Viva 4

A 59-year-old male presents to an outer metropolitan hospital, supported by a non-tertiary ICU, with severe respiratory failure.

He gives a history of a week of cough, myalgia, fevers and increasing shortness of breath.

What is your differential diagnosis?

What is your differential diagnosis?

It would help to separate the potential causes into common and uncommon, as well as into infectious and non-infectious. 

Common infectious causes in the immunocompetent host:

  • Bacterial pneumonia
    • Typical (S.pneumoniae, H.influenzae)
    • Atypical (eg. mycobacterial)
    • Community acquired vs. hospital acquired
  • Viral pneumonia

Common infectious causes in the immunocompromised host:

  • Fungal infection eg. Aspergillus
  • Viral infection, eg. CMV, VZV
  • PJP

Common non-infectious causes:

  • Pulmonary embolism
  • Bronchospasm: COPD or asthma
  • Pneumothorax
  • Pleural effusion for whatever reason
  • Heart failure, pulmonary oedema
  • Aspiration pneumonitis

Uncommon non-infectious causes:

  • Pulmonary vasculitis
  • Eosinophilic pneumonitis
  • Chemical pneumonitis (toxic exposure)
  • BOOP (COP)
  • Alveolar haemorrhage
  • Neuromuscular disease, with respiratory muscle weakness
  • Hyperthyroidism
  • Neurogenic pulmonary oedema
  • Mitral valve prolapse post MI
  • Lymphangitis carcinomatosis

(Much of this list of differentials is borrowed from Question 20 from the first  paper of 2014, where the candidates were asked for a broad list of differentials to explain a diffuse bilateral infiltrate in a patient with RA)

What history would be important to help you narrow down the diagnosis?

The candidate may begin to ramble interminably. Say, any six or seven of the following things might satisfy this question.

Patient's medical history of prognostic importance

  • smoking
  • COPD
  • heart disease, including CCF and pulmonary hypertension
  • exercise tolerance
  • immunesuppression, eg. corticosteroids
  • malignancy
  • vaccination history
  • history of exposure to TB, country of origin
  • end-stage organ failure, eg. cirrhosis or dialysis-dependent renal failure

Recent history of aetiological importance

  • swallowing difficulty, history of stroke
  • alcohol binges
  • haemoptysis
  • recent travel
  • recent gardening (Legionella)
  • recent bushwalking
  • exposure to birds or pets
  • recent chemotherapy
  • recent hospital stay
  • recent antibiotic use

Presenting history

  • rapidity of onset
  • associated symptoms eg. copious amounts of sputum, flu-like symptoms, hemoptysis, pleuritic chest pain, and so forth

Features which help narrow the organism

  • Recent hospital stay, nursing home residence (community acquired vs. nosocomial: determines the likelihood og Gram negative organisms, and influences antibiotic decisions)
  • Recent travel to regions of known Legionella epidemics
  • Exposure to birds (Chlamydia psittacii)
  • Exposure to groups with known drug-resistant pneumococcus, or similar
  • Risk factors for Pseudomonas infection
    • Structural lung disease, eg. bronchiectasis
    • Use of corticosteroids
    • Courses of broad-spectrum antibiotics
  • Specific immunosuppression:
    • Splenectomy (encapsulated organisms: S.pneumoniaeH.influenzae)
    • HIV (Pneumocystis, tuberculosis)
    • Neutropenia (fungi)

Much of this was borrowed from  Question 26 from the first paper of 2006, where the candidates were expected to "List  specific  historical  information " which might be useful in the diagnosis of severe pneumonia. The possible list of answers is vast. It would be easy to waste a lot of time on this, losing marks.

 
The history is unremarkable, except for a background of bullous pemphigoid, treated with 15mg/day of oral prednisolone.
Which investigations would you order?
  • CXR
  • Arterial blood gas
  • Blood cultures
  • FBC (for leucocyte morphology rather than their number)
  • EUC (to anticipate renal clearance problems)
  • LFTs (to anticipate hepatic clearance problems)
  • Blood culture
  • Sputum culture
  • Pleural fluid culture
  • Legionella urinary antigen
  • Pneumococcal urinary antigen
  • Bronchoscopic lavage specimen for culture
  • Respiratory viral swabs (NAT)
  • Inflammatory markers, eg. CRP and procalcitonin

 
A chest X ray is done, which demonstrates bilateral diffuse pulmonary infiltrates. 
An ABG  is collected (on 15L O2 via non-rebreather mask). How would you interpret this result?

Severe hypoxia (PF ratio = 78 if FiO2 is thought to be 100%)

Consistent with severe ARDS.

