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LIPOSUCTION TEXTBOOK
The Tumescent Technique By Jeffrey A. Klein MD

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LIPOSUCTION TEXTBOOK

Chapter 12:
Infections

Liposuction surgeons who use only local anesthesia seem to have a much lower rate of serious postoperative infections than those who use systemic anesthesia. For example, virtually every case of postliposuction necrotizing fasciitis has occurred in association with general anesthesia or heavy IV sedation.

The risk of postoperative infection is a multivariate function of characteristics of the surgeon, patient, procedure, surgical setting,1 and anesthetic agent.2,3 The risks of postoperative pneumonia and intravenous (IV) site infection are determined by anesthetic technique and the type of postoperative analgesia. General anesthesia is often associated with hypothermia, which in turn is associated with increased incidence of postoperative wound infections.4

The tumescent technique minimizes the risk of infections. For example, commercial lidocaine is bactericidal, and lidocaine neutralized with sodium bicarbonate has even more bactericidal action (see Chapter 17). Also, vasoconstriction, hemostasis, and rapid drainage of blood-tinged anesthetic solution minimize the incidence of hematomas and seromas, which further reduces the risk of infection. Nevertheless, localized minor postoperative cutaneous infections have occurred after tumescent liposuction (Figures 12-1 and 12-2).

Prophylactic Antibiotics

Many surgeons routinely recommend prophylactic antibiotics before tumescent liposuction, even though it has an extremely low incidence of infection. Presently, patients receive cephalexin, cefadroxil, or doxycycline, starting the day before surgery and continuing for 6 days.

My preference for preoperative antibiotics derives from a clinical research project on percutaneous absorption of hydrocortisone. After 6-mm suction blisters were created on the volar surface of both forearms, hydrocortisone cream was applied. The blisters were sequentially aspirated and the fluid assayed for hydrocortisone. One patient returned 1 day after the procedure with all eight deepithelialized blister wounds apparently infected. The patient had a sore throat on the day of the experimental procedure. The infections resolved with antibiotic therapy after cultures of her throat and blister wounds demonstrated streptococcal infection.

Pretreatment with antibiotics might minimize the risk of a similar event affecting a liposuction patient and causing liposuction incisions to become infected.

Antibiotics are associated with risks. In addition to allergic drug reactions, liposuction patients who take antibiotics are also at risk for Clostridium difficile–associated, pseudomembranous enterocolitis.

Cautious, proper use of prophylactic antibiotics together with constant adherence to rational infection prevention procedures will minimize the risk of postoperative infections. The risk for wound infection for surgical procedures categorized as clean and clean contaminated was 2.1% and 3.3%, respectively, in the United States from 1987 to 1991.5 I estimate that tumescent liposuction has an infection rate of less than one per 2000 cases.

Mitral Valve Prolapse

Mitral valve prolapse (MVP) is more common in females; as many as 7% of women may have echocardiographic evidence of MVP. The spectrum of clinical severity is wide ranging, from a minimal systolic click murmur to severe mitral regurgitation. The condition may progress over years, but most patients are asymptomatic for their entire lives (see Chapter 9).

MVP is the most common cause of isolated severe mitral regurgitation. The most common symptoms are dysrhythmias. Ventricular premature contractions and paroxysmal supraventricular or ventricular tachycardias may cause palpitations, lightheadedness, and syncope. Atypical chest pain may be vague, substernal, prolonged, poorly related to exertion, and unlike that of angina pectoris. Transient ischemic attacks may be caused by microemboli originating on the roughened mitral valve surface and should be treated with antiplatelet mediations such as aspirin and dipyridamole.

Infective endocarditis may occur in patients with severe MVP and mitral regurgitation. Preoperative antibiotic prophylaxis is appropriate for patients with MVP.

Predisposing Conditions

Excess fluid in the subcutaneous tissue after liposuction is free to move about, as evidenced by postoperative drainage and pitting edema. Bacteria that are suspended in collections of subcutaneous fluid can perform their pathogenic functions, such as multiplying and producing toxins. Because leukocytes must crawl from place to place and cannot swim and intercept invading bacteria, leukocytes are at a disadvantage when defending against an underwater attack from bacteria. Postoperative care that implements open drainage and bimodal compression will rapidly eliminate free subcutaneous fluid and thus minimize the incidence of postliposuction infection.

Infections with tumescent liposuction are extremely rare. As mentioned, certain factors associated with tumescent liposuction totally by local anesthesia minimize the risk of infection. These include the following:

  1. Profound tumescent hemostasis, open drainage, and bimodal compression minimize the risk of hematomas and seromas, which predispose to infection.
  2. Since lidocaine is bactericidal, diffuse infiltration of lidocaine directly into treated tissue reduces the risk of infection.
  3. With an alert, awake patient, diagnosis of inadvertent visceral penetration by a cannula is not delayed.
  4. Elimination of sutures minimizes foreign body reaction, wound inflammation, and incision site infections.
  5. Postoperatively, patients are instructed to shower and bathe daily.

Every liposuction patient is at risk for an infection, and therefore every reasonable precaution against infection should be considered. The most serious infections associated with liposuction include toxic shock syndrome, necrotizing fasciitis, cellulitis, staphylococcal abscess, and rapidly growing atypical mycobacteria (see later discussions).

Toxic Shock Syndrome

Toxic shock syndrome (TSS) is a potentially life-threatening manifestation of Staphylococcus aureus infection. Symptoms include high fever, diarrhea, nausea, vomiting, hypotension, oliguria, conjunctival hyperemia, and a diffuse erythematous rash. TSS has been reported in association with a case of liposuction and abdominoplasty and with a case of abdominal liposuction and fat transfer to the face to treat facial atrophy.6 Perioperative blood transfusions increase the rate of TSS infection from 4% to 25%.7

Abdominal Perforation and Peritonitis

Delayed diagnoses of abdominal perforation with necrotizing fasciitis, IV fluid overload with pulmonary edema, and pulmonary thromboembolism are the three most common fatal complications of liposuction.

With liposuction under general anesthesia, a high probability exists for delayed diagnosis of an inadvertent penetration of the abdominal cavity, with intestinal laceration. If a liposuction cannula causes a bowel perforation under general anesthesia, it might not be immediately appreciated. When the patient awakes after general anesthesia, any complaint of abdominal pain may be dismissed as the expected consequence of abdominal liposuction. Delay beyond 18 to 24 hours results in a serious risk of peritonitis, sepsis, or necrotizing fasciitis. Intraabdominal penetration with intestinal perforation by a liposuction cannula has a mortality rate probably exceeding 50%.

With liposuction totally by local anesthesia, little possibility exists for missing the proper diagnosis after a traumatic bowel perforation. A high suspicion of an intestinal perforation should be followed immediately with an evaluation by a general surgeon. Prompt diagnosis and surgical intervention greatly reduce the risk of a life-threatening infection.

Liposuction is contraindicated immediately after any surgical procedure of the abdomen (e.g., peritoneoscopy) that creates a tract into the peritoneal cavity.8,9 Similarly, a periumbilical hernia is a relative contraindication for abdominal liposuction.

Necrotizing Fasciitis

Necrotizing fasciitis is an infection of the subcutaneous fat (fascia) that usually extends to the overlying dermis.10 The most serious infectious complication of liposuction, it can result from a perforation of an abdominal viscus, inadequate sterilization of surgical instruments, or direct wound contamination by the patient or another person. Early diagnosis and aggressive treatment offer the best chance for survival. Thus the liposuction surgeon must know its clinical presentation and when to suspect the diagnosis and must be aggressive in investigating and confirming the diagnosis and then in implementing treatment.

