Septic shock management

10 min read Last updated April 9, 2026

Surgical approach (source control)

  • Aim: remove/contain the infective focus and reduce ongoing bacterial/toxin load
    • Drain pus/collections: percutaneous radiological drainage vs operative drainage
    • Debridement: necrotising soft tissue infection (NSTI) requires urgent wide debridement, repeat look operations common
    • Control contamination: perforated viscus (laparotomy/laparoscopy), washout, resection, stoma where needed
    • Remove infected devices: lines, prostheses where feasible, urinary obstruction relief (stent/nephrostomy)
    • Obtain cultures at source (pus/tissue) before antibiotics if this does not delay treatment
  • Timing: early source control when feasible (often within 6–12 h for uncontrolled intra-abdominal sepsis/NSTI), balance against need for initial resuscitation
    • Damage-control surgery may be appropriate in profound shock/coagulopathy/hypothermia/acidosis

Anaesthetic management (perioperative septic shock / emergency source control)

  • Type of anaesthesia: usually general anaesthesia, regional techniques often inappropriate in haemodynamic instability/coagulopathy
    • Neuraxial: avoid if septic shock, coagulopathy, thrombocytopenia, or evolving organ failure, consider only in stable sepsis with normal coagulation after senior discussion
  • Airway: endotracheal tube preferred (full stomach, reduced reserve, need for controlled ventilation/vasopressors), SGA generally not appropriate
    • RSI with haemodynamically stable induction strategy, anticipate difficult airway (oedema, sepsis, obesity)
  • Duration: depends on source control (e.g. laparotomy 1–4 h, NSTI debridement 1–3 h, drainage variable). Plan for prolonged ICU care post-op
  • Pain: usually moderate–severe (laparotomy/NSTI). Use multimodal analgesia, consider IV opioids, ketamine, lidocaine infusion, avoid NSAIDs if AKI/bleeding risk
    • Regional adjuncts: TAP blocks/rectus sheath blocks may help if coagulation acceptable, avoid neuraxial in unstable/coagulopathic patients
  • Monitoring and access: arterial line early, large-bore IV access, central venous access for vasopressors, urinary catheter, temperature monitoring
    • Consider cardiac output monitoring/echo to guide fluids/inotropes (especially if persistent shock)
  • Induction/maintenance: titrated doses (reduced requirements). Ketamine/etomidate often used, avoid large propofol doses. Maintain with volatile or TIVA with careful titration
    • Use vasopressor boluses/infusion ready before induction (e.g. metaraminol/phenylephrine, start noradrenaline early if needed)
  • Ventilation: lung-protective strategy, manage ARDS if present (low tidal volume, appropriate PEEP), avoid excessive fluids that worsen pulmonary oedema
  • Haemodynamic goals: MAP ≥ 65 mmHg (individualise), adequate perfusion, improving lactate/urine output, correct hypovolaemia then vasopressors
  • Perioperative antibiotics: ensure broad-spectrum antibiotics given promptly (ideally within 1 h of recognition), re-dose intra-op if prolonged/major blood loss
  • Post-op: ICU admission, ongoing vasopressors, ventilation, renal support, early nutrition, glycaemic control, VTE prophylaxis when safe

Definition and diagnosis

  • Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA increase ≥ 2 from baseline)
  • Septic shock: sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg AND lactate &gt, 2 mmol/L despite adequate fluid resuscitation
  • qSOFA (screening outside ICU): RR ≥ 22, altered mentation, SBP ≤ 100 (≥2 suggests high risk, not a diagnostic tool)
  • Clinical features: warm shock early (vasodilation, bounding pulse), cold shock later (low CO, mottling), fever/hypothermia, tachycardia, tachypnoea, oliguria, altered consciousness

Immediate approach (first hour)

