Viva 4

A 59-year-old male, accepted for admission to the ICU from the Emergency Department (ED) following a severe traumatic brain injury, and now sedated, intubated and ventilated, is escorted to ICU by an ED Consultant.

What are the critical features of the handover that you would want to know?

The trainee may rant extensively; there should be some sort of structure to the answer

Prognostically relevant information

  • Mechanism of injury
  • Age of the patient (poor outcome risk increases by 20-30% in the over-60s)
  • Pupillary abnormalities (70-90% mortality with bilaterally absent light reflex)
  • Presence of hypotension (doubles mortality)
  • Presence of hypoxia (doubles the likelihood of a poor neurological outcome)
  • GCS on presentation (65% mortality if the GCS is 3)
  • CT scan abnormalities (absence of abnormalities equates to a better prognosis)

Pragmatic information

  • Grade of intubation
  • Other findings of primary survey (i.e. any associated injuries)
  • Neurosurgical plan
  • Plans form other surgical teams
  • Family - what is their understanding of this situation

Patient history:

  • Age, other demographics
  • Comorbidities
  • Allergies
  • Regular medications (antiplatelets or anticoagulants?)

Management history:

  • What has been given for induction at intubation
  • When was the last muscle relaxant given
  • When was the last neurological assessment
  • What did the last gas show (O2, CO2, sodium)
  • What sedation is the patient currently on
  • Whether tetanus vaccination has been given
The ED consultant does not have any of those details, they were just asked to bring the patient up. They know that the CT had some sort of "bleed" on it. 
How will you assess this patient now that you are looking after them? 

There should again be some sort of system. Ideally, the system should resemble a primary survey.

A - assess the airway; is the tube in a good position?

B - assess the ventilator; are the settings appropriate?
      The PEEP should be minimised and there should be normoxia and normocapnea.
      - Is there any evidence of missed injuries, eg. subcutaneous emphysema, trachea off midline?

C - assess the haemodynamics:
      - what access is there? 
      - is the BP satisfactory?

D - What sedation is running? What are the neurological findings? Is there evidence of raised ICP?

E -  Expose the patient; is there any evidence of any other injuries?

The patient has previously been documented to have bilaterally reactive pupils, 3mm. On your examination the patient has a 7mm right-sided pupil and a 1mm left-sized pupil. 
What could account for this finding?

The patient appears to have some sort of brain herniation, which will be the first thing the exam candidate will say. With prompting, they should subsequently give some differentials for what might be the cause of a unilaterally different pupil. 

The patient has a unilateral mydriasis and a unilateral miosis.

Causes of unilateral mydriasis:

Midbrain lesion- ipsilateral damage to the Edinger-Westphal nucleus of the 3rd nerve (thus resulting in loss of parasympathetic input to the ipsilateral eye)
Uncal herneation - stretch of the 3rd nerve across the petroclinoid ligament; most likely
Direct trauma to the eyeball

Causes of unilateral miosis:

Horner's syndrome
Sympathetic damage at any level:

Ipsilateral thalamic lesion

Ipsilateral pontine lesion

Ipsilateral sympathetic chain lesion

The CT scan becomes available online. The neurosurgical team is not aware of this patient. 


Please describe this CT as you would describe it to the neurosurgical registrar over the phone.

There is a large right-sided extradural haematoma.

The haematoma looks acute (i.e. it is homogeneous in appearance).

There is significant midline shift to the left

There is effacement of most of the ventricular system 

There is evidence of obstructive hydrocephalus (dilatation of the temporal horn of the right lateral ventricle)

Given the eye findings, the patient is likely in the process of coning

The neurosurgical registrar suggest you "give something to shrink the brain" as they prepare to operate on the patient. Which osmotherapy agent will you choose, and why?
A Comparison of Mannitol and Hypertonic Saline Osmotherapy
  • Molecular weight: 182.17 g/mol
  • Reflection coefficient: 0.9
  • Sodium content: none
  • Osmolarity (20%): 1100 mOsm/L 20%: 
  • Molecular weight: 58.45 g/mol
  • Reflection coefficient: 1.0
  • Sodium content 3400 mEq/L
  • Osmolarity: 6800 mOsm/L
  • 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.
  • 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.
  • 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
  • Need for central venous access
  • 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 dose of [your agent of choice here] would you administer?

Hypertonic saline is usually given as 3% or 20%.

  • 3% saline is given as 3ml/kg, or ~ 210ml for a standard size 70kg patient
  • 20% saline is usually given as 10-20ml boluses 

Mannitol - the official dose is 0.5-1g/kg, but generally boluses of 20g tend to be given as a routine measure (which is easier to calculate, as it is a fifth of the 500ml bag).

