Discuss the Management of Septic Shock
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DISCUSS THE MANAGEMENT OF
SEPTIC SHOCK
DR SK OBIANO JNR
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OUTLINE
Definition of shock
Epidemiology
Classes of Shock
Definition of Septic shock
Pathophysiology of septic shock
Management of septic shock
Current trends
Controversies
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shock
Clinical manifestations of cellular dysfunction
due to inadequate tissue perfusion resulting in
cellular hypoxia as a result of decreased
circulatory blood volume.
Tissue requirement- 3mls/kg/min
70kg
Delivery- 1000mls/min
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Epidemiology
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Types of shock
Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock
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Septic shock
State of acute circulatory failure characterised
by persistent arterial hypotension despite
adequate fluid rescusitation
Or
Tissue hypoperfusion unexplained by other
causes.
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Definitions
Infection A microbial phenomenon characterized byan inflammatory response to the presence ofmicroorganisms or the invasion of normally sterile hosttissue by those organisms.
BacteremiaThe presence of viable bacteria in theblood.
SIRSsystemic level of acute inflammation, that may ormay not be due to infection, and is generally manifested
as a combination of vital sign abnormalities includingfever or hypothermia, tachycardia, and tachypnea.
Severe SIRSSIRS in which at least 1 major organ systemhas failed
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SepsisSIRS which is secondary to infection.
Severe sepsis Severe SIRS which is secondary to infection.
Shock It is a serious, life threatening medical conditioncharacterized by a decrease in tissue perfusion to a point that is
inadequate to meet cellular metabolic needs.
Septic shock sepsis induced hypotension despite adequatefluid resuscitationalong with perfusion abnormalities manifestedby a lactate greater than 4 mg/dL.
Multiple Organ Dysfunction Syndrome (MODS)The presence ofaltered organ function in an acutely ill patient such thathomeostasis cannot be maintained without intervention.
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Criteria for SIRS
Requires 2 of the following 4
features to be present:
o Temp >38 or 20
o Tachycardia (HR>90, in theabsence of intrinsic heartdisease)
o WBC > 12,000/mm3or10% band formson differential
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Criteria for Severe SIRS
Must meet criteria forSIRS, plus 1 of the
following:
oAltered mental statuso SBP40mmHg from baseline
o Impaired gas exchange (PaO2/FiO2ratio1.5 x control,o elevated fibrin degredation products
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Pathophysiology(septic shock)
Imbalance in oxygen supply and demand
Conversion from aerobic to anaerobic
metabolism
Appropriate and inappropriate metabolic and
physiologic responses
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Pathophysiology cont
Complex interaction between pathogen and
host immune systems
Localised sepsis- normal response
Response is systemic in septic shock
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Proinflammatory response to infection
Mediators
TNF Alpha, IL-1, IL-6
Complement system (C5 alpha)
Bacterial factors
Endotoxin, bacterial cell wall products, bacterial toxins
Immunosuppressive
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Infection
Inflammatory
Mediators
Endothelial
Dysfunction
Vasodilation
Hypotension Vasoconstriction Edema
Maldistribution of Microvascular Blood Flow
Organ Dysfunction
Microvascular Plugging
Ischemia
Cell Death
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Risk Factors for SIRS/Sepsis
1. Extremes of age
2. Indwelling lines/catheters
3. Immunocompromised states
4. Malnutrition5. Alcoholism
6. Malignancy
7. Diabetes8. Cirrhosis
9. Male sex
10.Genetic predisposition?
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Management
The initial treatment of sepsisand septic shock involves the
administration ofsupplemental oxygen andvolume infusion with isotonic
crystalloids
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Management of Sepsis-PRINCIPLES
Resuscitate: ABCs
Restore tissue perfusion
Identify and eradicate source of infection
Assure adequate tissue oxygenation
Activated Protein C
Steroids
Glucose Control Nutrition
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Clinical Manifestations
Recognition of Septic Shock:
Inflammatory triad-
Fever
Tachycardia flushed skin
Hypoperfusion
Altered sensorium
Urine output
Wide pulse pressure.......bounding
pulses
Warm
shock
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Clinical Manifestations
Hypotension
Cold and clammy skin
Mottling
Tachycardia
Cyanosis
Narrow pulse pressure
Hypoxemia
Acidosis.
Cold shock
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Localizing symptoms that are most useful clues tothe etiology sepsis: Head and neck infections - Severe headache, neck stiffness,
altered mental status, earache, sore throat, sinus pain ortenderness, cervical or submandibular lymphadenopathy
Chest and pulmonary infections- Cough (especially ifproductive), pleuritic chest pain, dyspnea
Abdominal and GI infections - Abdominal pain, nausea, vomiting,diarrhea
Pelvic and genitourinary infections - Pelvic or flank pain, vaginalor urethral discharge, dysuria, frequency, urgency
Bone and soft-tissue infections - Focal pain or tenderness, focalerythema, edema, fluctuance
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Work-up
Laboratory studies
o CBC
o Comprehensive chemistry panel
o Coagulation studies
o Blood & urine cultures
Imaging studies
o Chest radiography
o Abdominal radiography
o Others according to the suspected cause.
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Laboratory studies
CBC:
o The WBC count and differential.
o Hemoglobinconcentration dictates oxygen-carryingcapacity in blood.
o The goal is to maintain hematocrit >30% and hemoglobin >10 g/dL.
o Plateletsare an acute-phase reactant and are typicallyelevated in the setting of inflammation. However, plateletcounts may decrease in the setting of DIC.
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Comprehensive chemistry panel
Sodium and chloridelevels are abnormal in severe dehydration.
Decreased bicarbonatecan point to acute acidosis.
Increased BUN and creatinine levels can point to severedehydration or renal failure.