  • A–E assessment, call for help early, treat as time-critical
  • Oxygen to target SpO2 (usually 94–98%, 88–92% if risk of hypercapnic failure)
  • IV access (2 large-bore cannulae), bloods: FBC, U&amp,E, LFT, coagulation, CRP, lactate, glucose, ABG/VBG, group &amp, save/crossmatch if bleeding/surgery likely
  • Cultures: blood cultures (2 sets) before antibiotics if no significant delay, cultures from suspected source (urine/sputum/wound)
  • Antibiotics: broad-spectrum IV within 1 hour, tailor to likely source/local policy, de-escalate when cultures available
    • Consider early antifungal cover if high risk (e.g. immunosuppression, TPN, abdominal surgery, persistent shock despite antibiotics)
  • Fluids: balanced crystalloid initial bolus, typical starting point 30 mL/kg within first 3 h (individualise, smaller aliquots with frequent reassessment)
    • Avoid starches, albumin may be considered if large volumes required (ICU decision)
  • Vasopressors: if hypotension persists after initial fluid or if profound hypotension, start early (preferably via central line, peripheral short-term acceptable with close monitoring)
    • First-line: noradrenaline, target MAP ≥ 65 mmHg (higher if chronic hypertension/cerebral perfusion concerns)
  • Source control: urgent imaging and surgical/radiological intervention when indicated, do not delay for prolonged optimisation if ongoing uncontrolled sepsis

Haemodynamic management (ICU/perioperative)

  • Resuscitation endpoints: improving mentation, capillary refill, urine output ≥ 0.5 mL/kg/h, falling lactate, improving acid–base, avoid chasing CVP
  • Dynamic fluid responsiveness: passive leg raise, stroke volume variation (selected ventilated patients), echo (LV filling, RV function, IVC trends), mini-fluid challenges
  • Vasopressors: noradrenaline first-line, add vasopressin (e.g. 0.03 units/min) to reduce NA dose or refractory vasoplegia, adrenaline second-line alternative
  • Inotropes: dobutamine if myocardial dysfunction with low cardiac output and ongoing hypoperfusion despite adequate MAP/volume, consider adrenaline if combined inotropy/vasopressor needed
  • Steroids: hydrocortisone 200 mg/day (e.g. 50 mg QDS or infusion) if ongoing vasopressor requirement despite adequate fluids/vasopressors
  • Transfusion: restrictive strategy generally (Hb threshold ~70 g/L) unless active bleeding/ACS/ongoing ischaemia, correct coagulopathy for procedures/bleeding

Respiratory management

  • Early intubation/ventilation if work of breathing high, hypoxaemia, encephalopathy, severe acidosis, or for source control surgery
  • ARDS strategy: tidal volume 6 mL/kg predicted body weight, plateau pressure &lt, 30 cmH2O, appropriate PEEP, permissive hypercapnia if needed (avoid if raised ICP/severe pulmonary HTN)
  • Prone positioning for moderate–severe ARDS, consider neuromuscular blockade short-term in severe ventilator dyssynchrony

Renal, metabolic and supportive care

  • AKI: avoid nephrotoxins, optimise perfusion, monitor urine output/creatinine, consider RRT for refractory hyperkalaemia, acidosis, fluid overload, uraemic complications
  • Glycaemic control: treat severe hyperglycaemia, avoid tight control, typical ICU target 6–10 mmol/L (local policy)
  • Temperature: treat hypothermia, fever control for comfort/metabolic demand (paracetamol, cooling if needed)
  • Nutrition: early enteral feeding when feasible, consider thiamine if malnourished/alcohol dependence, stress ulcer prophylaxis if indicated
  • VTE prophylaxis: LMWH when bleeding risk acceptable, mechanical prophylaxis if contraindicated
  • Communication: early ICU involvement, sepsis pathway, documentation of time antibiotics/fluids/vasopressors started

Antimicrobial principles (anaesthetist/ICU focus)

  • Choose empiric antibiotics based on likely source, local resistance patterns, recent antibiotics, immunosuppression, healthcare exposure
  • Dose appropriately in shock: consider increased Vd and augmented renal clearance early, later AKI may require dose adjustment—use pharmacy/microbiology input
  • Therapeutic drug monitoring where appropriate (e.g. vancomycin, aminoglycosides)
  • De-escalate based on cultures and clinical response, define duration (often 5–7 days if source controlled, longer if deep-seated infection/endocarditis/osteomyelitis)

