Septic shock and source control

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The key judgement in septic shock is whether ongoing hypoperfusion reflects insufficient circulating volume, pathological vasodilatation, myocardial dysfunction, an uncontrolled focus or a different shock state. Bedside assessment and focused imaging are repeated as treatment changes the physiology. Fluids, vasopressors and inotropes are supports; they do not sterilise an infected collection.

Source control planning begins at recognition, not after prolonged antimicrobial failure. The responsible procedural specialty, radiology, microbiology and critical care should agree what intervention is required, how urgently it can occur, what imaging is essential and how the patient will be supported during transfer or anaesthesia. Delay must be explicitly justified and reviewed.

Antimicrobial therapy should cover the probable source and resistant-organism risks promptly, then narrow when microbiology and operative findings become available. Renal replacement, obesity, burns, capillary leak and rapid changes in kidney function complicate exposure; pharmacist and microbiologist involvement is part of shock management rather than an optional later review.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Uncontrolled bacterial focus

Perforation, abscess, infected obstruction, necrotic tissue or device biofilm can maintain a high microbial burden despite appropriate circulating antimicrobial concentrations.

Severe systemic infection

Pneumonia, abdominal infection, pyelonephritis and bloodstream infection may provoke profound vasodilatation and myocardial dysfunction without a drainable collection.

Host and treatment factors

Immune suppression, delayed recognition, resistant pathogens and altered drug exposure increase the likelihood that infection progresses to persistent circulatory failure.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pathological vasodilatation
Inflammatory mediators reduce vascular tone and responsiveness, lowering effective perfusion pressure despite a normal or increased cardiac output early in shock.
2
Endothelial leak
Capillary barrier dysfunction moves fluid into tissues, reducing effective circulating volume while causing pulmonary and peripheral oedema.
3
Myocardial and microvascular dysfunction
Impaired contractility and maldistributed microcirculatory flow limit tissue oxygen delivery even after macroscopic blood-pressure targets are reached.
4
Persistent microbial stimulus
Undrained infection continues releasing pathogen and damage signals, sustaining inflammation until the anatomical focus is controlled.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Persistent hypoperfusionRed flag

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

Undrained focusRed flag

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

Septic cardiomyopathyRed flag

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 shockRed flag

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

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial lactate and blood gasFirst step
Why
Track metabolic stress, ventilation and response without treating one number in isolation.
Interpretation and limitations
A falling lactate can support improvement, but beta-agonism, seizures and liver dysfunction affect clearance. Persistent elevation prompts renewed perfusion, source and diagnosis review.
02
Focused echocardiography and dynamic fluid assessment
Why
Distinguish likely fluid responsiveness, ventricular dysfunction and obstructive physiology at the bedside.
Interpretation and limitations
Static filling estimates are unreliable alone. Integrate passive-leg-raise or stroke-volume response, lung findings and cardiac function with the patient's trend.
03
Urgent source-directed CT or ultrasound
Why
Identify collections, obstruction, perforation, ischaemic tissue and device complications that need intervention.
Interpretation and limitations
Imaging should be the minimum necessary to enable treatment and must not create an unsafe delay in an unstable patient with an obvious surgical source.
04
Cultures from blood and the source
Why
Define the pathogen and resistance pattern and verify microbiological source control.
Interpretation and limitations
Collect before antibiotics when possible without delay, and obtain operative or drainage samples directly. Persistent positive blood cultures suggest ongoing focus, endovascular infection or ineffective therapy.
05
Renal, hepatic, coagulation and drug-exposure monitoring
Why
Detect organ failure and prevent underdosing or toxicity during rapidly changing physiology.
Interpretation and limitations
Creatinine may lag acute filtration changes. Use urine output, renal-replacement modality and therapeutic drug monitoring for agents such as aminoglycosides or glycopeptides.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Cardiogenic shock

Primary ventricular or valvular failure produces low output and congestion; focused echocardiography and the clinical context identify a dominant cardiac mechanism.

Haemorrhagic shock

Occult gastrointestinal, postoperative or retroperitoneal bleeding may coexist with fever or inflammation and requires haemoglobin trends and source-directed imaging.

Obstructive shock

Massive pulmonary embolism, tamponade and tension pneumothorax cause abrupt impaired filling or outflow and need immediate mechanism-specific treatment.

Anaphylaxis or adrenal crisis

Exposure timing, rash, bronchospasm, eosinophilia or endocrine history may reveal a distributive mimic requiring additional emergency therapy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Initial shockRestore perfusion while defining mechanismFirst stepSuspected infection with hypotension or hypoperfusion persisting during initial ABCDE management.

1EscalationEscalate 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.
2Start 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.
3AlternativeEscalationUse 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.

02Vasoactive escalationEscalate support step by stepEscalationMean arterial pressure or organ perfusion remains inadequate despite initial fluid assessment and noradrenaline.

1AlternativeConfirm line and pump delivery, reassess fluid responsiveness, source control and alternative or mixed shock; then titrate noradrenaline to the documented perfusion target.
2EscalationWhen noradrenaline requirements are escalating, add vasopressin under critical-care protocol; if pressure remains inadequate with both agents, add adrenaline rather than relying on unbounded noradrenaline escalation.
3For cardiac dysfunction with persistent hypoperfusion despite adequate volume status and arterial pressure, consider dobutamine added to noradrenaline or adrenaline alone. Consider intravenous corticosteroids for ongoing vasopressor-dependent septic shock under critical-care protocol.

