Synopsis
Recognise infection-associated acute organ dysfunction early, distinguish immediate physiological danger from lower-risk infection, and connect bedside findings to time-critical investigation, treatment and repeated reassessment.
- Sepsis is life-threatening organ dysfunction caused by a dysregulated response to infection; fever and a positive culture are neither necessary nor sufficient for the diagnosis.
- Begin with ABCDE, observations, NEWS2 and clinical trajectory. A normal temperature, modest inflammatory markers or apparently reassuring blood pressure does not exclude dangerous deterioration.
- Look deliberately for new confusion, increased oxygen requirement, tachypnoea, hypotension, poor peripheral perfusion, reduced urine output, non-blanching rash and inability to maintain normal activity.
- Identify likely source and host modifiers in parallel: recent procedures, devices, immune suppression, pregnancy, frailty, antimicrobial exposure, resistant-organism history and travel all change the pathway.
- Obtain blood cultures and appropriate source samples before antimicrobials when this causes no clinically significant delay; never postpone urgent treatment in a high-risk patient to complete sampling.
- For adults meeting high-risk criteria, NICE prioritises broad-spectrum intravenous antimicrobial treatment within one hour of risk recognition, selected from the suspected source, allergy history and local resistance data.
- Treatment is a cycle rather than a bundle completed once: stabilise, measure response, review source control, narrow therapy when results arrive and escalate when physiology fails to improve.
Key red flags
New hypotension, marked tachypnoea, increased oxygen need, altered mental state, mottled or ashen skin, cyanosis, non-blanching rash or very low urine output indicates threatened organ function and demands immediate senior assessment.
Older, frail, pregnant, immunosuppressed or recently treated patients may lack fever or tachycardia. Acute functional decline, delirium, reduced intake, falls or caregiver concern may be the earliest signal.
Pulmonary embolism, haemorrhage, pancreatitis, adrenal crisis, anaphylaxis, toxic ingestion and inflammatory disease can reproduce shock and raised inflammatory markers; parallel assessment prevents diagnostic closure.
Persistent shock, rising lactate, increasing oxygen need or worsening confusion after initial measures suggests inadequate resuscitation, wrong diagnosis, resistant infection or a source requiring urgent drainage or surgery.
Investigation priorities
Quantify physiological disturbance, find hypoglycaemia and establish a repeatable baseline.
Management branches
Suspected infection plus NICE high-risk criteria, shock, rapidly worsening organ dysfunction or strong clinician concern.
- Call senior help, perform ABCDE, secure monitoring and intravenous access, measure lactate and obtain cultures and source samples without delaying treatment.
- Give oxygen only when needed, use small reassessed crystalloid boluses for hypoperfusion, and administer source-appropriate broad-spectrum intravenous antimicrobials within the nationally recommended high-risk timeframe.
- Reassess after every intervention; measure urine output, repeat lactate when relevant, seek critical-care support for ongoing shock and arrange urgent source control when obstruction, infected material or a device is suspected.