5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

Acute Ventilatory Failure With Hypoxemia2 (Acute Respiratory Acidosis)

2See Fig. 5.3 and Table 5.5 and related discussion for the acute pH, PaCO2, and changes associated with acute and chronic ventilatory failure.

3When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular PaCO2 level.

Oxygenation Indices4

(Large Pleural Effusion)

5The DO2 may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the DO2 is normal, the O2ER is usually normal.

4, Arterial-venous oxygen difference; DO2, total oxygen delivery; O2ER, oxygen extraction ratio; QS/QT, pulmonary shunt fraction; , mixed venous oxygen saturation; VO2, oxygen consumption.

Hemodynamic Indices6

(Large Pleural Effusion)

6CO, Cardiac output; 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

•Blunting of the costophrenic angle

•Fluid level on the affected side (Fig. 24.3)

effusion itself. For example, if the heart failure is reversed or the lung infection is cured by antibiotics, the effusion usually resolves. When the cause of the pleural effusion is not readily evident, microscopic and chemical examination of pleural fluid may determine whether the effusion is a transudate or an exudate. If the fluid is a transudate, treatment is directed to the underlying problem (e.g., congestive heart failure, cirrhosis, nephrosis).

When an exudate is present, a cytologic examination may identify a malignancy. The fluid must be examined for its biochemical makeup (e.g., protein, sugar, various enzymes) and for the presence of bacteria. Examination of the effusion may reveal blood after trauma or surgery, pus in empyema, or milky fluid in chylothorax. The presence of blood in the pleural fluid in the absence of trauma or surgery suggests malignant disease, pulmonary embolization or infarction.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in pleural effusion is mostly caused by the atelectasis and pulmonary 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

Lung expansion techniques are often administered to offset the atelectasis associated with pleural effusions and are particularly helpful once the pleural fluid has been removed by thoracentesis or thoracostomy (see Lung Expansion Therapy Protocol, Protocol 10.3).

Mechanical Ventilation Protocol

Because acute ventilatory failure and hypoxemia may be seen in severe pleural effusions, continuous mechanical ventilation may be required to maintain an adequate ventilatory status. Continuous mechanical ventilation is justified when the acute ventilatory failure is thought to be reversible (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2).

Pleurodesis

A pleurodesis may be performed to cause irritation and inflammation (pleuritis) between the parietal and visceral layers of the pleural. During the pleurodesis procedure a sclerosant (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 the chest cavity. This procedure is performed to cause the surface of the lung to adhere to the chest wall, thus preventing or reducing recurrent pneumothorax or recurrent pleural effusions. An intense pleuritis is produced, which may be quite painful (pleurisy).

Case Study Pleural Disease

Admitting History

A 38-year-old woman had discharged herself from the hospital against medical advice 2 months before the admission discussed here. She had originally been admitted for severe right lower lobe pneumonia. After 5 days of treatment, she became angry because she was not allowed to smoke. She was a longtime, three-pack-per-day smoker. When a nurse found her smoking in her hospital bed while on a 2 L/min oxygen nasal cannula, the nurse quickly confiscated her cigarettes and matches.

The woman became upset. She told her doctor that this was the last straw and that she was going to leave the hospital on her own. Her doctor wanted her to remain so that a thorough follow-up could be performed for what was described as a “spot” on her lower right lung. The woman promised that she would make an appointment at the doctor's office the next week. She then got dressed and left. However, 2 days later, she felt so much better that she decided the spot on her lung was not an issue for concern. The woman told her friends that smoking one pack of cigarettes made her feel better than 5 days’ worth of nurses, doctors, and hospitals.

On the day of the admission discussed here, the woman appeared at her doctor's office without an appointment. She told the receptionist that something was very wrong. She thought that she had the flu and that it had been getting progressively worse over the previous 4 days. At the time of the office visit, she could speak in short sentences only and was unable to inhale deeply. Seeing that the woman was in obvious respiratory distress, the physician was notified. The doctor had the woman transported and admitted to the hospital a few blocks away.

Physical Examination

The woman appeared malnourished, exhibited poor personal hygiene, and had yellow tobacco stains around her fingers. She appeared to be in moderate to severe respiratory distress. Her nails and mucous membranes were cyanotic, and her shirt was wet from perspiration. She demonstrated an occasional hacking, nonproductive cough. She stated that she could not take a deep breath and that maybe the problem stemmed from “that spot” on her lung.

Her vital signs were blood pressure 130/60 mm Hg, heart rate 112 beats/min, and respiratory rate 36 breaths/min with shallow respirations. She was slightly febrile, with an oral temperature of 37.7°C (99.8°F). Palpation showed that the trachea was shifted slightly to the left. Dull percussion notes were found over the right middle and right lower lobes. Auscultation revealed normal vesicular breath sounds over the left lung fields and upper right lobe. No breath sounds could be heard over the right middle and right lower lobes.

