eMedicine Specialties > Emergency Medicine > Infectious Diseases

Toxic Shock Syndrome: Treatment & Medication

Author: Vicken Y Totten, MD, MS, FACEP, FAAFP, Assistant Professor, Case Western Reserve University School of Medicine; Director of Research, Department of Emergency Medicine, University Hospitals, Case Medical Center
Coauthor(s): Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Contributor Information and Disclosures

Updated: Jan 6, 2010

Treatment

Prehospital Care

  • Oxygen should be provided.
  • Aggressive fluid resuscitation should begin in the field, especially for the severely hypotensive patient.
  • If toxic shock syndrome (TSS) is suspected in a menstruating woman, prior to transport, she may be asked to remove her tampon, if possible. There is no research proving that this is necessarily part of prehospital care, but removing all easily removed potential sources of toxin production seems reasonable.
  • Again, if TSS is suspected in the field in a person with deep wound packing, that packing should probably be removed, although no controlled studies have demonstrated a benefit to prehospital packing removal.
  • Rapid transport to a hospital capable of managing severe shock is definitive prehospital management.

Emergency Department Care

Early goal-directed therapy (EGDT) is aimed at hemodynamic optimization within the first 6 hours. It has been shown to reduce mortality in patients with severe sepsis and septic shock.36

Endpoints for optimization are central venous pressure (CVP), mean arterial pressure (MAP), and central venous oxygen saturation (ScvO2).

  • Source control/removal of foreign bodies including wound packing or tampons, if not already removed 
    • This includes vaginal and nasal tampons and any fibrous foreign body in an abscess cavity.
    • Some authorities recommend irrigating the abscess cavity or vaginal vault with isotonic sodium chloride solution to remove necrotic material and excess bacterial load.
  • Start intravenous crystalloid infusion, O2, and place continuous cardiac and pulse oximetry monitors. Pulse oximetry, (pulse co-oximetry if available), cardiac and respiratory monitoring, and continuous exhaled carbon dioxide monitoring may be useful.
  • Obtain blood for above tests, also type and crossmatch. 
    • Optimizing delivered oxygen may require transfusion.
  • Culture all potential inciting sites.
  • Hemodynamic monitoring, including invasive arterial blood pressure monitoring
  • Oxygen and respiration 
    • Maximize tissue oxygenation and correct hypoxia and/or acidosis.
    • Assisted ventilation may be required to support oxygenation or if acute respiratory distress syndrome develops.
  • A Foley catheter should be placed to monitor urine output and to assess adequacy of resuscitation/end-organ perfusion.
  • Fluid resuscitation may need to be massive. 
    • As much as 10-20 L/day of crystalloid may be necessary, as patients may have significant insensible fluid losses. Endpoints of resuscitation, such as lactate, CVP, and urine output, should be monitored.
    • Some authors suggest that colloids may decrease the risk of pulmonary edema.
  • Start antibiotics. 
    • Antibiotics should be started as soon as the disease is suspected. Each hour of delay in antimicrobial administration over the ensuing 6 hours after onset of hypotension decreased survival an average of 7.6%.37
    • Antibiotics are best guided by the local biogram. See Medication for empiric suggestions.
    • Calculation of the Mortality in Emergency Department Sepsis Score (MEDS) may assist in further management.28
  • Admit to ICU setting.
ICU care and treatment
  • Continue care started in the ED, for example, intravenous fluids, O2, pressors, and monitoring.
  • Culture blood, urine, wounds, and cavities as indicated if not already performed.
  • Type and crossmatch: Optimizing delivered oxygen may require transfusion.
  • Calculate APACHE II score. Changes in score are an effective monitoring tool.
  • Treat malignant cardiac arrhythmias.
  • Initiate or continue early goal-directed therapy (EGDT).38  
    • Optimize within 6 hours
      • CVP
      • MAP
      • ScvO2
    • EGDT was associated with a 16% absolute risk reduction for in-hospital mortality, which, to date, is the largest mortality benefit demonstrated in a sepsis randomized controlled trial. Current consensus recommendations now advocate EGDT as best practice for the first 6 hours of severe sepsis resuscitation.
  • Hyperbaric oxygen therapy has been used in necrotizing soft-tissue infections, but the benefit of this intervention has not been proven in toxic shock syndrome (TTS).

Consultations

  • Intensivist: The high mortality and morbidity rates mandate care in an intensive care environment
  • Infectious disease: The worldwide emergence of MRSA and the changing sensitivities of streptococci and staphylococci suggest that local infectious diseases consultation is warranted.
  • Surgical: Prompt surgical consultation may be necessary for drainage, debridement, fasciotomy, or amputation of a clearly infected site, especially if necrotizing fasciitis is suspected.

