- Email: [email protected]
Postoperative Toxic Shock Syndrome After Excision of a Ganglion Cyst From the Ankle
Postoperative Toxic Shock Syndrome After Excision of a Ganglion Cyst From the Ankle K. Brandon Strenge, MD,1 Douglas B. Mangan, MD,2 and O. B. Idusuyi, MD, FACS3 Postoperative toxic shock syndrome (PTSS) after orthopedic surgery is rare, but early recognition and prompt intervention are essential to minimize morbidity and potential mortality. The diagnosis should be considered in all postoperative patients presenting with fever, hypotension, and systemic illness. The treating surgeon must have not only knowledge of the clinical entity, but also an extremely high index of suspicion, because the diagnosis can be elusive with surgical wounds appearing deceptively benign. Treatment consists of antibiotics, surgical wound debridement, and, more importantly, aggressive supportive care with intravenous fluids and intensive care surveillance. To date, the literature contains relatively few case reports of PTSS after orthopedic procedures, with even fewer cases encountered after foot and ankle surgery. This report describes a patient who developed the rare complication of PTSS after an elective ganglion cyst excision from the ankle. ( The Journal of Foot & Ankle Surgery 45(4): 275–277, 2006) Key words: toxic shock syndrome, ganglion, ankle
S ince its initial description by Todd et al (1) in 1978, toxic
Case Report
shock syndrome (TSS) has become notoriously associated with the use of highly absorbent intravaginal tampons in young menstruating women. However, the importance of TSS in the postoperative setting has also been recognized (2, 3), with case reports presented in the literature across many surgical specialties. The first reports of postoperative toxic shock syndrome (PTSS) as a complication of orthopedic procedures were presented in 1984 by Rovner et al (4) and Hermens (5), with a relatively small number of subsequent case reports in the orthopedic literature (6 –19). The complication has been described after foot and ankle surgery in only 2 instances: once after a triple arthrodesis for residual clubfoot deformity (5) and another after excision of an accessory navicular (20). This case report describes a patient who developed the rare complication of PTSS after an elective excision of a ganglion cyst from the ankle.
A 45-year-old male dentist presented to the foot and ankle clinic with a complaint of a recurrent ganglion cyst on the lateral aspect of the left ankle. Before presentation, two previous attempts at excision had been performed elsewhere. After each recurrence, the patient admitted to personally aspirating the cyst multiple times, and added that self-prescribed antibiotics were used to treat the development of localized cellulitis. The patient was scheduled and underwent elective excision of the recurrent ganglion cyst without difficulty. Intraoperatively, there were no overt signs of infection, but the excised tissue was sent for pathology and culture as per routine. The patient was discharged home the same day in a posterior splint with oral analgesics and instructions for follow-up. On the first postoperative day, the patient developed nausea with chills lasting approximately one hour, which then subsided. However, 3 days postoperatively, the patient presented to his local area hospital with complaints of persistent intermittent chills, nausea, and muscle pain. On admission by his primary care physician, his temperature was 40.2° C (104.4° F), and he had a blood pressure of 80/50. Lactated ringer’s solution was started for resuscitation along with 3.375 mg of piperacillin/tazobactam intravenously every 6 hours. Initial laboratory work revealed his white blood cell count to be 17.8 K/L, bilirubin 3.8 mg/dL, creatinine 1.7 mg/dL, and lactic acid 4.1 mmol/L. The
From Southern Illinois University, Department of Surgery, Division of Orthopedics and Rehabilitation, Springfield, IL. Address correspondence to: K. Brandon Strenge, MD, Resident, Southern Illinois University, Department of Surgery, Division of Orthopedics and Rehabilitation, PO Box 19679, Springfield, IL 62794. E-mail: [email protected]. 1 Resident. 2 Resident. 3 Associate Professor. Copyright © 2006 by the American College of Foot and Ankle Surgeons 1067-2516/06/4504-0013$32.00/0 doi:10.1053/j.jfas.2006.04.008
VOLUME 45, NUMBER 4, JULY/AUGUST 2006
275
