Elective cosmetic surgery procedures are associated

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1 Case Report Reza Jarrahy, MD; Jason Roostaeian, MD; Matthew R. Kaufman, MD; Cristopher Crisera, MD; and Jaco H. Festekjian, MD The authors are from the Division of Plastic and Reconstructive Surgery, UCLA Medical Center, Los Angeles, CA. Toxic shock syndrome (TSS) is a serious, potentially life-threatening condition resulting from an overwhelming immunological response to an exotoxin released by Staphylococcus aureus. TSS has rarely been described as a complication after elective aesthetic plastic surgery. We present here the case of a patient who underwent abdominoplasty after massive weight loss and had a near-fatal case of TSS 6 weeks after surgery. Prolonged use of closed suction drains may have been the ultimate source of virulent bacterial growth leading to systemic toxicity. To our knowledge, TSS has not been reported as a complication after abdominoplasty, nor has a case with such a delayed presentation of the disease been described. (Aesthetic Surg J 2007;27: ) Elective cosmetic surgery procedures are associated with risks common to all surgical techniques, including infectious, hemorrhagic, neurologic, and even lethal complications. Any thorough consultation must include a discussion of these risks when obtaining informed consent from patients. However, because of their rarity, potentially lethal complications from outpatient body contouring surgery are likely not elaborated on during preoperative counseling. We present here the case of a patient who underwent elective abdominoplasty and had toxic shock syndrome (TSS) 6 weeks after surgery, resulting in multisystem organ failure. TSS is an infectious disease caused by Staphylococcus aureus and group A Streptococcus species. If left untreated, it can rapidly pursue an aggressive course and even culminate in death. It has been identified as a potential outcome of many different surgical procedures. 1 To our knowledge, however, it has not been reported as a complication after abdominoplasty, nor has a case with such a delayed presentation of the disease been described. Case Report The patient was a 47-year-old woman with a medical history significant for morbid obesity complicated by non-insulin dependent diabetes mellitus, hypertension, hypercholesterolemia, gastroesophageal reflux disease, obstructive sleep apnea, and urinary stress incontinence. She underwent an uncomplicated laparoscopic Roux-en- Y gastric bypass 2 years before her initial consultation, losing 150 pounds in the interval. At presentation, her medical comorbidities had resolved with the exception of her hypertension and hypercholesterolemia, both of which were well controlled with oral medications. She presented with complaints of constant back pain caused by bilateral breast hypertrophy, grade 3 ptosis of the breasts, and excess lax skin of the proximal upper extremities. She also had excessive skin of the abdominal wall and abdominal wall laxity. She desired correction of her breast volume and shape and aesthetic contouring of her arms. The patient underwent bilateral mastopexy and brachioplasty under general anesthesia as an outpatient and had a normal recovery with a good result. One year after the surgery she presented again, complaining of recurrent dermal infections in the suprapubic crease underlying her large abdominal pannus. She requested removal of the excess tissue, as well as minor contour revisions to the previously operated breasts and subsequently underwent abdominoplasty with abdominal fascial plication, bilateral flank lipoplasty, and lipoplasty of the axillae bilaterally. Two closed suction drains were placed beneath the abdominal wall skin flap. She tolerated the procedure well, with no immediate perioperative complications. She was observed overnight and discharged on the morning of postoperative day 1 with instructions for drain and wound care. She was followed up regularly as an outpatient and had an unremarkable early recovery. The drains put out 50 to 80 ml 162 A ESTHETIC S URGERY J OURNAL ~ MARCH/APRIL 2007

