Toxic Shock Syndrome and Streptococcal Toxic Shock Syndrome

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					Toxic Shock Syndrome and
Streptococcal Toxic Shock
        Syndrome
     Tintinalli Chapter 142
    Toxic Shock Syndrome (TSS)
•   Life Threatening       • Pharyngitis
•   High fever             • Diarrhea
•   Profound hypotension   • Mucous membranes
•   Diffuse erythroderma     hyperemia
                       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.
               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.
             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.
             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.
           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.
             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
            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.
          Physical Examination
• 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
           Physical Examination
• 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
                                   performed
            Laboratory findings
• 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
  abnormalities
                           • Echocardiogram with wall
• Hyperbilirubinemia         motion abnormalities
          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
               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
                  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.
                  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.
Streptococcal Toxic Shock
        Syndrome
                      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.
                  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
                   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
             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.
            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.
        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.
           Laboratory findings
•   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
                            cultures
       Differential Diagnosis
• Same as in TSS with the addition of
  Clostridium Perfringens, C. Septicum and
  mixed organisms
                  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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posted:10/19/2011
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