The document outlines septic shock, including its definition, classification, epidemiology, pathogenesis, clinical features, investigation, treatment, complications, prognosis and prevention. Septic shock results from a systemic inflammatory response due to infection and can lead to multiple organ dysfunction. Prompt resuscitation, antibiotics, source control and organ support are crucial for treatment, but mortality remains high, especially in patients with multiple organ dysfunction or failure to respond to therapy. Early recognition and treatment of infection helps reduce risks of septic shock.

1. 5/24/2014 1
DR BASHIR YUNUSA
REGISTRAR SURGERY DEPT.
AKTH
26TH NOV.,2013

2. 
 INTRODUCTION
 AETIOLOGY/RISK FACTORS
 PATHOGENESIS
 CLINICAL FEATURES
 INVESTIGATION
 TREATMENT
 COMPLICTIONS
 PROGNOSIS
 PREVENTION
 FUTURE TRENDS
 CONCLUSION
 REFERENCES
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OUTLINE

3. 
DEFINITION Shock is the clinical manifestation of
failure of cellular function due to inadequate tissue
perfusion and consequent cellular hypoxia resulting
from a reduction in the effective circulating blood
volume.
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INTRODUCTION

4. 
It’s the most common cause of death among
surgical patients. Hence every surgeon must
understand the pathophysiology, diagnosis as well
as priority in management
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INTRODUTION

5. 
CLASSIFICATION
The most common and clinically applicable way of
classifying shock is that based on the initiating mechanism
 HYPOVOLEMIC –reduction in effective circulating volume
 CARDIOGENIC- failure of cardiac pump
 DISTRIBUTIVE – vasodilation and peripheral pooling of blood
 SEPTIC
 ANAPHYLACTIC
 NEUROGENIC
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INTRODUCTION

6. 
 SEPTIC SHOCK
Results from moderate to severe sepsis or tissue damage.
It is considered as part of a spectrum and a progression of
SIRS (systemic inflammatory response syndrome)
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INTRODUCTION

7. 
 DEFINATION OF TERMS;
 Bacteremia : transient invasion of circulation by
bacteria
 Septicemia: prolonged presence of bacteria in the
blood accompanied by systemic reaction
 SIRS (systemic inflammatory response syndrome ): it
is a syndrome characterized by the presence of two or
more of the following clinical criteria:
 Temperature(core) >38°C or<36°C
 Heart rate >90beats/min
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INTRODUCTION

8. 
 Respiratory rate >20b/min or PaC02 <32mmHg
 WBC >12000cells/ml or <4000cells/ml or >10%immature
band forms.
 Sepsis: SIRS with a clearly established focus of infection
 Severe sepsis: sepsis associated with organ dysfunction
and hypoperfusion.
 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.
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INTRODUCTION

9. 
 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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INTRODUCTION

10. 
 EPIDEMIOLOGY
 4.6 cases/1000 persons in a study in US
 200,000 cases annually with 50% mortality
 M>F(most studies M=52-66%)
 Extreme of ages are more affected
 13th leading cause of death in US
 Leading cause of death in ICU
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INTRODUCTION

11. 
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AETIOLOGY

12. 
 BACTERIA: gram –ve nearly 2/3, gram+ve 1/3 of the
gram –ve, E.coli is the commonest.
 GRAM -VE
 Klebsiella,
 Entrobacter,
 Serratia,
 Proteus,
 Mirabillis/Vulgari,
 Pseudomonas and
 Bacteroides
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AETIOLOGY

13. 
 GRAM +VE
 Streptococci
 Staph
 Clostridia and
 Pneumococci
 Viruses, Fungi and Parasites in a few especially
the immuno-compromised.
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AETIOLOGY

14. 
SOURCE
Endogenous –
 Skin- SSI
 urinary tract- UTI
 respiratory tract- LRTI
 GIT- bowel surgery, perforations
Exogenous.
 surgical instruments
 drapes
 imaging machines
 staff
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AETIOLOGY

15. 
 Age (<10 >70years)
 malnutrition,
 anemia,
 Primary disease: Malignancies, DM, CLD, CRF,
 Immunosuppression, Immunosupresssive agents,
 necrotic tissue
 hematoma
 poor surgical technique
 Catheriration
 Prolong hospitalisation
 Major surgeries, trauma, extensive burns
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RISK FACTORS

16. 
 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.
 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

17. 
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PATHOGENESIS

18. 
BACTERIA
GRAM-VE GRAM+VE
LIPOPOLYSACCHARIDE LIPOTEICHOIC ACID
(ENDOTOXIN) (PEPTIDOGLYCAN)
(MACROPHAGE,MONO,NEU,LYM,END)
FACTOR XII PRO-INFLAMMATORY CYTOKINES COMPLEMENT
COMPONENT
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PATHOGENESIS

