SEPSIS, SIRS & SEPTIC SHOCK

DR. JUAN CARLOS BECERRA MARTÍNEZ

CÁTEDRA DE MEDICINA INTERNA-MC3087

TECNOLÓGICO DE MONTERREY, CAMPUS GUADALAJARA

INTRODUCTION Sepsis is a clinical syndrome that complicates severe infection. It is

characterized by: Inflammation (vasodilation, leukocyte accumulation, increased microvascular

permeability)

Systemic inflammatory response syndrome (SIRS) is an identical clinical syndrome that complicates a noninfectious insult (eg, acute pancreatitis, pulmonary contusion).

The onset and progression of sepsis and SIRS focus on dysregulation of the inflammatory response, including the possibility that a massive and uncontrolled release of proinflammatory mediators initiates a chain of events that lead to widespread tissue injury.

This response can lead to multiple organ dysfunction syndrome (MODS), which is the cause of the high mortality associated with these syndromes.

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DEFINITIONS Infection: is the invasion of normally

sterile tissue by organisms.

Bacteremia: is the presence of viable bacteria in the blood.

Sepsis is defined as the presence (probable or documented) of infection together with SIRS.

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DEFINITIONSDIAGNOSTIC CRITERIA FOR SEPSIS include infection (documented or suspected) and some of the following:

1.- General variables Temperature >38.3 or <36ºC Heart rate >90 beats/min  Tachypnea >20 breaths/min Altered mental status Significant edema or positive fluid balance (>20 mL/kg over 24 hours) Hyperglycemia (plasma glucose >140 mg/Dl) in the absence of diabetes

2.- Inflammatory variables Leukocytosis (WBC count >12,000 microL–1) or leukopenia (WBC count <4000

microL–1) Plasma C-reactive protein more than two standard deviations above the normal

value Plasma procalcitonin more than two standard deviations above the normal value

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DEFINITIONS3.- Hemodynamic variables

Arterial hypotension (systolic blood pressure SBP <90 mmHg, MAP <70 mmHg, or an SBP decrease >40 mmHg

4.- Organ dysfunction variables Arterial hypoxemia (arterial oxygen tension [PaO2]/fraction of inspired oxygen [FiO2] <300) Acute oliguria (urine output <0.5 mL/kg/hr for at least two hours despite adequate fluid

resuscitation) Creatinine increase >0.5 mg/dL Coagulation abnormalities [INR] >1.5 or [aPTT] >60 seconds) Ileus (absent bowel sounds) Thrombocytopenia (platelet count <100,000 ) Hyperbilirubinemia (plasma total bilirubin >4 mg/dL)

5.- Tissue perfusion variables Hyperlactatemia (>1 mmol/L) Decreased capillary refill or mottling

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DEFINITIONSSEVERE SEPSIS: refers to:

Sepsis-induced hypotension (MAP <70 mmHg)Lactate above upper limits of laboratory normalUrine output <0.5 mL/kg/hr for more than two

hours despite adequate fluid resuscitationAcute lung injury with PaO2/FIO2 <250Creatinine >2 mg/dL Bilirubin >4 mg/dL Platelet count <100,000 microL–1

Coagulopathy (INR >1.5)

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DEFINITIONS SEPTIC SHOCK: 

Is defined as sepsis-induced hypotension persisting despite adequate fluid resuscitation, which may be defined as infusion of 30 mL/kg of crystalloids.

Septic shock is a type of vasodilatory or distributive shock [2,3]. In other words, it results from a marked reduction in systemic vascular resistance, often associated with an increase in cardiac output.

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DEFINITIONS Multiple organ dysfunction syndrome

(MODS):Refers to progressive organ dysfunction in an

acutely ill patient, such that homeostasis cannot be maintained without intervention. It is at the severe end of the severity of illness spectrum of both SIRS and sepsis.

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RISK FACTORS 50 percent of ICU patients

Bacteremia

Advanced age (≥65 years)

Immunosuppression – Comorbidities that depress host-defense (eg, neoplasms, renal failure, hepatic failure, AIDS, asplenism) and immunosuppressant medications

Diabetes and cancer – Diabetes and some cancers may alter the immune system

Community acquired pneumonia – Severe sepsis and septic shock develop in approximately 48%

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EPIDEMIOLOGY Incidence:   The increased rate of sepsis is thought to be a consequence of advancing age,

immunosuppression, and multidrug-resistant infection. Appears to be highest among African-American males. The incidence is also greatest during the winter, probably due to the increased

prevalence of respiratory infections. Older patients ≥65 years of age account for the majority (60 to 85 percent) of all

episodes of severe sepsis.