Necrotizing fasciitis can be suspected but not diagnosed clinically; it should be considered a surgical, anatomic, and pathologic diagnosis. Such a diagnostic process usually requires intense, aggressive efforts. A delay of an hour or two in the diagnosis can mean the difference between life and death.

Necrotizing fasciitis is a rare complication of liposuction surgery. Because the consequences can be rapidly fatal if not diagnosed and treated early, every liposuction surgeon must be aware of this potential problem.

There are two clinical types of necrotizing fasciitis. Type I is a polymicrobial or mixed infection caused by aerobic and anaerobic bacteria. It occurs most often after surgical procedures, in diabetic patients, or in those with severe peripheral vascular disease. The portal of entry can be the skin or a mucous membrane of the mouth, gastrointestinal (GI) tract, or urinary tract.

Severe bacterial infections have been reported in four French patients. Three had areas of skin necrosis, and one had septic shock. A pathogenic bacterium was identified in only two of the patients; one had group A Streptococcus and the other Peptostreptococcus.10a

Type II necrotizing fasciitis is caused by group A betahemolytic streptococci. In contrast with type I, patients with type II usually are younger, often do not have serious medical problems, but do have a history of recent surgery or trauma (blunt or penetrating).11 The skin is the portal of entry but frequently has no apparent break.

Epidemiology

In the general population, most spontaneous nonsurgical cases of necrotizing fasciitis involve some degree of impaired immunity, such as old age, peripheral vascular disease, diabetes, alcoholism, renal failure, liver disease, human immunodeficiency virus (HIV) infection, or immunosuppressive drugs, including chemotherapy, corticosteroids, and nonsteroidal antiinflammatory drugs (NSAIDs). The use of NSAIDs suppresses leukocyte function and early signs and symptoms of group A streptococcal infection, with a possible delay in treatment.

Bacterial contamination from localized infected skin wounds accounts for 80% of cases of necrotizing fasciitis. The remaining cases are the spontaneous result of hematogenous spread.

Mixed aerobic and anaerobic bacteria are present in 70% of all patients with necrotizing fasciitis, aerobic bacteria in 10%, and anaerobes in 20%.12 On average, three to five organisms are isolated per culture specimen. Polymicrobial infections usually reflect the flora present at the site of trauma or surgery, such as the lower GI tract, mouth, or nasal mucosa. The typical aerobic pathogens include group A Streptococcus pyogenes, Staphylococcus aureus, Escherichia coli, and other enterobacteriaceae. Anaereobic bacteria include Bacteroides, Clostridium, Peptostreptococcus, and Fusobacterium species. The initial antibiotic therapy for necrotizing fasciitis involves a broad-spectrum antibiotic. Then the medications are adjusted based on the results of culture and sensitivity.

Approximately 10% of all cases of necrotizing fasciitis are caused by a group A streptococci, with a mortality of 30%13 to 70%.14 Up to half these patients are otherwise healthy. An association with preexisting streptococcal pharyngitis is seen in 10% of patients. For this reason, preoperative oral antibiotics are begun the day before surgery.

Group A Streptococci

Invasive group A beta-hemolytic streptococcal infections can present with a spectrum of clinical manifestations, ranging from “streptococcal toxic shock–like syndrome” to necrotizing fasciitis. The necrotizing fasciitis is characterized by a rapid course with shock, sepsis, multiorgan failure, soft tissue infection, and a high mortality rate. Younger, healthy patients are most often affected after minor local trauma. High-dose antibiotic therapy, intensive care monitoring, and aggressive debridement of necrotic soft tissue are necessary to save the patient’s life.15

An association between group A beta-hemolytic streptococcal necrotizing fasciitis and varicella in children has been recognized for more than 50 years. Necrotizing fasciitis occurs after direct laceration or in contused areas with secondary hematogenous spread.16

Since the 1980s there has been an increased awareness of streptococcal TSS caused by highly invasive, group A beta-hemolytic streptococcal and of group A streptococcal infections associated with shock and organ failure, with or without necrotizing fasciitis.17 Purpura fulminans can also occur.18 Strains of these group A beta-hemolytic streptococci that cause invasive necrotizing fasciitis have been predominantly M-protein types 1 and 3 and produce pyogenic exotoxin A, B, or C or a combination of these.

Group A streptococcal necrotizing fasciitis has occurred in liposuction patients (see Case Reports 12-1 and 12-2) as well as with other cosmetic surgical procedures, including blepharoplasty19 and reduction mammoplasty.20

An important interaction between group A streptococci virulence and host defense mechanisms probably determines the ultimate manifestation of the disease. Two cases have been reported of cervical necrotizing fasciitis as the initial presentation of HIV infection.21 Similarly, group A streptococcal necrotizing fasciitis can occur with diabetes, alcoholism, chronic renal failure, and drug abuse.

Fatal postoperative infections are a risk of any surgery. Surgical training, surgical experience, or hospital surgical facilities cannot eliminate this risk. When an infection does occur, survival depends on earliest possible diagnosis and treatment. Any suspicion of necrotizing fasciitis requires an immediate (emergency) consultation by a general surgeon.

Although necrotizing fasciitis has been reported in association with a purported case of tumescent liposuction, a careful reading of the case report provides no evidence that the procedure was true tumescent liposuction.22 More likely the report represents a case of excessive liposuction of too many areas (thoracic roll/flanks/hips, abdomen, medial thighs, knees) done under systemic anesthesia.

Immunosuppressive Drugs

Immunosuppressive drugs may predispose to postoperative necrotizing fasciitis. Necrotizing fasciitis was reported in an 80-year-old female with blepharospasm and a low leukocyte count after chemotherapy for chronic myeloid leukemia following botulinum toxin injection.23 Antiinflammatory drugs such as NSAIDs, steroids, and combinations of these have been reported in association with group A streptococcal necrotizing fasciitis.24 With the exception of acetaminophen, antiinflammatory drugs and corticosteroids should be avoided during the first 3 to 4 days in the immediate postoperative period to minimize the risk of infections.25,26

NSAIDs suppress white blood cell function and can impair host immunity to streptococcal infection. Acetaminophen is preferred over NSAIDs for analgesia after liposuction.

Liposuction Causes

Liposuction patients are presumably healthy and have a robust immune system. Postliposuction necrotizing fasciitis can be considered an opportunistic infection, most often the result of either polymicrobial contamination or group A streptococcal infection. The polymicrobial form is often the result of the delayed diagnosis of a perforated intestine after abdominal liposuction under general anesthesia. Polymicrobial necrotizing fasciitis has been associated with internal ultrasound-assisted liposuction (internal UAL), perhaps as a result of ultrasound-induced tissue necrosis (see Chapter 29).

Other causes of necrotizing fasciitis include (1) improper sterilization of liposuction cannulas, (2) avascular tissue necrosis of skin or subcutaneous tissue from excessively superficial liposuction or ultrasonic injury, and (3) a pharyngeal carrier of streptococcus, such as the patient or operating room personnel.

Clinical Suspicion

Successful treatment of necrotizing fasciitis depends on a high degree of clinical suspicion and early diagnosis. Early presumptive clinical diagnosis of necrotizing fasciitis is the key factor in maximizing the rate of patient survival. The earliest clinical diagnosis of postoperative necrotizing fasciitis is made by the clinician using an attentive ear rather than a discerning clinical eye. A history of extreme pain is often the earliest hint of a serious problem.

