5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

FIGURE 25.2 (A) Chest radiograph of a patient with kyphoscoliosis. (B) Method of calculating the Cobb angle. Scoliosis is defined as a spinal curvature of 10 degrees or greater. Because the Cobb angle reflects curvature only in a single plane, it may fail to fully identify the severity of the scoliosis, especially when the patient has vertebral rotation and threedimensional spinal deformity.

Kyphosis

Kyphosis can occur at any age, although it is rare at birth. Known causes of kyphosis are (1) degenerative diseases of the spine (such as arthritis or disk degeneration), (2) fractures caused by osteoporosis (osteoporotic compression fractures), and (3) slipping of one vertebra forward on another (spondylolisthesis). Other disorders associated with the cause of kyphosis include certain endocrine diseases, connective tissue disorders, infections (e.g., tuberculosis), muscular dystrophy, neurofibromatosis, Paget disease, polio, spina bifida, and tumors. Kyphosis also may be caused by Scheuermann disease, which is the wedging together of several bones of the vertebrae in a row. The precise cause of Scheuermann disease is unknown.

Overview of the Cardiopulmonary Clinical Manifestations Associated With Kyphoscoliosis1

The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by atelectasis (see Fig. 10.7) and excessive airway secretions (see Fig. 10.11)—the major anatomic alterations of the lungs associated with kyphoscoliosis (see Fig. 25.1).

Clinical Data Obtained at the Patient's Bedside

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

•Stimulation of peripheral chemoreceptors (hypoxemia)

•Relationship of decreased lung compliance to increased ventilatory rate

•Stimulation of the J receptors

•Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Cyanosis

Digital Clubbing

Peripheral Edema and Venous Distention

Because polycythemia and cor pulmonale are late findings associated with kyphoscoliosis, the following may be seen:

•Distended neck veins

•Pitting edema

•Enlarged and tender liver

Cough and Sputum Production

Chest Assessment Findings

•Limited thoracic expansion

•Obvious thoracic deformity

•Tracheal shift

•Increased tactile and vocal fremitus

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•Dull percussion note

•Bronchial breath sounds

•Whispered pectoriloquy

•Crackles and wheezing

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

Moderate to Severe Kyphoscoliosis (Restrictive Lung Pathology)

Forced Expiratory Volume and Flow Rate Findings

Lung Volume and Capacity Findings

Arterial Blood Gases

Moderate Kyphoscoliosis

Acute Alveolar Hyperventilation With Hypoxemia2 (Acute Respiratory Alkalosis)

2See Fig. 5.2 and Table 5.4 and related discussion for the acute pH, PaCO2, and changes associated with acute alveolar hyperventilation.

Severe Kyphoscoliosis

Chronic Ventilatory Failure With Hypoxemia3 (Compensated Respiratory Acidosis)

3See Table 5.6 and related discussion for the pH, PaCO2, and changes associated with chronic ventilatory failure.

Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failure4

Because acute ventilatory changes are frequently seen in patients with chronic ventilatory failure, the respiratory therapist must be familiar with—and alert for—the following two dangerous arterial blood gas (ABG) findings:

•Acute alveolar hyperventilation superimposed on chronic ventilatory failure, which should further alert the respiratory therapist to record the following important ABG assessment: possible impending acute ventilatory failure

•Acute ventilatory failure (acute hypoventilation) superimposed on chronic ventilatory failure

4See Table 5.7, Table 5.8, and Table 5.9 and related discussion for the pH, PaCO2, and changes associated with acute ventilatory changes superimposed on chronic ventilatory failure

Oxygenation Indices5

Moderate to Severe Kyphoscoliosis

6The 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.

5, 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 Indices7

Moderate to Severe Kyphoscoliosis

7CO, 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.

Laboratory Findings

Severe and/or late-stage kyphoscoliosis (if the patient is chronically hypoxemic)

•Increased hematocrit and hemoglobin (polycythemia)

•Hypochloremia (Cl−)

•Hypernatremia (Na+)

Radiologic Findings

Chest Radiograph

•Thoracic deformity

•Mediastinal shift

•Increased lung opacity

•Atelectasis in areas of compressed (atelectatic) lungs

•Enlarged heart (cor pulmonale)

The extent of the thoracic deformity in kyphoscoliosis is demonstrated in anteroposterior and lateral radiographs. When present, a mediastinal shift is best shown on an anteroposterior chest radiograph. As the alveoli collapse, the density of the lung increases and is revealed on the chest radiograph as increased opacity (Fig. 25.3). In severe cases, cor pulmonale may be seen.

