Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome

Dr. Batizy, D.O. January 26, 2006

Toxic Shock Syndrome



Severe life threatening syndrome characterized by:

High fevers  Severe hypotension  Diffuse erythroderma  Mucous membrane hyperemia  Pharyngitis  Diarrhea


Toxic Shock Syndrome

    

May progress rapidly Multisystem disfunction Severe electrolyte disturbances Renal failure Shock

Toxic Shock Syndrome



  

Discovered in 1978 in apparently healthy children Staph aureus isolated TSS epidemic 1981 associated with increased tampon use Incidence has dropped significantly, Currently most cases are unrelated to menses Case Definition of Toxic Shock Syndrome, table 142142-1

Case Definition of Toxic Shock Syndrome, Table 142-1 142   

Fever temp >102.0 F (>38.9 C) Rash: diffuse macular erythroderma Hypotension Multisystem envolvement (three or more)
GI: vomiting or diarrhea at onset of illness  Muscular: sever myalgia or creatine phosphokinase level at least twice the upper limit of normal  Mucous membrane: vaginal, oropharyngeal, or conjunctival hyperemia


Renal: blood urea nitrogen or creatinine at least twice the upper limit of normal for laboratory or urinary sediment with pyuria (greater than or equal to 5 leukocytes per highpower field) in the absence of urinary tract infection Hepatic: total bilirubin, alanine aminotransferase enzyme, or asparate aminotransferase enzyme levels at least twice the upper limit of normal for laboratory Hematologic: platelets less than 100,000/ml

CNS: disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent Lab criteria: negative results on the following tests, if obtained:
Blood, throat, or cerebrospinal fliud cultures (blood culture may be positive for Staphlococcus aureus  Rise in titer to Rocky Mountain Spotted fever, leptospirosis, or measles


Case Definition of TSS



Case classification
Probable: five of six clinical findings are present  Confirmed: all six clinical findings are present, including desquamation, unless patient dies before desquamation occurs


Epidemiology


 

TSS initially a disease of young healthy menstruating women, comprised fifty percent of cases reported in 1986-87 1986Tampon use increased risk up to 33% In 2000, 135 reported cases, 3 were in men, and 2 fatalities were from menstrual-related TSS menstrual(MRTSS) FDA - Tampons now made of cotton and rayon, should be changed every 4-8 hrs 4-

Epidemiology


NonNon-menstrual related cases of Toxic Shock Syndrome (NMTSS)

Increasing since 1980  41% NMTSS  Men comprise one-tenth of population one


Mortality rate 3.3 x that of MRTSS in women

 

S. aureus isolated from 98% of women with TSS Women with MRTSS most likely colonized with Staph aureus before the onset of menstruation

Epidemiology


TSS associated with influenza or influenza-like influenzaillnesses mortality rate (43%) Nasal packing (nasal tampons) also associated with TSS

Pathophysiology
 

Most TSS associated with S. aureus TSST-1: toxic shock syndrome toxin, exotoxin TSSTInduce fever via the hypothalamus or via IL-1 and ILTNF  T-lymphocyte superantigenation and overstimulation  Induce interferon production  Enhance delayed hypersensitivity  Supress neutrophil migration and IG secretion  Enhance host suseptibility to exotoxins


Pathophysiology


Enterotoxins B and C
Similar chemical structure to TSST-1 TSST Seen primarily in NMTSS  Elicit similar clinical manifestations as TSST-1 TSST

Pathophysiology


Vaginal conditions favorable to TSST-1 TSSTTemp 39-40 C 39 Neutral pH  PO2 > 5%  Supplemental CO2  Menstruation neutralizes vaginal pH  Tampon use may increase O2 and CO2  Synthetic fibers in tampon composition  Synergistic relationship between S. aureus and E. coli


Pathophysiology
 

Vasodilation rapid and massive onset Hypotension

Decreased vasomotor tone, blood pooling, decreased vascular return  Nonhydrostatic leakage of fluid into the interstitium, contributing to hypotension and nonpitting edema of the head and neck  Depressed cardiac function  Total body water deficits from vomiting and diarrhea and fever