If necrotizing fasciitis is misdiagnosed and treated as cellulitis, the patient will not improve despite appropriate antibiotics. A mistaken diagnosis of deep venous thrombosis (DVT) will also delay appropriate treatment.

The earliest and most common initial symptom of necrotizing fasciitis is severe local pain greater than might be expected based on the skin’s clinical appearance. Therefore, when a postoperative liposuction patient telephones and complains of unusually severe pain, the surgeon must consider the possibility of necrotizing fasciitis. If the clinical history is not sufficient to exclude fasciitis, the surgeon is obligated to examine that patient as soon as possible.

If the surgeon cannot rule out the possibility of necrotizing fasciitis, an immediate consultation and evaluation by another surgeon should be considered. Necrotizing fasciitis is a surgical disease, and patients admitted to a nonsurgical service will have delayed surgical treatment. By the time that the skin has developed the typical woody consistency, discoloration, or bullae, the disease is usually far advanced and the chance of survival poor.

Early signs of necrotizing fasciitis, which may be subtle and difficult to see, include skin that first appears slightly red and edematous. The presence and proximity of a cutaneous wound or surgical incision site, no matter how small in size or trivial in appearance, may be the best evidence distinguishing infection from DVT.

Clinical Signs

The earliest visible clinical lesions appear pale, blue-gray, or purple.27 Often, bullae formation eventually appears. A rapidly spreading area of painful induration with dusky or bright-red ecchymoses and violaceous bullae often indicates an advanced stage of an invasive streptococcal infection. The presence of bullae and severe pain together with other risk factors should be sufficient to trigger an aggressive diagnostic workup with blood cultures, laboratory studies, soft tissue radiographs, aspiration of bullae and subcutaneous tissue for bacterial culture and Gram stain, and early surgical exploration.

By the time that the cuticular lesions are plainly visible, the disease is rather widespread. When skin lesions are visible, palpation of the affected subcutaneous tissue may reveal a hard, woody consistency. Crepitance is present in 30% of patients and is especially common in those with diabetes.

The diagnosis is easily made late in the course of necrotizing fasciitis. The late clinical signs and significant evidence of necrotizing fasciitis include (1) a hard tactile density that extends beyond the visible margins of the affected tissue, (2) rapid onset of bullae and necrotic skin, (3) crepitus palpation, (4) absence of ascending lymphangitis, (5) failure to respond after 24 to 48 hours of antibiotic treatment for cellulitis, and (6) lack of response to treatment for DVT.

Laboratory Diagnosis

Patients with necrotizing fasciitis often show elevated levels of serum creatinine, creatine phosphokinase, and aspartate transaminase. These laboratory findings, as well as polymorphonucleocytosis with a left shift, in the appropriate clinical setting, should be sufficient to justify prompt surgical exploration.

The definitive diagnosis requires direct surgical examination of the fascia. A biopsy is done for histologic analysis by frozen section, as well as careful cultures for aerobic and anaerobic bacteria. Early, accurate diagnosis of necrotizing fasciitis has been reported using a frozen-section tissue biopsy obtained at the bedside by an open incisional biopsy.28 Punch biopsies should not be used because of the risk of false-negative results caused by insufficient sampling. Histologic analysis typically shows severe intravascular coagulation within affected tissue.29

Blood cultures should be obtained before beginning therapy with IV antibiotics.

Gram-positive cocci found by fine-needle aspiration of subcutaneous fluid or skin bullae should lead to early surgical intervention.30 Needle aspiration for culture and sensitivity testing will help refine the optimal selection of antibiotics. The standard rapid streptococcal diagnostic kit typically used for the diagnosis of streptococcal pharyngitis has been reported to be a useful adjunct in the diagnosis of group A streptococcal necrotizing fasciitis.31

Standard radiographic views should be obtained as soon as possible but should not delay surgical exploration. Radiography typically shows gas and abscess formation in necrotizing fasciitis. Delayed surgical treatment is more common in the absence of suspicious radiographic findings. Negative x-ray findings also should not delay surgical exploration.

Magnetic resonance imaging (MRI) with gadolinium contrast is more accurate in predicting necrosis or pyomyositis than laboratory tests, such as myoglobinuria or elevation of serum creatine kinase or lactate dehydrogenase. MRI is extremely useful in confirming the diagnosis, determining the need for surgical intervention, and delineating the extent of the necrotizing fasciitis.32 MRI is also a valuable tool for establishing the diagnosis of group A streptococcal necrotizing fasciitis, but it should not delay early surgical intervention.33

Computed tomography (CT) can reveal asymmetric fascial swelling, fat stranding, gas tracking, and abscesses and thus can assist in the diagnosis of suspected necrotizing fasciitis.34

Treatment

As soon as the diagnosis of group A streptococcal necrotizing fasciitis is seriously considered, the patient should be immediately admitted for intensive care (e.g., burn unit) and for surgical exploration. The polymicrobial profile and the fulminating clinical course require initial treatment with high doses of IV antibiotics. IV fluid replacement and nutritional and blood pressure support are essential. Rapid confirmation of the tentative diagnosis is vital and must be followed immediately by aggressive surgical debridement.

Initial Antibiotic Therapy. High-dose IV antibiotic therapy should be initiated with broad-spectrum antibiotics. The antibiotic mix can be modified later according to the results of the preliminary bacterial culture and sensitivity testing. The choice of antibiotic therapy should be made after consultation with an infectious disease specialist. The Gram stain will guide initial therapy pending the results of the culture and sensitivity.

For group A streptococcal infections, clindamycin suppresses both toxin and M-protein synthesis and is more effective than penicillin.35 Combination therapy, consisting of clindamycin and an appropriate cephalosporin or vancomycin, is a reasonable initial treatment for gram-positive infections. Mixed gram-negative and gram-positive infections require antibiotics such as ticarcillin-clavulanate or ampicillin-sulbactam.

The ability of azithromycin, erythromycin, clarithromycin, or cefuroxime to modify the course of group A streptococcal or S. aureus soft tissue infection has been compared in a mouse model. All antibiotics were effective against S. aureus infections, with no significant differences among the four antibiotics. In contrast, in streptococcus-infected mice given azithromycin, fewer demonstrated dermonecrosis (P = 0.0004). The effectiveness of azithromycin in these mice may be related to the high and sustained tissue concentrations achieved with this antibiotic.36

Other therapeutic considerations include intramuscular gamma globulin. Hyperbaric oxygen treatment is controversial and has not been shown to be significantly helpful.

Surgical Treatment. Definitive treatment of necrotizing fasciitis requires surgical debridement and antibiotics. A clinical continuum exists between aggressive soft tissue infections (streptococcal necrotizing fasciitis) and less destructive local infections that produce systemic toxicity (streptococcal TSS). These two processes cannot be distinguished by clinical examination. Thus every patient with localized evidence of aggressive soft tissue infection should be explored surgically for evidence of a necrotizing process.

Immediate surgical exploration is imperative to visualize directly the fascia and underlying musculature and to obtain sufficient issue for the mandatory Gram stain and culture. Patients with necrotizing fasciitis who undergo surgery within 24 hours of admission have a 6% mortality rate. With further surgical delay, mortality can be as high as 70%.

Surgical incision, blunt dissection, and packing of the wound with wet gauze are done at least once daily. Additional incisions beyond the infected tissue are usually required to detect the extent of peripheral spread of infection. Widespread radical debridement and amputation are not unusual (Figure 12-3).

