5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

6CO, Cardiac output; CI, cardiac index; CVP, central venous pressure; LVSWI, left ventricular stroke work index; , mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

Radiologic Findings

Chest Radiograph

•Increased translucency (darker lung fields) on the side of pneumothorax

•Mediastinal shift to unaffected side in tension pneumothorax

•Depressed diaphragm on the affected side

•Lung collapse

•Atelectasis

Ordinarily, the presence of a pneumothorax is easily identified on the chest radiograph in the upright posteroanterior view. A small collection of air is often visible if the exposure is made at the end of maximal expiration because the translucency of the pneumothorax is more obvious when contrasted with the density of a partially deflated lung. The pneumothorax is usually seen in the upper part of the pleural cavity when the film is exposed, while the patient is in the upright position. Severe adhesions, however, may limit the collection of gas to a specific portion of the pleural space. Fig. 23.9A shows the development of a tension pneumothorax in the lower part of the right lung. Fig. 23.9B shows progression of the same pneumothorax 30 minutes later. Fig. 23.10 shows the classic body shape of a 19-year-old man who is 6 feet 5 inches tall and who experienced a spontaneous left-sided pneumothorax while playing a round of golf.

FIGURE 23.9 (A) Development of a small tension pneumothorax in the lower part of the right lung (arrow). (B) The same pneumothorax 30 minutes later. Note the shift of the heart and mediastinum to the left away from the tension pneumothorax. Also note the depression of the right hemidiaphragm (arrow).

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FIGURE 23.10 (A) A 19-year-old male patient, 6 feet 5 inches tall, who experienced a sudden spontaneous left-sided pneumothorax while playing a round of golf. A spontaneous pneumothorax is not uncommon in people who are tall and thin. (B) Chest radiograph of the same patient 45 minutes later in the emergency department. Note the slight shift of the heart and mediastinum to the right (toward the unaffected side), away from the tension pneumothorax, and the markedly depressed diaphragm on the patient's left side.

Fig. 23.11 shows a pneumothorax caused by a gunshot wound to the upper left chest/shoulder area.

(A) Fragments of a bullet faintly seen (white dots) in the upper left chest/shoulder area (see red arrow). (B) Four hours later, the patient clearly revealed a left pneumothorax (see red arrow). Note the increased radiodensity of the left upper lung suggesting the presence of compression atelectasis of the left upper lobe.

Faught.)

General Management of Pneumothorax

The management of pneumothorax depends on the degree of lung collapse. When the pneumothorax is relatively small

(15% to 20%), the patient may need only bed rest or limited physical activity. In such cases, reabsorption of intrapleural gas usually occurs within 30 days.

When the pneumothorax is larger than 20%, it should be evacuated. In less severe cases, air may simply be withdrawn from the pleural cavity by needle aspiration. In more serious cases, a thoracostomy chest tube attached to an underwater seal is inserted into the patient's pleural cavity. Because air rises, the tube is usually placed anteriorly near the lung's apex, above the rib to avoid injury to the vessels and nerves that run under the ribs in the costal grooves. Typically, a no. 28 to 36 gauge French thoracostomy tube is used for adults, with smaller sizes used for children. The tube permits evacuation of air and enhances the reexpansion and pleural adherence of the affected lung. The chest tube may or may not be attached to gentle suction. When suction is used, the negative pressure need not exceed –12 cm H2O; –5 cm H2O is

generally all that is needed. After the lung has reexpanded and bubbling from the chest tube has ceased, the tube is clamped and left in place without suction for another 24 to 48 hours.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. It should be noted, however, that the hypoxemia that develops in a pneumothorax is most commonly caused by the alveolar atelectasis and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 10.1).

Lung Expansion Therapy Protocol

With caution, lung expansion techniques are commonly administered to offset the atelectasis associated with a pneumothorax (see Lung Expansion Therapy Protocol, Protocol 10.3) in patients with chest tubes.

