Deranged Physiology » CICM Fellowship Exam » Past Papers » 2006, Paper 2 SAQs

Question 23

Created on Fri, 05/29/2015 - 02:32
Last updated on Fri, 04/28/2017 - 17:45
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Topic

Neurology and Neurosurgery

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A previously fit 36-year-old patient  has been admitted  to your Intensive Care Unit with an isolated severe head injury. 18 hrs after admission he develops polyuria. Outline the way in which you would evaluate this polyuria.

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College Answer

The causes of polyuria in this patient include

a)  Diabetes insipidus

b)  Mannitol or other diuretics

c)  Use of hypertonic saline

d)  Cerebral salt wasting syndrome

e)  Effects of ingested alcohol prior to the trauma

Evaluation and treatment

a)  DI : Serum and urine osmolality and Na measurements,

b)  If mannitol: check serum osmolar gap, and ensure it is < 320 mOsm/kg to prevent renal toxicity

c)  Hypertonic saline: Large urine outputs are a feature of hypertonic saline therapy and this can be confirmed by high serum and high urine Na.

d)  CSW: Low intravasc volume, low serum Na, high urine Na.

e)  Residual alcohol: based on index of suspicion, check serum osmolar gap and ethanol levels.

Discussion

LITFL do justice to this topic; theirs is a succinct and accurate answer. In addition to it, one may wish to read a relevant article by Bradshaw and Smith.

To paraphrase the already well-written college answer, the causes of polyuria following a head injury include the following:

  • Diabetes insipidus
  • Cerebral salt wasting
  • Appropriate post-resuscitation diuresis
  • Appropriate natriuresis following hypertonic saline infusion
  • Mannitol-induced diuresis
  • Hypothermic diuresis due to therapeutic cooling

A more detailed tabulated answer would look like this:

Polyuria in Traumatic Brain Injury

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

Risk factors for diabetes insipidus in traumatic brain injury:

  • Severe TBI (GCS < 8) - however, sources disagree whether this is a true association
  • a head Abbreviated Injury Score higher than 3
  • Base of skull fracture
  • Cerebral oedema on the CT
    • Particularly, oedema around the hypothalamus

 

An approach to the investigations and management of 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.

One should hope that the ADH-inhibiting effects of alcohol would have worn off after 18 hours, or else this gentleman had a minimum blood alcohol level of around 0.36% at the time of his injury (which is not entirely unreasonable).

The college did not ask for treatment options in their question, and so I have offered none.

References

Bradshaw, Kate, and Martin Smith. "Disorders of sodium balance after brain injury." Continuing Education in Anaesthesia, Critical Care & Pain 8.4 (2008): 129-133.

Robertson, Gary L. "Differential diagnosis of polyuria." Annual review of medicine 39.1 (1988): 425-442.