Introduction - definition of sepsis and septic shock -epidemiology - causative micro-organisms- Risk factors- Diagnosis- clinical manifestations - investigations - treatment - prevention

1. Septic Shock
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine

2. 2
 Describe clinical characteristics of
Septic shock
 Identify Causative agent-risky factors
 Review appropriate drug therapy
Objectives

3. 3
SHOCK
INTRODUCTION
Cause
RISK FACTORS
Diagnosis
Treatment & Prevention
CONTENTS

4. INTRODUCTION

5. 5
Definitions
Bacteremia :
 transient invasion of circulation by
bacteria
Septicemia:
 prolonged presence of bacteria in
the blood accompanied by systemic
reaction

6. 6
Definitions
 SIRS (systemic inflammatory response
syndrome ):
 It is a syndrome characterized by the presence
of two or more of the following clinical
criteria:
o Temperature(core) >38°C or<36°C
o Heart rate >90beats/min
o Respiratory rate >20b/min or PaC02
<32mmHg
o WBC >12000cells/ml or <4000cells/ml or
>10%immature forms.

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Definitions
 Sepsis:
 SIRS with a clearly established focus
of infection.
Severe sepsis:
 sepsis associated with organ
dysfunction and hypoperfusion.

8. 8
Definitions
 SEPTIC SHOCK
 Refers to severe sepsis which is not
responsive to intravenous fluid infusion for
resuscitation and requires inotropic or
vasopressor agent to maintain systolic blood
pressure.
 It is considered as part of a spectrum and a
progression of SIRS (systemic inflammatory
response syndrome)

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Definitions
 Multiple organ dysfunction syndrome
(MODS)
 Altered function of more than one organ
system in an acutely ill patient requiring
medical intervention to maintain
homeostasis

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EPIDEMIOLOGY
 More than 750,000 cases of sepsis
annually
 Accounts for 215,000 deaths each year
 This is more than AMI, lung cancer and
other common causes of in hospital death
 Approximate cost: $17 billion per year
 M>F
 Extreme of ages are more affected
 Leading cause of death in ICU

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AETIOLOGY
 BACTERIA:
 Gram –ve nearly 2/3, gram+ve 1/3
 GRAM –VE:
o E.coli is the commonest.
o Klebsiella, Entrobacter, Serratia, Proteus
o Pseudomonas
o Bacteroides

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AETIOLOGY

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AETIOLOGY
 BACTERIA:
 GRAM +VE
o Streptococci
o Staph
o Clostridia and Pneumococci
 Others:
 Viruses, Fungi and Parasites in a few
especially the immuno-compromised.

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AETIOLOGY
 SOURCE
 Endogenous
 Skin- Soty skin infections(SSI)
 urinary tract- UTI
 respiratory tract- LRTI
 GIT- bowel surgery, perforations
 Exogenous.
 surgical instruments ,imaging machines

15. RISK FACTORS

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RISK FACTORS
 Age (<10 >70years)
 malnutrition
 anemia
 Primary disease: Malignancies, DM,
CLD, CRF
 Immunosuppression,
Immunosuppressive agents

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RISK FACTORS
 necrotic tissue
 hematoma
 poor surgical technique
 Catherization
 Prolong hospitalization
 Major surgeries, trauma, extensive
burns

18. PATHOGENESIS

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PATHOGENESIS
 Micro-organisms or products of
tissue damage stimulates production
of pro-inflammatory cytokines
which in turn stimulate production of
secondary mediators of
inflammation in order to localize
infection and limit proliferation.

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PATHOGENESIS
 The production of the pro-inflammatory
cytokines is regulated to limit damage.
 However in poorly controlled sepsis or
extensive tissue damage, there is
excessive inflammatory response which is
poorly regulated

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PATHOGENESIS
 Effects of secondary mediators
i. Damage of vascular endothelium
ii. Vasodilation of microvasculature
iii. Activation of neutrophils(aggravates
endothelial damage)
iv. Diminished force of cardiac contraction
 These ultimately lead to peripheral
pooling of blood, extravasation of fluid,
hypotension, hypoxia and shock

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PATHOGENESIS

23. Diagnosis

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CLINICAL FEATURES
 EARLYSTAGE(compensated/warm
shock)
 Not associated with hypovolemia
 Febrile (38.2-41°C )
 Shivering and malaise
 Warm dry and flushed skin.
 Hyperventilation
 Rapid bounding pulse
 Wide pulse pressure

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CLINICAL FEATURES
 LATE STAGE(decompensated/ cold shock)
 Hypovolemia with superimposed sepsis
 Altered sensorium
 Cold clammy skin
 Weak pulse
 Hypothermia, hypotension
 Oliguria
 Jaundice
 Upper GI bleeding
 DIC(Disseminated intravascular coagulation)

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CLINICAL FEATURES
 LOCALISING INFECTION
 A good complete systemic
examination is done to detect any
focus of sepsis.

