Chapter IX: Part 9

Treatment is usually unsatisfactory. The hot, moist jacket, inhalations of vapors of warm water, of carbonate of ammonia, and of ether may be tried, counterirritants to the chest, and internally liquor ammonia acetatis and iodide of sodium would be indicated. When the membranes are somewhat loosened pilocarpin, or in weaker subjects apomorphine may assist their expulsion.

ACUTE CONGESTION OF THE LUNGS. PULMONARY HYPERÆMIA.

Active and passive congestions. Congestion of incipient pneumonia.
Congestion of over-exertion. Causes, lack of condition, fat, plethora,
gorged stomach, hot weather, cold rains, cold baths, infectious
diseases. Symptoms, dilated nostrils, labored breathing, deep lifting
of flanks, panting, pendent head, staring, fixed, bloodshot eyes,
pale—later dark red nasal mucosa, rapid pulse, palpitating heart, fine
crepitation, cold limbs, tremors, perspiration, obstinate standing,
till unable, blood from nose. Fulminant cases. Exposure cases. Course.
Termination. Resolution. Lesions, lungs black, gorged, do not
crepitate nor collapse, lessened buoyancy, cut surface, compressed
bronchioles and alveoli, right heart and veins gorged, blood black,
semi-liquid, petechiæ. Nature. Not yet inflammatory, blood
engorgement, no cell proliferation, migration, non-exudation,
pulmonary vaso-motor paresis, effect of blood pressure, of peptones,
etc., of exhaustion. Treatment, relieve respiratory muscles,
derivation to surface, stimulants, hot pediluvia and packs, relief of
vascular system, bleeding, heart stimulants, digitalis.

Congestion of the lungs occurs in all animals as the precursor of inflammation, but as death may occur without the supervention of actual inflammation a special notice appears to be demanded. The hyperæmia of the lungs may be seen in two forms, active and passive, the latter form being secondary to other diseases, such as valvular diseases of the left heart, by reason of which the blood is forced back on the lungs and creates mechanical congestion. The active form is a pathological process developed in the lung itself, and which often proves fatal through arrest of the circulation through this organ.

_Causes._ The pulmonary congestions preceding pneumonia are due to the same causes with that disease. The most typical, acute and deadly form of pulmonary congestion is usually due to _over-exertion in an animal that is fat and out of condition_. The English hunting field presents the most typical specimens. A horse that has just left the dealer’s hands, or that is plethoric, fat, soft and flabby, is ridden over a heavy country, and though he may perform well for a few miles, he soon hangs heavily on the bit, slackens his pace, and if not pulled up, staggers and falls “all of a heap.” A farm horse, taken from grass or other soft feeding, and entirely out of condition often suffers in the same way, in going perhaps for the veterinarian in case of urgent colic in one of its fellows. Cruzel draws attention to similar congestions from over-exertion in fat cattle, and Trasbot in wild stags and hogs when beechnuts and acorns were abundant, in pampered family horses and in plethoric farm animals generally. Excessive heat (heat apoplexy) is invoked as a cause, and the arrest of hæmatosis and consequent stagnation in the pulmonary capillaries are undoubtedly accessory causes, yet the majority of cases, and the most typical and fatal, occur in the winter season (the hunting season). On the other hand, chills from rains or cold draughts, especially when heated and exhausted, are common causes, and the disease often comes on more gradually, attaining its acme after five or six hours. A horse perspiring after a hard drive and left to face a cold blast unblanketed, or one plunged by accident into ice cold water for ten minutes (Trasbot) are examples of this kind. These cases are ushered in by violent rigors, whereas in those due to over-exertion this is much less marked and is usually only suggested by the coldness of surface and extremities. Another condition which contributes to pulmonary congestion is a full stomach. The plentitude of the abdominal organs leads to compression of the lungs and hampered circulation, and when to this is added over-exertion and exhaustion acute congestion is speedily induced.

