Orthopedics

Case Reports 

Wound Necrosis After Total Knee Arthroplasty

Vittorio Patella, MD; Domenico Speciale, MD; Silvio Patella, MD; Biagio Moretti, MD; Vito Pesce, MD; Antonio Spinarelli, MD

Abstract

Wound problems after total knee arthroplasty (TKA) are uncommon; however, quickly evolutive skin necrosis and deep infection is not uncommon. Several predisposing factors such as immunosuppression, malnutrition, steroid use, rheumatoid arthritis, multiple scars, and vascular disease can be involved in the onset of wound complications, as well as long tourniquet time and early knee flexion. Skin necrosis after TKA can be treated in different ways, including local wound care, debridement, and soft tissue coverage with muscle or skin grafts. Joint immobilization to minimize skin tension and antibiotic therapy can also be helpful. This article presents a rare case of skin necrosis occurring in a patient without any other apparent risk factor after TKA.

A 78-year-old woman underwent a cemented TKA in May 2005 for primary osteoarthritis. According to our standard protocol, at the time of admission in the clinic the patient’s general conditions were checked. An arteriovenous echo-color Doppler on the lower limbs showed a normal vascular situation, blood parameters were in the normal range, and no infections were demonstrated.

She had no comorbidities, but the medical history was positive for allergic diathesis, so in addition to the standard drugs we use for antibiotic, antithrombotic, ulcer prevention, and analgesic prophylaxis (cefazolin 2 g intravenous 1 hour preoperatively and at 6, 12, and 18 hours postoperatively; enoxaparin 4000 IU every 24 hours starting the night before surgery; omeprazole; tramadol; and paracetamol), the patient underwent corticosteroid and antistaminic therapy.

A midvastus approach was used with a medial parapatellar skin incision. The operation (skin to skin) took 60 minutes. A tourniquet was applied for 40 minutes, drainage was put in the medial compartment, and intermittent pneumatic leg compression was used.

Immediately postoperatively, the patient reported dyspnea and was treated with oxygen therapy and corticosteroids. This situation was rapidly solved, and the patient began the protocol for passive mobilization of the knee (knee bent at 90° of flexion in the first 3 hours after surgery, then extended for 1 hour, so passively mobilized in the range from 60° to 90° of flexion once for 90 minutes at 4 hours postoperatively, and then from 0° to 90° for 90 minutes every day of hospitalization). The drainage was removed 24 hours postoperatively, and graduated compression stockings took the place of the intermittent pneumatic compression.

On the third postoperative day, the patient had a fever (38.5°C/101.3°F) and was treated with paracetamol and antibiotic therapy. The next day, the surgical wound showed a secretion and the surrounding skin was painful, swollen, hot, and red (Figure 1). The following day, these signs worsened and the wound appeared superficially opened in its proximal and distal part, without any worsening of the general clinical condition.

In subsequent days the sides of the wound showed skin necrosis, integrity of deep layers, and evolutive inflammation signs in the surrounding skin. Treatment options for skin necrosis, including local wound care, swabs (all negative), and antibiotic therapy, were applied. The fever occurred occasionally during the following days, and the only altered parameter was the count of peripheral leukocytes (polymorphonuclear leukocytosis, a leukemia-like reaction). The possibility of a course of hyperbaric therapy was discussed, but was not recommended. All the swabs of the wound (bacteriological and mycological) and bacteremia of the following days were negative. Biopsy of the deep side of the wound revealed necrosis, an inflammatory reaction with a large presence of neutrophil leukocytes, and vessel thrombosis (Figure 2). A seroimmunologic search (ANCA, APCA, ASCA) was negative.

After 20 days the necrosis was no longer evolutive and was treated with local wound care devices (topic drugs: antibacterial, epithelial trophic) for 15 days and then by…

Wound problems after total knee arthroplasty (TKA) are uncommon; however, quickly evolutive skin necrosis and deep infection is not uncommon. Several predisposing factors such as immunosuppression, malnutrition, steroid use, rheumatoid arthritis, multiple scars, and vascular disease can be involved in the onset of wound complications, as well as long tourniquet time and early knee flexion. Skin necrosis after TKA can be treated in different ways, including local wound care, debridement, and soft tissue coverage with muscle or skin grafts. Joint immobilization to minimize skin tension and antibiotic therapy can also be helpful. This article presents a rare case of skin necrosis occurring in a patient without any other apparent risk factor after TKA.

