eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Toxic Shock Syndrome: Treatment & Medication

Author: Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Coauthor(s): Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
Contributor Information and Disclosures

Updated: Jan 27, 2009

Treatment

Medical Care

Seriously ill patients may require care in the ICU, including dialysis for renal failure, ventilatory support for acute respiratory distress syndrome (ARDS), and correction of coagulopathy using plasma and blood products as necessary. Treatment regimens for toxic shock syndrome (TSS) include the following:

  • Staphylococcal toxic shock syndrome
    • Aggressive fluid support with normal saline or colloids
    • Vasopressor/inotrope infusion as necessary
    • Antistaphylococcal antibiotics (nafcillin and clindamycin or vancomycin and clindamycin in patients with penicillin allergy)
    • Removal of tampons, nasal packing, and other foreign objects
    • Intravenous immunoglobulin (IVIG) therapy (sporadically reported to have salutary effects; controlled trials are inconclusive)
    • Aggressive supportive care in an ICU
  • Streptococcal toxic shock syndrome
    • Normal saline or colloids may be used. Intractable hypotension that results from diffuse capillary leaking may require large amounts of these fluids. Albumin replacement may be necessary in patients in whom albumin levels drop lower than 2 g/dL.
    • Perform vasopressor/inotrope infusion as necessary.
    • Surgical debridement is mandatory in the presence of tissue necrosis.
    • Use penicillin plus clindamycin for antibiotic treatment. Clindamycin therapy for streptococcal toxic shock syndrome produces better results than penicillin alone for the following reasons:
      • Clindamycin is affected less by the growth stage of an organism than penicillin, which acts only on organisms in the growth phase and not on those in the stationary phase.
      • Clindamycin suppresses toxin production by the organism.
      • Clindamycin suppresses cytokine production by monocytes.
      • Clindamycin inhibits the synthesis of penicillin-binding proteins.
      • Clindamycin has a longer postantibiotic effect than do beta-lactam antibiotics.
    • Studies have suggested a salutary effect of IVIG therapy. In one such comparative observational study of patients treated with IVIG, the mortality rate decreased to 34%, compared with a mortality rate of 67% in historical control subjects.6 In the future, double-blind trials may further clarify the role of IGIV in streptococcal toxic shock syndrome.7
    • Aggressive supportive care in an ICU is needed.
    • The role of hyperbaric oxygen in streptococcal toxic shock syndrome remains uncertain in the absence of any comparative clinical trials.

Surgical Care

  • Perform debridement of any necrotizing skin lesion, such as may be seen in patients with streptococcal toxic shock syndrome.
  • Remove tampons, if present, in patients with staphylococcal toxic shock syndrome.
  • Surgical debridement of necrotic tissue should be promptly performed in patients with necrotizing fasciitis and streptococcal toxic shock syndrome.

Consultations

  • Infectious diseases specialist
  • Surgeon, if debridement is considered
  • Other specialists and subspecialists, as the clinical situation dictates

Diet

  • No special diet is necessary.

Medication

The goal of medical therapy is to eradicate infection and to prevent complications.

Antibiotics

Antibiotics are used to kill the infective organisms in patients with toxic shock syndrome (TSS). Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Antibiotic therapy should be used for 10-14 days.


Nafcillin (Nafcil, Unipen)

IV penicillinase-resistant penicillin.

Adult

500 mg to 2 g IV/IM q4-6h; not to exceed 12 g/d

Pediatric

50-100 mg/kg/d IV/IM divided q6h; not to exceed 12 g/d

Associated with warfarin resistance when administered concurrently; effects may decrease with bacteriostatic action of tetracycline derivatives

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hepatic or renal impairment (decrease dose)


Vancomycin (Lyphocin, Vancocin)

IV antibiotic used to treat serious infection. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci.

Adult

500 mg IV q6h or 1 g q12h; adjust dose for renal insufficiency

Pediatric

Neonates:
<7 days and <1200 g: 15 mg/kg IV q24h
<7 days and >1200 g: 10-15 mg/kg IV q8-18h
>7 days and <2000 g: 10-15 mg/kg IV q8-24h
>7 days and >2000 g: 15-20 mg/kg IV q8h
Infants and children: 10 mg/kg IV q6h; not to exceed 1 g/dose

Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal failure and neutropenia; red man syndrome is caused by too-rapid IV infusion (ie, dose administered over a few minutes), but rarely occurs with dose administered over 2 h or PO or IP administration; red man syndrome is not allergic reaction; serum level peaks at 25-40 mcg/mL; trough level is 5-10 mcg/mL


Clindamycin (Cleocin)

Lincosamide antibiotic that inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes that cause RNA-dependent protein synthesis to arrest. Is coadministered with penicillin because it is less affected by the growth stage of organisms than penicillin. Suppresses toxin production by the organism. Suppresses cytokine production by monocytes. Inhibits the synthesis of penicillin-binding proteins and has a longer postantibiotic effect than do beta-lactam antibiotics.