patient was transferred back to our hospital the next day, or postoperative day 4, for definitive management. Examination at that time revealed the surgical incision to be intact without signs of drainage, but the area surrounding the entire left lateral malleolus was edematous and erythematous. Also, the patient’s face and trunk were flushed, slight erythema was found on the skin of all 4 extremities, and petechiae were noted on the posterior pharynx. A presumptive diagnosis of PTSS was made, and the patient was promptly admitted to the intensive care unit. After starting 1 g of vancomycin intravenously every 12 hours, an infectious disease consultation was immediately requested and 20 g of intravenous immune globulin was administered. The patient was brought to the operating room for irrigation and debridement of the lateral ankle wound the following day, after improvement was noted in his blood pressure. Intraoperatively, an effusion was found involving the subtalar joint, but no other gross signs of infection were encountered. The subtalar joint fluid, as well as tissue and bone samples, were sent for culture. The wound was left open in preparation for a repeat irrigation and debridement a few days later. Initial cultures taken during the ganglion cyst excision were reported with growth of methacillin-sensitive Staphylococcus aureus. This organism was also cultured from samples obtained at the debridement procedure; thus, vancomycin was discontinued and 2 g intravenous nafcillin every 6 hours was started. Within 24 hours of switching antibiotics, the erythroderma of the trunk and extremities began to resolve, along with fewer complaints of muscle pain and resolution of the pharyngeal petechiae. Three days post-debridement, the patient was brought back to the operating room for a repeat irrigation and debridement, with new tissue cultures obtained and wound closure over a surgical drain. The patient was transferred from the intensive care unit, and the drain was removed after 2 days. The white blood cell count improved to 10.2 K/L, and the final cultures did not produce any bacterial growth. The other laboratory values also normalized, with bilirubin decreasing to 0.6 mg/dL, creatinine increasing to 1.1 mg/dL, and lactic acid measuring 1.2 mmol/L. Ultimately, the patient was discharged with 2 g of intravenous cefazolin every 8 hours for a total of 2 weeks. Initial follow-up revealed a well-healed surgical site, free of erythema or drainage, and the patient went on to develop no further sequelae. As required by law, the case was reported to the local and state Departments of Public Health and Centers for Disease Control.
Discussion PTSS is a progressive, potentially lethal, multisystem disorder associated with postoperative wound infections. 276
THE JOURNAL OF FOOT & ANKLE SURGERY
Most cases result from the production of TSS toxin-1 by S aureus infections, although other enterotoxins have been identified as causative, including exotoxins A, B, and C elaborated by infections caused by Streptococcus pyogenes. Local wound infections produce the toxins, which are absorbed systemically, creating the characteristic multisystem dysfunction. A retrospective review by Raab et al (21) estimated the risk of developing PTSS after surgical procedures to be 0.003%. Interestingly, the disease is most prevalent in previously healthy patients 20 to 50 years of age. The disease process is believed to result from enterotoxins behaving as superantigens, excessively stimulating Tcells and inciting a massive inflammatory cascade. Normally, antigens are processed within the lysosomes of specific antigen-presenting cells, and the resulting peptides are presented to major histocompatibility complex (MHC) class II molecules, forming MHC-peptide complexes. These complexes are transported to the cell surface to interact with highly specific T-cell receptors, initiating a measured T-cell response, with activation of only about 0.01% to 0.1% of the total T-cell population. In contrast, enterotoxins bypass the classic antigen-processing procedures by binding directly to an invariant region of MHC, outside the MHC class II groove, and simultaneously interacting with the non-antigen–specific V-beta region of T-cell receptors. This superantigen interaction allows T-cell proliferation on a much more generalized basis, with up to 20% of the entire population stimulated. The excessive T-cell activation leads to a massive release of inflammatory mediators, most notably IL-1 and IL-6 as well as tumor necrosis factor alpha. These cytokines are directly responsible for producing the constellation of systemic symptoms characteristic of TSS and its multiorgan system failure, such as skeletal muscle breakdown. The muscle breakdown then results in myalgia and impairment of immune system function by interfering with polymorphonuclear leukocyte migration, potentially explaining the deceptively benign appearance of surgical wounds with the absence of purulence (22). Surgeons must rely on clinical symptoms for diagnosis of PTSS because no laboratory test is available. These presenting symptoms include: fever of more than 38.9° C, hypotension, diffuse erythematous macular rash associated with desquamation, myalgia, and symptoms implicating disease of 3 or more major organ systems. This constellation of symptoms has been organized into a formal criteria list for diagnosis in an effort to standardize the disease definition and facilitate case surveillance (Table 1) (23). Classically, PTSS presents within the first 48 hours postoperatively, but reports have indicated presentation to be as much as 13 days after the surgical procedure. The diagnosis can be elusive because surgical wounds can be deceptively benign in appearance, requiring the surgeon to have a high index of suspicion.
