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Flashcards in Diseases and Conditions Deck (23):
1

Air bronchogram sign

air bronchogram sign

Radiographic appearance of an air-filled bronchus as it passes through an area of increased anatomic density, as in pulmonary edema and pneumonia.

2

Silhouette sign

Loss of the normal radiographic silhouette or contour.

Something normally visible is hidden because of an change in the density of the surrounding tissue.

3

Atelectasis, Taber's

Signs and symptoms, Treatment

A collapsed or airless condition of the lung.

Signs and symptoms
Symptoms may not be present if the atelectasis is minor and the patient has previously healthy lungs. Dyspnea is common when the atelectasis is severe.

Treatment
Treatment varies with the cause. The patient with atelectasis due to persistent ventilation with small tidal volumes is given lung expansion therapy such as incentive spirometry. During mechanical ventilation, the patient should receive appropriate tidal volume, and positive end-expiratory pressure (PEEP) to increase FRC. Oxygen should be administered at the lowest setting that will prevent hypoxemia. The patient should be weaned from the ventilator and extubated as soon as possible. The patient with atelectasis due to mucus plugging needs bronchial hygiene therapy to assist with mucus removal. Artificial surfactant may be useful for the infant with premature lungs and atelectasis.

4

Empyema, Taber's
Definition, causes, diagnosis

A collection of pus in a body cavity, esp. the pleural space.

Causes
The disease is usually caused by the local spread of infection from a pneumonia or lung abscess but may be caused by organisms brought to the pleural space via the blood or lymphatic system or an abscess extending upward from below the diaphragm. Streptococcus pneumoniae, Staphylococcus aureus, and Klebsiella pneumoniae are the most common pathogens, but anaerobic organisms also can cause empyema.

Diagnosis
Empyema may be diagnosed indirectly by chest x-rays, computerized tomography, magnetic resonance imaging, or definitively by thoracentesis (insertion of a large-bore needle into the pleural space). Withdrawal of fluid from the pleural space provides material for a culture and sensitivity test of the organism and helps the infection resolve.

5

Empyema, Taber's
Treatment

The purulent exudate and fluid are drained via thoracentesis, and one or more chest tubes is inserted to underwater-seal chest drainage with suction. Surgical removal of the thick coating over the lung (decortication) or rib resection may be required to allow open drainage and lung expansion. Standard dressing precautions are used if the patient has open drainage. Medications such as urokinase may be injected into the pleural space to minimize fibrous adhesions and to help keep the chest tube stay patent; surgical drainage may be necessary. Intravenous antibiotic therapy is administered based on pathogen sensitivity. Oxygen is administered to treat associated hypoxia. To

6

Decortication, Taber's
Pulmonary Decortication, Taber's

The stripping away of a restrictive membrane from the surface of an entrapped organ or structure.

Pulmonary decortication
Surgical removal of restrictive tissue from the visceral pleura. It is used to treat an entrapped lung, e.g., in patients who have a malignant pleural effusion.

7

Thoracentesis, Taber's

Before the procedure, the patient is carefully examined, a history is taken, and radiological studies, such as chest x-rays or ultrasonograms, are reviewed. The procedure should be explained to the patient and sensation information provided (stinging with anesthesia instillation). The risks (bleeding, puncture of the lung with subsequent lung collapse, or introduction of infection), as well as the benefits and alternatives to the procedure, should be carefully reviewed. If the patient wishes to proceed, a consent form with the patient's signature must be completed. Allergies to local anesthetics are noted. Baseline vital signs will be obtained and supplemental oxygen administered. Cardiac monitoring is usually performed. A nurse or respiratory therapist may assist the physician and support the patient throughout the procedure. Equipment is assembled for the procedure, and, in most instances, the fluid is identified with ultrasound to avoid injury to the liver, lung, or other tissues. The patient is positioned to make pleural fluid accessible to the examiner.

