Fungal Diseases of the Lung

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Fungal Diseases of the Lung

Chapter Objectives

After reading this chapter, you will be able to:

• List the anatomic alterations of the lungs associated with fungal disease.

• Describe the causes of fungal disease.

• List the cardiopulmonary clinical manifestations associated with fungal disease.

• Describe the general management of fungal disease.

• 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

Anatomic Alterations of the Lungs

When fungal spores are inhaled, they may reach the lungs and germinate. When this happens, the spores produce a frothy, yeastlike substance that leads to an inflammatory response. Polymorphonuclear leukocytes and macrophages move into the infected area and engulf the fungal spores. The pulmonary capillaries dilate, the interstitium fills with fluid, and the alveolar epithelium swells with edema fluid. Regional lymph node involvement commonly occurs during this period. Because of the inflammatory reaction, the alveoli in the infected area eventually become consolidated (Figure 18-1). Airway secretions may also develop at this time.

image
FIGURE 18-1 Fungal disease of the lung. Cross-sectional view of alveoli infected with Histoplasma capsulatum. AC, Alveolar consolidation; M, alveolar macrophage; S, Fungal spore; YLS, yeastlike substance.

In severe cases, tissue necrosis, granulomas, and cavity formation may be seen. During the healing process, fibrosis and calcification of the lung parenchyma ultimately replace the granulomas. In response to the fibrosis and occasionally calcification, the lung tissue retracts and becomes firm. The apical and posterior segments of the upper lobes are most commonly involved. The anatomic changes of the lungs caused by fungal diseases are similar to those seen in tuberculosis.

Fungal diseases of the lung cause a chronic restrictive pulmonary disorder. The major pathologic or structural changes of the lungs associated with fungal diseases of the lungs are as follows:

Etiology and Epidemiology

Fungal spores are widely distributed throughout the air, soil, fomites, and animals, and even exist in the normal flora of humans. As many as 300 fungal species may be linked to disease in animals. In plants, fungal disease is the most common cause of death and destruction. In humans, most exposures to fungal pathogens do not lead to overt infection because humans have a relatively high resistance to them. Human fungal disease (also called mycotic disease or mycosis) can be caused, however, by primary or “true” fungal pathogens that exhibit some degree of virulence or by opportunistic or secondary pathogens that take advantage of a weakened immune defense system (e.g., in acquired immunodeficiency syndrome [AIDS] and human immunodeficiency virus [HIV] infection).

Primary Pathogens

Histoplasmosis

Histoplasmosis is the most common fungal infection in the United States. It is caused by the dimorphic fungus Histoplasma capsulatum. In the United States, the prevalence of histoplasmosis is especially high along the major river valleys of the Midwest (e.g., Ohio, Michigan, Illinois, Mississippi, Missouri, Kentucky, Tennessee, Georgia, and Arkansas). In fact, on the basis of skin test surveys it is estimated that 80% to 90% of the population throughout these areas shows signs of previous infection. Histoplasmosis is often called Ohio Valley Fever.

H. capsulatum is commonly found in soils enriched with bird excreta, such as the soil near chicken houses, pigeon lofts, barns, and trees where starlings and blackbirds roost. The birds themselves, however, do not carry the organism, although the H. capsulatum spore may be carried by bats. Generally, an individual acquires the infection by inhaling the fungal spores that are released when the soil from an infected area is disturbed (e.g., children playing in dirt).

When the H. capsulatum organism reaches the alveoli, at body temperature it converts from its mycelial form (mold) to a parasitic yeast form. The clinical manifestations of histoplasmosis are strikingly similar to those of tuberculosis. The incubation period for the infection is approximately 17 days. Only about 40% of those infected demonstrate symptoms, and only about 10% of these patients are ill enough to consult a physician. Depending on the individual’s immune system, the disease may take on one of the following forms: asymptomatic primary histoplasmosis, acute symptomatic pulmonary histoplasmosis, chronic histoplasmosis, and disseminated histoplasmosis.

Asymptomatic histoplasmosis is the most common form of histoplasmosis. Normally it produces no signs or symptoms in otherwise healthy individuals who become infected. The only residual sign of infection may be a small, healed lesion of the lung parenchyma or calcified hilar lymph nodes. The patient has a positive histoplasmin skin test result.

