Diabetes Insipidus

Original Editor - Rhiannon Clement
Top Contributors - Rhiannon Clement, Rucha Gadgil and Shaimaa Eldib

Introduction

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) . 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.

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. 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

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

DI affects around 1 in 25,000 people and can occur at any age. In 30% of cases, there is no known cause of DI.

Known causes of DI:

• 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:

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

Nephrogenic DI

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

Craniogenic DI

• 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

• 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

Individuals may present with:

• Polydipsia
• Polyuria
• hypernatremia ( increased sodium)
• Dehydration
• Hypotension (low blood pressure)

Diagnostic Procedures

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

An individuals hydration and fluid intake and output will need to be monitored closely.

add links to outcome measures here (see Outcome Measures Database)

Management / Interventions

add text here relating to management approaches to the condition

Resources

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