Nocturnal enuresis

Cite this article as:
Mary Hardimon. Nocturnal enuresis, Don't Forget the Bubbles, 2020. Available at:

Kristy is a 5-year old girl; her mother has brought her in due to her having started kindie. She has been invited to have a sleepover at a family friends house however she still wets the bed most nights of the week and is wondering about how to manage this.


Attaining continence – both daytime and nighttime – is a developmental milestone with a significant normal variation which is affected by both genetic and environmental factors.

At 5 years of age, approximately 15% of children continue to experience nocturnal enuresis (more commonly known as bedwetting). Every year beyond this, there is spontaneous resolution in ~15% of affected children (although it should be noted that the longer duration of NE, the lower the likelihood of spontaneous resolution).

Boys are more commonly affected than girls (2:1) and there is a strong family predisposition (both parents = 77%, single parent = 43%). Only one-third of those affected will seek medical attention.


What is nocturnal enuresis?

Nocturnal enuresis is episodes of urinary incontinence during sleep in children ≥5 years of age. It may be further subdivided into monosymptomatic (aka uncomplicated) and non-monosymptomatic (aka complicated or polysymptomatic).

  • Monosymptomatic: incontinence is present without other symptoms of lower urinary tract/gastrointestinal tract
  • Non-monosymptomatic: incontinence associated with other symptoms including but not limited to
    • Polyuria/oliguria (8/3 times per day respectively)
    • Urgency, hesitancy, intermittency
    • Straining/holding manoeuvres
    • Weak stream, dribbling
    • A feeling of incomplete emptying
    • Pain

When episodes additionally occur during the day, it is more appropriately referred to as diurnal enuresis/incontinence.

Incontinence should be classified as primary or secondary.

  • Primary: the child has never been dry
  • Secondary: the child has been dry for a period of at least 6 months


Why does nocturnal enuresis occur?

Nocturnal enuresis is the result of inappropriate emptying of the bladder by the child and is the result of a mismatch between the neurones of the bladder and the conscious state of the child. This may be due to a multitude of factors including:

  • Maturation delay
  • Genetic factors
  • Nocturnal polyuria – this may be due to fluid intake, reduced response to antidiuretic hormone (ADH) and/or reduced production of ADH
  • Disturbed sleep in the child (controversial)
  • Small bladder capacity
  • Detrusor overactivity

These factors may be primary to the child (eg. genetic factors) or secondary to an underlying condition (eg. polyuria secondary to undiagnosed diabetes insipidus)



How to evaluate a child with nocturnal enuresis?

It’s almost all in the history – search for red flags!


  • Onset
  • Previously dry?
  • Daytime symptoms (non-monosymptomatic NE)
  • Frequency, amount
  • Response to episodes
  • Fluid habits
  • Bowel habits
  • Sleep routines



  • Height/weight
  • BP
  • Tonsillar hypertrophy/adenoidal facies
  • Abdomen (distended bladder, faecal mass)
  • Spine
  • Lower limb neurology
  • Perianal/vulval inflammation (pinworms)


Do you need to do investigations?

Investigations are not necessary for all patients and should be guided by history and examination. Consider:

  • Blood sugar level (fingerprick)
  • Urinalysis (m/c/s, electrolytes)

Imaging and blood tests are not routinely indicated.


What are the treatment options?


Important things to remember in treatment:

  • Tricyclic medications are not recommended as they are less effective and have a higher risk of adverse effects
  • Intranasal desmopressin is not recommended due to the risk of hyponatraemia
  • There are high rates of relapse when desmopressin is discontinued (60 – 70%) therefore best used as a short term measure (eg. for going to camp) whilst awaiting spontaneous resolution
  • Desmopressin should not be used in those who are unable to adhere to fluid restrictions (due to risk of hyponatraemia)
  • Treatments with weak evidence include elimination diet, hypnosis, retention control (holding urine for progressively longer periods), biofeedback, acupuncture, scheduled awakenings, caffeine restriction


Take-home messages

  • It doesn’t require treatment in those under the age of 6
  • It is common  although undertreated despite treatment options (and families potentially being eligible for funding)
  • It is usually a primary disorder rather than secondary to an underlying medical condition (although maybe particularly exacerbated by constipation)
  • Investigations are not routinely required
  • Treatment requires a motivated family, with behavioural measures and bedwetting alarms being the first line of treatment.


Selected references

Tu, Baskin, Arnhym et al (2019) “Nocturnal Enuresis in Childre: Etiology and Evaluation”. UpToDate.

Tu, Baskin, FAAP (2019). “Nocturnal Enuresis in Children: Management”. UpToDate.

The Royal Childrens Hospital. (2019). “Enuresis – Bedwetting and Monosymptomatic Enuresis.” Melbourne. Retrieved from:

Thiedke C. “Nocturnal Enuresis”. American Family Physician (2003); April 1; 67(7): 1499 – 1506

Ramakrishnan K. “Evaluation and treatment of enuresis”. American Family Physician (2008); August 15; 78(4): 489 – 496.

Diabetes Insipidus

Cite this article as:
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?


Bottom Line

  • 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.


Biochemical abnormalities

  • 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%)


Selected references

Diabetes insipidus, Royal Children’s Hospital (Melbourne)

Diabetes insipidus, Medscape

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.

How to do the water deprivation test