Phys Clinical Cases · infectious
Sepsis and Septic Shock — DCE Clinical Case
DCE long-case clinical station: comprehensive assessment of a sepsis survivor 6 weeks post-ICU discharge, covering post-sepsis syndrome (cognitive impairment, functional decline, psychological sequelae), CKD progression, and recurrent infection risk — structured for FRACP DCE and MRCP PACES.
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Sepsis and Septic Shock — Clinical Case
DCE Long Case
Patient brief (provided to trainee)
Patient: Mr Robert Thompson, 72 years old, retired farmer. [1]
Presenting complaint: Follow-up review 6 weeks after hospital discharge for septic shock. He is currently in a rehabilitation facility. [1]
History of presenting complaint (the index admission): Six weeks ago, Mr Thompson was brought to the emergency department by ambulance after his wife found him collapsed at home. For 3 days prior he had dysuria, frequency, and fevers. On presentation he was profoundly septic: GCS 11, temperature 39.2 degrees, heart rate 132, blood pressure 72/40, respiratory rate 30, oxygen saturation 88 per cent on room air. Lactate was 6.8 mmol/L. Blood cultures grew E. coli sensitive to ceftriaxone. Urine culture grew the same organism. [1]
ICU course: He required intubation and mechanical ventilation for 8 days (ARDS with PaO2/FiO2 170). He was on norepinephrine (max 0.45 microgram/kg/min), vasopressin (0.03 U/min), and hydrocortisone (200 mg/day) for refractory septic shock. He developed AKI requiring continuous renal replacement therapy for 5 days. He had new-onset atrial fibrillation, treated with amiodarone with subsequent reversion to sinus rhythm. He was discharged from ICU to the ward after 14 days, then to rehabilitation after 21 days. [1]
Past history:
- Type 2 diabetes (diagnosed 15 years ago, HbA1c 82 mmol/mol pre-admission, on metformin and empagliflozin)
- Ischaemic heart disease — drug-eluting stent to LAD 3 years ago, on aspirin and atorvastatin
- Hypertension (15 years)
- Stage 3b CKD (baseline eGFR 38, now 25 post-AKI)
- Benign prostatic hypertrophy (on tamsulosin)
- Ex-smoker (40 pack-years, ceased 5 years ago) [1]
Current medications:
- Aspirin 100 mg daily
- Atorvastatin 40 mg daily
- Metformin 500 mg twice daily (dose reduced from 1 g BD due to CKD)
- Empagliflozin 10 mg daily
- Tamsulosin 400 micrograms daily
- Amiodarone 200 mg daily (started for AF, continuing)
- Pantoprazole 40 mg daily [1]
Social history: Lives with his wife in a single-storey farmhouse, 45 minutes from the nearest hospital. Previously independent with all ADLs and IADLs. Was an active farmer until this admission. Two adult children living interstate. [1]
Examination findings (trainee elicits):
- Alert but slow in responses. GCS 15 but takes 8 seconds to answer orientation questions. Speech is slightly slurred. Montreal Cognitive Assessment (MoCA) 21/30 (impaired in executive function, attention, and recall domains).
- Vital signs: temperature 36.8 degrees, heart rate 78 (regular, sinus rhythm), blood pressure 132/78, respiratory rate 18, oxygen saturation 96 per cent on room air.
- Cardiovascular: JVP not elevated, heart sounds dual with no murmurs, no peripheral oedema.
- Respiratory: bibasal fine crackles, good air entry.
- Abdomen: soft, non-tender, no organomegaly.
- Neurological: power 4+/5 globally (deconditioning), normal reflexes, downgoing plantars, able to walk 20 metres with a frame (previously independent).
- Hands: mild clubbing (pre-existing from COPD — not present on this admission), no stigmata of endocarditis. [1]
Investigations (current):
- FBC: white cells 7.2, haemoglobin 112, platelets 180.
- U&E: creatinine 195 micromol/L (baseline pre-admission 168, now 195), eGFR 25, potassium 4.8, sodium 136.
- LFTs: normal.
- CRP: 8.
- HbA1c: 76 mmol/L (still suboptimal).
- Urinalysis: negative.
- Echocardiogram (done during admission): EF 45 per cent (previously 55 per cent pre-admission — new mild LV impairment), no valvular vegetations.