Glucosecontrol is important in the management of sepsis, with
hyperglycemia associated with higher mortality.
LFTs and bilirubin, alkaline phosphatase, and lipase levels areimportant in evaluating multiorgan dysfunction or apotentialsource(eg, biliary disease, pancreatitis, hepatitis).
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Serum lactate
It is the best serum marker for tissue perfusion.
There is also evidence that lactate can be elevated in sepsisin the absence of tissue hypoxia due to mitochondrial
dysfunction and down-regulation of pyruvatedehydrogenase, which is the first step in oxidativephosphorylation.
Lactate levels >2.5 mmol/L are associated with an increase in
mortality.
It has been hypothesized that lactate clearance is a measureof tissue reperfusion and an indication of adequate therapy.
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Coagulation studies (PT/aPTT)
o PT and activated aPTT are elevated in DIC.
o Fibrinogen levels are decreased and FDP are increased in the setting of DIC.
Blood cultures
o Blood cultures should be obtained in patients who have suspected sepsis in order toisolate a specific organism and tailor antibiotic therapy.
o Positive in < 50% of cases of sepsis.
o A set of cultures from an indwelling intravenous catheter is especially important, asthese catheters are a frequent source of bacteremia.
Urinalysis and urine cultureo Urinary tract infection is a common source of sepsis, especially in elderly patients.
o Febrile adults without localizing symptoms or signs have a rate of occult urinary tractinfection of 10-15%.
Gram stain and culture, when applicable
o
Sputum specimen should be obtained if pneumonia is suspected.o Any abscess should be drained promptly, and purulent material sent to the microbiology
laboratory for analysis.
o CSF specimen should be obtained if meningitis is suspected.
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Imaging studies
CXRroutine in the workup of fever with an unclear etiology.
o Infiltrates are detected with a chest radiograph in about5% of febrile adults without localizing signs of infection.
Abdominal plain films should be obtained if clinicalevidence of bowel obstruction or perforation exists.
Abdominal ultrasonography is indicated when
evidence of acute cholecystitis or ascendingcholangitis exists
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Rescusitation
Patients with septic shock should betreated in an ICU
Airway: AMS, unable to protect airway
Breathing: Respiratory failure
Circulation: Restoration of blood pressure to
levels which perfuse core organs
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Restoration of tissue perfusion
Causes of poor tissue
perfusion
Leaky vessels
Decreased vascular tone Myocardial depression
Interventions
Volume infusion
Intravenous fluids
PRBCs
Vasopressors
Inotropes
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Intravenous FluidsPractice parameters for hemodynamic support of sepsis in adult patient in sepsis. Task Force of the ACCCM/SCCM.
Critical Care Medicine 1999
Administered in well-defined, rapidly infused
boluses
Continued until blood pressure, tissue
perfusion, and oxygen delivery acceptable or
presence of pulmonary edema
Colloid vs. Crystalloid: No evidence to
recommend one over the other.
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Patients with suspected septic shock require an initial crystalloid fluidchallenge of 20-30 mL/kg(1-2 L) over a period of 30-60 minutes withadditional fluid challenges at rates of up to 1 L over 30 minutes.
Crystalloid administration is titrated to aCVP goal between 8 and 12mm Hgor signs of volume overload (dyspnea, pulmonary rales, orpulmonary edema on the chest radiograph).
A fluid challenge refers to the rapid administration of volume over a
particular time period followed by an assessment of the response.
Patients withseptic shock often require a total 4-6 L or more ofcrystalloid resuscitation.
It is also important to monitor urine output (UOP) as a measure
of dehydration.
UOP
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Vasopressor agents
Vasopressor administration is required forpersistenthypotension once adequate intravascular volume expansionhas been achieved.
Persistent hypotension
is typically defined as systolic bloodpressure (SPB)
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One regimen for septic shock of unknown cause is
o gentamicin or tobramycin 5.1 mg/kg IV once/day
o 3rdgeneration cephalosporin cefotaxime2 g q 6 to 8 h orceftriaxone2 g once/day
o or ifpseudomonas is suspected ceftazidime 2 g IV q 8 h
Vancomycinmust be added if resistant staphylococci orenterococci are suspected.
If there is an abdominal source, a drug effective againstanaerobes should be included metronidazole
Antibiotics are continued for at least 5 days after shock resolvesand evidence of infection subsides
Abscesses must be drained and necrotic tissues (eg, infarctedbowel, gangrenous gallbladder, abscessed uterus) surgicallyexcised.
The patient's condition will continue to deteriorate despiteantibiotic therapy unless septic foci are eliminated.
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The patient's condition will continue todeteriorate despite antibiotic therapyunless septic foci are eliminated.
4 Ds
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Steroid therapy
It has theoretical benefits in the setting of severe sepsis byinhibiting the massive inflammatory cascade.
Recent guidline is that steroids should be administered only inpatients with septic shock whose hypotension is poorlyresponsive to fluid resuscitation and vasopressor therapy.
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Activated protein C
Recombinant drug with fibrinolytic and anti-inflammatory activity,seems beneficial for severe sepsis and septic shock if begun early;benefit has been shown only in patients with significant risk ofdeath.
Dose: 24 mcg/kg/h by continuous IV infusion for 96 h.
Bleeding is the most common complication;
Contraindications include:
hemorrhagic stroke within 3 mo, spinal or intracranial surgery within 2 mo,
acute trauma with a risk of bleeding
intracranial neoplasm.
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Blood sugar
Normalization of blood glucose improves outcome in criticallyill patients, even those not known to be diabetic.
A continuous IV insulin infusion (crystalline zinc 1 to 4 U/h) is
titrated to maintain glucose between 80 to 110 mg/dL .
This approach necessitates frequent (eg, q 1 to 4 h) glucosemeasurement.