septic shock
DESCRIPTION
TRANSCRIPT
04/10/2023 1
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
AETIOLOGY
04/10/2023
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
04/10/2023
GRAM +VE Streptococci Staph Clostridia and Pneumococci Viruses, Fungi and Parasites in a few
especially the immuno-compromised.
AETIOLOGY
04/10/2023
SOURCE
Endogenous – Skin- SSI urinary tract- UTI respiratory tract- LRTI GIT- bowel surgery, perforationsExogenous. surgical instruments drapes imaging machines staff
AETIOLOGY
04/10/2023
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
04/10/2023
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
04/10/2023
PATHOGENESIS
04/10/2023
BACTERIA
GRAM-VE GRAM+VE
LIPOPOLYSACCHARIDE LIPOTEICHOIC ACID(ENDOTOXIN) (PEPTIDOGLYCAN) (MACROPHAGE,MONO,NEU,LYM,END)
FACTOR XII PRO-INFLAMMATORY CYTOKINES COMPLEMENT COMPONENT
PATHOGENESIS
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
COMPLIMENT COMPONENT
C3a, C5a(ANAPHYLACTOXINS)
(HISTAMINE)
PROCOAGULATION
DAMAGE OF VASODILATION ACTIVATION OF DICVASCULAR OF MICROCIRCUL- NEUTROPHILSENDOTHELIUM TION
PAF
PATHOGENESIS
04/10/2023
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
04/10/2023
FACTOR XIIa
ENDOTHELIAL CELLS MACROPH. KININOGEN FACTOR XI(intrinsic pathway) TISSUE FACTOR
COAGULATION (extrinsic pathway) BRADYKININ CONSUMPTION OF COAGULATION FACTOR
HYPOTENSION DIC
PATHOGENESIS
04/10/2023
Pro-inflammatory cytokines reduces plasma levels of thrombomodulin, coagulation inhibitors like protein S, protein C, and ATIII. Microvascular coagulatio results which worsens DIC.
PATHOGENESIS
04/10/2023
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
04/10/2023
Hypovolemia Interstitial loss cellular hypoxia Cardiac depression Arteriovenous shunt septic shock
PATHOGENESIS
04/10/2023
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
04/10/2023
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
04/10/2023
LOCALISING INFECTIONA good complete systemic examination is done to detect any focus of sepsis.
CLINICAL FEATURES
04/10/2023
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
04/10/2023
Based on suspected source
CXR, Abd-X RAY, Abd-pelvic uss, CT Scan of various sites
INVESTIGATION
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
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
04/10/2023
ARDS ARF DIC Encephalopathy Liver failure MODS Death
COMPLICATION
04/10/2023
Poor prognostic factor Advanced age Immunosuppresion Infection with resistance organism, level of IL -
6 Need for inotrophs for > 24hrs Mods despite treatment
PROGNOSIS
04/10/2023
Early recognition Prompt treatment of infection Meticulous surgical technique Pre op antibiosis Aseptic technique Sterilization of surgical equipments Optimization of patient – eg DM
PREVENTION
04/10/2023
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
04/10/2023
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
04/10/2023
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