Acute symptomatic pulmonary histoplasmosis tends to occur in otherwise healthy individuals who have had an intense exposure to H. capsulatum. Depending on the number of spores inhaled, the individual signs and symptoms may range from a mild to serious illness. Mild signs and symptoms include fever, muscle and joint pain, headache, dry hacking cough, chills, chest pain, weight loss, and sweats. People who have inhaled a large number of spores may develop a severe acute pulmonary syndrome, a potentially life-threatening condition in which the individual becomes extremely short of breath. The acute pulmonary syndrome is often referred to as spelunker’s lung because it frequently develops after excessive exposure to bat excrement stirred up by individuals exploring caves. During this phase of the disease, the patient’s chest radiograph generally shows single or multiple infection sites resembling those associated with pneumonia.

Chronic pulmonary histoplasmosis is characterized by infiltration and cavity formation in the upper lobes of one or both lungs. This type of histoplasmosis often affects people with an underlying lung disease such as emphysema. It is most commonly seen in middle-aged white men who smoke. Signs and symptoms include fatigue, fever, night sweats, weight loss, a productive cough, and hemoptysis—similar to signs and symptoms of tuberculosis. Often the infection is self-limiting. In some patients, however, progressive destruction of lung tissue and dissemination of the infection may occur.

Disseminated histoplasmosis may follow either self-limited histoplasmosis or chronic histoplasmosis. It is most often seen in very young or very old patients with compromised immune systems (e.g., patients with HIV infection). Even though the macrophages can remove the fungi from the bloodstream, they are unable to kill the fungal organisms. As a result, disseminated histoplasmosis can affect nearly any part of the body, including eyes, liver, bone marrow, skin, adrenal glands, and intestinal tract. Depending on which body organs are affected, the patient may develop anemia; pneumonia; pericarditis; meningitis; adrenal insufficiency; and ulcers of the mouth, tongue, or intestinal tract. If untreated, disseminated histoplasmosis is usually fatal.

Screening and Diagnosis

Coccidioidomycosis

Coccidioidomycosis is caused by inhalation of the spores of Coccidioides immitis, which are spheric fungi carried by wind-borne dust particles. The disease is endemic in hot, dry regions. In the United States, coccidioidomycosis is especially prevalent in California, Arizona, Nevada, New Mexico, Texas, and Utah. About 80% of the people in the San Joaquin Valley are coccidioidin skin test positive. Because the prevalence of coccidioidomycosis is high in these regions, the disease is also known as California Disease, Desert Fever, San Joaquin Valley Disease, and Valley Fever. The fungus has been isolated in these regions from soils, plants, and a large number of vertebrates (e.g., mammals, birds, reptiles, amphibians).

When C. immitis spores are inhaled, they settle in the lungs, begin to germinate, and form round, thin-walled cells called spherules. The spherules, in turn, produce endospores that make more spherules (the spherule-endospore phase). The disease usually takes the form of an acute, primary, self-limiting pulmonary infection with or without systemic involvement. Some cases, however, progress to disseminated disease.

Clinical manifestations are absent in about 60% of the people who have a positive skin test result. In the remaining 40%, most of the patients demonstrate coldlike symptoms such as fever, chest pain, cough, headaches, and malaise. In uncomplicated cases, patients generally recover completely and enjoy lifelong immunity. In approximately 1 in 200 cases, however, the primary infection does not resolve and progresses with varied clinical manifestations. Chronic progressive pulmonary disease is characterized by nodular growths called fungomas and cavity formation in the lungs. Disseminated coccidioidomycosis occurs in about 1 in 6000 exposed persons. When this condition exists, the lymph nodes, meninges, spleen, liver, kidney, skin, and adrenals may be involved. The skin lesions (e.g., bumps on the face and chest) are commonly accompanied by arthralgia or arthritis, especially in the ankles and knees. This condition is commonly called desert bumps, desert arthritis, or desert rheumatism. Death is most commonly caused by meningitis.