2 of clear serous fluid each day during the first several weeks after the operation. Four weeks after surgery, the patient presented with a 4 6-cm area of erythema in the left lower quadrant, overlying the incision, which was mildly tender to palpation. She had no fever, leukocytosis, or any other signs or symptoms consistent with a deep tissue or intraabdominal infection. There was no change in the serous quality of her drain output. An ultrasound examination of the abdomen revealed three noncontiguous areas of fluid accumulation beneath the abdominal wall, none greater than 1 cm in diameter. She was admitted to the hospital with a diagnosis of abdominal wall cellulitis and was treated with intravenous antibiotics. Her cellulitis and focal abdominal wall tenderness resolved after 72 hours of antibiotic therapy, and she was discharged home on the fourth day of admission with an additional 1-week course of oral antibiotics. She continued to do well at home until 2 weeks later (6 weeks after surgery), when she presented to the emergency department complaining of recurrent abdominal wall erythema associated with severe and diffuse tenderness, fever, chills, nausea, a vesicular rash of the anterior and posterior trunk, and a generalized sense of malaise. The patient was febrile and appeared toxic on arrival, and subsequently became obtunded, tachycardiac, and hypotensive. On physical examination, her entire abdominal wall was erythematous. The fluid in her drains appeared murky and contained exudative debris. A computed tomographic scan of the abdomen revealed fluid under the abdominoplasty flap, as well as diffuse edema of the abdominal wall but no evidence of an abscess or subcutaneous emphysema. The patient quickly progressed to respiratory failure, necessitating endotracheal intubation and mechanical ventilation. She suffered an anterior wall myocardial infarction and had heart failure requiring multiple intravenous inotropic agents. Serum electrolytes revealed that the patient had acute kidney failure, and she was placed on continuous hemodialysis. Cultures of the fluid in her drains subsequently grew out S aureus. She was admitted to the intensive care unit for management of toxic shock syndrome. A small incision was made in the lower abdominal surgical wound at the bedside to explore the abdominal wall. There was no purulence, and the fascia appeared healthy. The suction drains were removed, and the wound was packed open. Cultures from the wound also grew S aureus. The patient was started on broad-spectrum antibiotics and Xigris, a recombinant form of human-activated protein C, to which she responded well. She was weaned from cardiopulmonary support and extubated 5 days after admission. Her renal function returned to normal within 1 week, and hemodialysis was stopped. She was discharged home 11 days after admission. The patient continued to do well at home, with stable cardiopulmonary function, but she required ongoing treatment for some of the late sequelae of toxic shock syndrome, including bilateral sensorineural hearing loss and skin desquamation. The open wound in the lower abdominal incision was allowed to heal by secondary intention, which generated a significant contour irregularity. This scar was effectively revised after it had matured completely. Preoperative photographs, taken after her brachioplasty and mastopexy, and postoperative photographs are presented (Figure). Discussion TSS is a rare but severe acute illness characterized by fever, widespread vesicular rash, and potential progression to multisystem organ failure. Early sporadic cases of a staphylococcal-induced scarlet fever were reported as early as However, the syndrome was first formally described in 1978 by Todd, 2 who detailed a major systemic illness associated with noninvasive S aureus infections in pediatric patients. In the early 1980s, TSS received significant attention in the medical literature and in the popular media because of an outbreak of the disease among healthy young women associated with the use of high-absorbency tampons. 4 While the syndrome was initially thought only to be associated with S aureus, by the late 1980s, invasive group A Streptococcus species were also found to cause a very similar disease process. 5 The incidence of TSS is currently reported to be between 1-2/100, In a Center for Disease Control review of 5296 cases of S aureus TSS reported from 1979 to 1996, including both menstrual and nonmenstrual cases, the median age for all patients with TSS was 22 years; 93% of patients were female. In nonmenstrual cases 18.3% developed after surgical procedures, 11.5% occurred postpartum or after abortion, and 23.1% originated from nonsurgical cutaneous lesions. Between 1979 and 1996, there was a significant decline in the number of menstrual TSS cases reported, but essentially no change in the number of nonmenstrual cases. The case fatality rate for menstrual TSS declined from 5.5% to 1.8% during the study period, whereas nonmenstrual TSS decreased from 8.5% to 6% during the same period. 6 The annual incidence of nonmenstrual cases of TSS now exceeds that of menstrual cases. However, it is disturbing to note that the incidence of both may be rising. 7 The current theory behind the pathogenesis of both A ESTHETIC S URGERY J OURNAL ~ MARCH/APRIL