Rapidly Growing Mycobacteria

Rapidly growing mycobacteria (RGM) are diagnostically distinguished from other mycobacteria, such as Mycobacterium tuberculosis, by their relatively rapid growth in culture. RGM usually infect skin and subcutaneous tissue, but disseminated disease and localized pulmonary and osteoarticular infections also occur.37-39

The three clinically important species of atypical RGM are Mycobacterium chelonei (chelonae), M. fortuitum (recently divided into three subspecies), and M. abscessus (see following discussion). A fourth pathogenic, rapid grower is M. mucogenicum. Appearing as diphtheroid on Gram stain, these RGM require several days to 2 weeks to grow on initial culture plating. On subculture, however, regrowth always occurs in 5 days or less.

The RGM are important nosocomial pathogens associated with traumatic and postsurgical skin and subcutaneous wound infections. The rapidly growing acid-fast bacteria are clinically indistinguishable, and biochemical separation is usually of interest only for epidemiologic purposes.

The RGM are increasingly recognized as a source of chronic nosocomial infections. The first description of a nosocomial infection caused by RGM was a 1938 report of a postinjection cutaneous abscess.40 Subsequently, numerous reports have attributed postinjection cutaneous abscesses to RGM.41-50 RGM also have been associated with deep surgical wounds involving the sternum and endocarditis.51,52 Automated endoscope-disinfecting machines may become highly contaminated with mycobacteria that resist usual disinfection, causing contamination of bronchoscopes and GI endoscopes.53,54

Taxonomic and Clinical Distinctions

Previously the rapidly growing mycobacteria were divided into two species: M. fortuitum and M. chelonae (chelonei), with M. chelonae subdivided into two subspecies, M. chelonae chelonae and M. chelonae abscessus. Before 1992, many clinical studies did not distinguish between M. chelonae and M. abscessus. After 1992, based on deoxyribonucleic acid (DNA) homology studies, the RGM have been divided into the three distinct species (chelonei, abscessus, fortuitum).55,56 Less than 70% DNA homology exists between M. chelonei and M. abscessus. DNA studies are important in epidemiologic investigations of mycobacterial outbreaks.57-59

Important clinical differences are seen between M. chelonei and M. abscessus. M. chelonei has often been associated with disseminated skin disease in patients with corticosteroidinduced immunosuppression.60 In contrast, besides being associated with surgical wound infections, M. abscessus has been responsible for more than 90% of chronic otitis media infections after placement with tympanotomy tubes.61 Whereas M. chelonei is highly resistant to cefoxitin, M. abscessus tends to be susceptible to cefoxitin.62,63 Both are uniformly susceptible to clarithromycin.

Liposuction Equipment

RGM are unique in that subcultures grow rapidly (within a few days), whereas the initial culture from tissue biopsies may take several weeks before cultures grow. Atypical RGM infections associated with liposuction are most likely the result of inadequately sterilized surgical equipment. These mycobacteria are notoriously resistant to chemical disinfectants. All surgical instruments must be adequately steam sterilized (Case Report 12-3).

Ubiquitous in the environment, RGM have been cultured from tap water, distilled water, and the walls, furniture, and other surfaces within hospitals and medical clinics. M. chelonei and M. fortuitum are highly resistant to antibiotics and disinfectants. In particular, RGM are not killed by antibacterial liquids used for “cold sterilization.” Nine liposuction patients in eight different hospitals in Caracas, Venezuela, were reported to have acquired RGM infections as a result of cold sterilization of liposuction cannulas. All infections manifested within 2 months after liposuction.64

Steam autoclaving is the only reliable method of sterilization. All liposuction cannulas must be steam sterilized under the high pressure of a medical autoclave. Other forms of sterilization are inadequate and below liposuction standards of care.

An international standard of care mandates that all liposuction cannulas be sterilized using a steam autoclave. Similarly, all aspiration tubing, infiltration tubing, syringes, collection canisters, collection bottles, and needles must either be disposable, single-use items or be adequately sterilized in a steam autoclave. Patients expect that all surgical instruments and equipment have been adequately sterilized. It is improper to reuse any tubing, needles, canisters, syringes, or cannulas that have not been adequately steam sterilized.

Cold sterilization of a liposuction cannula, tubing, syringes, canisters, and needles does not meet the internationally accepted standard of care. As noted, cold sterilization does not sterilize certain species of mycobacteria, such as the atypical RGM. Postoperative RGM infections are always a risk, but careful sterilization of instruments and aseptic technique will minimize such risks.

Clinical Presentation

Atypical RGM should be suspected in a postliposuction patient who manifests persistent lesions within a liposuctioned area despite empiric treatment with antistaphylococcal antibiotics. The onset may be delayed for several weeks or months after surgery, and new lesions may continue to appear for many months. At least one patient developed new lesions a year after liposuction surgery. Patients receiving long-term oral corticosteroid therapy appear to be predisposed to cutaneous infections with atypical mycobacteria.

The typical lesion in a liposuction patient is a pink or skin-colored papule or subcutaneous inflammatory nodule that progressively increases in size. As lesions grow progressively larger, they appear more inflamed and erythematous and become abscessed and fluctuant. After aspiration or routine swabbing of an abscess, routine bacterial culture and sensitivity tests show no growth.

Lesions typically appear clinically as tender, erythematous, subcutaneous and cutaneous nodules that progress to focal or interconnected abscesses. Surgery may be delayed weeks to months after clinical appearance of the lesions (Figures 12-4 to 12-8).

Hematogenous spread is uncommon except in immunosuppressed patients. The apparent spread of atypical RGM beyond the site of liposuction has been observed in at least one patient (Figure 12-8, C).

Postoperative RGM infections probably are underdiagnosed among cosmetic surgical patients, including liposuction patients. The diagnosis of postliposuction RGM infection requires a high degree of clinical suspicion and the clinical ability to recognize the characteristic cutaneous lesions. Before the surgeon can initiate the process of obtaining tissue for RGM culture, the surgeon must recognize the clinical possibility of a postoperative RGM infection. The diagnosis of postliposuction RGM infections might be missed for the following reasons:

  1. Many surgeons are unfamiliar with the typical dermatologic appearance of cutaneous RGM. Unless laboratory personnel are provided with a clinical differential diagnosis that includes RGM, the laboratory might not use the specific culture and tissue smear techniques.
  2. Many surgeons might be unaware of the optimal laboratory methods used to confirm the clinical diagnosis of RGM infection. Obtaining tissue for RGM culture requires special technique (see following section).
  3. A high incidence of false-negative mycobacterial cultures occurs among patients with postliposuction RGM infection. I have diagnosed RGM in seven patients, all of whom had liposuction by the same surgeon. In fact, this surgeon had 34 liposuction patients who developed postoperative cutaneous lesions consistent with RGM infection, although positive cultures were obtained from only 12 patients. If positive cultures were required to treat RGM infection, many patients might not be adequately treated.

In my experience with patients who have had positive cultures for RGM, acid-fast bacteria (AFB) have not been detected after routine histologic processing with stains for AFB. Occasionally, a patient suspected of having a RGM infection will have negative RGM cultures but a positive tissue smear for AFB.

Laboratory Diagnosis

Culture and antimicrobial drug sensitivity testing are important and require special procedures. Culture of a RGM is necessary for an accurate diagnosis. Because mycobacteria are often resistant to antibiotics, obtaining good antibiotic sensitivity data is essential.