Medication

  • Oxygen/respiration38  
    • Supplement and optimize tissue oxygenation, but avoid supranormal oxygen delivery because of potential toxicity (Surviving Sepsis Campaign).
    • Intubation and mechanical ventilation may be needed. However, a low tidal volume and limitation of inspiratory plateau pressure may reduce acute lung injury and minimize acute respiratory distress syndrome.
    • If acute lung injury/acute respiratory distress syndrome develop, consider a minimal amount of positive end-expiratory pressure.
    • Semirecumbent bed position unless contraindicated.
  • Intravenous fluids 
    • Crystalloid is recommended. No research has proven the benefit of one crystalloid over another.
    • Controversy remains about the benefit, if any, of colloids over crystalloids, in shock.39
    • Aggressive fluid administration to normalize flow and perfusion is indicated. This may result in congestive heart failure (CHF) and edema. Central intravenous access for delivery of fluid and for pressure monitoring may be required.
    • Supplement cross-matched blood to a target hemoglobin level of 7-9 g/dL.
    • Fresh frozen plasma and platelets should be provided as needed for signs of coagulopathy or disseminated intravascular coagulation.
  • Antibiotics 
    • Cover both staphylococci and streptococci until a definitive diagnosis is made.
    • Continue antibiotics for a minimum of 7 days; 10 days may be preferable.
    • TSS requires penicillinase-resistant antibiotics.
    • Because of the increasing resistance of streptococci to penicillin G, clindamycin often is considered the drug of first choice for invasive group A streptococcal infections such as streptococcal TSS.
  • Pressors 
    • Pressors may be needed. The Surviving Sepsis Campaign supported norepinephrine and dopamine over other pressors;40 Patel et al disagrees and recommends vasopressin.41
    • Vasopressin, epinephrine, norepinephrine, dopamine, dobutamine, and others remain in common clinical use, with norepinephrine the preferred inotrope in septic shock.
    • Low-dose or "renal dose" dopamine has not been shown to be helpful; consider dobutamine inotropic therapy when relevant and indicated.
  • Steroids 
    • Short courses of high-dose glucocorticoids decrease survival during sepsis, but a 5- to 7-day course of physiologic hydrocortisone with subsequent tapering increases survival rate and shock reversal in patients with vasopressor-dependent septic shock.42
    • Long course of low-dose corticosteroids reduced 28-day all-cause mortality and intensive care unit and hospital mortality in sepsis; it has not been shown helpful specifically in TSS but may be.43
  • Immunoglobulins 
    • The use of intravenous immunoglobulin G (IVIG) has been shown to be effective in neutralizing the TSS toxin and therefore aids in recovery. The dose is 1 g/kg and should be given within 6 hours if no rapid response to therapy. IVIG has doubled 30-day survival.44
    • Different batches from different manufacturers may have different efficacy.45
    • Staphylococcal superantigens are not inhibited as efficiently as streptococcal superantigens by IVIG, and, hence, a higher dose of IVIG may be required for therapy of staphylococcal toxic shock syndrome in order to achieve protective titers and clinical efficacy.46
    • Alimentation/hyperalimentation: Numerous studies over the years have shown that stressed patients recover better when they have a source of nutrition.
  • Antioxidants: These have shown some clinical benefit. 
    • Glutathione (GSH) has been used for this purpose.47
    • Short-term intravenous infusion of N -acetyl-L-cysteine (NAC) has also been used.48
  • Recombinant activated protein C: Recommended by the Surviving Sepsis Campaign for patients with severe sepsis and with high risk for death who meet the inclusion and exclusion criteria.38

Antibiotics

Semisynthetic penicillins have been widely used for toxic shock syndrome (TSS). Growing evidence suggests that the protein synthetase inhibitor, clindamycin, a bacteriostatic agent, may be more efficacious in this illness. Accordingly, these authors recommend treating patients suspected of TSS initially with clindamycin, 900 mg IV q8h for adults (13 mg/kg IV q8h for children) in combination with a linezolid (600 mg IV q12h) or daptomycin (6 mg/kg q24h). Vancomycin is another agent to be considered at 1 g q12h instead of clindamycin, but with vancomycin resistance being reported, the authors prefer clindamycin.


Linezolid (Zyvox)

Prevents formation of functional 70S initiation complex, which is essential for bacterial translation process. Bacteriostatic against enterococci and staphylococci and bactericidal against most strains of streptococci. Used as alternative in patients allergic to vancomycin and for treatment of vancomycin-resistant enterococci.

