Fig. 4.1
A 34-year-old male presented to the clinic with chronic ankle pain from numerous inversion ankle injuries. Radiographs revealed a large osseous fragment (figure) over the anterior medial aspect of the ankle. After several months of conservative therapy, it was decided that the patient would undergo arthroscopic debridement of the ankle and removal of loose body. The ankle was debrided arthroscopically, but it was decided during the surgery to remove the fragment via medial ankle arthrotomy. The fragment was removed, and patient was instructed to be non-weight bearing. He presented to the clinic 1 week later ambulating on the affected extremity. A hematoma was present over the medial aspect of the ankle. There was minimal erythema/edema over the hematoma. It was decided to treat in a conservative fashion. For 1 week, he was placed in a posterior splint and instructed to place warm compresses over the dressings. At 1 week, there was increased erythema/edema, and patient was taken to the OR for incision and drainage (Fig. 4.2). Deep cultures were positive for E. coli. One month following surgery, patient was healed with casting and 2 weeks of oral antibiotics
Fig. 4.2
Seroma . A 61-year-old male underwent arthroscopic ankle stabilization. Against medical advice, patient took off his splint and began ambulating. At his 2-week postoperative appointment, he developed a small seroma (a) over the medial portal. Treatment included Betadine dressing with posterior splint for 1 week. One week following his Betadine dressing, there was still small amount of fluid originating from the seroma. The surrounding area had no erythema/edema or purulence. The seroma was treated by placement of full-thickness 3-0 nylon sutures without any debridement (b). The patient was placed in a cast, and this was changed on a weekly basis (total of 3 weeks). The incision healed and the sutures removed. The patient started his physical therapy regimen and has had no further complications
Allergic reactions can be type I anaphylaxis or type IV contact sensitivity. Reactions can occur to any substance or medication used during the surgical procedure. Thus, it is imperative to obtain an accurate history of your surgical patient to minimize potential reactions. Local anesthetics, skin preparation agents, topical antibiotics, and adhesives are among some of the most common offenders.
Local anesthetics are injected often preemptively for intraoperative analgesia and to reduce the amount of general anesthetics required. Local anesthetics fall into one of the two major groups: ester- or amide-type anesthetics. The esters cross-react with para-aminobenzoic acid (PABA) esters and other related compounds and thus have been associated with a higher incidence of allergic reactions. The amide anesthetics which include lidocaine, bupivacaine, etidocaine, and prilocaine are most commonly used in foot and ankle surgery. There have been much fewer incidences of allergic reactions to these drugs.
Skin preparation agents such as povidone-iodine have been shown to cause an acute contact dermatitis in sensitized patients. The iodophor compound slowly releases the iodine. The contact dermatitis consisting of vesicle formation and weeping may develop in the area of the surgical incision and thus predispose the patient to a secondary infection. Treatment typically consists of application of wet dressing and topical steroids. If severe, systemic steroids may be required to treat the adverse reaction. Chlorhexidine gluconate tends to cause little skin irritation and has a very weak sensitizing potential while providing a prolonged bactericidal effect.
Topical antibiotics can produce contact sensitivity. The most common sensitizer is neomycin which causes sensitivity reaction in 6–8% of patients. Bacitracin is often found in many over-the-counter products with neomycin, but alone, it does not appear to be a potent sensitizer. When examining patients with a contact dermatitis, one may mistake it for an infection. It is important to look for vesicle formation and involvement of the skin up to the incision. Typically, a dressing reaction or tape reaction will not involve the incision.
Adhesive allergy can cause severe reaction in many patients. Reactions can include rapid severe blistering or more chronic erythema with skin irritation. It is best to avoid adhesives all together including steri-strips and adhesive products such as Mastisol and Benzoin tincture and hold bandages in place with elastic wraps instead (Fig. 4.3).
Fig. 4.3
(a) and (b) Allergic reaction to Steri-Strip adhesive after bunion surgery. Patient was treated with topical corticosteroids and dry dressings for seepage until symptoms resolved in about 7 days
Surgical site infections (SSIs) are a serious impediment to surgical incision healing. According to the Centers for Disease Control (CDC) , approximately 300,000 are reported each year and have associated costs both economically and in terms of mortality and morbidity [1]. SSIs occur within 30 days of surgery or within 1 year if an implant is used and the infection involves that site. SSIs are classified into superficial and deep . Superficial incision infection involves only the skin and subcutaneous tissue at the incision. Deep incision infection involves the deep tissues including the muscle and fascia (Fig. 4.4). Factors have been identified for both categories of infection in multiple studies. Superficial infections are most commonly seen in patients with previous operations, prolonged duration of surgery, low albumin, and chronic obstructive pulmonary disease, whereas deep infections have been most common in patients with low albumin and previous operations.
