Tessa Davis. Diabetes Insipidus, Don't Forget the Bubbles, 2013. Available at:
A 5-year-old girl is on the ward following resection of a craniopharyngioma. The nurses call you because her urine output has increased dramatically over the last few hours. You check her sodium and it’s 150.
Is your brain hurting just thinking about it?
- Suspect diabetes insipidus if there is polyuria, polydipsia in the presence of a high serum Na and low urinary Na
- Manage with vasopressin and appropriate hydration
- Watch for hyponatraemia following the commencement of treatment
- This can be a life-long condition and ease of management will depend on whether the patient has an intact thirst centre
What is DI?
In diabetes insipidus, the body produces no (or very little) anti-diuretic hormone. This means that the patient cannot concentrate the urine and ends up with dehydration and electrolyte imbalance.
What causes it?
ADH is a hormone that regulated fluids and sodium retention.
In cranial DI the pituitary does not properly signal for the release of ADH when needed (i.e. when dehydrated) and so there is no ADH to instigate fluid retention. Due to dehydration, the body then tries to retain sodium.
Cranial DI causes include: surgery (trans-sphenoidal); traumatic brain injury; idiopathic; autoimmune; tumours (suprasellar, lung, breast, lymphoma, leukaemia); hypoxic brain injury; brain stem death; profound hyponatraemia; radiotherapy; drugs – amiodarone, lithium; inflammatory conditions – sickle cell, sarcoid, Wegener’s, histiocytosis X; infections – TB, abscess, encephalitis, meningitis; vascular disease – CVA, SAH, Sheehan’s syndrome.
In nephrogenic DI, ADH is being produced but the kidneys are not responding to it. This is a different condition and will not be dealt with in this post.
How can I recognise it?
The symptoms of DI can include polyuria, polydipsia and dehydration or weight loss.
In some patients, the thirst centre is not intact and so they will no have symptoms of polydipsia.
- Urine output >4ml/kg/hr for 2 hours
- Serum Na>145
- Osmolality: serum >295 mOsmol/kg H2O And urine <450 mOsmol/kg H2O
- Weight loss of >5%
Additional studies such as plasma ADH, urine specific gravity and a water deprivation test can assist with diagnosis. Urine specific gravity is a particularly handy test as it can be done there and then without going to the lab.
Water deprivation test
- This test aims to check if the kidneys can concentrate urine in the presence of ADH
- The patient is fluid deprived for 8 hours or until 5% of body weight is lost
- Measure plasma osmolality every 4 hours. and urine volume and osmolality every 2 hours.
- After the 8 hours, the patient is given IM vasopressin unless there is a clear indication of DI prior to this
- urine and serum osmolality are checked over the following 4 hours
- In cranial DI the urine osmolality will initially be low (<300 mmol/kg) and after vasopressin it will rise to >800
- In nephrogenic DI giving the vasopressin will not make any difference to the osmolality
What is the treatment?
Management in ICU
If the patient has a high serum Na, high urine output and low urine osmolality in the post-op period, treatment should be considered (usually in discussion with the endocrine team).
Treatment is based around a combination of rehydration and vasopressin.
Vasopressin can be given IN, orally or IV.
The aim is to keep the Na at 135-140. If the Na>150 the amount of vasopressin should be increased.
The other aim is to maintain hydration and a normal urine output (target 2-3 mls/kg/hr).
Be careful of hyponatraemia from over-treatment and also of bringing the sodium down too fast (this can cause cerebral oedema).
If the Na<135 then either stop the vasopressin or give some hypertonic saline. Consider fluid restriction or frusemide if the Na continues to fall and is <130. These patients can have seizures due to hyponatraemia post commencement of vasopressin if it’s not tightly monitored.
Calculating sodium replacement
(Target sodium – current sodium) x 0.6 x weight = mmol Na required to reach target
Sodium content of fluids[wpsm_comparison_table id=”9″ class=”center-table-align”]
Ongoing DI management
Daily serum electrolytes and osmolality, and daily urine osmolality are required until stable.
Make sure sodium is above 145 mmol/L prior to administration of vasopressin.
Should have 1-2 hrs of diuresis (greater than 4ml/kg/hour) prior to administration of next dose to avoid hyponatraemia.
Patients should be weighed daily and keep a strict fluid balance chart.
What is cerebral salt wasting (CSW)?
This is rare but can occur following cranial surgery.
It causes polyuria and dehydration but with high urinary sodium (i.e. hyponatraemic dehydration).
The urine:serum osmolality ratio will be greater than 1.
CSW is managed with fluid replacement and salt replacement of urinary sodium losses (as guided by the serum sodium).
What’s the prognosis?
DI can be transient or permanent.
Pratheesh et al (2013) did a retrospective analysis of 102 children who were status post removal of craniopharyngioma (and compared them to adults)
- DI was more common post-op in children than adults (80% v 63%)
- Triphasic response (fluctuating serum sodium levels) was more common in children
- Children had a higher incidence of permanent DI (55.6%)
Pratheesh R, Swallow DM, Rajaratnam S, Jacob KS, Chacko G, Joseph M, et al. Incidence, predictors and early post-operative course of diabetes insipidus in paediatric craniopharygioma: a comparison with adults. Childs Nerv Syst. 2013;29(6):941-9.