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Toxic Shock Syndrome after Surgery: Case Presentation and Systematic Review of the Literature

Celie, Karel-Bart MD*; Colen, David L. MD; Kovach, Stephen J. III MD

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Plastic and Reconstructive Surgery - Global Open: May 2020 - Volume 8 - Issue 5 - p e2499
doi: 10.1097/GOX.0000000000002499



Septic shock is a serious condition, carrying a mortality of up to 50% and representing the second leading cause of deaths in noncardiac intensive care units (ICUs).1,2 First reported in 1978, toxic shock syndrome (TSS) is a particularly insidious subtype of septic shock.3 Although less well-known, it carries a significant mortality rate, higher even than meningococcal septicemia.4 Unlike classic presentations of sepsis, patients with TSS often lack evidence of an overt infection or even bacteremia. Nonetheless, they may rapidly progress to shock and multiorgan failure. The systemic inflammatory response is predominantly caused by exotoxins and enterotoxins that are produced by pathologic strains of bacteria—most commonly SA and beta-hemolytic group A Streptococcus (GAS) species.4

Although there is some awareness of TSS among health-care professionals and even the general public, early reports have led to an association between TSS and the prolonged use of tampons. Changes in tampon manufacturing led to a decrease in the incidence of menstrual TSS, with menstrual TSS accounting for only 55% of TSS in women in the United States by 1986.5 Indeed, 1 French surveillance study in 2008 demonstrated that 65% of staphylococcal TSS cases were nonmenstrual and that these carried a mortality of 22% compared to 0% in menstrual TSS.6

As the epidemiology of TSS has evolved over the recent decades, the relative rate of TSS has risen in postoperative patients.7 Given the paucity of typical signs of sepsis in TSS, its rapid progression, and the high mortality conveyed by this condition, the aim of this paper is to provide an overview of this syndrome as it may present in patients after surgery. We present a case describing our experience with postoperative TSS and a systematic review of the literature.

Patient Presentation

A 57-year-old man with a history of hypertension and daily tobacco use first presented to our institution with a basal cell carcinoma of the frontal and parietal scalp (Fig. 1A). He underwent en bloc excision resulting in a significant calvarial defect requiring titanium mesh cranioplasty and anterolateral thigh (ALT) fasciocutaneous, perforator flap from the right thigh for soft tissue coverage (Fig. 1B and C). The ALT donor site could not be completely closed, so split-thickness skin grafts from the right medial thigh were used. The patient received 3 perioperative doses of cefazolin over the course of 24 hours. The donor site was dressed with Xeroform, Kerlix gauze, and a compressive wrap. The gauze and wrap was removed on postoperative day 5; the Xeroform was left in place over the split-thickness skin graft donor site until the skin reepithelialized. His postoperative course was unremarkable and on postoperative day 7 he was discharged.

Fig. 1.
Fig. 1.:
Initial patient presentation and surgery. A, Preoperative image demonstrating fungating scalp mass. B, Defect following excision of mass and titanium mesh cranioplasty. C, Postoperative image demonstrating ALT flap coverage of defect with a single drain in place.

On postoperative day 9, the patient presented to the emergency department with a 24-hour history of fevers, severe pain on the right lower extremity, and emesis. His mental status was at baseline. On physical examination, he was found to have a fever of 103°F and mean arterial pressures less than 65 mm Hg. Physical examination of the patient’s ALT flap was unremarkable. The right thigh donor site demonstrated mild erythema and edema around the wound margins, but was without any purulent drainage or tissue necrosis. Hypotension was unresponsive to a total of 6 L of intravenous (IV) fluid. Blood cultures were drawn, and he was started on broad-spectrum IV antibiotics. He required emergent intubation in the emergency department and was admitted to the ICU where he required the maximum dose of vasopressors. His lactate peaked at 4.6 mmol/L; his white blood cell count (WBC) at the end of the day of his admission was 32 × 103 cells/μL (up from 10 × 103 cells/μL that same morning). Imaging demonstrated some soft tissue swelling in the right thigh but no fluid collections or evidence of gas along fascial planes. A bedside incision and drainage of his right thigh donor site revealed only viable muscle and subcutaneous tissue without evidence of purulent drainage.

Over the following days, the patient suffered 1 pulseless electrical activity arrest and significant multiorgan dysfunction: his WBC peaked at 51 × 103 cells/μL, urine production fell to 15 mL/h with rising creatinine (0.5 to 4.4 mg/dL), and creatine phosphokinase levels rose to 1,890 U/L. However, with supportive care and antimicrobial treatment, he gradually improved, and on the third day after admission was successfully weaned off vasopressors and extubated. Withdrawal of vasopressors resulted in return of the free flap Doppler signal and right foot (lost due to pressor requirements); however, the left foot remained ischemic.

Blood cultures were persistently negative for growth of organisms. The patient experienced desquamation of the palms of his hands (Fig. 2) and the soles of his feet on the 19th day after admission. He underwent a left below-knee amputation on the 25th day after admission. He was discharged 34 days after admission and was in good health at last follow-up.

Fig. 2.
Fig. 2.:
Desquamation occurred approximately 19 days after surgery. A and B demonstrate the patient’s hands with panel B showing desquamation of the palms. The patient had removed some of the desquamated skin on his palms when the pictures were taken.


We performed a systematic review of the literature to assess reports of TSS after surgery. We searched the PubMed databased using the phrase “toxic shock syndrome” (title) and “surgery” (all fields). We also performed a manual search using the phrase “toxic shock syndrome after surgery.” The criteria for “surgery” that were applied included any procedure that disrupted the epithelial/mucosal barrier by way of intentional instrumentation. Cases of TSS that occurred more than 60 days after surgery were excluded. Non-English language articles and commentaries were excluded. Cases of TSS due to the sole use of nasal packing, facial peels, or burns were excluded. Descriptive statistics and figures were generated using GraphPad Prism version 7.00 for Mac OS X, GraphPad Software, La Jolla, CA, USA.