Adult

600 mg IV q6h or 900 mg IV q8h
150-450 mg PO q6h

Pediatric

25-40 mg/kg/d IV/IM divided q6-8h; not to exceed 4.8 g/d IV

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, and antibiotic-associated colitis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal pseudomembranous colitis


Penicillin G (Pfizerpen)

A beta-lactam antibiotic that acts by inhibiting cell wall synthesis in susceptible organisms.

Adult

1-2 million U IV q4-6h

Pediatric

25,000-50,000 U/kg IV q6h

Probenecid can increase effects; coadministration of tetracyclines can decrease effects

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hypersensitivity reactions occur in 1-4% of patients, including anaphylaxis in 0.004-0.015%; Coombs-positive hemolytic anemia, drug fever, serum sickness, and maculopapular eruption may be noted; seizures occasionally are observed when high-dose therapy is used in patients with renal failure

Immunoglobulin

This agent is a purified preparation of gamma globulin. It is derived from large pools of human plasma and comprises 4 subclasses of antibodies, approximating the distribution in human serum. Immunoglobulin therapy is intended to neutralize the toxins that cause TSS.


Immunoglobulin intravenous (Carimune NF, Gammagard S/D, Gammar-P)

Actions include neutralizing circulating myelin antibodies through anti-idiotypic antibodies, down-regulating proinflammatory cytokines (including interferon gamma), blocking Fc receptors on macrophages, suppressing inducer T and B cells, and augmenting suppressor T cells. Also blocks the complement cascade and promotes remyelination. May increase CSF IgG (10%).
IVIG has been shown to have high concentration of TSST-1 and the staphylococcal enterotoxins implicated in the pathogenesis of TSS. These antibodies may interfere with the binding of toxins that cause TSS.

Adult

400 mg/kg IV as single dose infused over several hours

Pediatric

Administer as in adults

Globulin preparation may interfere with immune response to live virus vaccine (MMR) and reduce efficacy (do not administer within 3 mo of vaccine)

Documented hypersensitivity; IgA deficiency; anti-IgE/IgG antibodies

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Check serum IgA before IVIG (use IgA-depleted product, eg, Gammagard S/D); infusions may increase serum viscosity and thromboembolic events; infusions may increase risk of migraine headaches, aseptic meningitis (10%), urticaria, pruritus, or petechiae (2-30 d postinfusion)
Increases risk of renal tubular necrosis in elderly patients and in patients with diabetes, volume depletion, and preexisting kidney disease; changes in laboratory test results associated with infusions include elevated antiviral or antibacterial antibody titers for 1 mo, 6-fold increase in ESR for 2-3 wk, and apparent hyponatremia

Vasopressors

Vasopressors are used to correct hypotension. These agents augment both coronary and cerebral blood flow.


Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced by higher doses. After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. Satisfactory maintenance dose is <20 mcg/kg/min in more than 50% of patients.

Adult

1-5 mcg/kg/min IV; not to exceed 50 mcg/kg/min

Pediatric

Administer as in adults

Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia


Norepinephrine (Levophed)

Used in protracted hypotension following adequate fluid-volume replacement. Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility, heart rate, and vasoconstriction. As a result, systemic blood pressure and coronary blood flow increases. After obtaining a response, the rate of flow should be adjusted and maintained at a low normal blood pressure, such as 80-100 mm Hg systolic, sufficient to perfuse vital organs.

Adult

2 mcg/kg/min IV; titrate to effect

Pediatric

0.1 mcg/kg/min IV; titrate to effect

Effects increase when administered concurrently with tricyclic antidepressants, monoamine oxidase inhibitors, antihistamines, guanethidine, methyldopa, or ergot alkaloids; atropine may block reflex tachycardia caused by norepinephrine and enhances pressor response

Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia and area of infarction may be increased

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Correct blood-volume depletion, if possible, before administering norepinephrine therapy; extravasation may cause severe tissue necrosis, thus, should be administered into large veins; caution in occlusive vascular disease


Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher doses, may cause increased heart rate, exacerbating myocardial ischemia.

Adult

5-20 mcg/kg/min IV continuous infusion

Pediatric

Administer as in adults

Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Following myocardial infarction, use with extreme caution; hypovolemic state should be corrected before administration

More on Toxic Shock Syndrome

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Treatment & Medication: Toxic Shock Syndrome
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Multimedia: Toxic Shock Syndrome
References
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Further Reading

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Keywords

toxic shock syndrome, TSS, acute respiratory distress syndrome, conjunctival hyperemia, cyanosis, endophthalmitis, erythroderma, hypotension, leptospirosis, measles, menses, menstruation, myocarditis, myositis, perihepatitis, peritoneal effusions, peritonitis, pleural effusions, Rocky Mountain spotted fever, soft tissue necrosis, staphylococcal infection, staphylococcal TSS, Staphylococcus aureus, S aureus, streptococcal infection, streptococcal TSS, Streptococcus pyogenes, S pyogenes, tampon use, TSS toxin-1, TSST-1, vaginal hyperemia

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Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
Vinod K Dhawan, MD, FACP, FRCP(C) is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada
Disclosure: Pfizer Inc None None

Medical Editor

David Jaimovich, MD, Chief Medical Officer, Joint Commission International and Joint Commission Resources
David Jaimovich, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

 
 
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