Viva 6

As the duty Intensivist you have been called to review a patient on the orthopaedic ward in a small private hospital.The patient is a 56-year-old male who had a total knee replacement 6 days ago. He has a past history of obesity and hypertension. Yesterday he complained of an episode of shortness of breath and was seen by his surgeon.

This morning he has collapsed unconscious whilst being assisted into the shower, the nurses have now placed him back into bed and called for urgent review because of ongoing hypoxia, hypotension and tachycardia.

What are the possible explanations for this shock state?

This is a low-budget cut and paste job from the article on the approach to undifferentiated shock.

Differential Diagnosis of Shock

Artifactual or spurious

  • Inaccurately measured blood pressure
  • Noradrenaline line is not connected

Mechanical support failure

  • IABP augmentation failure
  • VA ECMO malfunction

Hypovolaemic

  • Inadequate fluid intake
  • Loss of fluid
    • Vomiting
    • Diarrhoea
    • Ileostomy losses
    • Sweating
    • Polyuria
    • Burns
    • Pancreatitis
    • Ascites
    • Post-operative "third spacing"
  • Loss of blood
    • Traumatic or surgical
    • Gastrointestinal
    • Uterine (postpartum)
    • Retroperitoneal or abdominal
    • Fractures
    • Pulmonary / intrathoracic

Non-mechanical failure of the circulation

  • Extreme anaemia
  • Extreme hypoxia
  • Mitochondrial toxicity (eg. cyanide poisoning)
  • Inappropriately high metabolic demand (eg. malignant hyperthermia)

Cardiogenic

  • Ischaemia
  • Sudden "valve failure", eg. infective endocarditis
  • Septal or ventricular rupture
  • Myocarditis
  • Cardiac contusion (commotio cordis)
  • Drug overdose (of negative inotropes)
  • Rate problem: too fast or too slow
  • AF (loss of atrial kick)
  • Severe acidosis (myocardial depression)

Distributive

  • Septic shock
  • Toxic shock syndrome
  • Anaphylaxis
  • Angioedema
  • Neurogenic (i.e. loss of sympathetic tone)
  • Adrenal insufficiency
  • Thyroid insufficiency (myxoedema)
  • Drug overdose (of vasodilators)
  • CO2 excess
  • Reperfusion "post arrest" syndrome

Obstructive

  • Intracardiac obstruction:
    • Pulmonary embolism
    • Valve obstruction (thrombosis, myxoma)
    • LVOT or RVOT obstruction
    • Amniotic fluid embolism
  • Extracardiac obstruction
    • Cardiac tamponade
    • Tension pneumothorax
    • Dynamic hyperinflation
    • Excessive positive pressure ventilation
    • Restrictive pericarditis
    • Chest compression (traumatic asphyxia)
Describe your immediate management of this patient.

Primary survey:

  • Assess airway patency
    • Exclude airway obstruction and asphyxia
  • Assess breathing:
    • Oxygenation (saturation probe)
    • Ventilation (end tidal CO2, chest auscultation)
    • Exclude tension pneumothorax and massive haemothorax
  • Assess circulation
    • Peripheral and central temperature/capillary refill
    • Vital signs (heart rate, blood pressure)
    • Equipment check
      • Exclude artifactual shock and equipment failure as the cause of shock, eg. comically mis-matched BP cuff size
    • Head-to-toe exposure
      • Exclude externally obvious haemorrhage
      • Exclude anaphylaxis/angioedema
    • Point of care TTE: rapid assessment with cardiac echo
      • Exclude cardiac tamponade
      • Exclude massive PE
  • Establish venous access
  • Collect a series of generic laboratory investigations, most importantly an ABG
  • Assess neurology (i.e. neurological reason for this shock state)

Empiric resuscitation:

