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 n either sex equally and 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 (NDI)

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

Craniogenic DI (CDI)

• 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) in patients with increased urine output
• 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

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:

Dehydration / Over hydration

Fluid balance

• Oliguria (very low urine output)
• Increased thirst

Weight loss

• Possible 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
• Reduced alertness
• Fatigue

Generalised weakness

Muscle spasms / pain

Management / Interventions

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

Medical Management

• Correct underlying cause

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.

MSK / rehabilitation

Current advice suggests that patients should follow the ACSM

Women's health

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

Paediatric:

Children with acute injury to the nervous system and craniogenic DI have a high mortality . 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 .

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

Nutrition advice

Resources

add appropriate resources here