Key Points
- Stabilize ABCs; begin targeted evaluation without delaying life-saving therapy.
- Use system-specific risk tools to guide testing and disposition.
- Order high-yield tests first; escalate imaging when indicated.
- Start evidence-based initial therapy and reassess frequently.
Algorithm
- Primary survey and vitals; IV access and monitors.
- Focused history/physical; identify red flags and likely etiologies.
- Order system-appropriate labs and imaging (see Investigations).
- Initiate guideline-based empiric therapy (see Pharmacology).
- Reassess response; arrange consultation and definitive management.
Clinical Synopsis & Reasoning
Sepsis represents dysregulated host response with life‑threatening organ dysfunction; prioritize rapid recognition using qSOFA/SOFA elements, attention to mentation, perfusion, and lactate trends. Clinically, integrate history for potential sources (pulmonary, urinary, abdominal, device‑related), examine for shock phenotypes, and obtain paired blood cultures without delaying therapy. Point‑of‑care ultrasound refines volume status and source hypotheses (e.g., pneumonia, cholecystitis, obstructive uropathy). Early identification of patients likely to decompensate guides ICU triage and invasive monitoring.
Treatment Strategy & Disposition
Initiate balanced crystalloid resuscitation targeting MAP ≥65 mmHg and improving capillary refill/lactate; start time‑appropriate empiric antibiotics within 60 min tailored to suspected source and local resistance. If hypotension persists after 30 mL/kg or sooner when indicated, begin norepinephrine and titrate to perfusion targets; add vasopressin for catecholamine‑sparing effects. Pursue urgent source control (drainage, device removal, debridement) and de‑escalate antimicrobials with culture data. Disposition hinges on shock and organ failure—ICU for vasopressors/respiratory support; otherwise step‑down/ward with protocolized reassessment.
Epidemiology / Risk Factors
- Risk factors vary by condition and patient profile
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| CBC | Baseline hematology | Abnormal counts | |
| BMP | Electrolytes/renal | Derangements |
Vasopressor Strategy (Adult)
| Step | Agent | Notes |
|---|---|---|
| First line | Norepinephrine | Target MAP ≥65 mmHg |
| Add-on | Vasopressin | Catecholamine sparing |
| Escalation | Epinephrine | Consider for refractory shock |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Hydrocortisone (refractory shock) | Glucocorticoid | Hours | Adjunct in pressor-refractory septic shock | Hyperglycemia, infection risk |
| Norepinephrine | α1-adrenergic agonist | Minutes | First-line vasopressor to target MAP ≥65 mmHg | Arrhythmia, ischemia |
| Vasopressin (adjunct) | V1 receptor agonist | Minutes | Catecholamine-sparing add-on in refractory shock | Ischemia at high dose |
| Balanced crystalloids | Plasma volume expansion | Immediate | Initial resuscitation (e.g., 30 mL/kg) | Fluid overload; monitor oxygenation |
| Broad empiric antibiotics | Bactericidal (varies) | Variable | Start within 1 hour; de-escalate to source | Allergy, resistance |
Prognosis / Complications
- Prognosis depends on severity, comorbidities, and timeliness of care
Patient Education / Counseling
- Explain red flags and when to seek emergent care.
- Reinforce medication adherence and follow-up plan.
Notes
Use balanced crystalloids when available. Consider hydrocortisone in refractory shock. Start VTE and stress-ulcer prophylaxis per protocol and address glycemic control.