Diabetes Insipidus

Question 1

What is Diabetes Insipidus?

Answer 1

1. A disorder of the POSTERIOR PITUITARY gland in which water loss is caused by either an antidiuretic hormone deficiency (ADH) or an inability of the kidney to respond to ADH.
   o The result of DI is the excretions of large volume of dilute urine because the distal tubules and collecting ducts do not reabsorb water; this leads to POLYURIA, DEHYDRATION and DISTURBED FLUID AND ELECTROLYTE IMBALANCE

Question 2

Causes of Diabetes Insipidus

Answer 2

1. Primary Neurogenic: caused by a defect in the hypothalamus or the pituitary gland resulting in a lack of ADH production or release
    If the posterior pituitary gland is not releasing enough ADH, the kidneys aren’t getting the signal to reabsorb the water
2. Secondary Neurogenic: result of tumors in or near the hypothalamus or pituitary gland, head trauma, infectious process or brain surgery
3. Nephrogenic: the posterior pituitary gland is doing its job fine releasing ADH, but there’s some problem in the kidneys and they are not responding to that signal
    The kidneys are not reabsorbing more water
    Could be due to kidney infection, or kidney damage (nephrotoxic medication)
4. Drug-related: caused by lithium carbonate and demeclocycline
    These drugs can interfere with the response of the kidneys to ADH

Question 3

Signs and Symptoms of Diabetes Insipidus

Answer 3

1. Key Symptoms:
   o Polyuria: excessive urination
   o Polydipsia: excessive thirst
2. Symptoms Related to Dehydration:
   o Cardiovascular:
    Hypotension
    Tachycardia
    Weak peripheral pulses
    Hemoconcentration
   o Kidney/Urine Symptoms:
    Increased urine output
    Dilute, low specific gravity
   o Skin Symptoms:
    Poor turgor
    Dry mucous membrane
   o Neurologic Symptoms:
    Decreased cognition
    Ataxia
    Increased thirst
    Irritability

Although increased fluid intake prevents serious volume depletion, the patient who is deprived of fluids or who cannot increase oral fluid intake may develop SHOCK from fluid loss

Question 4

History Assessment

Answer 4

1. Ask about a history of recent surgery, head trauma, or drug use (lithium)
    Although increased fluid intake prevents serious volume depletion, the patient who is deprived of fluids or who cannot increase oral fluid intake may develop SHOCK from fluid loss

Question 5

Diagnosis

Answer 5

1. 24-hour Fluid Intake and Output
   o 24-hour fluid intake and output is measured without restricting foods or fluid intake.
   o DI is considered if urine output is more than 4 L during this period and is greater than the volume ingested
   o Amount of urine excreted in 24 hours by patients with DI may vary from 4 to 30 L/day
   o Urine is dilute with a LOW SPECIFIC GRAVITY (less than 1.005) and LOW osmolarity (50 to 200 mOsm/kg) or LOW osmolality (50 to 200 mOsm/L)
2. Water Deprivation Test (Desmopressin Stimulation Test)
   o No drinking- (fluid deprivation) 8 hour
   o Give Desmopressin to assess response
   o Measure Urine after deprivation
   > Volume and Osmolality levels? (Normal or no)

Question 6

Laboratory

Answer 6

1. Specific gravity: will be very low, or under 1.005 (very diluted)
2. Urine Osmolarity: Very low because it’s DILUTED; under 200 (decrease sodium in urine)
3. Blood Osmolarity: Will be over 300
4. Sodium: Levels will be very high (HYPERNATREMIA)
5. BUN: Normal (if kidneys are functioning)
6. Creatinine: Normal (if kidneys are functioning)
7. pH: unchanged
8. ADH: released by the posterior pituitary gland in response to low blood volume in the body (low BP) or HYPERNATREMIA or increased blood osmolarity
   o ADH will cause the kidneys to reabsorb more water, which helps to bring up that BP, bring up blood volume and dilute the blood so that the blood osmolarity is back to normal level
   o DECREASED ADH

Question 7

Intervention: Drug Therapy

Answer 7

1. DESMOPRESSIN
    A synthetic form of vasopressin, replaces antidiuretic hormone (ADH) and decreased urination
    Given orally, sublingual or intranasally in metered spray
2. VASOPRESSIN
    Essentially the same as ADH
    If we give the patient vasopressin, we expect their kidneys to reabsorb water
    If we give vasopressin and the kidneys do not reabsorb water, then we know it a kidney problem and we have NEPHROGENIC DIABETES INSIPIDUS
3. Teaching
    Mild DI: only one or two doses in 24 hours
    Severe DI: one or two metered doses two or three times daily
    Severe Dehydration: ADH may be given IV or IM
    Ulceration of the mucous membranes, allergy, sensation of chest tightness, and lung inhalation of the spray occur with the use of INTRANASAL preparation
    If patient has an upper respiratory infection, ORAL or SUBCUTANEOUS vasopressin is used

Question 8

Intervention: Early Detection of Dehydration

Answer 8

1. Measure fluid INTAKE and OUTPUT
2. Check URINE SPECIFIC GRAVITY
3. DAILY WEIGHTS
4. Urge patient to drink fluids in an amount equal to urine output
5. If fluids are given IV (hypotonic solution; 0.45% saline), ensure the patency of the access catheter and accurately monitor the amount infused HOURLY

Question 9

Intervention: Lifelong Drug Therapy

Answer 9

1. The patient with permanent DI requires lifelong drug therapy
2. Check his or her ability to assess symptoms and adjust dosages as prescribed for changes in condition
3. Teach that polyuria and polydipsia indicate the need for another dose

Question 10

Intervention: Drug Therapy for DI induces Water Retention and can Cause Fluid Overload

Answer 10

1. Teach patient to weigh themselves daily to identify weight gain
2. Stress the importance of using the same scale and weighing at the same time of the day while wearing a similar amount and type of clothing
3. If weight gain of more than 2.2 lbs along with other signs of water toxicity (persistent headache, acute confusion, nausea, vomiting), instruct them to go immediately to the ER or call 911
4. Instruct the patient to wear a medical alert bracelet identifying the disorder and drug