Septic shock and source control — Rapid

Synopsis

Manage persistent infection-associated circulatory failure as a resuscitation and source-control emergency, integrating fluids, vasoactive support, antimicrobial delivery and definitive procedural treatment.

Septic shock is not simply sepsis with a low blood pressure: it is persistent circulatory and metabolic failure with substantially increased mortality despite initial resuscitation.
Reassess fluid responsiveness after small boluses; repeated unmeasured litres can worsen pulmonary oedema, abdominal pressure and tissue congestion without restoring effective perfusion.
Vasoactive sequence: start noradrenaline as first-line; if the dose is escalating, add vasopressin rather than continuing noradrenaline alone, then add adrenaline if mean arterial pressure remains inadequate despite both.
Source control: drain pus, relieve obstruction, debride necrosis or remove an infected device as soon as practical and safe—ideally within 6 hours when an intervention is required.
Antibiotic penetration, spectrum, dose and infusion strategy must be reviewed in shock because capillary leak, augmented or impaired renal clearance and extracorporeal support change exposure.
Follow response using mental state, skin perfusion, urine output, lactate trend, haemodynamics and organ function; no single blood-pressure value proves adequate resuscitation.

Key red flags

Persistent hypoperfusion

Hypotension, prolonged capillary refill, cool or mottled skin, oliguria, altered consciousness and rising lactate despite initial treatment indicate continuing circulatory failure.

Undrained focus

Localised pain, swelling, fluctuance, peritonism, obstructive jaundice, hydronephrosis, device inflammation or persistent bacteraemia suggests an anatomical focus that antimicrobials alone cannot control.

Septic cardiomyopathy

Poor contractility, pulmonary congestion or inadequate output despite restored vascular tone may reflect infection-associated myocardial dysfunction and requires echocardiographic and critical-care assessment.

Mixed shock

Haemorrhage, embolism, adrenal failure, cardiogenic disease and distributive sepsis can coexist after surgery or critical illness; discordant physiology should trigger parallel evaluation.

Investigation priorities

Serial lactate and blood gasFirst step

Track metabolic stress, ventilation and response without treating one number in isolation.

Management branches

Initial shockRestore perfusion while defining mechanism

Suspected infection with hypotension or hypoperfusion persisting during initial ABCDE management.

Escalate to critical care, obtain monitored vascular access, cultures and lactate, start source-directed intravenous antimicrobials and give reassessed crystalloid boluses when fluid responsiveness is plausible.
Start noradrenaline promptly through a locally approved monitored route; peripheral initiation is appropriate when it avoids delay, with frequent site checks and planned secure access. Aim initially for mean arterial pressure around 65 mmHg; for adults aged 65 years or over, use the 60–65 mmHg range unless individual physiology requires otherwise.
Use bedside perfusion, urine output, lactate trend and focused cardiac assessment to select further fluid, vasoactive, inotropic or alternative shock treatment. Use an arterial line when vasopressor doses are intermediate or high, escalating, multiple, frequent blood sampling is required or cuff readings are inconsistent.

Key medicines

Noradrenaline infusionFirst-line vasopressor: start as a monitored continuous intravenous infusion and titrate to the documented perfusion target under the local critical-care protocol; do not delay initiation solely while waiting for central access.Use a dedicated secure line and frequent peripheral-site checks until central access is appropriate. Extravasation causes tissue injury; excessive vasoconstriction can worsen peripheral or mesenteric ischaemia.

Balanced isotonic crystalloidGive a small intravenous bolus under the local resuscitation protocol, then repeat only after a documented dynamic or clinical response assessment; stop when fluid responsiveness is absent or congestion develops.Cumulative positive balance can worsen lung oedema and tissue congestion; use particular caution with cardiac, renal or hepatic failure and do not force fluid into a non-responsive patient.

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