Diabetes Insipidus

Original Editor - Rhiannon Clement
Top Contributors - Rhiannon Clement and Rucha Gadgil

Introduction[edit | edit source]

Diabetes is a greek work meaning "siphon", and inspidus is the latin for "no taste".

The term for diabetes was coined for patients who pass of more fluid than they consume (therefore siphon) [1]. The urine was tested for sweetness. In the case of sweet urine the condition was names diabetes mellitus (latin for honey), and is the result of excess sugar in the urine and blood. In history this would be determined by examining the colour, sediment, odour and even the taste of the urine[1].

In the case of diabetes insipidus there is an increase in urine production, but without the sweet taste.

Johann Peter Frank is credited with first making the distinction between diabetes mellitus and diabetes insipidus (DI)in 1794[2]. The two main symptoms as excessive thirst (polydipsia) and excessive urination (polyuria).

Since then, DI has been attributed to a dysfunction in the production or action of the hormone vasopressin (AVP), also known as anti-diuretic hormone (ADH), affecting the individual's kidneys ability to retain water. The human body is made up of around 60-70% water, with the brain needing around 70-80% water. The blood requires around 50% water in the circulation to safely balance salts in our body. Therefore, in sever cases, it can be dangerous to the individual if DI is not identified and treated correctly to prevent too much, or too little hydration.

The presence or development of DI can have an impact on the physiotherapy management and rehabilitation of individuals in a number of clinical areas, as discussed below.

Clinically Relevant Anatomy[edit | edit source]

The regulation of water in the blood is clinically important for regulating electrolytes and blood pressure. The video below by Khan Academy discusses hydration and blood osmolarity and the triggers that alert the brain of the need for production of ADH.

The video below focuses on endocrinology and the posterior pituitary gland. It discusses the trigger and release of both oxytocin and ADH.

Mechanism of Injury / Pathological Process[edit | edit source]

DI affects around 1 in 25,000 [3] people and can occur n either sex equally and at any age [4]. In 30% of cases, there is no known cause of DI.

Known causes of DI:[edit | edit source]

  • Genetics (defects to the AVPR2 gene)
  • Head injury
  • Infection
  • Loss of blood
  • Tumour
  • Brain surgery/ radiotherapy (up to 20% of people who have surgery on their pituitary gland develop signs and symptoms of DI. A small number may be permanent)
  • Hormone release during pregnancy

Types of DI:[edit | edit source]

DI can be nephrogenic (defected function of the kidneys) or craniogenic (defected function in the brain), or the result of electrolyte imbalances.

Nephrogenic DI (NDI)[edit | edit source]

Kidneys fail to recognise ADH. Can be defect with kidneys themselves or a genetic condition. Causes include:

  • Kidney disease
    • Can affect kidneys response to vasopressin. Polycystic kidney disease is most common.
  • Medication induced DI
    • E.g. lithium, foscarnet, clozaoine [4]
Craniogenic DI (CDI)[edit | edit source]
  • Dysfunction with production of hormones (such as ADH) at the hypothalamus or secretion from the pituitary gland.This can result from:
    • idiopathic causes
    • brain tumour
    • head injury
    • infection (such as TB, HIV, encephalitis or meningitis)
    • Brain malfunctions
    • surgery / radiotherapy
  • Gestational DI
    • Hormones released during pregnancy can interfere with, or even destroy vasopressin.
Electrolyte imbalances[edit | edit source]
  • Hypercalcemia
    • Too much calcium in the body interferes with communication between kidneys and vasopressin
  • Hypokalemia
    • Kidney cells, as all cell in the body, requires sufficient potassium to functions properly.

All types can range from mild to severe.

The video below illustrates the types of DI further, as well as discussing presentation, diagnosis and some medical management of the disease.

Clinical Presentation[edit | edit source]

Individuals may present with:

  • Polydipsia
  • Polyuria
  • hypernatremia ( increased sodium) in patients with increased urine output
  • Dehydration
  • Hypotension (low blood pressure)

Individuals who are medicated with vasopressin supplements (e.g. desmopressin) may be at risk of retaining water. Resulting presentation may be[5]:

  • Confusion
  • Disorientation
  • Nausea
  • Vomiting
  • hyponatremia
  • Hypertension
  • Inability to identify sensory information

In rare cases, over hydration can cause swelling in the brain, which can be fatal. Therefore, the fluid balance of individuals being medically managed needs to be closely monitored.

Diagnostic Procedures[edit | edit source]

A number of test can be used to diagnose DI and distinguish type:

  • Blood test for kidney function
  • Blood osmolality
    • Patient will have low urine osmolarity and high serum osmolarity.
  • Water deprivation test (desmopressin stimulation test)
Water Deprivation Test
Urine osmolarity After 8 hrs water depriation After ADH
Cranial DI Low High
Nephrogenic DI Low Low
Primary polydipsia High (test stopped as cannot be DI)

Outcome Measures[edit | edit source]

Due to the possible dangerous implications of an individual becoming dehydrated or overly hydrated, it is important to closely monitor the individuals hydration and fluid intake and output using some of the outcome measures below:[6] If the patient is medicated (e.g. with vasopressin supplement) they need to be closely monitored for over hydration.