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CLINICAL FEATURES

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INVESTIGATION
 INVESTIGATION GOES HAND-IN-HAND
WITH RESUSITATION
I. Full blood count(FBC): there is leukocytosis
after initial leucopenia. Thrombocytopenia
II. Septic work up
 Blood culture
 Sputum (microscopy-Culture & sensitivity)
 Urine(microscopy-Culture & sensitivity)
 Wound swab (microscopy-Culture & sensitivity)
 any exudate (microscopy-Culture & sensitivity)

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INVESTIGATION
 Based on suspected source
 CXR, Abd-X RAY, Abd-pelvic US, CT
Scan of various sites

30. TREATMENT

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TREATMENT
 Septic shock is a medical emergency
that requires prompt and efficient
resuscitation.
 If possible patient should be admitted
to ICU

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TREATMENT
 AIMS:
 Improve hemodynamic state
 Restore tissue perfusion thereby increase
O2 delivery to tissue.
 Administer O2
 Combat the bacteria and cytokines
 Eliminate septic focus

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TREATMENT
I. RESUSITATION
 VOLUME REPLACEMENT
 IV access
 Crystalloids started(readily available ): 1L
in 30- 45min. Then re-assess, and repeat
as appropriate.
 Monitor the hourly urine output(30-
50ml/hr)

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TREATMENT
 Vasopressor
 After adequate fluid resuscitation or about
4L, with signs of fluid overload(basal
crepitation, high CVP) and persistent
hypotension.
 Norepinephrine:
o 1st line for septic shock refractory to
volume replacement
 Dopamine

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TREATMENT
 Inotropic therapy
 A dobutamine infusion up to 20
micrograms/kg/min be administered or
added to vasopressor in the presence of
a. myocardial dysfunction
b. signs of hypoperfusion,

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TREATMENT
II. OXYGEN ADMINISTRATION
 In a cleared and patent airway, O2 is
delivered via a face mask to increase
O2 saturation. Increasing uptake and
delivery to tissue.

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TREATMENT
III. ANTIBIOTIC
 Give in large doses IV to combat
infection.
 Initial empiric anti-infective therapy
 Empirical IV Broad spectrum bactericidal
& anaerobe coverage
o (3rd generation cephalosporin)
Ceftriaxone 50-100mg/kg up to 2gm daily
+ Metronidazole 500mg 8hrly

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TREATMENT
 Antimicrobial regimen should be
reassessed daily
 Empiric combination therapy should
not be administered for more than 3–
5 day.
 Move to the most appropriate single
therapy should be performed as soon
as the susceptibility profile is known
.

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TREATMENT
 Duration of therapy typically 7–10
days
 Antiviral therapy should be initiated
as early as possible in patients with
sepsis of viral origin.

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TREATMENT
IV. STEROIDS:
 Hydrocortisone 2-6g daily for 2days
is beneficial if given at the onset.
 Has anti-inflammatory and has
antishock effects
V. NSAIDS:
 Has anti-inflammatory effect

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TREATMENT
VI. O2 Free radical scavengers
 superoxide dismutase
 Vitamin C, allopurinol, α-tocopherol
 Used to decrease tissue damage and
MOD in septic shock if given
prophylactically.

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TREATMENT
VII.Glycemic control- soluble insulin
 to maintain blood sugar – 80- 120mg/dl
 found to ↓morbidity/mortality
VIII.NALOXONE:
 it raises the blood pressure
IX. PREVENTION OF FURTHER
COAGULATION
 Recombinant human activated protein C

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TREATMENT
X. SURGERY
 resuscitative & therapeutic
 If septic focus is responsible for the shock
it should be dealt with as soon as possible
especially if response to therapy is poor.
E.g. debridement, drainage of abscess

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MONITORING
 Clinical signs:
 Sensorium- consciousness regained, calm.
 Conjunctiva becomes pink
 venous /capillary feeling
 warm dry skin.
 Urine output (best indicator): Hourly urine
output(0.5-1ml/kg /h)
 PR and BP: Quarterly pulse and BP
 Central venous pressure (10-15cmH2O)
 Lung and jugular veins
 Arterial blood gases/ pulse oximeter (oxygen
saturation :80-100mmHg)

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COMPLICATION
 ARDS
(Acute respiratory distress syndrome)
 ARF(Acute renal failure)
 DIC
 Encephalopathy
 Liver failure
 MODS
 Death

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PROGNOSIS
 Poor prognostic factor
 Advanced age
 Immunosuppression
 Infection with resistance organism
 Need for inotropes for > 24hrs
 MODs despite treatment

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PREVENTION
 Early recognition
 Prompt treatment of infection
 Meticulous surgical technique
 Pre operative antibiotics
 Aseptic technique
 Sterilization of surgical equipments
 Optimization of patient : e.g DM

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CONCLUSION
 Septic shock is an emergency with
high mortality even in the best centers
 Early recognition and immediate
treatment is the key to good outcome
 Early detection of those at risk and
prevention is the safest and cheapest
way of reducing the morbidity and
mortality associated with it .

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thanksF o r W a t c h i n g