septic shock

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SEPTIC SHOCK

DR BASHIR YUNUSAREGISTRAR SURGERY DEPT.

AKTH26TH NOV.,2013

04/10/2023

INTRODUCTION AETIOLOGY/RISK FACTORS PATHOGENESIS CLINICAL FEATURES INVESTIGATION TREATMENT COMPLICTIONS PROGNOSIS PREVENTION FUTURE TRENDS CONCLUSION REFERENCES

OUTLINE

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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.

INTRODUCTION

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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

INTRODUTION

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CLASSIFICATIONThe 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

INTRODUCTION

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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)

INTRODUCTION

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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

INTRODUCTION

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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.

INTRODUCTION

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Multiple organ dysfunction syndrome

(MODS) - Altered function of more than one organ system in an acutely ill patient requiring medical intervention to maintain homeostasis

INTRODUCTION

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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

INTRODUCTION

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AETIOLOGY

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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

AETIOLOGY

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GRAM +VE Streptococci Staph Clostridia and Pneumococci Viruses, Fungi and Parasites in a few

especially the immuno-compromised.

AETIOLOGY

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SOURCE

Endogenous – Skin- SSI urinary tract- UTI respiratory tract- LRTI GIT- bowel surgery, perforationsExogenous. surgical instruments drapes imaging machines staff

AETIOLOGY

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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

RISK FACTORS

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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.

PATHOGENESIS

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PATHOGENESIS

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BACTERIA

GRAM-VE GRAM+VE

LIPOPOLYSACCHARIDE LIPOTEICHOIC ACID(ENDOTOXIN) (PEPTIDOGLYCAN) (MACROPHAGE,MONO,NEU,LYM,END)

FACTOR XII PRO-INFLAMMATORY CYTOKINES COMPLEMENT COMPONENT

PATHOGENESIS

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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.

PATHOGENESIS

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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.

PATHOGENESIS

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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

PATHOGENESIS

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COMPLIMENT COMPONENT

C3a, C5a(ANAPHYLACTOXINS)

(HISTAMINE)

PROCOAGULATION

DAMAGE OF VASODILATION ACTIVATION OF DICVASCULAR OF MICROCIRCUL- NEUTROPHILSENDOTHELIUM TION

PAF

PATHOGENESIS

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EFFECT OF COPLIMENT COMPONENT

vasodilatation and increase permeability Endothelial damage C5a causes aggregation of platelet and

leucocytes thereby acting as procoagulant leading to DIC

PATHOGENESIS

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FACTOR XIIa

ENDOTHELIAL CELLS MACROPH. KININOGEN FACTOR XI(intrinsic pathway) TISSUE FACTOR

COAGULATION (extrinsic pathway) BRADYKININ CONSUMPTION OF COAGULATION FACTOR

HYPOTENSION DIC

PATHOGENESIS

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

PATHOGENESIS

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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

PATHOGENESIS

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Hypovolemia Interstitial loss cellular hypoxia Cardiac depression Arteriovenous shunt septic shock

PATHOGENESIS

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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

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LATE STAGE (decompensated/ cold shock)Hypovolemia with superimposed sepsis

altered sensorium cold clammy skin Feeble pulse hypothermia, hypotension Oliguria Jaundice upper GI bleeding DIC

CLINICAL FEATURES

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LOCALISING INFECTIONA good complete systemic examination is done to detect any focus of sepsis.

CLINICAL FEATURES

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NOTE THAT RESUSCITATION TAKES PRECEDENCE OVER

INVESTIGATIONS, WHICH SHOULD NOT DELAY INTERVENTION

INVESTIGATION GOES HAND-IN-HAND WITH RESUSITATION1. 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

INVESTIGATION

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Based on suspected source

CXR, Abd-X RAY, Abd-pelvic uss, CT Scan of various sites

INVESTIGATION

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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

TREATMENT

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RESUSITATION1. 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)

TREATMENT

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VasopressorAfter adequate fluid resuscitation or about 4L, with signs of fluid overload(basal crepitation, high CVP) and persistent hypotension. Norepinephrine – α & β1st line for septic shock refractory to volume

replacementVasoconstriction & reflex bradycardia 5-20mcg/min Dopamine – systemic vasoconstriction, inotropic, renal vasodilatation 2-20mcg/m

TREATMENT

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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

TREATMENT

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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

TREATMENT

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6. O2 Free radical scavengers

superoxide dismutase Vitamin C, allopurinol, α-tocopherolThey 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.

TREATMENT

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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.

TREATMENT

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10. SURGERY resuscitative & therapeuticIf 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

TREATMENT

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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

MONITORING

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ARDS ARF DIC Encephalopathy Liver failure MODS Death

COMPLICATION

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Poor prognostic factor Advanced age Immunosuppresion Infection with resistance organism, level of IL -

6 Need for inotrophs for > 24hrs Mods despite treatment

PROGNOSIS

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

PREVENTION

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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.

FUTURE TREND

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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 .

CONCLUSION

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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

REFERENCES