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Diabetes Insipidus

 

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Diabetes insipidus is a disorder of the posterior lobe of the pituitary gland due to a deficiency of vasopressin, the antidiuretic hormone (ADH). it is characterized by polydipsia and polyuria. Diabetes insipidus may be (1) secondary, related to head trauma, brain tumor, or surgical ablation or irradiation of the pituitary gland or infection of the central nervous system or metastatic tumors (lung or breast); (2) nephrogenic (faliure of the renal tubules to respond to ADH), possibly related to hypokalemia, hypercalcemia, and a variety of medications (eg, lithium, demeclocycline); (3) primary (hereditary), with symptoms possibly beginning t birth (defect in pituitary gland).

The disease cannot be controlled by limiting the intake of fluids because loss of high volumes of urine continues even without fluid replacement. Attempts to restrict fluids cause the patient to experience an insatiable carving for fluid and to develop hypernatremia and severe dehydration.

Clinical Manifestations

  • Polyuria: enormous daily output of very dilute urine (specific gravity 1.001 to 1.005). Primary diabetes insipidus may have ab abrupt onset or an insidious onset in adults.
  • Polydipsia: patient experiences intense thirst, drinking 2 to 20 liters of fluid daily, with a special craving for cold water.
  • Polyuria continues even without fluid replacement.

Assessment and Diagnostic Findings

  • Fluid deprivation test: fluids are withheld for 8 to 12 hours until 3% to 5% of the body weight is lost. Inability to increase specific gravity and osmolality of the urine during test is characteristic of diabetes insipidus.
  • Urine specific gravity, serum osmolality, and serum sodium levels may be obtained.

Medical Management

Objectives of the therapy are to ensure adequate fluid replacement, to replace vasopressin, and to search for and correct the underlying intracranial pathology. Treatment for diabetes insipidus of nephrogenic origin involves using thiazide diuretics, mild salt depletion, and prostaglandin inhibitors (eg. ibuprofen, indomethacin, and aspirin).

Vasopressin Replacement

  • Desmopressin (DDAVP), administered intranasally, 1 or 2 administrations daily to control symptoms.
  • Lypressin (Diapid), absorbed through nasal mucosa into blood; duration may be short for patients with severe disease.
  • Intramuscular administration of ADH (vasopressin tannate in oil) every 24 to 96 hours to reduce urinary volume (shake vigorously or warm; administer in the evening, rotate injection sites to prevent lipodystrophy)

Fluid Conservation

  • Clofibrate, a hypolipidemic agent, has an antidiuretic effect on patients who have some residual hypothalamic vasopressin.
  • Chlorpropramide (Diabinese) and thiazide diuretics are used in mild forms to potentiate the aciton of vasopressin; may cause hypoglycemic reactions.

Nursing Management

  • Encourage and support patient undergoing studies for possible cranial lesion.
  • Instruct patient and family members about follow-up care and emergency measures.
  • Advise patient to wear a medical identification bracelet and to carry medication information about the disorder at all times.
  • Use caution with administration of vasopressin if coronary artery disease is present because of vasoconstrictive action of this drug.

 

Reference:

Joyce Young Johnson et. al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition

Lippincott Williams & Wilkins pp.297-299

 

 

 

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Medical Surgical

Addison’s Disease (Primary Adrenocortical Insufficiency)

Wikipedia

Addison’s disease is caused by a deficiency of cortical hormone. It results when the adrenal cortex function is inadequate to meet the patient’s need for cortical hormones. Autoimmune or idiopathic atrophy of the adrenal glands is responsible for 80% to 90% of cases. Other causes include surgical removal of both adrenal glands or infection (tuberculosis or histoplasmosis) of the adrenal glands. Inadequate secretion of adrenocorticotrophic¬† hormone (ACTH) from the primary pituitary gland results in adrenal insufficiency. Symptoms may also result from sudden cessation of exogenous adrenocortical hormone therapy, which interferes with normal feedback mechanisms.

Clinical Manifestations:

Clinical manifestations include muscle weakness, anorexia, gastrointestinal symptoms, fatigue, emaciation, dark pigmentation of the skin and mucous membranes, hypotension, low blood glucose, low serum sodium and high serum potassium. The onset usually occurs with nonspecific symptoms. Mental changes (depression, emotional lability, apathy and confusion) are present in 60% to 80% of patients. In severe cases, disturbance of sodium and potassium metabolism may be marked by depletion of sodium and water and severe, chronic dehydration.