3 A C B D E F Figure. A, C, E, Preoperative views of a 47-year-old woman who had undergone brachioplasty and mastopexy following massive weight loss. B, D, F, Postoperative views taken after recovery from S aureus mediated TSS. Results are 4 months after abdominoplasty with abdominal fascial plication, bilateral flank lipoplasty, lipoplasty of the axillae bilaterally, and minor contour revisions to the breasts. 164 Aesthetic Surgery Journal ~ MARCH/APRIL 2007 Volume 27, Number 2

4 Staphylococcus and Streptococcus TSS is that the offending organisms produce powerful immunostimulatory exotoxins, which in turn contribute to the end-stage organ damage. The toxins belong to a large family of pyrogenic toxins that are known to non-selectively stimulate T-cell activation and proliferation. These toxins are referred to as super antigens (SAGs) because of their ability to stimulate nearly 20% of all circulating T-cells, compared with the ability of conventional antigens to stimulate, on average, only 1 in 10,000 T-cells. 8, 9 The immense expansion of T-cells results in a massive release of cytokines, including TNF-, interleukin-1, and interleukin-6. These are responsible for most of the severe consequences of TSS, such as vascular collapse, hypotension, and shock. 10 The diagnostic criteria for Staphylococcus and Streptococcus TSS established by the CDC are presented in the Table. The signs and symptoms of TSS develop rapidly and overwhelmingly, even in healthy individuals. In postsurgical cases, the onset of symptoms often occurs on the second postoperative day, but initial symptoms have been reported to present up to 65 days after surgery. 11 Because of cytokine-mediated increases in vascular permeability, TSS is characterized by vasodilation and subsequent Table. CDC definitions for staphylococcal and streptococcal TSS hypotension, hypoalbuminemia, and generalized edema. Disseminated intravascular coagulation is also commonly associated with TSS, and, if unchecked, the disease may progress to multisystem organ failure, including myocardial suppression, pulmonary failure with acute respiratory distress syndrome, kidney failure, and liver failure. 10 The treatment of TSS is characterized by immediate and aggressive multisystem support. The goal of the initial resuscitation period is to maintain systemic blood pressure through the use of intravenous fluids and vasopressors. Depending on the systems involved, mechanical ventilation, inotropic support, hemodialysis, and even liver transplantation may be required. 12 In conjunction with this supportive care, a source of infection should be sought and a determination of any potential benefit of surgical intervention should promptly be made. While it remains unclear whether antibiotics alter the overall course of TSS, the use of broad-spectrum antimicrobial agents is recommended. Therapy is narrowed to cover target organism(s) once they are identified. 13 Antibiotics that target protein synthesis mechanisms, such as clindamycin, have been shown to halt exotoxin production in vitro and are therefore preferred. 14 Staphylococcal TSS CDC case definition for toxic shock syndrome requires presence of the following 5 clinical criteria: Temperature >38.8 C Low blood pressure Widespread red flat rash Shedding of skin, especially on palms and soles, 1-2 weeks after onset of illness Abnormalities in 3 or more of the following organ systems: Gastrointestinal: vomiting or diarrhea Muscular: severe muscle pain Hepatic: decreased liver function Renal: raised urea or creatinine levels Hematologic: bruising due to low blood platelet count Central nervous system: disorientation or confusion Mucous membranes: red eyes, mouth, and vagina due to increased blood flow to these areas Streptococcal CDC case definition for Streptococcal TSS requires isolation of group A streptococci and hypotension with 2 or more of the following clinical criteria: Renal impairment: decreased urine output Coagulopathy: bleeding problems Liver problems Rash that may shed, especially on palms and soles, 1-2 weeks after onset of illness Difficulty breathing Soft tissue necrosis including necrotizing fasciitis, myositis and gangrene A ESTHETIC S URGERY J OURNAL ~ MARCH/APRIL

5 It has been suggested that treatment with intravenous immunoglobulin can decrease mortality rates in cases of S aureus TSS caused by neutralization of the SAGs, 15 but there have been no controlled experimental trials of intravenous immunoglobulin therapy in human beings to test this theory. Recently, the use of human-activated protein C has been proposed as a means to decrease mortality rates in patients with TSS because of its ability to stem the progress of the inflammatory response. 