Viva 2

You are the Duty Intensivist at a large neurosurgical centre and receive a call from a General Practitioner in a small rural Emergency Department. She reports that a man in his 40s has been assaulted and beaten unconscious with a crowbar outside a pub.

Upon his arrival at the hospital she intubated him immediately for a low GCS. On examination he has obvious facial and head injuries with a BP of 180/100. No other injuries are immediately apparent but there is no CT scanner.

After speaking to your neurosurgical registrar who has accepted the patient, the GP is now seeking an urgent patient transfer to your intensive care unit.

What initial questions would you ask the GP prior to transfer to provide you with an assessment of the patient?

The trainee should come up with a list of questions to ask, of which the most important should be:

Details of history:

  • How long was the patient unconscious
  • What is the pre-intubation GCS in detail (E, V, M)
  • What other bakcgorund history is known
  • Allergies and medications (eg. anticoagulants, antiplatelet drugs)

Details of examination

  • Are the pupils equal or unequal
  • What are the other observations, apart from the already known blood pressure
  • Specifically, what are the oxygen saturation, heart rate and temperature
  • Is there any suspicion that the C-spine may be injured

Transfer-related details

  • What is the weight of the patient
  • What are the currently running infusions
  • What is the neurosurgical plan on arrival
The GP reports that the GCS prior to intubation was 3, and that the pupils are unequal.
What advice would you give?

The trainee should offer some basic first-tier management strategies. Question 6 from the second paper of 2015 lists the following measures:

Stereotypical first steps in management:

  • Normoxia: keep the PaO2 above 60 mmHg
  • Normotension: measure the MAP, and keep the systolic above 90mmHg
  • Intracranial Pressure monitoring: keep it under 20mmHg
  • Cerebral perfusion pressure: keep it 50-70mmHg
  • Cerebral oxygenation monitoring:keep the SjO2 >50%, and PbrO2 >55mmHg
  • Managing increased intracranial pressure for which there is a variety of methods​
    • Position the head (45 °head up, facing straight)
    • Loosen the ETT ties
    • Remove the C-spine collarn(if one was applied)
    • Decrease PEEP as much as possible
    • Maintain a low-normal PaCO2 (35-40 mmHg)
    • Increase sedation
      • Propofol sedation to decrease distress and thus decrease ICP
      • Benzodiazepines may be of use (but they do not decrease the CMRO2 as much as propofol)
    • Paralysis with neuromuscular junction blocker
    • Osmotherapy of some sort:
      • Mannitol 20% 
      • Hypertonic saline 

For full marks, ask for doses of the drugs.

What is the rationale behind your choice of sedative? How does sedation help in this scenario?
  • Sedation improves control of intracranial pressure and is a "neuroprotective measure", because:
    • It decreases cerebral metabolic demand (CMRO2)
    • Thereby, it decreases cerebral blood flow and thus intracranial pressure (by altering the intracranial blood content)
    • It allows the use of neuromuscular junction blockers
    • It ablates the sympathetic response to raised intracranial pressure, which can be destructve)
    • It decreases the sympathetic response to pain
    • It reduces patient distress
  • Propofol is the first choice
    • Widely available
    • Familiar and predictable
    • Decreases CMRO2: in one study (Vandesteen et al, 1988) cerebral blood flow decreased by 27.6% and cerebral vascular resistance by 51%.... Cerebral oxygen consumption decreased by 18.25%.
  • A barbiturate, eg. thiopentone, is the next best choice
    • Also widely available
    • Also decreases CMRO2
    • Undesirable effects include long clearance halflife and some immunosuppressant effects 
  • Midazolam is a distant third choice
    • It is relatively long acting
    • It has little effect on CMRO2 (certainly less than propofol)
  • Opiates
    • For humanitarian reasons (the head: it hurts)
    • To decrease the ICP rise in response to noxious stimuli
    • To ablate the cough reflex (coughing also causes ICP to rise)
    • A potential sedative-sparing effect (it is thought that there is some sort of additive benefit on the CMRO2)
Can you explain your use of osmotherapy in this context? What is your rationale?

Osmotic effects: 

  • Osmotherapy solutions change (increase) the osmolality of extracellular fluid
  • The change in extracellular osmolality results in the shift of fluid from the intracellular to the extracellular compartment
  • This has the effect of decreasing the volume of intracranial parenchyma 
  • The water which has shifted into the extracellular compartment then undergoes removal by osmotic diuresis
  • The reduction in intracranial parenchymal volume is not sustained because the neurons will respond by generating idiogenic osmoles

Non-osmotic effects:

  • Osmotherapy agents increase systemic blood volume, which leads to:
    • haemodilution
    • increased cardiac output
    • increased blood pressure.
  • Mannitol also reduces blood viscosity and supposedly improves rheology of red cells
  • Improved intracranial blood flow should result from this
  • The improvement in blood viscosity also decreases intracerebral blood volume
What is the evidence for the use of osmotherapy in traumatic brain injury?