Acute congestions are noticed as an accompaniment of other diseases, but these are mostly either the localization in the lung of a specific morbid process (anthrax, influenza, distemper, strangles), or it is due to auto-poisoning, as when the cutaneous transpiration is suppressed by a coating of glue, or to embolism.

_Symptoms._ In the horse which fails under severe exertion there are the dilated nostrils, the labored breathing, the deep, almost convulsive action of the flanks, the hanging on the reins, the slacking of the pace, the unsteadiness of gait, and lastly the fall. There may now be noticed the protruded bloodshot eyes, the agonized expression of countenance, the extended head, the pallor, and later the blueness of the nasal mucous membrane, the short, panting breathing, accompanied by a roaring noise alike in inspiration and expiration, and the small, weak, rapid pulse often imperceptible at the jaw. If the animal has been stopped short of having fallen, or if he is able to get upon his feet, he stands with his limbs apart to secure his stability, and with the elbows turned out to facilitate the expansion of the chest. As the breathing becomes panting the respirations are less deep, the ribs are maintained permanently drawn outward, and the flanks rise and fall to a limited extent only but with great rapidity (eighty to one hundred per minute). Auscultation may detect at first an increase in the pitch of the respiratory murmur, and the presence of the finest possible _crepitation sound_. Soon the murmur decreases uniformly. The extremities are cold, and in this coldness the general surface to some extent participates even though it may be covered by perspiration. Tremors or rigors are present. The heart is felt behind the left elbow to beat tumultuously. If blood is drawn it flows in a thin, black, tary stream.

In some cases blood more or less frothy is discharged from the nostrils as the result of rupture of pulmonary vessels.

In the fulminant cases in =cattle= respiration is rapid, even panting, wheezing, the expiration attended by a hoarse grunt, sometimes nasal hemorrhage, great prostration, profuse perspiration, a stupor sets in and the animal falls and dies, with more or less struggling.

In the cases which develop more slowly, and as the result of cold and chill whether in horses or cattle, there is dullness, anorexia, prostration, increasing rapidity and oppression of the breathing, a small, frequent, hoarse cough, and at first distinct pallor of the conjunctiva and pituitary mucosa, with more or less trembling. The head is extended on the neck, toward an open door or window, if available, until prostration and stupor forbid. The pulse is small, thready, often almost imperceptible and much accelerated, while the heart beats are strong, violent, tumultuous. For a time the respiration may be not more than double the normal rythm, but it tends to more or less rapid increase with wheezing or stertorous sounds and shaken by trembling of the respiratory muscles. The nasal discharge is slight and grayish often with streaks of blood. If it increases the cough becomes looser and softer. Quite early the respiratory murmur decreases over the whole lung and a blowing sound from the bronchia or larnyx is heard on the upper middle third of the chest. This may be complicated by a mucous râle, or when hæmorrhage has supervened by a loud rattling. Percussion shows a lack of resonance over the whole lung, not so flat and definitely circumscribed as in pneumonia but a partial flatness of sound over the whole chest. In pneumonia a limited area of lung is absolutely solidified (hepatized) while the remaining lung is practically normal, whereas in acute congestion often the whole lung is gorged with blood but for some time no part of it is entirely divested of air.

Another marked feature is the maintenance at first of the normal temperature with only a slight rise of about 1°. This serves to distinguish congestion of the lungs from sunstroke (heat anhæmatosis) in which the temperature usually rises to 108° or 110° F or higher. The temperature rises however as the disease advances and merges into pneumonia. Another distinguishing feature from sunstroke is the early pallor of the mucous membranes which in heat apoplexy are strongly congested. In congestion they become dark red only with the advance of the disease and the advent of asphyxia. These features serve also to distinguish acute pulmonary congestion from contagious fevers, pneumonia and other inflammations of internal organs.

_Course._ _Termination._ The more acute (fulminant) forms are promptly fatal. In the exhausted system the lungs have become uniformly gorged with blood, which can no longer be forced through the capillaries by the right heart, the heart in turn is overdistended with blood and ceases to beat and death ensues in a few minutes.