The patient's skin is prepared per protocol, the area is draped, and local anesthesia is injected subcutaneously. After allowing a short time for this to become effective, the thoracentesis needle is inserted above the rib to avoid damaging intercostal vessels, which run in a neurovascular bundle beneath each rib. The patient is advised not to move, cough, or take a deep breath during the procedure to reduce the risk of injury. When the needle contacts the fluid pocket, fluid can be withdrawn by gravity drainage or with suction. When indicated after removal of the thoracentesis needle or cannula, a larger bore thoracostomy tube may be inserted to provide additional drainage.

During thoracentesis, health care professionals should assess the patient for difficulty in breathing, dizziness, faintness, chest pain, nausea, pallor or cyanosis, weakness, sweating, cough, alterations in vital signs, oxygen saturation levels, or cardiac rhythm. An occlusive dressing should be applied to the puncture site as the needle or cannula is removed, preventing air entry. The fluid obtained is labeled and sent for diagnostic tests as ordered (typically Gram stain, cultures, cell count, measurements of fluid chemistries, pH, and, when appropriate, cytology). The amount, color, and character of the fluid is documented, along with the time of the procedure, the exact location of the puncture, and the patient's reaction. After the procedure, a chest x-ray is often obtained to assess results or determine if any injury has occurred, e.g., pneumothorax. The patient should be positioned comfortably. Vital signs are monitored until stable, then as needed. The patient is advised to call for assistance immediately, if difficulty in breathing or pleuritic pain is experienced.

8

ARDS, Taber's

Definition, etiology

Acute Respiratory Distress Syndrome

Respiratory insufficiency marked by progressive hypoxemia due to severe inflammatory damage causing abnormal permeability of the alveolocapillary membrane. The alveoli fill with fluid, which interferes with gas exchange.

Etiology
ARDS may result from direct trauma to the lungs, e.g., near drowning, aspiration of gastric acids, severe lung infection or systemic disorders, e.g., shock, septicemia, disseminated intravascular coagulation (DIC) cardiopulmonary bypass, or reaction to blood transfusions. Widespread damage to the alveolocapillary membranes is initiated through the aggregation and activity of neutrophils and macrophages and the activation of complement. Cytokines, oxygen-free radicals, and other inflammatory mediators damage the walls of capillaries and alveoli, producing diffuse inflammatory interstitial and alveolar edema, fibrin exudates, and hyaline membranes that block oxygen delivery to the blood.

9

ARDS, Taber's

Diagnosis, symptoms, prognosis

Diagnosis
Diagnosis is based on a history of a recent event associated with the onset of ARDS, the presence of noncardiogenic pulmonary edema on the chest radiograph, and persistent hypoxemia and a PaO2/FIO2 ratio of

10

ARDS, Taber's

Treatment

Treatment
Endotracheal intubation, mechanical ventilation with positive end-expiratory pressure (PEEP), supplemental oxygen, and tidal volumes of 4 to 8 ml/kg optimize respiratory outcomes. PEEP increases intrathoracic pressure, keeping alveoli open during exhalation. This reduces the pressure required to open alveoli during inhalation, improves gas exchange, and reduces oxygen need. The patient should be monitored and treated for acidosis, cardiac arrhythmias, DIC, oxygen toxicity, renal failure, and sepsis.