Mechanical Ventilation Protocol

Because acute ventilatory failure may develop with severe pneumothorax, continuous monitoring and use of mechanical ventilation with positive end-expiratory pressure (PEEP) may be required to maintain adequate ventilatory status (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2). When mechanical ventilation is needed, a tube thoracotomy (preventive thoracotomy) is required to offset the possible development of a tension pneumothorax.

Pleurodesis

On occasion, a thoracentesis may be performed before a procedure called pleurodesis. During the pleurodesis procedure a sclerosant agent (talc, tetracycline, or bleomycin sulfate) is injected into the chest cavity. The chemical substance or medication causes an intense inflammatory reaction over the outer surface of the lung and inside of the chest cavity. This procedure is performed to cause the surface of the lung to adhere to the chest cavity, thus preventing or reducing recurrent pneumothorax or recurrent pleural effusions. An intense pleuritis is produced, which may be quite painful (pleurisy).

Case Study Spontaneous Pneumothorax

Admitting History and Physical Examination

This patient was a 20-year-old man, a university student who was in excellent health until 5 hours before admission. He was sitting quietly in his dorm room studying for an examination when he suddenly developed a sharp pain in his left lower thoracic region. It was most acute in the anterior axillary line. The pain was exacerbated by deep inspiration and radiated anteriorly, almost to the midline. It did not radiate into the shoulder or neck. The patient became mildly dyspneic and had episodes of nonproductive cough that seemed to increase the chest pain. These symptoms worsened, and at 1 a.m. his roommate drove him to the university hospital emergency department (ED).

On examination, the patient was a tall, thin, well-nourished young man in moderately acute distress. His trachea was shifted to the right of the midline. His blood pressure was 150/82 mm Hg, pulse 96 beats/min, and respirations 28 breaths/min and shallow. On room air, his SpO2 was 90%. The left side of the chest was hyperresonant to percussion, and

the breath sounds were described as “distant.” The patient was not cyanotic. The ED physician was momentarily busy with another patient and asked the respiratory therapist on duty to assess the patient's respiratory status.

The respiratory therapist assigned to the ED during the night shift made the following assessments and plans.

Respiratory Assessment and Plan

S Sudden left chest pain worsened by cough; shortness of breath

O Normal vital signs. Left chest hyperresonant. Trachea shifted to the right. Breath sounds on left “distant.” Room air SpO2 90%.

A Probable left spontaneous tension pneumothorax (history and objective indicators)

P Notify physician (who was in the next room). Request stat CXR and ABG. Oxygen Therapy Protocol (partial rebreathing mask). Obtain supplies for tube thoracostomy and place at the patient's bedside.

The patient stated that he was more comfortable on the oxygen mask, but that some left-sided chest pain was still present. His physical findings were unchanged from his initial evaluation. The chest radiograph confirmed the diagnosis of a 50% left-sided pneumothorax, lung collapse, and mediastinal shift to the right. The arterial blood gas values on a partial rebreathing mask were pH 7.53, PaCO2 29 mm Hg, HCO3– 21 mEq/L, PaO2 56 mm Hg, and SaO2 92%. The physician was

still busy with the patient in the next room.

With this new information, the respiratory therapist charted the following.

Respiratory Assessment and Plan

S “This oxygen mask helps a little.”

O Persistent symptoms and physical findings as in SOAP-1 above. CXR: 50% left tension pneumothorax. Mediastinum shifted to right. ABGs pH 7.53, PaCO2 29, HCO3– 21, PaO2 56, and SaO2 92% (on partial rebreathing mask).

A

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a.1 and 4 only

b.2 and 3 only

c.3 and 4 only

d.2, 3, and 4 only

6.The physician usually elects to evacuate the intrathoracic gas when the pneumothorax is greater than:

a.5%

b.10%

c.15%

d.20%

7.During treatment of a pneumothorax with a chest tube and suction, the negative (suction) pressure usually need not exceed:

a.−6 cm H2O

b.−8 cm H2O

c.−10 cm H2O

d.−12 cm H2O

8.A patient with a severe tension pneumothorax demonstrates which of the following on the affected side?