Case Report

A 78-year-old woman underwent a cemented TKA in May 2005 for primary osteoarthritis. According to our standard protocol, at the time of admission in the clinic the patient’s general conditions were checked. An arteriovenous echo-color Doppler on the lower limbs showed a normal vascular situation, blood parameters were in the normal range, and no infections were demonstrated.

She had no comorbidities, but the medical history was positive for allergic diathesis, so in addition to the standard drugs we use for antibiotic, antithrombotic, ulcer prevention, and analgesic prophylaxis (cefazolin 2 g intravenous 1 hour preoperatively and at 6, 12, and 18 hours postoperatively; enoxaparin 4000 IU every 24 hours starting the night before surgery; omeprazole; tramadol; and paracetamol), the patient underwent corticosteroid and antistaminic therapy.

A midvastus approach was used with a medial parapatellar skin incision. The operation (skin to skin) took 60 minutes. A tourniquet was applied for 40 minutes, drainage was put in the medial compartment, and intermittent pneumatic leg compression was used.

Immediately postoperatively, the patient reported dyspnea and was treated with oxygen therapy and corticosteroids. This situation was rapidly solved, and the patient began the protocol for passive mobilization of the knee (knee bent at 90° of flexion in the first 3 hours after surgery, then extended for 1 hour, so passively mobilized in the range from 60° to 90° of flexion once for 90 minutes at 4 hours postoperatively, and then from 0° to 90° for 90 minutes every day of hospitalization). The drainage was removed 24 hours postoperatively, and graduated compression stockings took the place of the intermittent pneumatic compression.

On the third postoperative day, the patient had a fever (38.5°C/101.3°F) and was treated with paracetamol and antibiotic therapy. The next day, the surgical wound showed a secretion and the surrounding skin was painful, swollen, hot, and red (Figure 1). The following day, these signs worsened and the wound appeared superficially opened in its proximal and distal part, without any worsening of the general clinical condition.

Figure 1: Surgical wound fourth day after surgery Figure 2: Skin necrosis and wound inflammation 10 days after surgery Figure 3: Autologous skin grafting
Figure 1: Surgical wound fourth day after surgery. Figure 2: Skin necrosis and wound inflammation 10 days after surgery. Figure 3: Autologous skin grafting.

In subsequent days the sides of the wound showed skin necrosis, integrity of deep layers, and evolutive inflammation signs in the surrounding skin. Treatment options for skin necrosis, including local wound care, swabs (all negative), and antibiotic therapy, were applied. The fever occurred occasionally during the following days, and the only altered parameter was the count of peripheral leukocytes (polymorphonuclear leukocytosis, a leukemia-like reaction). The possibility of a course of hyperbaric therapy was discussed, but was not recommended. All the swabs of the wound (bacteriological and mycological) and bacteremia of the following days were negative. Biopsy of the deep side of the wound revealed necrosis, an inflammatory reaction with a large presence of neutrophil leukocytes, and vessel thrombosis (Figure 2). A seroimmunologic search (ANCA, APCA, ASCA) was negative.

 
Figure 4: Wound healing 30 days after skin grafting
Figure 4: Wound healing 30 days after skin grafting.

After 20 days the necrosis was no longer evolutive and was treated with local wound care devices (topic drugs: antibacterial, epithelial trophic) for 15 days and then by vacuum-assisted closure (Kinetic Concepts Inc, San Antonio, Texas) therapy. After 60 days the patient underwent an autologous skin grafting (Figure 3). The result was excellent, and after 30 days the wound was healed (Figure 4). There was also a full functional recovery of the autonomous ambulation and of the knee motion and stability, reaching a good passive and active ROM (0°-0°-90°). The pain was absent and the local status of the knee and of the grafting was very good. In December 2005 the patient was lost to follow-up because she died of a brain hemorrhage.