On clinical suspicion, one or more inflammatory nodules or abscesses should be biopsied. Fluid aspirated from a cutaneous RGM abscess is often negative on culture. The highest probability of obtaining a positive culture requires tissue obtained using at least a 4-mm punch biopsy. The tissue sample should be obtained using local anesthesia consisting of extremely dilute lidocaine and epinephrine; for example, a dilution of less than 1 mg of lidocaine (1 ml of 1% lidocaine and epinephrine) in 10 ml of normal (0.9%) saline (nonbacteriostatic) should be adequate, while also minimizing the antibacterial effects of lidocaine. Bacteriostatic saline should not be used to dilute the lidocaine and should not be substituted for lidocaine for local anesthesia. Although the benzyl alcohol in bacteriostatic saline does produce brief cutaneous local anesthesia after intradermal injection, it might also inhibit the growth of RBG on culture media.

The biopsy specimen should be transported immediately to the laboratory in a sterile, chemical-free test tube containing preservative-free normal saline, which is then placed on ice. Placing the test tube in a plastic bag containing a few ice cubes should suffice.

The selection of the microbiology laboratory to perform the RGM culture and smear should be based on its experience with mycobacteria. Typically the county or regional public health laboratory will have this expertise because of its experience with M. tuberculosis. One should telephone the laboratory in advance to arrange for reception of the specimen and its expeditious processing.

It is important to notify the laboratory when an atypical mycobacterium is suspected because of the special procedures and growth requirements of RGM. Routine culture procedures for M. tuberculosis might suppress the growth of atypical mycobacteria. For example, the optimal temperature for culturing rapid growing atypical mycobacteria is 28° to 30° C (82° to 86° F), which is lower than that normally used for incubation. The laboratory decontamination process used for M. tuberculosis is too harsh for rapidly growing acid-fast bacteria, and false-negative results are likely unless special procedures are used. Bactec AFB (Becton-Dickinson) is a growth medium that uses a carbon radiometric method to identify acid-fast bacteria.

Treatment

The optimal treatment for cutaneous infection from RGM is not yet well defined. In general, cutaneous abscesses should be incised and drained, with extreme care not to contaminate the environment.

One well-studied outbreak of M. abscessus infection was associated with local injections of lidocaine given in a single physician’s office.65 Over 5 months, 350 (18%) of approximately 2000 patients injected with lidocaine developed localized cutaneous abscesses or cellulitis; of the 210 abscesses cultured, 205 were positive for M. abscessus. Therapy with combined surgical excision and 3 to 6 months of treatment with clarithromycin was successful for 95% of 148 patients. In contrast, therapy was successful for less than one third of patients treated with surgery or clarithromycin alone. Clarithromycin may be the drug of choice for disseminated infection by M. chelonei.66

A minimum of 6 months of antibiotic treatment is recommended because of drug resistance. In otherwise healthy patients who have only a few localized foci of infection or abscesses, treatment with oral antibiotics with incision and drainage may be sufficient. In most cases, clarithromycin is the drug of choice for localized cutaneous and subcutaneous infections. The reference laboratory at the University of Texas Health Center at Tyler has found that about 20% of the cultured organisms are sensitive to either ciprofloxacin or doxycycline. Some physicians prescribe doxycycline as a second oral antibiotic even if it has not been effective with in vitro testing. An occasional mycobacterium is sensitive to cefoxitin.

The recommended dose of clarithromycin for RGM associated with liposuction is 500 mg orally, twice daily, for at least 6 months. Some clinicians recommend polydrug therapy (e.g., doxycycline, 100 mg twice daily, with clarithromycin) to minimize the possibility of developing drug resistance.

More serious or extensive infections may require daily IV antibiotic treatment with either tobramycin or amikacin. The nephrotoxicity and ototoxicity of these aminoglycoside antibiotics require careful evaluation before committing a patient to prolonged use.

M. chelonei wound infections have been reported after cosmetic plastic surgery employing contaminated gentian-violet skin-marking solution.67 Treatment required repeated incision and drainage, as well as long-term antibiotics.

The clinical course can be prolonged and frustrating, with new lesions continuing to appear even after months of antibiotic treatment for RGM. At the conclusion of treatment, clinically apparent lesions should be biopsied again and tissue submitted for culture.

Viruses

HIV-positive patients may have a relatively increased risk for perioperative infections after liposuction. Thus HIV infection is a relative contraindication for cosmetic surgery.

Furthermore, protease inhibitor drugs are metabolized by cytochrome P450 3A4, which also metabolizes lidocaine. The potential for an adverse drug interaction between protease inhibitors and lidocaine is another relative contraindication for tumescent liposuction.

Hepatitis C virus (HCV) was identified relatively recently, and much is still unknown about its mode of transmission. No available immunization protects health care workers from hepatitis C. Because HCV infections can lead to fatal chronic infections and have been associated with malignant hepatomas, liposuction may be contraindicated in an HCV-positive patient. Medical staff should not be exposed to a potentially fatal infection merely for a cosmetic surgical procedure.

Laboratory tests for hepatitis C antibody are available, but a certain percentage of HCV-positive tests are false-positive results. A positive test should be followed up by a more specific immunologic test.

Dermatologic Aseptic Technique

Different specialties have different approaches to aseptic surgical technique. In skin cancer surgery, for example, surgeons who use local anesthesia for office-based surgery certainly use different techniques than those who use general anesthesia or heavy IV sedation in a hospital setting.

Dermatologic surgical aseptic technique often does not conform to hospital operating room standards. Many dermatologic surgeons do not always wear masks, caps, or full sterile gowns when excising large skin cancers and performing complex repairs. Nevertheless, hospital infection control nurses would be envious of dermatologists’ low rate of postoperative wound infections.

I experienced one troubling postliposuction wound infection, a small staphylococcal abscess on the medial thigh. I had mistaken the focal erythema, warmth, tenderness, and swelling for a postoperative panniculitis and treated the patient with prednisone, 10 mg daily. Within a few days an abscess developed, which was incised and drained on an outpatient basis. Subsequently the wound healed rapidly, and the patient had no visible scar or evidence of the postoperative infection.

Many years ago, when incisions were closed by sutures, I also encountered postoperative inflammation at an incision site on the distal medial knee on six occasions.

Dermatologic surgeons may find standard hospital operating room procedure and aseptic technique somewhat irrational as applied to liposuction. For example, before liposuction of multiple areas, nurses scrub the patient, and the surgeon dons a mask, hat, sterile surgical gown, and pair of sterile surgical gloves. Frequently, however, the surgeon wears the same pair of gloves throughout the procedure.

No matter how well a patient’s skin is prepared with an aseptic scrub, bacteria readily contaminate a surgeon’s glove after a few minutes of touching, squeezing, and grabbing the patient’s skin. When such a contaminated glove grasps the shaft of a cannula, it is increasing the risk of a surgical infection. From my perspective, wearing a sterile surgical gown is not as important as changing gloves more frequently and not touching the shaft of a liposuction cannula.

Box 12-1 lists other measures to reduce the risk of infection after liposuction.