FIGURE 25.3 Severe kyphoscoliosis in a 14-year-old male patient.

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FIGURE 25.5 The SpineCor brace is composed of soft, elastic corrective bands that wrap around the patient's body and resist the body's movement back to the abnormal position.

Surgery

In general, surgery is performed to correct unacceptable deformity and prevent further curvature. Surgery is usually recommended in patients who have curvatures of the spine greater than 40 to 50 degrees. As a general rule, the surgery is extensive and invasive; even the best surgical techniques do not completely straighten the patient's spine. Also, surgery often does not improve ventilatory function. Surgical procedures include the following.

Spinal Fusion

Spinal fusion is the most widely performed surgery for scoliosis. A spinal fusion, followed by casting, involves placing pieces of bone between two or more vertebrae. The bone sections are taken from the patient's pelvis or rib. Eventually the bone pieces and the vertebrae fuse together. This procedure has now been largely replaced by rod instrumentation.

Rod Instrumentation

In 1962, Paul Harrington introduced a metal spinal system that involved the insertion of a metal rod (the Harrington rod) after a fusion procedure, hooks, screws, and wires to prevent the curve from moving for 3 to 12 months and to allow the fusion to become solid (Fig. 25.6). The system provides disruption to the concave side of the spine and compression to the convex side. This action enhances stabilization, reduces any rotational tendency, and applies force to the spine to correct the curvature. Although the Harrington rod improved up to 50% of the curvature in patients who elected to have the procedure, it is now obsolete. Its major shortcomings were that it failed to produce a posture that allowed the skull to be in proper alignment with the pelvis and it did not address rotational deformity. Currently, the Cotrel-Dubousset system is the most common technique for this procedure. The Cotrel-Dubousset technique has been shown to work well in improving pelvic area sagittal imbalance and rotational defects. The Cotrel-Dubousset technique has shown relatively good success (e.g., it reduces or prevents the rib hump) and exhibits low rates of infection. The long-term success of this technique is still being studied.

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by the hospital.

Physical Examination

Although chronically ill, the patient appeared to be well nourished; the lateral curvature of her spine was twisted significantly to the left. She also demonstrated forward (anterior) bending of the thoracic spine. She appeared older than her stated age, and she was in obvious respiratory distress. The patient stated that she was having trouble breathing. Her skin was cyanotic. She had digital clubbing, and her neck veins were distended, especially on the right side. The woman demonstrated a frequent and strong cough. During each coughing episode, she expectorated a moderate amount of thick, yellow nonodorous sputum.

When the patient generated a strong cough, a large unilateral bulge appeared at the right anterolateral base of her neck, directly posterior to the clavicle. The patient referred to the bulge as her “Dizzy Gillespie pouch1.” The physician thought the bulge was a result of her severe kyphoscoliosis, which had in turn stretched and weakened the suprapleural membrane that normally restricts and contains the parietal pleura at the apex of the lung. Because of the weakening of the suprapleural membrane, any time the woman performed a Valsalva maneuver for any reason (e.g., for coughing), the increased intrapleural pressure herniated the suprapleural membrane outward. Despite the odd appearance of the bulge, the doctor did not consider it a serious concern.

The patient's vital signs were blood pressure 160/100 mm Hg, heart rate 90 beats/min, respiratory rate 18 breaths/min, and oral temperature 36.3°C (97.3°F). Palpation revealed a trachea deviated to the right and 2+ cervical venous distention, more on the right. Dull percussion notes were produced over both lungs; coarse crackles were also heard bilaterally. There was 2+ pitting edema below both knees. A pulmonary function test (PFT) conducted that morning showed vital capacity (VC), functional residual capacity (FRC), and residual volume (RV) were all 45% to 50% of predicted values.

Although the patient's electrolyte levels were all normal, her hematocrit was 58% and her hemoglobin level was 18 g%. A chest radiograph examination revealed a severe thoracic spinal deformity, a mediastinal shift, an enlarged heart with prominent pulmonary artery segments bilaterally, and bilateral infiltrates in the lung bases consistent with pneumonia and

atelectasis. The patient's arterial blood gas values (ABGs) on room air were pH 7.52, PaCO2 58 mm Hg, 46 mEq/L, PaO2 49 mm Hg, and SaO2 88%. The physician requested a respiratory care consultation and stated that mechanical

ventilation was probably not an option and would not be his choice at this time per the patient's request and his knowledge of the case.