Discussion

Poor wund healing and skin necrosis after TKA is an uncommon but devasting complication. The consequences of wound complication are numerous, but many failures can be prevented. The risk seems to be largest in the presence of factors that affect local vascularity to the soft tissues, such as prior scars or peripheral vascular disease, and systemic immunologic factors such as steroid use, immunosuppressive disorders, and malnutrition predisposing risk factors.1,2 Kim et al3 observed skin necrosis in 13 of 27 patients who underwent TKA for bony ankylosis.

Skin vascularity over the knee affects the rate of healing postoperatively and the risk of necrosis. Ries4 measured transcutaneous skin oxygen tension and found that the oxygen tension decreases for the first 2 to 3 days after surgery, then increases. In addition, the lateral skin edge is more hypoxic than the medial edge. The medial parapatellar incision is more parallel to the skin cleavage lines than the vertical midline incision and is associated with less tension during flexion. Although the skin depends heavily on the terminal branches of the anterior anastomosis, there is a better blood supply originating medially.5,6 Since the beginning of TKA in 1971, most surgeons recommend a straight, anterior midline approach for TKAs in patients without previous scars of the knee.7

Constant passive motion decreases skin oxygen tension further. Aggressive knee flexion in the early postoperative period and higher tourniquet pressures induce skin hypoxia. Less aggressive rehabilitation in the immediate postoperative period and the perioperative administration of systemic oxygen may minimize these problems.8,9 Yashar et al10 reported that high-flexion constant passive motion (70°-100° flexion started in the recovery room) was associated with increased knee flexion during hospitalization, but wound necrosis requiring medial gastrocnemius coverage occurred in 1 of 104 patients.

If poor wound healing or skin necrosis occurs after TKA, early recognition of the problem minimizes the risk of deep infection. There is no consensus as to what stage of the complication intervention should occur, but adequate wound care, including identification of infection, debridement, and early appropriate defect coverage, should be the main points to consider.

Whether to observe and wait or operate early is the question. It is essential not to ignore the early stage of complication but also to make decisions about therapy without concrete knowledge. Necrotic skin must be removed. If the aspiration has yielded a negative culture and cell count, an arthrotomy may not be necessary. In patients exposed to multiple risk factors concerning wound complications, avoidance or delayed use of constant passive motion and early range-of-motion exercises might be beneficial in reducing the development of skin necrosis.11 In our patient we delayed the use of passive motion until the acute inflammatory reaction was solved. During this period the patient achieved prudent assisted mobilization.

As described by Wadia et al,12 a high index of suspicion, negative cultures, and a failure of response to antibiotics should alert the treating clinician to the diagnosis of pyoderma gangrenosum.

A specific management protocol has to be applied to each knee on the basis of the size and depth of the wound, the presence of infection, and the quality of soft tissue. Primary treatment is local wound care, debridement, and then skin grafting or coverage with a fasciocutaneous flap, pedicled muscle flap, or free muscle transfer.11,13 The medial gastrocnemius flap has become the most utilitarian of the available reconstructive methods. A lateral gastrocnemius flap is a good option in patients with lateral soft tissue deficiency. These flaps may be used in conjunction with a skin graft as needed, but it is futile to turn any flap over an active infection.14 The patient in this study did not require any muscle flap coverage. The limitations of such a procedure may outweigh the potential risks, and arthrodesis and amputation are appropriate alternatives.

In our patient, successful wound healing and a functioning TKA were eventually achieved. Skin necrosis developed on the wound, but the integrity of the deep planes in all phases of the pathogenesis allowed us to follow the evolution of the necrosis with a nonsurgical procedure and then cover the nonepithelial area with autologous skin grafting.

There are many local and systemic strategies to optimize wound healing after TKA. Postoperative wound complications (draining and/or necrosis) must be differentiated from deep infection because the 2 problems require distinctly different modes of treatment. It is useful to perform an aspiration prior to initiating antibiotic treatment and then treat the wound with accurate local care; this reduces the seriousness of inflammation infection and prepares the patient for all following and possible treatment.1,9 In our patient the wound was prepared first with vacuum-assisted closure (Kinetic Concepts Inc) therapy and then with skin grafting with an excellent result.