References

  1. Nichols RL: Surgical wound infection, Am J Med 91 (suppl 3B):54S-64S, 1991.
  2. Bennett SN, McNeil MM, Bland LA, et al: Postoperative infections traced to contamination of an intravenous anesthetic, propofol, N Engl J Med 333:147-154, 1995.
  3. Nichols RL, Smith JW: Bacterial contamination of an anesthetic agent, N Engl J Med 333:184-185, 1995.
  4. Kurz A, Sessler DI, Lenhardt R: Perioperative normothermia to reduce the incidence of surgical-wound infection and shortened hospitalization, N Engl J Med 334:1209-1215, 1996.
  5. Culver DH, Horan TC, Gaynes RP, et al: Surgical wound infection rates by wound class, operative procedure, and patient risk index, Am J Med 91 (suppl 3B):152S-157S, 1991.
  6. Rhee CA, Smith RJ, Jackson IT, et al: Toxic shock syndrome associated with suction-assisted lipectomy, Aesthetic Plast Surg 18:161-163, 1994.
  7. Wheatley T, Veitch PS: Effect of blood transfusion on postoperative immunocompetence, Br J Anaesth 78:489-492, 1997.
  8. Talmor M, Hoffman LA, Lieberman M: Intestinal perforation after liposuction: a case report and review of the literature, Ann Plast Surg 38:169-172, 1997.
  9. Ovrebo KK, Grong K, Vindenes H: Small intestinal perforation and peritonitis after abdominal suction lipoplasty, Ann Plast Surg 38:642-644, 1997.
  10. Stone DR, Gorbach SL: Necrotizing fasciitis: the changing spectrum, Dermatol Clin 15:213-220, 1997.
  11. Vermeulen C, Serra M, Roujeau JC: Deaths related to liposuction, N Engl J Med 341:1000-1001, 1999 (letter).
  12. Stevens DL: Myositis and fasciitis. In Root RK, editor: Clinical infectious diseases, New York, 1999, Oxford University Press.
  13. Brook I, Frazier EH: Clinical and microbiologic features of necrotizing fasciitis, J Clin Microbiol 33:2382-2387, 1995.
  14. Stevens DL, Tanner MH, Winship J, et al: Severe group A streptococcal infections associated with a toxic shock–like syndrome and scarlet fever toxin A, N Engl J Med 321:1-7, 1989.
  15. Schwartz B, Elliott JA, Butler JC, et al: Clusters of invasive group A streptococcal infections in family, hospital, and nursing home settings, Clin Infect Dis 15:277-284, 1992.
  16. Broll R, Eckmann C, Kujath P, Bruch HP: [Streptococcal toxic shock–like syndrome], Chirurg 69:806-812, 1998.
  17. Nothwang J, Ulrich C: Necrotising fasciitis: cryptogenic infection following posttraumatic immunopathy? Arch Orthop Trauma Surg 118:167-171, 1998.
  18. Stevens DL: The flesh-eating bacterium: what’s next? J Infect Dis 179 (suppl 2):S366-S374, 1999.
  19. Sellers BJ, Woods ML, Morris SE, Saffle JR: Necrotizing group A streptococcal infections associated with streptococcal toxic shock syndrome, Am J Surg 172:523-527, 1996.
  20. Jordan DR, Mawn L, Marshall DH: Necrotizing fasciitis caused by group A streptococcus infection after laser blepharoplasty, Am J Ophthalmol 125:265-266, 1998.
  21. Eugster T, Aeberhard P, Reist K, Sakmann K: [Necrotizing fasciitis caused by beta-hemolytic streptococci with fatal outcome—a case report], Swiss Surg 3:117-120, 1997.
  22. Mohammedi I, Ceruse P, Fontaine P, et al: [Cervical necrotizing fasciitis disclosing HIV infection], Ann Otolaryngol Chir Cervicofac 114:228-230, 1997.
  23. Gibbons MD, Lim RB, Carter PL: Necrotizing fasciitis after tumescent liposuction, Am Surg 64:458-460, 1998.
  24. Latimer PR, Hodgkins PR, Vakalis AN, et al: Necrotizing fasciitis as a complication of botulinum toxin injection, Eye 12:51-53, 1998.
  25. Chaplain A, Gouello JP, Dubin J: [Acute cervical necrotizing fasciitis of pharyngeal origin: possible role of steroidal and non-steroidal anti-inflammatory agents: apropos of 5 cases], Rev Laryngol Otol Rhinol (Bord) 117:377-380, 1996.
  26. Birkinshaw R, O’Donnell J, Sammy I: Necrotizing fasciitis as a complication of steroid injection, J Accid Emerg Med 14:52-54, 1997.
  27. Browne BA, Holder EP, Rupnick L: Nonsteroidal antiinflammatory drugs and necrotizing fasciitis, Am J Health Syst Pharm 53:265-269, 1996.
  28. Misago N, Narisawa Y, Ryu S, et al: Necrotizing fasciitis due to group A streptococci: a clinicopathological study of six patients, J Dermatol 23:876-882, 1996.
  29. Majeski J, Majeski E: Necrotizing fasciitis: improved survival with early recognition by tissue biopsy and aggressive surgical treatment, South Med J 90:1065-1068, 1997.
  30. Stamenkovic I, Lew PD: Early recognition of potential fatal necrotizing fasciitis, N Engl J Med 310:1689-1693, 1984.
  31. Lille ST, Sato TT, Engrav LH, et al: Necrotizing soft tissue infections: obstacles in diagnosis, J Am Coll Surg 182:7-11, 1996.
  32. Ault MJ, Geiderman J, Sokolov R: Rapid identification of group A streptococcus as the cause of necrotizing fasciitis, Ann Emerg Med 28:227-230, 1996.
  33. Brothers TE, Tagge DU, Stutley JE, et al: Magnetic resonance imaging differentiates between necrotizing and non-necrotizing fasciitis of the lower extremity, J Am Coll Surg 187:416-421, 1998.
  34. Drake DB, Woods JA, Bill TJ, et al: Magnetic resonance imaging in the early diagnosis of group A beta streptococcal necrotizing fasciitis: a case report, J Emerg Med 16:403-407, 1998.
  35. Wysoki MG, Santora TA, Shah RM, Friedman AC: Necrotizing fasciitis: CT characteristics, Radiology 203:859-863, 1997.
  36. Stevens DL: Invasive group A streptococcal disease, Infect Agents Dis 5:157-166, 1996.
  37. Barg N: Comparison of four antibiotics in a murine model of necrotizing cutaneous infections caused by toxigenic Streptococcus pyogenes and Staphylococcus aureus, J Antimicrob Chemother 42:257-260, 1998.
  38. Rotman DA, Blauvelt A, Kerdel FA: Widespread primary cutaneous infection with Mycobacterium fortuitum, Int J Dermatol 32:512-514, 1993.
  39. Wallace RJ, Swenson JM, Silcox VA, et al: Spectrum of disease due to rapidly growing mycobacteria, Rev Infect Dis 5:657-679, 1983.
  40. Rodriguez-Barradas MC, Clarridge J, Darouiche R: Disseminated Mycobacterium fortuitum disease in an AIDS patient, Am J Med 93:473-482, 1992.
  41. da Costa Cruz JC: Mycobacterium fortuitum um novo bacilo acido-resistente patogenica para o homem, Acta Med (Rio de Janeiro) 1:298-301, 1938.
  42. Vandepitte J, Desmyter J, Brochier J, Gatti F: Une nouvelle affection à mycobactéries, l’abcès post-injection à M. fortuitum, Ann Soc Belg Med Trop 42:555-560, 1962.
  43. Vandepitte J, Desmyter J, Gatti F: Mycobacteria, skin, and needles, Lancet 2:691, 1969 (letter).
  44. Owen M, Smith A, Coultras J: Granulomatous lesions occurring at site of injection of vaccines and antibiotics, South Med J 56:949-952, 1963.
  45. Inman PM, Beck A, Brown AE, Stanford JL: Outbreak of injection abscesses due to Mycobacterium abscessus, Arch Dermatol 100:141-147, 1969.
  46. Borghans JGA, Stanford JL: Mycobacterium chelonei in abscesses after injection of diphtheria-pertussis-tetanus-polio vaccine, Am Rev Respir Dis 107:1-8, 1973.
  47. Gremillion DH, Mursch SB, Lerner CJ: Injection site abscesses caused by Mycobacterium chelonei, Infect Control 4:25-28, 1983.
  48. Abscesses in an allergy practice due to Mycobacterium chelonae, Ga Epidemiol Rep 6:2, 1990.
  49. Wegner JD, Spika JS, Smithwick RW, et al: Outbreak of Mycobacteria chelonae infection associated with the use of jet injectors, JAMA 264:373-376, 1990.
  50. Toth EL, Boychuk LR, Kirkland PA: Recurrent infection of continuous subcutaneous insulin infusion sites with Mycobacterium fortuitum, Diabetes Care 18:1284-1285, 1995.
  51. Centers for Disease Control and Prevention: Infection with Mycobacteria abscessus associated with intramuscular injection of adrenal cortex extract—Colorado and Wyoming, 1995-1996, MMWR 45:713-715, 1996.
  52. Kuritsky JN, Bullen MG, Broome CV, et al: Sternal wound infections and endocarditis due to organisms of the Mycobacterium fortuitum complex, Ann Intern Med 98:938-939, 1983.
  53. Hoffman PC, Fraser DW, Robicsek F, et al: Two outbreaks of sternal wound infections due to organisms of the Mycobacterium fortuitum complex, J Infect Dis 143:533-541, 1984.
  54. Fraser VJ, Jones M, Murray PR, et al: Contamination of flexible fiberoptic bronchoscopes with Mycobacterium chelonae linked to automated bronchoscope disinfection machine, Am Rev Respir Dis 145:853-855, 1992.
  55. Maloney S, Welbel S, Daves B, et al: Mycobacterium abscessus causing pseudoinfection traced to an automated endoscope washer: utility of epidemiologic and laboratory investigation, J Infect Dis 163:1150-1153, 1991.
  56. Lévy-Frébault V, Grimont F, Grimont PAD, David HL: Deoxyribonucleic acid relatedness study of Mycobacteria fortuitum–Mycobacteria chelonae complex, Int J Syst Bacteriol 36:458-460, 1986.
  57. Kusunoki S, Ezaki T: Proposal of Mycobacterium peregrinum sp nov, nom rev, and elevation of Mycobacterium chelonae subsp abscessus (Kusunoki et al) to species status: Mycobacterium abscessus comb nov, Int J Syst Bacteriol 42:240-245, 1992.
  58. Hector JSR, Pang Y, Mazurek GH, et al: Large restriction fragment patterns of genomic Mycobacterium fortuitum DNA as stain-specific markers and their use in epidemiologic investigation of four nosocomial outbreaks, J Clin Microbiol 30:1250-1255, 1992.
  59. Wallace RJ Jr, Zhang Y, Brown BA, et al: DNA large restriction fragment patterns of sporadic and epidemic nosocomial strains of Mycobacterium chelonae and Mycobacterium abscessus, J Clin Microbiol 31:2697-2701, 1993.
  60. Wallace RJ Jr, Silcox VA, Tsukamura M, et al: Clinical significance, biochemical features, and susceptibility patterns of sporadic isolates of Mycobacterium chelonae–like organism, J Clin Microbiol 31:3231-3239, 1993.
  61. Wallace RJ Jr, Brown BA, Onyi GO: Skin, soft tissue, and bone infections due to Mycobacterium chelonae chelonae, importance of prior corticosteroid therapy, frequency of disseminated infections, and resistance to oral antimicrobials other than clarithromycin, J Infect Dis 166:405-412, 1992.
  62. Franklin DJ, Starke JR, Brady MT, et al: Chronic otitis media after tympanostomy tube placement caused by Mycobacterium abscessus: a new clinical entity? Am J Otol 15:313-320, 1994.
  63. Swenson JM, Wallace RJ Jr, Silcox VA, Thornsberry C: Antimicrobial susceptibility of five subgroups of Mycobacterium fortuitum and Mycobacterium chelonae, Antimicrob Agents Chemother 28:807-811, 1995.
  64. Wallace RJ Jr, Brown BA, Onyi G: Susceptibilities of Mycobacterium fortuitum biovar fortuitum and the two subgroups of Mycobacterium chelonae to imipenem, cefmetazole, cefoxitin, and amoxicillin-clavulanic acid, Antimicrob Agents Chemother 35:773-775, 1991.
  65. Centers for Disease Control and Prevention: Rapidly growing mycobacterial infection following liposuction and liposculpture—Caracas, Venezuela, 1996-1998, JAMA 281: 504-505, 1999.
  66. Villanueva A, Calderon RV, Vargas BA, et al: Report on an outbreak of postinjection abscesses due to Mycobacterium abscessus, including management with surgery and clarithromycin therapy and comparison of strains by random amplified polymorphic DNA polymerase chain reaction, Clin Infect Dis 24:1147-1153, 1997.
  67. Wallace RJ Jr, Tanner D, Brennan PJ, Brown BA: Clinical trial of clarithromycin for cutaneous (disseminated) infection due to Mycobacterium chelonae, Ann Intern Med 119:482-486, 1993.
  68. Safranek TJ, Jarvis WR, Carson LA, et al: Mycobacteria chelonae wound infections after plastic surgery employing contaminated gentian violet skin-marking solution, N Engl J Med 317:197-201, 1987.

