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 - gram-

negative 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
THANKS