Two hundred ninety-four titles were identified through PubMed. Four additional unique titles were identified through a manual search. All 298 titles were screened, and 222 titles were excluded based on predetermined criteria. The remaining 76 articles were reviewed in-depth. (see Supplemental Digital Content 1, Nine titles were excluded following this in-depth review. Reasons for exclusion included the comorbid presence of necrotizing fasciitis, unclear timelines or outcomes, and unclear relation between TSS and a surgical procedure. A total of 67 articles describing 96 patients were included in our qualitative review (Fig. 3).

Fig. 3.
Fig. 3.:
Descriptive statistics of collected variables. A, Frequency distribution of patient age (in 5-year increments). Most patients were between 21 and 40 years of age. B, Distribution of days to onset of TSS symptoms or admission. The red bars represent the median (4 days) ± the interquartile range (6.75 days). C, Number of reports by decade. Most reports were published within the first decade since recognition of TSS. D, Frequency distribution of surgical procedure specialties preceding onset of TSS.

In our review series, 38 (39.6%) patients were men and 58 (60.4%) were women. The mean reported patient age was 34.1 years with an SD of 15.5 years and a range from 4 to 73 years; the most commonly reported age group was that between 26 and 30 years of age (Fig. 4A). The median number of postoperative days to onset of symptoms or hospital admission for TSS was 4 days, with an interquartile range of 6.75 days and a range from 1 to 44 days (Fig. 4B). Of the 96 patients, 73 (76%) did not suffer permanent complications. The remaining 23 (24%) patients suffered permanent complications, including additional procedures (eg, hysterectomy, cholecystectomy, skin grafting), amputations, reduced range of motion at a joint, or eventual death (Table 1). Nine (9.38%) patients in our review series eventually expired due to TSS (Table 1). The medical histories of 59 (61.5%) patients were considered noncontributory by the authors of their respective reports (Table 1). An even number of reports of postoperative TSS were published in the past 2 decades (excluding the case presented herein), 19 (28.4%) reports were published between 1990 and 1999, and 26 (38.8%) reports were published between 1980 and 1989 (Fig. 4C). Most of the surgical procedures preceding onset of TSS fell within the domain of plastic surgery, followed by orthopedic surgery and otolaryngology, respectively (Fig. 4D).

