Edema of Undetermined Origin

Aliya N. Husain MBBS

Vinay Kumar MD

*The contributions of Dr. Lester Kobzik to the previous editions of this text are gratefully acknowledged. Dr. Anirban Maitra is also acknowledged for his contributions to this chapter.

Normal Lung

The lungs are ingeniously constructed to carry out their cardinal function: the exchange of gases between inspired air and blood. Developmentally, the respiratory system is an outgrowth

from the ventral wall of the foregut. The midline trachea develops two lateral outpocketings, the lung buds. The right lung bud eventually divides into three branches—the main bronchi—

and the left into two main bronchi, thus giving rise to three lobes on the right and two on the left. The lingula on the left is the middle lobe equivalent; however, the left lung is smaller than

the right. The right main stem bronchus is more vertical and more directly in line with the trachea than is the left. Consequently, aspirated foreign material, such as vomitus, blood, and

foreign bodies, tends to enter the right lung rather than the left. The main right and left bronchi branch dichotomously, giving rise to progressively smaller airways. Accompanying the

branching airways is the double arterial supply to the lungs, that is, the pulmonary and bronchial arteries. In the absence of significant cardiac failure, the bronchial arteries of aortic origin

can often sustain the vitality of the pulmonary parenchyma when pulmonary arterial supply is blocked, as by emboli.

Progressive branching of the bronchi forms bronchioles, which are distinguished from bronchi by the lack of cartilage and submucosal glands within their walls. Further branching of

bronchioles leads to the terminal bronchioles, which are less than 2 mm in diameter. The part of the lung distal to the terminal bronchiole is called the acinus; it is approximately spherical,

with a diameter of about 7 mm. As illustrated in Figure 15-5A , an acinus is composed of respiratory bronchioles (emanating from the terminal bronchiole), which give off several alveoli

from their sides. These bronchioles then proceed into the alveolar ducts, which immediately branch into alveolar sacs, the blind ends of the respiratory passages, whose walls are formed

entirely of alveoli, which are the site of gas exchange. The alveoli open into the ducts through large mouths. In the correct plane of section, therefore, all alveoli are open and have

incomplete walls. A cluster of three to five terminal bronchioles, each with its appended acinus, is usually referred to as the pulmonary lobule. As will be seen subsequently, this lobular

architecture assumes importance in distinguishing the major forms of emphysema.

From the microscopic standpoint, except for the vocal cords, which are covered by stratified squamous epithelium, the entire respiratory tree, including the larynx, trachea, and bronchioles,

is lined by pseudostratified, tall, columnar, ciliated epithelial cells, heavily admixed in the cartilaginous airways with mucus-secreting goblet cells. The bronchial mucosa also contains

neuroendocrine cells that exhibit neurosecretory-type granules and contain serotonin, calcitonin, and gastrin-releasing peptide (bombesin). Numerous submucosal, mucus-secreting glands

are dispersed throughout the walls of the trachea and bronchi (but not the bronchioles).

The microscopic structure of the alveolar walls (or alveolar septa) consists, from blood to air, of the following ( Fig. 15-1 ):

• The capillary endothelium lining the intertwining network of anastomosing capillaries.

• A basement membrane and surrounding interstitial tissue separating the endothelial cells from the alveolar lining

epithelial cells. In thin portions of the alveolar septum, the basement membranes of epithelium and endothelium are fused, whereas in thicker portions, they are separated by an interstitial

space (pulmonary interstitum) containing fine elastic fibers, small bundles of collagen, a few fibroblast-like interstitial cells, smooth muscle cells, mast cells, and, rarely, lymphocytes and

monocytes.

• Alveolar epithelium, which contains a continuous layer of two principal cell types: flattened, platelike type I pneumocytes (or membranous pneumocytes) covering 95% of the

alveolar surface and rounded type II pneumocytes. Type II cells are important for at least two reasons: (1) They are the source of pulmonary surfactant, contained in osmiophilic

lamellar bodies seen with electron microscopy, and (2) they are the main cell type involved in the repair of alveolar epithelium after destruction of type I cells.

• Alveolar macrophages, loosely attached to the epithelial cells or lying free within the alveolar spaces, derived from blood monocytes and belonging to the mononuclear

phagocyte system. Often, they are filled with carbon particles and other phagocytosed materials.

Figure 15-1Microscopic structure of the alveolar wall. Note that the basement membrane (yellow) is thin on one side and widened where it is continuous with the interstitial space.

Portions of interstitial cells are shown.

Figure 15-2Various forms of atelectasis in adults.

TABLE 15-1-- Classification and Causes of Pulmonary Edema

Hemodynamic Edema

Increased hydrostatic pressure (increased pulmonary venous pressure)

••Left-sided heart failure (common)

••Volume overload

••Pulmonary vein obstruction

Decreased oncotic pressure (less common)

••Hypoalbuminemia

••Nephrotic syndrome

••Liver disease

••Protein-losing enteropathies

Lymphatic obstruction (rare)

Edema Due to Microvascular Injury (Alveolar Injury)

Infections: pneumonia, septicemia

Inhaled gases: oxygen, smoke

Liquid aspiration: gastric contents, near-drowning

Drugs and chemicals: chemotherapeutic agents (bleomycin), other medications (amphotericin B), heroin, kerosene, paraquat

Shock, trauma

Radiation

Transfusion related

Edema of Undetermined Origin

High altitude

Neurogenic (central nervous system trauma)

the clinical setting, pulmonary congestion and edema are characterized by heavy, wet lungs. Fluid accumulates initially in the basal regions of the lower lobes because hydrostatic pressure

is greater in these sites (dependent edema). Histologically, the alveolar capillaries are engorged, and an intra-alveolar granular pink precipitate is seen. Alveolar microhemorrhages and

hemosiderin-laden macrophages ("heart failure" cells) may be present. In long-standing cases of pulmonary congestion, such as those seen in mitral stenosis, hemosiderin-laden

macrophages are abundant, and fibrosis and thickening of the alveolar walls cause the soggy lungs to become firm and brown (brown induration). These changes not only impair normal

respiratory function, but also predispose to infection.

Date: 2016-04-22; view: 694