Synonyms.—Apneumatosis; Collapse of the Lung.
Definition.—A collapse of the air-vesicles of the whole or part of a lung, and which may be either congenital or acquired.
Etiology.—Congenital.—This form is usually due to causes that prevent a prompt and complete establishment of the function of respiration at birth, rather than disease of the pulmonary organs. Thus a protracted labor, a compression of the cord, or a placental separation, a premature birth, or a plugging of the bronchioles by mucous or liquor amnii, where the child draws into the larynx these secretions during an inspiratory effort before the mouth has cleared the maternal outlet, may give rise to atelectasis.
When acquired, it is always a secondary affection, and is usually due to obstruction or compression.
Cases due to obstruction are those preceded by measles, whooping-cough, diphtheria, influenza, bronchitis, or broncho-pneumonia; the bronchioles becoming filled with a viscid mucus or muco-pus, the air fails to enter the vesicles, and as soon as the air already present escapes, or is absorbed, collapse takes place.
When due to compression, it is from pleural or pericardial effusions, anasarca, cardiac hypertrophy, or abnormal growths. Conditions weakening the respiratory functions also favor atelectasis; thus paralysis of the pneumogastric nerve, enfeebled vitality, as in rickets, poor chest development, feeble inspiratory muscles, and when the environment tends to lower vital force.
Pathology.—The collapse may involve quite a large area, diffuse atelectasis, or it may be confined to small patches, lobular atelectasis, the former being more marked when congenital. The affected portions are airless, do not crepitate, and sink when placed in water. They are slightly depressed from the general surface of the lung, are dense, and of a dark bluish or purplish color; when cut, a dark liquid may be pressed from their surface.
If the disease is recent, the collapsed portions, after death, may be inflated through the bronchus; but if of long standing, the vessel is totally destroyed. The pleura usually remains normal.
Symptoms.—The symptoms are chiefly those of imperfect breathing and defective aeration of the blood, the severity of which depends upon the rapidity of development and amount of lung tissue involved. In congenital cases, the child comes into the world more or less asphyxiated, the respiration is labored, and the child is more or less cyanotic. It appears feeble, sleeps most of the time, nurses with difficulty, or not at all, and has a feeble cry, or moans in its sleep. The surface is cool; the temperature normal, or subnormal. Muscular twitching may be the forerunner of convulsions and death.
In acquired cases, the primary lesion may so overshadow the atelectatic condition as to be entirely overlooked, especially when but few vesicles are involved. If preceded by bronchitis or broncho-pneumonia, which is generally the case, and if the lesion be extensive, there will be a sudden aggravation of all the symptoms. The breathing becomes very rapid, is shallow and arhythmic. The patient is restless, the nose, ears, and finger-tips become blue, the extremities are cold, and the temperature is often subnormal.
The physical signs depend upon the extent of the collapsed tissue; thus, if the patches are small and involve both lungs, the signs are negative, while if large patches are involved, the physical signs are those of a consolidated lung.
Diagnosis.—In the congenital form, where marked enough to give rise to characteristic symptoms, the diagnosis is comparatively easy. The acquired form, however, is often quite difficult, associated as it is with capillary bronchitis, catarrhal pneumonia, and lobar pneumonia.
The sudden appearance of grave symptoms in bronchitis—such as quick, shallow breathing, rapid pulse, cyanotic discoloration, with fall of temperature—is the most important diagnostic feature. The absence of fever would be important in distinguishing it from pneumonia.
Prognosis.—If congenital, and the child be feeble or premature, or the fetal circulatory openings remain unclosed, the prognosis is unfavorable; if, however, the lesion is slight and restorative measures are early used, the prospects are more hopeful.
In acquired atelectasis, the prognosis is usually grave, though not necessarily fatal. When the result of whooping-cough or severe broncho-pneumonia, there is usually a fatal termination.
Treatment.—In infants, the air-passages should be cleared, and, where possible, artificial respiration should be practiced, and the child prevented from remaining too quiet. Its sleep should be disturbed at frequent intervals, and crying and coughing provoked, thus securing forced inspiration. In premature births, the incubator has been suggested as a possible means in prolonging life until nature can carry on the vital processes unaided by artificial heat.
In the acquired form, in addition to the measure used for the primary lesion, capillary bronchitis, lobar pneumonia, whooping-cough, etc., the patient should be instructed to change his position frequently, to avoid lying on the back for more than a few minutes at a time, and to practice full inspiration at frequent intervals. In extreme cases, inhalation of oxygen is to be advised.