Table 1. - Select Variables from Case Reports Meeting Inclusion Criteria of Our Systematic Review
Study Year Patient Age Patient Sex Surgical Procedure Days to Onset Complications/Additional Procedures Mortality Culture Results
Elkbuli et al18 2018 31 F Cesarean section 17 Hysterectomy and bilateral salpingectomy No Clostridium sordellii
Tomura et al8 2017 35 M Right lumbar melanoma excision 6 None No
Komuro et al61 2017 33 F Cesarean section 37 None No
Suga et al62 2016 40 F Mastectomy, SLNB, and immediate subpectoral implant-based reconstruction 10 None No
54 F Mastectomy, SLNB, and immediate subpectoral implant-based reconstruction 8 None No
Chan et al63 2015 5 F Open reduction and K-wiring of lateral condyle fracture 14 None No Pin sites grew enterotoxin A, G, I, and TSST-1-producing SA
Rimawi et al64 2014 23 F Cesarean section 7 Hysterectomy No Alpha-toxin-producing Clostridium septicum
Yadav et al65 2014 25 M Inguinal hernia repair 2 None No
Shimizu et al66 2014 46 M ORIF and fasciotomy for left tibia/fibula fracture 21 None No
Hung and Rajeev20 2013 24 F Total thyroidectomy 2 None No
Al-ajmi et al16 2012 39 F Laparoscopic left salpingectomy 1 Yes Blood grew GAS
31 F Elective tubal ligation 1 Bilateral salpingectomy No Intraperitoneal fluid grew GAS
Tare et al67 2010 36 F Left mastectomy with DIEP flap reconstruction 8 Yes Wound fluid grew TSST-1-producing MRSA
Vendemia and Rohde43 2009 55 F Right tissue expander placement with AlloDerm 35 None No Periprosthetic wound culture grew TSST-1-producing SA
Shoji et al68 2007 61 M Thoracotomy with mediastinal lymph node dissection 5 None No
Jarrahy et al69 2007 47 F Abdominoplasty 44 Anterior wall MI, heart failure, bilateral sensorineural hearing loss No Drain fluid grew SA
Kastl et al70 2007 35 M Rectal mucosal biopsy 1 None No Rectal swab grew pyogenic exotoxin (SpeA, B, F, G, J)-producing GAS
Strenge et al39 2006 45 M Excision of ganglion cyst 3 None No Wound cultures grew SA
Agerson and Wilkins21 2005 40 F TRAM flap reconstruction of right breast; right salpingo-oophorectomy; left tubal ligation 15 None No Abdominal wall abscess grew GAS and Klebsiella
Goksugur et al71 2003 52 M Laparotomy with lymph node sampling 2 None No Blood and wound cultures grew SA
Odom et al72 2001 56 F L2 corpectomy with L1 to L3 interbody fusion and debridement of abscess 2 None No Abscess grew SA*
Gwan-Nulla et al73 2001 48 M Sigmoid colectomy with end colostomy 18 None No Wound culture grew SA
Chadwell et al41 2001 47 M Bilateral polypectomy, total ethmoidectomy, sphenoidotomy, frontal sinusotomy, and right antrostomy 18 None No Nasal stents and blood cultures grew TSST-1-producing SA
Umeda et al11 2000 27 F Suction-assisted lipectomy 2 Meshed skin autograft over 22% TBSA due to repeat debridement No Wound cultures grew SA
Rutishauser et al22 1999 43 M Elective herniotomy 2 Right orchiectomy No Wound cultures grew GAS
55 F Tetanus vaccine administration 4 None No Blood cultures grew GAS
Kato et al74 1999 23 F Internal fixation of humerus fracture 4 Reduced elbow ROM No Wound grew enterotoxin C and TSST-1-producing SA
Birdsall et al75 1999 14 F Closed reduction of proximal humerus and fixation with K wires 14 None No Blood and wound cultures grew TSST-1-producing SA
Kotlarz et al76 1998 62 F Mastoidectomy 3 None No Wound cultures grew enterotoxin B-producing SA
Holm and Mühlbauer44 1998 58 F Bilateral exchange of silicone implants (subglandular) 4 None No 2-mL periprosthetic fluid grew SA
Bitti et al19 1997 29 F Cesarean section 2 - Yes Intraperitoneal cultures grew Clostridium sordellii
Younis et al77 1996 5 M Functional endonasal sinus surgery 10 None No Direct sinus cultures grew toxin-producing SA
7 F Functional endonasal sinus surgery 5 None No Direct sinus cultures grew toxin-producing SA
32 M Functional endonasal sinus surgery 35 None No Blood and sinus cultures grew toxin-producing SA
8 M Functional endonasal sinus surgery 7 None No Blood and sinus cultures grew toxin-producing SA
27 M Functional endonasal sinus surgery 10 None No Direct sinus cultures grew toxin-producing SA
Mills and Swiontkowski23 1996 29 M Tibial hardware removal 2 - Yes Bullous fluid grew 3+ GAS
Grimes et al78 1995 4 F Removal of Steinmann pins from iliac crest 9 - Yes Wound cultures grew SA
4 F Right femoral valgus osteotomy 22 None No Pin sites grew SA
Poblete et al45 1995 21 F Elective augmentation mammaplasty (subglandular) 6 Bilateral transmetacarpal amputations; bilateral BKAs No Blood cultures grew enterotoxin B-producing SA
Graham et al13 1995 42 F Oophorectomy 2 None No 12 out of 12 patients had negative blood cultures
64 F Lumbar sympathectomy 2 None No
15 M Patellar realignment 5 None No
40 F Hysterectomy 4 None No
28 M Excision of navicular bone 4 None No
45 F Cholecystectomy 8 None No
48 F Cholecystectomy 9 None No
26 M Pilonidal cystectomy 5 None No
61 F Breast biopsy 2 None No
26 F Chest tube placemen 4 None No
29 M Nasal septoplasty 1 None No
66 M Percutaneous angioplasty 1 None No
