discuss the management of septic shock

8/12/2019 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.

discuss the management of septic shock

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