Blastomycosis

Blastomycosis (also called Chicago disease, Gilchrist’s disease, and North American blastomycosis) is caused by Blastomyces dermatitidis. Blastomycosis occurs in people living in the south-central and midwestern United States and Canada. The infection occurs in 1 to 2 out of every 100,000 people in these areas. Cases also have been reported in Central America, South America, Africa, and the Middle East. B. dermatitidis inhabits areas high in organic matter, such as forest soil, decaying wood, animal manure, and abandoned buildings. Blastomycosis is most common among pregnant women and middle-aged African-American men. The disease also is found in dogs, cats, and horses.

The primary portal of entry of B. dermatitidis is the lungs. The acute clinical manifestations resemble those of acute histoplasmosis, including fever, cough, hoarseness, aching of the joints and muscles, and, in some cases, pleuritic pain. Unlike histoplasmosis, however, the cough is frequently productive, and the sputum is purulent. Acute pulmonary infections may be self-limiting or progressive. When the condition is progressive, nodules and abscesses develop in the lungs. Extrapulmonary lesions commonly involve the skin, bones, reproductive tract, spleen, liver, kidney, or prostate gland. The skin lesions may, in fact, be the first signs of the disease. It often begins on the face, hands, wrists, or legs as subcutaneous nodules that erode to the skin surface. Dissemination of the yeast also may cause arthritis and osteomyelitis, and involvement of the central nervous system causes headache, convulsions, coma, and mental confusion. Standardized testing procedures for blastomycosis are not available. The diagnosis of blastomycosis can be made from direct visualization of the yeast in sputum smears. Culture of the fungus also can be performed. An accurate blastomycin skin test is not available.

Opportunistic Pathogens

Opportunistic yeast pathogens such as Candida albicans, Cryptococcus neoformans, and Aspergillus also are associated with lung infections in certain patients.

C. albicans occurs as normal flora in the oral cavity, genitalia, and large intestine. C. albicans infection of the mouth is characterized by a white, adherent, patchy infection of the mouth, gums, cheeks, and throat. In patients with HIV infection, C. albicans often causes infection of the mouth, pharynx, vagina, skin, and lungs.

C. neoformans proliferates in the high nitrogen content of pigeon droppings and is readily scattered into the air and dust. Today, Cryptococcus is most often seen in patients with HIV infection and persons undergoing steroid therapy.

Aspergillus may be the most pervasive of all fungi—especially Aspergillus fumigatus. Aspergillus is found in soil, vegetation, leaf detritus, food, and compost heaps. Persons breathing the air of granaries, barns, and silos are at greatest risk. Aspergillus infection usually occurs in the lungs. It is almost always an opportunistic infection and poses a serious threat to patients with HIV infection.

imageOVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Fungal Diseases of the Lungs

The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by Alveolar Consolidation (see Figure 9-9) and, in severe cases, with fibrosis, Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10)—the major anatomic alterations of the lungs associated with fungal diseases of the lungs (see Figure 18-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Moderate to Severe)* (Restrictive Lung Pathology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC FEVT FEV1/FVC ratio FEF25%-75%
↓ N or ↓ N or ↑ N or ↓
FEF50% FEF200-1200 PEFR MVV
N or ↓ N or ↓ N or ↓ N or ↓

image

LUNG VOLUME AND CAPACITY FINDINGS

VT IRV ERV RV  
N or ↓ ↓ ↓ ↓  
VC IC FRC TLC RV/TLC ratio
↓ ↓ ↓ ↓ N

image

Arterial Blood Gases

Oxygenation Indices*

Moderate to Severe Stages

*C(a-image)O2, Arterial-venous oxygen difference; DO2, total oxygen delivery; O2ER, oxygen extraction ratio; image, pulmonary shunt fraction; image, mixed venous oxygen saturation; image, oxygen consumption.

Hemodynamic Indices‡

Severe Fungal Disease

CVP RAP image PCWP CO SV
↑ ↑ ↑ N N N
SVI CI RVSWI LVSWI PVR SVR
N N ↑ N ↑ N

image

‡CO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; image, 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.