TABLE 1 Major Criteria for Diagnosis of Toxic Shock Syndrome (23)
References
● ● ● ●
1. Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock syndrome associated with phage-group-I Staphylococci. Lancet 2:1116 –1118, 1978. 2. Bartlett P, Reingold AL, Graham DR, Dan BB, Selinger DS, Tank GW, Wichterman KA. Toxic shock syndrome associated with surgical wound infections. JAMA 247:1448 –1450, 1982. 3. Reingold AL, Dan BB, Shands KN, Broome CV. Toxic-shock syndrome not associated with menstruation: a review of 54 cases. Lancet 1:1– 4, 1982. 4. Rovner RA, Baird RA, Malerich MM. Fatal toxic shock syndrome as a complication of orthopaedic surgery: a case report. J Bone Joint Surg 66A:952–954, 1984. 5. Hermens KA. Toxic shock syndrome as a complication of orthopedic surgery. J Bone Joint Surg 66A:1321, 1984. 6. Croall J, Chaudhri S. Non-menstrual toxic shock syndrome complicating orthopedic surgery. J Infect 18:195–196, 1989. 7. Cruse CW, Hall WL. Toxic shock syndrome: a problem in the surgical patient. J Fla Med Assoc 75:87–90, 1988. 8. Dreghorn CR, Graham J, Rae PS. Toxic shock syndrome following repair of a ligament of the knee. Injury 18:356 –357, 1987. 9. Grayson MJ, Saldana MJ: Toxic shock syndrome complicating surgery of the hand. J Hand Surg Am 12:1082–1084, 1987. 10. Grimes J, Carpenter C, Reinker K. Toxic shock syndrome as a complication of orthopaedic surgery. J Pediatr Orthop 15:666 – 671, 1995. 11. Irvine GW. Postoperative toxic shock syndrome following osteoplasty of the hip: a case report. J Bone Joint Surg 67A:504, 1985. 12. Irvine GW, Kling TF, Hensinger RN. Postoperative toxic shock syndrome following osteoplasty of the hip. J Bone Joint Surg 66A:955– 958, 1984. 13. Knudson P, Charney M, Salcido D. Post-traumatic toxic shock syndrome. J Trauma 28:121–123, 1988. 14. Long WT, Filler BC, Cox E, Stark HH. Toxic shock syndrome after a human bite to the hand. J Hand Surg Am 13:957–959, 1988. 15. Paterson MP, Hoffman EB, Roux P. Severe disseminated staphylococcal disease associated with osteitis and septic arthritis. J Bone Joint Surg 72B:94 –97, 1990. 16. Silver MA, Simon GL. Toxic shock syndrome in a male postoperative patient. J Trauma 21:650 – 651, 1981. 17. Smith PA, Hankin FM, Louis DS. Postoperative toxic shock syndrome after reconstructive surgery of the hand. J Hand Surg Am 11:399 – 402, 1986. 18. Spearman PW, Barson WJ. Toxic shock syndrome occurring in children with abrasive injuries beneath casts. J Pediatr Orthop 12:169 – 172, 1992. 19. Turker R, Lubicky JP, Vogel LC. Toxic shock syndrome in patients with external fixators. J Pediatr Orthop 12:658 – 662, 1992. 20. Graham DR, O’Brien M, Hayes JM, Raab MG. Postoperative toxic shock syndrome. Clin Infect Dis 20:895– 899, 1995. 21. Raab MG, O’Brien M, Hayes JM, Graham DR. Postoperative toxic shock syndrome. Am J Orthop 24:130 –136, 1995. 22. Resnick SD. Toxic shock syndrome: recent developments in pathogenesis. J Pediatr 116:321–328, 1990. 23. Wharton M, Chorba TL, Vogt RL, Morse DL, Buehler JW. Case definitions for public health surveillance. MMWR Morb Mortal Wkly Rep 39:1– 43, 1990. 24. Bergdoll MS, Crass BA, Reiser RF, Robbins RN, Davis JP. A new staphylococcus enterotoxin, enterotoxin F, associated with toxicshock-syndrome Staphylococcus aureus isolates. Lancet 1:1017–1021, 1981.
