1

The Foot & Ankle Journal 1 (5): 3

The efficacy of bioengineered alternative tissue (BAT) for lower extremity ulcers (diabetic and non-diabetic) is well described in the literature. What is not present in the literature is a concise description of how to manage these fragile biological tissues after application. This paper introduces the BRAIN principle for adjuvant management of wounds after application of bioengineered alternative tissues. Based on the experience of the author, utilizing the principles found in the BRAIN protocol have not only demonstrated improved BAT incorporation rates, it also increased the rate of wound closure.

Key words: Diabetic wounds, bioengineered alternative tissues, wound healing

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org) 

Accepted: April 1, 2008
Published: May 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0105.0003

Bioengineered Alternative Tissues (BAT’s) have revolutionized the science of wound healing. These new technologies offer the wound care specialist an important tool in the battle to prevent nearly 90,000 amputations that occur annually among diabetic patients. [7] However, this technology is of little value when not used as a part of a comprehensive approach to wound healing. This includes assessing nutrition, metabolic status, vascular status, off loading options, and choosing the right wound healing product.

As new bioengeenered alternative tissue products enter the market it is important to consider patient expectations and treat the patient with the best product available for their specific wound. While there are procedures described for many of the better-known BAT’s on the market, they differ in many respects. The table in the study demonstrates the differing protocols for “after-care” following applications of these products. (Table 1)

Table 1 Application and Aftercare Instructions to Providers from the Manufacturer.

Choosing the right BAT along with the appropriate topical wound care agent is critical not only to improve healing times, but to also lower costs.

It has been estimated that 15 to 20 percent of individuals with diabetes will suffer from lower extremity ulceration during their lifetime. [8] Furthermore, half of the diabetic patients who have had a leg amputated will loose the other leg in three to five years. In 1997 it was estimated that total costs for both direct and indirect health care for the persons with diabetes was $98 billion. Of this total, direct medical costs including hospitalization, medical care, and dressing supplies, accounts for $44.1 billion. [9] What is more startling is the annual $5 billion dollar price tag estimated for the cost of dressings for these conditions. With the increased cost of wound care, the wound care specialist should consider using protocols that not only maximize wound healing, but also minimize the risk of BAT failure by providing the best tools to maintain the optimum environment for the wound.

While it is not the purpose of this paper to review every type of BAT on the market, it is vital to understand the characteristics of these products in order to understand how they work and how they should be adjunctively managed after application.

For purposes of defining terms, BAT’s are products that have been produced artificially or modified in some way that alters the biology and its interaction with the wound bed with the goal of creating an optimal environment to stimulate healing.

These tissues include both allograft, xenografts and manufactured/engineered biologic products like Apligraf® (Organogenesis, Inc., Canton, MA). The purpose of these tissues has been well established in the medical literature. However, the primary goal in using a BAT is to stimulate granulation of a chronic wound and augment the wound’s intrinsic healing pathway, thus creating a bridge to epithelialization of the wound.

The literature has well described the process of preparing the wound bed for application of a BAT. The TIME acronym as proposed by the International Wound Bed Preparation Advisory Board provides an exceptional framework for the physician to improve the opportunity for wounds to heal. The TIME principle in essence describes an approach to remove the barriers to the wound-healing process in order to optimize wound repair and healing. Removal of these barriers will not only help to establish a well-vascularized wound bed, but they will also be vital for the incorporation and success of a BAT. (Table 2). [10]

Table 2   International Wound Bed Preparation Advisory Board – TIME principles.

While the principles of TIME described above remains important a new set of principles are needed to assure the BAT has the best chance of incorporation and healing the wound in a timely manner.

Thus, the following acronym called BRAIN is proposed. (Table 3)

Table 3   The BRAIN principles to maximize BAT incorporation and wound healing.

The BRAIN Principle

B (Bioburden)

Despite having properly prepared the wound bed before application of the bioengineered tissue through debridement, among other modalities, maintenance of the bioburden after BAT application remains important. Non-cytotoxic antimicrobials should be considered to prevent colonization after application of bioengineered tissues.

Proper assessment to the needs of the wound is vital after application of the BAT in order to reduce the chances of infection. In the event of a clinical infection of a chronic wound, aggressive treatment is recommended to prevent limb loss. The following are recommendations that should be considered after application of a BAT for the prevention of infection:

1. Sharp debridement is the fundamental component in preparing the chronic wound for the BAT, whether it is an allograft or a bioengineered skin equivalent, like Apligraf®. Sharp debridement too early after application of the BAT may result in destruction of the bioengineered tissue or disruption of the materials the BAT was able to establish in the wound bed. Debridement post BAT application should only be considered if there is necrotic or infected tissue present.