Cederna79 1995 47 F TRAM flap reconstruction of left breast 7 33% of TRAM flap lost; latissimus flap required for coverage No Small amounts of serous fluid from breast and abdomen grew SA
Miller36 1994 45 M L1 laminectomy and discectomy 3 None No Serosanguinous fluid in deep tissue layer yielded light growth of SA
Rhee et al10 1994 36 F Abdominoplasty with suction-assisted lipectomy 3 None No Wound and drain cultures grew SA
43 F Suction-assisted lipectomy 4 None No
Abram et al42 1994 30 M Functional endonasal sinus surgery 1 None No Nasal cultures grew SA
32 F Functional endonasal sinus surgery 1 None No Nasal cultures grew SA
14 F Second-stage endonasal clean-out 1 None No Nasal and throat cultures grew SA
25 F Functional endonasal sinus surgery 21 None No Throat cultures grew SA
8 M Second-stage endonasal clean-out 5 None No Nasal cultures grew SA†
Miller et al80 1994 61 F Endoscopic bilateral ethmoidectomy, sphenoidotomy, maxillary antrostomy, and septoplasty 25 None No Sinus cultures grew SA
Bosley et al9 1993 14 F Mole excision 1 Cardiac arrest, PE Yes Wound culture grew TSST-1-producing SA
Gosain and Larson48 1992 33 F Bilateral breast reconstruction with latissimus dorsi musculocutaneous flaps; immediate silicone implants 28 None No
Shlasko et al12 1991 29 M Pilonidal cystectomy 3 None No
Croall et al81 1989 27 M MCL repair 8 None No Synovial fluid grew enterotoxin B-producing SA
Frame et al82 1988 17 M Prominent ear correction 3 Wound cultures grew TSST-1-producing SA
Tobin et al47 1987 39 F Left permanent prosthesis, right mastectomy with immediate implant-based reconstruction 5 None No Wound cultures grew TSST-1-producing SA
57 F L subpectoral tissue expander 3 None No
29 F Herniorrhaphy and septorhinoplasty 1 None No Nasal cultures grew TSST-1-producing SA
Grayson and Saldana32 1987 20 M Tenolysis of FDS and FDP 35 None No Wound fluid grew enterotoxin B-producing SA
Murphy et al83 1987 40 F Lumpectomy 2 None No Wound discharge grew enterotoxin C-producing SA
Dreghorn et al84 1987 26 M Repair of MCL 5 Reduced ROM at knee No Synovial fluid grew SA
Jacobson and Kasworm33 1986 27 F Septoplasty 1 Right BKA, left Syme’s amputation, Volkmann’s contracture of left forearm No Vaginal and maxillary sinus cultures grew TSST-1-producing SA
34 M Septoplasty 1 None No
29 F Septoplasty 1 None No Nasal cultures grew SA
Wagner and Toback40 1986 26 F Septoplasty 2 None No Nasal cultures grew SA
Giesecke and Arnander46 1986 33 F Bilateral primary augmentation mammoplasty (subglandular) 2 None No Periprosthetic fluid grew enterotoxin F-producing SA
Vanderheyden et al85 1986 30 F Cesarean section 5 None No
Smith et al34 1986 30 M Extensor tenosynovectomy and side-to-side juncture (EDC ring to small finger) 4 None No Wound cultures grew TSST-1-producing SA
Shaffer et al86 1986 44 M Orthotopic liver transplant and right adrenalectomy 16 None No Wound cultures grew SA
Farber et al15 1984 19 M Arthroscopy 1 Cardiopulmonary arrest requiring bypass Yes Synovial fluid grew exotoxin C-producing SA
Beck et al87 1984 73 M Cholecystectomy 28 Yes Small sinus tract grew enterotoxin F-producing SA
Spotkov et al88 1984 21 F Diagnostic laparotomy for bleeding cyst of corpus luteum 7 None No Wound drainage grew enterotoxin A, F-producing SA
Toback et al89 1983 21 M Septorhinoplasty 1 None No Nasal cultures grew SA
Aganaba et al35 1983 26 M Orchidectomy 4 None No Deep wound culture grew enterotoxin F-producing SA
Moyer et al90 1983 18 F Patellar shaving procedure 3 None No Synovial cultures grew SA
60 M Arthrotomy and patellectomy 2 Cholecystectomy No Synovial cultures grew SA
Bresler91 1983 35 F Removal of R breast implant 7 None No Periprosthetic fluid grew SA
Barnett et al92 1983 32 F Right subglandular breast prosthesis exchange 7 None No Periprosthetic fluid grew SA
Thomas et al93 1982 25 F Submucous resection and rhinoplasty 1 None No
Bartlett et al94 1982 31 F Removal of granulation tissue (bilateral augmentation incisions failed to heal) 1 Yes
53 F Vesico-urethral suspension 4 None No Suture abscess grew SA
McClelland et al95 1982 36 M Wide excision with STSG 20 None No
Knudsen et al96 1981 21 F Bilateral primary augmentation mammoplasty 4 None No Right breast cavity grew SA
Silver et al97 1981 34 M Amputation of left index finger due to trauma 3 None No 0.25 cc serous fluid expressed from incision grew SA
*Blood cultures eventually grew SA, but this was too remote from onset of toxic shock symptoms.
†Stool testing was also positive for Clostridium difficile in the patient.
BKA, below-knee amputation; DIEP, deep inferior epigastric artery perforator; EDC, extensor digitorum communis; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; GAS, group A Streptococci; MCL, medial collateral ligament; MI, myocardial infarction; ORIF, open reduction, internal fixation; ROM, range of motion; SA, Staphylococcus aureus; SLNB, sentinel lymph node biopsy; STSG, split-thickness skin graft; TBSA, total body surface area; TRAM, transverse rectus abdominis myocutaneous.