ABNORMAL LABORATORY TEST AND PROCEDURE RESULTS

Radiologic Findings

Chest Radiograph

During the early stages of many pulmonary fungal infections, localized infiltration and consolidation with or without lymph node involvement are commonly seen (Figure 18-2). Single or numerous spheric nodules may be seen (Figure 18-3). During the advanced stages, bilateral cavities in the apical and posterior segments of the upper lobes are often seen (Figure 18-4). In disseminated disease a diffuse bilateral micronodular pattern and pleural effusion may be seen. Fibrosis and calcification of healed lesions can be identified. Finally, because right-sided heart failure may develop as a secondary problem during the advanced stages of fungal disease, an enlarged heart may be seen on the chest radiograph. These radiologic findings are very similar to those seen in pulmonary TB.

image
FIGURE 18-2 Acute inhalational histoplasmosis in an otherwise healthy patient. This young man developed fever and cough after tearing down an old barn. The study shows bilateral hilar adenopathy and diffuse nodular opacities. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of diseases of the chest, ed 4, Philadelphia, 2005, Elsevier.)
image
FIGURE 18-3 Histoplasmoma, showing a well-defined spheric nodule. The central portion of the nodule shows calcification. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of diseases of the chest, ed 4, Philadelphia, 2005, Elsevier.)
image
FIGURE 18-4 Chronic cavitary histoplasmosis. Note the striking upper zone predominance of the shadows. Numerous large cavities. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of diseases of the chest, ed 4, Philadelphia, 2005, Elsevier.)

General Management of Fungal Disease

The antifungal agents are the first line of defense in treating fungal lung infections. In general, the drug of choice for most fungal infections is intravenously administered polyene amphotericin B (Fungizone). Although ketoconazole was used as a first-line agent against common fungal organisms, it has largely been replaced by the trizoles, fluconazole and itraconazole. The echinocandins, a relatively new class of antifungal agents, are now available (Table 18-1).

Table 18-1

Antifungal Agents

Agents Common Uses (Microorganisms)
Polyenes  
Amphotericin B (Fungizone) Cryptococcus neoformans, Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis, Candida species, Aspergillus species
Amphotericin B colloidal dispersion (Amphotec) Candida species, Aspergillus species, mucormycosis, C. neoformans
Azoles  
Ketoconazole (Nizoral) Candida species, C. neoformans, H. capsulatum, B. dermatitidis
Fluconazole (Diflucan) Candida species, Aspergillus species, C. neoformans, H. capsulatum
Itraconazole (Sporanox) B. dermatitidis, C. immitis, Sporothrix schenckii
Echinocandins  

Aspergillus species, Candida species Other Antifungals   Flucytosine (Ancobon) Aspergillus species, Candida species, C. neoformans Griseofulvin (Fulvicin) Tinea corporis, tinea cruris, tinea barbae Terbinafine (Lamisil) Tinea corporis, tinea pedis, tinea manuum

image

Modified from Gardenhire DS: Rau’s respiratory care pharmacology, ed 7, St Louis, 2008, Elsevier.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. Because of the hypoxemia associated with the fungal pulmonary condition, supplemental oxygen may be required. Because of the alveolar consolidation produced by a fungal disorder, capillary shunting may be present. Hypoxemia caused by capillary shunting is often refractory to oxygen therapy. In addition, when the patient demonstrates chronic ventilatory failure during the advanced stages of fungal disease, caution must be taken not to overoxygenate the patient (see Oxygen Therapy Protocol, Protocol 9-1).

CASE STUDY

Fungal Diseases of the Lungs

Admitting History

A 56-year-old cattle driver was admitted to the arthritis clinic of a small hospital just outside Phoenix because of joint pain. The man stated that the tenderness in his joints prevented him from riding his horse for any extended period. He was born on a cattle ranch in New Mexico and spent most of his adult life working as a cattle driver in Arizona, New Mexico, and Colorado. He had always considered himself an “outdoors” kind of man. He loved the range, wide open spaces, clear air, and beauty of the desert.

In his early 20s he traveled to the East Coast to attend college. While there, he became withdrawn and depressed and felt confined. After 1 year he dropped out of college and returned to New Mexico. Shortly after returning home, his symptoms of depression disappeared. He worked on a large cattle ranch, made several new friends, and was content with the fact that he “belonged on the open range.” He never married or settled down in one place he could call home. He often said that the great outdoors was his home. He never owned an automobile. In fact, he often said that the only things of real value he owned were a roan quarter horse and a saddle.