2. Application of a topical antimicrobial agent for use on the wound bed prior to application of the BAT (at least 2 weeks prior), in order to decrease bacterial colonization, should be considered for both cellular engineered tissues and allografts. Use of a silver containing antimicrobial agent, as a part of wound bed preparation should not be a problem, as the silver will be inactivated by wound fluid among other wound components. Application of a topical antimicrobial agent post application of a BAT remains controversial

Living skin equivalents like Apligraf® should not be used in conjunction with any silver-based topical antimicrobial agent as these can be, at certain levels, cytotoxic to keratinocytes and fibroblasts.11 While there is debate about other types of topical agents used on or with a living skin equivalent like Apligraf®, I have used Bacitracin ointment as well as AmeriGel®

Hydrogel Saturated Gauze Dressing (Amerx Health Care Corporation, Clearwater, FL) pre and post application of Apligraf® pose no adverse clinical effects. Agents that are known to be cytotoxic to living skin equivalents include: Dakin’s solution, Mafenide Acetate, Scarlet Red Dressing, Tincoban, Zinc Sulfate, Povidone-iodine solution, Polymyxin/Nystatin and Chlorhexidine.

3. Care must be taken to control swelling and edema with careful compression over the BAT site taking care not to compromise circulation. Edema can significantly compromise wound healing and incorporation of the BAT.

4. Systemic antibiotics should be considered in the presence of malodorous drainage, friable necrotic tissue, increased levels of wound exudate, increasing pain, surrounding cellulitis, crepitus, necrosis and lymphadenopathy. Fever, chills, malaise, leukocytosis, and an elevated erythrocyte sedimentation rate are also common systemic manifestations of wound infection. Superficial contaminants are not always representative of the wound status, as healing wounds will have some contamination. Macerated tissue culture or curettage is a reliable way to determine the etiology of a serious wound infection. Infected wounds will typically respond to aggressive debridement with appropriate systemic antibiotic therapy. Indiscriminate use of oral antibiotics will not decrease infection rates, but can result in resistance. Gram-negative bacterial infections can be severe and need to be treated aggressively. [12]

R (Reduction of pressure and shear force)

In order for incorporation of the BAT to take place in the chronic wound, excess pressure, motion and shearing must be eliminated. Unless the bioengineered tissue maintains adherence to the wound bed with proper pressure redistribution, BAT incorporation will fail. The medical literature is replete with articles that stress the importance of offloading during wound healing. [13]

Although there are many devices on the market that can be employed to remove plantar pressure {Bledsoe® Walker (Bledsoe Brace Systems, Grand Prairie, TX), DH Walker® (Royce Medical, Inc., Camarillo, CA) or total contact casting}, care must further be taken when applying the BAT to the wound site.

Although most BAT manufacturers recommend some type of anchoring of the bioengineered tissue to the wound (i.e. sutures, staples, etc.), specific protocols are lacking. The following are recommendations to consider for the development of your protocols:

1. Determine the best and the most secure application method based upon the quality of the tissues and the location of the BAT. Plantar pressures will deteriorate the BAT unless properly offloaded and secured. With dorsal wounds, anything creating pressure or shear over the site will also result in the failure of the BAT.

2. Although suturing the BAT to the wound bed is ideal, in cases of severe tissue atrophy or poor skin perfusion, Steri-Strips™ (3M, St Paul, MN) should be considered to prevent worsening of the wound site.

3. If sutures or staples are employed, be careful to make sure the bioengineered tissue has been adequately fenestrated in order to prevent hematoma or seroma formation under the BAT.

4. Plantar ulcers MUST be offloaded in order for the BAT to incorporate. Ideally, no pressure should be applied to the wound site, if possible. Surgical shoes with a Velcro®(Velcro Industries B.V., Manchester, NH) latch should be considered for dorsal foot wounds in order to prevent rubbing or shearing forces.

5. Regular shoes, flip-flops or any like footwear are contraindicated after application of any BAT and should NOT be employed.

A (Adapting to the moisture needs of the wound and the bioengineered tissue.)