Fig. 4.
Fig. 4.:
Schematic of normal T-cell activation and abnormal T-cell activation induced by superantigen. Note that more inflammatory markers are secreted downstream than are shown in the figure.


The mortality rate in our review (9.38%) is lower than that of other reports; this may reflect publication bias and advances in ICU care over time. The average time between TSS diagnosis/treatment and death was 6.78 days, with a range from 12 hours to 18 days. Mortality tended to occur early (<2 days) when due to the shock itself or late (>14 days) due to systemic complications such as cardiopulmonary arrest. Notably, the surgical procedures that most commonly preceded TSS were those that extensively involved the skin (plastic surgery, orthopedic surgery) or mucosal surfaces (otolaryngology), suggesting that sites colonized with toxin-producing bacteria may result in presentation only after disruption of the integrity of the epithelial or mucosal barrier.

Although our patient suffered TSS after extensive surgery, it is important to note that postoperative TSS may present even after relatively simple procedures. Two papers describe TSS in patients following the removal of skin lesions.8,9 Suction-assisted lipectomy,10,11 pilonidal cyst excision,12,13 surgical biopsy,13,14 arthroscopy,15 and elective tubal ligation16 represent just some of the procedures in our review. Furthermore, our review of the literature demonstrates that patients affected by postoperative TSS are often young and in otherwise good health.

The virulence factors responsible for TSS are produced mainly by Gram-positive organisms, especially SA and GAS. However, they are also known to be produced by some Gram-negative bacteria, Mycoplasma spp., and certain viruses.4,17 In our series of postoperative TSS, most causative organisms, if identified, were GAS or SA—however, 2 reports described very virulent TSS following obstetrical procedures that led to the isolation of Clostridium sordellii.18,19 One of these patients died.19 Six reports included in our review reported cultures that grew beta-hemolytic Streptococcus.14,16,20–23 Streptococcal TSS carries a much higher mortality than staphylococcal TSS, with a mortality rate of up to 80% reported in some of the literature.4,24


Despite rapid deterioration, patients with TSS may not present with evidence of infection. This is because only a critical mass of toxin-producing bacteria with concomitant epithelial or mucosal disruption is needed. It is the toxins produced by the bacteria that cause the presentation as opposed to a runaway infection by any 1 microorganism.

The word exotoxin refers to virulence factors that are genetically encoded and secreted. They are usually heat labile (but not always, eg, SEB, a type of bacterial superantigen17) and are highly toxic. The term enterotoxin refers to exotoxins that have an effect on the gastrointestinal (GI) tract, thereby producing GI symptoms (a prominent feature in most cases of TSS). The causative toxins behind TSS are usually referred to as “superantigens,” a term first used in the 1980s to describe the mechanism by which streptococcal enterotoxin B stimulates T-cell populations.25 Nearly all superantigens are exotoxins, and most are also enterotoxins.26 Of note, the staphylococcal TSS toxin 1 (TSST-1) is responsible for nearly 95% of menstrual TSS and up to 50% of nonmenstrual TSS, making it the most common causative toxin.4,27

The pathogenicity of superantigens is due to the nonconventional activation of T-cells by antigen-presenting cells (APCs). Normally, APCs present processed peptide fragments to T-cell receptors (TCRs) by way of specific peptide-binding grooves in the major histocompatibility class II (MHC II) protein. This selective process results in the activation of only about 0.01% of the T-cell population.4 By contrast, superantigens bind as unprocessed proteins to both the MHC class II protein and TCR (Fig. 4). They are thought to bind to the variable Vβ region of the TCR (although some bind to the α chain), and bind distant from the normal peptide-binding groove on the MHC II protein.4,26,28 This results in the aberrant activation of up to 20%–30% of the T-cell population. Once a superantigen has cross-linked that T-cell and APC, there is a rapid increase in cytokine expression by both cell types. This is thought to be primarily due to the activation of nuclear factor κB.29

Superantigens are extremely potent, with human T-cell sensitivity noted at as little as 1 fg/mL in vitro.17 GI symptoms have been noted with ingestion of less than 1 μg of staphylococcal enterotoxin.30

Clinical Presentation

It has been suggested that the onset of postoperative TSS most commonly occurs by the second postoperative day.26,31 Our review demonstrated widespread variability in the timeline of postoperative TSS; though, Figure 3B shows that most cases became apparent within 10 days.

