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Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome

Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome. Tintinalli Chapter 142. Life Threatening High fever Profound hypotension Diffuse erythroderma. Pharyngitis Diarrhea Mucous membranes hyperemia. Toxic Shock Syndrome (TSS). TSS.

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Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome

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  1. Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome Tintinalli Chapter 142

  2. Life Threatening High fever Profound hypotension Diffuse erythroderma Pharyngitis Diarrhea Mucous membranes hyperemia Toxic Shock Syndrome (TSS)

  3. TSS • It can progress to multisystem dysfunction, renal failure and shock. • Initially associated with Staph Aureus infections. • In 1981 there was an epidemic of TSS associated with extended tampon use. • Over the last decade streptococcal toxic shock syndrome has emerged (STSS). • See Table 142-1 for the CDC definition.

  4. Epidemiology • The proportion of non-menstrual-related TSS (NMTSS) has increased since 1980 although the absolute number of cases has remained constant. • Nonsurgical skin lesions are more frequently associated with NMTSS in children 2 years or older • S. Aureus has been isolated from the vaginas of 98 percent of women with TSS presumably due to colonization.

  5. Epidemiology • TSS has also been reported following influenza and influenza-like illnesses with significant mortality rate (43 percent). • Nasal packing is also associated with TSS, with 20 to 40 percent of the population carrying S.Aureus in the nasal vestibule. • Body art/piercing is also another route.

  6. Pathophysiology • Toxic Shock Syndrome Toxin (TSST-1) is the primary mediator by acting on hypothalamus, IL-1 and TNF to produce fever, stimulates T-lymphocytes, enhances delayed hypersensitivity, suppresses neutrophil migration and enhances susceptibility to endotoxins. • The amount of TSST-1 is enhanced by temperature of 39-400C, neutral pH, pO2 greater than 5 percent, and supplemental CO2 , conditions that are met during menses and introduction of tampons or intravaginal devices.

  7. Pathophysiology • There is massive vasodilatation and movement of fluid to the extravascular space. • Hypotension occurs due to decreased vasomotor tone, decreased venous return, decreased intravascular volume, depressed cardiac function, and total body water deficit due to diarrhea, fever, vomiting.

  8. Clinical Features • Consider TSS with unexplained febrile illness, erythroderma, hypotension and diffuse organ pathology. • Usually present between the third and fifth day of menses. • In postoperative cases, onset is on POD #2. • Mild TSS is characterized by fever and chills, myalgias, abdominal pain, sore throat, nausea, vomiting and diarrhea. • Usually self limited

  9. Clinical Features • Severe TSS is an acute-onset multisystem disease with symptoms, signs and laboratory abnormalities. • Headache is the most common complaint. • Patients may have a prodrome consisting of malaise , myalgias, headache, n/v and diarrhea. • Fever develops suddenly in 1-4 days. • Diffuse proximal myalgia are present in majority of patients.

  10. Hypotension or an orthostatic decrease in SBP of 15 mm Hg May be obtunded, disoriented Non pitting edema of face and extremities Pharyngitis with strawberry red tongue (1/3 of the patients) Profound muscle weakness and tenderness Abdominal tenderness Profuse watery diarrhea associated with incontinence Conjunctiva hyperemia Vaginitis with strawberry cervix Oliguric Physical Examination

  11. Rash of TTS is diffuse blanching erythroderma described as painless “sunburn” Fades within 3 days followed by full-thickness desquamation, especially on palms and soles 6-14 days after onset of illness. Neuro exam is non specific Pt may present with disorientation, hysteria, agitation, somnolence, and seizures If clinical picture is unclear, CT and lumbar puncture should be performed Physical Examination

  12. Leukocytosis Lymphocytopenia Mild anemia Azotemia Myoglobinuria Sterile pyuria and red blood cell casts Liver function abnormalities Hyperbilirubinemia Metabolic acidosis Hypokalemia, hypophosphatemia, hyponatremia Hypocalcemia-check Mg Ventricular arrhythmias, bundle brunch block, first AV block Echocardiogram with wall motion abnormalities Laboratory findings