Lactic acidosis consistent with ARDS and sepsis

The patient becomes more hypoxic and drowsy. He is intubated. Following intubation, peak airway pressure remains high and his oxygenation does not improve beyond SpO2 85% on 100% FiO2
Describe your initial ventilator settings, and the rationale behind them.
How would you decide on which level of PEEP to use?
  • Use an arbitrarily high PEEP: set to 15-20cmH2O (CT studies support the use of a PEEP of around 16 cmH2O)
  • Use the ARDSNet PEEP/FiO2 escalation tables (setting the PEEP according to the severity of the oxygenation failure)
  • Titrate PEEP according to maximum compliance, i.e. set the PEEP which achieves the highest static compliance (this has the advantage of being tailored to each specific patient)
  • Set the PEEP to slightly above the lower inflection point of the pressure volume curve (therefore avoiding cyclic atelectasis)
  • Use a staircase recruitment (or derecruitment) manoeuvre to find the lowest PEEP at which the maximal oxygenation is maintained (this has the advantage of having a very pragmatic endpoint, SpO2)
  • Titrate PEEP to achieve the smallest intrapulmonary shunt using a PA catheter with continuous SvO2 monitoring
  • Titrate PEEP to achieve the lowest arterial minus end-tidal CO2 gradient (i.e. the PEEP at which dead space is minimal)
  • Use the transpulmonary pressure calculated from oesophageal balloon manometry, using oesophageal pressure (Pes) as a surrogate for pleural pressure (where TPP = Pplat - Pes). Adjust PEEP so that TPP at end-expiration is 0-10.
  • Using electrical impedance tomography, titrate PEEP to achieve the highest electrical impedance in the thorax (i.e. the greatest amount of aerated lung)
  • Use sequential CT scans to visually determine a PEEP at which the greatest volume of lung is recruited during end-expiration
What additional ventilation strategies could you employ if the patient becomes more hypoxic?
What are the non-ventilator strategies available to help in the management of this condition?
  • Pulmonary vasodilators - nitric oxide or prostacycline
  • Minimization of dead space ventilation - Remove as much tubing as you can.
  • Low-carbohydrate high-fat nutrition - Keep them off the carbs, and don't overfeed. (little evidence for this)
  • Neuromuscular blockade may improve survival
  • Sedation decreases energy expenditure and improves ventilator synchrony
  • Fluid management should have a goal of neutral balance (keep em dry)
  • ECMO may improve survival (CESAR, 2009) but again there were problems with methodology.

The candidate - at some stage- needs to mention retrieval for this patient. The viva stem says that the patient is in some sort of non-tertiary ICU, so advanced stuff like ECMO or HFOV is probably out of the question.

What are the advantages and disadvantages of prone ventilation?

Rationale for prone ventilation

  • Improved V/Q matching
  • More homogeneous ventilation
    • More uniform distribution of pleural pressure;
    • Thus, more uniform compliance;
    • Thus, more uniform distribution of plateau pressure;
    • Thus, less cyclical atelectasis and alveolar overdistension.
  • Less compression of the lungs by the heart and by the abdominal content.
  • Increased FRC by about 300-400ml
  • Improved drainage of secretions
  • Improved response to recruitment manoeuvres: prone patients seem to require less PEEP (8cm vs 14cm) to sustain the post-recruitment improvement in oxygenation.
  • Improved mechanics of the chest wall in obesity

Limitations of prone ventilation

  • Limitations and contraindications by patient factors
    • Open abdomen, wounds or burns over the ventral body surface
    • Spinal or pelvic instability
    • Massive abdominal distension, eg. pancreatitis
  • Limitations of logistics:
    • difficulty of positioning and increased nursing workload
    • poor control of airway safety
      • In fact, poor control of all drains and tubes of any sort
      • There is a known risk of airway compromise
      • If the tube falls out, it is difficult to reintubate
    • poorer pressure area care
    • Difficult (impossible) central insertion while prone
    • Pressure prone areas include eyes, lips (frm the ETT), bridge of nose, shoulders, ulnar nerves at the elbow, breasts (particularly large ones and those that contain implants), pelvis (particularly interior superior iliac spines), penises and scrotums, and the knees.
  • Limitations of physiology
    • Poor NG feed tolerance
    • Facial oedema
    • Raised intraabdominal and intracranial pressure
  • Limitations of imagination
    • ECG electrode position will change, and so potentially "ECG changes" may appear
    • Up to 50% of ARDS patients do not benefit from prone position, and so this manoeuvre may be a time-wasting exercise, delaying the decision to start ECMO.

(This comes from Question 7 from the second paper of 2012, which is mainly about the causes of non-resolving pneumonia. The discussion is elaborated further in the community-acquired pneumonia chapter.) 

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

Khilnani, G. C., and C. Bammigatti. "Acute Respiratory Failure-Algorithmic Approach-Diagnosis and management." Medicine Update (2005): 548.

UpToDate: Evaluation of the adult with dyspnea in the emergency department

Metlay, Joshua P., Wishwa N. Kapoor, and Michael J. Fine. "Does this patient have community-acquired pneumonia?: Diagnosing pneumonia by history and physical examination." Jama 278.17 (1997): 1440-1445.

Blanco, Silvia, and Antoni Torres. "Differential Diagnosis of Pulmonary Infiltrates in ICU Patients."www.antimicrobe.org

Gattinoni, Luciano, Eleonora Carlesso, and Massimo Cressoni. "Selecting the ‘right’positive end-expiratory pressure level." Current opinion in critical care 21.1 (2015): 50-57.

Grasso, Salvatore, et al. "ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure." American journal of respiratory and critical care medicine 176.8 (2007): 761-767.

De Campos, T. "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network." N Engl J Med342.18 (2000): 1302-130g.

Lamm, W. J., Michael M. Graham, and Richard K. Albert. "Mechanism by which the prone position improves oxygenation in acute lung injury." American journal of respiratory and critical care medicine 150.1 (1994): 184-193.