Of the 96 patients in our review, at least 52 were described as presenting with symptoms that included nausea, vomiting, or diarrhea. This highlights the enterotoxic nature of many superantigens. Furthermore, some manner of pain was frequently reported. For example, 2 reports described patients with severe hand and wrist pain following hand surgery, whereas another described nasal pain in a septoplasty patient.32–34 The pain in TSS has been described as severe and relentless, making it a common impetus for patients to seek medical attention.4

A benign-appearing wound is another common feature of postoperative TSS, and this frequently leads to a delay in diagnosis.4,26,28 Several case reports in our review explicitly noted the normal appearance of surgical wounds, even if these later grew the causative pathogen. For example, 1 report described a normal looking wound that eventually grew enterotoxin F-producing SA from deep swabs.35 Another described an unremarkable wound that yielded “light” growth of SA from minimal serosanguinous fluid within the deep tissue layers.36 Notably, the death of a 14-year-old girl was reported following TSS that developed after mole excision.9 The authors note that although the surgical wound appeared dry and normal, debrided tissue eventually grew TSST-1 producing SA.9

After onset of symptoms, multiorgan failure can occur within as little as 8–12 hours.4 Multiorgan failure is a prominent feature of the clinical case definitions proposed by the Centers for Disease Control and Prevention. These were first developed in 1980 and have undergone only slight modifications, with the most recent update occurring in 2011.37 However, strict adherence to Centers for Disease Control and Prevention criteria may only identify the most severe cases of TSS. The authors noted that a changing understanding of TSS pathophysiology and presentation over time has demonstrated a wider range of severity than originally suggested and that advances in supportive care have likely begun to prevent the most severe manifestations of the disease.37

Less than 5% of staphylococcal TSS present with positive blood culture.4,38 One series of 12 patients who developed postoperative TSS did not show a single patient with positive blood cultures.13 Most commonly, SA was eventually isolated from the surgical wound,11,34,39 and sometimes from nasal40–42 or rectal14 swabs. If foreign bodies were involved in the initial surgery, tissue or fluid around the foreign body frequently grew SA. For example, in cases that involved breast prostheses, SA was frequently isolated from periprosthetic fluid.43–46 In contrast, streptococcal TSS more commonly presents with concomitant bacteremia.4 This was the case for 2 out of 6 reports of streptococcal TSS in our review.16,22

Lastly, a late but characteristic feature of TSS is a peeling rash known as desquamation. This classically occurs on the palms of the hands or the soles of the feet (Fig. 2); however, several case reports indicated that it may also develop on the trunk or over regions affected by rash.9,10 Although typically desquamation occurs within 10–21 days of symptom onset,4 there was widespread variability in our report ranging from 347 to 3548 days postoperatively. In the series of 12 postoperative TSS patients described earlier, 11 developed desquamation.13


Treatment for TSS involves source control, supportive care, and antibiotic treatment. Source control is a principle that is particularly relevant to postoperative patients, as surgical wounds must be considered a potential source despite the lack of typical signs of infection.4 Once sepsis is diagnosed, antibiotic treatment should be started within an hour,26 and the requisite cultures should be acquired before this. We recommend that wound cultures accompany exploration of the wound early on in addition to standard blood cultures if a postoperative patient presents with symptoms suggestive of TSS. Initial surgical interventions should involve visual inspection for fascial involvement, debridement of any necrotic tissue, surgical biopsy for histopathology, and deep bacterial cultures.49 If packing or any foreign objects are present, they should be removed. If suspicion for staphylococcal TSS is high, a nasal swab may be considered.

Appropriate initial antibiotic therapy has been shown to reduce mortality in sepsis,50 and empiric therapy should be targeted at SA and GAS species. Given the potential for Methicillin-resistant Staphylococcus aureus (MRSA), vancomycin, or linezolid should be considered in cases of suspected staphylococcal TSS.51 Linezolid has the added benefit of reducing exotoxin release, including TSST-1.4,52 In cases of suspected streptococcal TSS, penicillin G remains an antibiotic of choice. This is because despite decades of use, Streptococcus pyogenes remains exquisitely sensitive to penicillin.4,49,53 In addition to linezolid, clindamycin, erythromycin, rifampin, and fluoroquinolones have all been demonstrated to reduce bacterial exotoxin release by up to 90%.51 Clindamycin is a common choice in combination with vancomycin or penicillin G.4,51

Resuscitation and supportive care should be performed according to current sepsis guidelines.54 This includes maintaining a target mean arterial pressure of 65 mm Hg in patients requiring vasopressors and administering at least 30 mL/kg of IV crystalloid within the first 3 hours.54

The IV administration (usually 1–2 g/kg) of polyclonal, neutralizing intravenous immune globulin (IVIG) has long been proposed as a potential adjunct in the treatment of TSS. These immunoglobulins can block the activation of T-cells by both staphylococcal and streptococcal superantigens,4 in addition to improving bacterial opsonization, phagocytosis, and destruction.49,55 An observational cohort study in 1999 reported a mortality benefit conveyed by IVIG in cases of streptococcal TSS,56 although this study may have been confounded by the fact that IVIG recipients were also more likely to receive surgery. Results from the INSTINCT trial, which was a randomized, double-blinded, placebo-controlled trial, were published in 2017. They demonstrated no significant difference between the placebo and intervention groups with regard to both functional status and mortality.57 However, a recent meta-analysis demonstrated a reduction in mortality from 33.7% to 15.7% in patients with clindamycin-treated streptococcal TSS who received IVIG.58 Therefore, there may be a role for IVIG in streptococcal TSS, although further evidence is needed. The utility of IVIG in staphylococcal TSS has been even less well determined. There is currently a European, multicenter, placebo-controlled, randomized trial underway that aims to assess the utility of IVIG in pediatric patients with TSS.59 It hopes to enroll 156 patients and is expected to complete in 2022. Of note, the Infectious Disease Society of America has pointed to the heterogeneity between preparations of IVIG, which may result in variance between studies.49,60


TSS is a rapidly progressive, potentially fatal complication of surgery that frequently presents with a benign-appearing wound. As the incidence of gram-positive sepsis increases, and as MRSA colonization becomes more common in populations, surgeons must be aware of the potential subclinical presence of toxin-producing strains. Importantly, our review shows that TSS should not be excluded despite young patient age, patient health, or relative simplicity of a procedure. Symptoms such as fever, rash, pain out of proportion to examination, and diarrhea or emesis should prompt inclusion of TSS in the differential diagnosis. It is our hope that the case presented herein, and the systematic review, will aid surgeons in the earlier recognition and treatment of this dangerous syndrome.


