A 65 year old previously healthy man has presented to the Emergency Department with chest pain and shortness of breath. Vital signs are Glasgow Coma Score 15, respiratory rate 30 breaths/minute, oxygen saturation 96% on 8 L O2 via nasal prongs, heart rate 120 bpm and BP 180/40 mmHg.
He has an established IV access.
You are requested by the ED physician to review him and possibly take over his care. Outline your initial plan of management
The rest of the viva focussed on approach to the evaluation of chest pain and management of aortic dissection and its complications.
(I made one minor change to the college stem - because the patient ends up with an aortic regurgitation, I made the systolic BP 40mmHg, to raise suspicion of AR. In the original stem the diastolic was 130. - AY)
Plan of management could be fairly nebulous here. Not much information was given.
The major issues are:
- Complaints of shortness of breath
- Complaints of chest pain
A well- structured answer would include:
- First, a primary survey (i.e. does this patient need intubation immediately)
- Then, some history and examination, concurrently with investigations and early management
- History of the chest pain
- Examination looking for features of heart failure, including valve pathology
- Bloods including troponin
- Early basic management
- Pain relief (morphine)
- GTN to control BP and decrease preload
The history is of sudden onset severe central chest pain, maximal at onset and radiating to the back. Background is of heavy tobacco use and hypertension.
There is a diastolic murmur on auscultation.
The bloods demonstrate acute kidney injury (Creatinine >200 from a normal baseline).
The ABG is as shown:
(show them the ABG)
What is your interpretation of this ABG?
- There is no acidaemia.
- The gas exchange is grossly impaired (on 8L O2, pO2 of 116 is too low - there is a raised AA gradient. if he was on a Venturi mask at 50%, the A-a gradient would be 204)
- There is a mild metabolic acidosis (SBE -4.4)
- The respiratory compensation is excessive - the expected CO2 is ~ 35mmHg; thus there is also a respiratory alkalosis
- The anion gap is 17.3 if you include the potassium, which is mildly elevated
- The delta ratio is ~ 1.1, i.e. this is mainly a high anion gap acidosis
- There is a lactic acidosis, which accounts for the high anion gap (and some of which is well buffered).
In summary, there is a high anion gap metabolic acidosis and a respiratory alkalosis which can be attributed to the pain and hypoxia.
The CXR demonstrates interstitial pulmonary oedema.
The ECG is as shown:
(show them the ECG)
What is your interpretation of this ECG?
(it's rapid AF with no ischaemic features)
What are the differentials for this presentation?
The trainee shoudl have captured that the combination of "sudden", "maximal at onset" and "radiating to the back" with a normal ECG should make one think of aortic dissection; just in case it wasn't obvious enough I threw in specifically the diastolic murmur of AR.
- Aortic dissectioon
- Unstable angina with pulmonary oedema due to diastolic failure
- Pericarditis or myocarditis
- Pancreatitis with "leaky lung" ARDS
- Pulmonary embolism
- Musculoskeletal pain with pulmonary oedema due to diastolic failure
The cardiology team suspect aortic dissection. What are the risk factors for this condition?
I paraphrase Table 9 from the ACCF/AHA guidelines:
- Weight lifting
- Deceleration or torsional injury
- Coarctation of the aorta
- Marfan syndrome
- Ehlers-Danlos syndrome
- Bicuspid aortic valve (including prior aortic valve replacement)
- Inflammatory vasculitis ("Aortitis")
- Polycystic kidney disease
- Chronic corticosteroids
- Infections involving the aortic wall
What imaging options are available to confirm aortic dissection?
- TTE (not ideal but easier to arrange)
- TOE (better, but requires more phonecalls)
- CT angiogram
- DSA aortogram
The cardiologist involved is proficient with TOE and offers to perform one at the bedside. What are the advantages and disadvantages of TOE for diagnosis of aortic dissection?