On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S “I'm having trouble breathing.”

O Well-nourished appearance; severe anterior and left lateral curvature of the spine; cyanosis, digital clubbing, and distended neck veins—especially on the right side; strong cough: frequent, adequate, and productive of moderate amounts of thick yellow sputum; 2+ pitting edema below both knees; vital signs BP 160/100, HR 90, RR 18, T 36.3°C (97.3°F); trachea deviated to the right; both lungs: dull percussion notes, coarse crackles; PFT: VC, FRC, and RV 45% to 50% of predicted; Hct 58%, Hb 18 g%; CXR: Severe thoracic and spinous deformity, mediastinal shift, cardiomegaly, and bilateral infiltrates in the lung bases consistent with

pneumonia or atelectasis; ABGs (room air) pH 7.52, PaCO2 58, 46, PaO2 49; SaO2 88%. A

•Severe kyphoscoliosis (history, CXR, physical examination)

•Atelectasis and consolidation (CXR)

•Acute alveolar hyperventilation superimposed on chronic ventilatory failure with moderate hypoxemia (ABGs)

•Impending ventilatory failure

•Increased work of breathing (elevated blood pressure, heart rate, and respiratory rate)

•Cor pulmonale (CXR and physical examination)

•Excessive bronchial secretions (sputum, coarse crackles)

•Infection likely (thick, yellow sputum)

•Good ability to mobilize secretions (strong cough)

P Initiate Oxygen Therapy Protocol (Venturi mask at FIO2 0.28). Airway Clearance Therapy

Protocol (obtain sputum for culture; DB&C instructions and oral suction PRN). Lung Expansion Therapy Protocol (incentive spirometry qid and PRN). Notify physician of admitting ABGs and impending ventilatory failure. Monitor closely.

10 Hours After Admission

The patient's condition had not improved, and she was transferred to the intensive care unit. The physician had trouble titrating the cardiac drugs and decided to insert a pulmonary artery catheter, a central venous catheter, and an arterial line. Because of the woman's cardiac problems, several medical students, respiratory therapists, nurses, and doctors were constantly in and out of her room, performing and assisting in various procedures. As a result, working with the patient for any length of time was difficult, and the intensity of respiratory care was less than desirable. Eventually, the patient's cardiac status stabilized, and the physician requested an update on the woman's pulmonary condition.

The respiratory therapist working on the pulmonary consultation team found the patient in extreme respiratory distress. She was sitting up in bed, appeared frightened, and stated that she was extremely short of breath. A pulmonary artery catheter (Swan-Ganz) had been inserted previously. Both of her sisters were in the room; one sister was putting cold towels on the patient's face while the other sister was holding the patient's hands. Both sisters were crying softly. The woman's skin appeared cyanotic, and perspiration was visible on her face. Her neck veins were still distended. She demonstrated a weak, spontaneous cough. Although no sputum was noted, she sounded congested when she coughed. Dull percussion notes and coarse crackles were still present throughout both lungs. Her vital signs were blood pressure 180/120 mm Hg, heart rate 130 beats/min, respiratory rate 26 breaths/min, and rectal temperature 37.8°C (100°F).

Several of the patient's hemodynamic indices were elevated: CVP, RAP, PA, RVSWI, and PVR.2 Her oxygenation indices were increased QS/QT and O2ER. Decreased DO2 and . Her VO2 and were normal.3 No recent chest

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radiograph was available. Her ABGs on an FIO2 of 0.28 were pH 7.57, PaCO2 49 mm Hg, 43 mEq/L, PaO2 43 mm Hg, and SaO2 87%. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S Severe dyspnea; “I'm extremely short of breath.”