1. Wheeler AP, Bernard GRTreating patients with severe sepsis. N Engl J Med. 2008;340:207–214.
2. Martin GS, Mannino DM, Eaton S, et al.The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med. 2009;348:1546–1554.
3. Todd J, Fishaut M, Kapral F, et al.Toxic-shock syndrome associated with phage-group-i staphylococci. Lancet. 1978;2:1116–1118.
4. Lappin E, Ferguson AJGram-positive toxic shock syndromes. Lancet Infect Dis. 2009;9:281–290.
5. Gaventa S, Reingold AL, Hightower AW, et al.Active surveillance for toxic shock syndrome in the United States, 1986. Rev Infect Dis. 1989;11suppl 1S28–S34.
6. Descloux E, Perpoint T, Ferry T, et al.One in five mortality in non-menstrual toxic shock syndrome versus no mortality in menstrual cases in a balanced French series of 55 cases. Eur J Clin Microbiol Infect Dis. 2008;27:37–43.
7. Hajjeh RA, Reingold A, Weil A, et al.Toxic shock syndrome in the United States: surveillance update, 1979–1996. Emerg Infect Dis. 1999;5:807–810.
8. Tomura Y, Osada SI, Akama T, et al.Case of toxic shock syndrome triggered by negative-pressure wound therapy. J Dermatol. 2017;44:e315–e316.
9. Bosley AR, Bluett NH, Sowden GToxic shock syndrome after elective minor dermatological surgery. BMJ. 1993;306:386–387.
10. Rhee CA, Smith RJ, Jackson ITToxic shock syndrome associated with suction-assisted lipectomy. Aesthetic Plast Surg. 1994;18:161–163.
11. Umeda T, Ohara H, Hayashi O, et al.Toxic shock syndrome after suction lipectomy. Plast Reconstr Surg. 2000;106:204–207; discussion 208.
12. Shlasko E, Harris MT, Benjamin E, et al.Toxic shock syndrome after pilonidal cystectomy. Report of a case. Dis Colon Rectum. 1991;34:502–505.
13. Graham DR, O’Brien M, Hayes JM, et al.Postoperative toxic shock syndrome. Clin Infect Dis. 1995;20:895–899.
14. Kastl S, Horstkotte MA, Schäfer HJ, et al.“Anal angina”–pelvic sepsis and streptococcal toxic shock syndrome after rectoscopy and mucosal biopsy. Int J Colorectal Dis. 2008;23:225–226.
15. Farber BF, Broome CV, Hopkins CCFulminant hospital-acquired toxic shock syndrome. Am J Med. 1984;77:331–332.
16. Al-ajmi JA, Hill P, O’ Boyle C, et al.Group A streptococcus toxic shock syndrome: an outbreak report and review of the literature. J Infect Public Health. 2012;5:388–393.
17. Fraser JD, Proft TThe bacterial superantigen and superantigen-like proteins. Immunol Rev. 2008;225:226–243.
18. Elkbuli A, Diaz B, Ehrhardt JD, et al.Survival from clostridium toxic shock syndrome: case report and review of the literature. Int J Surg Case Rep. 2018;50:64–67.
19. Bitti A, Mastrantonio P, Spigaglia P, et al.A fatal postpartum Clostridium sordelli associated toxic shock syndrome. J Clin Pathol. 1997;50:259–260.
20. Hung JA, Rajeev PStreptococcal toxic shock syndrome following total thyroidectomy. Ann R Coll Surg Engl. 2013;95:457–460.
21. Agerson AN, Wilkins EGStreptococcal toxic shock syndrome after breast reconstruction. Ann Plast Surg. 2005;54:553–556.
22. Rutishauser J, Funke G, Lütticken R, et al.Streptococcal toxic shock syndrome in two patients infected by a colonized surgeon. Infection. 1999;27:259–260.
23. Mills WJ, Swiontkowski MFFatal group a streptococcal infection with toxic shock syndrome: complicating minor orthopedic trauma. J Orthop Trauma. 1996;10:149–155.
24. McCormick JK, Yarwood JM, Schlievert PMToxic shock syndrome and bacterial superantigens: an update. Annu Rev Microbiol. 2001;55:77–104.
25. White J, Herman A, Pullen AM, et al.The V beta-specific superantigen staphylococcal enterotoxin B: stimulation of mature T cells and clonal deletion in neonatal mice. Cell. 1989;56:27–35.
26. Silversides JA, Lappin E, Ferguson AJStaphylococcal toxic shock syndrome: mechanisms and management. Curr Infect Dis Rep. 2010;12:392–400.
27. Bohach GA, Fast DJ, Nelson RD, et al.Staphylococcal and streptococcal pyrogenic toxins involved in toxic shock syndrome and related illnesses. Crit Rev Microbiol. 1990;17:251–272.
28. Pinchuk IV, Beswick EJ, Reyes VEStaphylococcal enterotoxins. Toxins (Basel). 2010;2:2177–2197.
29. Trede NS, Castigli E, Geha RS, et al.Microbial superantigens induce NF-kappa B in the human monocytic cell line THP-1. J Immunol. 1993;150:5604–5613.
30. Tranter HSFoodborne staphylococcal illness. Lancet. 1990;336:1044–1046.
31. Strausbaugh LJToxic shock syndrome. Postgrad Med. 1993;94:107–118.
32. Grayson MJ, Saldana MJToxic shock syndrome complicating surgery of the hand. J Hand Surg Am. 1987;12:1082–1084.
33. Jacobson JA, Kasworm EMToxic shock syndrome after nasal surgery. Case reports and analysis of risk factors. Arch Otolaryngol Head Neck Surg. 1986;112:329–332.
34. Smith PA, Hankin FM, Louis DSPostoperative toxic shock syndrome after reconstructive surgery of the hand. J Hand Surg Am. 1986;11:399–402.
35. Aganaba T, Evans RP, O’Neill PToxic shock syndrome after orchidectomy. Br Med J (Clin Res Ed). 1983;286:685.
36. Miller SDPostoperative toxic shock syndrome after lumbar laminectomy in a male patient. Spine (Phila Pa 1976). 1994;19:1182–1185.
37. DeVries AS, Lesher L, Schlievert PM, et al.Staphylococcal toxic shock syndrome 2000–2006: epidemiology, clinical features, and molecular characteristics. Diep BA, ed. PLoS One. 2011;6:e22997–e22998.
38. Murray RJRecognition and management of Staphylococcus aureus toxin-mediated disease. Intern Med J. 2005;35suppl 2S106–S119.
39. Strenge KB, Mangan DB, Idusuyi OBPostoperative toxic shock syndrome after excision of a ganglion cyst from the ankle. J Foot Ankle Surg. 2006;45:275–277.
40. Wagner R, Toback JMToxic shock syndrome following septoplasty using plastic septal splints. Laryngoscope. 1986;96:609–610.
41. Chadwell JS, Gustafson LM, Tami TAToxic shock syndrome associated with frontal sinus stents. Otolaryngol Head Neck Surg. 2001;124:573–574.
42. Abram AC, Bellian KT, Giles WJ, et al.Toxic shock syndrome after functional endonasal sinus surgery: an all or none phenomenon? Laryngoscope. 1994;1048 pt 1927–931.
43. Vendemia N, Rohde CToxic shock syndrome after prosthetic breast reconstruction with alloderm. Plast Reconstr Surg. 2009;124:173e–174e.
44. Holm C, Mühlbauer WToxic shock syndrome in plastic surgery patients: case report and review of the literature. Aesthetic Plast Surg. 1998;22:180–184.
45. Poblete JV, Rodgers JA, Wolfort FGToxic shock syndrome as a complication of breast prostheses. Plast Reconstr Surg. 1995;96:1702–1708.
46. Giesecke J, Arnander CToxic shock syndrome after augmentation mammaplasty. Ann Plast Surg. 1986;17:532–533.
47. Tobin G, Shaw RC, Goodpasture HCToxic shock syndrome following breast and nasal surgery. Plast Reconstr Surg. 1987;80:111–114.
48. Gosain AK, Larson DLToxic shock syndrome following latissimus dorsi musculocutaneous flap breast reconstruction. Ann Plast Surg. 1992;29:571–575.
49. Schmitz M, Roux X, Huttner B, et al.Streptococcal toxic shock syndrome in the intensive care unit. Ann Intensive Care. 2018;8:88.
50. MacArthur RD, Miller M, Albertson T, et al.Adequacy of early empiric antibiotic treatment and survival in severe sepsis: experience from the MONARCS trial. Clin Infect Dis. 2004;38:284–288.
51. Gottlieb M, Long B, Koyfman AThe evaluation and management of toxic shock syndrome in the emergency department: a review of the literature. J Emerg Med. 2018;54:807–814.
52. Coyle EA, Cha R, Rybak MJInfluences of linezolid, penicillin, and clindamycin, alone and in combination, on streptococcal pyrogenic exotoxin a release. Antimicrob Agents Chemother. 2003;47:1752–1755.