Temperature ⬎38.9°C Systolic blood pressure ⬍90 mm Hg Diffuse erythroderma followed by desquamation in 1 to 2 weeks Involvement of at least 3 of the following organ systems: Gastrointestinal: vomiting or diarrhea Musculoskeletal: myalgia or creatinine phosphokinase ⬎5 times normal level Mucous membranes: conjunctival injection, vaginal, or oropharyngeal hyperemia Renal: BUN or creatinine ⬎2 times normal level or pyuria without evidence of UTI Hepatic: bilirubin or transaminases ⬎2 times normal level Blood: platelet count of ⬍100,000/L CNS: confusion without focal neurologic deficits ● Serologic exclusion of Rocky Mountain spotted fever, measles, and leptospirosis Probable diagnosis: Desquamation plus 3 other major criteria Or All five major criteria in the absence of desquamation Abbreviations: BUN, blood urea nitrogen; UTI, urinary tract infection; CNS, central nervous system.
Treatment involves early wound exploration and excisional debridement coupled with aggressive fluid resuscitation and electrolyte correction, as well as closely monitored supportive care, often in the intensive care unit with mechanical ventilation. Anti-staphylococcal antibacterial agents should be given intravenously to eliminate the infectious origin and decrease the risk of bacteremia. However, antibiotic therapy will not alter the systemic effects of toxins responsible for multiorgan system failure and, as such, is usually not necessary more than 2 to 3 weeks. Intravenous administration of gamma globulin has also been advocated by some as being therapeutically beneficial, because a high percentage of patients with TSS have low or no antibody titers to staphylococcal enterotoxins (24). Summary PTSS after orthopedic surgery is rare, with only a few reported cases after foot and ankle surgery in the literature. This case represents the first report of PTSS after excision of a ganglion cyst from the ankle. Early recognition and intervention are essential to minimize morbidity and potential mortality from this condition. The diagnosis should be considered in all postoperative patients presenting with fever, hypotension, and systemic illness, even in those with no obvious clinical signs of surgical wound infection. Surgeons must have knowledge of this clinical entity and an extremely high index of suspicion to correctly diagnose PTSS and initiate treatment consisting of antibiotics and, most importantly, aggressive supportive care.
VOLUME 45, NUMBER 4, JULY/AUGUST 2006
277
S ince its initial description by Todd et al (1) in 1978, toxic
Case Report
shock syndrome (TSS) has become notoriously associated with the use of highly absorbent intravaginal tampons in young menstruating women. However, the importance of TSS in the postoperative setting has also been recognized (2, 3), with case reports presented in the literature across many surgical specialties. The first reports of postoperative toxic shock syndrome (PTSS) as a complication of orthopedic procedures were presented in 1984 by Rovner et al (4) and Hermens (5), with a relatively small number of subsequent case reports in the orthopedic literature (6 –19). The complication has been described after foot and ankle surgery in only 2 instances: once after a triple arthrodesis for residual clubfoot deformity (5) and another after excision of an accessory navicular (20). This case report describes a patient who developed the rare complication of PTSS after an elective excision of a ganglion cyst from the ankle.