Addisonian Crisis

This medical emergency develops as the disease progresses. Signs and symptoms include:

  • Cyanosis, fever, and classic signs of circulatory shock: pallor, apprehension, rapid and weak pulse, rapid respirations, and low blood pressure
  • Headache, nausea, abdominal pain, diarrhea, confusion and restlessness
  • Slight overexertion, exposure to cold, and acute infections, decrease salt intake and may lead to circulatory collapse, shock and death
  • Stress of surgery or dehydration from preparation for diagnostic tests or surgery may precipitate addisonian or hypotensive crisis
  • Decreased blood glucose and sodium levels, increased serum potassium (hyperkalemia), and leukocytosis.

Assessment and Diagnostic Findings

Primary adrenocortical insufficiency:

  • greatly increased plasma ACTH (>22.0 pmol/L)
  • serum cortisol low normal or lower than normal (<165 nmol/L)
  • decreased blood glucose (hypoglycemia)
  • decreased sodium levels (hyponatremia)
  • increased serum potassium (hyperkalemia)
  • increased white cell count (leukocytosis)

Medical Management

Immediate treatment is directed toward combating shock.

  • Restore blood circulation, administer fluids, monitor vital signs, and place patient in a recumbent position with legs elevated
  • Administer intravenous hydrocortisone, followed by 5% dextrose in normal saline
  • Vasopressor amines may be required if hypotension persists
  • Antibiotics may be prescribed for infection
  • Oral intake may be initiated as soon as tolerated
  • If adrenal gland does not regain function, lifelong replacement of corticosteroids and mineralocorticoids is required
  • Dietary intake should be supplemented with salt during times of gastrointestinal losses of fluids through vomiting and diarrhea

NURSING PROCESS: The Patient with Addison’s Disease

Assessment

Assessment focuses on fluid imbalance and stress

  • Check blood pressure from a lying to standing position; check pulse rate
  • Assess skin color and turgor
  • Assess history of weight changes, muscle weakness, and fatigue
  • Ask patient and family about onset of illness or increased stress that may have precipitated crisis

Diagnosis

Nursing Diagnoses

  • Deficient fluid volume related to inadequate fluid intake and fluid loss secondary to inadequate adrenal hormone secretion
  • Deficient knowledge about need for hormone replacement and dietary modification

Collaborative Problems/Potential Complications

Addisonian crisis

Planning and Goals

Goals may include improving fluid balance, improving response to activity, decreasing stress, increasing knowledge about need for hormone replacement and dietary modifications, and ensuring absence of complications.

Nursing Interventions

Restoring Fluid

  • Record weight changes daily
  • Assess skin turgor and mucous membranes
  • Instruct patient to report increased thirst
  • Monitor lying, sitting, and standing blood pressures frequently
  • Assist patient in selecting, and encouraging patient to consume, food and fluids that assist in restoring and maintaining fluid and electrolyte balance (eg, foods high in sodium during gastrointestinal disturbances and very hot weather). Include a dietitian for added guidance.
  • Assist patient and family in learning to administer hormone replacement and to modify dosage during illness and stress
  • Provide written and verbal instructions about mineralocorticoid and glucocorticoid therapy.

Improving Activity Intolerance

  • Avoid unnecessary activities and stress that might precipitate a hypotensive episode
  • Detect signs of infection or presence of stressors that may have triggered the crisis
  • Provide a quiet, nonstressful environment during acute crises; carry out all activities for patient
  • Explain all procedures to reduce fear and anxiety
  • Explain rationale for minimizing stress during acute crisis

Monitoring and Managing Complications (Addisonian Crisis)

  • Assess for signs and symptoms of crisis: circulatory collapse and shock
  • Avoid physical and psychological stress, including exposure to cold, overexertion, infection, and emotional distress
  • Initiate immediate treatment with intravenous fluid, glucose, and electrolytes, especially sodium; corticosteroid supplements; and vasopressors
  • Avoid patient exertion; anticipate and take measures to meet patient’s needs
  • Monitor symptoms, vital signs, weight, and fluid and electrolyte balance to evaluate return to precrisis state
  • Identify factors that led to crisis

 

Reference:

Joyce Young Johnson et.al Handbook for Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 11th edition

Lippincott Williams & Wilkins pp; 21 – 24