Fig. 23.1
Cellulitis of medial ankle
Fig. 23.2
(a, b). Recurrent cellulitis in a patient who had undergone fixation for a tibial plateau fracture. The patient developed osteomyelitis and required implant removal
Acute and Chronic Soft Tissue and Wound Complications
Since there is a natural inflammatory process during wound healing, it may be challenging to differentiate an actual infection from the natural healing process. Normal tissue healing and repair undergoes an inflammatory stage where immune cells such as macrophages consume bacteria and necrotic tissue. This is followed by a stage where precursor cells differentiate into the appropriate cells in the healing of the soft tissue layer. Lastly, the new tissue needs to mature and become stronger through a process known as remodeling, which may take over a year. Clinically, the skin may appear warm and erythematous, have a scab or eschar over the incision or wound, feel indurated, and be tender to palpation. The method of skin closure itself may cause local skin irritation seen more commonly with skin staples as opposed to suture material. The erythema in this case is usually confined to the area around the staples and there is a sharp demarcation between color of the irritated skin and normal surrounding skin. There is also no associated drainage with this condition as may be the case with an infection. In the case of a cellulitis, the erythema is more diffuse and has less of a distinct border in the vicinity of the incision.
Another complication that may be seen acutely is wound edge necrosis. Patient-based factors such as poor nutrition or diabetes may impair the body’s ability to heal an incision leading to wound dehiscence. In this scenario, the body cannot heal from the trauma caused to the skin even in a controlled setting. An extrinsic cause would be tissue strangulation and ischemia from sutures being tied too tightly or having too much tension across the incision or wound. This can lead to wound dehiscence if the necrosis is severe enough (Fig. 23.3).
Fig. 23.3
Wound dehiscence and necrosis within 2 weeks of a primary knee arthroplasty
In such a case, or if the dehiscence is from another cause, it is important to determine the depth of the dehiscence, whether it is superficial and above the fascia or deep extending beyond the fascia. If the dehiscence is superficial, then monitoring the wound and providing local wound care or negative pressure wound therapy to assist in wound closure via secondary intention healing will suffice. If the fascia is involved, wound exploration and revision closure may help avoid prolonged healing and infection.
When the fascial layer is not closed properly or if the closure fails, a hernia can develop. This complication is known to occur after iliac crest bone graft harvest [26]. It can also occur in the thigh or lower leg. This may cause localized pain to the patient and it may be cosmetically displeasing depending on the location and the person’s body habitus.
Additional complications involving soft tissues include walled off fluid collections. One is a collection of serous fluid that superficial, known as a seroma, and the other is an abscess, which implies a collection of purulent material. A seroma may develop around a foreign body or fill in a void in soft tissues that may be created surgically or after trauma. The body may not reabsorb the reactive fluid or a foreign body may irritate the local surrounding tissues and cause the fluid to accumulate as the body protects itself. Both types of fluid collections can cause pain or a mass effect, and seromas may become secondarily infected. If located near the spine, it can cause spinal cord compression.
Both collections will be difficult to see on plain radiographs and warrant more advanced imaging such as ultrasound, CT scans, or MRI with and without contrast. The clinician must take into account the patients presenting symptoms such as systemic signs of infection during the workup of this collection. Labs such as CBC with differential, ESR, and CRP are a good start to check if an inflammatory process is occurring in the body and, at the very least, can serve as a baseline for future trending. If the lab values are elevated, once treatment is initiated, the CRP usually decreases first, within 48–72 h, if the treatment was correct. Radiographically guided percutaneous drainage of abscesses can decompress some of these fluid collections and save the patient a formal irrigation and debridement in the operating room with general anesthesia.
Nonunion or Fixation Failure
Most fractures heal when treated appropriately, but some fractures will fail to heal and develop what is termed a “nonunion.” Certain features are typically necessary for fractures to heal, such as sufficient stabilization, vascularity (or blood flow), absence of infection with appropriate soft tissue coverage, and sufficient host nutrition. On the other hand, there may be risk factors for nonunion as well. These include hypothyroidism, diabetes mellitus, smoking, vitamin D deficiency, and chemotherapeutic agents. The point at which a slowly healing fracture is distinguished from a nonunion can be a function of a clinician’s discretion and may vary from bone to bone. As an example, a typical description of a humeral shaft nonunion is “no evidence of radiographic healing 6 months after an injury” [27].
Three types of nonunion are described: hypertrophic, atrophic, and oligotrophic. A hypertrophic nonunion demonstrates callus around the fracture site. However, the callus does not bridge the fracture site. This scenario is attributed to a lack of stability. The body has the biological capacity to form new bone demonstrated by the callus, but excessive fracture motion prevents the bone from uniting across the fracture site. With an atrophic nonunion, the exact opposite is true. The stability may be adequate, but the local or systemic biologic response to form new bone is lacking, therefore no callus forms. The host’s nutritional status may be inadequate and unable to provide the necessary factors for new bone generation [28]. Oligotrophic nonunions show some capacity to heal, but is insufficient given the needs at the fracture site. One example would be a poor reduction or alignment of a fracture that may be solved by revision of the fracture reduction and more stability.
When fractures do not unite, under physiologic stresses, any metallic implant will mechanically fatigue over time. If the bone does not fail at the bone-implant interface, ultimately the implant will fail. Identifying a failure to progress toward union may allow a surgeon to intervene prior to fixation failure and correct the problem preemptively. Thus, the determination of a “delayed union” may allow fixation implant retention, and a less extensive surgical intervention may allow for successful fracture healing.