A 45-year-old male dentist presented to the foot and ankle clinic with a complaint of a recurrent ganglion cyst on the lateral aspect of the left ankle. Before presentation, two previous attempts at excision had been performed elsewhere. After each recurrence, the patient admitted to personally aspirating the cyst multiple times, and added that self-prescribed antibiotics were used to treat the development of localized cellulitis. The patient was scheduled and underwent elective excision of the recurrent ganglion cyst without difficulty. Intraoperatively, there were no overt signs of infection, but the excised tissue was sent for pathology and culture as per routine. The patient was discharged home the same day in a posterior splint with oral analgesics and instructions for follow-up. On the first postoperative day, the patient developed nausea with chills lasting approximately one hour, which then subsided. However, 3 days postoperatively, the patient presented to his local area hospital with complaints of persistent intermittent chills, nausea, and muscle pain. On admission by his primary care physician, his temperature was 40.2° C (104.4° F), and he had a blood pressure of 80/50. Lactated ringer’s solution was started for resuscitation along with 3.375 mg of piperacillin/tazobactam intravenously every 6 hours. Initial laboratory work revealed his white blood cell count to be 17.8 K/L, bilirubin 3.8 mg/dL, creatinine 1.7 mg/dL, and lactic acid 4.1 mmol/L. The
From Southern Illinois University, Department of Surgery, Division of Orthopedics and Rehabilitation, Springfield, IL. Address correspondence to: K. Brandon Strenge, MD, Resident, Southern Illinois University, Department of Surgery, Division of Orthopedics and Rehabilitation, PO Box 19679, Springfield, IL 62794. E-mail: [email protected]. 1 Resident. 2 Resident. 3 Associate Professor. Copyright © 2006 by the American College of Foot and Ankle Surgeons 1067-2516/06/4504-0013$32.00/0 doi:10.1053/j.jfas.2006.04.008
VOLUME 45, NUMBER 4, JULY/AUGUST 2006
275
patient was transferred back to our hospital the next day, or postoperative day 4, for definitive management. Examination at that time revealed the surgical incision to be intact without signs of drainage, but the area surrounding the entire left lateral malleolus was edematous and erythematous. Also, the patient’s face and trunk were flushed, slight erythema was found on the skin of all 4 extremities, and petechiae were noted on the posterior pharynx. A presumptive diagnosis of PTSS was made, and the patient was promptly admitted to the intensive care unit. After starting 1 g of vancomycin intravenously every 12 hours, an infectious disease consultation was immediately requested and 20 g of intravenous immune globulin was administered. The patient was brought to the operating room for irrigation and debridement of the lateral ankle wound the following day, after improvement was noted in his blood pressure. Intraoperatively, an effusion was found involving the subtalar joint, but no other gross signs of infection were encountered. The subtalar joint fluid, as well as tissue and bone samples, were sent for culture. The wound was left open in preparation for a repeat irrigation and debridement a few days later. Initial cultures taken during the ganglion cyst excision were reported with growth of methacillin-sensitive Staphylococcus aureus. This organism was also cultured from samples obtained at the debridement procedure; thus, vancomycin was discontinued and 2 g intravenous nafcillin every 6 hours was started. Within 24 hours of switching antibiotics, the erythroderma of the trunk and extremities began to resolve, along with fewer complaints of muscle pain and resolution of the pharyngeal petechiae. Three days post-debridement, the patient was brought back to the operating room for a repeat irrigation and debridement, with new tissue cultures obtained and wound closure over a surgical drain. The patient was transferred from the intensive care unit, and the drain was removed after 2 days. The white blood cell count improved to 10.2 K/L, and the final cultures did not produce any bacterial growth. The other laboratory values also normalized, with bilirubin decreasing to 0.6 mg/dL, creatinine increasing to 1.1 mg/dL, and lactic acid measuring 1.2 mmol/L. Ultimately, the patient was discharged with 2 g of intravenous cefazolin every 8 hours for a total of 2 weeks. Initial follow-up revealed a well-healed surgical site, free of erythema or drainage, and the patient went on to develop no further sequelae. As required by law, the case was reported to the local and state Departments of Public Health and Centers for Disease Control.
