Pediatric Toxic Shock Syndrome - Causes, Diagnosis, and Management.

Introduction:

Toxic shock syndrome in children is caused by toxin-producing strains of staphylococcal infection. These toxins are released into the bloodstream and impair the functioning of various vital organs, leading to death. Staphylococcus aureus and Streptococcus pyogenes are the two important bacterial strains responsible for toxic shock syndrome. The toxic condition was first discovered in 1978 in children and adults. The majority of the cases are caused due to involvement of staphylococcus aureus bacteria, especially in teenage girls and young women using vaginal tampons during menstruation.

What Is Pediatric Toxic Shock Syndrome?

Pediatric toxic shock syndrome is an uncommon, potentially life-threatening infectious medical emergency. Clinical manifestations appear when toxins are released into the bloodstream by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes bacteria, affecting vital organs like the heart, liver, and kidneys. Wounds, surgical incisions, nasal packs, scrapes, burns, or other exposed areas of injured skin present as major risk factors for the development of the infection.

What Are the Types of Bacteria Causing Toxic Shock Syndrome?

• Staphylococcus Aureus: This bacteria is a normal habitant of the human body and resides on the skin. It gains entry into the bloodstream when the immune system is compromised and can enter through wounds and small tears in the vagina caused due to tampon usage.

• Streptococcus Pyogenes: The bacteria usually infect people who have a previous history of scarlet fever, impetigo, and other group A streptococcus infections.

• Clostridium Sordellii: This bacteria normally is found in the vagina and enters the host during menstruation, childbirth, and other gynecological procedures. The infection can also affect drug abusers.

What Happens When the Bacteria-Causing Toxic Shock Syndrome (TSS) Enters Into the Body?

• TSS is a superantigen-initiated disease. The toxins produced by the bacterial strains act as superantigens.

• Superantigens are proteins that bypass conventional steps in antigen-mediated immune response, thereby activating the immune system.

• Superantigens cause T-cell activation by binding to T-cell receptors and MHC class II molecules on antigen-presenting cells, releasing cytokines, tumor necrosis factor-α (TNFα), interleukin (IL)-6, interferon-γ, and IL-2 which are the pro-inflammatory chemical substances.

• T-cell activation also results in bringing more T and B cells (immune cells) to the site of infection, activating the antigen-presenting cells and resulting in the further release of inflammatory mediators like IL-1 and TNFα.

• Clinical manifestations like fever, hypotension, tissue injury, and shock occur due to the extreme levels of cytokines in the blood.

What Are the Clinical Features Of Toxic Shock Syndrome?

TSS caused by Staphylococcus aureus and or Streptococcus pyogenes are both associated with features of acute illness such as fever, hypotension, sudden occurrence of renal failure, and involvement of the multisystem organ system. However, clinical features in both cases differ from each other in various aspects, which are summarized as follows,

Staphylococcal Toxic Shock Syndrome:

1. Fever.

2. Diffuse rashes.

3. Desquamation (loss of upper layer of skin) of palms and soles after one to two weeks.

4. Hypotension.

5. Nausea and vomiting.

6. Extreme myalgia, excess creatinine phosphokinase levels.

7. Vaginal and other mucous membrane hyperemia.

8. Elevated serum urea nitrogen and creatinine levels.

9. Altered mental status.

Streptococcal Toxic Shock Syndrome:

1. Fever.

2. Hypotension.

3. Osteomyelitis (an infection of the bone).

4. Cellulitis or abscess (a bacterial skin infection).

5. Endocarditis or pericarditis (inflammation of the inner or outer layer of the heart).

6. Myositis (inflammation of the muscles).

7. Necrotizing fasciitis (an aggressive bacterial infection affecting deeper layers of the skin).

8. Respiratory distress syndrome.

9. Generalized erythematous macular rashes (reddish, small, discolored flat patches on the skin).

What Are the Risk Factors for Developing TSS?

• Increased usage of absorbent tampons.