The hospital had no past medical record on the patient. The man reported, however, that although he was rarely ill, he had gone to see a doctor while in Colorado about a year ago for severe “cold” symptoms, which included fever, cough, chest pain, headaches, and a general feeling of fatigue. He was a nonsmoker, although he did chew tobacco for a short time in his teens. The patient verified that he consumed alcohol regularly on Friday and Saturday nights. The man estimated that on average he consumed between 6 and 10 beers per outing and sometimes more. Despite the patient’s somewhat rugged living conditions and alcohol consumption, he was not overweight and was in reasonably good physical condition.

Physical Examination

The patient appeared to be a well-developed, well-nourished white man in moderate respiratory distress. He complained of soreness and stiffness in all his joints. He also stated that he thought he had a “bad cold” and that he was short of breath.

The patient’s knees and ankle joints were warm, swollen, and tender to the touch. Although his skin appeared weathered and tan, his lips and nail beds were cyanotic. He demonstrated a frequent cough productive of a moderate amount of thick, yellow sputum. Although the cough was strong, he experienced difficulty raising sputum during each coughing episode. His vital signs were as follows: blood pressure 160/90, heart rate 90 bpm, respiratory rate 18/min, and oral temperature 37.8° C (100° F). Palpation revealed a few erythematous lesions on his anterior chest, of which he was unaware. In addition, a walnut-sized erythematous lesion was present on the patient’s left cheek. Percussion of the chest was not remarkable. Auscultation revealed bilateral crackles and rhonchi in the lung apices.

The patient’s chest x-ray film showed scattered infiltrates consistent with fibrosis and calcification and multiple spheric nodules throughout both lungs. In the upper lobes of both lungs, two to three small, 1- to 3-cm cavities were visible. On room air the patient’s arterial blood gas values (ABGs) were as follows: pH 7.51, Paco2 29, image 22, and Pao2 64 mm Hg. The patient was admitted to the hospital. Concerned about the patient’s respiratory status, the physician requested a respiratory care consultation. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S “I feel short of breath, and my joints are swollen and painful.”

O Cyanosis; cough: frequent and strong, producing moderate amounts of thick, yellow sputum; vital signs: BP 160/90, HR 90, RR 18, T 37.8° C (100° F); palpation: red lesions on anterior chest and left cheek; auscultation: bilateral crackles and rhonchi in lung apices; CXR: bilateral fibrosis and calcification and spheric nodules; two to three 1- to 3-cm cavities in both upper lobes; ABGs (room air): pH 7.51, Paco2 29, image 22, Pao2 64

A 

P Initiate Oxygen Therapy Protocol (2 L/min per nasal cannula) and Bronchopulmonary Hygiene Therapy Protocol (C&DB instruction, PD to both upper lobes q shift × 3 days). Order sputum culture (routine, AFB, and fungal). Encourage fluid intake. Monitor (oximeter, I&O).

5 Days after Admission

After microscopy of the patient’s sputum and a spherulin skin test, the diagnosis of coccidioidomycosis was written in the patient’s chart. The patient had been receiving amphotericin B intravenously for 2 days. A complete pulmonary function study revealed a moderate-to-severe restrictive disorder, with a moderate obstructive component as well.

When the respiratory practitioner entered the patient’s room, the man was sitting up in bed, appearing cyanotic, short of breath, and fatigued. He stated that he was becoming tired of people in white outfits coming in and out of his room, day and night, with “needles, pills, and bills.” He further stated that he still could not get a good breath of air. In fact, he said it was more difficult for him to breathe today than it had been on the day he entered the hospital.

The patient still had a frequent, strong cough productive of moderate amounts of thick, opaque sputum. His vital signs were as follows: blood pressure 165/95, heart rate 96 bpm, respiratory rate 24/min, and temperature 37° C (98.6° F). Auscultation revealed persistent bilateral tight wheezes, and bilateral crackles and rhonchi in the apices of both lungs. A current chest x-ray film was not available. His hemoglobin oxygen saturation measured by pulse oximetry (Spo2) was 88%. His ABGs were as follows: pH 7.54, Paco2 27, image 21, and Pao2 55. At this time, the following SOAP was charted.