Adult

600 mg IV q12h for 7-10 d

Pediatric

Preterm neonate <7 days: 10 mg/kg PO/IV q12h for 7-10 d
Term neonates to 12 years: 10 mg/kg PO/IV q8h for 7-10 d
>12 years: Administer as in adults

May cause hypertension when used concomitantly with adrenergic agents including pseudoephedrine, sympathomimetic agents, vasopressors, or dopaminergic agents (reduce dose of dopamine or epinephrine if concurrent use required); serotonin syndrome may occur if used concomitantly with serotonergic agents including tricyclic antidepressants, meperidine, dextromethorphan, trazodone, venlafaxine, and selective serotonin reuptake; may cause myelosuppression or pseudomembranous colitis

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

Has mild MAO inhibitor properties and has potential to have same interactions as other MAO inhibitors; caution in uncontrolled hypertension, pheochromocytoma, carcinoid syndrome, or untreated hyperthyroidism, and in patients who are at increased risk for bleeding, have preexisting thrombocytopenia, receive concomitant medications that may decrease platelet count or function, or who may require >2 wk of therapy (monitor platelet counts); unnecessary use may lead to development of resistance to drug; may cause peripheral or optic neuropathy


Nafcillin (Unipen)

Treats infections caused by penicillinase-producing staphylococci, and, therefore, it is used for penicillin G-resistant staphylococcal infections. Not for use in treatment of penicillin G-susceptible staphylococci. Use parenteral therapy initially in severe infections, with very high doses for very severe infections. Change to oral therapy as the condition improves. Because of the occasional occurrence of thrombophlebitis associated with the parenteral route, especially in elderly patients, administer parenterally only for a short term (24-48 h), and change to oral route as soon as clinically possible.

Adult

1-2 g IV q4h for 7-10 d

Pediatric

50-200 mg/kg/d IV divided q4-6h for 7-10 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

To optimize therapy, determine causative organisms and susceptibility; use >10-d treatment to eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever); obtain cultures after treatment to confirm infection eradication


Clindamycin (Cleocin)

DOC for invasive group A streptococcal infections (eg, STSS). Lincosamide for treatment of serious skin and soft-tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Adult

900 mg IV q8h for 7-10 d

Pediatric

13 mg/kg IV q8h for 7-10 d

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; 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 colitis


Daptomycin (Cubicin)

First of new antibiotic class called cyclic lipopeptides. Binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis, and ultimately causing bacterial death.
Indicated to treat complicated skin and skin structure infections caused by S aureus (including methicillin-resistant strains), S pyogenes, S agalactiae, S dysgalactiae, and E faecalis (vancomycin-susceptible strains only).

Adult

CrCl >30 mL/min: 6 mg/kg IV q24h infused over 30 min for 7-10 d
CrCl <30 mL/min: 6 mg/kg IV q48h (including hemodialysis or CAPD) for 7-10 d

Pediatric

<18 years: Not established
>18 years: Administer as in adults

Coadministration with tobramycin slightly increases daptomycin Cmax and AUC and decreases tobramycin Cmax and AUC; may experience additive effects with other drugs causing myopathy (eg, HMG CoA reductase inhibitors)

Pregnancy

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

Precautions

Decrease dose with renal function <30 mL/min; pseudomembranous colitis may occur; may cause muscle pain or weakness (monitor CPK levels and discontinue daptomycin with elevated CPK and unexplained myopathy, or marked CPK elevation [10-times upper limits of normal]); not indicated for pneumonia (higher death rate in daptomycin-treated patients during phase III trials); not compatible with dextrose-containing solutions


Vancomycin (Vancocin)

Used in prophylaxis. Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.
To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in patients with renal impairment.
Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients who are undergoing gastrointestinal or genitourinary procedures.

Adult

1 g IV q12h for 7-10 d

Pediatric

40 mg/kg/d IV divided tid/qid for 7-10 d

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, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h administration or as PO or IP administration; red man syndrome is not an allergic reaction

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References
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Further Reading

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Keywords

toxic shock syndrome, TSS, toxic shock, toxic shock syndrome symptoms, toxic shock syndrome causes, toxic shock syndrome treatment, endotoxin, exotoxin,   exotoxin A, SPEA, exotoxin B, SPEB, streptococcal toxic shock syndrome, staphylococcal toxic shock syndrome, pyrogenic toxin superantigens, menstrual toxic shock, nonmenstrual toxic shock

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Contributor Information and Disclosures

Author

Vicken Y Totten, MD, MS, FACEP, FAAFP, Assistant Professor, Case Western Reserve University School of Medicine; Director of Research, Department of Emergency Medicine, University Hospitals, Case Medical Center
Vicken Y Totten, MD, MS, FACEP, FAAFP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine
Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Mark L Plaster, MD, JD, Executive Editor, Emergency Physicians Monthly
Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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