11

ARDS, Taber's

Patient care

To avert ARDS, respiratory status must be monitored in at-risk patients. Recognizing and treating early signs and symptoms can be crucial to a patient's survival. Ventilation rate, depth, and rhythm must be monitored and subtle changes noted. The onset of ARDS is marked by the onset of a rapid, shallow breathing pattern, and pulse oximetry must be monitored continuously for subtle changes. If shock ensues and blood is shunted away from body surfaces, resulting in cool skin, O2 readings may become inaccurate, necessitating use of arterial blood gas monitoring for respiratory alkalosis (early) and mixed metabolic and respiratory acidosis (later). Serial chest x-rays should be obtained to assess for bilateral consolidation progressing to lung “whiteout.” The patient must also be observed for chest wall retractions on inspiration, use of accessory breathing muscles, and level of dyspnea. The patient's consciousness level, cardiac rate and rhythm, blood pressure, arterial blood gas (ABG) values, serum electrolyte levels, and chest radiograph results must be monitored. Fluid balance must be closely watched by 1) measuring intravenous (IV) fluid intake, urinary output, and central venous pressure; 2) weighing the patient daily; and 3) assessing for peripheral edema. A patent airway must be maintained, and oxygen therapy with continuous positive airway pressure or mechanical ventilation with PEEP must be provided by the respiratory therapist as prescribed by the attending physician. Routine management of a mechanically ventilated patient includes 1) monitoring breath sounds, chest wall movement, vital signs and comfort, and ventilator settings and function; 2) suctioning the endotracheal tube and oropharynx; and 3) assessing changes in pulse oximetry and ABG values.

Cardiac output may be decreased because PEEP increases intrathoracic pressure and reduces venous return. For this reason, health care professionals must monitor blood pressure, urine output, mental status, peripheral pulses, and pulmonary capillary wedge pressure to determine the effects of positive-pressure ventilation on hemodynamics. Inotropic drugs must be administered as prescribed if cardiac output falls. Hemoglobin levels and oxygen saturation values must also be monitored closely because packed red blood cell transfusion may be required if hemoglobin is inadequate for oxygen delivery. The nurse and respiratory therapist (RT) must observe for signs and symptoms of barotrauma, e.g., subcutaneous emphysema, pneumothorax, and pneumomediastinum. If mechanical ventilation is used, sedation may help calm the patient and reduce the incidence of poor synchronization between the patient and the ventilator. Nutritional support should begin early to promote pulmonary cell regeneration and to provide proteins needed for successful weaning from a ventilator. Enteral nutrition is preferred over parenteral because it reduces the risk of infection. A formula that is lower in carbohydrates helps decrease CO2 formation during metabolism in ARDS patients retaining CO2. Fluid replacement should maintain sufficient circulating volume without causing overhydration as determined by central venous pressure readings. Nursing measures must be used to prevent problems of immobility. Prone positioning may be prescribed to improve oxygenation while lessening the risk of barotrauma, but it complicates some elements of nursing care. Prone positioning, if prescribed (usually for 4 to 6 hours daily), is often labor-intensive and requires several staff members to position the patient and therefore is best accomplished on day shift when more staff are available in an emergency. To limit the patient's fear and isolation, the procedure should be explained to the patient, assuring him or her of its safety. Sedation or analgesia are prescribed 30 to 60 minutes before turning the patient on his or her abdomen. To reduce compression of the lungs by the heart and mediastinum, a specialty bed may be used, or a pronator device (a padded metal frame that is placed against the patient's chest and abdomen, with belt buckles that secure and protect the head, chest, and abdomen during the procedure) is strapped to the patient. To use this device, the side rails on the patient's bed are lowered, and the patient is pulled close to the edge of the bed farthest from the ventilator. The patient's face is turned away from the ventilator, his or her arm tucked under the body, and the leg farthest from the ventilator crossed over the other leg at the ankle to aid in turning the patient. The patient can then be turned by one staff member on each side of the bed and one (usually an RT) at the head, who protects the endotracheal tube, IV lines, and other attachments. The prone patient's blood pressure and heart and respiratory rates must be closely monitored for evidence of position tolerance, and the RT may confirm correct endotracheal tube position by capnography. Vital signs should return to baseline within 5 min after prone positioning, repositioning the patient in the supine position if there is any drop in O2 saturation, deterioration in ABG results, or uncontrollable patient anxiety. Once in the prone position, the patient's feet and elbows should be padded to prevent pressure injuries. The patient's head should be repositioned every hour to prevent necrosis of facial skin and to provide oral care and airway suctioning. Range of motion exercises should be performed at least every 2 hr. The patient should be repositioned to the supine position after 4 or 6 hr, as prescribed. Strict asepsis must be observed in dressing changes, suctioning, hand hygiene, and oral care. The patient must be routinely assessed for fever, changes in sputum color, and elevated white blood cell count. Response to therapy must be evaluated and adverse reactions noted. The family must be encouraged to talk to the patient even though he or she may not be able to respond verbally.