The patient undergoes a craniectomy and evacuation of haematoma. He returns from the operating theatre with the post-op orders asking for "neuroprotective measures".  What do you understand by this statement?

"Neuroprotective measures" are therapeutic and prophylactic strategies which are employed to prevent secondary brain injury.

Maintaining cerebral oxygen supply:

  • 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 strategies:
    • Draining the EVD ( about 20ml/hr, max)
    • Positioning the head straight
    • Removing the C-spine collar
    • Sedation :
      • Propofol sedation to decrease distress and thus decrease ICP
      • Barbiturate coma if other methods of lowering ICP have failed
      • Analgesia to prevent increased ICP in response to suctioning and routine care
    • Paralysis
    • Osmotherapy
    • Controversial measures
      • Decompressive craniectomy
      • Hypothermia
      • Dexamethasone

Decreasing cerebral oxygen demand:

  • Sedation
    • Propofol sedation to decrease distress and thus decrease ICP
    • Barbiturate coma if medical and surgical methods of lowering ICP have failed
  • Analgesia - opioid selection is irrelevant, but opiate boluses increase ICP
  • Seizure prophylaxis is infrequently indicated, and the course is 7 days only
What do you understand by the term, "secondary brain injury"?

Secondary brain injury is the preventable negative effect of several associated physiological variables on the neurological outcome from a primary brain injury.

Those variables are:

  • Increased ICP
  • Hypotension
  • Hypoxia
  • Hypercapnea/hypocapnea
  • Hypoglycaemia and hyperglycaemia
  • Hyponatremia and hypernatremia
  • Hyperthermia
  • Seizures

Some are due to the injury itself, whereas others (eg. hyper and hypoglycaemia) are factors which have been found to be associated with a poorer outcome, and are though to play a contributing role

Your registrar rings you four hours later and tells you that the patient's urine output is rising. How will you investigate and manage this?

Polyuria following traumatic brain injury has several differentials:

Serious differentials:

  • Central diabetes insipidus
  • Mannitol diuresis
  • Hypertensive diuresis
  • Hypothermic diuresis
  • Normal response to fluid loading

Unlikely differentials:

  • Hyperglycaemia
  • Nephrogenic diabetes insipidus
  • Cerebral Salt Wasting Syndrome
  • Post-obstructive diuresis
  • Recovery phase of acute tubular necrosis

An approach to the investigations and management of this polyuria:

Once the polyuria is discovered:

  • Collect a baseline serum sodium and serum osmolality
  • Observe urine output: watch for 3 consecutive hours of 300ml/hr urine output

After 3 hours of obervation:

  • If the serum sodium is rising, collect a urine specimen for urinary sodium and osmolality
  • Continue to observe. The sodium may safely approach 155mmol/L.

If the serum sodium continues to rise, with low urinary sodium and urine osmolality under 300mOsm/kg, consider 0.5μg of DDAVP.

  • If DDAVP has been given, monitor sodium at frequent regular intervals for the next 24-48 hours.
  • The registrar describes the following findings:
Over the subsequent three days the patient becomes progressively more and more hyponatremic. The neurosurgical team think this cerebral salt wasting and the endocrinology team think this is SIADH. How do you tell the difference?
  • CSW is defined as a renal loss of sodium during intracranial disorders, in the presence of normal renal function.
  • It is characterised by natriuresis, polyuria and hypovolemia.
  • It is a diagnosis of exclusion.

In both disorders, ADH levels are elevated and urinary sodium is raised above 20mmol/L

In SIADH, the body fluid volume is normal or elevated, and therefore the ADH secretion is inappropriate.

In cerebral salt wasting the body fluid volume is low

In CSW the patient should also be polyuric. The renal function must be normal to meet the definition. In SIADH, the urine output should be low. 

The fractional excretion of urate and phosphate is usually normal or low in SIADH and usually high in CSW.

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:

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

 Brain Trauma Foundation Guidelines.

Cerdà-Esteve M, Cuadrado-Godia E, Chillaron JJ, Pont-Sunyer C, Cucurella G, Fernández M, Goday A, Cano-Pérez JF, Rodríguez-Campello A, Roquer J Cerebral salt wasting syndrome: review. .Eur J Intern Med. 2008 Jun;19(4):249-54

Verbalis, Joseph G. "Hyponatremia with intracranial disease: not often cerebral salt wasting." The Journal of Clinical Endocrinology & Metabolism 99.1 (2014): 59-62.