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Puerperal Toxic Shock Syndrome Treated with Extracorporeal Membrane Oxygenation (ECMO)
Abstract Number: T-52
Abstract Type: Case Report/Case Series
Puerperal group A streptococcal (GAS) infections were very common before 1900, rare between 1900 and 1980, and are now occurring more frequently with more virulent bacteria.1 We present a parturient with GAS toxic shock syndrome (TSS) who recovered after abdominal hysterectomy and extracorporeal membrane oxygenation (ECMO).
A healthy 21 yo G2P1 presented in term spontaneous labor. She delivered a healthy male infant vaginally. Estimated blood loss was < 500mL, and post-partum hemorrhage never occurred. She was tachycardic, hypotensive, afebrile, and leukocytopenic soon after delivery. On postpartum day (PPD) 2, the patient had a normal chest x-ray and lower extremity Dopplers. “Ground glass” opacities in the left lung were noted on chest CT. Ultrasound showed an empty uterus. The uterine fundus was tender. Mask oxygen was required for normal oxygen saturation. On PPD 3, blood and urine cultures were drawn for presumed sepsis. Broad-spectrum antibiotics and ICU transfer were initiated. Metabolic acidosis and leukocytopenia were present. ECHO revealed global left ventricular dysfunction and a mildly enlarged right ventricle. CT scan of the abdomen showed an enlarged uterus and peritoneal fluid. Her clinical status worsened. She was intubated and started on IV pressors. Cultures grew GAS. She met diagnostic criteria for TSS (hypotension plus failure of 2 organ systems)1. Ceftriaxone and clindamycin replaced the broad-spectrum antibiotics. On PPD 4, laparotomy revealed necrosis and hemorrhage of the uterus, fallopian tubes, and ovaries, and TAH-BSO was performed. Bilevel ventilation improved oxygenation. A repeat ECHO showed biventricular dysfunction and an ejection fraction of 25%. Her severe acute respiratory distress syndrome (ARDS) was refractory to conventional treatment. ECMO was started on PPD 7 and continued for 19 days. She was discharged on PPD 47 with a gastrostomy tube and a tracheostomy. She was later readmitted for tracheostomy complications and new onset seizure disorder.
GAS-TSS, while rare, has a mortality rate of 30-81%.1 Some GAS produce exotoxin A, which directly stimulates T-cells to release massive amounts of cytokines.1 These cytokines rapidly induce severe multi-organ failure despite effective antibiotic treatment.1 Penicillin and clindamycin, in combination, are recommended. While GAS is more sensitive to penicillin, clindamycin decreases exotoxin production, enhances phagocytosis, and is associated with increased survival.2 IVIG, which was not used in our patient, may neutralize exotoxin A, decreasing the likelihood and/or severity of TSS.2 Earlier recognition of our patient's sepsis might have led to a less complicated clinical course.
1. Schummer W, Schummer C. Infect Dis Obstet Gynecol 2002;10:217-222.
2. Aronoff DM, Mulla ZD. Infect Dis Obstet Gynecol 2008;2008:796892.