A 20 year old female in ICU following a diffuse axonal head injury develops a severe exacerbation of intracranial hypertension on day 3. She is mechanically ventilated, paralysed and sedated. Investigations during a subsequent episode of marked polyuria are summarised below.
Test |
Value |
Normal Range |
pH* |
7.50 |
(7.36 –7.44) |
PaCO2* |
28 mm Hg |
(36 – 44) |
HCO3-* |
21 mmol/L |
(23 – 26) |
Standard base excess |
-1.5 mmol/L |
(-2 .0 to +2.0) |
Sodium* |
147 mmol/L |
(135 – 145) |
Potassium |
3.2 mmol/L |
(3.2 – 4.5) |
Chloride |
110 mmol/L |
(100 –110) |
Urea |
3.0 mmol/L |
(3.0 – 8.0) |
Creatinine |
65 mmol/L |
(50 – 100) |
Glucose |
4.0 mmol/L |
(3.0 – 6.0) |
Measured plasma osmolality* |
333 mosmol/kg |
(280 –290) |
Urine osmolality |
410 mosmol/L |
(50– 1200) |
a) What is the most likely explanation for the polyuria? Give the reasoning behind your answer.
a) What is the most likely explanation for the polyuria? Give the reasoning behind your answer.
Mannitol therapy
There is increased measured plasma osmolality with an elevated osmolar gap. The gap is 44 mosmol/kg, if we use a calculated osmolality of 1.86 × ([Na] + [K]) + [urea]
+ [glucose]. If we use the simple formula of 2 × [Na] + [urea] + [glucose] for
calculated osmolality, the gap is 32 mosmol/kg. (There are also other formulae which are more difficult to remember). In the setting of treatment for an exacerbation of intracranial hypertension, the increased osmolar gap is likely to be due to mannitol administration. The high urinary osmolality rules out diabetes insipidus, and supports the diagnosis of mannitol induced polyuria
This question is identical to Question 22.1 from the second paper of 2011, and Question 3 from the second paper of 2007 (which contains an answer with a more complete interpretation of this issue).