Respiratory therapists play a key role in the care of patients with ARDS. They initiate mechanical ventilation as prescribed by the attending physician and monitor arterial blood gases and pulse oximetry to ensure adequate oxygenation. They adjust the tidal volume, respiratory rate, and PEEP levels to optimize tissue oxygenation. They also help determine when the patient may be ready for weaning from mechanical ventilation by periodic assessment of the patient's cardiopulmonary status.

12

Emphysema, Taber's

Definition, etiology

1. Pathological distention of interstitial tissues by gas or air. The distention can be palpated or seen radiographically. Causes include leaking tracheostomy tubes or open pneumothoraces.
2. A chronic obstructive pulmonary disease marked by an abnormal increase in the size of air spaces distal to the terminal bronchiole, with destruction of the alveolar walls. These changes result in a loss of the normal elastic properties of the lungs and difficulty exhaling air. Alveolar septa are destroyed, and portions of the capillary bed are eliminated. Residual volume increases.

Etiology
Tobacco smoking is the most common cause of the tissue destruction found in emphysema. Exposure to environmental dust, smoke, or particulate pollution may also contribute to the disease. A small number of people with emphysema may have developed it as a result of alpha-1-antitrypsin deficiencies, a group of genetic illnesses in which there is inadequate protection against destructive enzyme activity in the lung. Complications include cor pulmonale, recurrent respiratory infections, and respiratory failure.

13

Emphysema, Taber's

Patient care

The patient's oxygenation, weight, and the results of electrolyte and complete blood count measurements are monitored. The patient is evaluated for infection and other complications and for the effects of the disease on functional capabilities. Prescribed medications are administered by parenteral or oral route or by inhalation.

The patient is encouraged to intersperse normal activities with rest periods. Respiratory infections may be devastating to the emphysema patient; some of them can be prevented by avoiding crowds and contact with infectious persons; by using correct pulmonary hygiene procedures, including thorough hand hygiene; and by obtaining influenza and pneumococcal immunizations. Patients are taught breathing techniques to control dyspnea. Frequent small meals of easy-to-chew, easy-to-digest, high-calorie, high-protein foods and food supplements are encouraged. Small meals conserve patient energy, prevent fatigue, and also reduce intra-abdominal pressure on the diaphragm and reduce dyspnea.

When patients with emphysema are hospitalized, the respiratory therapist and physician monitor the results of arterial blood gas assays, pulmonary function studies, and breath sounds. Once stabilized, the patient often benefits from participation in a pulmonary rehabilitation program to promote improved lung function and more efficient breathing techniques. The

14

Collapse versus atelectasis

In general, the term collapse is used to describe a markedly decreased lung, lobe, or segment volume.

Atelectasis is often used to describe less severe changes.

Fuzzy and interchangeable terms.

15

Bronchiectasis, Taber's

Chronic dilation of a bronchus or bronchi, usually in the lower portions of the lung, caused by the damaging effects of a long-standing infection.

Causes
The condition may be acquired or congenital and may occur in one or both lungs. Bronchiectasis has three forms (cylindrical, varicose, and saccular), which may occur individually or together. Acquired bronchiectasis usually occurs secondary to an obstruction or an infection such as bronchopneumonia, chronic bronchitis, tuberculosis, cystic fibrosis, or whooping cough. The incidence has decreased with antibiotic treatment of acute infections.

Signs and Symptoms
Chronic cough, foul-smelling, mucopurulent, or bloody sputum, fever, shortness of breath, wheezing, and malaise are common symptoms and signs.

Diagnosis
Radiography is used to confirm the diagnosis. High-resolution lung CT reveals abnormal widening of small and medium-sized bronchi with mucosal thickening.

