Septic Shock Management Guidelines (Surviving Sepsis Campaign)

Fluid Resuscitation

Give at least 30 mL/kg of intravenous crystalloid within the first 3 hours of recognizing sepsis‑induced hypoperfusion. This early bolus improves tissue perfusion and is a core recommendation of the SSC. 1
Balanced crystalloids or normal saline may be used as the initial fluid of choice. No superiority has been demonstrated, allowing clinician discretion. 2
Continue fluid challenges only while objective signs of hemodynamic improvement are present, using dynamic variables (e.g., pulse‑pressure variation, stroke‑volume variation) or static markers (arterial pressure, heart rate, urine output). This approach limits unnecessary fluid overload. 1
Add albumin when large volumes of crystalloids are required to maintain adequate MAP. Albumin supplementation can help achieve target pressures without excessive crystalloid volume. 1
Avoid hydroxyethyl starches (and gelatins) because they increase the risk of acute kidney injury and mortality. Strong contraindication in septic shock. 1

Obtain blood cultures before starting antibiotics, but never delay antimicrobial administration to wait for cultures. Prompt therapy is critical for survival. 4
Administer broad‑spectrum antibiotics within 1 hour of septic shock recognition to cover likely bacterial, fungal, and viral pathogens. Early coverage reduces mortality. 4
De‑escalate to narrower‑spectrum agents once the causative pathogen and susceptibilities are identified. This minimizes collateral damage and resistance. 7
Perform daily assessments for antimicrobial de‑escalation. Ongoing review supports optimal stewardship. 2

Rapidly identify or exclude anatomic infection sources that require emergent intervention. Early source control is linked to better outcomes. 1
Implement required source‑control procedures as soon as medically and logistically feasible. Timely drainage or surgery improves hemodynamics. 1
Prefer the least physiologically invasive method (e.g., percutaneous drainage over open surgery) when feasible. Minimally invasive approaches reduce procedural risk. 1
Remove intravascular catheters promptly after establishing alternative vascular access if they are a potential infection source. Catheter removal reduces ongoing sepsis risk. 1

Target an initial mean arterial pressure (MAP) of ≥ 65 mmHg. This MAP threshold balances organ perfusion with vasopressor exposure. 1
Use norepinephrine as the first‑line vasopressor. It has the best efficacy‑safety profile in septic shock. 1
Add epinephrine if norepinephrine alone cannot achieve the MAP target. Epinephrine provides additional pressor support. 1
Add vasopressin at 0.03 units/min to norepinephrine when hypotension persists, either to raise MAP or to reduce norepinephrine dose. Low‑dose vasopressin augments vasoconstriction without excess catecholamine exposure. 1
Do not use vasopressin as the sole initial vasopressor. Combination therapy is recommended. 1
Reserve vasopressin doses > 0.03–0.04 units/min for salvage therapy only. Higher doses carry increased adverse effects. 1
Consider dopamine only in highly selected patients with low risk of tachyarrhythmias and absolute or relative bradycardia. Routine use is discouraged. 1
Avoid phenylephrine except in specific scenarios (e.g., refractory tachyarrhythmias with norepinephrine, high‑output shock with persistent hypotension, or as salvage). Phenylephrine lacks inotropic support. 1

Start dobutamine (up to 20 µg/kg/min) when myocardial dysfunction (elevated filling pressures, low cardiac output) or ongoing hypoperfusion persists despite adequate volume and MAP. Dobutamine improves cardiac output in septic cardiomyopathy. 4
Do not pursue supranormal cardiac index targets; aim for physiologic adequacy instead. Over‑optimization has not shown benefit. 9

Prefer dynamic over static preload markers to predict fluid responsiveness when applicable. Dynamic indices better identify patients who will benefit from fluids. 10
Monitor cardiac output or stroke volume in patients who do not respond to initial therapy. Ongoing cardiac output assessment guides further interventions. 10
Place an arterial catheter for continuous pressure monitoring in shock refractory to initial therapy or when vasopressors are required. Continuous MAP data enable precise titration. 9
Measure central venous pressure in patients who already have a central venous catheter. CVP can assist in assessing volume status when other data are unavailable. 10
Use bedside echocardiography as the first‑line imaging modality to classify the type of shock. Rapid cardiac assessment informs targeted therapy. 10

Maintain MAP ≥ 65 mmHg. Consistent with SSC hemodynamic goals. 1
Achieve urine output ≥ 0.5 mL/kg/h. Adequate renal perfusion marker. 8
Normalize lactate levels in patients with elevated lactate, using lactate clearance as a marker of tissue perfusion recovery. Lactate reduction correlates with improved outcomes. 4

Do not give intravenous hydrocortisone if adequate fluid resuscitation and vasopressor therapy have restored hemodynamic stability. Steroids are reserved for refractory cases. 4
Consider hydrocortisone 200 mg/day plus fludrocortisone in refractory septic shock when vasopressors cannot achieve target MAP. Combination therapy may reduce vasopressor requirements. 9
Do not use the ACTH stimulation test to select patients for hydrocortisone therapy. Test does not predict response. 9
Taper hydrocortisone once vasopressors are no longer needed. Gradual withdrawal avoids adrenal insufficiency. 9

Target a hemoglobin of 7–9 g/dL in the absence of tissue hypoperfusion, ischemic coronary disease, or acute hemorrhage. Restrictive transfusion strategy is safe. 4
Provide prophylaxis for deep‑vein thrombosis in all septic shock patients unless contraindicated. VTE prevention is standard ICU care. 5
Administer stress‑ulcer prophylaxis to patients with risk factors for gastrointestinal bleeding. Reduces incidence of stress‑related mucosal injury. 5
Start insulin therapy when two consecutive glucose readings exceed 180 mg/dL, targeting an upper glucose limit of ≤ 180 mg/dL. Tight glucose control improves outcomes without hypoglycemia risk. 5

Never delay antimicrobial therapy to obtain cultures; obtain cultures promptly but proceed with antibiotics without waiting. Delay increases mortality. 4
Avoid low‑dose dopamine for renal protection; it offers no benefit and may cause harm. Evidence does not support renal‑protective effect. 9
Prevent fluid overload by stopping fluid administration once hemodynamic improvement ceases. Excess fluids worsen outcomes. 1
Do not use hydroxyethyl starches or gelatins; they are associated with higher mortality and acute kidney injury. Strong contraindication. 1

Discuss goals of care and prognosis with patients and families early, but no later than 72 hours after ICU admission. Early communication aligns treatment with patient values. 8

All statements are derived from cited Surviving Sepsis Campaign recommendations.