53. Macris MH, Hartman N, Murray B, et al.Studies of the continuing susceptibility of group A streptococcal strains to penicillin during eight decades. Pediatr Infect Dis J. 1998;17:377–381.
54. Rhodes A, Evans LE, Alhazzani W, et al.Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43:304–377.
55. Mouthon L, Kaveri SV, Spalter SH, et al.Mechanisms of action of intravenous immune globulin in immune-mediated diseases. Clin Exp Immunol. 1996;104suppl 13–9.
56. Kaul R, McGeer A, Norrby-Teglund A, et al.Intravenous immunoglobulin therapy for streptococcal toxic shock syndrome--a comparative observational study. The Canadian Streptococcal Study Group. Clin Infect Dis. 1999;28:800–807.
57. Madsen MB, Hjortrup PB, Hansen MB, et al.Immunoglobulin G for patients with necrotising soft tissue infection (INSTINCT): a randomised, blinded, placebo-controlled trial. Intensive Care Med. 2017;43:1585–1593.
58. Parks T, Wilson C, Curtis N, et al.Polyspecific intravenous immunoglobulin in clindamycin-treated patients with streptococcal toxic shock syndrome: a systematic review and meta-analysis. Clin Infect Dis. 2018;67:1434–1436.
59. Effectiveness of Intravenous Immunoglobulins (IVIG) in Toxic Shock Syndromes in Children (IGHN2). Accessed January 7, 2019
60. Stevens DL, Bisno AL, Chambers HF, et al.Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59:e10–e52.
61. Komuro H, Kato T, Okada S, et alToxic shock syndrome caused by suture abscess with methicillin-resistant Staphylococcus aureus (MRSA) with late onset after Caesarean section.IDCases. 2017;10:12–14.
    62. Suga H, Shiraishi T, Takushima A, et alToxic shock syndrome caused by methicillin- resistant Staphylococcus aureus (MRSA) after expander-based breast reconstruction.Eplasty. 2016;16:e2.
      63. Chan Y, Selvaratnam V, Garg NToxic shock syndrome post open reduction and Kirschner wire fixation of a humeral lateral condyle fracture.BMJ Case Re 2015;2015:bcr2015210090.
        64. Rimawi B, Graybill W, Pierce J, et al.Necrotizing fasciitis and toxic shock syndrome from clostridium septicum following a term cesarean delivery. Case Reports Obstetrics Gynecol. 2014;2014:724302.
          65. Yadav R, Bhattarai B, Gupta R, et alToxic shock syndrome following inguinal hernia repair: a rare condition.J Coll Medical Sci. 20149. doi:10.3126/jcmsn.v9i2.9689
            66. Shimizu T, Yamamoto Y, Hosoi T, et alMRSA toxic shock syndrome associated with surgery for left leg fracture and co-morbid compartment syndrome.J Acute Dis. 2014;3:82–84.
              67. Tare M, Durcan J, Niranjan NA case of toxic shock syndrome following a DIEP breast reconstruction.J Plastic Reconstr Aesthetic Surg. 2010;63:e261–262.
                68. Shoji F, Yoshino I, Osoegawa A, et al.Toxic shock syndrome following thoracic surgery for lung cancer: report of a case. Surg Today. 2007;37:587–589.
                69. Jarrahy R, Roostaeian J, Kaufman MR, et alA rare case of staphylococcal toxic shock syndrome after abdominoplasty.Aesthet Surg J. 2007;27:162–166.
                70. Kastl S, Horstkotte MA, Schäfer H-J, et al“Anal angina”--pelvic sepsis and streptococcal toxic shock syndrome after rectoscopy and mucosal biopsy.Int J Colorectal Dis. 2008;232225–226.
                71. Goksugur N, Ozaras R, Tahan V, et alToxic shock syndrome due to Staphylococcus aureus sepsis following diagnostic laparotomy for Hodgkin’s disease.J Eur Acad Dermatol Venereol. 2003;17:732–733.
                72. Odom S, Stallard J, Pacheco H, et al.Postoperative staphylococcal toxic shock syndrome due to pre-existing staphylococcal infection: case report and review of the literature. Am Surg. 2001;67:745–747.
                73. Gwan–Nulla DN, Casal RSToxic shock syndrome associated with the use of the vacuum-assisted closure device.Ann Plas Surg. 2001;47:552–554.
                  74. Kato N, Nemoto K, Amako MToxic shock syndrome after a closed comminuted fracture surgery at the distal end of the humerus.J Shoulder Elb Surg. 1999;8:165–169.
                    75. Birdsall P, Milne DToxic shock syndrome due to percutaneous Kirschner wires.Injury. 1999;30:509–510.
                    76. Kotlarz J, Crane JToxic shock syndrome after mastoidectomy.Otolaryngology Head Neck Surg. 1998;118:701–702.
                      77. Younis R, Lazar RDelayed toxic shock syndrome after functional endonasal sinus surgery. Arch Otolaryngol Head Neck Surg1996;122:83–85.
                      78. Grimes J, Carpenter C, Reinker KToxic shock syndrome as a complication of orthopaedic surgery.J Pediatr Orthop. 1995;15:666–671.
                      79. Cederna JToxic shock syndrome after transverse rectus abdominis musculocutaneous flap breast reconstruction.Ann Plast Surg. 1995;34:73–75.
                      80. Miller SPostoperative toxic shock syndrome after lumbar laminectomy in a male patient.Spine. 1994;19:1182–1185.
                      81. Croall J, Chaudhri SNon-menstrual toxic shock syndrome complicating orthopaedic surgery.J Infect. 1989;18:195–196.
                      82. Frame J, Hackett MToxic shock syndrome after a minor surgical procedure.Lancet. 1988;1:1330–1331.
                      83. Murphy P, Holmes W, Wilson T, et al.Non-menstrual associated toxic shock syndrome. Ulster Med J. 1987;56:146–148.
                      84. Dreghorn C, Graham J, Rae PToxic shock syndrome following repair of a ligament of the knee.Injury. 1987;18:356–357.
                      85. Vanderheyden J, Renard J, Dehaen M, et al.Non-menstrual toxic shock syndrome. A case report and a review of non-menstrual toxic shock syndrome in Western Europe. Eur J Obstet Gynecol Reprod Biol. 1986;22:243–248.
                      86. Shaffer D, Jenkins R, Karchmer A, et al.Toxic shock syndrome complicating orthotopic liver transplantation--a case report. Transplantation. 1986;42:434–437.
                      87. Beck S, Fenton P, Rollinson PA fatal case of toxic-shock syndrome following cholecystectomy.Medicine Sci Law. 1984;24:269–270.
                        88. Spotkov J, Ruskin JToxic shock syndrome with staphylococcal wound abscess after gynecologic surgery.South Med J. 1984;77:806.
                          89. Toback J, Fayerman JToxic shock syndrome following septorhinoplasty. Implications for the head and neck surgeon.Arch Otolaryngol. 1983;109:627–629.
                          90. Moyer M, Edwards L, BergdollNosocomial toxic-shock syndrome in two patients after knee surgery.Am J Infect Control. 1983;11:83–87.
                          91. Bresler MToxic shock syndrome due to occult postoperative wound infection.West J Med. 1983;139:710–713.
                          92. Barnett A, Lavey E, Pearl R, et alToxic shock syndrome from an infected breast prosthesis. Ann Plast Surg. 1983;10:408–410.
                            93. Thomas S, Baird I, Frazier RToxic shock syndrome following submucous resection and rhinoplasty.JAMA. 1982;247:2402–2403.
                            94. Bartlett P, Reingold A, Graham D, et alToxic shock syndrome associated with surgical wound infections.JAMA. 1982;247:1448–1450.
                            95. McClelland J, Craig C, Hall WToxic shock syndrome in a man.South Med J. 1982;75:1027–1028.
                            96. Knudsen F, Olesen A, Højbjerg T, et al.Toxic shock syndrome. Br Med J (Clin Res Ed). 1981;282:399.
                            97. Silver M, Simon GToxic shock syndrome in a male postoperative patient.J Trauma. 1981;21:650–651.

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