  13. Differential diagnosis • Kawasaki disease –primarily in children • Staphylococcal scalded skin syndrome(SSSS)-only pathologic specimens or serologic evidence of exfoliative toxin will differentiate it from TSS. • Streptoccocal Scarlet fever-”sandpaper” is characteristic • Rocky Mountain spotted fever-rash is petechial and delayed in onset • Toxic epidermal necrolysis • Septic Shock • See table 142-2

  14. Treatment • Most important aspect is management of circulatory shock • Pt may require 4-20 L of crystalloid/FFP in the first 24 hours • Vasopressors as needed (Dopamine) • CBC, CMP, Coags, UA, CXR, Echo, ABG, Blood cultures • Foreign bodies should be removed

  15. Treatment -Early consultation with surgeon or gynecologist for possible drainage -Antibiotics are recommended although they haven’t shown to affect the outcome of acute illness. -Nafcillin or oxacillin 2g IV q 4 h is recommended because of better beta-lactamase activity compared to Cefazolin. -If PCN-allergic, clindamycin, vancomycin or first-generation cephalosporin. -Parenteral antibiotics should be given for 3 days at least or until clinical improvement.

  16. Treatment • Oral antibiotics should be given for additional 10-14 days. • Methylprednisolone and IV immunoglobulin have shown some improvement in some cases of TSS. • Most patients become afebrile and normotensive within 48 hrs. • Pt not treated with beta-lactamase stable antimicrobial drugs can have a recurrence of the disease.

  17. Streptococcal Toxic Shock Syndrome

  18. STSS • Identical in definition to TSS except that it is associated with severe soft tissue infection and cultures must be positive for Strep Pyogenes. • Emerged in late 1980s • Defined as group A Strep infection (GAS), early shock with organ failure and invasive soft tissue infection. • GAS known as “flesh-eating bacteria” is associated with streptococcal necrotizing fasciitis and streptococcal myositis. • See table 142-3 for complete definition.

  19. STTS • Affects usually individuals between the ages 20-50 without predisposing illnesses • Diabetes, alcohol, advanced age, drug abuse, NSAIDS, immunodeficiency appear to be risk factors • Rarely develops from symptomatic pharyngitis

  20. STTS • 2000-3000 new cases every year with mortality at 30 to 80 percent • 70 percent of STTS will progress to necrotizing fasciitis or myositis with mortality of 60 percent and 85 to 100 percent respectively despite aggressive treatment

  21. Pathophysiology • Streptococcal pyogenic exotoxins (SPEs) are the primary mediator. • SPEs like TSS-mediated exotoxins induce interleukins, TNF, T-cells. • Portal of entry includes vagina, pharynx, mucosa, and skin. • Cases have been developed from burns lacerations, abrasions, hematomas, minor muscle injuries, orthopedic procedures, and recent infections with influenza and varicella.

  22. Clinical Features • Pain is most common initial symptom. • Fever is the most common early sign. • 20 percent of patients have prodromal influenza-like symptoms. • Swelling, erythema at the site of infection may be seen. • Very difficult to distinguish STSS from TSS.

  23. Physical Examination • Fever • Shock within 4 to 8 h of admission • Vesicles and bullae at the site of infection with violaceous or blue discoloration is an ominous sign for the development of necrotizing fasciitis. • ARDS develops in 55 percent of patients. • Rash develops in 10 percent of patients.

  24. Mild leukocytosis Profound bandemia Elevated LFTs Thrombocytopenia-may progress to DIC Renal failure-dialysis is required commonly Elevated creatinine kinase if necrosis Positive GAS blood cultures Laboratory findings

  25. Differential Diagnosis • Same as in TSS with the addition of Clostridium Perfringens, C. Septicum and mixed organisms

  26. Treatment • Initial treatment is with fluids and vasopressors. • Antibiotics should be started in ED • IV Pen G 24 million U/d in divided doses plus Clindamycin 900 mg IV q 8 h. • If PCN-allergic Erythromycin 1 g IV q 6 or Rocephin 2 g IV qd with Clindamycin • IV immunoglobulin has improved 30 day survival rates. • Aggressive exploration and debridement of infection sites is mandatory-seek surgery consultation immediately

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