Dehydration / Over hydration[edit | edit source]
  • Fluid balance
    • Chart oliguria (very low urine output) - patient could be retaining too much fluid
    • Polyuria (increased urine output)
    • Chart fluid intake
    • Numerical / visual rating scale for thirst
  • Weight loss
    • Possibly due to fluid loss
  • Blood pressure / cardiac changes
    • Dehydration can cause: low BP
    • Tachycardia
  • Changes to secretions
    • Dry oral mucosa
    • Increased secretions viscosity
  • Monitoring electrolytes (calcium levels and sodium levels)
    • Those who are not medicated may have high sodium levels. Signs may include:
      • cognitive dysfunction: confusion, lethargy, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks.
  • GCS / Alertness (if hydration status or electrolytes become deranged, this can impact on the individuals alertness)
    • GCS <8 has been independently associated with development of craniogenic DI [4]
    • Reduced alertness
    • Fatigue
  • Generalised weakness
    • Passive range of motion
    • Active range of motion
    • Oxford scale
    • Upper limb and lower limb functional assessment
  • Muscle spasms / pain
    • Numerical rating scale
    • visual rating scale

Management / Interventions[edit | edit source]

Medical Management

  • Correct underlying cause - e.g. balance electrolytes, treat kidney disease or infection

Mild cases may be managed conservatively

  • nutritional advice: eat a varied diet, drink fluids when thirsty, avoid diuretics (such as caffine and alcohol).

More severe cases may be medically managed

  • Desmopressin to replace reduced production in CDI, or to increase amount in NDI.

Nutritional advice:

The effective management of DI is important for the individuals participation in all areas of physiotherapy, including:

MSK / rehabilitation[edit | edit source]

Symptoms of fatigue, muscle pains and spasms and general weakness can have an impact on the individuals engagement in exercise and rehabilitation. Current advice suggests that patients should follow the ACSM advice on daily exercise, and for the individual to find an activity that they enjoy and will participate in regularly.

However, it is also very important that these patients are able to rehydrate effectively and have toilet facilities available to them.

It may be beneficial to direct patients towards resources, such a for information on access to toilet cards and further advice around managing their condition (see resources below). There are also support networks available for individuals, to meet others with this rare condition.

Oncology[edit | edit source]

Brain tumours can cause symptoms of diabetes insipidus, and in some individuals the symptoms of DI may be the first sign that something has changed. Individuals who present with DI will often have an MRI and frequent checkups to determine if a tumour might be a factor in the development of the disease.

Individuals may also experience symptoms of DI after radiotherapy, due to damage to cells.

Neurosurgery[edit | edit source]

This may also be the case after surgery to the brain.

An increase in the need to drink and urinate can be very uncomfortable for individuals and have an impact on their participation in activities of daily living. Therefore it is important that they have adequate ongoing support at home, such as the resources listen below.

Orthopaedics and head injury[edit | edit source]

Similarly, individuals can be affected by symptoms of DI after head injury.

Women's health and Pregnancy[edit | edit source]

Gestational DI occurs in about 1 in 30,000 pregnancies (42), due to degradation of AVP by the enzyme aminopeptidase[4]. This typically presents in the third trimester and resolves 2-3 weeks postpartum [4]. This is likely to be masked by other contributors to increased urine frequency and pelvic floor dysfunction.

Pre-eclapmptic toxaemia (PET) and haemolysis, elevated liver enzymes and low platelets (HELLP) can exacerbate diabetes insipidus due to a reduction in vasopressinase metabolism[7].

ICU / ward based therapy[edit | edit source]

Individuals on ICU who are sedated will be unable to tell anyone when they feel any of the symptoms above, therefore it is even more important to monitor objective signs of hydration. If they are taking desmopressin, this is particularly important, due to possible fatal effects of water intoxication.

Any deviation in hydration may impact on the patients respiratory function, e.g. thick and sticky secretions that are difficult to clear. Overdose of desmopressin itsef can cause difficulty in breathing.

Derangement in electrolytes can also limit patients ability to mobilise or participate in rehabilitation.

Paediatric[edit | edit source]

Children with acute injury to the nervous system and craniogenic DI have a high mortality [4]. DI occurs in 12.5% of individuals with blunt head injury, and 40.9% of patients with penetrating head injury.

Wolfram syndrome often results in DI and type 1 diabetes mellitus in children [4].

Particular symptoms in children might include fever, irritability, sleep disturbance, growth disturbances, failure to thrive [4].

Resources[edit | edit source]

The pituitary Foundation

Diabetes Insipidus.org

References[edit | edit source]

  1. 1.0 1.1 diabetes.co.uk
  2. Fitz R. A Case of Diabetes Insipidus Arch Intern Med (1914) XIV(5): 706-721
  3. Di Lorgi et al. Diabetes Insipidus - Diagnosis and Mangement (2012) Horm Res paediatr 77:69-84
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Kalra S. Diabetes Insipidus: The Other Diabetes Indian journal of Endocrinology and Metabolism (2016) 20(1):9-21
  5. Semeco M. What Happens if you Drink Too Much Water Medical News Today (2020) [Online: https://www.medicalnewstoday.com/articles/318619] <Accessed 31/10/20>
  6. Lukisch I. Hypernatremia Clinical Presentation Medscape 2018 [online: https://emedicine.medscape.com/article/241094-clinical#b1] <accessed 31/10/20>
  7. Quigley et al Diabetes Insipidus in Pregnancy. The Obstetrician and Gynaecologisy 2018 20:41-8