Selasa, 19 Juni 2012
Sepsis and septic shock
Definitions
Systemic
inflammatory response syndrome (SIRS)—Two or more of the following, due to either an
infectious or a noninfectious etiology:
- Temperature >380C or >360C
- Respiratory rate >24 breaths/ min
- Heart rate >90 beats/ min
- WBC count >12,000/uL or <4000/uL, or >10% bands
Sepsis—SIRS witha proven or
suspected microbial etiology
Severe
sepsis—Sepsis
withone or more signs of organ dysfunction
Septic
shock—Sepsis
witharterial blood pressure<90 mmHg or 40 mmHg below pt’s normal blood pressure for at least 1
hdespite fluid resuscitation
Etiology
•
Blood cultures are positive in 20–40% of sepsis cases and in 40–70% of septic
shock cases. Of cases with positive blood cultures,-40% are due to gram-positive bacteria, 35% to
gram-negative bacteria, and 7% to fungi.
•
Any class of microorganism can cause severe sepsis.
•
A significant proportion of cases have negative microbiologic data.
Epidemiology
and Risk Factors
The incidence of severe sepsis and septic shock is
increasing in the United States, with >300,000
cases each year. Two-thirds of cases occur in pts hospitalized for other
reasons. Sepsis is a contributing factor in >200,000 deaths eachyear in the United
States.
The higher incidence of sepsis is due to the aging of the
population, longer survival of pts withch ronic diseases, medical treatments
(e.g., with steroids or antibiotics), and invasive procedures (e.g., catheter
placement). Gram-negative sepsis is associated withunderlying diabetes
mellitus, lymphoproliferative disorders, cirrhosis of the liver, burns,
neutropenia, and indwelling urinary cathe ters. Gram-positive sepsis is
associated withindwelling mechanical devices and intravascular catheters, IV
drug use, and burns. Fungal sepsis is associated with neutropenia and
broad-spectrum antimicrobial therapy.
Pathogenesis
and Pathology
Local
and Systemic Host Responses
•
Recognition of microbial molecules by tissue phagocytes triggers
production and release of cytokines and other mediators that increase blood
flow to the infected site, enhance the permeability of local blood vessels,
attract neutrophils to the infected site, and elicit pain.
•
Through intravascular thrombosis (the hallmark of the local immune
response), the body attempts to wall off invading microbes and prevent the
spread of infection and inflammation. Key features of the systemic immune
response include intravascular fibrin deposition, thrombosis, and DIC; the
underlying mechanisms are the activation of intrinsic and extrinsic clotting
pathways, impaired function of the protein C–protein S inhibitory pathway,
depletion of antithrombin and protein C, and prevention of fibrinolysis by
increased plasma levels of plasminogen activator inhibitor 1.
Organ Dysfunction and Shock
•
Endothelial injury:
Widespread endothelial injury is believed to be the major mechanism for
multiorgan dysfunction.
•
Septic shock: The
hallmark is a decrease in peripheral vascular resistance despite increased
levels of vasopressor catecholamines. Cardiac output and blood flow to
peripheral tissues increase, and oxygen utilization by these tissues is greatly
impaired.
Clinical
Features
- Hyperventilation
- Encephalopathy (disorientation, confusion)
- Hypotension
- DIC, acrocyanosis, ischemic necrosis of peripheral tissues (e.g., digits)
- Skin: hemorrhagic lesions, bullae, cellulitis. Skin lesions may suggest specific pathogens—e.g., petechiae and purpura with Neisseria meningitidis, ecthyma gangrenosum in neutropenic pts with Pseudomonas aeruginosa.
- Gastrointestinal: nausea, vomiting, diarrhea, ileus, cholestatic jaundice
- Hypoxemia: ventilation-perfusion mismatchand increased alveolar capillary permeability withincreased pulmonary water content
Major Complications
• Cardiopulmonary manifestations:
Acute
respiratory distress syndrome (progressive diffuse pulmonary infiltrates and
arterial hypoxemia) develops in -50%
of pts withsevere sepsis or septic shock.
Hypotension:
Normal or increased cardiac output and decreased systemic vascular resistance
distinguish septic shock from cardiogenic or hypovolemic shock.
Myocardial
function is depressed withdecreased ejection fraction.
• Renal manifestations: oliguria, azotemia, proteinuria, renal failure due to acute
tubular necrosis
• Coagulation: thrombocytopenia in 10–30% of pts. With DIC, platelet counts usually
fall below 50,000/uL.
• Neurologic manifestations: polyneuropathy with distal motor weakness in prolonged
sepsis
Laboratory Findings
• Leukocytosis
with a left shift, thrombocytopenia
• Prolonged
thrombin time, decreased fibrinogen, presence of D-dimers, suggestive of DIC
• Hyperbilirubinemia,
increase in hepatic aminotransferases, azotemia, proteinuria
• Metabolic
acidosis, elevated anion gap, elevated lactate levels, hypoxemia
Diagnosis
Definitive
diagnosis requires isolation of the microorganism from blood or a local site of
infection. Culture of infected cutaneous lesions may help establish the
diagnosis. Lacking a microbiologic diagnosis, the diagnosis is made on clinical
grounds.
Treatment
1.
Antibiotic treatment
2.
Removal or drainage of a focal source of infection
·
Remove indwelling intravascular catheters and send tips for
quantitative culture; replace Foley and other drainage catheters.
·
Rule out sinusitis in pts withnasal intubation.
·
Perform CT or MRI to rule out occult disease or abscess.
3.
Hemodynamic, respiratory, and metabolic support
a.
Maintain intravascular volume withIV fluids. Initiate treatment with 1–2 L of
normal saline administered over 1–2 h, keeping pulmonary capillary wedge
pressure at 12–16 mmHg or central venous pressure at 8–12 cmH2O, urine output
at >0.5 mL/kg per hour, mean arterial blood pressure at >65 mmHg, and cardiac index
at >4 (L/min)/m2. Add
inotropic and vasopressor therapy if needed. Maintain central venous O2 saturation
at _70%,
using dobutamine if necessary.
b.
Maintain oxygenation withventilator support as indicated.
c.
Monitor for adrenal insufficiency or reduced adrenal reserve. Pts witha plasma
cortisol response of <9 ug/dL
to an ACTH challenge may have improved survival if hydrocortisone (50 mg q6h
IV) and 9-alpha fludrocortisone (50 ug/d via nasogastric tube) are administered for 7 days.
4.
Other treatments (investigational): Antiendotoxin, anti-inflammatory, and anticoagulant
drugs are being studied in severe sepsis treatment. The anticoagulant
recombinant activated protein C (aPC), given as a constant infusion of 24 ug/kg per hour for 96 h, has
been approved for treatment of severe sepsis or septic shock in pts with APACHE
II scores of >25 preceding aPC infusion and low risk of hemorrhagic
complications. The long-term impact of aPC is uncertain, and long-term survival
data are not yet available. Other agents have not improved outcome in clinical
trials.
Shock Algorithm Guidelines
Prognosis
In
all, 20–35% of pts withsevere sepsis and 40–60% of pts with septic shock die
within 30 days, and further deaths occur within the first 6 months. The severity
of underlying disease most strongly influences the risk of dying.
Prevention
In
the United States, most episodes of severe sepsis and septic shock are
complications of nosocomial infections. Thus the incidence of sepsis would be
affected by measures to reduce those infections (e.g., limiting the use and
duration
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