- Can assess valves
- Decent sensitivity (35-80%) and specificity(39-96%)
- Performed at the bedside- no risk of transfer
- Contrast not required
- Allows detection of tamponade
- Allows assesment of proximal coronary arteries
- Able to detect intramural haematoma
- Accuracy is operator dependent
- Requires sedation
- May cause hypertension
- Limited by a blind spot caused by interposition of the trachea and left main bronchus between the oesophagus and aorta
- Unable to visualise the abdominal aorta, which is important here.
The renal function is off and the lactate is high; the candidate should be able to identify a need for an urgent CT of the abdomen.
What would be the advantages of CT with IV contrast in this situation?
- Easily available
- High sensitivity (83-94%) and specificity (87-100%)
- Information about end-organ ischaemia
- Imaging of the vascular tree allows planning of surgical or endovascular approach
- ECG-gated CT = cardiac motion artifact is abolished
- Able to exclude conditions which mimic aortic dissection
A CT is performed. It demonstrates an aortic dissection extending from the aortic root down to the common iliac. SMA and one of the renal arteries are under-perfused.
How would you classify this dissection?
This is a Type A dissection.
Other classification systems exist:
The Stanford classification system divides dissections into 2 categories, those that involve the ascending aorta and those that do not.
- Type A: All dissections involving the ascending aorta
- Type B: All dissections that do not involve the ascending aorta
The DeBakey classification system categorizes dissections based on the origin of the intimal tear and the extent of the dissection:
- Type I: Dissection originates in the ascending aorta and propagates distally to include at least the aortic arch and typically the descending aorta (surgery usually recommended).
- Type II: Dissection originates in and is confined to the ascending aorta (surgery usually recommended).
- Type III: Dissection originates in the descending aorta and propagates most often distally (nonsurgical treatment usually recommended).
- Type IIIa: Limited to the descending thoracic aorta.
- Type IIIb: Extending below the diaphragm.
What complications might be expected from this condition?
- About 40% die immediately. They are underidentified, as few are subjected to autopsy.
- About 1% die per hour thereafter.
- About 5-20% will die shortly after their definitive surgery.
- Cardiac failure due to aortic regurgitation
- Cardiac failure due to cardiac tamponade
- Myocardial ischemia or infarction
- Ischemic stroke
- Paraplegia due to spinal ischemia
- Aortopulmonary fistula with haemorrhage
- Mesenteric ischaemia
- Renal ischaemia
- Limb ischaemia
What immediate management would you recommend?
- Intubation and positive pressure ventilation to decrease myocardial workload
- Urgent blood pressure control with β-blockers, eg. metoprolol or esmolol
( SNP is a good second agent)
- Reasonable targets are a heart rate less than 60 bpm and a systolic blood pressure between 100 and 120 mm Hg (2010 guidelines)
- Urgent surgical consultation for aortic root repair
- Urgen general /vascular surgical consultation for compromised mesenteric circulation
The patient is transferred to theatre for an urgent repair of the aortic root. Seven hours later he is admitted to your ICU post-operatively.
What details would you like to know from the anaesthetist at handover?
- Details of the operation
- Intubation grade
- Haemodynamic stability perioperatively
- Duration of bypass
- Duration of deep hypothermic arrest
- Duration of crossclamp
- Weaning off bypass
- Any arrhythmias post weaning
- How much blood product was transfused
- Post-procedure TOE results
- Drain output at the time of admission to ICU
- last ACT
- What was done in the abdomen
This was taken almost verbatum from the Starship Children's Hospital PICU handover checklist, an excellent example of such checklists.
The patient underwent an emergency Bentall procedure. What complications might you anticipate in this patient?
The 2012 article by Joo et al and the English language copy of Almeida et al (2011) is an excellent resource for this.
- Acute MI (thrombosis of reimplanted coronaries)
- Stroke (ejected atheroma)
- Infaction of the spinal cord
- AF or ventricular arrhythmia
- Nosocomial pneumonia (~ 40%)
- Worsening renal failure, likely requiring dialysis
- Worsening gut ischaemia
- Poor feed tolerance (gut is poorly perfused)
- Mortality risk is 10-20%
- High risk of prolonged ICU stay