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Critical Care Medicine›Condition·Updated Jul 11, 2026·v1

Sepsis

Sepsis is a medical emergency requiring immediate recognition, resuscitation, and source control. The 1-hour bundle, balanced crystalloids, norepinephrine, and the ABCDEF bundle are evidence-based cornerstones. Mortality remains high, and long-term PICS surveillance is essential.

High Evidence590 references·2,892 words·12 min read·v1
sepsisseptic shockcritical careresuscitationantibioticsvasopressorsSOFAqSOFAABCDEF bundlesource controllactateprocalcitoninPICS

Quick Reference

RxDrug of choiceNorepinephrine (first-line vasopressor for septic shock, initiate early if MAP <65 mmHg after fluids)
AltAlternativesVasopressin (0.03 U/min) as second-line; epinephrine as third-line; hydrocortisone 200 mg/day IV for refractory shock
⊘AvoidHydroxyethyl starches, activated protein C (drotrecogin alfa), low-dose dopamine, vitamin C/thiamine/hydrocortisone combination, non-dihydropyridine CCBs, and supranormal oxygen delivery targets
DxTest of choiceSerum lactate (initial and serial clearance); blood cultures (two sets before antibiotics); procalcitonin for de-escalation guidance
ScKey scoreSOFA score (≥2 increase defines sepsis; trajectory over 48-72h predicts mortality); qSOFA (≥2 for rapid bedside screening in non-ICU settings)
→When to referRefractory shock (norepinephrine >0.5 µg/kg/min), need for source control (surgery/IR), ECMO consideration, goals-of-care discussions with multiple poor prognostic factors
Early recognition (qSOFA), 1-hour bundle (antibiotics, balanced crystalloids, norepinephrine), source control within 12 hours, and ABCDEF bundle for post-resuscitation care are the pillars of sepsis management.
Sepsis is life-threatening organ dysfunction from a dysregulated host response to infection [41]. Defined by Sepsis-3 as acute [[SOFA]] score increase ≥2 points due to infection, it carries high mortality. Septic shock is a subset with vasopressor requirement and lactate >2 mmol/L after fluids. This concise guide covers recognition, resuscitation, source control, organ support, and post-ICU care.

Overview and Recommendations

Background

  • •Sepsis is life-threatening organ dysfunction from a dysregulated host response to infection, defined by Sepsis-3 as an acute increase in SOFA score ≥ 2 points. Septic shock requires vasopressors to maintain MAP ≥ 65 mmHg and lactate > 2 mmol/L after adequate fluids, with hospital mortality > 40%.
  • •It affects approximately 49 million people annually worldwide, causing 11 million deaths. Hospital-treated incidence is 189 per 100,000 person-years, with mortality of 26.7% for all sepsis and 41.9% for ICU-treated cases. Incidence is rising due to aging populations and improved recognition.
  • •Pathophysiology begins with pathogen recognition via Toll-like receptors, triggering a cytokine storm (TNF-α, IL-1, IL-6) that causes vasodilation, capillary leak, and microcirculatory failure. Endothelial activation leads to coagulopathy and DIC, while mitochondrial dysfunction (cytopathic hypoxia) impairs oxygen utilization. Later, immune paralysis (lymphocyte apoptosis, reduced HLA-DR) increases vulnerability to secondary infections, driving late mortality.
  • •Risk factors include extremes of age (neonates, elderly >65 years), immunosuppression (HIV, chemotherapy, transplant), indwelling devices, recent hospitalization, and comorbidities like diabetes and hypertension. One in eight patients with infection and organ failure does not meet SIRS criteria; qSOFA (altered mentation, RR ≥ 22, SBP ≤ 100 mmHg) is a more specific bedside screening tool.
  • •Sepsis subphenotypes identified by organ dysfunction trajectory, rapidly worsening, delayed worsening, rapidly improving, and delayed improving, carry distinct mortality risks. Molecular phenotyping (hyperinflammatory vs. hypoinflammatory) may guide future therapy but current management remains standardized.