O Extreme respiratory distress; cyanosis and perspiration noted; distended neck veins; weak, spontaneous cough; sounds of pulmonary congestion but no sputum produced; bilateral dull percussion notes, coarse crackles; vital signs BP 180/120, HR 130, RR 26, T 37.8°C (100°F); hemodynamics: increased CVP, RAP, PA, RVSWI, and PVR; oxygenation indices: increased

QS/QT, and O2ER and decreased DO2 and . VO2 and normal. ABGs worse on FIO2

0.28: pH 7.57, PaCO2 49, 43, PaO2 43; SaO2 87%. A

•ABGs worse: on FIO2 of 0.35

•Acute alveolar hyperventilation superimposed on chronic ventilatory failure with moderate to severe hypoxemia (ABGs and history)

•Impending ventilatory failure

•Severe kyphoscoliosis (history, physical examination, CXR)

•Increased work of breathing, worsening (increased blood pressure, heart rate, and respiratory rate)

•Excessive bronchial secretions (coarse crackles, congested cough)

•Atelectasis and consolidation (previous CXR)

•Pulmonary hypertension (hemodynamic indices)

•Continued critically ill status but chances of avoiding ventilatory failure improving P Up-regulate Oxygen Therapy Protocol (Venturi oxygen mask at 0.35). Up-regulate Airway

Clearance Therapy Protocol (add chest physical therapy [CPT] and postural drainage [PD] qid). Contact physician regarding impending ventilatory failure. Discuss possibility of noninvasive mechanical ventilation and therapeutic bronchoscopy with physician. Monitor and reevaluate in 30 minutes.

24 Hours After Admission

At this time the respiratory therapist found the patient watching the morning news on television with her two sisters. The woman was situated in a semi-Fowler's position eating the last few bites of her breakfast. The patient stated that she felt “so much better” and that “finally I have enough wind to eat some food.”

Although her skin still appeared cyanotic, she did not look as ill as she had the day before. On request, she produced a strong cough and expectorated a small amount of white sputum. Her vital signs were blood pressure 140/85 mm Hg, heart rate 83 beats/min, respiratory rate 14 breaths/min, and temperature normal. Chest assessment findings demonstrated coarse crackles and dull percussion notes over both lung fields. The coarse crackles were less intense, however, than they had been the day before.

Although the patient's hemodynamic and oxygenation indices were better than they had been the day before, she still had room for improvement. Her hemodynamic parameters, still abnormal, revealed an elevated CVP, RAP, PA, RVSWI, and PVR. All other hemodynamic indices were normal. Her oxygenation indices still showed an increased QS/QT and O2ER and a

decreased DO2 and . Her VO2 and were normal. The patient's chest radiograph, taken earlier that morning, showed some clearing of the pneumonia and atelectasis described on admission. Her ABGs on an FIO2 of 0.35

were pH 7.45, PaCO2 73 mm Hg, 49 mEq/L, PaO2 68 mm Hg, and SaO2 94%. On the basis of these clinical data, the following SOAP was recorded.

Respiratory Assessment and Plan

S “I feel so much better. I finally have enough wind to eat some food.”

O Cyanotic appearance; cough: strong, small amount of white sputum; vital signs: BP 140/85, HR 83, RR 14, T normal; coarse crackles, and dull percussion notes over both lung fields; coarse crackles improving; hemodynamic and oxygenation indices improving, but still an elevated CVP, RAP, PA, RVSWI, and PVR and still an increased QS/QT and O2ER and a decreased

DO2 and . CXR: Improvement of the bilateral pneumonia and atelectasis. ABGs worse on

FIO2 0.35: pH 7.45, PaCO2 73, 49, PaO2 68; SaO2 94%. A

•Generally slightly improved overall status (history, CXR, hemodynamic and oxygenation indices, ABGs)

•ABGs worse on FIO2 0.35 (likely close to the patient's normal baseline values)

•Significant improvement in problem with excessive bronchial secretions (coarse crackles, cough)

•Improvement in atelectasis and consolidation (CXR)

•Chronic ventilatory failure with mild hypoxemia (ABGs)

•Persistent pulmonary hypertension (hemodynamic indices)

P Down-regulate Oxygen Therapy Protocol and Airway Clearance Therapy Protocol. Continue

to monitor closely and reevaluate ABGs on reduced FIO2. Recommend pulmonary rehabilitation

and patient and family education (noninvasive positive pressure ventilation cuirass ventilation, possibly rocking bed, bilevel positive airway pressure, or positive expiratory pressure).

Discussion

This case contains an excessive amount of extraneous historical and personal material. This was done to demonstrate, in part, how the respiratory therapist must cut through to the core of the case in the SOAP note, no matter how interesting the other information may be. Care of the patient with symptomatic advanced kyphoscoliosis consists of treatment of the conditions that can complicate it (e.g., bronchitis, pneumonia, atelectasis, pleural effusion) and treatment of the underlying condition itself.