Discussion PTSS is a progressive, potentially lethal, multisystem disorder associated with postoperative wound infections. 276
THE JOURNAL OF FOOT & ANKLE SURGERY
Most cases result from the production of TSS toxin-1 by S aureus infections, although other enterotoxins have been identified as causative, including exotoxins A, B, and C elaborated by infections caused by Streptococcus pyogenes. Local wound infections produce the toxins, which are absorbed systemically, creating the characteristic multisystem dysfunction. A retrospective review by Raab et al (21) estimated the risk of developing PTSS after surgical procedures to be 0.003%. Interestingly, the disease is most prevalent in previously healthy patients 20 to 50 years of age. The disease process is believed to result from enterotoxins behaving as superantigens, excessively stimulating Tcells and inciting a massive inflammatory cascade. Normally, antigens are processed within the lysosomes of specific antigen-presenting cells, and the resulting peptides are presented to major histocompatibility complex (MHC) class II molecules, forming MHC-peptide complexes. These complexes are transported to the cell surface to interact with highly specific T-cell receptors, initiating a measured T-cell response, with activation of only about 0.01% to 0.1% of the total T-cell population. In contrast, enterotoxins bypass the classic antigen-processing procedures by binding directly to an invariant region of MHC, outside the MHC class II groove, and simultaneously interacting with the non-antigen–specific V-beta region of T-cell receptors. This superantigen interaction allows T-cell proliferation on a much more generalized basis, with up to 20% of the entire population stimulated. The excessive T-cell activation leads to a massive release of inflammatory mediators, most notably IL-1 and IL-6 as well as tumor necrosis factor alpha. These cytokines are directly responsible for producing the constellation of systemic symptoms characteristic of TSS and its multiorgan system failure, such as skeletal muscle breakdown. The muscle breakdown then results in myalgia and impairment of immune system function by interfering with polymorphonuclear leukocyte migration, potentially explaining the deceptively benign appearance of surgical wounds with the absence of purulence (22). Surgeons must rely on clinical symptoms for diagnosis of PTSS because no laboratory test is available. These presenting symptoms include: fever of more than 38.9° C, hypotension, diffuse erythematous macular rash associated with desquamation, myalgia, and symptoms implicating disease of 3 or more major organ systems. This constellation of symptoms has been organized into a formal criteria list for diagnosis in an effort to standardize the disease definition and facilitate case surveillance (Table 1) (23). Classically, PTSS presents within the first 48 hours postoperatively, but reports have indicated presentation to be as much as 13 days after the surgical procedure. The diagnosis can be elusive because surgical wounds can be deceptively benign in appearance, requiring the surgeon to have a high index of suspicion.
TABLE 1 Major Criteria for Diagnosis of Toxic Shock Syndrome (23)
References
● ● ● ●
1. Todd J, Fishaut M, Kapral F, Welch T. Toxic-shock syndrome associated with phage-group-I Staphylococci. Lancet 2:1116 –1118, 1978. 2. Bartlett P, Reingold AL, Graham DR, Dan BB, Selinger DS, Tank GW, Wichterman KA. Toxic shock syndrome associated with surgical wound infections. JAMA 247:1448 –1450, 1982. 3. Reingold AL, Dan BB, Shands KN, Broome CV. Toxic-shock syndrome not associated with menstruation: a review of 54 cases. Lancet 1:1– 4, 1982. 4. Rovner RA, Baird RA, Malerich MM. Fatal toxic shock syndrome as a complication of orthopaedic surgery: a case report. J Bone Joint Surg 66A:952–954, 1984. 5. Hermens KA. Toxic shock syndrome as a complication of orthopedic surgery. J Bone Joint Surg 66A:1321, 1984. 6. Croall J, Chaudhri S. Non-menstrual toxic shock syndrome complicating orthopedic surgery. J Infect 18:195–196, 1989. 7. Cruse CW, Hall WL. Toxic shock syndrome: a problem in the surgical patient. J Fla Med Assoc 75:87–90, 1988. 8. Dreghorn CR, Graham J, Rae PS. Toxic shock syndrome following repair of a ligament of the knee. Injury 18:356 –357, 1987. 9. Grayson MJ, Saldana MJ: Toxic shock syndrome complicating surgery of the hand. J Hand Surg Am 12:1082–1084, 1987. 