PULMONARY ŒDEMA.
Causes, pneumonia, extra force of right heart or weakness of left, insufficiency of mitral valves, deflection of blood by obstruction in one portion of lung, pressure of tumor on pulmonary veins. Malignant œdema. Malignant catarrh. Bright’s disease. Anæmia. Parasitism. Symptoms, abnormal heart sound, or urinary secretion. Parasitism. Percussion shows flat sound auscultation lowered, respiratory murmur, heightened blowing. No crepitation. Expectoration serous. Prognosis grave. Treatment, attacks primary disease. Posture. Elimination. Dry capping. Heart tonic.
A dropsy of the lung tissue may supervene in weak conditions, in the course of inflammatory disease of the lungs; it may also depend on an imperfect balance in the forces of the right and left heart respectively, which leads to the habitual throwing of blood pressure back upon the lungs. Still more frequently the congestion and dropsy depends on insufficiency of the mitral valves by reason of which a reflux of blood toward the lungs takes place at each heart beat. The pressure of tumors on the pulmonary veins may have a similar action. Obstruction of circulation in one portion of lung may cause an extra blood pressure on an adjacent one, and œdema so caused may be found especially in cattle and pigs in which the interlobular connective tissue is specially abundant. This may be seen in miliary tuberculosis in cattle, and it probably contributes to produce the extraordinary liquid collections that characterize lung plague. In cattle also malignant œdema may affect the lung, and an œdematous condition is sometimes met with in malignant catarrh. Bright’s disease is another cause, the uræmic dropsy finding a favorite seat of election in the loose lung tissue unsupported by solid tissues. The anæmia resulting from parasitism like distomatosis may similarly affect the lung.
The symptoms of pulmonary œdema will usually be complicated by those of the affection causing it. Thus modification of the first heart sound or of the urinary secretion, or the existence of parasitism, would furnish valuable indications.
The physical signs of lung disease vary. If pneumonia is present it is betrayed by its characteristic symptoms. In the absence of inflammation there is dullness on percussion over the affected area, and on auscultation an absence of the respiratory murmur, and perhaps abnormal clearness of bronchial, cardiac and other sounds from deeper parts. It differs from pneumonia in the absence of fever and of any crepitation surrounding the consolidated portion. The expectoration is serous or watery, rather than rusty or purulent.
The prognosis is always grave in proportion to the incurable nature of the primary disease. Chronic valvular or Bright’s disease, miliary tuberculosis or malignant tumors would render the case hopeless, while in acute pneumonia, or nephritis or parasitism there may be some hope. The treatment will largely consist in the therapeutics of the primary disease, yet we may also seek to relieve the dangerous symptoms of œdema. The frequent change of position may serve to limit hypostatic accumulation. Diuretics or purgatives in strong patients will favor absorption. Pilocarpin more than any other agent secures temporary absorption but cannot be continued owing to its depressing effects. Digitalis is often valuable in improving the heart’s action, and acting freely on the kidneys. Dry capping on the chest acts as a derivative.
ATELECTASIS. COLLAPSE OF LUNG.
Atelectasis in bronchitis, congenital, etc. Airless condition in the absence of exudation. Causes, congenital persistence in butcher animals. Blocking of air tubes by exudate—ball valve. Desquamation of ciliated epithelium. Compression by hydrothorax, pneumothorax, and false membrane. Symptoms. Percussion flatness, juvenile respiration elsewhere, blowing sounds loud. Drum-like sounds on emphysema and pneumothorax. Cyanosis. Lesions, depressed, flesh-like, non-crepitating lobules or lobuletes, sink in water, dilatable. Treatment, rouse respiratory centres, douches, cold and warm, slapping, electricity, forced inspiration, diet, massage. Treat attendant disease.
This has been already referred to as a result of bronchitis, but it deserves special mention as a sequel of that affection, and in various domestic animals, as an independent condition. The condition is one of consolidation of lung by the complete exclusion of air, but without any infiltration of its substance by inflammatory exudate or dropsical effusion. The tissue remains in its normal state apart from the fact that its bronchioles and air sacs are undilated. The affected portion has a solid dark fleshy appearance. The collapsed portion often represents one lobule or group of lobules which communicate with a single bronchium.
Causes. In some instances the conditions remain from birth, the lobule never having been called into use. This is seen especially in cattle and other meat producing animals, in which active breathing is systematically suppressed in the interests of rapid growth and the deposition of fat. In the improved breeds the lungs remain larger than the exigencies of the life demand, and large portions remain out of use. In bronchitis the condition is acquired, and is mainly dependent on the blocking of a bronchial tube with tenacious mucus or a desiccated mass. The pathological lesions of bronchitis favor this since one of the earliest changes in the inflamed mucosa is the desquamation of the columnar epithelium. This removal of much of the cilia and the paralysis of much of what is left annihilates for a time the normal method of clearing away the secretion, and this being now produced in excess blocks the tubes. This secretion virtually acts like a ball valve in favoring the exit of the air during the convulsive expiration of coughing, and hindering its entrance during the succeeding inspiration. The bronchia and bronchioles decrease in size to near their termination, so that, as forced out in coughing, the secretion enters the larger tube and allows the exit of air, which as drawn back in inspiration it enters the smaller tube and closes it against any possible ærial entrance. Mendelssohn and Traube demonstrated this action by introducing a shot into a dog’s lung, and in two days the left lung was found collapsed and the right one the seat of complementary emphysema. The violence and frequency of the cough therefore bears a ratio to the occurrence and extent of atelectasis. Other causes are the compression of the lower lobes of the lung by hydrothorax, by pneumothorax (developed by lacerated lung or perforated chest wall) or by a false membrane contracting in process of organization.