The patient's chest radiograph showed a large, right-sided pleural effusion. The right costophrenic angle demonstrated severe blunting, the right hemidiaphragm was depressed, and the right middle and lower lung lobes were partially collapsed and showed changes consistent with pneumonia. The patient was immediately placed on a nonrebreathing mask,

and an arterial blood gas (ABG) sample was drawn. The results were pH 7.48, PaCO2 24 mm Hg, 17 mEq/L, PaO2 37 mm Hg, and SaO2 73%. The doctor, assisted by the respiratory therapist, performed a thoracentesis, and slightly more

than 2 L of yellow fluid was withdrawn.1 The patient then was started on intravenous antibiotics. A portable radiograph of the chest was ordered, and a respiratory therapy consultation was requested. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S “I can't take a deep breath.”

O Malnourished appearance with poor personal hygiene; cyanosis with an occasional hacking, nonproductive cough; vital signs BP 130/60, HR 112, RR 36 and shallow, temperature 37.7°C (99.8°F); trachea slightly shifted to the left; dull percussion notes over the right middle and

•Atelectasis and consolidation in right middle and right lower lung lobes (previous CXR)

•Normal acid-base status with mild hypoxemia (ABGs)

P Maintain present level of Lung Expansion Therapy Protocol and Oxygen Therapy Protocols. Monitor and reevaluate each shift. Provide patient with smoking cessation materials and suggest pulmonary function testing as an outpatient.

Discussion

This case illustrates a patient with postpneumonic pleural effusion, one of the pleural diseases that generally can be improved with appropriate therapy—in this case, the removal of a large amount of yellow fluid via a thoracentesis. This portion of the case study provides a good opportunity to introduce the concept of reexpansion pulmonary edema. It is a rare complication resulting from rapid emptying of air or liquid from the pleural cavity performed by either thoracentesis or chest drainage. The condition usually appears unexpectedly—and dramatically—within the first few minutes to an hour after the fluid or air removal. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24 to 48 hours and persist for 4 to

5days.

During the first assessment, the respiratory therapist recognized that the patient had significant respiratory morbidity.

Indeed, the patient had an extensive right-sided pneumonia and pleural effusion and partially collapsed right middle and lower lobes. Clearly the patient was in respiratory distress. The patient's acute alveolar hyperventilation and severe hypoxemia were a direct result of the partial collapse of the lung lobes. Because of the extremely low PaO2 noted on the

initial ABG sample, the presence of lactic acid was very likely. In fact, this was confirmed by the respiratory therapist with

the PCO2//pH nomogram. Understanding that ate​lectasis was the main pathophysiologic mechanism in this case

(see Fig. 10.7), the therapist correctly assessesed the situation as one that required careful monitoring and began the Lung Expansion Therapy Protocol (Protocol 10.3) (e.g., PEP or CPAP therapy) and the Oxygen Therapy Protocol (Protocol 10.1) (with a high concentration of oxygen).

Given the patient's history, the respiratory therapist also would be interested in the results of the cytologic studies for malignancy in both the sputum and thoracentesis fluid. Frequently, blood gas values do not improve immediately after a thoracentesis, despite the fluid removal, because the atelectasis under the pleural effusion takes some time (hours or days) to dissipate. For this reason, the Lung Expansion Therapy Protocol, after thoracentesis, was appropriate.

At the time of the second assessment, the patient was beginning to improve, although she still had signs of right middle and lower lobe consolidation (see Fig. 10.8). Good breath sounds were heard over the left lung and upper right lung, although bronchial breath sounds reflecting consolidation were still noted on the right. The respiratory therapist was appropriately concerned that atelectasis was still present, and in such a case the therapist should increase the Lung Expansion Therapy Protocol (Protocol 10.3). In this case, the therapist selected a CPAP mask at 10 cm H2O every 2 hours

for 15 minutes. The therapist could have also intensified use of incentive spirometry, carefully used intermittent positivepressure breathing, or extended the amount of time the patient was using the CPAP mask.

In the last assessment the patient continued to do fairly well, although she was far from returning to baseline values. The pneumonia, atelectasis, and mild hypoxemia, which persisted despite supplemental oxygen therapy, suggested the need for continued significant (though unchanged) therapy. This case demonstrates that in-place therapy often does not need to be changed at each assessment. Indeed, this guide may apply to as many as 50% to 60% of accurately performed serial assessments. For pedagogic reasons, this option has not been exercised often in this text. However, this third assessment (in a patient with pleural effusion and underlying atelectasis and pneumonia) is a good case in point.

Self-Assessment Questions

1.Which of the following is(are) associated with exudative effusion?