Figure 12-1 Early staphylococcal infection on left medial thigh first presented as simple local inflammation. Previous attempt to aspirate fluid for bacterial culture was unsuccessful. Staphylococcal abscess eventually developed and was diagnosed. Outpatient treatment consisted of incision and drainage and oral antibiotics, with almost no residual scarring.

Figure 12-2 Inflammation of medial knee after liposuction was early cellulitis or sterile inflammatory seroma. Bacterial culture was negative, but condition resolved with oral antibiotics. Infections are rare with tumescent local anesthesia.

Figure 12-3 Sequelae of necrotizing fasciitis. Large granulating wound on abdomen is healing by secondary intention after aggressive surgical debridement of necrotizing fasciitis. Infection was precipitated by excessive superficial liposuction, which devascularized skin, causing large bullae and subsequent full-thickness dermal necrosis. Large area of denuded, necrotic, devitalized skin has high risk for infection.

Figure 12-4 Rapidly growing, atypical, mycobacterial infection. Thirty-four patients, all of whom had liposuction by the same surgeon, developed Mycobacterium chelonei infections. Infected lesions appear within skin overlying areas treated by liposuction, such as this woman’s abdomen.

Figure 12-5 This patient demonstrates range of characteristic postliposuction lesions of atypical mycobacteria, varying from Kaposi-like nodules and erythematous fluctuant subcutaneous abscesses to superficial ulcerations. Tissue cultured at room temperature grew Mycobacterium chelonei.

Figure 12-6 This patient had one nonspecific, subtle, pink, scaly plaque on lower abdomen for more than 5 months after liposuction surgery. Bacterial cultures were negative, and common antibiotics were of no apparent benefit. Tissue smear and stain for acid-fast bacteria (bacilli) were positive, whereas tissue cultures and fixed-tissue, histologic Fite stain were negative.