Evaluation

  • •Suspect sepsis in any patient with infection plus altered mentation, tachypnea, or hypotension. Calculate qSOFA: 1 point each for GCS < 15, RR ≥ 22, SBP ≤ 100 mmHg. A score ≥ 2 should trigger immediate escalation of care.
  • •Measure serum lactate immediately. A level > 2 mmol/L indicates tissue hypoperfusion; > 4 mmol/L defines severe shock and mandates urgent resuscitation. Repeat lactate at 2-4 hours; failure to clear (decrease < 10% or persistent elevation) is associated with higher mortality.
  • •Obtain two sets of blood cultures (aerobic and anaerobic) before initiating antibiotics. Do not delay antibiotics more than 45 minutes if cultures are difficult to obtain. Collect other cultures (urine, sputum, wound, CSF) based on suspected source.
  • •Assess organ dysfunction using the SOFA score (or quick bedside assessment: MAP, PaO₂/FiO₂, creatinine, bilirubin, platelets, GCS). An increase ≥ 2 points from baseline confirms sepsis.
  • •Order chest radiograph for pneumonia; CT abdomen/pelvis with IV contrast if intra-abdominal source suspected; bedside ultrasound for cholecystitis, hydronephrosis, or abscess.
  • •Consider echocardiography if hemodynamic instability persists despite fluids and vasopressors, to rule out right ventricular dysfunction (present in ~50% of septic patients, associated with 3-fold higher 28-day mortality) or endocarditis.
  • •Check procalcitonin (PCT) to support bacterial etiology and guide antibiotic de-escalation. Serial PCT with drop > 80% from peak or to ≤ 0.5 µg/L suggests stopping antibiotics. CRP is less specific but can be used if PCT unavailable.
  • •In refractory septic shock, assess for critical illness-related corticosteroid insufficiency (CIRCI) with random cortisol < 10 µg/dL or delta < 9 µg/dL after cosyntropin stimulation.
  • •Evaluate for DIC with platelet count, PT/PTT, fibrinogen, D-dimer. Purpura fulminans (sudden extensive purpuric lesions) signals meningococcemia or pneumococcal sepsis and requires immediate aggressive management.
  • •Reassess fluid responsiveness after initial bolus using dynamic measures (passive leg raise, pulse pressure variation) before administering additional fluids. A positive passive leg raise test predicts response to further boluses.