Pathogens: Gram positive bacteria are most frequently identified in patients with sepsis in the United

States, although the number of cases of Gram negative sepsis remains substantial.

Disease severity: The most common manifestations of severe organ dysfunction were acute respiratory distress syndrome, acute renal failure, and disseminated intravascular coagulation.

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MORTALITY High mortality rate:

SIRS: 7%Sepsis: 16%Severe sepsis: 20%Septic shock: 46%

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PROGNOSTIC FACTORSHost response: 

Failure to develop a fever was more common among non-survivors of sepsis

Leukopenia was similarly more frequent among non-survivors Risk factors for mortality:

Atrial fibrillation Older age AIDS Liver disease Cancer Alcohol dependence Immune suppression

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PROGNOSTIC FACTORSSite of infection:

Urinary tract infection generally being associated with the lowest mortality rates (30%)

Highest mortality in those with sepsis from ischemic bowel (78%)

Type of infection:

Nosocomial pathogens has a higher mortality than sepsis due to community-acquired pathogens

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PROGNOSTIC FACTORSAntimicrobial therapy:  

Early institution of adequate antibiotic therapy was associated with a 50 percent reduction in the mortality

Restoration of perfusion: Failure to aggressively try to restore perfusion

early may also be associated with mortality.

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Management of severe sepsis and septic shockTherapeutic priorities:

1. Early initiation of supportive care to correct hypoxemia and hypotension.

2. Distinguishing sepsis from systemic inflammatory response syndrome (SIRS)

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EARLY MANAGEMENT

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EARLY MANAGEMENT1.- Stabilize respiration:

Supplemental oxygenIntubation and mechanical ventilation: for airway

protectionChest radiographs and arterial blood gas

analysis should be obtained following initial stabilization

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EARLY MANAGEMENT2.- Assess perfusion:

Hypotension: systolic blood pressure [SBP] <90 mmHg, mean arterial pressure <70 mmHg, decrease in SBP >40 mmHg).

Signs of poor end-organ perfusion: the skin may become cool, tachycardia >90 per min, obtundation, and oliguria or anuria. 

Elevated lactate: is consistent with severe sepsisOthers:

○ Low platelet count○ Elevated INR○ Elevated creatinine and bilirubin levels

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EARLY MANAGEMENT3.- Establish venous access:

As soon as possible in patients with suspected sepsis.

The majority will require central venous access: ○ Can be used to infuse intravenous fluids, medications

(particularly vasopressors), and blood products○ Laboratory studies○ Hemodynamic monitoring (central venous

oxyhemoglobin saturation (ScvO2). Pulmonary artery catheters (PACs): may be helpful to

guide circulatory resuscitation.

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EARLY MANAGEMENT4.- Intravenous fluids:

Volume:  rapid, large volume infusions of intravenous fluids are indicated as initial therapy for severe sepsis or septic shock (restore MAP in 6 hrs).

Choice of fluid: Evidence found no convincing difference between using albumin solutions and crystalloid solutions.

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EARLY MANAGEMENT5.- Vasopressors:

Intravenous vasopressors are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic pulmonary edema:Norepinephrine: prefered DopamineDobutamine (diminished cardiac output)

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EARLY MANAGEMENT6.- Goals of initial resuscitation

(MAP) ≥65 mmHg

Urine output ≥0.5 mL/kg/hour

Central venous pressure (CVP) 8 to 12 mmHg

Central venous (superior vena cava) oxyhemoglobin saturation (ScvO2) ≥70%

Mixed venous oxyhemoglobin saturation (SvO2) ≥65% (if a pulmonary artery catheter is being used).

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EARLY MANAGEMENT7.- CONTROL OF THE SEPTIC FOCUS

8.- Additional therapies:Glucocorticoids (controversial)NutritionIntensive Insulin Therapy

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JAMA. 2015;314(7):708-717.

JAMA. 2015;314(7):708-717.

Artículo de revisión recomendado

JAMA. 2015;314(7):708-717.