16

Pulmonary fibrosis, Taber's

The formation of scar tissue in the parenchyma of the lungs, following inflammation of the alveoli. The disease results in difficulty breathing caused by impaired gas exchange.

SYN: diffuse interstitial pulmonary fibrosis; pulmonary fibrosis; Hamman syndrome

SYMPTOMS AND SIGNS
Dyspnea, cough, exertional fatigue, and generalized weakness are common. Signs of the illness include pulmonary crackles, finger clubbing, cyanosis, and evidence of right ventricular failure (such as lower-extremity swelling). The disease typically progresses to end-stage lung disease and death within 7 years of diagnosis.

DIAGNOSIS
A biopsy of the lung is needed to make the diagnosis.

TREATMENT
Corticosteroids (such as prednisone) may be helpful in 10% to 20% of patients. Lung transplantation can be curative if a donor organ is available.

17

Pulmonary fibrosis can be localized or generalized, give examples of each

Localized: tuberculous scarring, radiation fibrosis

Generalized: silicosis, sarcoidosis

Pulmonary fibrosis results in diminution of volume.

18

Cicatrization atelectasis

(sĭk″ă-trĭ-zā′shŭn)

Healing by scar formation.

Atelectasis due to scar formation, usually due to radiation.

19

Adhesive atelectasis

Atelectasis due to diminished surfactant.

Respiratory distress syndrome of the newborn causes profound generalized atelectasis caused by surfactant deficiency.

20

Hypoventilation atelectasis

Hypoventilation atelectasis is frequent after general anesthesia or heavy sedation. It most often involves the lung base or causes generalized decrease in lung volume.

21

Goodpasture's Disease

This patient likely has Goodpasture's (anti-glomerular basement membrane) disease. Diffuse "ground glass" regions are visible within the lungs on the CT, consistent with alveolar hemorrhage (which is in agreement with the patient's history of hemoptysis). Goodpasture's disease is characterized by autoantibodies against collagen type-IV, resulting in damage to the kidney and lung. Renal biopsy may be used to visualize the antibodies on the basement membrane (useful for diagnosis), where anti-collagen type-IV IgG will smoothly label the entire glomerular membrane (this is in contrast to the puncta visible with immune deposits in diseases like post-infectious glomerulonephritis). Renal biopsies may also be used to determine the extent of kidney damage (useful for prognosis and management).

Anti-collagen type-IV antibody serology is the definitive confirmation of the diagnosis. Chest MRI, lung function tests, and creatine clearance test are unnecessary because the presence of anti-GBM antibodies is highly determinant of the immune-mediated nature of the disease.

Major Takeaway:
Goodpasture's disease is characterized by autoantibodies against type-IV collagen, resulting in damage to the lung and kidney. Definitive diagnosis may be made by detection of these antibodies. Nonetheless, renal biopsies are useful to confirm diagnosis and determine severity of renal injury.

22

ANCA-positive vasculitis

The correct answer is ANCA (Antineutrophil cytoplasmic antibody)-positive vasculitis because the disease presents with acute glomerulonephritis and pulmonary hemorrhage (causing the cough and hemoptysis in the patient)

23

Goodpasture's Treatment

Plasmapheresis combined with prednisone and cyclophosphamide

This patient has Goodpasture syndrome, an autoimmune disease that targets a certain site (alpha-3 chain of type IV) of collagen in the lungs and kidneys. Pulmonary symptoms, which often occur first, include cough, shortness of breath, and hemoptysis. Renal symptoms include hypertension, hematuria, proteinuria, and peripheral edema. Other findings consistent with Goodpasture syndrome include presence of anti-glomerular basement membrane (GBM) antibodies, as well as glomerulonephritis.

The goal of treatment is to mitigate activity of anti-GBM antibodies. The recommended treatment for Goodpasture syndropopme is plasmapheresis combined with immunosuppressive medications, namely prednisone and cyclophosphamide. Plasmapheresis removes anti-GBM antibodies and other mediators of inflammation (such as complement), while immunosuppressive agents minimize new antibody formation.