Sepsis and Septic Shock — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Robert Thompson is a 72-year-old retired farmer who presents with a 3-day history of dysuria, fevers, and rigors, found collapsed at home by his wife. He has type 2 diabetes (HbA1c 78 mmol/mol), ischaemic heart disease with a prior stent, stage 3b chronic kidney disease (baseline eGFR 38), and benign prostatic hypertrophy. [1]

His main problems are:

1. Septic shock from an upper urinary tract infection with bacteraemia — confirmed by blood cultures growing E. coli, lactate 6.2 on presentation
2. Acute kidney injury (AKI stage 2, creatinine 265 from baseline 168) secondary to septic and nephrotoxic injury
3. Acute respiratory distress syndrome (ARDS) — PaO2/FiO2 180 on day 2, requiring lung-protective ventilation
4. Hyperglycaemia (BSL 22 mmol/L on presentation) — stress hyperglycaemia in a poorly controlled diabetic
5. New atrial fibrillation with rapid ventricular response on day 3 of admission
6. Post-sepsis cognitive impairment and functional decline — now in rehabilitation, 6 weeks post-ICU discharge [1]

His management to date has followed the Surviving Sepsis Campaign Hour-1 Bundle: broad-spectrum antibiotics within 45 minutes of recognition, 2.5 litres of balanced crystalloid, norepinephrine titrated to MAP 65, and then vasopressin and hydrocortisone added for refractory shock. He was ventilated for 8 days with lung-protective settings, received continuous renal replacement therapy for 5 days with partial renal recovery, and was discharged to the ward after 14 days in ICU. He is now in rehabilitation for deconditioning, cognitive impairment, and mobility limitation." [1]

Examiner probing questions and model answers

Q1: "Walk me through your vasopressor escalation in the first 6 hours." [1]

"I started norepinephrine at 0.08 microgram/kg/min immediately after the initial fluid bolus, as his MAP was 58 despite 2.5 litres of Hartmann's. I titrated norepinephrine to achieve a MAP of 65 mmHg or above — the SSC 2021 target. By the 2-hour mark he needed 0.25 microgram/kg/min, and his MAP was still 62, so I added vasopressin at a fixed dose of 0.03 U/min. By 4 hours his norepinephrine requirement had risen to 0.4 microgram/kg/min despite the vasopressin, and his MAP was 60 — at that point, because he had refractory septic shock on two vasopressors, I started hydrocortisone 200 mg per day as a continuous infusion. The APROCCHSS trial supported this — it showed a mortality benefit for hydrocortisone plus fludrocortisone in patients with septic shock on vasopressors. I did NOT add epinephrine at this stage because the hydrocortisone typically takes 12 to 24 hours to reduce vasopressor requirements. Over the next 12 hours his MAP improved to 68, and I was able to wean the norepinephrine progressively over the following 48 hours. I avoided dopamine because the SOAP II trial showed it causes more arrhythmias than norepinephrine without any mortality benefit." [1]

Q2: "How did you assess fluid responsiveness before giving further fluids?" [1]

"After the initial 30 mL/kg, I used a passive leg raise with real-time stroke volume measurement using point-of-care echocardiography. I measured LVOT VTI before and after the leg raise — there was less than a 10 per cent increase in VTI, indicating he was NOT fluid responsive. This is important because he already had evidence of pulmonary oedema on his chest X-ray. Further fluids would have worsened his ARDS without improving his cardiac output. I also noted that his pulse pressure variation was only 5 per cent on the ventilator, confirming he was not preload-responsive. I relied on norepinephrine for blood pressure support and targeted a conservative fluid strategy after the initial resuscitation, as recommended by the SSC 2021 guidelines and supported by the CLASSIC trial." [1]

Q3: "He developed ARDS on day 2. What ventilation strategy did you use?" [1]

"I used lung-protective ventilation: tidal volume 6 mL per kg of predicted body weight — not actual body weight — targeting a plateau pressure below 30 cm of water. I allowed permissive hypercapnia down to a pH of 7.20 to avoid injurious tidal volumes. I titrated PEEP using a FiO2/PEEP ladder. On day 3 his PaO2/FiO2 ratio dropped to 140, so I initiated prone positioning for 16 hours per day, as the PROSEVA trial showed a 28-day mortality reduction with early prolonged prone positioning in severe ARDS. I also used a conservative fluid strategy — targeting a negative fluid balance with furosemide once he was stable — because the FACTT trial showed this improved lung function and reduced ventilator days." [1]

Q4: "He developed atrial fibrillation on day 3. How did you manage that in the context of septic shock?" [1]

