Miscellaneous Chest Diseases

Chapter 26

Miscellaneous Chest Diseases

Dennis M. Marchiori

ACUTE RESPIRATORY DISTRESS SYNDROME

EXTRINSIC ALLERGIC ALVEOLITIS

PNEUMOCONIOSES

PNEUMOTHORAX

SARCOIDOSIS

Acute Respiratory Distress Syndrome

Background

Acute respiratory distress syndrome (ARDS) occurs when the pulmonary system is affected as a result of more generalized, multiorgan capillary damage.1 The pathogenic sequence appears related to inappropriate activation of the complement cascade,2,3 resulting in increased capillary permeability and pulmonary edema. Eventually fluid spills into the alveolar spaces, leading to hemorrhaging, reduced surfactant levels, and a resultant smaller functional area for gas exchange. A wide range of factors and conditions are associated with the development of ARDS (Box 26-1).

Box 26-1   Partial List of Factors Associated with Adult Respiratory Distress Syndrome2,26,31

• Amniotic fluid embolism

• Arterial embolism

• Aspiration

• Drug abuse

• Eclampsia

• Fat embolism

• Fractures

• Heat stroke

• High-altitude pulmonary edema

• Pancreatitis

• Pulmonary contusions

• Radiation pneumonitis

• Shock

• Smoke inhalation

• Transplantation

Imaging Findings

No changes are detectable radiographically during the initial stage of ARDS unless caused by pneumonia, aspiration, or another pulmonary condition, in which case the pulmonary findings of the concurrent disease may be noted. The latter stages of the disease are marked by alveolar filling. Patchy areas of incomplete lung consolidation are noted at first (Fig. 26-1), which eventually become more uniform, generalized, and homogenous. The radiographically detectable features gradually resolve during the ensuing weeks. Pleural effusion is rare.

image
FIG 26-1 Diffuse pulmonary consolidations with air bronchograms (arrows) are the result of ARDS after viral pneumonia. This appearance is radiologically indistinguishable from pulmonary alveolar edema and diffuse pneumonia. From Reed JC: Chest radiology: plain film patterns and differential diagnoses, ed 5, St. Louis, 2003, Mosby.

Clinical Comments

ARDS is characterized by rapidly progressing respiratory distress.4,5 Alveolar filling is followed by acute respiratory failure requiring mechanical ventilation and oxygen administration. The eventual clinical outcome depends heavily on whether the patient develops a nosocomial infection, hemorrhage, sepsis, lung barotrauma, or another major complication.3

Key Concepts

• ARDS involves increased capillary permeability that is caused by a wide variety of systemic and pulmonary insults.

• The radiographic features are related to excessive fluid accumulation in the alveolar spaces and present as varying degrees of lung consolidation.

Extrinsic Allergic Alveolitis

Background

Extrinsic allergic alveolitis (EAA), also known as hypersensitivity pneumonitis, is a nonatopic, nonasthmatic allergic lung disease. EAA manifests as an occupational lung disease caused by the inhalation of organic dusts; this then produces granulomatous and interstitial lung changes. Table 26-1 lists several etiologic agents.

TABLE 26-1

SELECTED PROVOCATIVE AGENTS OF EXTRINSIC ALLERGIC ALVEOLITIS

Disease Provocative agent
Bagassosis Moldy sugar cane
Bird fancier’s lung Avian excreta
Farmer’s lung Moldy hay
Humidifier lung Contamination from humidifying, heating, and air conditioning systems
Malt worker’s lung Moldy malt
Maple bark stripper’s lung Moldy maple bark
Mushroom worker’s lung Mushroom spores
Sequoiosis Redwood dust
Suberosis Moldy cork dust

Imaging Findings

The radiographic presentation of EAA is the same regardless of the type of organic dust inhaled,6 but varies according to intensity of exposure.7 The early stages of EAA are characterized by reversible, multiple, small (1- to 3-mm), nodular radiodensities scattered bilaterally throughout the lung zones; although less common, the lung apices may be spared (Fig. 26-2).812 Repeated exposures may result in a chronic interstitial (honeycomb) pattern11 with upper lobe predominance.

image
FIG 26-2 EAA presenting with (A) bilateral diffuse infiltrate and (B) small pulmonary nodules on a computed tomogram after exposure to pigeon droppings. From Swensen SJ: Radiology of thoracic diseases: a teaching file, St. Louis, 1993, Mosby.

Clinical Comments

Acute EAA is characterized by sudden onset of malaise, chills, fever, cough, dyspnea, and nausea within hours after exposure to the offending agent. Subacute and chronic forms are characterized by a persistent cough and slowly progressing dyspnea, anorexia, and weight loss. The patient’s history of exposure preceding the clinical symptoms is important for a proper diagnosis.

Key Concepts

• EAA comprises a group of diseases caused by the inhalation of organic dusts.

• The radiographic appearance is marked by the presence of small radiopaque nodules scattered throughout the lung fields.

• Chronic forms of the disease often develop a chronic interstitial pattern.

Pneumoconioses

Background

Pneumoconioses are a group of diseases caused by inhalation of inorganic dust and its accumulation in the lung.7 The dust deposits cause a nonneoplastic lung reaction that may be seen on radiographs. Asbestos, silicon, talc, beryllium, and coal dust incite a fibrogenic tissue reaction throughout the lung.13 Tin, barium, iron, and other inert particles do not incite fibrogenic changes but do cause particle-laden macrophages to accumulate in the lung.14 These reactions are called benign pneumoconioses (even though their radiographic appearance can be dramatic) because they are less aggressive.

Imaging Findings

The chest radiograph is the primary means of determining the presence and extent of pneumoconiosis.15 The International Labor Office (ILO) has established a classification system for the radiographic appearance of pneumoconioses16,17 that focuses on the size and shape of the lung nodules. The classification also includes a detailed categorization of pleural thickening.

The radiographic appearance of pneumoconiosis depends on the type and amount of dust inhaled and individual immunologic lung reactions (Table 26-2).18,19

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Feb 2, 2016 | Posted by in RESPIRATORY IMAGING | Comments Off on Miscellaneous Chest Diseases

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