Any BAT must stay hydrated in order to achieve wound incorporation. Early desiccation of the wound bed and the surrounding tissues will ultimately lead to BAT failure and subsequent slower healing times. The concept of keeping wounds moist in order to accelerate wound healing has been known now for over 50 years. [14,15] Contrary to conventional wisdom, keeping the wound site and the BAT moist does not increase the risk of infection. In fact, a moist wound environment has been shown to improve wound healing by up to 50% compared with exposure to air. [16]

Many factors will determine the amount of wound fluid present in the wound bed. Venous ulcers, for instance, are more likely to produce more moisture than an ulcer on the top of the foot. Close assessment of the moisture balance in the wound is critical for the success of the BAT. Fluid from chronic wounds will block cellular proliferation and angiogenesis, and will ultimately impair wound healing through the build up of excessive amounts of matrix metalloproteinases (MMPs) that break down critical matrix proteins. [17]

The dressing choice after the application of the BAT to the wound site is vital in order to properly adapt to the moisture needs of the wound. Here are some considerations:

1. Upon review of many bioengineered tissue dressing protocols, as provided by the manufacturers of the top BAT’s on the market, regular gauze is recommended as a secondary dressing in nearly all. (Table 1) Although the purpose of the gauze is understood to provide some level of absorption of drainage from the wound, this concept is not ideal for several reasons. No matter how much hydrogel or mineral oil you use under a regular piece of dry gauze, most of this will be absorbed by the gauze and thus provide minimal moisture to the wound bed over time.

Regular gauze alone, even with a nonadherent dressing of some sort, cannot provide consistent and long lasting moisture to the wound site. Hydrogels and hydrogel impregnated gauzes formulated with substrates allowing for longer and controlled moisture balance reduces the incidence of adhesion to the BAT and wound site. Saline or glycerin-based hydrogels or hydrogel impregnated gauzes frequently result in premature desiccation and should be avoided.

2. In those cases where excessive wound fluid is evident, more frequent dressing changes is recommended.

3. In cases of severe exudate and draining from the wound site, the presence of infection needs to be addressed and antibiotics should be prescribed.

4. The ideal wound dressing will remove the excess amounts of wound exudates while retaining a moist environment that accelerates wound healing.

Keep in mind that healing wounds are always characterized by high mitogenic activity, low inflammatory cytokines (less chronic wound fluid), low proteases, mitotically competent cells and a moist environment.

I ( Incorporation and Identification)

Successful incorporation of a BAT hinges upon the molecular environment of the wound. Incorporation of the acellular BAT into the wound bed through a collagen matrix allows for the recruitment of cells into the wound and facilitates the induction and expression of growth factors and cytokines necessary for wound healing. The balance between collagen degradation and synthesis can be disrupted by disease states like diabetes. This can result in defective collagen metabolism and disrupted wound healing.

In contrast, cellular BAT’s are designed to accelerate tissue regeneration by stimulating the recipient’s own wound bed derived skin cells. [18,19] Some authors have called the BAT an interactive “drug” delivery system by the transfer of MMPs and cytokines from the BAT into the wound. [20] Acellular BAT’s work by effectively providing a cover for the wound that prohibits desiccation and fluid loss within the wound, thus decreasing the bacterial burden and promoting angiogenesis and allowing vascular ingrowth into the dermal layer of the allograft.

Identification and correction of factors that can cause tissue damage is essential after application of a BAT. Keep in mind that cellular bioengineered alternative tissues work by biochemically balancing the wound environment to promote tissue regeneration. This provides the “primordial soup” of mediators and growth factors. [21]

Among the many things that can impair wound healing (systemic steroids, non-steroidal anti-inflammatories, immunosuppressive drugs), several other factors must be recognized:

1. Localized edema from venous insufficiency or lymphedema must be addressed before and after application of a BAT. Compression therapy or a referral to a certified lymphedema specialist should be considered.

2. Low albumin can have a significant impact on wound healing. A deficiency in serum albumin, which accounts for more than 50% of total serum proteins, impairs the inflammatory and proliferative stages of wound healing while also decreasing wound perfusion.22 A dietary or nutritional consult should be ordered to maximize the body’s own potential to heal.

3. Autonomic Neuropathy resulting in over drying of the wound and surrounding tissues will impair wound healing in many ways. Desiccation within the wound site will slow epithelial cell migration and thus prevent the incorporation of the BAT.

4. Infection within the wound site can present many challenges to the incorporation of the BAT. Infection must be treated without delay through either debridement, antibiotics, wound cleansing, or wound disinfection.