19. 
 Anti-inflammatory and immunosuppressive
cytokines IL-10 which aided by IL-4 inhibits the
activity of the pro-inflammatory cytokines to limit
damage.
 In severe sepsis they become immunosuppressive to
patient.
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PATHOGENESIS

20. 
 PRO-INFAMMATORY CYTOKINE
TNF-α, IL-1β, IL-6, IL-8
CELL MEMBRANE PHOSPHOLIPID
PHOSPHOLIPASE A2
ARACHIDONIC ACID
CYCLO-OXYGENASE LIPO-OXYGENASE
SECONDARY MEDIATORS OF INFLAMMATION
PGI2, PGE2, TXA2, LT, PAF,NO, KININS, IL-1,IL-6, OXYGEN
FREE RADICAL, PROTEASES.
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PATHOGENESIS

21. 
 Effects of secondary mediators
 Damage of vascular endothelium
 Vasodilation of microvasculature
 Activation of neutrophils(aggravates endothelial
damage)
 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

22. 
 COMPLIMENT COMPONENT
C3a, C5a(ANAPHYLACTOXINS)
(HISTAMINE)
PROCOAGULATION
DAMAGE OF VASODILATION ACTIVATION OF DIC
VASCULAR OF MICROCIRCUL- NEUTROPHILS
ENDOTHELIUM TION
PAF
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PATHOGENESIS

23. 
 EFFECT OF COPLIMENT COMPONENT
 vasodilatation and increase permeability
 Endothelial damage
 C5a causes aggregation of platelet and leucocytes
thereby acting as procoagulant leading to DIC
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PATHOGENESIS

24. FACTOR XIIa
ENDOTHELIAL CELLS MACROPH.
KININOGEN FACTOR XI(intrinsic pathway)
TISSUE FACTOR
COAGULATION (extrinsic pathway)
BRADYKININ CONSUMPTION OF COAGULATION
FACTOR
HYPOTENSION DIC
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PATHOGENESIS

25. 
 Pro-inflammatory cytokines reduces plasma
levels of thrombomodulin, coagulation inhibitors
like protein S, protein C, and ATIII. Microvascular
coagulatio results which worsens DIC.
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PATHOGENESIS

26. 
 Hence there is acute inflammation, vasculitis,
haemorrhage, capillary thrombosis and necrosis are
seen in several vital organs.
 Net effect:
 Maldistribution of blood flow at microvasculature
 Arteriovenous shuting O2 utilization
 Interstitial loss effective vol.
Hypovolemia
 Myocardial depression
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PATHOGENESIS

27. 
 Hypovolemia
 Interstitial loss cellular hypoxia
 Cardiac depression
 Arteriovenous shunt
septic shock
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PATHOGENESIS

28. 
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CLINICAL FEATURES
 It could be in inn patients receiving treatment
for another condition
 EARLYSTAGE(compensated/warm shock )
Not associated with hypovvolemia
 febrile (38.2-41°C )
 Shivering and malaise
 warm dry and flushed skin.
 hyperventilation
 rapid bounding pulse
 wide pulse pressure

29. 
 LATE STAGE
(decompensated/ cold shock)
Hypovolemia with superimposed sepsis
 altered sensorium
 cold clammy skin
 Feeble pulse
 hypothermia, hypotension
 Oliguria
 Jaundice
 upper GI bleeding
 DIC
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CLINICAL FEATURES

30. 
 LOCALISING INFECTION
A good complete systemic examination is done to
detect any focus of sepsis.
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CLINICAL FEATURES

31. 
 NOTE THAT RESUSCITATION TAKES PRECEDENCE OVER
INVESTIGATIONS, WHICH SHOULD NOT DELAY
INTERVENTION
 INVESTIGATION GOES HAND-IN-HAND WITH
RESUSITATION
1. FBC: there is leucocytosis after initial leucopenia.
Throbocytopenia
2. Septic work up
 Blood culture
 Sputum m/c/s
 Urine m/c/s
 Wound swab m/c/s
 Endocervical swab m/c/s or any exudate
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INVESTIGATION

32. 
Based on suspected source
 CXR, Abd-X RAY, Abd-pelvic uss, CT
Scan of various sites
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INVESTIGATION

33. 
 Septic shock is a medical emergency that requires prompt
and efficient resuscitation
 If possible patient should be admitted to ICU
 AIMS:
 Improve haemodynamic 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

