Overview
Definition:
Toxic Shock Syndrome (TSS) is a severe, multisystem illness characterized by fever, rash, hypotension, and multi-organ involvement, typically caused by toxin-producing strains of *Staphylococcus aureus* or *Streptococcus pyogenes*
Clindamycin is crucial for its role in toxin suppression, in addition to its bactericidal activity, which is vital in managing certain forms of TSS.
Epidemiology:
TSS can occur in any age group but is less common in infants and very young children
It is associated with the use of certain tampons, surgical packing, and in children, with skin infections, wounds, or viral infections like varicella
Incidence varies, but prompt recognition and management are critical due to high morbidity and mortality.
Clinical Significance:
TSS is a medical emergency requiring immediate diagnosis and aggressive treatment
Understanding the role of antibiotics like clindamycin in not only eradicating the bacteria but also suppressing toxin production is paramount for effective patient outcomes, especially in critically ill pediatric patients.
Clinical Presentation
Symptoms:
Sudden onset of high fever (typically >38.5°C or 101.3°F)
Diffuse erythematous rash, often described as sunburn-like, which may desquamate 1-2 weeks after onset
Hypotension or orthostatic hypotension
Vomiting and diarrhea
Myalgias
Pharyngitis
Conjunctival injection
Mental status changes.
Signs:
Generalized erythroderma
Mucous membrane hyperemia (oral, conjunctival, vaginal)
Hypotension (systolic blood pressure <90 mmHg in adults, or <5th percentile for age in children)
Tachycardia
Signs of multi-organ dysfunction including decreased urine output, elevated liver enzymes, thrombocytopenia, elevated creatinine, and altered mental status.
Diagnostic Criteria:
Clinical diagnosis is often based on revised diagnostic criteria
Key features include fever (>38.5°C), rash, hypotension, and involvement of at least three organ systems (e.g., gastrointestinal, musculoskeletal, renal, hepatic, hematologic, central nervous system, or cardiovascular)
Microbiologic evidence of *S
aureus* or *S
pyogenes* is supportive but not always present.
Diagnostic Approach
History Taking:
Detailed history focusing on the onset and progression of symptoms
Recent infections (e.g., skin, respiratory, genitourinary)
Use of menstrual products or wound care
Any recent surgeries or trauma
Exposure to ill contacts
Vaccinations and underlying medical conditions.
Physical Examination:
Thorough physical exam to assess vital signs (temperature, heart rate, blood pressure, respiratory rate)
Skin examination for rash characteristics and distribution, looking for any focal source of infection
Examination of mucous membranes for erythema
Systemic examination to identify signs of organ dysfunction.
Investigations:
Complete blood count (CBC) with differential may show leukocytosis with a left shift
Thrombocytopenia is common
Comprehensive metabolic panel (CMP) to assess renal and hepatic function, electrolytes
Coagulation studies (PT, PTT, INR)
Blood cultures to identify bacteremia
Wound cultures, throat swabs, or vaginal swabs if indicated
Inflammatory markers like CRP may be elevated
Urinalysis to assess for renal involvement.
Differential Diagnosis:
Scarlet fever (caused by streptococcal exotoxins, but usually presents with a different rash morphology and without severe hypotension)
Kawasaki disease (typically chronic fever, conjunctivitis, rash, but more prolonged course and distinct criteria)
Meningococcemia (rapidly progressive sepsis with petechial or purpuric rash)
Stevens-Johnson syndrome/Toxic Epidermal Necrolysis (distinctive mucocutaneous involvement)
Viral exanthems.
Management
Initial Management:
Immediate hospitalization, often in an intensive care unit (ICU)
Hemodynamic support with intravenous fluids (crystalloids) to maintain blood pressure
Vasopressors may be required if hypotension persists despite fluid resuscitation.
Medical Management:
Aggressive antimicrobial therapy is crucial
Clindamycin is preferred for *S
aureus* TSS due to its ability to inhibit protein synthesis and thereby toxin production (especially TSST-1 and exfoliative toxins), in addition to its bacteriostatic/bactericidal activity
Standard regimen: Clindamycin 10-15 mg/kg/dose IV every 8 hours for 7-14 days
Vancomycin may be used in areas with high rates of methicillin-resistant *S
aureus* (MRSA) or if *S
aureus* is isolated and susceptible to vancomycin
For *Streptococcus pyogenes* TSS, penicillin G is the drug of choice, often combined with clindamycin for toxin suppression
Other antibiotics may be considered based on sensitivities
Intravenous immunoglobulin (IVIG) may be beneficial in severe cases, particularly streptococcal TSS, to neutralize circulating toxins.
Surgical Management:
Identification and drainage of any infected focus (e.g., abscess, infected wound, osteomyelitis)
Removal of foreign bodies (e.g., tampons, surgical packing) if implicated
Surgical debridement of necrotic tissue may be necessary in severe wound infections.
Supportive Care:
Close monitoring of vital signs, fluid balance, and organ function
Respiratory support if indicated (e.g., mechanical ventilation)
Renal replacement therapy if acute kidney injury is severe
Nutritional support
Pain management
Close follow-up of desquamation and skin healing.
Complications
Early Complications:
Acute Respiratory Distress Syndrome (ARDS)
Acute kidney injury
Hepatic failure
Myocardial dysfunction
Disseminated Intravascular Coagulation (DIC)
Shock
Seizures
Coma
Limb ischemia due to vascular compromise.
Late Complications:
Desquamation of skin, particularly on palms and soles, which can be extensive and painful
Long-term sequelae from organ damage, though usually reversible with prompt treatment
Psychological impact on patients and families.
Prevention Strategies:
Patient education on proper tampon use (change frequently, do not use superabsorbent tampons continuously)
Strict hygiene during wound care and after surgery
Prompt medical attention for any signs of infection
Early recognition and management of suspected cases.
Prognosis
Factors Affecting Prognosis:
Promptness of diagnosis and initiation of treatment
Severity of illness at presentation
Presence of multi-organ failure
Age of the patient
Underlying health status
Causative organism (streptococcal TSS generally carries a poorer prognosis than staphylococcal TSS).
Outcomes:
With timely and aggressive management, the mortality rate has significantly decreased
However, TSS remains a life-threatening condition
Patients can recover fully, but prolonged hospitalization and intensive supportive care are often required
Recurrence is possible if the underlying source of infection or predisposing factor is not completely addressed.
Follow Up:
Close outpatient follow-up is essential to monitor for any residual organ dysfunction, skin healing, and to address any psychosocial needs
Education for patients and families regarding signs of recurrence and when to seek immediate medical attention is crucial.
Key Points
Exam Focus:
Remember clindamycin's dual role: bactericidal/bacteriostatic AND toxin suppression
Recognize the diagnostic criteria for TSS
Differentiate TSS from other febrile illnesses with rash
Understand the importance of hemodynamic support and source control.
Clinical Pearls:
Always consider TSS in a febrile child with a diffuse rash and hypotension, especially if gastrointestinal symptoms are present
Don't forget to look for a focal source of infection
IVIG can be a valuable adjunct in severe cases, particularly streptococcal TSS.
Common Mistakes:
Delayed recognition of TSS due to its mimicry of other common illnesses
Inadequate fluid resuscitation
Failure to initiate appropriate antibiotic therapy promptly, especially clindamycin for toxin suppression
Overlooking a treatable source of infection.