In the less acute cases the patient survives twenty-four hours and upward, the whole lung not being equally implicated but only certain lobules, usually the lower, or the congestion, if uniform in all the lung, being less extreme.

In favorable cases recovery takes place in one or two days. There is a return of life and appetite, a gradual improvement in pulse and breathing, the respirations becoming deeper and longer, and in a few hours all the more violent symptoms may have disappeared. With a more gradual improvement recovery may still be complete in four or five days.

_Lesions._ When the subject has died suddenly the appearances are essentially those of uniform engorgement of the pulmonary capillaries with blood. The general aspect is a dark red, varying from reddish brown to black, the darkest shades corresponding to circumscribed areas of actual hæmorrhage. In the worst cases the whole mass may appear like black currant jelly. The lungs do not collapse when the chest is opened, they are more or less friable at various points, and different portions will sink or float in (not on) water, according as it may be more or less airless. A dark liquid blood exudes freely from the torn or cut surface. Sections of the lung tissue hardened and examined under the microscope show the alveoli and bronchioles devoid of exudate, but having their cavities compressed and obliterated by the pressure of the swollen mucosa, and its investing blood clot. The heart is overdistended with fluid blood. In asphyxiated cases the general venous system is filled with black, liquid blood, and the serosæ spotted with petechiæ.

_Nature._ The nature of this disease is variously understood. It differs from inflammation in the absence of active cell proliferation, and migrations of inflammatory exudation, and of fever at all proportionate to the extent of the lesions. All these may and do supervene if the patient survives but they are practically absent for a length of time at the outset. Some attribute it to paresis of the vaso-motor centres for the lungs, as the result of their over stimulation and of the retrocession of blood from the chilled surface to the internal organs. But congestions caused by cutting the cervical branch of the sympathetic nerve or the sciatic plexus are not marked by a similar blood extravasation and destruction of tissue. The delicate structure of the lung tissue and the comparative absence of mechanical support will account for this in part, the great force of the circulation overloading the capillaries, under the impulse of the heart so closely adjacent, has doubtless a certain effect, and the venous nature of the blood thus forced into the lungs and calculated to arrest all normal function has a potent influence. If we add to this, for the _over-exertion_ cases, the sudden advent into the circulatory stream of unchanged peptones and other ingredients of the portal blood of highly fed and plethoric animals we find a sufficiently pathogenic combination. In all acute cases however the adiposity, poor condition and susceptibility to speedy exhaustion must be given their full share of responsibility.

_Treatment._ Girths, saddles and anything else that may hamper the movement of the chest must be at once removed and the horse’s head turned to the wind, an active stimulant given and the legs well rubbed and loosely flannel bandaged. The nature of the stimulant is of less consequence than its prompt administration. Two ounces of chloroform, of sulphuric ether, or of sweet spirits of nitre; half a pint of whisky, brandy or gin; or a pint of any of the more stimulating wines may be given, diluted in warm water so as to remove their irritating qualities. A drink of warm gruel will often go far to restore warmth to the surface and to unload the overtaxed lungs. Frequent large injections of warm water have a similar effect. Active hand rubbing of the legs and the wrapping of them loosely in flannel bandages previously warmed at the fire is equally valuable. If a roomy, well ventilated, loose box can be obtained the horse should be led to it gently and a light but warm rug placed upon the body. Valuable derivation may be obtained from pediluvia, the feet and legs up to the knees and hocks being put in buckets of water as hot as the hands can bear, and at the same time actively rubbed. If this is impossible the legs may be wrapped in bandages and wet with hot water every few minutes. Or this soothing derivative agent may be applied as well to the surface of the chest. A blanket wrung out of hot (nearly boiling) water until it no longer drops is wrapped round the body and covered up with two or three dry rugs. A second smaller rug is wrung and placed on the neck and covered by a sufficiency of hoods to keep in the heat. The legs are meanwhile hand rubbed and bandaged and the other measures above recommended carried out to restore the circulation in the surface and extremities. The time honored practice of bleeding freely from the jugular vein is one of the most effective means of relieving the overcharged heart and lungs, and should be resorted to at the earliest possible moment. The blood will at first flow in a small, dark stream, but as the circulation obtains relief the jet will increase in volume and the general symptoms will improve. From four to six quarts may be taken with advantage from an ordinary horse. This is not a pneumonia but an overloaded heart and lungs, threatening speedy death and which the abstraction of blood promptly relieves.