Soft tissue defects after TKA are a severe problem that can even result in the loss of the prosthesis or limb. Well-planned strategies are necessary for sufficient soft tissue reconstruction, resulting in optimal functional and aesthetic results. Early recognition and treatment (surgical debridement, local wound care, and soft tissue reconstruction) allowed us to achieve this result. For best results, interdisciplinary treatment by orthopedic surgeons, plastic surgeons, microbiologists, and physiotherapists is mandatory.

References

  1. Vince KG, Abdeen A. Wound problems in total knee arthroplasty. Clin Orthop Relat Res. 2006; (452):88-90.
  2. Møller AM, Pedersen T, Villebro N, Munksgaard A. Effect of smoking on early complications after elective orthopaedic surgery. J Bone Joint Surg Br. 2003; 85(2):178-181.
  3. Kim YH, Cho SH, Kim JS. Total knee arthroplasty in bony ankylosis in gross flexion. J Bone Joint Surg Br. 1999; 81(2):296-300.
  4. Ries MD. Skin necrosis after total knee arthroplasty. J Arthroplasty. 2002; 17(4 suppl 1):74-77.
  5. Johnson DP, Houghton TA, Radford P. Anterior midline or medial parapatellar incision for arthroplasty of the knee. A comparative study. J Bone Joint Surg Br. 1986; 68(5):812-814.
  6. Colombel M, Mariz Y, Dahhan P, Kénési C. Arterial and lymphatic supply of the knee integuments. Surg Radiol Anat. 1998; 20(1):35-40.
  7. Insall J. A midline approach to the knee. J Bone Joint Surg Am. 1971; 53(8):1584-1586.
  8. Johnson DP. The effect of continuous passive motion on wound-healing and joint mobility after knee arthroplasty. J Bone Joint Surg Am. 1990; 72(3):421-426.
  9. Johnson DP, Eastwood DM, Bader DL. Biomechanical factors in wound healing following knee arthroplasty. J Med Eng Technol. 1991; 15(1):8-14.
  10. Yashar AA, Venn-Watson E, Welsh T, Colwell CW Jr, Lotke P. Continuous passive motion with accelerated flexion after total knee arthroplasty. Clin Orthop Relat Res. 1997; (345):38-43.
  11. Kovacs L, Zimmermann A, Juhnke P, Taskov C, Papadopulos NA, Biemer E. Soft tissue defects as a complication in knee arthroplasty. Surgical strategies for soft tissue reconstruction [in German]. Orthopade. 2006;35(2):162-168.
  12. Wadia F, Malik MH, Porter ML. Postoperative wound breakdown caused by pyoderma gangrenosum after bilateral simultaneous total knee arthroplasty. J Arthroplasty. 2007; 22(8):1232-1235.
  13. Nahabedian MY, Mont MA, Orlando JC, Delanois RE, Hungerford DS. Operative management and outcome of complex wounds following total knee arthroplasty. Plast Reconstr Surg. 1999; 104(6):1688-1697.
  14. Menderes A, Demirdover C, Yilmaz M, Vayvada H, Barutcu A. Reconstruction of soft tissue defects following total knee arthroplasty. Knee. 2002; 9(3):215-219.

Authors

Drs Patella (Vittorio), Speciale, Patella (Silvio), Moretti, Pesce, and Spinarelli are from the Italian Society of Orthopedic Surgeons, Unità Operativa Ortopedia e Traumatologia II-University of Bari, Bari, Italy.

Drs Patella (Vittorio), Speciale, Patella (Silvio), Moretti, Pesce, and Spinarelli have no relevant financial relationships to disclose.

Correspondence should be addressed to: Antonio Spinarelli, MD, Unità Operativa Ortopedia e Traumatologia II, Azienda Ospedaliera Policlinico Bari, 11 Giulio Cesare Square, 70124, Bari, Italy.

10.3928/01477447-20080801-22

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