A case of toxic shock
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A Case of Toxic Shock?. Edward L. Goodman, MD September 18, 2002. Outline. Case Presentation Relevant Epidemiology Differential Diagnosis Pathophysiology Management. Case Presentation. July 18, 2002 CC: SOB, Hypotension, Dizzy

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A case of toxic shock

A Case of Toxic Shock?

Edward L. Goodman, MD

September 18, 2002


Outline

Outline

  • Case Presentation

    • Relevant Epidemiology

  • Differential Diagnosis

  • Pathophysiology

  • Management


Case presentation

Case Presentation

  • July 18, 2002

  • CC: SOB, Hypotension, Dizzy

  • HPI: 74 WM two day hx of chills, fever, SOB and weakness. Tender in right thigh

    • GERD surgery 5/6/02 complicated by necrotizing pancreatitis and open wound after laparotomy

    • Wound Care Department managing open wound as outpatient


History 2

History 2

  • PMH

    • IDDM

    • HBP

    • PUD

    • Hyperlipidemia,

    • Diverticulosis

    • Prostate Ca S/P XRT and Lupron


A case of toxic shock

Exam

  • Alert but confused

  • BP 80’s, tachycardia

  • Healing open abdominal wound

  • Faint, generalized erythema

  • Tender demarcated erythema swollen right thigh

  • Tinea pedis


Imaging

Imaging


Lab results

Lab Results


Epidemiology

Epidemiology

  • 2001 Outbreak Group A Streptococcal infections of complex wounds

    • 28 cases/10 isolates were available and typed

    • Epidemic strain identified

      • Identical emm (M protein) type

      • Levofloxacin/clindamycin resistant

        • Virtually all patients had been on these drugs

    • 52 control patients selected to compare with 10 cases


Rr 297 95 ci 14 6000 p 0 001

RR 297 (95% CI 14 - 6000)p<0.001


Epidemiology continued

Epidemiology - continued

  • Multivariate analysis

    • No relationship to sex, type of wound or underlying condition

    • Age >60 related

  • Thus, strong link to exposure to a specific group of HCW

  • Subsequent extensive HCW cultures negative

    • Implicated group

    • Many others

  • Epidemic ceased July 2001


Epidemiology continued1

Epidemiology - continued

  • July 12, 2002 first case of GAS infection of a complex wound in 12 months

    • Four suspected HCW cultured again

    • One grew GAS from two sites - asymptomatic

    • One environmental isolate positive

    • All four isolates were identical but different M type from 2001 strain

  • Our patient was exposed to the implicated HCW!


Initial therapy

Initial Therapy

  • Received Cefotaxime by ER staff

  • Admitting Team started IV Pen G and Clindamycin

  • IVIG daily x 5 days

  • Vigorous support

  • Surgery consulted early and often

    • No surgery required!


Imaging1

Imaging


Hoadley dj case records of the mgh nejm 2002 347 831 839

Hoadley DJ, Case Records of the MGH, NEJM 2002;347:831-839


Discussion

Discussion

  • Was there reason to infer a GAS etiology?

    • Clinical appearance

    • Relevant epidemiology

    • (No cultures were positive for GAS)

    • Strongly positive anti DNAse B suggests recent or current infection

  • Did he have invasive GAS infection?

  • Did he have features of GAS TSS?

    • See Case Definition


Discussion1

Discussion

  • Antibiotics

    • Penicillin

    • Clindamycin

  • Role of IVIG


Penicillin s ineffectiveness

Penicillin’s ineffectiveness

  • High mortality in invasive GAS when Penicillin used

    • 81% mortality in myositis

    • Animal data on inoculum effect

  • High concentrations of GAS in deep sites

    • Stationary phase reached quickly

    • PBPs not expressed in stationary phase


Clindamycin

Clindamycin

  • No inoculum effect

  • Suppresses toxin synthesis

  • Facilitates phagocytosis by inhibiting M protein synthesis

  • Suppresses proteins involved in cell wall synthesis

  • Longer post antibiotic effect (PAE)

  • Suppress LPS induced monocyte synthesis of TNF-alpha


Tss and ivig

TSS and IVIG

  • Shock from gram positive toxins

    • Superantigens

      • Enterotoxins

      • TSST-1

      • SPEA

    • Superantigens bind to

      • MHC II

      • ß chain of T cell receptor

    • Resulting in

      • T cell proliferation

      • Cytokine production


A case of toxic shock

IVIG

  • Blocks in vitro T cell activation

  • Contains superantigen neutralizing antibodies


Effects of ivig kaul et al cid 1999 28 800

Effects of IVIGKaul et al, CID 1999;28:800


Conclusion

Conclusion

  • Severe pain and fever – think of GAS

  • Know the epidemiology of your institution

  • Consult a surgeon promptly

  • Add Clindamycin to beta lactam therapy for necrotizing or serious GAS infections

  • Consider IVIG for TSS


References

References

  • Bisno AL, Stevens DL. Streptococcal Infections of Skin and Soft Tissues. New Eng J Med 1996; 334:240-245.

  • Case Records of the MGH. New Eng J Med 1995; 333: 113-119.

  • Case Records of the MGH. New Eng J Med 2002; 347:831-837.

  • Disease Prevention News. TDH. March 27, 2000;60: No.7.

  • Kaul R, McGeer A et al. Intravenous Immunoglobulin Therapy for Streptococcal Toxic Shock Syndrome – A Comparative Observational Study. Clin Infect Dis 1999; 28:800-807.


References continued

References - continued

  • Kazatchkine MD, Kaveri, SV. Immunomodulation of Autoimmune and Inflammatory Diseases with Intravenous Immune Globulin. New Eng J Med 2001; 345: 747-755.

  • Stevens DL. The Flesh-Eating Bacterium: What’s Next. J Infect Dis 1999;179(Suppl 2): S366-374


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