Investigations and imaging

  • Bedside: ABG with lactate, ECG, CXR, urine dip/culture, point-of-care ultrasound (heart, lungs, IVC, abdomen)
  • Imaging for source: CT abdomen/pelvis with contrast (if stable enough), ultrasound for biliary/urinary obstruction, echocardiography if endocarditis suspected
  • Serial lactate and clinical reassessment guide response, lactate clearance is a useful trend, not a sole target

Test yourself…

Define sepsis and septic shock (Sepsis-3).

Definitions should be precise and include haemodynamic/lactate criteria for septic shock.

  • Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection, operationalised as SOFA increase ≥ 2 from baseline.
  • Septic shock: sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg AND lactate &gt, 2 mmol/L despite adequate fluid resuscitation.
You are called to ED: 70-year-old with suspected perforated diverticulitis, BP 78/40, HR 125, lactate 6. Outline your first-hour management.

Structure as A–E plus sepsis bundle: cultures, antibiotics, fluids, vasopressors, source control, monitoring.

  • A–E, call for senior/ICU/surgical review, high-flow O2, monitor ECG/NIBP/SpO2, consider early arterial line.
  • Access/bloods: 2 large-bore IVs, ABG/VBG with lactate, FBC/U&amp,E/LFT/coag/CRP, group &amp, save/crossmatch.
  • Cultures: 2 sets blood cultures and source cultures if feasible without delaying treatment.
  • Antibiotics: broad-spectrum IV immediately (within 1 h), per local intra-abdominal sepsis policy, document time given.
  • Fluids: balanced crystalloid in 250–500 mL boluses with frequent reassessment, aim ~30 mL/kg within 3 h if responsive and no overload.
  • Vasopressors: start noradrenaline early if MAP remains low, peripheral start acceptable short-term while obtaining central access, target MAP ≥ 65.
  • Source control: urgent CT and expedite theatre/interventional radiology, do not delay definitive control once resuscitation underway.
What fluid would you choose for initial resuscitation and why? What are the risks of over-resuscitation?

Expect discussion of balanced crystalloids, avoidance of starch, and harms of fluid overload.

  • Initial choice: balanced crystalloid (e.g. Hartmann’s/Plasma-Lyte) rather than 0.9% saline to reduce hyperchloraemic acidosis and renal vasoconstriction risk.
  • Avoid hydroxyethyl starch (increased AKI and mortality signals in critical illness).
  • Albumin: may be considered if very large volumes of crystalloid required (ICU-led decision).
  • Over-resuscitation risks: pulmonary oedema/ARDS worsening, abdominal compartment syndrome, tissue oedema impairing healing/anastomoses, dilutional coagulopathy, increased venous pressures and organ congestion.
Which vasopressor is first-line in septic shock? How do you start it safely in theatre/ED?

Include noradrenaline, MAP target, central vs peripheral administration, and practical setup.

  • First-line: noradrenaline, titrate to MAP ≥ 65 mmHg (individualise).
  • Start via central line ideally, if urgent, start peripherally through a large-bore cannula in a proximal vein with close observation and plan to convert to central access promptly.
  • Use infusion pump with clearly labelled concentration, have vasopressor boluses available for induction, continuous arterial BP monitoring if possible.
When would you add vasopressin or hydrocortisone in septic shock?

Refractory vasoplegia and persistent vasopressor requirement are key triggers.

  • Add vasopressin (e.g. 0.03 units/min) when noradrenaline requirements are escalating or high, to reduce catecholamine dose and treat vasoplegia.
  • Give hydrocortisone 200 mg/day when shock remains vasopressor-dependent despite adequate fluids and vasopressors.
How would you use echocardiography to guide management in septic shock?

Demonstrate ability to differentiate vasoplegia from cardiogenic component and assess fluid responsiveness.