1.Diminished breath sounds

2.Hyperresonant percussion note

3.Dull percussion notes

4.Whispered pectoriloquy

a.2 only

b.1 and 2 only

c.3 and 4 only

d.1, 2, and 4 only

9.When a patient has a large tension pneumothorax, which of the following occur(s)?

a.pH increases

b.PaCO2 increases

c. decreases

d.PaCO2 decreases

10.When a patient has a large tension pneumothorax, which of the following occur(s)?

a.PVR decreases

b. increases

c.CVP decreases

d.CO increases

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C H A P T E R 2 4

Pleural Effusion and Empyema

CHAPTER OUTLINE

Anatomic Alterations of the Lungs Pleural Anatomy and Pathophysiology

Etiology and Epidemiology

Common Causes of Transudative Pleural Effusion Common Causes of Exudative Pleural Effusion

Other Pathologic Fluids That Separate the Parietal From the Visceral Pleura

Overview of the Cardiopulmonary Clinical Manifestations Associated With Pleural Effusion and Empyema

General Management of Pleural Effusion

Respiratory Care Treatment Protocols

Case Study: Pleural Disease

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

•List the anatomic alterations of the lungs associated with pleural diseases.

•Describe the causes of pleural diseases.

•Describe the use of thoracentesis and pleural fluid examination in the etiology of pleural diseases.

•List the cardiopulmonary clinical manifestations associated with pleural diseases.

•Describe the general management of pleural diseases.

•Describe the clinical strategies and rationales of the SOAPs presented in the case study.

•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

KEY TERMS

Chylothorax

Congestive Heart Failure

Decortication

Empyema

Exudative Pleural Effusion

Fungal Diseases

Hemothorax

Hepatic Hydrothorax

Lateral Decubitus Radiograph

Left-Sided Heart Failure

Light Criteria

Loculated Pleural Effusion

Malignant Mesothelioma

Meniscus Sign

Nephrotic Syndrome

Parapneumonic Pleural Effusion

Peritoneal Dialysis

Pigtail Catheter

Pleural Effusion

Pleurisy

Pleurodesis

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FIGURE 24.2 Balance of forces regulating pleural fluid formation. The amount of fluid in the pleural pace depends on the balance of hydrostatic and oncotic pressures between the parietal and visceral pleura and the pleural space. Because hydrostatic pressures are higher on the parietal pleura than on the visceral pleura and the oncotic pressures are equivalent, pleural fluid is primarily produced from the parietal pleura. Likewise, the lymphatic vessels on the parietal pleura are responsible for the majority of pleural fluid resorption.

Evaluation of pleural effusions is of key importance in the diagnosis of potentially significant conditions. The use of point-of-care ultrasonography now joins portable chest radiology as a tremendous aid to evaluation of these patients in critical care units. The technique can be used to localize the effusion, and thus there are fewer complications compared with “blind” needle aspiration. A chest physician is usually involved in this procedure to help the timely evaluation of the effusion, to decrease the likelihood of possible complications, and to ensure appropriate follow-up.

Etiology and Epidemiology

Pleural effusion affects more than 1.5 million people each year in the United States. Congestive heart failure, cancer, and pneumonia account for the majority of cases. Early signs and symptoms include pleuritic chest pain, “chest pressure,” dyspnea, and cough. Chest pain can occur early when there is intense inflammation of the pleural surfaces. Chest pressure does not usually develop until the effusion reaches the moderate (500 to 1500 mL) to large (more than 1500 mL) category. Dyspnea rarely occurs in small effusions unless significant pleurisy is present. A cough is usually directly related to the degree of atelectasis caused by the effusion.

