Guidelines of Sepsis

Guidelines for Management of Severe Sepsis and Septic Shock: 

Guidelines for Management of Severe Sepsis and Septic Shock

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Severe sepsis is the number one cause of death in the non-coronary ICU, the third leading cause of death by infectious diseases. Cases of severe sepsis are predicted to increase in the future due to many factors including: an increase in the number of immunocompromised and elderly patients, the continued use of invasive medical procedures, and the emergence of antibiotic resistant microorganisms.

ACCP/SCCM consensus Conference definition: 

Infection : Microbial phenomenon characterized by an inflammatory response to the microorganisms or the invasion of normally sterile host tissue by those organisms. ACCP/SCCM consensus Conference definition

Systemic inflammatory response syndrome (SIRS): : 

Systemic inflammatory response syndrome (SIRS): A systemic response that can result from a wide variety of clinical insults including both infectious and non-infectious (e.g. trauma, burns, or pancreatitis) etiologies manifested by two or more of the following conditions: Temperature >38°C or <36°C Heart rate >90 beats/min Respiratory rate >20 breaths/min or PaCO 2 <32 mmHg White blood cell count > 12000/ uL or < 4000/uL or > 10% immature (band) forms.

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Sepsis: Infection with concomitant SIRS ( > 2 more clinical symptoms) Severe sepsis: Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Septic shock: A subset of severe sepsis with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental status. Multiple organ dysfunction syndrome : Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention .

Pathophysiology: 

Pathophysiology Severe sepsis can be defined as an overlapping triad of over active systemic inflammation coupled with overactive coagulation and impaired fibrinolysis. Pro-inflammatory mediators such as: IL-1, IL-6, IL-8, TNF, platelet activating factor (PAF).

Management of sepsis: 

Management of sepsis A) Early goal-directed therapy (EGDT): Has been shown to improve survival for emergency department patients presenting with septic shock. The goals should include: Central venous pressure (CVP) 8-12 mmHg. Mean arterial pressure (MAP) > 65 mmHg. U.O.P > 0.5 ml/kg/h. Central venous (superior vena cava) or mixed venous oxygen saturation (Scv O2) > 70%.

During the first 6 hr of resuscitation of severe sepsis if Scv O2 of 70% is not achieved with fluids to a CVP of 8-12 mmHg then  packed RBCs transfusion to achieve an hematocrit of 30% and/or administration of dobutamine infusion (up to a maximum of 20 µg/kg/min) to achieve this goal. : 

During the first 6 hr of resuscitation of severe sepsis if Scv O2 of 70% is not achieved with fluids to a CVP of 8-12 mmHg then  packed RBCs transfusion to achieve an hematocrit of 30% and/or administration of dobutamine infusion (up to a maximum of 20 µg/kg/min) to achieve this goal.

B) Diagnosis: 1) Appropriate cultures (blood, urine, CSF, respiratory secretions). 2) Diagnostic studies (U/S, CT).: 

B) Diagnosis: 1) Appropriate cultures (blood, urine, CSF, respiratory secretions). 2) Diagnostic studies (U/S, CT). C) Antibiotic therapy: Should be started within the 1st hour. Should be broad enough. Duration of therapy should be 7 to 10 days. D) Source control: as Drainage of an abscess. Debridement of infected necrotic tissue. Removal of infected device.

E) Vasopressors: Norepinephrine or dopamine. Vasopressin in patients with refractory shock (infusion rates 0.01-0.04 U/min).: 

E) Vasopressors: Norepinephrine or dopamine. Vasopressin in patients with refractory shock (infusion rates 0.01-0.04 U/min). F) Inotropic therapy: In low COP patients dobutamine may be used. G) Steroids: I.V. hydrocortisone 200-300 mg/day for 7 days in 3 or 4 divided doses or by infusion is recommended in patients with septic shock.

H) Recombinant activated protein C (rhAPC): Drotrecogin alpha (xigris). It is recommended in patients at high risk of death.: 

H) Recombinant activated protein C (rhAPC): Drotrecogin alpha (xigris). It is recommended in patients at high risk of death. It inactivate factors Va and VIIIa  preventing the generation of thrombin which decrease inflammation by inhibiting platelet activation, neutrophil recruitment and mast-cell degranulation. APC has direct anti inflammatory properties, including blocking of the production of cytokines by monocytes and blocking cell adhesion. Also has anti apoptotic actions that may contribute to its efficacy.

It is contraindcated in patients with:: 

It is contraindcated in patients with: Active internal bleeding. Recent hemorrhagic stroke (within 3 months). Recent intracrannal or intraspinal surgery.

I) Mechanical ventilation of sepsis induced acute lung injury (ALT)/ acute respiratory distress syndrome (ARDS):: 

I) Mechanical ventilation of sepsis induced acute lung injury (ALT)/ acute respiratory distress syndrome (ARDS): Low tidal volume 6ml/kg is the goal in conjunction with maintaining the endinspiratory plateau pressures less than 30 cm H2O. Permissive hypercapnea can be tolerated in patients with ALI/ARDS if required to minimize plateau pressures and tidal volumes. A minimum amount of PEEP should be set to prevent lung collapse at end expiration. Prone position should be considered in ARDS patients requiring potentially injurious levels of FIO2 or PEEP.

J) Sedation, analgesia, and neuromuscular blockade in sepsis. Intermittent bolus sedation or continuous infusion sedation with daily interuption.: 

J) Sedation, analgesia, and neuromuscular blockade in sepsis. Intermittent bolus sedation or continuous infusion sedation with daily interuption. K) Glucose control: Intensive insulin therapy that maintained the blood glucose level at 80-110 mg/dL resulted in lower morbidity and mortality. Mechanism: Correction of hyperglycemia may improve bacterial phagocytesis. Anti apoptotic effect of insulin by activating the phosphatidylinositol 3- kinase pathway.

L) Renal replacement: In acute renal failure, continuous veno-venous hemofiltration or intermittent hemodialysis.: 

L) Renal replacement: In acute renal failure, continuous veno-venous hemofiltration or intermittent hemodialysis. M) Deep vein thrombosis prophylaxis: Low dose low molecular weight heparin. Mechanical prophylactic device (graduated compression stockings). N) Stress ulcer prophylaxis: Should be given to all patients with severe sepsis H2 receptor inhibitors are more efficacious than sucralfate.

REFERENCES: 

REFERENCES Intensive Care Medicine (2004), 30: 536-555. The New England Journal Medicine (2003), 348: 138-150.

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