Management

  • •Initiate the 1-hour sepsis bundle immediately upon recognition of hypotension (MAP < 65 mmHg) or lactate ≥ 4 mmol/L: measure lactate, obtain blood cultures, start broad-spectrum antibiotics, begin 30 mL/kg crystalloid bolus, and start norepinephrine if MAP < 65 persists.
  • •Administer 30 mL/kg of balanced crystalloids (e.g., lactated Ringer's) within the first 3 hours. Balanced crystalloids reduce mortality compared to 0.9% saline in sepsis (NNT = 20). Avoid hydroxyethyl starches (increase mortality and need for RRT).
  • •Start norepinephrine as first-line vasopressor if MAP < 65 mmHg persists after initial fluid bolus. Target MAP 65-70 mmHg. Early norepinephrine (within 1-2 hours) improves shock control at 6 hours and reduces cardiogenic pulmonary edema and new-onset arrhythmias.
  • •If norepinephrine exceeds 0.25-0.5 µg/kg/min, add vasopressin 0.03 U/min. Vasopressin spares norepinephrine but has no proven mortality benefit. Consider epinephrine as third-line agent.
  • •For refractory shock despite norepinephrine and vasopressin, add hydrocortisone 50 mg IV every 6 hours (200 mg/day). This accelerates shock reversal but does not improve survival and may increase superinfection. Avoid vitamin C/thiamine/hydrocortisone combination (no benefit; vitamin C alone may cause harm).
  • •Choose empiric antibiotics based on suspected source, local epidemiology, immune status, and prior antibiotic exposure. For septic shock with high mortality risk (>25%), consider combination therapy (e.g., antipseudomonal beta-lactam plus aminoglycoside or fluoroquinolone). De-escalate using cultures and PCT.
  • •Achieve source control within 12 hours of diagnosis: drainage of abscesses, debridement of necrotic tissue, removal of infected catheters, surgical intervention for intra-abdominal infections. Failure to control source is an independent risk factor for mortality.
  • •Provide lung-protective ventilation for ARDS: tidal volume 6 mL/kg predicted body weight, plateau pressure ≤ 30 cm H₂O, SpO₂ 92-96%. Use high-flow nasal cannula after extubation to reduce reintubation.
  • •Implement the ABCDEF bundle: Assess and treat pain, daily spontaneous awakening and breathing trials, analgesia-first sedation (target RASS 0 to -2), delirium monitoring (CAM-ICU or ICDSC), early mobility and exercise, and family engagement. Each element reduces mortality and delirium.
  • •For delirium, avoid benzodiazepines. Use dexmedetomidine or propofol for sedation. Haloperidol (1-2 mg IV q6-8h) may be used for incident delirium with QTc monitoring.
  • •Provide VTE prophylaxis with LMWH (e.g., enoxaparin 40 mg subcutaneously daily) or unfractionated heparin (5000 U subcutaneously twice daily). In high-risk patients (e.g., COVID-19 with coagulopathy), consider therapeutic-dose enoxaparin with caution for bleeding.
  • •Start stress ulcer prophylaxis with a PPI (e.g., pantoprazole 40 mg IV daily) in mechanically ventilated patients. Discontinue when oral intake resumes and no longer ventilated.
  • •Initiate enteral nutrition within 48 hours of ICU admission if hemodynamically stable. Avoid overfeeding. Immunonutrition with eicosapentaenoic acid, gamma-linolenic acid, and antioxidants may reduce mortality but evidence is limited.
  • •Monitor for ICU-acquired weakness using MRC sum score (score < 35 defines paresis). Begin early physical and occupational therapy as soon as hemodynamically stable.
  • •Do not use: supranormal oxygen delivery goals, activated protein C (drotrecogin alfa, withdrawn), low-dose dopamine for renal protection, or routine albumin (no survival benefit). Do not delay antibiotics to obtain cultures; the 1-hour window is critical.
  • •Refer to intensivist for any sepsis with organ dysfunction. Consult surgery or interventional radiology for source control. Consider ECMO for refractory shock in selected patients. Involve palliative care when multiple poor prognostic factors are present (advanced cancer, frailty, high lactate, persistent organ failure).
  • •Discharge criteria: resolution of organ dysfunction (SOFA improving), stable hemodynamics off vasopressors for ≥ 24 hours, no ongoing infection, adequate oral intake, and plan for post-ICU follow-up to screen for PICS at 2-4 weeks using validated tools (MoCA, HADS, IES-R, 6-minute walk test).

Board Review — High Yield

  • •qSOFA, Bedside score: altered mentation, RR≥22, SBP≤100; score ≥2 identifies high-risk patients with poor outcomes.
  • •Sepsis-3 definition, Organ dysfunction = acute increase in SOFA ≥2 points; septic shock = vasopressor requirement + lactate >2 mmol/L after fluids.
  • •1-hour bundle, Measure lactate, obtain blood cultures, give broad-spectrum antibiotics, start 30 mL/kg crystalloid, begin norepinephrine if MAP<65.
  • •Balanced crystalloids, Associated with lower 30-day mortality vs saline in sepsis (SMART trial; NNT=20).
  • •Norepinephrine first-line, Target MAP 65-70 mmHg; early use improves shock control and reduces complications.
  • •Source control within 12 hours, Independent predictor of survival; failure increases mortality (OR 2.1).
  • •ABCDEF bundle, Each component reduces mortality and delirium: Assess pain, SAT/SBT, choice of sedation, delirium monitoring, early mobility, family engagement.
  • •Procalcitonin-guided de-escalation, Reduces antibiotic duration by ~1 day without increasing mortality; stop when PCT drops >80% or ≤0.5 µg/L.
  • •Corticosteroids, Consider in refractory shock; faster reversal but no survival benefit; avoid in SRS2 endotype (increased mortality).
  • •Post-ICU syndrome (PICS), Screen at 2-4 weeks post-discharge for cognitive, physical, and mental health impairments using MoCA, HADS, IES-R, 6-minute walk.

Deep Dive — Evidence Details

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