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Pulmonary Emphysema

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Pulmonary emphysema is defined as a nonuniform pattern of abnormal, permanent distention of the air spaces  with destruction of the alveolar walls and eventually a reduced pulmonary capillary bed. It appears to be the end stage of a process that has progressed slowly for many years. Smoking is the major cause. In a few patients, there is familial predisposition associated with a plasma protein abnormality ( deficiency in alpha-1 antitrypsin), making the person sensitive  to environmental factors ( air pollution, infectious agents, allergens). Emphysema  manifests commonly in the fifth decade of life and is classified as follows:

  • Panlobular (panacinar): characterized by destruction of respiratory bronchiole, alveolar duct, and alveoli; air spaces within the lobule are enlarged  with little inflammatory disease.
  • Centrilobular (centriacinar): cause pathologic changes in the center of the secondary lobule, producing chronic hypoxemia, hypercapnia, polycythemia, and episodes of right-sided heart failure.

Both types of emphysema can occur together.  

Clinical Manifestations

  • Dyspnea with insidious onset progressing to severe dyspnea with slight exertion (major symptom)
  • Chronic cough, hyperinflated “barrel chest” due to air trapping, muscle wasting, and pursed-lip breathing
  • On ausculatation, diminished breath sounds with crackles, wheezes, rhonchi, and prolonged expiration.
  • Hyperresonance with percussion and a decrease in fremitus .
  • Anorexia, weight loss, weakness, and inactivity.
  • Hypoxemia and hypercapnia, morning headaches in advanced stages.
  • Inflammatory reactions and infections from pooled secretions.

Assessment and Diagnostic Method Evaluation entails primarily chest x-rays,  chest computed tomography CT) scans, pulmonary function tests, pulse oximetry, blood gases, and complete blood count.

Complications Right-sided heart failure  (cor pulmonale) leading to central cyanosis and respiratory failure

Medical ManagementThe major goals of medical management are to improve quality of life, slow progression of the disease, and treat obstructed airways to relieve hypoxia. Treatment is directed at improving ventilation, decreasing work of breathing and preventing infection.

  • Smoke cessation
  • Physical therapy to conserve and increase pulmonary ventilation
  • Maintenance of proper environmental conditions to facilitate breathing
  • Psychological support
  • Ongoing program of patient education ans rehabilitation
  • Bronchodilators and metered-dose inhalers (aerosol therapy, dispensing particles in fine mist)
  • Treatment of infection (antimicrobial therapy at the first sign of respiratory infection).
  • Oxygenation in low concentrations for severe hypoxemia

Reference: Joyce Young Johnson, Brunner & Suddarth’s Textbook for Medical-Surgical Nursing 11th edition Lippincott Williams & Wilkins pp. 331-333

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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