In summary:

  • The 2007 Brain Trauma Foundation guidelines gave recommendations in support fo mannitol
  • The new BTF guidelines (4th edition)  have withdrawn some of their support, and merely restated the old recommendation.
  • This is because the study quality was sub-optimal
  • There were two RCTs and one cohort study in 
  • None met the criteria for level II or III recommendation
  • The ongoing use of osmotherapy derives support from the concept that ICP-guided therapy has a mortality benefit, but itself has been challenged.
The GP only has mannitol in stock. What are the pharmacolgical properties of mannitol?
  • Molecular weight: 182.17 g/mol
  • Reflection coefficient: 0.9
  • Sodium content: none
  • Osmolarity (20%): 1100 mOsm/L 20%:
What are the advantages and disadvantages of using mannitol?

Advantages of mannitol:

  • Still fairly cheap
  • Rapid effect
  • Seems to have some sort of rheological benefit (increaes red cell deformability)
  • Acts as a transient volume expander
  • May have a better effect on cerebral blood flow for a given reduction in ICP.
  • Safe endpoint (serum sodium) is easily monitored with ABGs.

Disadvantages of mannitol:

  • Unstable in storage: at low temperatures and at altitude, it precipitates.
  • Medium for bacteria and fungus.
  • Causes a brief state of volume overload
  • Causes torrential diuresis and hypovolemia
  • Causes hyponatremia while in the serum, and hypernatremia after the inevitable diuresis
  • Endpoint is serum osmolality(320), which is cumbersome to measure
  • May cause ICP to "rebound" after prolonged use
How does hypertonic saline compare to mannitol? What are the advantages and disadvantages of hypertonic saline?

Advantages of hypertonic saline:

  • Cheap
  • Stable in storage
  • Very rapid effect
  • Seems to have some sort of intrinsic anti-inflammatory effect
  • May also have some rheological benefits
  • At least as potent as mannitol when it comes to reducing intracranial pressure
  • Less potential for hypovolemia than with mannitol- the diuretic effect is less potent
  • May have a better effect on cerebral blood flow for a given reduction in ICP.
  • Safe endpoint (serum sodium around 145-155) is easily monitored with serial ABGs

Disadvantages of hypetonic saline

  • Need for central venous access (sclerosant)
  • No standards for which concentration to use, or how to give it
  • Hypokalaemia
  • Hyperchloraemic acidosis
  • Should not be used if the patient is chronically hyponatremic
  • Possible seizures due to wild fluctuations in serum sodium
  • Increase in circulating volume with risk of fluid overload.
  • Coagulopathy (APTT and INR)
  • Altered platelet aggregation.
  • May affect normal brain more that injured brain which theoretically may worsen herniation
What is the evidence to support the use of one osmotherapy agent over another?
  • No mortality benefit
  • No difference in efficacy
  • Francony et al, 2008: both substances "equally and durably reduced the ICP" in a case series of 20 stable TBI patients.
  •  Kamel et al (2011)Rickard et al (2013): meta-analysis; small but statistically significant mortality difference in favour of hypertonic saline.
  • BTF guidelines: no specific recommendation for one agent over another
  • Pragmatic interpretation of the evidence: these agents should be viewed as equivalently efficacious and the decisoon to use one over another should be guided by patient factors (eg. hyponatremia)

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. 


Oh's Intensive Care manual has two excellent chapters to dedicate to this topic:

  • Chapter 43 (pp. 563) Cerebral protection by Victoria Heaviside and Michelle Hayes, and
  • Chapter 67 (pp. 765) Severe head injury by John A Myburgh.

However, the discerning reader will recognise this book as an antique, and look instead to the frequently updated Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury.

(see also the new 4th edition of the BTF guidelines)

Diringer, Michael N. "New trends in hyperosmolar therapy?.Current opinion in critical care 19.2 (2013): 77.

Francony, Gilles, et al. "Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure*." Critical care medicine 36.3 (2008): 795-800.

Kamel, Hooman, et al. "Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: A meta-analysis of randomized clinical trials*."Critical care medicine 39.3 (2011): 554-559.