Toxic shock syndrome: Clinical sciences

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A 28-year-old previously healthy woman presents to the emergency department with fever, hypotension, diffuse macular erythema with scaling, and desquamation of her palms and soles. Prior to her symptoms, she was undergoing treatment for a wound infection after elective cholecystectomy. She is admitted to the ICU and receives IV fluids, norepinephrine, and broad spectrum antibiotic therapy with vancomycin, cefepime, and clindamycin. On hospital day three, she shows clinical improvement, though she still requires a small amount of norepinephrine to maintain her blood pressure. Blood cultures now demonstrate methicillin-susceptible S. aureus. Antibiotics are changed to cefazolin and clindamycin. Given the clinical presentation, what is the primary reason to continue clindamycin?  

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Toxic shock syndrome, or TSS for short, is a rare form of septic shock caused by bacteria like Streptococcus pyogenes or Staphylococcus aureus. Based on the causative agent, TSS is subdivided into two main types called streptococcal TSS and non-streptococcal TSS.

TSS typically results from a skin and soft tissue infection, or a contaminated foreign body, such as retained surgical packing.

At these points, bacteria produce toxins that can reach the bloodstream and spread throughout the body, eventually activating T lymphocytes. This triggers the release of inflammatory cytokines, causing fever, hypotension, and multiple organ failure.

Now, when a patient presents with a chief concern suggesting toxic shock syndrome, the first step is to perform an ABCDE assessment. Patients with toxic shock syndrome are generally unstable, so initiate acute medical management to stabilize the airway, breathing, and circulation.

Admit your patient to the ICU, and initiate continuous vital sign monitoring. Next, obtain IV access and consider placing catheters for invasive hemodynamic monitoring, including an arterial line and a central venous catheter, or CVC.

Patients with toxic shock syndrome often have profound hypotension, so begin IV fluid resuscitation.

In some cases, to maintain hemodynamic stability, you may need to add vasopressors, targeting a mean arterial pressure or MAP of 65 millimeters of mercury or above.

Lastly, obtain blood cultures and begin broad-spectrum IV antibiotics.

Keep in mind that achieving hemodynamic stability, obtaining blood cultures and starting broad spectrum antibiotics is known as the “1-hour sepsis bundle”, and it should be performed within the first hour of patient presentation.

Now, here’s a clinical pearl! You should obtain a blood lactate level in the first hour to check for organ hypoperfusion. These levels are then monitored serially to guide hemodynamic resuscitation efforts. If lactate levels are high initially, it suggests organ hypoperfusion and indicates the need for aggressive hemodynamic support. On the flip side, if lactate levels decline with treatment, that helps determine when hemodynamic support can be withdrawn.

Okay, once you stabilize the patient, perform a focused history and physical examination and order labs, including CBC and CMP. The history typically reveals nonspecific systemic symptoms, such as fever, myalgias, and headache; as well as gastrointestinal symptoms, like nausea, vomiting, and diarrhea.

Additionally, the patient could report a rash over the entire skin. In some cases, history might reveal severe pain at the site of a recent soft tissue infection, or other risk factors for infection, like recent tampon use or surgery.

On the flip side, the physical exam typically shows hypotension and macular erythroderma, which is a diffuse reddening of the skin due to widespread inflammation. Later in the course of the illness, the rash may desquamate, or flake off, so keep in mind that you may or may not see desquamation when the patient initially presents!

Finally, labs may reveal elevated lactate, leukocytosis, low hemoglobin and hematocrit, thrombocytopenia, as well as elevated creatinine and the hepatic transaminases, AST and ALT.

Here’s another clinical pearl! As with all cases of septic shock, it’s important to identify the source of infection in TSS. In many cases, a detailed history and physical examination will reveal the source of the infection. However, in some situations, you might need imaging to locate the focus of infection, especially if you suspect retained foreign bodies.

Now, with these findings, you should suspect toxic shock syndrome, so your next step is to collect cultures from the suspected source of infection!

Soft tissue infections and retained foreign bodies are the most common cause of TSS, but don’t forget other potential infections, such as pneumonia, pharyngitis, and meningitis!

So depending on the patient's presentation, you may need to send cultures from the throat, sputum, genitourinary tract, a skin lesion or wound, or cerebrospinal fluid.

If the suspected source is a necrotizing soft tissue infection, consult the surgical team to evaluate for an emergent operative exploration, debridement, and wound cultures.

Now here’s another clinical pearl! TSS is a clinical diagnosis, which means that no single finding or test is sufficient for diagnosis. Instead, you should look at the combination of clinical and laboratory findings in order to diagnose TSS.

One easy way to do so is using the Centers for Disease Control and Prevention or CDC’s case definitions for streptococcal toxic shock syndrome and non-streptococcal toxic shock syndrome. These case definitions were designed for public health surveillance, and not for individual patient diagnosis, but they can be a helpful tool at the bedside because they list the classic features of toxic shock syndrome.