5. Hyperglycemia must be addressed in order to have successful incorporation of the BAT. Although the wound care specialist may not be able to directly influence this factor, all efforts need to be made to communicate with the primary care provider and patient to gain better control the patient’s blood sugar. Behavior modification regarding diet and exercise is always an immense challenge in the diabetic population. [23]

N ( Nonadherent Dressing)

It has been said that the choice of the wound dressing at one stage of the wound may well influence subsequent events in the later phases of healing. [24] In reviewing the protocols set forth by most BAT manufacturers, the one common denominator among all of them is the recommendation of a “nonadherent dressing” as the primary dressing to be used over the bioengineered tissue. (Table 1)

While the goal of the nonadherent dressing is to prevent trauma or adhesion of the secondary dressing to the BAT (or underlying tissues), few of these products possess the characteristics ideal for covering a bioengineered tissue. While it is possible for several different types of dressings to be employed over the BAT at once (i.e. petrolatum impregnated gauze, antibiotic cream, hydrogel, mineral oil followed by an absorptive 4” X 4” pad or a foam), this is impractical and expensive.

Ideal Characteristics of the Primary Dressing for Coverage over a BAT:

1. Nonadhesive
2. Antimicrobial
3. Ability to absorb exudate
4. Maintains moisture on the BAT and within the wound site
5. Non-cytotoxic
6. Cost-effective

Of the myriad of different dressing options available that meet some of the criteria mentioned above, the AmeriGel® Hydrogel Saturated Gauze Dressing is an excellent option that meets most if not all of the characteristics above.

Case Example using the BRAIN Principal

A 47 year-old diabetic patient with profound peripheral neuropathy developed a blister on the plantar aspect of her right heel that became recalcitrant to conservative treatment. The patient’s wound was debrided weekly and had Promogran™ (Johnson & Johnson Wound Management, Somerville, NJ) applied to the site until the wound developed a healthy granular base. Apligraf® was chosen to close the wound, secured in place by Steri-Strips™. AmeriGel® Hydrogel Saturated Gauze Dressing covered the BAT to provide an antimicrobial barrier. A dry sterile secondary dressing was then applied. The bioburden of the BRAIN principle had been accomplished. (Fig. 1)

Figure 1  The Bioburden of the wound has been addressed with debridement and diligent local wound care.

To achieve the reduction of pressure and shear force, a Bledsoe® boot was utilized along with a wheel chair. Due to the patient’s severe neuropathy, as well as other balance concerns, the patient could not use crutches. The primary and secondary dressings remained dry and intact for one week. (Fig. 2)

Figure 2  Reduction of pressure and shear force is essential for incorporation of the BAT.

Once the AmeriGel® Hydrogel Saturated Gauze Dressing was removed, the absorptive capability was evident as well as its ability to maintain a moist wound environment. (Fig. 3) This demonstrates adapting to the moisture needs of the BAT and of the wound.

Figure 3  Adapting to the moisture needs of the wound.  Here, a healthy moisture balance has been achieved using AmeriGel® Hydrogel Saturated Gauze Dressing after BAT application.

The patient returned at two weeks and Incorporation was achieved. The wound had already started to reduce in size and was considered to be a healthy granulating wound. There was no evidence of bleeding or absence of tissue caused by traumatic dressing changes. (Fig. 4)

Figure 4  Incorporation of the Apligraf®.  Reduction of wound size is already appreciated.

At 4 weeks and 4 days, after daily applications of the AmeriGel® Hydrogel Saturated Gauze Dressing and dry sterile gauze as the secondary dressing, the wound was healed.

The nonadherent secondary dressing played a significant role in healing this wound quickly and without the need for subsequent applications of the BAT. (Fig. 5)

Figure 5  Nonadherence of the surrounding secondary dressings will help ensure the viability of the BAT.  Using the AmeriGel® Hydrogel Saturated Gauze Dressing as a secondary dressing provides a non adherent and antimicrobial barrier to facilitate rapid wound healing.

Conclusion

Effective management of lower extremity ulcerations using bioengineered alternative tissues requires a multidisciplinary approach, patient involvement and the right use of the proper adjunctive tools available to the wound care specialist.

Diabetic foot ulceration is a limb and life threatening condition that requires the establishment of sound, evidence-based protocols. It is the hope of the author that protocols be established in every wound care clinic that are based upon patient outcomes, cost and ease of use for the wound care specialist and the patient.

A protocol as described above certainly may be modified depending on many factors that may or may not be present in the wound, however the core principles as presented in the acronym BRAIN should provide a road map to maximizing the effectiveness of bioengineered tissues before, during and after BAT application.

References

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Address correspondence to: Jonathan Moore, DPM, MS, Cumberland Foot & Ankle Center. 117 Tradepark Drive, Somerset, KY 42503

1Cumberland Foot & Ankle Center. 117 Tradepark Drive, Somerset, KY 42503.

© The Foot & Ankle Journal, 2008

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