“Toxic Shock Syndrome Management” – Help From Dr. Farkas Of PulmCrit

The big point of Dr. Farkas’ two posts on Toxic Shock Syndrome (TSS)

is to think of it early because the treatment is different from garden variety septic shock. Read carefully the two cases in each of the two posts as they contain clinical clues that can help you think of TSS.

You’ll need to give dual  antibiotic toxin suppressive therapy, IVIG, hemodynamic support (with pressors), respiratory support, and source control. See Conclusions below for Dr. Farkas’ summary.

The following post [which as always are just my study notes to help me remember topics I review] are excerpts from  Toxic Shock Syndrome Management: A tale of two patients
January 12, 2015 by Dr. Josh Farkas of PulmCrit [link is to the PulmCrit Table of Contents]:

[Toxic Shock Syndrome] is potentially quite lethal, with many series of streptococcal toxic shock syndrome reporting mortality in the range of 30-50%.  However, recent observational studies suggest that treatment with modern critical care, toxin-suppressive antibiotics, and IVIG may reduce the mortality to 10% (Linner 2014).
After last week’s post on diagnosis, this post explores management.  Treatment primarily consists of high-quality sepsis care, but there are some important points that are unique to TSS.  This is illustrated in two examples.

Patient #1

Ten years ago, a 30-year-old woman presented to Genius General Hospitalwith a diffuse erythematous rash, diarrhea, nausea, and vomiting.  She had developed flu-like symptoms and spent some days at home trying to rehydrate herself.  When she could no longer get out of bed, she presented to the emergency department and was found to be in septic shock with renal failure.  She was admitted to the ICU, resuscitated with fluid and vasopressors, and treated with broad-spectrum antibiotics including clindamycin.  Intravenous immunoglobulin (IVIG) was not given because of the lack of proven mortality benefit in the literature.  Her initial ICU course was marked by anuria and a moderate requirement for vasopressors (about 10-15 mcg/min norepinephrine).  Imaging studies questioned an ovarian abscess, perhaps related to her intrauterine device (IUD).  Due to failure to improve, she was taken to the operating room for surgical exploration.  Following intubation she developed pulseless electrical activity and could not be resuscitated.  Autopsy revealed an ovarian abscess containing group A streptococcus.
In reflecting on this case, perhaps the most notable feature is how the patient really didn’t look that sick.  She was mentating adequately without significant distress for several hours in the ICU.  This seems to be a common error in treating young TSS patients: they may not appear to be very sick and thus don’t receive sufficiently aggressive intervention.  A very similar case was recently reported by Cho 2013.

Patient #2

More recently, a 35-year-old woman presented to an outside hospital with diffuse erythematous rash, hypotension, renal failure (creatinine 2 mg/dL), and severe thigh pain. She remained hypotensive despite four liters of fluid resuscitation. Upon transfer to the Genius General Hospital ICU, she was found to have a mean arterial pressure (MAP) in the low 50s with tachycardia, moderate tachypnea, and a lactate of 10 mM. Peripheral norepinephrine was immediately started to stabilize her MAP, requiring 15 mcg/min to achieve a MAP>65 mm. She was started on clindamycin, linezolid, piperacillin-tazobactam, and IVIG (one gram/kg). Although she wasn’t in severe distress, she was intubated using 1.4 mg/kg Rocuronium and 0.4 mg/kg ketamine. Despite fluid resuscitation, following intubation her vasopressor requirement increased to norepinephrine 40 mcg/min and vasopressin 0.04 units/min. Stress dose hydrocortisone was started. CT scan of the thigh revealed focal soft tissue swelling. Surgical exploration was performed to evaluate for necrotizing fasciitis or any drainable abscess, however neither was found.

Please see Dr. Farkas’ post for all the details of therapy. Here is Dr. Farkas conclusion:


TSS is unusual in its ability to cause severe septic shock in previously normal young people.  Given that patients often have high physiologic reserve, they may initially look deceptively OK, masking the severity of their illness.  This often causes delays in instituting sufficiently aggressive management.  In addition to aggressive supportive care, specific therapies including IVIG and toxin-suppressive antibiotics may be very important.  The following checklist includes some interventions which should be considered when treating a patient with TSS.
  • Hemodynamic support
    • Early norepinephrine to establish a MAP>65mm
    • Fluid resuscitation
    • Low threshold to add vasopressin and stress-dose hydrocortisone if not responding well to norepinephrine
    • Serial echocardiography to identify occurance of septic cardiomyopathy
  • Respiratory support
    • Consider pre-emptive intubation (e.g., for severe shock or respiratory distress).  Meticulous attention required to peri-intubation hemodynamics.
  • Dual toxin-supressive antibiotic therapy
    • Clindamycin 900 mg IV q8 hours first dose STAT
    • Linezolid 600 mg IV q12 hours first dose STAT
  • Intravenous immunoglobulin (IVIG)
    • Standard course: 1 g/kg IVIG on day #1, then 0.5 g/kg IVIG on days #2 and #3
    • Consider higher dose IVIG (2 g/kg) for refractory shock or necrotizing fasciitis
  • Source control
    • Early surgical consultation for debridement/drainage of any focus of infection
    • Definitive imaging if needed to search for a focus of infection (e.g. CT scan, pelvic ultrasound, etc.)
    • Exclude retained tampon, nasal packing, or foreign body


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