Toxic Shock Syndrome and
Streptococcal Toxic Shock
Tintinalli Chapter 142
Toxic Shock Syndrome (TSS)
• Life Threatening • Pharyngitis
• High fever • Diarrhea
• Profound hypotension • Mucous membranes
• Diffuse erythroderma hyperemia
• 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.
• 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
• S. Aureus has been isolated from the vaginas of 98
percent of women with TSS presumably due to
• 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.
• 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.
• There is massive vasodilatation and
movement of fluid to the extravascular
• 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.
• Consider TSS with unexplained febrile illness,
erythroderma, hypotension and diffuse organ
• Usually present between the third and fifth day of
• 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
• Severe TSS is an acute-onset multisystem disease
with symptoms, signs and laboratory
• 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
• Hypotension or an • Profound muscle
orthostatic decrease in weakness and tenderness
SBP of 15 mm Hg • Abdominal tenderness
• May be obtunded, • Profuse watery diarrhea
disoriented associated with
• Non pitting edema of face incontinence
and extremities • Conjunctiva hyperemia
• Pharyngitis with • Vaginitis with strawberry
strawberry red tongue (1/3 cervix
of the patients) • Oliguric
• Rash of TTS is diffuse • Neuro exam is non
blanching erythroderma specific
described as painless • Pt may present with
“sunburn” disorientation, hysteria,
• Fades within 3 days agitation, somnolence, and
followed by full-thickness seizures
desquamation, especially • If clinical picture is
on palms and soles 6-14 unclear, CT and lumbar
days after onset of illness. puncture should be
• Leukocytosis • Metabolic acidosis
• Lymphocytopenia • Hypokalemia,
• Mild anemia hypophosphatemia,
• Azotemia hyponatremia
• Myoglobinuria • Hypocalcemia-check Mg
• Sterile pyuria and red • Ventricular arrhythmias,
blood cell casts bundle brunch block, first
• Liver function AV block
• Echocardiogram with wall
• Hyperbilirubinemia motion abnormalities
• 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
• Rocky Mountain spotted fever-rash is petechial
and delayed in onset
• Toxic epidermal necrolysis
• Septic Shock
• See table 142-2
• Most important aspect is management of
• 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,
• Foreign bodies should be removed
-Early consultation with surgeon or gynecologist for
-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
-If PCN-allergic, clindamycin, vancomycin or first-
-Parenteral antibiotics should be given for 3 days at
least or until clinical improvement.
• Oral antibiotics should be given for additional 10-
• 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
Streptococcal Toxic Shock
• 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
• GAS known as “flesh-eating bacteria” is
associated with streptococcal necrotizing fasciitis
and streptococcal myositis.
• See table 142-3 for complete definition.
• 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
• 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
• Streptococcal pyogenic exotoxins (SPEs) are the
• SPEs like TSS-mediated exotoxins induce
interleukins, TNF, T-cells.
• Portal of entry includes vagina, pharynx, mucosa,
• Cases have been developed from burns
lacerations, abrasions, hematomas, minor muscle
injuries, orthopedic procedures, and recent
infections with influenza and varicella.
• Pain is most common initial symptom.
• Fever is the most common early sign.
• 20 percent of patients have prodromal
• Swelling, erythema at the site of infection
may be seen.
• Very difficult to distinguish STSS from
• 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
• ARDS develops in 55 percent of patients.
• Rash develops in 10 percent of patients.
• Mild leukocytosis • Renal failure-dialysis
• Profound bandemia is required commonly
• Elevated LFTs • Elevated creatinine
• Thrombocytopenia- kinase if necrosis
may progress to DIC • Positive GAS blood
• Same as in TSS with the addition of
Clostridium Perfringens, C. Septicum and
• 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
• Aggressive exploration and debridement of
infection sites is mandatory-seek surgery