1.Few blood cells

2.Inflammation

3.Thin and watery fluid

4.Disease of the pleural surfaces

a.2 only

b.4 only

c.1 and 3 only

d.2 and 4 only

2.Which of the following is probably the most common cause of a transudative pleural effusion?

a.Pulmonary embolus

b.Congestive heart failure

c.Hepatic hydrothorax

d.Nephrotic syndrome

3.A hemothorax is said to be present when the hematocrit of the pleural fluid is at least:

a.20%

b.30%

c.40%

d.50%

4.What percentage of patients with pulmonary emboli develop pleural effusion?

a.0% to 20%

b.20% to 30%

c.30% to 50%

d.50% to 60%

5.Which of the following is(are) associated with pleural effusion?

a.Increased RV

b.Decreased RV/TLC ratio

c.Increased VT

C H A P T E R 2 5

Kyphoscoliosis

CHAPTER OUTLINE

Anatomic Alterations of the Lungs

Etiology and Epidemiology

Scoliosis

Congenital Scoliosis

Neuromuscular Scoliosis

Idiopathic Scoliosis

Diagnosis of Scoliosis

Kyphosis

Overview of the Cardiopulmonary Clinical Manifestations Associated With Kyphoscoliosis

General Management of Scoliosis

Conservative Treatment

Braces

Surgery

Other Approaches

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Airway Clearance Therapy Protocol

Lung Expansion Therapy Protocol

Case Study: Kyphoscoliosis

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

•List the anatomic alterations of the lungs associated with kyphoscoliosis.

•Describe the causes of kyphoscoliosis.

•List the cardiopulmonary clinical manifestations associated with kyphoscoliosis.

•Describe the general management of kyphoscoliosis.

•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

Adolescent Scoliosis

Boston Brace

Cervicothoracolumbosacral Orthosis (CTLSO)

Charleston Bending Brace

Cobb Angle

Cor Pulmonale

Congenital Scoliosis

Cotrel-Dubousset Technique

“Dizzy Gillespie Pouch”

Harrington Rod

Idiopathic Scoliosis

Infantile Scoliosis

Juvenile Scoliosis

Kyphoscoliosis

Kyphosis

• A condition caused by poor muscle control, muscle weakness, or paralysis because of diseases such as cerebral palsy, muscular dystrophy, spina bifida, or poliomyelitis.

Idiopathic Scoliosis

• Scoliosis from an unknown cause that appears in a previously straight spine. When kyphoscoliosis arises without a known cause (80% to 85% of cases), it is referred to as idiopathic kyphoscoliosis.

Other possible causes include hormonal imbalance, trauma, extraspinal contractures, infections involving the vertebrae, metabolic bone disorders (e.g., rickets, osteoporosis, osteogenesis imperfecta), dwarfism, joint disease, and tumors.

Depending on the child's age at the time of onset, idiopathic scoliosis is classified as infantile, juvenile, or adolescent. In infantile scoliosis the curvature of the spine develops during the first 3 years of life. In juvenile scoliosis the curvature occurs at 4 years of age to the onset of adolescence. In adolescent scoliosis the spinal curvature develops after the age of 10 years. Adolescent scoliosis is the most common. Early signs of scoliosis (i.e., appearing when a child is approximately 8 years of age) include uneven shoulder height, prominent shoulder blade(s), uneven waist height, elevated hips, and leaning to one side.

Risk factors include the following:

•Gender: Girls are more likely to develop curvature of the spine than boys.

•Age: The younger the child is when the diagnosis is first made, the greater the chance of curve progression.

•Angle of the curve: The greater the initial curvature of the spine, the greater the risk that the curve progression will worsen.

•Location: Curves in the middle to lower spine are less likely to progress than those in the upper spine.

•Height: Taller people have a greater chance of curve progression.

•Spinal problems at birth: Children with scoliosis at birth (congenital scoliosis) have a greater risk for worsening of the curve with aging.

Diagnosis of Scoliosis

Scoliosis is diagnosed by the patient's medical history, physical examination, x-ray evaluation, and curve measurement. Clinically, scoliosis is commonly defined according to the following factors related to the curvature of the spine:

•Shape (nonstructural scoliosis and structural scoliosis): Nonstructural scoliosis is a curve that develops side-to-side as a C- or S-shaped curve. This form of scoliosis results from a cause other than the spine itself (e.g., poor posture, leg length discrepancy, pain). A structural scoliosis is a curvature of the spine associated with vertebral rotation. Structural scoliosis involves the twisting of the spine and appears in three dimensions.

•Location: The curve of the spine may develop in the upper back area where the ribs are located (thoracic), the lower back area (lumbar), or in both areas (thoracolumbar).

•Direction: Scoliosis can bend the spine left or right.

•Angle: A normal spine viewed from the back is zero degrees—a straight line. Scoliosis is defined as a spinal curvature of greater than 10 degrees (i.e., bending toward the ground when in the upright position). The degree of the lateral curvature is expressed by the Cobb angle, which is calculated from a radiograph as shown in Fig. 25.2.