Pathophysiology


ILIL-1


Hypoalbuminemia, hypoferrinemia, and proteolysis manifest as peripheral edema, anemia, and rhabdomyolysis seen in TSS

TNF
Acidosis, shock, and multisystem organ failure  Multisystem organ failure


Direct result from toxin  Rapid onset of hypotension and decreased perfusion


Small amts of TSST-1 and enterotoxins B and C can TSSTbe detected in pts with TSS up to 1 year

Clinical Features


TSS must be considered when



Unexplained febrile illness with erythroderma, hypotension, and diffuse organ pathology

Pts with NMTSS present 3rd to 5th days of menses Postoperative NMTSS approx 2 days

Clinical Features


Mild TSS:
Fever  Chills  myalgias  Abdominal pain  Sore throat  Nausea  Vomiting  Diarrhea  Self-limiting Self

Clinical Features


Severe
Acute onset  Early multiorgan envolvement  Prodrome


Headache, malaise, myalgias, nausea, vomiting, and diarrhea  Sudden onset of fevers and chills 1-4 days prior to 1presentation


Orthostatic lightheadedness, profuse watery diarrhea, sore throat, paresthesias, photophobia, abdominal pain, and cough

Clinical Presentation


PE
Hypotension  Pt appears acutely ill  Change in mental status  Oliguria  Nonpitting edema of face and extremities  Watery diarrhea  Pharygitis strawberry red tongue  Tender erythematous external genitalia diffuse vaginal hyperemia, strawberry cervix, scant purulent cervical discharge, bilat adenexal tenderness


Clinical Features


Rash diffuse painless blanching erythroderma, fades in three days Followed by full-thickness desquamation fullparticularly of palms and soles of feet Severely affected patients may have hair and nail loss 2-3 months later 2-

Clinical Features
  

Focal neuro findings are rare Varying degrees of altered consciousness Toxic encephalopathy - confusion, disorientation, agitation, hysteria, somnolence, and seizures CT and LP will help deliniate

Clinical Features


Lab findings
        

Leukocytosis lymphocytopenia Anemia ARF: azotemia, myoglobinuria, sterile pyuria, RBC casts Liver abnormalities Metabolic acidosis 2nd to hypotension Electrolyte abnormalities Arrhythmias ARDS

Differential Diagnosis
      

Acute pyelonephritis Septic shock Acute rheumatic fever Scarlet fever: strep or staph etiologies Leigionares disease PID HUS

Differential Diagnosis
         

Acute viral syndrome Leptospirosis SLE Rocky Mountain Spotted fever Tick typhus Gastroenteritis Kawasaki disease Reye syndrome Toxic epidermal necrolysis Erythema multiforme

Treatment
  

  

Aggressive shock management Continuous monitoring: central Aggressive fluid replacement 4-20 L of crystalloid and FFP Ventilatory management if ARDS develops Complete blood work and cultures Removal of foreign bodies, i.e. tampon or nasal packing Antistaphlococcal penicillin or cephalosporin

Treatment
   

Antistaphlococcal penicillin or cephalosporin Nafcillin or oxacillin 2g IV every 4hrs Cefazolin 2g IV every 6hrs Oral anti-staphlococcal ABx for the next 10 -14 antidays

Treatment


Pt not treated with -lactamase-stable abx can lactamasehave recurrence MRTSS recurrence occurs in second month after the initial disease, recurring on the same day of the menstrual cycle Initial episode is the most severe

Streptococcocal Toxic Shock Syndrome



Group A Strep
Soft tissue infection, early shock, multisystem organ failure, higher mortality than TSS, Flesh eating bacteria  Most serious Strep necrotizing fasciitis and myositis


STSS


Most commonly affects 20 50 yr olds without prior illness

STSS


Risk factors
Extremes of age  Diabetes  EtOH  Drug abuse  NSAIDS  Immunodeficiency  Rarely develops from symptomatic pharyngitis