16 A particular clinical dilemma in the management of TSS lies in the fact that in postsurgical patients an infected surgical wound may have a completely benign appearance until after the disease has become fulminant: a potentially lethal delay in diagnosis. As a result, the surgeon must have a high index of suspicion for the presence of the disease, coupled with a low threshold for taking the patient to the operating room for exploration and debridement of grossly involved tissue. The use of closed suction drains has not been shown to definitively result in increased rates of postoperative infections, but they have been associated with decreases in seroma and hematoma formation in numerous surgical procedures. 17 In this case, it is possible that the prolonged use of drains provided a conduit for exogenous bacterial infection. It would be expected, however, that an infection from an intraoperative break in sterile technique would manifest sooner than 4 weeks postoperatively, when our patient initially presented with cellulitis. The benign appearance of the wound at that time, and its immediate response to intravenous antibiotics, underscore the fact that TSS may have a misleadingly indolent course until it becomes a fulminant, life-threatening disease. It is further possible that our initial treatment of the abdominal wall cellulitis with narrow-spectrum antibiotics might have contributed to selection and growth of the more virulent strain of Staphylococcus, ultimately leading to TSS. Conclusions We have presented a case of S aureus mediated TSS after abdominoplasty. Prolonged use of closed suction drains may have been the ultimate source of virulent bacterial growth leading to systemic toxicity. Despite its rarity, we recommend that surgeons have a high index of suspicion for the presence of this disease and institute early and aggressive means of removing or debriding any source of infection, as any delay in treatment may have dire consequences. We also recommend removal of drains as promptly as possible in the postoperative period. References 1. Odom SR, Stallard JD, Pacheco HO, Ho H. Postoperative staphylococcal toxic shock syndrome due to pre-existing staphylococcal infection: case report and review of the literature. Am Surg 2001;67: Todd JK, Kapral FA, Fishaut M, Welch TR. Toxic shock syndrome associated with phage group I staphylococci. Lancet 1978;2: McCormick JK, Yarwood JM, Schlievert PM. Toxic shock syndrome and bacterial superantigens: an update. Annu Rev Microbiol 2001;55: Shands KN, Schmid GP, Dan BB, Blum D, Guidotti RJ, et al. Toxicshock syndrome in menstruating women: association with tampon use and Staphylococcus aureus and clinical features in 52 cases. N Engl J Med 1980;303: Cone LA, Woodard DR, Schlievert PM, Tomory GS. Clinical and bacteriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med 1987;317: Hajjeh RA, Reingold A, Weil A, Shutt K, Schuchat A, Perkins BA. Toxic shock syndrome in the United States: surveillance update, Emerg Infect Dis 1999;5: Schlievert PM, Tripp TJ, Peterson ML. Reemergence of staphylococcal toxic shock syndrome in Minneapolis-St. Paul, Minnesota, during the surveillance period. J Clin Microbiol 2004;42: Poindexter NJ, Schlievert PM. Toxic-shock-syndrome toxin 1-induced proliferation of lymphocytes: comparison of the mitogenic response of human, murine, and rabbit lymphocytes. J Infect Dis 1985;151: Marrack P, Kappler J. The staphylococcal enterotoxins and their relatives. Science 1990;248: Kotb M. Bacterial pyrogenic exotoxins as superantigens. Clin Microbial Rev 1995;8: Bartlett P, Reingold AL, Graham DR, Dan BB, Selinger DS, Tank GW, et al. Toxic shock syndrome associated with surgical wound infections. JAMA 1982;247: McGilvray ID, Rotstein OD. Management of infection in the surgical patient: an update. Surg Technol Int 2003;11: Bochud PY, Bonten M, Marchetti O, Calandra T. Antimicrobial therapy for patients with severe sepsis and septic shock: an evidencebased review. Crit Care Med 2004;32(suppl):S Schlievert PM, Kelly JA. Clindamycin-induced suppression of toxic-shock syndrome-associated exotoxin production. J Infect Dis 1984;149: Norrby-Teglund A, Ihendyane N, Kansal R, Basma H, Kotb M, Andersson J, et al. Relative neutralizing activity in polyspecific IgM, IgA, and IgG preparations against group A streptococcal superantigens. Clin Infect Dis 2000;31: Brueckmann M, Wizenmann J, Hoffmann U, Seeger M, Bewig B. Clinical and laboratory effects of recombinant human activated protein C in the treatment of a patient with sepsis-induced multiple organ failure. Thromb Res 2003;109: Reid RR, Dumanian GA. A minimalist approach to the care of the indwelling closed suction drain: a prospective analysis of local wound complications. Ann Plast Surg 2003;51: Accepted for publication December 21, Reprint requests: Jason Roostaeian, MD, 1485 North Bundy Dr, Los Angeles, CA Copyright 2007 by The American Society for Aesthetic Plastic Surgery, Inc X/$32.00 doi: j.asj Aesthetic Surgery Journal ~ MARCH/APRIL 2007 Volume 27, Number 2