Diabetes Insipidus

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Definition

Diabetes insipidus is a disorder of the posterior lobe of the


pituitary gland characterized by a deficiency of antidiuretic
hormone (ADH), or vasopressin.

Great thirst (polydipsia) and large volumes of dilute urine


characterize the disorder.
Types of Diabetes insipidus
A) Central diabetes insipidus
B) Nephrogenic diabetes insipidus
Causes
Central diabetes insipidus
• Head trauma or surgery
• Pituitary or hypothalamic tumor
• Intracerebral occlusion or infection
Nephrogenic diabetes insipidus
• Systemic diseases involving the kidney
• Multiple myeloma
• sickle cell anemia
• Polycystic kidney disease
• Pyelonephritis
• Medications such as lithium
Pathophysiology
Central diabetes insipidus
Loss of vasopressin-producing cells

Causing deficiency in antidiuretic hormone (ADH) synthesis or release

Deficiency in ADH, resulting in an inability to conserve water, leading


to extreme polyuria and polydipsia
Nephrogenic diabetes insipidus

• Depression of aldosterone release or inability of the nephrons


to respond to ADH, causing extreme polyuria and polydipsia
Signs and symptoms
• Polyuria with urine output of 5 to 15 L daily Polydipsia,
especially a desire for cold fluids

• Marked dehydration, as evidenced by dry mucous


membranes, dry skin, and weight loss

• Anorexia and epigastric fullness

• Nocturia and related fatigue from interrupted sleep


Diagnostic test

1. High serum osmolality, usually above 300 mOsm/kg of water


Low urine osmolality, usually 50 to 200 mOsm/kg of water

2. low urine-specific gravity of less than 1.005

3. Increased creatinine and blood urea nitrogen (BUN) levels


resulting from dehydration

4. Positive response to water deprivation test: Urine output


decreases and specific gravity increases
Protocol (Phase 1):
• The test should be initiated at 10 PM at which time serum and urine
specimens are collected for the determination of sodium and
osmolality. The patient should also be weighed at this time. No oral
intake is allowed until the test is terminated.
• At 6 AM, the following morning, the patient should be weighed
again. Weight should be measured and urine should be collected
hourly for measurement of volume and determination of osmolality.
• Once urine osmolality becomes stable (a change <30 mOsm/kg for
two consecutive hours) specimens are collected for serum sodium,
osmolality, and ADH levels.
Protocol (Phase 2):
• Five units of aqueous vasopressin (ADH) is given
subcutaneously, and urine osmolality is measured one
hour later. The test can then be terminated.
Goals of management
The objectives of therapy are :
(1)To replace ADH (which is usually a long-term therapeutic
program)
(2) To ensure adequate fluid replacement
(3) To identify and correct the underlying cause
Treatments
• Replacement vasopressin therapy with intranasal or I.V.
desmopressin acetate
• Correction of dehydration and electrolyte imbalances
• Administration of thiazide diuretics to deplete sodium
and increase renal water reabsorption
• Restriction of salt and protein intake
Nursing management
Nursing Assessment
• Polyuria of 4 to 24 L per day
• Polydipsia
• Dehydration
• Decreased skin turgor, dry mucous membranes
• Inability to concentrate urine
• A low urinary specific gravity: 1.006 or less
• Fatigue
• Muscle pain and weakness
• Headache
• Postural hypotension that may progress to vascular collapse
without rehydration
• Tachycardia
Nursing Interventions
• Monitor vital signs and neurological and cardiovascular status.

• Monitor electrolyte values and for signs of dehydration.

• Monitor intake and output, weight, and specific gravity of urine.

• Maintain the intake of adequate fluids, and monitor for signs of


dehydration.
• Instruct the client to avoid foods or liquids that produce diuresis.

• Administer vasopressin or desmopressin acetate as prescribed ,

these are used when the ADH deficiency is severe or chronic. may
be administered by injection, intra nasally, or orally).

• Instruct the client to wear a Medic-Alert bracelet.

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