In the first assessment, the SOAP documented excessive bronchial secretions and a likely infection because of the thick yellow sputum and recent history. The patient exhibited good ability to mobilize the secretions as charted by a strong cough. The chest radiograph confirmed atelectasis and consolidation, although the report did not precisely identify its location in the chest itself. Although acute alveolar hyperventilation on top of chronic ventilatory failure was present, the possibility of impending ventilatory failure was real. The therapist's decisions to oxygenate the patient with a low FIO2

(0.28), administer airway clearance therapy, and be prepared for ventilator support were all appropriate (see the second SOAP note). The patient's cor pulmonale, but not her polycythemia, would have been expected to improve rapidly as overall oxygenation improved. Improvement in her polycythemia would take some time. The digital clubbing and cor pulmonale suggested that the hypoxemia was long-standing.

At the time of the second assessment, the intensity of the patient's respiratory distress was increasing. This was verified by the continued observation of the high pulse and respiratory rate, excessive airway secretions, dull percussion notes, acute alveolar hyperventilation on top of chronic ventilatory failure with moderate to severe hypoxemia, atelectasis on the chest x-ray, and poor response to oxygen therapy. Undoubtedly, impending ventilatory failure was more likely.

Atelectasis is often refractory to oxygen therapy, suggesting that therapeutic bronchoscopy might have been worthwhile. At that point in time, the up-regulation of the Oxygen Therapy Protocol (Protocol 10.1) and Airway Clearance Therapy Protocol (Protocol 10.2) were all justified by the clinical indicators. Note that use of any prognostication is discouraged in SOAP notes, and the therapist's recording that “chances of avoiding respiratory failure were improving” (at the end of the second SOAP note) is in general not appropriate.

In the last assessment, the clinical manifestations associated with the patient's disorder had all improved substantially, except for the increased PaCO2, thought (again) to be related to “a return to baseline values” may have represented

wishful thinking, and his decision to monitor it closely was appropriate. The down-regulation of the Oxygen Therapy Protocol and Airway Clearance Therapy Protocol was appropriate. The recommendation of pulmonary rehabilitation and family education was appropriately considered.

It is correct that the patient's ABGs were most likely at the patient's baseline level, because the pH was in the normal range. In fact, according to the pH (normal, but on the alkalotic side of normal) the patient's usual PaCO2 was most likely

somewhat higher than the last assessment value. This case nicely demonstrates how a patient with a severe, chronic restrictive lung disorder—in this case, kyphoscoliosis—can, over time, demonstrate ABGs with very high PaCO2 levels, a

normal pH (which has been corrected by an increased level provided by kidney compensation), and a low PaO2

level. In other words, the patient with severe kyphoscoliosis may demonstrate ABG findings that reflect chronic ventilatory failure (compensated respiratory acidosis) with hypoxemia, very similar to the patient with severe chronic obstructive pulmonary disease (i.e., emphysema and chronic bronchitis) who displays chronic ventilatory failure ABGs.

Comparison with baseline values (if available) would have been appropriate at such a time, and consideration of cuirass ventilation, a rocking bed, or positive expiratory pressure to assist nocturnal ventilation might be in order. Oxygenation can easily be assessed by oximetry at home. This case is an excellent example of the value of hemodynamic monitoring (specifically the normal PCWP) in differentiating left-sided from right-sided cardiac failure.

Self-Assessment Questions

1.What kind of curvature of the spine is manifested in kyphosis?

a.Posterior

b.Anterior

c.Lateral

d.Medial

2.Kyphoscoliosis affects approximately what percentage of the US population?

a.2%

b.5%

c.10%

d.15%

3.Which of the following is associated with kyphoscoliosis?

a.Decreased RV/TLC ratio

b.Increased VT

c.Decreased RV

d.Increased TLC

4.Which of the following is associated with kyphoscoliosis?

a.Bronchial breath sounds

b.Hyperresonant percussion note

c.Decreased tactile and vocal fremitus

d.Diminished breath sounds

5.During the advanced stages of kyphoscoliosis, the patient commonly demonstrates which of the following arterial blood gas values?

1.Increased

2.Decreased pH

3.Increased PaCO2

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