A pleural effusion can be classified by (1) the origin of the fluid—that is, serous fluid (hydrothorax), blood (hemothorax), chyle (chylothorax), pus (pyothorax or empyema), or urine (urinothorax)—or (2) by the pathophysiology of the pleural effusion—that is, transudative pleural effusion or exudative pleural effusion. A transudate develops when fluid from the pulmonary capillaries moves into the pleural space. The fluid is thin and watery, containing a few blood cells and little protein. The pleural surfaces are not involved in producing the transudate. In contrast, an exudate develops when the pleural surfaces are diseased. The fluid has a high protein content and a great deal of cellular debris. Exudate is usually caused by inflammation, infection, or malignancy.

Table 24.1 contains the criteria for differential diagnosis of transudates and exudates that largely rely on the Light criteria. Careful, systematic analysis of pleural fluid will reveal the diagnosis as one or the other in about 75% of the patients and give good evidence of its causes (with additional Gram stain and cultures) and with microscopic examination for abnormal (e.g., malignant) cell types.

TABLE 24.1

Pleural Fluid Analysis in Differential Diagnoses of Transudates and Exudates

*Based on the original Light criteria for diagnosis of exudates from Feller-Kopman, D., & Light, R. W. (2018). Pleural disease: A review article. The New England Journal of Medicine, 378(8), 740-751; Light, R. W. (2006). Parapneumonic effusions and empyema. Proceedings of the American Thoracic Society, 3, 75-80.

Common Causes of Transudative Pleural Effusion

Congestive Heart Failure

Congestive heart failure is the most common cause of pleural effusion. Both rightand left-sided heart failure can result in pleural effusion. In general, left-sided heart failure is more likely to produce pleural effusion than right-sided heart failure. In left-sided heart failure, an increase in hydrostatic pressure in the pulmonary circulation can decrease the rate of pleural fluid absorption through the visceral pleura and cause fluid movement through the visceral pleura into the pleural space. In right-sided heart failure (cor pulmonale), an increase in the hydrostatic pressure in the systemic circulation can increase the rate of pleural fluid formation and decrease lymphatic drainage from the pleural space because of the elevated systemic venous pressure.

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Hepatic Hydrothorax

Hepatic hydrothorax is defined as a pleural effusion, usually greater than 500 mL, in patients with cirrhosis (particularly when ascitic fluid is present in the abdomen) and without primary cardiac, pulmonary, or pleural disease. It develops most likely because of diaphragmatic defects that have been opened by increased peritoneal pressure—thus allowing the passage of fluid from the peritoneal space to the pleural space. Hepatic hydrothorax may be difficult to manage in endstage liver failure and often fails to respond to therapy. Because of the location of the liver, the pleural effusion in these patients is generally right-sided.

Peritoneal Dialysis

As in the pleural effusion that occurs as a result of abdominal ascites (see above), on rare occasions a pleural effusion may develop as a complication of peritoneal dialysis in the treatment of severe chronic kidney disease. Peritoneal dialysis uses the patient's peritoneum in the abdomen as a membrane across which fluids and dissolved substances (electrolytes, urea, glucose, albumin, and other small molecules) are exchanged with the blood. When the peritoneal dialysis is stopped, the pleural effusion usually disappears rapidly.

Parapneumonic Pleural Effusions

Effusions that occur as a result of underlying pulmonary infection are termed parapneumonic effusions (e.g., those following a pneumococcal or staphylococcal pneumonia) abutting up to the visceral pleural surface. In patients with these effusions an invasive procedure more than a simple diagnostic thoracentesis may be necessary. This is true when the effusion occupies more than 50% of the hemithorax and presents as a loculated pleural effusion (bound down to the pleural surfaces) or shows a positive Gram stain or culture of the fluid and the purulent pleural fluid shows a pH less than 7.20 or a glucose value below 60 mg/dL.

If a needle thoracentesis is not successful in removing the fluid, a chest tube should be inserted, perhaps with the use of video-assisted thoracic surgery (VATS). After this, consideration of use of intrapleural fibrinolytics may be considered. Failing that, a full thoracotomy and decortication (a so-called “pleural peel”) may need to be performed and/or open drainage of the parapneumonic effusion may be required.

