Diabetes insipidus

The inability to produce concentrated urine due to either antidiuretic hormone deficiency or resistance, which leads to extreme thirst and polyuria. The diagnosis may be confirmed using a water deprivation test.

How long is the history of thirst or polyuria? 

Sudden onset is typical with central DI, though familial nephrogenic DI presents in early childhood and psychogenic polydipsia may have a very long history.

Does the patient complain of excessive thirst? 

Diabetes insipidus is typified by unquenchable thirst for any fluid, with polyuria and nocturia.

What do they like to drink and what volumes are involved? 

Ask specifically whether the patient prefers certain drinks for example tea or coffee. This is common with habitual drinking, whereas in diabetes insipidus the thirst is for any available liquid - usually water.

Habitual over-drinking or psychogenic polydipsia may in time lead to chronic dilution and loss of collecting tubule concentrating capacity. This mimics the biochemistry of DI and may require a formal water deprivation test to elucidate. 

Arrange for the patient to keep a diary of their intake prior to attending clinic. This is useful to quantify the volumes involved at first assessment.

Do they drink at night or at particular times? 

Ask whether they take a glass of water to bed with them, how large it is and whether they drink this in one go, or just sip it during the night. Patients with DI will drink very large volumes and tend to finish a glass in one gulp rather than sipping it over a period of time.

Patients who drink habitually may drink in certain situations for example when bored or anxious, but do not tend to drink when busy, or during the night.

Do they get up at night either to drink or to pass urine? 

Ask the patient exactly what it is that wakes them. If they drink immediately on waking, before using the toilet, this is typical of DI. If they wake to use the toilet, and then have a drink afterwards, this is less indicative of DI.

How many times do they get up at night to pass urine and what volumes are involved? 

Prostate pathology may lead to nocturia though volumes are low and other symptoms are usually obvious. Nocturia in DI typically involves very large volumes but passes in a smaller number of visits.

Do they have any prostatic symptoms? 

Patients with prostatic hyperplasia may present with nocturia but also tend to complain of poor stream and other obstructive symptoms.

Does the thirst occur at any particular times of day? 

In patients already taking replacement therapy, nasal desmopressin tends to control symptoms for approximately 16 hours.

Symptoms occurring before this time require an increase in the size or frequency of desmopressin dose.

Is there any history of head injury? 

DI occasionally occurs following head injuries.

Does the patient suffer with extreme anxiety or have a psychiatric history? 

Psychogenic polydipsia is more common in patients with anxiety and other psychiatric disorders.

Is the patient known to have pituitary or neurological disease? 

Central DI is commonly seen with peripituitary disease, or after surgery for intrinsic pituitary tumours.

DI may also occur with structural neurological lesions, for example septo-optic dysplasia.

Has the patient developed visual symptoms, a headache or neuralgia? 

Loss of acuity or failing vision at night are worrying features suggesting optic nerve involvement. Visual field loss, for example homonymous hemianopia, indicates chiasmal impingement from a pituitary or peripituitary lesion. 

Headaches present on waking and worse on coughing or leaning forward are suggestive of increased intracranial pressure which demands urgent imaging with an MRI scan. Pain across one section of the head or face only, are more suggestive of cranial nerve involvement particularly with disease in the cavernous sinus.

Has the patient lost or gained weight? 

Weight loss may indicate the development of hypopituitarism but should also alert the clinician to the possibility of malignant disease, germ cell tumours or peri-pituitary metastases.

Does the patient feel well in themselves? Have they noticed a loss of energy, fatigue, nausea or dizziness? 

Vague symptoms of tiredness, nausea and dizziness may indicate the development of hypopituitarism with ACTH or TSH deficiency.

Has there been any change in bowel habit? 

This could indicate the possibility of underlying malignancy or a loss of thyroid function.

Has there been any change in menstrual cycle or any new hot flushes? 

Oligomenorrhoea may occur with modest elevations of prolactin.

Amenorrhoea and hot flushes indicate loss of the gonadotropin release.

Has the patient's libido changed, or have they developed erectile dysfunction? 

Loss of libido may have many causes but in this circumstance suggests a loss of gonadotropin release.

Symptoms of erectile dysfunction may not be forthcoming and should be specifically asked about, as should early morning erections.

Are there any features to suggest underlying malignancy or connective tissue disorder? 

DI does not tend to occur with intrinsic pituitary disease. Stalk dysfunction may occur in isolation or with para sellar lesions such as germ cell tumours and metastases. DI may also occur when granulomatous and inflammatory conditions affect the posterior pituitary such as Wegener’s granulomatosis, sarcoidosis, tuberculosis or auto-immune disease.

Hypercalcaemia may also occur in malignancy and cause nephrogenic DI.

Are there features to suggest elevated prolactin? 

Hyperprolactinaemia is common with non-functioning and para-sellar tumours due to disinhibition of prolactin release.

Ask about breast swelling, galactorrhoea, oligomenorrhoea, libido and erectile function.

Are they taking any prescribed or non-prescribed medications? 

Lithium is a common cause of nephrogenic DI.

Diuretics may also complicate the presentation and history, and can lead to hypokalaemia leading to transient loss of concentrating capacity and nephrogenic DI.

Indigestion remedies and dietary supplements may be associated hypercalcaemia which may also lead to nephrogenic DI.

Is there a family history of DI?

There are various forms of familial nephrogenic DI which tend to present in infancy.