Respiratory Assessment and Plan

S “I still can’t get a good breath of air.”

O Respiratory distress: cyanotic, short of breath; positive spherulin skin test; coccidioidomycosis organisms seen in sputum smear; frequent strong cough: moderate amount of thick, opaque sputum; vital signs: BP 165/95, HR 96, RR 24, T normal; bilateral crackles and rhonchi in the lung apices; Spo2 88%; ABGs: pH 7.54, Paco2 27, image 21, Pao2 55

A 

P Up-regulate Oxygen Therapy Protocol (3 L/min nasal cannula). Add Aerosolized Medication Protocol; up-regulate Bronchopulmonary Hygiene Therapy Protocol (2 mL 10% acetylcysteine with 0.2 mL albuterol q6h followed by C&DB and PD to both upper lobes). Add supervised use of flutter valve 2 times per shift. Request repeat CXR. Continue to monitor and reevaluate.

10 Days after Admission

On this day, the respiratory therapist found the patient walking up and down the corridor talking to various staff members and patients. The man appeared to be in no respiratory distress. He stated that he was breathing much better and was ready to ride his horse a long distance in any direction away from the hospital.

No spontaneous cough was noted. When asked to generate a cough, the patient produced a strong, nonproductive cough. His vital signs were as follows: blood pressure 135/88, heart rate 80 bpm, respiratory rate 14/min, and normal temperature. Auscultation revealed persistent bilateral crackles in the apices of both lungs. A recent chest x-ray film was not available. His pulse oximetry on room air showed an Spo2 of 91%. His ABGs were as follows: pH 7.44, Paco2 34, image 23, and Pao2 71. On the basis of these clinical data, the following SOAP note was written.

Respiratory Assessment and Plan

Discussion

Respiratory care practitioners (RCPs) who work in the Southwest, where coccidioidomycosis is endemic, would probably anticipate this diagnosis in the patient with bilateral pulmonary infiltrates, swollen tender joints, and the skin rash typical of this lesion. Others could not be blamed if they missed this potential diagnosis until the coccidioidal skin test came back positive and the sputum fungal smear demonstrated the presence of the coccidioidomycosis organism. In this case, the patient demonstrated the clinical manifestations associated with the following two anatomic alterations of the lungs: Increased Alveolar-Capillary Membrane Thickness (e.g., bilateral fibrosis and calcification; see Figure 9-10) and Excessive Bronchial Secretions (e.g., cough, sputum, and rhonchi; see Figure 9-12).

The first assessment—that the patient is hypoxemic despite alveolar hyperventilation and that he has alveolar fibrosis and cavity formation—is correct. For the hypoxemia, oxygen therapy is appropriate and should be started with a nasal oxygen cannula at 1 to 2 L/min and then regulated with a pulse oximeter. In treating this patient, as with any other pneumonia, the assessing RCP should quickly obtain sputum, Gram stain, and acid-fast bacillus and fungal preparations; this step was appropriately done in this case. The treating RCP would do well to understand the use of tuberculin and fungal testing in such patients and to understand that, as with other pneumonic infiltrates, the therapist’s impact once such testing was done would probably be minimal.

In the second assessment, the offending organism has been isolated and appropriate therapy with intravenous amphotericin B started. The patient is still hypoxemic, and up-regulation of his Oxygen Therapy Protocal (perhaps to 3 or 4 L/min, or with a nonrebreathing mask if the former is unsuccessful) is indicated. Because the patient is still wheezing and coughing up thick, opaque sputum and because his dyspnea is not relieved so far, up-regulation of the Bronchopulmonary Hygiene Therapy Protocol and addition of the Aerosolized Medication Protocol with a trial of bronchodilator therapy and mucolytic therapy are in order. Because the patient is not improving, a repeat chest x-ray examination appears to be indicated.

At the last assessment 10 days after the patient’s admission to the hospital, clear improvement is noted. Oximetry reveals good peripheral oxygen saturation, and the blood gases are much improved. Now is the time for the treating therapist to reduce the intensity of the patient’s respiratory care, and this step is illustrated in the appropriate response for this section of the case study. Follow-up pulmonary function testing 6 to 12 months after the abatement of acute illness would be worthwhile.

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