03Source-control candidateConvert diagnosis into a procedureImaging or examination identifies pus, obstruction, perforation, devitalised tissue or a removable infected device.

1Contact the responsible surgical, interventional-radiology or specialty team immediately and communicate physiology, imaging, anticoagulation, microbiology and current organ support.
2DefinitiveAgree and deliver the fastest safe definitive action as soon as practical—ideally within 6 hours when source-control intervention is required—obtain direct specimens during the procedure and continue antimicrobials and resuscitation during transfer.
3After intervention, document adequacy of drainage or debridement, review cultures and spectrum, and investigate residual or secondary foci if shock or bacteraemia persists.

04Refractory stateReassess every assumptionHypoperfusion continues despite antimicrobial delivery, initial source action and vasoactive support.

1Verify access, pump delivery, dose adjustment, fluid balance and source-control completion, and repeat focused examination and imaging for missed collections or complications.
2Evaluate mixed shock, myocardial dysfunction, abdominal compartment physiology, adrenal issues and occult bleeding with critical-care and specialty input.
3Use advanced organ support and therapeutic drug monitoring as indicated, while setting explicit physiological goals, review times and communication with the patient or family.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Restores vascular tone in persistent septic vasodilatation after initial fluid assessment.

Noradrenaline infusion

First-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.

Tests and treats a fluid-responsive component of infection-associated hypoperfusion.

Balanced isotonic crystalloid

Give 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.

Adds non-catecholamine vasoconstriction before a further catecholamine when first-line support is insufficient.

Vasopressin then adrenaline

Stepwise escalation: add vasopressin when noradrenaline requirements are escalating; if mean arterial pressure remains inadequate despite noradrenaline plus vasopressin, add adrenaline. Use critical-care protocol concentrations and titration.

Multiple vasoactive infusions require secure access, continuous haemodynamic and rhythm monitoring and repeated assessment for peripheral, mesenteric and cardiac ischaemia.

Provides inotropic support when low cardiac output contributes to continuing hypoperfusion.

Dobutamine

For septic shock with cardiac dysfunction and persistent hypoperfusion despite adequate volume status and arterial pressure, start and titrate only under a critical-care protocol; adrenaline alone is an alternative strategy.

May cause tachyarrhythmia, increased myocardial oxygen demand, hypotension and lactate elevation; reassess benefit against perfusion and echocardiographic findings.

May shorten shock duration in selected patients who continue to require vasopressor support.

Intravenous corticosteroid

Consider for ongoing vasopressor-dependent septic shock under the local critical-care protocol; the current international recommendation does not prescribe one universal regimen.

Review hyperglycaemia, neuromuscular weakness, secondary infection, delirium and gastrointestinal risk; do not allow steroid consideration to delay source control or vasoactive support.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Multiple-organ failure

Sustained hypoperfusion and inflammation impair kidneys, lungs, liver, brain, heart and coagulation, often requiring prolonged critical-care support.

Limb or gut ischaemia

Severe shock, microthrombosis and high vasopressor exposure can compromise vulnerable circulations and demand repeated peripheral and abdominal assessment.

Treatment-related injury

Fluid overload, line infection, extravasation, antimicrobial toxicity and procedure complications can add harm during otherwise necessary emergency treatment.

Persistent or recurrent infection

Incomplete drainage, retained foreign material or unrecognised secondary foci can cause continuing bacteraemia, relapse and selection of resistant organisms.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuously monitor rhythm, oxygenation and blood pressure while recording perfusion targets and vasoactive response. Use an arterial line when vasopressor doses are intermediate or high, escalating, multiple, frequent sampling is needed or cuff readings are inconsistent.
During peripheral vasopressor administration, use a dedicated secure vein and inspect the site frequently for pain, blanching, swelling or extravasation; follow the local immediate extravasation and access-escalation pathway.
Measure hourly urine output and serial lactate, mental state, capillary refill and peripheral temperature; interpret concordant trends rather than a single surrogate.
Review cumulative fluid input, balance, lung examination and oxygen requirement after each bolus to identify loss of fluid responsiveness or emerging overload.
Track the source-control plan with a named team, agreed intervention time and post-procedure assessment of drain output, imaging and bloodstream-culture clearance.
Review antimicrobial dose, renal-replacement settings, weight, albumin, organ function and therapeutic levels every day during unstable pharmacokinetics.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Blood pressure is not perfusion

A target pressure can coexist with cold peripheries, oliguria or impaired mentation; resuscitation endpoints must reflect organ perfusion and the patient's chronic baseline.

Fluid is a monitored intervention

A bolus has an indication, dose, response and stopping rule. Lack of physiological benefit is evidence to change strategy rather than repeat automatically.

The procedure has pharmacological value

Draining infected material reduces microbial burden, improves penetration and provides high-value cultures that can permit safer antimicrobial narrowing.

Creatinine lags exposure

Rapid renal change can produce antimicrobial accumulation or underexposure before serum creatinine reaches equilibrium, making trend and drug-level interpretation essential.

11Common pitfallsFrequent interpretation and management errors.

01
Treating a target mean arterial pressure as proof that organ perfusion is adequate.
02
Repeating fluid boluses without documenting a physiological response or stopping rule.
03
Calling source control only after several days of broadening antibiotics.
04
Using a fixed vasopressor dose without monitored titration and line-safety arrangements.
05
Failing to consider haemorrhagic, obstructive or cardiogenic components in an apparently septic patient.