PNEUMONIA

PNEUMONIA

 

Introduction

Pneumonia is an acute infection of the alveolar spaces of the lungs. The term includes any inflammatory condition of the lung in which some or all of the alveoli are filled with fluid and blood cells.

            The patient experienced bacterial pneumonia. This is a common type of pneumonia, caused most frequently by pneumococci. This disease begins with infection in the alveoli; the pulmonary membrane becomes inflamed and highly porous so that fluid and even red and white blood cells leak out of the blood into the alveoli. Thus, the infected alveoli become progressively filled with fluid and cells, and the infection spreads by extension of bacteria from alveolus to alveolus. Eventually, large areas of the lungs, sometimes whole lobes or even a whole lung, become “consolidated,” which means that they are filled with fluid and cellular debris ( 2000).

            The patient had a history of acute febrile illness associated with chill, chest pain and cough, especially with expectoration of viscid, rusty sputum which is practically diagnostic of pneumonia itself. The diagnosis is confirmed after physical examination of the patient discloses tachycardia, tachypnea, cyanosis, and signs of consolidation.

 

Cellular Pathophysiology

            Pneumococci reach the lungs via the respiratory passages. They lodge in the alveoli, proliferate, and initiate an inflammatory process that begins with an outpouring of protein-rich fluid into the alveolar spaces. This fluid acts as a culture medium for the pneumococci and as a vehicle for their spread to other alveoli, segments (lobules), and lobes (1998).

            Pathologically, the early stage of pneumonia (the first 12 to 48 hours) is called red hepatization because of the liver-like, reddish appearance of the consolidated lung that results from the characteristic widespread dilation of pulmonary blood vessels and the extravasation of erythrocytes into the alveoli ( 1998).

            A few hours after the pulmonary capillaries dilate and the edema fluid pours into the alveoli, polymorphonuclear leukocytes enter the alveolar spaces, rapidly fill the alveoli, and consolidate the lung (grey hepatization). Surface phagocytosis occurs, without antibodies, by leukocytic trapping of the bacteria against an alveolar wall or another leukocyte; the process is more active when large numbers of leukocytes are present ( 1998). Tissue sections show few pneumococi in the consolidated lung, but many in the advancing margin of the lesion where edema fluid is abundant and leukocytes are sparse (1994).

            The macrophage reaction occurs next, as large mononuclear cells enter the alveoli, engulf any remaining pneumococci, and phagocytized the cellular debris of the exudate. This process continues until resolution is complete, which is indicated by physical examination and x-ray evidence that the lungs are clear (1994).

            The pathogenesis of other bacterial pneumonias resembles that of pneumococcal infections, but abscess formation may occur when infection is caused by organisms that destroy pulmonary tissue.

 

Systemic Pathophysiology

            The patient who has pneumonia would experience a sudden, with a shaking chill, sharp pain in the involved hemothorax on the onset. Along with this are the appearance of cough with early sputum production, fever, and headache. All these symptoms are usually present as an effect of the cellular events that took place: red hepatization, grey hepatization, surface phagocytosis, and macrophage reaction.

            All these cellular events lead to changes in the gas exchange functions of the lungs. In pneumonia, the gas exchange functions of the lungs change in different stages of the disease. In the early stages, the pneumonia process might well be localized to only one lung, with alveolar ventilation reduced while blood flow through the lung continues normally (2001). This results in two major pulmonary abnormalities: (1) reduction in the total available surface area of the respiratory membrane and (2) decreased ventilation-perfusion ratio. Both these effects cause hypoxemia (low blood oxygen) and hypercapnia (high blood carbon dioxide).

           

Human Pathophysiology

            The effect of the resulting decreased ventilation-perfusion ratio in the patient with pneumonia is that the blood passing through the aerated lung becomes 97 per cent saturated with oxygen, whereas that passing through the unaerated lung is about 60 per cent saturated, causing the mean saturation of the blood in the left heart and in the aorta to be about 78 per cent, which is far below normal ( 2000).

            Oxygen is one of the most necessary nutrients in the body. Whenever the availability of oxygen to the tissues decreases, such as in pneumonia, the blood flow through the tissues increases markedly.

            Pneumococcal pneumonia is the most common bacterial pneumonia; many of its features are similar to those of pneumonia caused by other organisms. The disease is generally sporadic. Healthy carriers are usually responsible for the infection of others, but there is no practical way to identify carriers and eliminate the organisms (1998).

 

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