Figure 12-7 Pink-purple fluctuant periumbilical lesion is one of several on this patient with atypical mycobacterial infection. This woman and those in Figures 12-4 to 12-6 were treated by same liposuction surgeon, who soaked cannulas in chemical disinfectant rather than using steam sterilization.

Figure 12-8 Atypical mycobacteria (M. fortuitum). These two patients had liposuction by the same surgeon. A, Incision and drainage (I&D) of abscesses may accelerate healing of mycobacterial abscesses. B, Scars from aggressive I&D of lesions. Not all infections require surgical drainage. Some minor infections may be treated with 6-month course of oral clarithromycin. Aggressive infections may require months of IV therapy with amikacin and gentamicin. C, After abdominal liposuction, this patient developed a new subcutaneous abscess on left breast consistent with distant spread of M. fortuitum beyond site of original surgery. New lesion appeared several months after patient had completed 6 months of oral clarithromycin and IV amikacin therapy.

CASE REPORT 12-1 Fatal Necrotizing Fasciitis
A 25-year-old male had liposuction of the abdomen, flanks, and posterior thighs by systemic anesthesia in a hospital outpatient facility. Immediately after liposuction, the treated areas were infiltrated with 1000 ml of lactated Ringer’s solution (LR) containing bupivacaine and 200 mg of triamcinolone. The incision sites were closed with sutures, and Reston foam was applied to the overlying skin. The patient had risk factors for HIV infection, but there was no laboratory determination of HIV status.
The day after surgery the patient complained of pain in the thighs that was so severe that he could not sleep. Physical examination by the surgeon was unremarkable, and the patient was treated with acetaminophen, codeine, and diazepam. Two days after surgery the patient became lethargic and intermittently incoherent; on examination he was tachypneic and dehydrated with mottled skin. He was admitted to the hospital, but despite debridement of necrotic tissue, he died the next day, 4 days after surgery, from fulminant streptococcal necrotizing fasciitis, septicemia, and renal failure.
Discussion. Severe pain was the presenting symptom for this case of necrotizing fasciitis. Despite rigorous aseptic operating room conditions, this patient died from a streptococcal infection. The surgeon, the surgical staff, and the patient’s roommate all had negative bacterial cultures.
Reston foam is applied to skin over areas treated by liposuction to minimize bruising; its application may hinder a subsequent clinical examination of the skin. The indication for postliposuction intralesional triamcinolone is not well defined. Some physicians might be concerned about a corticosteroid adversely affecting phagocytosis and cellular immune response. Antibiotics were not taken the day before surgery, but whether this might have prevented the infection cannot be known. Unusual infections are a risk with any surgery, despite every reasonable precaution.

 

CASE REPORT 12-2 Streptococcal Necrotizing Fasciitis
A 28-year-old female 152 cm (5 feet) tall and weighing 70 kg (154 pounds) with previous abdominal liposuction had liposuction of the abdomen, hips, and anterolateral thighs for her second liposuction procedure. After subcutaneous infiltration of 2500 ml of LR with lidocaine and epinephrine, liposuction removed 2750 ml of aspirate. Incisions were closed with 6-0 nylon, and Reston foam and a compression garment were applied.
Approximately 36 hours after liposuction the patient was seen at midnight because of continued burning pain in her left outer thigh, which had not improved with ice packs and Vicodin. Skin examination revealed normal-appearing skin comparable to her right leg, but she had tenderness over the outer thigh. She was given 8 mg of morphine and a Compazine suppository to take home.
Later that morning (approximately 48 hours after surgery) the patient was brought to the surgeon’s office because of bleeding from the right thigh. Examination showed swelling and bluish discoloration of the left thigh. In particular the medial thigh had necrotic skin, and needle aspiration yielded serous fluid and air (or gas). Also, discoloration and bleb formation were seen on the left hip and buttock area beyond the area of liposuction. Blood pressure was 70/palpable.
The surgeon correctly diagnosed necrotizing fasciitis, andthe patient was transferred to a major medical center for definitive care.The patient survived severe streptococcal necrotizing fasciitis after left hip disarticulation and extensive debridement of the abdomen, left buttock, back, flank, and right anterior thigh.
Discussion. Although the specific type of liposuction was not specified, the surgeon may have used ultrasonicassisted liposuction (UAL) on the abdomen. UAL has been recommended for use in areas that have previously been treated by liposuction, such as the abdomen in this case. Intense ultrasonic energy can cause local tissue necrosis, injure nutrient blood vessels and lymphatic vasculature, and impair the normal inflammatory response to bacterial contamination. UAL may predispose to necrotizing fasciitis.
In both these cases of group A streptococcal necrotizing fasciitis, incisions were closed with sutures, Reston foam was applied, and compression garments were used. The first hint of prodromal necrotizing fasciitis was intense pain requiring narcotic analgesia. The early clinical appearance of the skin was unremarkable, and the correct diagnosis was delayed until the appearance of visible skin changes. Reston foam might have obscured an adequate early clinical examination of the skin.

 

CASE REPORT 12-3 Mycobacterial Infection
A surgeon had at least 34 liposuction patients develop postoperative clinical signs of cutaneous and subcutaneous RGM infections. Twelve of these patients had positive RGM cultures; other patients had negative cultures but positive tissue smears with stains for acid-fast bacteria. Most patients had typical clinical skin lesions that did not respond to antistaphylococcal antibiotics but did respond to antimicrobial therapy directed at RGM.
During this same period, no other forms of postliposuction bacterial infections were seen, as often occurs when a surgeon attempts to sterilize surgical instruments by soaking them in a cold antiseptic solution. RGM are notoriously resistant to chemical sterilization and liquid disinfectants.
Discussion. Apparently the surgeon was using liposuction cannulas that contained a rubber O-ring that functioned as a gasket between the cannula and its handle. Because rubber O-rings do not tolerate the high temperatures of a steam autoclave, the surgeon opted to sterilize his cannulas by soaking them in a cold antiseptic solution. It was also alleged that the surgeon’s office procedures for steam autoclave sterilization were inadequate and that the surgeon reused aspiration tubing after washing it with tap water. During an epidemiologic investigation an identical strain of RGM was cultured from the office tap water.

 

BOX 12-1 Minimizing the Risk of Infections
1.   Perform open drainage and bimodal compression to reduce free fluid in the subcutaneous space and thus decrease the risk of rapidly spreading an infection.
2.   Do not allow anything to touch a cannula shaft other than the skin at the incision site and the subcutaneous fat. Use a fresh, unused, sterile gauze pad to wipe off the cannula. Once the surgeon’s gloved hand has touched the patient’s skin, it should not touch the cannula shaft.
3.   Change gloves more frequently, for example, each time the patient is placed in a different position or each time a new area is treated.
4.   Use sterile, disposable, single-use suction tubing to connect the liposuction cannula handle to the suction apparatus.
5.   Always autoclave cannulas. It is never sufficient simply to soak a cannula in a cold sterilizing solution.
6.   Immediately before tumescent liposuction of a given area, scrub the area with surgical soap and disinfectant, such as chlorhexidine gluconate. Scrub the area again if the patient touches the surgical area or if contamination is suspected.
7.   Encourage patients to shower and wash with antibacterial soap every day after surgery.
8.   Avoid placing incisions too close to the perineal area during liposuction of the inner thighs.
9.   Begin antibiotic prophylaxis with oral medication the day before surgery.
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