  • Ventilate the intubated patient with low-moderate PEEP (0.1cmH2O/kg)
  • Commence fluid bolus: 10ml/kg.
  • Commence/escalate vasopressor infusion: no evidence to decide which is best (Metaraminol? Peripheral noradrenaline?).
Which details would you like to know from history, examination and immediate investigations?
  • Rapid focused history
    • Immediate events preceding the collapse
    • Drug administration history
    • Recent interventions
    • Relevant background history
    • Collateral from recently attending staff/family
  • Repeat focused examination and investigations
    • ECG
    • CXR
    • ABG with special attention to lactate
    • Head to toe examination
      • Fluid status
      • Sources of sepsis
      • Toxidromes
      • Abdominal examination, looking for AAA, retroperitoneal haematoma and pancreatitis
    • Bedside abdominal and chest ultrasound, looking for collections
    • Formal (skilled) TTE, looking for valvular dysfunction, LVOT obstruction, regional wall motion abnormalities and septal defects
  • Laboratory investigations
    • Full blood count
    • Electrolytes and urea
    • Inflammatory markers
    • Cardiac injury biomarkers
A rapid bedside TTE is performed at your request. This is the parasternal long axis view:

Please interpret this image in context of this patient scenario.

That's a dilated RV due to a massive PE. The image was borrowed witout any permission from radiologykey.comThe right ventricle (top) is massively dilated and compressing the left ventricle, the figure comments say.

A diagnosis of massive PE is made. The primary team ask for advice regarding thrombolysis. What is the rationale for thrombolysis in PE?
 

PE in general is managed with anticoagulation alone. In addition to this, clot burden may be decreased by either systemic thrombolysis, catheter-directed thrombolysis, clot fragmentation or surgical embolectomy. The rationale for this is the improvement of pulmonary blood flow, and thus improved hemodynamic performance of the systemic circulation. A long-term benefit of thrombolysis is the prevention of severe pulmonary hypertension which inevitably develops in the wake of large-scale pulmonary emboli.

Thus, thrombolysis may:

  • Decrease clot burden
  • Improve systemic haemodynamics by improving LV filling
  • Prevent further RV injury
  • Prevent progression to pulmonary hypertension
What are the indications and contraindications for thrombolysis in acute PE?
Contraindications for Thrombolysis in PE
Absolute Relative
  • any prior intracranial hemorrhage,
  • known structural intracranial cerebrovascular disease (eg, arteriovenous malformation),
  • known malignant intracranial neoplasm,
  • ischemic stroke within 3 months,
  • suspected aortic dissection,
  • active bleeding or bleeding diathesis,
  • recent surgery encroaching on the spinal canal or brain, and
  • recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury.
  • age >75 years;
  • current use of anticoagulation;
  • pregnancy;
  • noncompressible vascular punctures;
  • traumatic or prolonged cardiopulmonary resuscitation (>10 minutes);
  • recent internal bleeding (within 2 to 4 weeks);
  • history of chronic, severe, and poorly controlled hypertension;
  • severe uncontrolled hypertension on presentation (systolic blood pressure >180 mm Hg or diastolic blood pressure >110 mm Hg);
  • dementia;
  • remote (>3 months) ischemic stroke; and
  • major surgery within 3 weeks.
Would you offer this patient thrombolysis?

The correct answer is probably "yes". According to the 2011 AHA statement, "Recent surgery, depending on the territory involved, and minor injuries, including minor head trauma due to syncope, are not necessarily barriers to fibrinolysis"

What is the evidence and society recommendations for the use of thrombolysis in this patient?
  • Thrombolysis is seen as a mandatory first-line step in the treatment of massive PE. 
  • However, this is based on rather poor evidence.
  • Originally the guidelines were formed on the basis of only one study. The first randomised trial for thrombolysis in massive PE comes from 1995, and was performed in a group of only 8 patients. All 4 patients receiving thrombolysis had survived without pulmonary hypertension at 2 years follow-up; whereas all the heparin-treated patients had died.
  • Thrombolysis appears to reduce mortality by 55% according to a 2004 meta-analysis (including data from 748 patients). This meta-analysis (Wan et al, 2004) contained a small sub-group (n = 154) of haemodynamically unstable PE patients, and within this small subgroup thrombolytic therapy reduced the risk of their composite endpoint of death and recurrent PE (from 19% to 9%). On the basis of this, all current guidelines seem to recommend thrombolysis for haemodynamically unstable massive PE.
What is the timeframe within which thrombolysis is expected to be effective?
  • Greatest benefit is seen when it is given within 48 hours; however some benefit is still seen even when it is given as late as 6-14 days after the acute event.
  • Most patients respond within 36 hours
  • The haemodynamic benefits of thrombolysis are confined to the first few days after the treatment  (at one week after treatment the benefits are no longer apparent).
The patient's family ask about the risk of complications from thrombolysis. What are the risks you would like to discuss with them?

