Dr. Farkas’ posts on toxic shock syndrome [Resources (1) and (2) (links are directly to Dr. Farkas’ blog posts)] contain much information that I wasn’t aware of. This post is simply my study notes of the very basics of Toxic Shock Syndrome [Note to myself – If you are considering the possibility of Toxic Shock Syndrome you will want to review completely both of Dr. Farkas posts]
Toxic shock syndrome (TSS) is critical to recognize because it can be rapidly lethal and yet is usually treatable. TSS is a relatively new disease, first described in 1978. The prevalence has increased over the last few decades due to shifts in the circulating strains of Group A streptococcus (Low 2013). However, awareness of this disorder remains low.
Case #1 Rory Stauton
Rory Staunton was a very high-profile case of delayed diagnosis of streptococcal TSS. He initially suffered minor trauma playing basketball, and later presented to his pediatrician with fever, vomiting, severe leg pain, tachypnea, and tachycardia. Initially he was misdiagnosed as having gastroenteritis. He was later evaluated at the emergency department of a prominent medical center and discharged home, only to return days later with worsening shock. He died, and his case launched a campaign to improve sepsis awareness. While it’s easy to place blame, this case is not uncommon. Most cases of TSS are diagnosed late. Early differentiation of TSS from gastroenteritis or influenza is a bit like finding a needle in a haystack. However, a clear understanding of TSS can facilitate early diagnosis. The constellation of severe extremity pain out of proportion to exam, nausea/vomiting, fever, and tachycardia in this case might have suggested a streptococcal necrotizing soft tissue infection complicated by TSS.
A 60-year-old man presented to Genius General Hospital with cellulitis, hypotension, and acute renal failure. Examination disclosed a toxic-appearing man with confluent erythematous cellulitis involving his left calf. He was treated with volume resuscitation, norepinephrine, vancomycin, and piperacillin-tazobactam. However, his hemodynamics worsened, he developed increasing confusion, and was intubated due to tachypnea and agitation. Given that the severity of his septic shock seemed out of proportion to his cellulitis, he was treated emperically for TSS with clindamycin and intravenous immunoglobulin (IVIG). Following administration of IVIG he was promptly weaned off vasopressors. The next day he was extubated, and continued to improve rapidly. Blood cultures eventually returned positive for Group A Streptococcus.
Pathophysiology of Toxic Shock Syndrome
Some streptococcal and staphylococcal strains secrete a toxin which causes widespread activation of T lymphocytes. Activating this many leukocytes causes massive cytokine release, creating a syndrome that mimics septic shock. Most people acquire antibodies to these toxins. Toxic shock syndrome occurs if toxigenic bacteria colonize or invade a person without protective antibodies. This often causes the disease to occur in younger people who have not yet encountered these toxins and lack immunity to them.
Practical Approach to
DiagnosingSuspecting Toxic Shock SyndromeDiagnosing TSS is challenging, and in some cases it is impossible to ever reach a definitive diagnosis. Some patients will not develop positive cultures, leaving TSS as a diagnosis of exclusion. Alternative possibilities such as meningococcemia, primary adrenal insufficiency, and other foci of infection must be carefully evaluated.It is essential to treat TSS as early as possible. Thus, in situations of diagnostic uncertainty, empiric treatment for TSS should be started while continuing to evaluate for alternative diagnoses. Rather than conceptualizing the diagnostic process as an all-or-none phenomena, it may be more useful to imagine varying levels of suspicion leading to different empiric treatments. If there is any suspicion of TSS, it is reasonable to initiate toxin-suppressive antibiotics [clindamycin and linezolid – discussed in Dr. Farkas’ post Toxic Shock Syndrome Management: A tale of two patients]. Since intravenous immunoglobulin is expensive, a higher level of suspicion is required to initiate this treatment as well.
Conclusion: Red Flags For TSSUnfortunately, TSS may manifest differently in different patients. TSS should be considered in many situations, especially the following:
- Systemic illness plus a diffuse blanchable erythematous rash.
- Younger person initially develops a gastroenteritis-like illness and subsequently progresses to septic shock without alternative explanation.
- Severe focal soft tissue pain out of proportion to examination plus systemic toxicity (e.g., high fever or elevated shock index).
- Peripartum septic shock.
- Septic shock due to proven or probable Group A streptococcal infection (e.g., cellulitis, necrotizing fasciitis), with sepsis severity out of proportion to the infectious source.
Please remember that the above are simply excerpts for my study notes. There are so much more critical information in Dr. Farkas’ post that you should go there now and review it fully.
(2) Toxic Shock Syndrome Management: A tale of two patients January 12, 2015 by Dr. Josh Farkas of PulmCrit
(3) Toxic shock syndrome: major advances in pathogenesis, but not treatment [PubMed Abstract]. Crit Care Clin. 2013 Jul;29(3):651-75. doi: 10.1016/j.ccc.2013.03.012.
(4) Streptococcal Toxic Shock Syndrome Caused by Group G Streptococcus, United Kingdom [PubMed Abstract] [Full Text HTML] [Full Text PDF]. Emerg Infect Dis. 2017 Jan;23(1):127-129. doi: 10.3201/eid2301.161009.
(5) Toxic shock syndrome – the seven Rs of management and treatment [PubMed Abstract]. J Infect. 2017 Jun;74 Suppl 1:S147-S152. doi: 10.1016/S0163-4453(17)30206-2.
(7) Fatal streptococcal toxic shock syndrome from an intrauterine device [PubMed Abstract]. J Emerg Med. 2013 Apr;44(4):777-80. doi: 10.1016/j.jemermed.2012.03.020. Epub 2013 Feb 8.