34. 
 RESUSITATION
1. VOLUME REPLACEMENT
 Iv access with 2 wide bore cannulas are secured,
samples taken for FBC, EUCr, GXM
 Crystalloids started(readily available ): 1L in 30-
45min. Then re-assess, and repeat as appropriate.
 Urethral catheter is passed to empty the bladder then
to monitor the hourly urine output(30-50ml/hr)
 Central venous catheter is inserted(10-15cmH20)
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TREATMENT

35. 
 Vasopressor
After adequate fluid resuscitation or about 4L, with
signs of fluid overload(basal crepitation, high CVP) and
persistent hypotension.
 Norepinephrine – α & β
1st line for septic shock refractory to volume
replacement
Vasoconstriction & reflex bradycardia 5-20mcg/min
 Dopamine – systemic vasoconstriction, inotropic,
renal vasodilatation 2-20mcg/m
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TREATMENT

36. 
2. OXYGEN ADMISTRATION
In a cleared and patent airway, O2 is delivered via a
face mask to increase O2 saturation. Increasing uptake
and delivery to tissue.
3. ANTIBIOTIC
 Give in large doses IV to combat infection. Empirical
 IV Broad spectrum bactericidal & anerobe coverage
(3rd generation cephalosporin)
Ceftriaxone 50-100mg/kg up to 2gm daily +
Metronidazole 500mg 8hrly
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TREATMENT

37. 
4. STEROIDS: Inhibits conversion of membrane
phospholipid to arachidonic acid hence inhibiting release of
secondary mediators.
 Hydrocortisone 2-6g daily for 2days is beneficial if given
at the onset.
5. NSAIDS: e.g. Ibuprofen inhibits
 the COX pathway there by PG and TBX synth.
 Prevent neutrophil aggregation and
activation
 ↓production of superoxide radicals
 Stabilizes lysozomal membranes enzymes
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TREATMENT

38. 
6. O2 Free radical scavengers
 superoxide dismutase
 Vitamin C, allopurinol, α-tocopherol
They have been shown to decrease tissue damage and
MOD in septic shock if given prophylactically.
7. Glycemic control- soluble insulin (GKI) to maintain
blood sugar – 80- 120mg/dl has been found to
↓morbidity/mortality.
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TREATMENT

39. 
8. NALOXNE: it raises the blood pressure
9. PREVENTION OF FURTHER COAGULATION
 Atiii and C₁-estrase inhibitor
 Recombinant human activated protein C
inhibits thrombosis and inflammation, promotes
fibrinolysis, and modulates coagulation and
inflammation.
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TREATMENT

40. 
10. SURGERY
 resuscitative & therapeutic
If septic focus is responsible for the shock it should be
dealt with as soon as possible especially if respose to
therapy is poor. E.g debridement, drainage of
abscess
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TREATMENT

41. 
 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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MONITORING

42. 
 ARDS
 ARF
 DIC
 Encephalopathy
 Liver failure
 MODS
 Death
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COMPLICATION

43. 
Poor prognostic factor
 Advanced age
 Immunosuppresion
 Infection with resistance organism, level of IL -6
 Need for inotrophs for > 24hrs
 Mods despite treatment
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PROGNOSIS

44. 
 Early recognition
 Prompt treatment of infection
 Meticulous surgical technique
 Pre op antibiosis
 Aseptic technique
 Sterilization of surgical equipments
 Optimization of patient – eg DM
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PREVENTION

45. 
 Monoclonal antibodies to IL-1, IL-6, TNF Clinical trials have not been
rewarding.
 Recombinant activate protein C – inhibits va & viiia
also TNF- ά, IL-1,IL-6 although it is associated with high risk of bleeding.
Research has focused on modifying the host response to sepsis via a number of
approaches, including the following:
 Antibodies against gram-negative endotoxin
 Gamma globulins
 Monoclonal antibodies against tumor necrosis factor
 Blockade of eicosanoid production
 Blockade of interleukin (IL)–1 activity
 Inhibition of nitric oxide (NO) synthase
 These approaches have met with modest success in animal experiments,
but at present, they cannot be recommended for general use in humans.
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FUTURE TREND

46. 
 Septic shock is an emergency with high mortality
even in the best centers
 Early recognition and energetic 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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CONCLUSION

47. 
 E.A.Badoe .et al 4th edition.
 Bailey and loves 25th editon
 Sabiston textbook of surgery 18th edition
 PubMed.gov US national library of med.
 Wikipedia, encyclopedia. Septic shock
 Medscape e-medicine. Septic shock
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REFERENCES