  • Assess LV function: septic cardiomyopathy may cause reduced EF/low stroke volume → consider inotrope (dobutamine) if hypoperfusion persists.
  • Assess RV size/function and pulmonary pressures: RV failure/PEEP-related strain may limit fluid tolerance and require ventilator adjustment/inotropes.
  • Volume status/response: IVC trends (limited), LV filling, passive leg raise with stroke volume change, small fluid challenges with echo-derived SV/VTi.
  • Exclude alternative causes of shock: tamponade, massive PE, severe valvular pathology.
Outline an induction plan for emergency laparotomy in septic shock.

Key points: preparation, haemodynamic support, reduced induction dose, RSI, post-induction deterioration management.

  • Preparation: senior help, ICU bed, blood available, antibiotics confirmed, warming, arterial line (ideally pre-induction), vasopressor infusion ready and running if needed.
  • Pre-oxygenate, RSI due to full stomach, consider apnoeic oxygenation, gentle ventilation if needed.
  • Induction agent: titrated ketamine or etomidate, avoid large propofol doses, use reduced opioid dose initially if profoundly unstable.
  • Muscle relaxant: rocuronium or suxamethonium as appropriate, secure ETT, confirm with capnography.
  • Expect post-induction hypotension: treat with vasopressor boluses and infusion escalation, reassess volume status, consider calcium if massive transfusion/citrate load.
Discuss lactate in septic shock: causes, interpretation, and how you use it.

Lactate is a marker of severity and impaired clearance, not solely hypoxia.

  • Raised lactate mechanisms: tissue hypoperfusion/anaerobic metabolism, adrenergic-driven glycolysis, impaired hepatic clearance, mitochondrial dysfunction.
  • Use trends: serial lactate and clinical perfusion markers to assess response, aim for lactate clearance but avoid treating the number alone.
  • Persistent hyperlactataemia prompts reassessment: inadequate source control, ongoing hypoperfusion, occult bleeding, cardiogenic component, seizures, beta-agonists/adrenaline effects.
What are the key differences between septic shock and anaphylactic shock in theatre?

FRCA viva often tests differential diagnosis of sudden hypotension under anaesthesia.

  • Timing: anaphylaxis often abrupt after drug/latex exposure, septic shock usually evolving (though may decompensate at induction).
  • Features: anaphylaxis—bronchospasm, urticaria/angioedema, flushing, raised airway pressures, sepsis—fever/hypothermia, known infection, high lactate, warm peripheries early.
  • Management overlap: ABC, fluids, vasopressors, anaphylaxis requires IM/IV adrenaline as primary, tryptase sampling, allergist follow-up.
Describe organ dysfunction patterns in sepsis and how they influence your anaesthetic plan.

Link pathophysiology to drug handling and perioperative risk.

  • Cardiovascular: vasoplegia ± septic cardiomyopathy → reduced anaesthetic requirements, high risk of induction collapse, need invasive monitoring and vasopressors.
  • Respiratory: ARDS risk → lung-protective ventilation, cautious fluids, higher PEEP, consider postoperative ventilation.
  • Renal/hepatic: altered clearance → careful dosing of opioids/sedatives/antibiotics, avoid nephrotoxins, plan for RRT.
  • Coagulation: DIC/thrombocytopenia → avoid neuraxial, anticipate bleeding, correct coagulopathy for surgery/lines.
  • CNS: encephalopathy/delirium risk → avoid oversedation, ensure analgesia, consider ICU sedation strategy.
What is the &#039,sepsis bundle&#039, and what elements are time-critical?

Answer in a pragmatic UK hospital manner: early recognition, cultures, antibiotics, fluids, lactate, vasopressors, source control.

  • Time-critical: measure lactate, obtain blood cultures, give broad-spectrum antibiotics within 1 hour, start IV fluids, start vasopressors early if hypotension persists, and escalate for source control.
  • Ongoing: monitor urine output, repeat lactate, reassess fluid responsiveness, review antibiotics with microbiology, plan imaging and definitive control.

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