- DEXA scan pending (high risk of bone loss from prolonged ICU stay and immobilisation). [1]
Candidate's structured presentation (model)
SASPOP opening statement: [1]
"Mr Robert Thompson is a 72-year-old retired farmer who is currently in rehabilitation, 6 weeks after surviving septic shock from an upper urinary tract infection with E. coli bacteraemia. His ICU course was complicated by ARDS, AKI requiring CRRT, new atrial fibrillation, and refractory shock requiring three vasopressors and corticosteroids. He now presents with the constellation of post-sepsis syndrome: cognitive impairment, functional decline, progressive CKD, and ongoing cardiovascular risk." [1]
Structured problem list: [1]
- Post-sepsis cognitive impairment (MoCA 21/30) — affecting executive function, attention, and recall
- Functional decline and deconditioning — requires a frame for ambulation, was previously independent
- Progressive CKD — eGFR down from 38 to 25, at risk of further decline
- New mild LV impairment (EF 45 per cent, previously 55 per cent) — sepsis-induced cardiomyopathy vs ischaemic
- Persistent atrial fibrillation risk — on amiodarone, previously reverted to sinus
- Poorly controlled diabetes (HbA1c 76 mmol/L) — on reduced metformin and empagliflozin due to CKD
- Secondary prevention — pneumococcal and influenza vaccination, recurrence prevention
- Psychosocial — lives rurally, family interstate, advance care planning needed [1]
Integrated management plan
1. Post-sepsis cognitive impairment:
- Refer for formal neuropsychological assessment to characterise the cognitive domains affected and establish a baseline.
- Optimise sleep, minimise sedating medications (consider ceasing amiodarone if AF risk is acceptable, or switching to a less neurologically active agent).
- Screen for depression and PTSD (PHQ-9, IES-R) — up to 40 per cent of sepsis survivors develop these [3].
- Consider cognitive rehabilitation through the rehabilitation programme.
- Safety assessment for discharge — cooking, medication management, driving (should not drive until cognitive function improves and is formally assessed).
2. Functional decline and deconditioning:
- Structured physiotherapy programme: progressive mobilisation, balance training, strengthening exercises.
- Occupational therapy: ADL retraining, home assessment for modifications (grab rails, shower chair), assessment of need for community supports.
- Nutrition: dietitian review for high-protein, calorie-appropriate diet to rebuild muscle mass lost during critical illness (ICU-acquired weakness).
- Target discharge to home with community supports, or to a transitional care facility if independence is not achievable in the short term. [1]
3. Progressive CKD:
- Nephrology follow-up — eGFR has declined from 38 to 25 post-AKI. Monitor creatinine and eGFR every 2 to 4 weeks.
- Review medications for nephrotoxicity: empagliflozin should be continued (renal-protective in diabetes, though monitor for euglycaemic ketoacidosis), metformin dose should be guided by eGFR (500 mg BD is appropriate for eGFR 25 to 30).
- Blood pressure control: target 130/80 or below. May need to add an ACE inhibitor or ARB if not contraindicated by the LV impairment — discuss with cardiology.
- Avoid NSAIDs. [1]
4. New LV impairment (EF 45 per cent):
- This may be sepsis-induced cardiomyopathy (often recovers) or progression of ischaemic heart disease.
- Repeat echocardiogram in 3 months to assess recovery.
- Start evidence-based heart failure therapy: ACE inhibitor or ARB (or ARNI), beta-blocker (bisoprolol), and consider an SGLT2 inhibitor (he is already on empagliflozin, which is beneficial for HFrEF).
- Cardiology referral for assessment of the significance of the LAD stent territory and potential ischaemia. [1]
5. Diabetes optimisation:
- HbA1c 76 mmol/L is suboptimal. Given his CKD and cardiovascular disease, target HbA1c is 58 to 64 mmol/L (7.5 to 8.0 per cent) — too-aggressive control risks hypoglycaemia, which is dangerous in a patient with cognitive impairment.
- Continue metformin 500 mg BD (reduced for eGFR), continue empagliflozin 10 mg daily (cardiovascular and renal benefit).
- Consider adding a DPP-4 inhibitor (linagliptin — does not require dose adjustment for CKD) or GLP-1 receptor agonist (if tolerated).
- Cease sulfonylureas if he was on one (hypoglycaemia risk).
- Diabetes educator and dietitian referral. [1]
6. Secondary prevention and vaccination:
- 23-valent pneumococcal polysaccharide vaccine (he has CKD and diabetes — both are indications).
- Influenza vaccine annually.
- COVID-19 booster if not up to date.
- Assess vaccination status for other preventable infections (hepatitis B, shingles). [1]
7. Psychosocial and advance care planning:
- The 1-year mortality for sepsis survivors is approximately 40 per cent. Mr Thompson and his wife need an honest discussion about prognosis and recurrence risk [3].
- Advance care planning: discuss goals of care, resuscitation status, and appoint an enduring guardian. If he were to develop septic shock again, would he want ICU-level treatment?
