6.2 Sepsis & Septic Shock Guidelines

Sepsis & Septic Shock Guidelines

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. It is a medical emergency that requires rapid identification and prompt, protocolized management to reduce mortality. The AGACNP must be intimately familiar with the updated Surviving Sepsis Campaign (SSC) Guidelines and the clinical application of these recommendations in the acute care setting.

Defining Sepsis and Septic Shock

The previous continuum of "SIRS to Severe Sepsis" has been replaced. The current definitions focus on organ dysfunction:

• Sepsis: A suspected or documented infection accompanied by an acute increase in the Sequential Organ Failure Assessment (SOFA) score of 2 points or more. The SOFA score incorporates respiratory (PaO2/FiO2), hematologic (platelets), hepatic (bilirubin), cardiovascular (MAP/vasopressor requirement), neurologic (Glasgow Coma Scale), and renal (creatinine/urine output) parameters.
• Septic Shock: A subset of sepsis where underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. It is clinically defined by persisting hypotension requiring vasopressors to maintain a Mean Arterial Pressure (MAP) ≥ 65 mmHg AND a serum lactate level > 2 mmol/L (18 mg/dL) despite adequate volume resuscitation.

The "Hour-1 Bundle"

The cornerstone of modern sepsis management is the implementation of the "Hour-1 Bundle," which emphasizes that resuscitation should begin immediately upon recognition of sepsis. Elements of the bundle include:

1. Measure Lactate: Lactate is a marker of tissue hypoperfusion. If the initial lactate is elevated (>2 mmol/L), it should be remeasured within 2-4 hours to guide resuscitation and confirm clearance.
2. Obtain Blood Cultures: At least two sets of blood cultures (aerobic and anaerobic) must be drawn prior to the administration of antibiotics, provided this does not significantly delay antimicrobial therapy (should not delay >45 minutes).
3. Administer Broad-Spectrum Antibiotics: Empirical therapy should target the most likely pathogens based on the suspected source, local antibiograms, and patient risk factors (e.g., MRSA, Pseudomonas). Each hour of delay in appropriate antibiotic administration significantly increases mortality in septic shock.
4. Administer Intravenous Fluids: For sepsis-induced hypoperfusion or an initial lactate ≥ 4 mmol/L, a minimum of 30 mL/kg of IV crystalloid should be administered within the first 3 hours. Balanced crystalloids (e.g., Lactated Ringer's) are generally preferred over normal saline to reduce the risk of hyperchloremic metabolic acidosis and acute kidney injury.
5. Apply Vasopressors: If hypotension persists during or after fluid resuscitation, vasopressors must be initiated to maintain a target MAP ≥ 65 mmHg.

Vasoactive Therapy and Hemodynamic Support

The choice and titration of vasoactive medications are critical competencies for the AGACNP:

• Norepinephrine remains the first-line vasopressor for septic shock.
• Vasopressin (up to 0.03 units/min) is the recommended second-line agent. It is often added to norepinephrine rather than escalating the norepinephrine dose, particularly to reduce adrenergic side effects like tachycardia and ischemia.
• Epinephrine is considered a third-line agent if MAP is inadequate despite norepinephrine and vasopressin.
• Dobutamine may be added in cases of documented myocardial dysfunction (decreased cardiac output) or persistent hypoperfusion despite adequate intravascular volume and MAP. It should be used cautiously as it can cause vasodilation and worsen hypotension.

Source Control and Adjunctive Therapies

Source Control: Identification and eradication of the infectious source (e.g., drainage of an abscess, removal of an infected catheter, surgical debridement) are as important as resuscitation. Source control should be achieved as rapidly as possible.

Corticosteroids: The use of corticosteroids in septic shock remains nuanced. Current guidelines suggest utilizing intravenous hydrocortisone (typically 200 mg/day, often given as 50 mg IV q6h or as a continuous infusion) ONLY if adequate fluid resuscitation and vasopressor therapy are unable to restore hemodynamic stability. Corticosteroids are not recommended for sepsis in the absence of shock.

Glycemic Control: Target a blood glucose level of 144-180 mg/dL using a protocolized approach. Avoid strict glucose control (targeting 80-110 mg/dL) as it has been associated with an increased incidence of severe hypoglycemia without improving mortality.

Stress Ulcer Prophylaxis: Recommended for patients with septic shock or those with specific risk factors for gastrointestinal bleeding (e.g., mechanical ventilation >48 hours, coagulopathy).

Venous Thromboembolism (VTE) Prophylaxis: Pharmacologic prophylaxis (e.g., Low Molecular Weight Heparin or unfractionated heparin) is recommended unless contraindicated, often combined with mechanical prophylaxis.

Dynamic Assessment of Fluid Responsiveness

The initial 30 mL/kg bolus is just the beginning. Further fluid administration should be guided by dynamic, rather than static, measures of fluid responsiveness. Static measures like Central Venous Pressure (CVP) are poor predictors of responsiveness.

• Passive Leg Raise (PLR): An auto-transfusion of venous blood from the lower extremities to the central circulation. A transient increase in stroke volume or cardiac output (>10%) indicates the patient is fluid responsive.
• Stroke Volume Variation (SVV) / Pulse Pressure Variation (PPV): Useful in mechanically ventilated patients (with specific criteria: fully adapted to vent, tidal volume ≥ 8 mL/kg, sinus rhythm). High variation (>12-13%) suggests fluid responsiveness.
• Echocardiography: Point-of-care ultrasound to assess Left Ventricular Outflow Tract (LVOT) Velocity Time Integral (VTI) before and after fluid challenges or PLR.