Toxic Shock Syndrome Medication

  • Author: Ramesh Venkataraman, MBBS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Jul 16, 2010
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity, prevent complications, and eradicate the infection.

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Antibiotics

Class Summary

Antimicrobial therapy must cover all likely pathogens in the context of the clinical setting.

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Clindamycin (Cleocin)

 

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). As much as 20% of group B streptococci may be resistant. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.

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Aqueous penicillin G (Pfizerpen)

 

Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

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Nafcillin (Nafcil, Unipen, Nallpen)

 

Initial therapy for suspected penicillin G–resistant staphylococcal infections. Use parenteral therapy initially in severe infections.

Due to thrombophlebitis, particularly in elderly patients, administer parenterally only for short term (1-2 d); change to oral route as clinically indicated.

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Vancomycin (Lyphocin, Vancocin, Vancoled)

 

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of patients with septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci (eg, MRSA). For abdominal penetrating injuries, combine with an agent active against enteric flora and/or anaerobes.

Use creatinine clearance to adjust dose in patients with renal impairment.

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Oxacillin (Bactocill, Prostaphlin)

 

Bactericidal antibiotic that inhibits cell wall synthesis. Used in the treatment of infections caused by penicillinase-producing staphylococci. May be used to initiate therapy when staphylococcal infection is suspected.

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Contributor Information and Disclosures
Author

Ramesh Venkataraman, MBBS  Consultant, Critical Care Medicine, Apollo Hospitals, India

Ramesh Venkataraman, MBBS is a member of the following medical societies: American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, Indian Medical Association, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC  Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Cory Franklin, MD  Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Director, Division of Critical Care Medicine, Cook County Hospital

Cory Franklin, MD is a member of the following medical societies: New York Academy of Sciences and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Richard B Brown, MD, FACP  Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM  Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

References

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Description of M proteins and streptococcal toxins.
Group A streptococci cause beta hemolysis on blood agar.
Group A streptococci on Gram stain of blood isolated from a patient who developed toxic shock syndrome. Courtesy of T. Matthews.
This schematic shows interaction among T-cell receptor, superantigen, and class II major histocompatability complex. The binding of superantigen to class II molecules and T-cell receptors is not limited by antigen specificity and lies outside the normal antigen binding sites.
Progression of soft tissue swelling to vesicle or bullous formation is an ominous sign and suggests streptococcal shock syndrome. Courtesy of S. Manocha.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The leg was incised to exclude underlying necrotizing infection. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. This patient also had streptococcal pharyngitis. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The patient had diffuse erythroderma, a characteristic feature of the syndrome. Courtesy of Rob Green, MD.
A 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The patient had diffuse erythroderma, a characteristic feature of the syndrome. The patient improved with antibiotics and intravenous gammaglobulin therapy. Several days later, a characteristic desquamation of the skin occurred over palms and soles. Courtesy of Rob Green, MD.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
A 58-year-old patient presented in septic shock. On physical examination, progressive swelling of the right groin was observed. On exploration, necrotizing cellulitis, but not fasciitis, was present. The cultures grew group A streptococci. The patient developed severe shock (toxic shock syndrome). The CT scanning helped evaluate the extent of infection and exclude other pathologies, such as psoas abscess, osteomyelitis, and inguinal hernia.
Necrotizing cellulitis of toxic shock syndrome.
Soft tissue infection secondary to group A streptococci, leading to toxic shock syndrome.
Extensive debridement of necrotizing fasciitis of the hand.
The hand is healing following aggressive surgical debridement of necrotizing fasciitis of the hand (see Image 15).
Necrosis of the little toe of the right foot and cellulitis of the foot secondary to group A streptococci.
 
 
 
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