CC: transfer for further evaluation

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CC transfer for further evaluation PI 31 y/o
BF with PMH of panic attacks who had a recent
episode 4 days PTA . Pt developed N/V,
decreased in appetite, fatigue, and diarrhea.
Normal urine output. Denies F/C, URI, GU
symptoms. Weakness progressed so
she called EMS and was sent to OSH.
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PI In ED T 103, BUN 73, Cr 5.9. CXR
showed infiltrate. Rocephin and
azithromycin were started. Despite
aggressive hydration, her Cr went up gt6
so she was transferred to NCBMC.
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PI Pt was found to have anemia,
thrombocytopenia. HUS and TTP were ruled out.
HD was started. Pt had low grade fever.
Thrombocytopenia improved but WBC
increased from 17.1 to 48.8. C/O SOB, fatigue
and pleuritic chest pain. CXR showed
pleural fluid which was tapped -exudative.

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• ID was consulted for ? Empyema and leukocytosis.

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PMH As above PSH Tubal ligation,
cholecystectomy, hysterectomy. All
None SHX healthy 11 y/o son, no ETOH, no drug,
no tobacco FHX Father HD due to ETOH
abuse ROS Otherwise negative.
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PE T 99.2 P 116 RR 22 BP 153/95
PO 95 2LNC GA AO X 3, Afebrile, in
mild dyspnea HEENT mild pale conjunctiva, no
jaundice Neck supple, no JVD Chest
bibasilar crackles, decreased BS at bases Heart
tachycardia, nl S1, S2
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Abd BS, soft, mild tender at LUQ,
LLQ, no rebound tenderness Ext 1
edema LN no lymphadenopathy NS
no focal deficit Skin no rashes IV
dialysis catheter Rt femoral- OK
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Diagnostic data
CBC WBC 48.3 Hb 8.3 Hct 24.8 MCV 81 Plt
173 band 14 BMP Na 135 K 4.6 Cl 97 HCO3 19
BUN 59 Cr 5.1 LFT WNL INR 1.74 PTT
41.4 UA WBC 6-12 RBC TNTC prot gt 300
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Pleural fluid

• WBC 7750 Polys 84 M 16
• Protein 3 gm
• LDH fluid/serum 706/517 (gt0.6)
• Glu fluid/serum 81/108 (gt0.5)

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CXR
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ULTRASOUND No hydronephrosis, borderline
enlarged both kidneys, small amount of free
fluid adjacent to Rt kidney.
CULTURE BC NG UC NG
TTE mild LVH, mild pul HTN, no pericardial
effusion.
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ANA dsDNA C4, C3 complement ANCA HIV
Ab HBsAg HBcAb HCV Anti HBs IgG ASO titer
Negative WNL WNL Negative NR Negative Positive Neg
ative Negative WNL
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Blood culture from OSH
Group A Beta hemolytic Streptococcus Sensitive to
PCN, Cephalosporins, Clinda, Quinolone
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Strep Toxic Shock Syndrome

• Severe invasive group A streptococcal infection
• Prevalence 3.5 per 100,000 since
• mid-1980s
• Beta-hemolytic
• Aggressive soft tissue infection, shock, ARDS,
  and renal failure

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Portal of Entry

• Skin, vagina, pharynx
• Cannot be ascertained in 45
• Infection begins within 24-72 hrs at a site of
  minor local trauma.

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Characters

• M protein- virulence factor
• M types 1, 3, 12, 28 shock and multiorgan
  failure
• Pyrogenic exotoxins A and or B
• SPEA / SPEB
• Seven exogenic pyrotoxins
• SSA, MF(mitogenic factor), M-3

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Clinical Presentation

• 20 influenza-like syndrome
• F/C, myalgia, N/V, diarrhea
• Fever is the most common sign
• 55 confusion
• 50 are normotensivve on admission, but become
  hypotensive within 4 hrs.
• 80 have signs of soft tissue infection

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Clinical Presentation

• 20 endophthalmitis, perihepatitis, peritonitis,
  postpartum sepsis, myocarditis
• 10 a diffuse, scarlatina-like erythema