10. Grimes J, Carpenter C, Reinker K. Toxic shock syndrome as a complication of orthopaedic surgery. J Pediatr Orthop 15:666 – 671, 1995. 11. Irvine GW. Postoperative toxic shock syndrome following osteoplasty of the hip: a case report. J Bone Joint Surg 67A:504, 1985. 12. Irvine GW, Kling TF, Hensinger RN. Postoperative toxic shock syndrome following osteoplasty of the hip. J Bone Joint Surg 66A:955– 958, 1984. 13. Knudson P, Charney M, Salcido D. Post-traumatic toxic shock syndrome. J Trauma 28:121–123, 1988. 14. Long WT, Filler BC, Cox E, Stark HH. Toxic shock syndrome after a human bite to the hand. J Hand Surg Am 13:957–959, 1988. 15. Paterson MP, Hoffman EB, Roux P. Severe disseminated staphylococcal disease associated with osteitis and septic arthritis. J Bone Joint Surg 72B:94 –97, 1990. 16. Silver MA, Simon GL. Toxic shock syndrome in a male postoperative patient. J Trauma 21:650 – 651, 1981. 17. Smith PA, Hankin FM, Louis DS. Postoperative toxic shock syndrome after reconstructive surgery of the hand. J Hand Surg Am 11:399 – 402, 1986. 18. Spearman PW, Barson WJ. Toxic shock syndrome occurring in children with abrasive injuries beneath casts. J Pediatr Orthop 12:169 – 172, 1992. 19. Turker R, Lubicky JP, Vogel LC. Toxic shock syndrome in patients with external fixators. J Pediatr Orthop 12:658 – 662, 1992. 20. Graham DR, O’Brien M, Hayes JM, Raab MG. Postoperative toxic shock syndrome. Clin Infect Dis 20:895– 899, 1995. 21. Raab MG, O’Brien M, Hayes JM, Graham DR. Postoperative toxic shock syndrome. Am J Orthop 24:130 –136, 1995. 22. Resnick SD. Toxic shock syndrome: recent developments in pathogenesis. J Pediatr 116:321–328, 1990. 23. Wharton M, Chorba TL, Vogt RL, Morse DL, Buehler JW. Case definitions for public health surveillance. MMWR Morb Mortal Wkly Rep 39:1– 43, 1990. 24. Bergdoll MS, Crass BA, Reiser RF, Robbins RN, Davis JP. A new staphylococcus enterotoxin, enterotoxin F, associated with toxicshock-syndrome Staphylococcus aureus isolates. Lancet 1:1017–1021, 1981.
Temperature ⬎38.9°C Systolic blood pressure ⬍90 mm Hg Diffuse erythroderma followed by desquamation in 1 to 2 weeks Involvement of at least 3 of the following organ systems: Gastrointestinal: vomiting or diarrhea Musculoskeletal: myalgia or creatinine phosphokinase ⬎5 times normal level Mucous membranes: conjunctival injection, vaginal, or oropharyngeal hyperemia Renal: BUN or creatinine ⬎2 times normal level or pyuria without evidence of UTI Hepatic: bilirubin or transaminases ⬎2 times normal level Blood: platelet count of ⬍100,000/L CNS: confusion without focal neurologic deficits ● Serologic exclusion of Rocky Mountain spotted fever, measles, and leptospirosis Probable diagnosis: Desquamation plus 3 other major criteria Or All five major criteria in the absence of desquamation Abbreviations: BUN, blood urea nitrogen; UTI, urinary tract infection; CNS, central nervous system.
Treatment involves early wound exploration and excisional debridement coupled with aggressive fluid resuscitation and electrolyte correction, as well as closely monitored supportive care, often in the intensive care unit with mechanical ventilation. Anti-staphylococcal antibacterial agents should be given intravenously to eliminate the infectious origin and decrease the risk of bacteremia. However, antibiotic therapy will not alter the systemic effects of toxins responsible for multiorgan system failure and, as such, is usually not necessary more than 2 to 3 weeks. Intravenous administration of gamma globulin has also been advocated by some as being therapeutically beneficial, because a high percentage of patients with TSS have low or no antibody titers to staphylococcal enterotoxins (24). Summary PTSS after orthopedic surgery is rare, with only a few reported cases after foot and ankle surgery in the literature. This case represents the first report of PTSS after excision of a ganglion cyst from the ankle. Early recognition and intervention are essential to minimize morbidity and potential mortality from this condition. The diagnosis should be considered in all postoperative patients presenting with fever, hypotension, and systemic illness, even in those with no obvious clinical signs of surgical wound infection. Surgeons must have knowledge of this clinical entity and an extremely high index of suspicion to correctly diagnose PTSS and initiate treatment consisting of antibiotics and, most importantly, aggressive supportive care.
VOLUME 45, NUMBER 4, JULY/AUGUST 2006
277