Management Of Septic Shock

MANAGEMENT OF SEPTIC SHOCK

Dr. Swati singh Uduth SOKOTO NIGERIA

Septic Shock   Introduction.   Incidence  Pathophysiology    Differential Diagnosis  Clinical Manifestations   Management 

  Conclusion

Introduction.   What is shock?

     Shock is a state of acute disruption

of circulatory function, resulting in insufficiency of tissue perfusion, oxygen utilization and cellular energy production.  

   

Introduction.

 SIRS   The systemic inflammatory response

to a variety of severe clinical insults.Manifested by 2 or more of the following conditions:   Temperature  >38 0 C  or  <36 0c  HR   >90 beats/min  Respiratory Rate  >20 breaths/min or

PaCO2 <32 torr (<4.3 kPa)  WBC   >12,000 or  <4,000 cells/mm3 or >10% bands   

Introduction.  SEPSIS   The presence of SIRS associated with a confirmed infectious process. 

 Severe Sepsis  Sepsis with either hypotension or

systemic manifestations of hypoperfusion

 Lactic acidosis, oliguria, altered

mental status



Septic Shock  Sepsis with hypotension despite adequate

fluid resuscitation, associated with hypoperfusion abnormalities Septic shock is shock resulting from SIRS that is caused by micro-organisms - gramnegative in nearly two-thirds of cases and gram-positive in one-third- and viruses, fungi and parasites in a few.  It may lead to MODS.

Multiple Organ Dysfunction Syndrome (MODS)  Progressive distant organ failure

(initially uninvolved) following severe infectious or noninfectious insults (severe burn, multiple trauma, shock, acute pancreatitis)





Incidence / Magnitude of Problem   300,000 to 500,000 cases of

bacteremia each year in the US with  associated 20-30% mortality.      200,000 bouts of septic shock.   Sepsis is the leading cause of death in noncoronary intensive care   units.    Mortality has changed little over the

last 20 years.

Reasons Underlying Rising Incidence of Sepsis  Increased patient age                      Increased use of   



cytotoxic/immunosuppresive drug therapy   Increased incidence of concomittent medical illness    Increased use of invasive devices for diagnosis and therapy   Rising incidence of infections due to organisms other than Gram negative bacteria (Gram + bacteria, fungi, and possibly viruses)   Perhabs, the emergence of antibiotic resistant organisms

Individual Host Risk Factors  Extremes of age        Chronic disease        Substance abuse        Immunosuppressive therapy       Vascular catheterization       Prosthetic devices and urinary catheters       Tracheal intubation      

 



Bone, RC.  The Pathogenesis of Sepsis.  Ann Int  Med 1991(115): 457-69.

predisposing conditions in Septic Shock.

Pathophysiology (Microbial Triggers)  Gram-negative  bacteria:lipopolysaccharide 

 Gram-positive bacteria:  Lipoteichoic acid/cell wall muramyl

peptides– Superantigens  Staphylocococal Toxic Shock Syndrome Toxin, TSST  Streptococcal pyrogenic exotoxin, SPE

PATHOGENESIS OF SEPTIC SHOCK

PATHOGENESIS OF SEPTIC SHOCK

Differential Diagnosis of Septic Shock  Other Nonseptic Causes of Hyperdynamic

Shock.                 

overdosage of drugs with vasodilator properties Toxic Shock Syndrome primary/secondary adrenal insufficiency anaphylactic reactions severe anemia severe liver disease AV fistulas thyroid storm severe thiamine deficiency

 The forms of shock generally associated with a

vasocostricted peripheral circulation.      hypovolemic shock         cardiogenic shock         obstructed circulation due to embolism or

Clinical Manifestations.   Recognition of Septic Shock:  Inflammatory triad Fever 38.3" to 41° C.  Tachycardia  flushed   dry  Warm skin     Shock  Hypoperfusion  Altered sensorium    Urine output  Wide pulse pressure.......bounding pulses

Clinical Manifestations 

 Hypotension  Cold and clammy skin  Mottling  Tachycardia                                   

Cold shock Cyanosis Narrow pulse pressure Hypoxemia Acidosis.

. Staging of Septic Shock  I. Compensated / Preshock /

Hyperdynamic   II.Decompensated / Organ

hypoperfusion   III. End organ failure / Irreversible

Investigations  1. White blood cell count. There is

leucocytosis after initial leucopaenia. Thromocytopaenia occurs.  2. Culture of blood, urine or any exudate is done to identify the infecting organism and its antibiotic sensitivity.  3. Imaging (Chest x-ray, Ultrasound, CT Scan) is done if pockets of pus are suspected.  4. EUCr, Urinalysis, Clotting profile,

Therapies of Sepsis/Septic Shock  Antibiotics (early administration) 

 Hemodynamic support 

(fluid resuscitation) Restore tissue perfusion   Normalize cellular metabolism



– Vasopressor agents  Dopamine, norepinephrine, dobutamine

Source control  Surgical debridement of infected,

devitalized tissue  Catheter replacement 

 Supplemental oxygen (treatment of

acute respiratory distress syndrome, ARDS) 

 Nutritional support 

Fluid Therapy  Fluid challenge over 30 min  500–1000 ml crystalloid  300–500 ml colloid ,albumin

containing solutions

 Repeat based on response and

tolerance  

Antibiotics:  Antibiotics are given in large

doses IV to combat infection  A useful combition is gentamicin 80mg with clindrtmycin 600mg  cefuroxime 3-6mg with metronidazole 500mg. Bactericidal  antibiotics may cause temporary deterioration in the haemodynamic state.

Corticosteroids:  Hydrocortisone 2-6g daily for 2 days

is beneficial if given at the outset.  inhibit conversion of membrane

phospholipids to arachidonic acid  inhibiting further release of prostaglandins, prostacyclin, thromboxane A, and leukotrienes.

 They also inhibit  TNF synthesis and release and

normalize oxyhaemoglobin dissociation curve if affected and thereby improve oxygen delivery to

Controversial Current Therapies for Septic Shock 

Anti-inflammatory agents  – Ibuprofen (blocks synthesis of prostaglandins and thromboxane).  – Prostaglandin E1  – Pentoxifylline 

 Oxygen Scavengers (reduce tissue damage in septic shock)

 – N-acetylcysteine 

Controversial Current Therapies for Septic Shock  Drugs modifying coagulation  – Anti-thrombin III 

 Drugs enhancing host defenses  – Intravenous immunoglobulin (IVIG)  – Interferon-gamma  – immunonutrition 

Controversial Current Therapies for Septic Shock  Other drugs

Growth hormone, antibiotics, fresh frozen plasma, anesthetic sedative and analgesic agents, catecholamines 



 Hemofiltration, plasma filtration,

plasma exchange 

Experimental Therapies of Sepsis/Septic Shock  Anti-endotoxin therapies 

 IL-1 recepter antagonist 

 Anti-TNF-alpha, soluble Recombinant

TNF



 PLA2 inhibitors, PAF inhibitors 

 NO inhibitors 

 Anti-coagulants (APC) 

Conclusions  • Early recognition of sepsis is

critical:  – By emergencist in the A/E  – Good physical exam and clinical

judgment

 • Early treatment of sepsis is

crucial:  – Antibiotics  – Fluid resuscitation under clinical

and noninvasive monitoring  – Concept of the « 3 first golden hours close monitoring can significantly reduce the

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