Deformity/Malunion
“Deformity” is a broader term when describing how a bone did not heal properly. “Deformity” includes leg-length discrepancy, whereas “malunion” encompasses varus, valgus, rotation, procurvatum, and recurvatum. When reconstructing a bone or a limb, it is important to restore its proper alignment, length, and rotation. Restoring these three factors restores the normal mechanics to the bone with the muscles attached to and acting upon it; the joints above and below that particular bone will consequently be affected.
If, for example, someone sustains a tibia or femur fracture that heals in varus, there are increased joint forces through the medial compartment of the knee, which already sustains 70–80 % of the weight-bearing load of the knee. In order to enable gait, the patient will compensate at the ankle joint, causing a valgus deformity and predisposing the ankle to osteoarthritis from abnormal wear of its cartilage. Gait can also be affected by a sagittal plane deformity such as recurvatum (apex posterior) or procurvatum (apex anterior) deformity of the tibia because the knee cannot fully extend for a proper heel strike or may not generate enough power during toe-off entering the next stride.
Certain bones and joints may tolerate greater levels of deformity. The humerus can tolerate 4–6 times the acceptable deformity of a tibia with acceptable functional outcomes. One such reason has to do with the ability of the glenohumeral joint (shoulder) to compensate for deformity of the humerus since it has such a large range of motion and will still be able to accomplish the goal of positioning the hand where it is necessary in space. Altered forces in the lower extremity, by contrast, rapidly manifest in problems due to the increased demands of weight-bearing during ambulation.
Long-term consequences of deformity and malunion can lead to pain, joint contractures, ligamentous instability or imbalance (contractures and laxity on opposite sides of the joint), and ultimately joint degeneration. Uncorrected deformity with persistent pain and dysfunction may be treatable with joint replacement (arthroplasty). In the setting of joint arthroplasty, the surgery may be more technically difficult if ligaments are imbalanced, and the joint may not perform well without the use of special equipment and possibly customized implants.
Arthritis and Avascular Necrosis
There are several types of arthritis: inflammatory, osteoarthritis, posttraumatic, and septic. Osteoarthritis has four characteristic radiographic signs, which are asymmetric joint space narrowing, subchondral sclerosis, osteophytes, and subchondral cysts. Patients may present with complaints of pain, limited motion, stiffness, especially after periods of immobilization, and limited function. On exam the patient may have an erythematous, warm, edematous, tender joint, with an effusion. The most important condition to rule out in this circumstance is an acutely septic joint. Fevers are typically absent in the setting of an osteoarthritic or posttraumatic arthritic flare and inflammatory markers can be normal. If the patient’s history and clinical picture are unclear, performing a joint aspiration and sending the synovial fluid for gram stain and culture, crystals (to rule out gout), and cell count can rule out infection.
Part of the radiographic workup in posttraumatic arthritis and osteoarthritis especially in the lower extremity weight-bearing joints are weight-bearing radiographs. Avascular necrosis (AVN) results from a vascular insult to the bone’s blood supply. Risk factors include hypercoagulable disorders, chronic alcohol usage, steroids, chemotherapeutic agents, HIV/AIDS, and excessive soft tissue stripping from a trauma or iatrogenic soft tissue stripping. The use of alendronate ® delayed subchondral bone collapse in the femoral head for 2 years with findings of AVN on MRI and bone scan [29]. However, only 10 % of members of the American Association of Hip and Knee Surgeons (AAHKS) treat pre-collapse hip AVN with bisphosphonates [30].
There is questionable efficacy of bisphosphonates for shoulder and knee AVN as well as unknown effects in smaller areas and bones such as scaphoid, lunate, and capitellum. Presenting symptoms of avascular necrosis can be swelling, pain at rest, pain with motion, and restricted motion due to abnormal mechanics of the joint containing the bone with AVN. Treatment consists of identifying reversible causes or underlying disorders and rendering the proper treatment for those. Immobilization or at least decreasing the stress on the affected bone is another initial step of treatment. MRI is more sensitive in detecting avascular necrosis compared to plain radiographs.
Heterotopic Ossification
Bone may form in areas not associated with normal growth or fracture healing. This pathologic condition is known as heterotopic ossification (H.O.). The abnormal bone usually forms in areas of muscle issue, creating painful or limited joint motion. It is most well known for formation about the hip and elbow after trauma or surgery. Risk factors include head or spinal cord trauma and soft tissue damage (i.e., iatrogenic from surgery or from the trauma itself) and in the setting of burn injuries.
There are two methods employed prophylactically to decrease the risk of heterotopic ossification formation in high-risk patients. The first is with nonsteroidal anti-inflammatory drug (NSAID) therapy, and the second is radiation therapy [31, 32]. Indomethacin is commonly administered for 6 weeks. Radiation therapy is performed within a day preoperatively or the first 48–72 h postoperatively (at least in the setting of acetabular surgery).
Workup of heterotopic ossification is performed with plain radiographs and bone scan at times. In the event of surgery, a CT scan of the affected area can help with surgical planning.
When heterotopic ossification causes significant pain or functional limitations, surgical excision is indicated. Outcomes are generally very favorable, but may vary depending on anatomic location. H.O. may involve or abut other crucial structures, such as skin, neurovascular structures, and ligaments. In complex cases, an experienced practitioner must approach surgery cautiously and with careful consideration of risks and anticipated outcomes. Heterotopic ossification can take 6 months to a year or more to fully “mature” before it is excised, or the risk of recurrence may be high (Fig. 23.4).