Bleeding would be the major risk.

  • In the a 2004 meta-analysis, it was found that in comparison to heparin alone thrombolysis doubles the risk of major bleeding from 12% to 22% (which makes some sort of perverse sense, as it tends to halve PE-associated mortality).
  • Real-world registry data suggests that this risk of bleeding is probably underestimated by clinical trial data, given how spotlessly perfect their patient selection is (whereas at the coalface, in the ED and ICU, a fair few patients are retrospectively, posthumously, discovered to have had some contraindication to thrombolysis).
  • This 
  • In short, the risk of death from bleeding is significant, and should be presented to the patient and family as a real possibility.
What alternatives could you present to the family? What would be the advantages and disadvantages of these alternatives?

Catheter-based interventions are possible, but the patient is too unstable to undergo a prolonged interventional radiology procedure. These might include:

  • Aspiration thrombectomy
  • Thrombus fragmentation
  • Rheolytic thrombectomy (using a high velocity saline jet to break up the clot)
  • Catheter-directed thrombolysis

The risks are:

  • Perforation or dissection of a pulmonary artery
  • Pulmonary haemorrhage
  • Right atrial or ventricular perforation
  • Cardiac tamponade
  • Arrhythmias

Surgical embolectomy is a possibility, but good outcomes are only seen when a strong and organised purpose-built team is looking after the process, rather than some ad-hoc on-call cardiothoracic surgeon. Furthermore, the patients need to be carefully selected, and the sort of patient most in need of embolectomy are also the patients least likely to be selected for surgery (i.e. they are in florid cardiogenic shock, or worse yet they failed thrombolysis and are now full of alteplase). Apparently, in this enlightened age the rate of survival after surgical embolectomy is 85% at 1 month. 

The family agree to thrombolysis. What dose of which agent would you use?
  • The dose of alteplase is 0.9mg/kg:
    • 10% of the dose over 1 minute;
    • 90% of the dose over the subsequent hour
    • Maximum dose is 90mg.

In case the candidate has different agents in mind, this is the table from AHA's 2011 statement:

Fibrinolytic doses table from AHA guidelines (2011)

Thrombolysis is administered, and the patient is stabilised on a heparin infusion. A large DVT is found in the ipsilateral femoral vein. The orthopaedic team ask about the utility of an IVC filter. What advice would you give them?

The 2011 AHA statement also has something to say about this. Specifically, the advice is largely  based on the PREPIC trial (Decousus et al, 1998). In summary, "the beneficial effects of IVC filters to prevent recurrent PE in patients with DVT at high risk for PE were offset by an increased incidence of recurrent DVT with no effect on overall mortality". The specific statements which need to be offered to the surgeons should probably echo the AHA recommendations, which are as follows:

  • Placement of the filter may be considered in massive PE, but the level of evidence which supports this recommendation is poor, and it is generalyl only recommended for patients with very poor cardiopulmonary reserve (i.e. those who would surely die if another PE of any size were to occur).
  • IVC filters shoudl not be put in routinely as an adjuvant to anticoagulation
When would you use an IVC filter in this setting?
  • If contraindications to anticoagulation develop, insert the filter (eg. bleeding)
  • If recurrent PEs occur in spite of anticoagulation, insert the filter.

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station. 

References

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Corl, Keith, Sameer Shah, and Eric Gartman. "Ultrasound Evaluation of Shock and Volume Status in the Intensive Care Unit." Ultrasound in the Intensive Care Unit. Springer New York, 2015. 65-76.

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Wan, Susan, et al. "Thrombolysis compared with heparin for the initial treatment of pulmonary embolism a meta-analysis of the randomized controlled trials." Circulation 110.6 (2004): 744-749.

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