Toxic shock syndrome (TSS): Nursing

Toxic shock syndrome, or TSS, is an acute condition caused by a bacterial infection. TSS can be life threatening, as it involves multiple organ systems.

TSS is caused by the immune response to bacterial toxins produced by Staphylococcus aureus or Group A Streptococcus species, like Streptococcus pyogenes.

The most widely recognized risk factor for developing TSS is improper use of tampons during menstruation, but some contraceptive methods, such as a sponge or diaphragm, can also pose a risk. However, TSS can also present in other settings such as soft tissue infections, post-surgical infections, burns, or retained foreign objects such as nasal packing and dialysis catheters.

Now, let’s look at the pathophysiology of TSS. For example, TSS can happen when a tampon or a contraceptive device is left in the vagina for too long.

During menstruation, menstrual blood accumulates and provides a good medium for the bacteria to grow on.

Both Staphylococcus aureus and Streptococcus pyogenes produce exotoxins that are able to cross the vaginal mucosa through a mucosal break or via the uterus and enter the bloodstream.

For Staphylococcus aureus, the main culprit is called toxic shock syndrome toxin 1, or TSST 1 for short. That should be easy to remember! Streptococcus pyogenes, on the other hand, has an M protein in its structure that can overstimulate the immune system, causing TSS.

Alternatively, bacteria can also grow in infected tissues such as wounds or burns, and from there, they enter the bloodstream.

Once in the bloodstream, these toxins over activate some immune cells called T cells, which further leads to the overactivation of cytokines and inflammatory cells.

The end result of this is a massive systemic inflammatory response, which can cause capillary leakage, meaning fluid leaks out of the capillaries as well as severe end-organ failure, including liver dysfunction and renal failure, as well as acute respiratory distress syndrome and impaired coagulation, which can progress to disseminated intravascular coagulation.

Clinical manifestations of TSS typically develop within five days after the onset of menstruation.

For non-menstrual cases of TSS, the onset of illness can be preceded by pain, as well as signs of local inflammation and sloughing off of skin. Once in full swing, TSS manifestations include fever, chills, edema, hypotension, a diffuse rash that often looks like sunburn, and myalgias.

Additionally, there can be hyperemia, meaning redness and inflammation, of the eyes, oropharynx or vagina.

Left untreated, it causes multiple organ system dysfunction. Signs of liver dysfunction include jaundice, while signs of renal impairment can include oliguria or anuria; and acute respiratory distress syndrome can manifest as dyspnea, or shortness of breath.

Additionally, there can be severe hypotension, bleeding, vomiting or diarrhea; and signs of sepsis or disseminated intravascular coagulation.

Diagnosis of TSS starts with the client’s history and physical assessment.

Laboratory tests typically include a CBC, which can show anemia, thrombocytopenia, or leukocytosis with a left shift, meaning more immature WBCs are present in the blood; a comprehensive metabolic panel or CMP, which can show high levels of creatinine and elevated BUN, as well as elevated bilirubin and liver enzymes. Creatine phosphokinase or CPK, can be higher than two times the upper limit of normal, while coagulation studies can show prolonged coagulation times.

Blood cultures should also be obtained, as well as cultures from any suspected source. In clients with fever and altered mental status, a lumbar puncture should be performed to evaluate for meningitis.

Treatment of TSS starts with removing the source of infection.

Supportive therapy should be provided, including IV fluids to restore fluid and electrolyte balance, vasopressors such as norepinephrine to correct the hypotension, as well as IV immunoglobulins to neutralize the activity of the toxins.

Initially, broad spectrum antibiotics that are effective against both staphylococcal and streptococcal TSS should be provided.

After identification, antibiotics should be optimized and narrowed in spectrum depending on the identified bacteria.

So, for TSS caused by group A Streptococcus species, clindamycin is usually effective, while for TSS caused by methicillin sensitive Staphylococcus aureus, a beta-lactamase-resistant penicillin such as nafcillin or oxacillin can be used; or vancomycin if the client is allergic to penicillin.