STSS


20002000-3000 cases annually; with 500 to 1500 cases of necrotizing fasciitis

Mortality rate of 30 80%  70% of cases progress to necrotizing fasciitis


Surgical intervention  Mortality


 

Strep fasciitis 60% Strep Myositis 85-100% 85-

Case Definition of Streptococcocal Toxic Shock Syndrome



An illness with
 

Hypotension Multiorgan involvement with two or more of the following:

     

Renal impairment Coagulopathy Liver involvement ARDS Generalized erythematous macular rash that may desquamate Soft tissue necrosis

Case Definition of Streptococcal Toxic Shock Syndrome



Laboratory Criteria


Isolation of group A streptococcus

Case Classification
Probable clinical case definition in the absence of another identified etiology with isolation of group A strep from a nonsterile site  Confirmed clinical case definition with isolation of group A streptococcus from an otherwise sterile site


STSS


Epidemiology
Incidence 1-5 per 100,000  STSS associated Necrotizing Fasciitis 13-46% 13

Pathophysiology


GAS invasive infections more virulent exotoxins than TSS



SPE Streptococcal pyogenic exotoxins



SPE A Scarlet fever toxin most potent and commonly isolated SPE in STSS cases SPE A and B pyrogenicity, superactivation of T-cells, synthesis Tof TNF, IL-1 and IL-6, leading to acidosis, shock, organ failure ILIL-

STSS


Patients without immunity to M-type SPE A and MB producing strains of GAS are most susceptible to STSS Portal of entry
Vagina, pharynx, mucosa, and skin, most are unidentifiable  Commonly begins at site of minor skin trauma


STSS


Clinical Features
 

Pain most common with preceding local tenderness May present as

        

Peritonitis PID Pneumonia Pericarditis Fever Severe pain Swelling Redness Compartment syndrome

STSS


PE
Fever  Shock on admission or within 4-8hrs 4 Vesicles and/or bullae at infection site  ARDS  Less commonly erythematous rash


Labs
Mild increase in WBC  LFT 2x normal


STSS


Labs
Decreased platelets  Disseminated intravascular coagulopathy  Renal dysfunction requiring dyalysis  Blood cultures - +GAS 60%  Tissue cultures 90%


STSS


Diagnosis


Differential is the same as for TSS with the addition of invasive and noninvasive GAS infections, necrotizing fasciitis, myositis, serious infections caused by C. perforingens and C. septicum, and mixed septicum, aneorbic and aerobic organisms Aggressive shock management with early use of vasopressors

Treatment


STSS


IV ABx should be started in the ED once cultures have been taken. Inability to obtain Cx should not delay administration of IV ABx
Pen G 24 million U/d divided  Clindamycin 900mg IV q 8hr  Erythromycin 1g IV q 6 hr in PCN allergic pts  Ceftriaxone 2g IV q 24 hr with Clindamycin 900mg IV q 8hr  IVIG 2g/kg q 48 hr in patients without IGA deficiency improve 30 day mortality


STSS


Surgery


Prompt consultation in addition to IV ABx

Exploration  Debridement  70% of cases require debridement, fasciotomy, or amputation


TSS and STSS



1.) Toxic Shock Syndrome is only a disease of young healthy menstruating women. T/F 2.) The rash of TSS is a diffuse, blanching, erythroderma, classically described as a painless sunburn, that fades within 3-4 days of its 3appearance and is followed by full-thickness fulldesquamation of the palms and soles during convalescence. T/F

TSS and STSS



3.) STSS is defined as any group A streptococcocal (GAS) infection with invasive soft tissue infection, early onset of shock, and organ failure. T/F 4.) STSS associated with GAS invasive infections most commonly affects individual between the ages of 20 50 with a predisposing illness. T/F Answers: 1.) F, 2.) T, 3.) T, 4.) F

TSS and STSS



Tintinalli et al; Emergency Medicine: A Medicine: Comprehensive Study Guide. Chap. 142, pg. 913913-918.