• Surgical wounds.

• Local infection of the skin or deep tissue.

• Increased usage of a diaphragm or contraceptive sponge.

• Previous abortions and childbirth.

How Is Toxic Shock Syndrome Diagnosed?

The diagnostic criteria include the following clinical features:

• Rapidly dropping blood pressure.
• Shock.
• Impaired kidney function.
• Bleeding problems.
• Easily bruising skin owing to low blood platelet count.
• Red, flat rash that covers large areas of the body.
• Liver dysfunction.
• Desquamation of the skin.
• Breathing difficulties.

The diagnostic tests are as follows:

1. Blood tests are investigated to detect an increase in immature neutrophils, thrombocytopenia, anemia, and disseminated intravascular coagulation.

2. Hypocalcemia, hypoproteinemia, and elevated creatinine phosphokinase levels give a clue to the diagnosis.

3. Urine tests detect increased elevated blood urea nitrogen and creatinine levels.

4. Abnormal liver function tests reveal increased ALT (alanine transaminase) levels, AST (aspartate transaminase) levels, and total bilirubin levels.

5. A culture of mucous membranes like the vagina, cervix, or throat is done to isolate beta-hemolytic streptococcus bacteria.

6. If toxins have caused multi-organ involvement, it is imperative to investigate a CT (computed tomography) scan or chest X-ray to assess the extent of disease progression and manage the case effectively.

How Is Toxic Shock Syndrome Treated?

• TSS in a child is treated by maintaining hemodynamic stability and administration of specific antimicrobials to eliminate bacterial infection.

• The hypovolemic shock caused by capillary leakage, vasodilatation, and fluid loss should be managed as soon as possible by fluid resuscitation.

• Isotonic sodium chloride (crystalloid solution) and Ringer’s lactate (colloidal solution) are the main treatments of choice given to correct the fluid imbalance.

• Patients should be continuously resuscitated with multiple liquid boluses to counteract the volume depletion and capillary leakage.

• Dobutamine, Dopamine, and Norepinephrine are the inotropic agents used as adjuncts to fluid resuscitation for adequate perfusion of vital organs.

• Renal failure and respiratory distress syndrome should be managed in time.

• Infections caused by Streptococcus pyogenes and Staphylococcus aureus should be started with parenteral antibiotic coverage initially until the laboratory tests confirm the diagnosis, as the infections resemble each other.

• Infected wounds must be debrided at regular time intervals to prevent bacterial colonization. The abscesses need to be drained and debrided regularly to prevent secondary infections.

• Nafcillin, Oxacillin, and first-generation Cephalosporins are the drugs of choice to treat staphylococcus infection.

• Prompt antimicrobial therapy for ten to 14 days must be administered to eliminate the organism and avoid re-infections

• Streptococcus pyogenes infection is treated by administering Intravenous Penicillin G (200 000 to 400 000 U/kg/day) in four to six divided doses.

• Intravenous Clindamycin (25 to 40 mg/kg/day) is divided into three or four doses and is given as an adjunct to Penicillin to treat streptococcus infections.

• Intravenous immunoglobulin (IVIG) of 1 to 2 g/kg is given once daily as an adjunct to antimicrobial therapy as IVIG inactivates staphylococcal and streptococcal superantigens by decreasing cytokine production and inhibition of T-cell stimulation.

• Toxoids are given as they aid in producing toxin-specific neutralizing antibodies, which cause neutralization of superantigens, and hence, potential complications of streptococcal infections can be avoided.

Conclusion:

Pediatric toxic shock syndrome is a serious emergency that requires immediate medical care, failing which leads to increased fatality rates. TSS treatment protocols in children should include meticulous hemodynamic stabilization and appropriate antimicrobial therapy to eliminate the bacteria. Supportive therapy and aggressive fluid resuscitation play important roles in tissue perfusion. With a timely diagnosis and aggressive management, pediatric toxic shock syndrome can have better outcomes.