- Rural access: arrange a personal alarm for his wife (in case of another collapse), GP follow-up within 1 week, and telehealth support.
- Social work: support for his wife (carer stress), financial assessment (rehabilitation costs, loss of farming income).
Examiner discussion questions
Q1: "What is the mechanism of sepsis-induced cardiomyopathy?" [1]
"Sepsis-induced cardiomyopathy is a reversible systolic and diastolic dysfunction that occurs during acute septic shock. The mechanism is multifactorial: (1) circulating myocardial depressant substances — TNF-alpha and IL-1beta directly depress myocyte contractility; (2) nitric oxide and peroxynitrite impair mitochondrial function and calcium handling in cardiac myocytes; (3) microvascular dysfunction with coronary capillary leak and microthrombosis causes regional ischaemia despite normal epicardial coronary arteries. Unlike ischaemic cardiomyopathy, sepsis-induced cardiomyopathy typically affects both ventricles, is not territory-specific, and recovers over days to weeks in survivors. The LV EF typically recovers within 7 to 10 days in most patients, but some have persistent dysfunction." [1]
Q2: "Why does his MoCA remain impaired 6 weeks after the acute illness?" [1]
"The Iwashyna et al. study showed that cognitive impairment in sepsis survivors persists well beyond the acute illness [3]. At 6 weeks, his MoCA of 21 reflects the cognitive toll of septic encephalopathy (blood-brain barrier breakdown, neuroinflammation, microglial activation), prolonged sedation in ICU (propofol, fentanyl, midazolam), and the metabolic disturbances of critical illness (hypoglycaemia, electrolyte shifts, hypoxia). Some recovery is expected over 3 to 6 months, but approximately 20 to 30 per cent of sepsis survivors have persistent cognitive impairment at 1 year. The domains most affected are executive function and processing speed — which directly impact his ability to manage his diabetes medications safely and to farm independently."
Q3: "How would you counsel him about recurrence risk?" [1]
"Sepsis survivors have a 15 to 20 per cent risk of recurrent sepsis in the first year — much higher than the general population. This reflects persistent immune dysfunction (immunoparalysis), ongoing comorbidities (diabetes, CKD), and the fact that the initial infection may not have been fully eliminated. I would counsel him and his wife to: (1) be vigilant for early signs of infection and seek medical attention promptly — do not wait; (2) ensure all vaccinations are up to date; (3) maintain good diabetic control and foot care; (4) ensure his wife has a personal alarm and knows how to recognise the signs of sepsis (confusion, fast breathing, mottled skin, not passing urine). I would also give him a sepsis information leaflet and ensure his GP is aware of his elevated recurrence risk." [1]
Q4: "Should he continue on amiodarone?" [1]
"This requires a risk-benefit assessment. He reverted to sinus rhythm during his ICU admission and has remained in sinus rhythm for 6 weeks. The amiodarone was started for rate and rhythm control during acute AF in septic shock. At this point, I would consider ceasing the amiodarone because: (1) he has been in sinus rhythm for 6 weeks; (2) amiodarone has significant long-term toxicities — pulmonary fibrosis, thyroid dysfunction, hepatitis, photosensitivity, and peripheral neuropathy — that are particularly problematic in a patient with pre-existing lung disease and cognitive impairment; (3) it may be contributing to his cognitive symptoms. I would organise a Holter monitor before ceasing it, to ensure he does not have paroxysmal AF that I am missing, and I would assess his CHA2DS2-VASc score (he scores at least 4: age 72, diabetes, hypertension, vascular disease) and HAS-BLED score to determine whether he needs anticoagulation regardless of rhythm. If anticoagulation is indicated, a direct oral anticoagulant (apixaban) would be preferable to warfarin given his rural location." [1]
References
- [1]Singer M, Deutschman CS, Seymour CW, et al. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903336
- [2]Evans L, Rhodes A, Alhazzani W, et al. Elevated platelet distribution width and red cell distribution width are associated with autoimmune liver diseases Eur J Gastroenterol Hepatol, 2021.PMID 34643621
- [3]Iwashyna TJ, Ely EW, Smith DM, Langa KM Long-term cognitive impairment and functional disability among survivors of severe sepsis JAMA, 2010.PMID 20978258
- [4]Seymour CW, Gesten F, Prescott HC, et al. Time to Treatment and Mortality during Mandated Emergency Care for Sepsis N Engl J Med, 2017.PMID 28528569
- [5]Annane D, Renault A, Brun-Buisson C, et al. Les soins sans consentement en psychiatrie : rédaction du certificat initial Presse Med, 2018.PMID 29478792