Septic shock management

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 > 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&E, LFT, coagulation, CRP, lactate, glucose, ABG/VBG; group & 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 < 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
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 > 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&E/LFT/coag/CRP; group & 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 'sepsis bundle' 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.

0 comments