a rare but life-threatening condition

caused by bacteria getting into the

body and releasing harmful toxins
Etiology:

• staphylococcus
• streptococcus
• Clostridium sordellii
 Difference
between toxic
shock & septic
shock
Septic shock Toxic shock syndrome
(TSS)
occur as the result of an resulting from certain bacterial
abnormal immune response to a infections
bacterial infection

A flood of antibodies can lead Toxins produced by either

to widespread inflammation staphylococcal (staph) or
throughout a child's body, streptococcal (strep) bacteria
causing poor blood flow to may cause toxic shock
organs. In the most severe syndrome in children.
cases, the child's blood pressure
may drop, leading to a
weakened heart and organ
failure
 flu-like muscle
symptoms ache
macular
rash
Vomiting,
Hypotension diarrhea

sore
throat end- Fever
organ failure
Epidemiology:

occur at a lower incidence in children

than in adults. ... Mortality associated
with streptococcal TSS is 5-10% in
children, much lower than in adults (30-
80%), and is 3-5% for staphylococcal TSS
in children
Pathophysiology:
 There are several possible exotoxins that may be
responsible for causing toxic shock syndrome:
Toxic shock syndrome toxin type-1

Staphylococcal enterotoxin B Staphylococcal

enterotoxin E
Staphylococcal enterotoxin C
Staphylococcal
Staphylococcal enterotoxin D enterotoxin H
These superantigens bypass the normal pathway
for activation of T cells resulting in over-activation
of cytokines and inflammatory cells.
Monitoring:
 Hypo
albuminemia
Hypocalcemia Creatine
phosphokinase

Metabolic Monitor
acidosis Blood
counts
Pulse
oximitry Renal
function
 1- Recognition 2- Resuscitation
3- Removal of source of
infection

4- Rational 5- Role of
6- Review
choice of adjunctive
of progress
antibiotics treatment

7- Reduce risk of secondary cases in close

contacts
 Early recognition of TSS is critical to ensure
appropriate treatment is implemented promptly

It is important to have a high index of suspicion for

TSS in patients presenting with sepsis syndromes,
especially where the patients present with other
features compatible with TSS such as erythematous
rash, conjunctivitis or early signs including liver function
tests or abnormal
clotting or where there is a soft tissue focus of
infection
 The rapid progression from onset to multi-
organ system failure in Toxic Shock
Syndrome necessitates applying
aggressive fluid support
and respiratory and often inotropic support
 Deep seated soft tissue infections including
necrotizing fasciitis, myositis and cellulitis are
commonly the source of infection particularly in
streptococcal Toxic Shock Syndrome and
responsible for perpetuating the illness.

Controlling the source of infection by surgical

debridement of wounds and drainage of
abscesses are a priority in the initial on-going
managing
Rational choice of antibiotics:

Broad spectrum antibiotics should be

administered as soon as possible, Preferably following
a blood culture.
Current recommendations for empiric
treatment advocate the use of flucloxacillin.
 Group A
streptococcal penicillin.
infection
methicillin • Flucloxacillin
sensitive • Beta lactamase
staph. resistant penicillin
 5- Role of adjunctive treatment

• These include inhibition

Clindamycin of superantigen toxin
production.

• Better tissue
penetration and longer
post anti-biotic effect
than penicillin and the
potentiation of
phagocytosis.
IVIG • anti-inflammatory
• immunomodulatory
properties
but there is lack of
definitive evidence from
randomised controlled
tirlas for the efficacy!!!
 6- Review progress

• continued search for any focus of infection that

may require surgical intervention.

• Antibiotics should be rationalised based on

culture results.

• Duration of antibiotics for S.aures bacteraemia

should be a minimum of 7 to 14 days total IV
Abs with no switch to oral therapy.
• The US CDC recommends prophylaxis for
contacts with any risk factors for
disease.

• The optimal antibiotic regimen is

penicillin V 250mg (<10 years old) or 500 mg
(>10 years old) twice daily for 10 days plus
rifampicin 10mg/kg twice daily for 4 days.

• An alternative regimen is cephalexin 250mg four

times daily for 10 days.
Case presentation
 F.A, 1 Year old, 8 kg, FT, NVD, The second Sibling of
contagious marriage, Negative Abortion, without
known allergy

Presented to ER with:
Complain &
Fever
presentation: Cough
Dyspnea
Palpitation they defined it as “Atrial Flutter”
And received adenosine three times upon it
Shocked received shock therapy
DCL
 History of the
present illness:

Two days ago

Two weeks ago
• Complained of fever,
• Started with fever and
dyspnea, irritability,
cough
palpitation
• Diagnosed as pharyngitis
• CXR Showed chest
infection
Past History

• No previous PICU admission

• No previous hospital admission
On admission
to ICU

• The patient was DCL to

unconscious
• He was RD3 and dyspnea
increased, so patient ventilated
 Vitals on
INVESTIGATION
admission

Na : 134
BP: 90/60 K : 4.4
RR: 43 CA : 8
HR: 170 Albumin: 2.6
TIC : 24.8
CRP: 237
INR : 3
Toxic shock
syndrome
 Event 1

Shock improved &

patient regain
Vancomycin plus dalacin conscious but was
sedated

• CRP dec to 132

• Converted from
A/C to CPAP
 Event 2

Cultures was requested prior to admission, And its results was :

1. Blood culture MRSA 2. ETA culture Acnitobacter Sensitive

to:
Sensitive to Amikin
Vancomycin Gentamicin
Dalacin Imipenam
ciprofloxacin Colistin
Except ciprofloxacin and other
quinolones wasn’t done in the culture
Cultures was requested prior to admission, And its results was :

ETA culture Klebsiella

Sensitive to:
Amikin
Ciprofloxacin
Colistin
Imipenam
Meropenam
 Cultures was requested prior to admission, And its results was :

So we
Urine culture recommened
Wound swab Showed proteus the use of
Showed MRSA mirabilis Sensitive to Ciprofloxacin
Tienam Amikin
Amikin nebulization
Ciprofloxacin
 Event 2

Patient still ventilated although patient on

appropriate antibiotics but still hard to be
weaned and infection on CXR and clinical
status was still bad
 Event 3

1. vancomycin trough
level was 8 below the
“trough reference range“ So, We have
2. Patient was feverish shifted to
3. CRP was elevating. linezolid
4. Vancomycin taken for
16 days.
 Patient was on fentanyl
& there’s a drug drug interaction
between fentanyl and linezolid
“Serotonin syndrome “
So we recommended discontinuing
fentanyl infusion
 Event 4

So micafungin was
Result of ETA fungal
added as it shows
culture is:
the lowest MIC
Candida infection
therefore more
effective to be used
 Event 5
As

• Bad CXR
ETA CULTURE • Worsening Of
showed ventilator settings
acinetobacter • Previous ETA culture
with acinetobacter
MDR with proper antibiotic
intake
• Patient condition was
critical according to
physician notes
 So we
recommended new
combination and it
was approved:
Colistin plus rifampin