Nephrotic Syndrome

Pleural effusion is commonly seen in patients with nephrotic syndrome. It is generally bilateral. The effusion is a result of the decreased plasma oncotic pressure that develops in patients with this disorder.

Pulmonary Embolism or Infarction

Between 30% and 50% of patients with pulmonary arterial emboli develop pleural effusion. Two distinct mechanisms are responsible. First, obstruction of the pulmonary vasculature can lead to right-sided heart failure, which in turn can lead to pleural effusion. Second, increased permeability of the capillaries pulmonary infarction in the visceral pleura develops in response to the ischemic infarction caused by the pulmonary emboli.

Common Causes of Exudative Pleural Effusion

Empyema

The accumulation of pus in the pleural cavity is called empyema. Empyema commonly develops as a result of inflammation. Thoracentesis may confirm the diagnosis and determine the specific causative organism. The pus is usually removed by thoracostomy tube drainage. Open thoracotomy drainage may occasionally be necessary.

Malignant Pleural Effusions

About two-thirds of malignant pleural effusions occur in women. Malignant pleural effusions are highly associated with breast cancer. The pleural effusion is usually caused by a disturbance of the normal Starling forces regulating reabsorption of fluid in the pleural space, secondary to obstruction of mediastinal lymph nodes draining the parietal pleura. Tumors that metastasize frequently to these nodes (e.g., lung cancer, breast cancer, and lymphoma) cause most malignant effusions.

Malignant mesothelioma arises from the mesothelial cells that line the pleural cavities. Individuals who have had chronic exposure to asbestos have a much greater risk for developing mesothelioma. The pleural fluid is exudative and generally contains a mixture of normal mesothelial cells, differentiated and undifferentiated malignant mesothelial cells, and a varying number of lymphocytes and polymorphonuclear leukocytes.

Bacterial Pneumonias

Up to 40% of patients with bacterial pneumonia have an accompanying pleural effusion. Most pleural effusions associated with pneumonia resolve without any specific therapy. Approximately 10%, however, require some sort of therapeutic intervention. If appropriate antibiotic therapy is not instituted, bacteria invade the pleural fluid from the lung parenchyma. Eventually, pus will accumulate in the pleural cavity (empyema). Pleural effusion also can be produced by viruses, Mycoplasma pneumoniae and Rickettsia, although the pleural effusions are usually small.

Tuberculosis

Pleural effusion may develop from extension of a caseous tubercle into the pleural cavity. It also is possible that the inflammatory reaction that develops in tuberculosis obstructs the lymphatic pores in the parietal pleura. This in turn leads to an accumulation of protein and fluid in the pleural space. Pleural effusion caused by tuberculosis is generally unilateral and small to moderate in size (see Chapter 19, Tuberculosis).

Fungal Diseases

Patients with fungal diseases occasionally have secondary pleural effusions. Common fungal diseases that may produce pleural effusions are histoplasmosis, coccidioidomycosis, and blastomycosis (see Chapter 18, Pneumonia, Lung Abscess Formation, and Important Fungal Diseases).

Pleural Effusion Resulting From Diseases of the Gastrointestinal Tract

Pleural effusion is sometimes associated with diseases of the gastrointestinal tract such as pancreatitis, subphrenic abscess, intrahepatic abscess, esophageal perforation, abdominal operations, and diaphragmatic hernia.

Pleural Effusion Resulting From Collagen Vascular Diseases

Pleural effusion occasionally develops as a complication of collagen vascular diseases. Such diseases include rheumatoid pleuritis, systemic lupus erythematosus, Sjögren syndrome, familial Mediterranean fever, and Wegener granulomatosis.

Other Pathologic Fluids That Separate the Parietal From the Visceral Pleura

In addition to transudates and exudates, other pathologic fluids can separate the parietal pleura from the visceral pleura.