"New-onset atrial fibrillation is very common in septic shock — it occurs in 25 to 40 per cent of patients and is associated with worse outcomes. The first step was to correct reversible causes: his potassium was 3.2 (corrected to 4.0), he was on a high norepinephrine dose (excess catecholamine drive), and he had intravascular volume shifts. I achieved rate control with an amiodarone infusion — 300 mg IV over 1 hour, then 900 mg over 24 hours — because beta-blockers can destabilise a patient in shock and calcium channel blockers are contraindicated in heart failure. Amiodarone is the preferred agent in the critically ill because it has both rate-control and some antiarrhythmic effect, and it does not significantly depress cardiac output. I did NOT anticoagulate initially because he had thrombocytopenia (platelets 45) and an elevated INR (1.6) from his septic coagulopathy. Once his coagulopathy resolved and he was stable, I initiated prophylactic-dose enoxaparin for VTE prevention and assessed for the need for therapeutic anticoagulation using the CHA2DS2-VASc score." [1]

Q5: "He is now 6 weeks post-discharge with cognitive impairment and poor mobility. What is your plan?" [1]

"This is post-sepsis syndrome. The Iwashyna study showed that severe sepsis survivors have a threefold increase in moderate-to-severe cognitive impairment, independent of age and baseline function [7]. They also acquire 1 to 2 new ADL dependencies per episode, and up to 30 per cent require new institutional care. His plan includes: (1) formal cognitive assessment with a Montreal Cognitive Assessment and referral to a neuropsychologist; (2) structured rehabilitation — physiotherapy for mobility and deconditioning, occupational therapy for ADLs; (3) psychological screening for PTSD, anxiety, and depression — up to 40 per cent of sepsis survivors develop these; (4) secondary prevention: pneumococcal and influenza vaccination, glycaemic optimisation, review of his diabetes management; (5) nephrology follow-up for his AKI — he has partial recovery but is at risk of CKD progression; and (6) advance care planning — he and his family need to understand the elevated 1-year mortality (approximately 40 per cent for sepsis survivors) and the risk of recurrence."

Q6: "What is your approach to antimicrobial de-escalation in this patient?" [1]

"I de-escalated from empiric therapy to targeted therapy as soon as culture and sensitivity results were available — which was at 48 hours. The blood cultures grew E. coli sensitive to ceftriaxone, so I narrowed from piperacillin-tazobactam to ceftriaxone 2 g IV daily. I used a total duration of 7 days for the urinary source with good source control — a urinary catheter was changed on admission, and he had no perinephric abscess on imaging. I used procalcitonin trending to support the decision to stop — a procalcitonin below 0.5 ng/mL or a greater than 80 per cent fall from peak supports antibiotic cessation. The principle of antimicrobial stewardship is to use the narrowest-spectrum effective agent for the shortest effective duration — this reduces resistance selection, Clostridioides difficile infection risk, and drug toxicity." [1]

Short Case Discussion

Bedside assessment of the critically ill septic patient

Examiner instruction: "You are called to review a patient on the ward who was admitted 4 hours ago with community-acquired pneumonia. The nursing staff are concerned that the patient is deteriorating. Describe your systematic approach to assessment." [1]

Candidate's model answer: [1]

"I would use a systematic ABCDE approach to assess this critically ill patient: [1]

A — Airway: Is the patient maintaining their own airway? Are they able to speak in full sentences? Stridor, gurgling, or snoring suggests airway compromise. [1]

B — Breathing: Respiratory rate (is it elevated above 22, which is a qSOFA criterion?), oxygen saturation, work of breathing (use of accessory muscles, tracheal tug, intercostal recession), chest auscultation (unilateral findings suggesting consolidation, effusion, or pneumothorax). A respiratory rate above 25 in a ward patient is a red flag for deterioration. [1]

C — Circulation: Heart rate, blood pressure, capillary refill time (above 3 seconds suggests impaired perfusion), skin temperature (cool peripheries suggest vasoconstriction), mottling score (knee mottling is a sign of poor perfusion and predicts mortality in septic shock), and urine output via catheter. [1]

D — Disability: GCS, pupils, blood glucose (hypoglycaemia is easily missed and dangerous in sepsis), and a brief neurological exam. Altered mentation in sepsis is septic encephalopathy — an independent predictor of mortality. [1]

E — Exposure: Full examination for the source — skin for cellulitis or necrotising infection, abdomen for peritonitis, line sites for erythema or pus, perianal area in neutropenic patients (but NO digital rectal examination). [1]

If I identify signs of sepsis or deterioration, I would immediately activate the rapid response team, apply the Hour-1 Bundle, and arrange ICU review. The key is not to delay — each hour of untreated septic shock increases mortality by approximately 4 per cent." [1]