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Laboratory findings

• Mild leukocytosis, increased immature neutrophils
• Elevated creatinine ( shock, myoglobinuria,hemoglo
  binuria)
• blood culture in 60
• Elevated CK
• Hypoalbuminemia, hypocalcemia

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Clinical Presentation

• Renal dysfunction occurs in all pts by 48-72 hrs
• Cr returns to baseline within 4-6 weeks
• ARDS occurs in 55
• MR 30-70

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Differential Diagnosis

• Staphylococcal TSS esp. female during period,
  recent surgery, local staph abscess --bacteremia
  is uncommon.
• Gram negative sepsis- uncommon in healthy
  pts---RF after hypotension.
• RMSFsevere HA and rash, petechiae
• Acute meningococcemiarash and meningitis
• Heat stroke---history

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• Without rash, any pts from community with shock
• h/o trauma, severe pain , fever
• BC positive in 8-24 hrs
• Presumptive therapy should be initiated pending
  culture

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Antibiotic Therapy

• PCN
• Clinical failure when
• -high concentrations of GAS
• -transition from the logarithmic to the
• stationary phase

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Antibiotic Therapy

• Clindamycin
• Not affected by inoculum size or stage of growth
• Suppresses the synthesis of toxins, PBP
• Longer postantibiotic effect than beta-lactams

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Antibiotic Therapy

• Clindamycin 900 mg IV Q 8 hrs
• PCN G 4 mu IV Q 4 hrs clindamycin
• Clindamycin and azithromycin are more active in
  an experimental model of necrotizing fasciitis
  and myonecrosis

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Surgical Therapy

• Prompt and aggressive exploration

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Intravenous immunoglobulin (IVIG)

• Is IVIG efficacious in the treatment of
  Strep TSS?

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Intravenous immunoglobulin therapy for
streptococcal toxic shock syndrome a
comparative observational study. The Canadian
Streptococcal Study Group.
Kaul R McGeer A Norrby-Teglund A Kotb M
Schwartz B O'Rourke K Talbot J Low DE Clin
Infect Dis 1999 Apr28(4)800-7
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• 21 pts with strep TSS
• December 1994-April 1995
• Treated with a median dose of 2 gm of IVIG/kg
• Compared with 32 pts between 1992-1995 who did
  not receive IVIG

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Result

• Outcome was 30-day survival
• 67 in IVIG group and 34 in controls.
• Multivariate analysis- IVIG and a lower APACHE II
  score were asso. with survival.
• OR for survival ass. with IVIG was 8.1. (95 CI,
  1.6-45P.009)

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Conclusion

• IVIG enhance the ability of pt plasma to
  neutralize bacterial mitogenicity and reduced T
  cell production of IL-6 and TNF.
• IVIG may be an effective adjunctive therapy.

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• Intravenous immunoglobulin G therapy in
  streptococcal toxic shock syndrome a European
  randomized, double-blind, placebo-controlled
  trial.

Darenberg J, Ihendyane N, Sjolin J, Aufwerber E,
Haidl S, Follin P, Andersson J, Norrby-Teglund
A StreptIg Study Group. Clin Infect Dis. 2003
Aug 137(3)333-40. Epub 2003 Jul 17.
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• 21 enrolled pts
• 10 IVIG recipients and 11 placebo recipient
• Primary end point was mortality at 28 days
• 3.6 fold higher MR in placebo group. (P0.3)

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Result

• Significant decrease in the sepsis-related organ
  failure assessment score at days 2 (P0.02) and 3
  (P0.04) in IVIG group
• Significant increase in plasma neutralizing
  activity against superantigens in IVIG group
  after treatment(P0.03)

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Result

• Analyses of 1 revealed a trend toward a reduced
  MR in IVIG group (10 vs 36)
• Sig. improvement of organ dysfunction during day
  1-3 in IVIG group
• Sig. increase in SA-neutralizing activity after
  IVIG administration
• BUT no difference in cytokine level in 2 groups
  (both decreased)

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Conclusion

• Considering low incidence of disease which is a
  major obstacle of a prospective study and high
  MR, it seems reasonable to recommend IVIG as
  adjunctive therapy until further data are
  available.