College answer

a) Interpretation of raised troponin- should not be used in isolation in this patient. The measured 
value of troponin is high and should not be ignored or dismissed. If unexpected, repeat the 
test. Symptoms of chest pain are not easy to elicit in the ventilated patient. Troponin leak in 
this setting may be due to myocarditis associated with sepsis, acute cardiomyopathy.
Takotsubo disease given high dose vasopressor or a STEMI or NSTEMI or right ventricular 
disease. Elevated troponin in renal failure should also be considered if relevant. Elevated 
troponins are associated with poor outcomes in septic patients.

b) Management plan- Comprehensive clinical assessment especially cardiovascular and 
haemodynamic assessment. Look for recent, rapid increase in vasopressor requirement, 
signs of cardiogenic shock. Review ECG for any evidence of STEMI or other new changes, 
Review CXR for new pulmonary oedema/heart failure. Echo- transthoracic or if available TOE 
is mandatory to look for any regional wall motion abnormalities that may be new. Evidence of 
global changes on echocardiography may indicate acute cardiomyopathy e.g. Myocarditis. 
Look for classic changes of Takatsubo’s.
Further management will be determined by ECG and echo findings. Cardiology review, 
anticoagulation, careful consideration of thrombolysis or angioplasty if STEMI or regional 
changes on echo with consideration given to haemodynamic instability and challenges of 
transfer and management in cardiac catheter lab. Role of IABP in global hypokinesis related 
to acute cardiomyopathies. 
Troponin increases in septic patients is thought to be associated with poor prognosis 

Additional Examiners’ Comments:
Candidates were not expected to reproduce the template, but to demonstrate a reasonable and 
structured approach to the issue.

Discussion

Interpretation of a raised troponin in septic shock:

• It may be totally meaningless:
  • ​Cardiac troponins are elevated in 85% of patients with sepsis in the absence of acute coronary syndrome.
  • Overinterpretation can increase the cost and duration of hospital stay (Suarez et al, 2016)
• It may represent an acute coronary syndrome:
  • Sepsis is a high-output cardiac failure state, and may unmask some sort of (previously subclinical) coronary artery disease.
  • Any proinflammatory state can give rise to an increased risk of MI (Donzé et al, 2014)
• ​It may identify patients with septic cardiomyopathy:
  • Significant myocardial depression is observed in up to 60% of septic patients (Vieillard-Baron et al , 2008)
  • This may be associated with a raised troponin
  • A raised troponin does not identify patients who need inotropes
• It may be a predictor of increased mortality:
  • Raised troponin predicts increased mortality,  with a risk ratio of around 1.9. (Sheyin et al, 2015)

Assessment and management plan:

• History
  • Detailed interrogation of the bedside records to determine whether any critical events had taken place recently, eg. sudden increase in vasopressor doses or episodes of unexplained tachycardia
  • Exploration of the past medical history, specifically looking for previous history of ischaemic heart disease
• Examination, to look for...
  • New murmurs
  • Features more consistent with cardiac failure than with distributive shock, eg. oedema, pulsatile liver, displaced apex beat, elevated JVP, cool extremities.
• ECG, to look for...
  • Changes associated with ischaemia, eg. ST segments and T waves
  • New bundle branch block
  • Arrhythmia, eg. new onset AF
• Biochemistry
  • ABG, to assess for metabolic acidosis (as this can cause myocardial depression)
  • Electrolyte values, to exclude embarrassingly correctable causes of low cardiac output eg. severe ionised hypocalcemia or hypophosphataemia
  • A repeat troponin value, and serial measurements to follow
• TTE, to assess
  • Global systolic function
  • Regional wall motion
  • Valve function
  • Diastolic function
• Management:
  • This would depend on the findings of the abovelisted investigations.
  • If the TTE is essentially normal, it may be that no further management is required beyond regular aspirin.
  • If there is global systolic dysfunction, inotropes may be called for. At this stage, one may decide to use some sort of advanced haemodynamic monitor (eg. PA catheter, PiCCO etc) so that one may be better able to titrate their vasoactive drugs.
  • If there are ECG changes and/or regional wall motion abnormalities, one may be able to make a diagnosis of acute MI. This poses several treatment options:
    • Conservative management with antiplatelet drugs and heparin infusion (which may be impossible in the context of severe sepsis, where DIC has already made the patient thrombocytopenic and coagulopathic)
    • Angiography and revascularisation (risky in the context of severe sepsis, particularly insofar as stent deployment is concerned)
    • Coronary artery bypass grafting (essentially out of the question given the severe shock state)