Fig. 4.4
A 27-year-old female sustained Weber C ankle fracture . The first image (a) shows the patient 3 weeks following surgery when patient presented with increased pain and edema on the medial incision. There was a small area of incision dehiscence and clinical signs of infection. Patient started on IV antibiotics, and after 48 h of minimal improvement, patient was taken to the operating room. (b) Patient had two sequential debridements in the operating room 48 h apart. Hardware was retained until union was achieved as confirmed with CT. Upon union, the hardware was removed and a wound VAC was placed. Patient healed over the next 4 weeks via secondary intention
The most common pathogen in SSI per CDC is Staphylococcus aureus , which accounts for 30% of infections. This is followed by coagulase-negative Staphylococcus at 13.7%, Enterococcus spp. at 11.2%, E. c ol at 9.6%, and Pseudomonas aeruginosa at 5.6% [2]. It is important to identify the pathogen if possible in treating an SSI in order to administer appropriate antibiotic therapy. It is also important to choose the appropriate prophylactic antibiotic and administer it consistently with the Surgical Infection Prevention Collaborative and the Surgical Care Improvement Project to minimize the surgical wound infection and bacterial load at the surgical site prior to incision.
The guidelines currently state antibiotic administration should be within 60 min prior to injection or incision. The typical prophylactic antibiotic choice in orthopedic surgery is 1 g IV cephalexin and 2 g IV if over 80 kg. In patients with a known allergy to cephalosporins, either 600 or 900 mg of clindamycin can be administered. In patients with previous methicillin-resistant Staphylococcus aureus (MRSA) or sensitivity to clindamycin, 1 g IV vancomycin should be administered over 60 min prior to surgical incision. Intraoperatively, antibiotic should be readministered in any surgical case lasting over 3 h.
Risk factors for SSI can be broken into intrinsic and extrinsic, and several studies have identified both [3–6]. Intrinsic risks are inherent to the patient such as systemic disease, whereas extrinsic risks are due to surgeon, technique, and perioperative issues such as greater blood loss, hypothermia, use of blood products, and surgery time over 2 h.
Understanding which risk factors we can mediate and minimize will help decrease the incidence of SSIs and subsequent incision morbidity. Thus, thorough patient evaluation is vital and proper patient selection important.
Wound dehiscence is almost always related to another complicating issue with the most common being hematoma, wound infection, or premature suture removal. Healing may be affected by wound tension, external trauma, underlying medical comorbidities, and external factors such as smoking. Issues such as hematoma aspiration and early suture removal for infection drainage or hematoma/seroma aspiration can also lead to wound failure (Fig. 4.5).
Fig. 4.5
Anterior ankle incision with proximal wound dehiscence. Note fibrotic tissue in the wound. This required serial debridement and local wound care and went on to heal by secondary intention
Management of the dehisced wound depends on the cause. Typically, wound dehiscence can be treated by local wound care and allowing healing by secondary intention. However, some surgeons may choose to be more aggressive depending on the state of the wound, the patient, and the type of surgery that was performed. If a soft tissue procedure was performed and a superficial wound dehiscence is now present, often with local debridement in the office and ongoing wound care, the wound will heal. Often, one must limit motion of the affected area as well to minimize wound disruption. It is important to minimize excessive fibrous tissue formation along the edges of the incision. This can often require serial, weekly debridements in the office. If a wound dehiscence occurs over an area with retained hardware, typically, it is in the patient’s best interest to address these surgically due to the underlying risk of infection and sequelae of contamination of exposed hardware.
A wound that opens and is recognized within 24 h may be able to be repaired primarily unless there is nonviable material at the base or margins of the incision. The wound should be closed under aseptic technique using the least traumatic suture material (e.g., monofilament nylon). The use of prophylactic antibiotics is controversial and is left to the surgeon’s discretion.
Necrosis of a wound is almost always the result of another complication such as hematoma/seroma, increased tension, infection, or inadequate vascularity. Any of these complications can cause full-thickness tissue loss and require further intervention and repair. When using tissue flaps, necrosis can occur if the dimensions of the flap are not appropriate (i.e., flaps should be no more than three times the width of its base 3:1 length-to-base ratio). Inadvertent cutting, cautery use, or ligation of arterial feeders can also compromise tissue blood flow and viability. Wound tension can lead to ischemia and subsequent necrosis as well. Tobacco use may cause tissue hypoxemia and lead to tissue necrosis. When necrosis occurs, early debridement should be performed only if there is evidence of infection; otherwise, the necrosis should be allowed to fully demarcate prior to debridement (Fig. 4.6).