The longer the bleeding is delayed the less effective it is. It should not supersede the other measures already recommended. There is no real paradox in both bleeding and giving stimulants in such a case, as the essential condition is one of weakness, and if the abstraction of blood has been of use in relieving the clogged heart and lungs, the depression under which these have labored may be still further overcome by agents calculated to rouse their suspended vitality.

Trasbot strongly recommends large doses of tartar emetic and iodide of potassium to reduce the blood pressure in the lungs, an advice which will be received with hesitation by those who dread the already paretic condition of the heart. His combination of iodide of potassium with digitalis will be more confidently resorted to. One drachm of the former may be given with a half drachm of the latter twice daily.

With the advent of marked fever and other signs of pneumonia, the treatment for that disease should be resorted to.

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.

_Symptoms._ As a congenital condition in the improved meat producing animals the condition is rarely recognized in life and cannot be said to be a defect. The collapsed lobule being farther removed from the air may be a more favorable field for the growth of pathogenic bacteria, but on the other hand these do not so readily penetrate it as if the tubes were open. When the collapse is more extensive, the contrast in the flatness on percussion and indistinctness of the respiratory murmur on the affected side, and the marked resonance and loud murmur on the other, may serve to identify the affection. In extensive, traumatic cases this contrast is much more prominently marked, as the expanded portions have to take on extra compensatory work and are not infrequently rendered emphysematous. The drum-like sound in percussion of such parts, and in the upper part of the chest in pneumothorax are pathognomonic of these conditions. Again in hydrothorax the horizontal upper level of the area of dulness betrays a liquid cause. Severe cases are marked by cyanosis.

The _lesions_ seen in atelectasis consist in depressed areas of a dark fleshy color on the surface of the lung, usually sharply limited by the borders of the lobules, and in strong contrast with the bulging, light colored lobules adjacent, which are often emphysematous. The collapsed lobule may usually be dilated when air is forced into the bronchium, but if it has been of some standing this is often difficult or impossible. If it has resulted from bronchitis or compression of a previously inflated lung it will often float in (not on) water, from a little retained air, but in congenital atelectasis it is airless and sinks to the bottom.

When _treatment_ is demanded it will vary according to the cause. In congenital atelectasis the respiratory centres must be roused. The new born animal may be sprinkled alternately with ice cold and hot water, or the chest may be slapped with the palm of the hand or a wet towel. The nostrils must be cleared of mucus, and the lungs inflated by blowing or bellows, the larynx being pressed back against the gullet to prevent inflation of the stomach. If available electricity may be applied to the chest walls. These measures may be repeated at intervals and the systemic weakness overcome by nourishing food, stimulants and friction of the skin.

In acquired atelectasis we should seek to correct the disease to which it owes its existence. In bronchitis the measures already indicated for the liquefaction and removal of the expectoration will be in order; in hydrothorax a judicious paracentesis and in pneumothorax the aspiration of the gas, and the closure of any traumatic opening through which that gas has gained access.

HÆMOPTYSIS.

Causes, over-exertion in plethoric, glanders, pulmonary tubercle,
petechial fever, embolism, aneurism, ulcerated new formations,
anthrax, septicæmia, hæmorrhagic diathesis. Symptoms. Inappetence,
cough, cold limbs, rigor, hard pulse, jugular pulse, violent heart
beats, unsteady gait. Discharge, bloody, crimson, frothy, with cough,
without acid, excited breathing, debility. Indications from
pre-existing disease. Treatment, quiet, elevated head, cold
irrigation, ice bags, acetate of lead, opium, ergot, matico, tannin,
iron, oil of turpentine, laxatives, cool stable.

The term _hæmoptysis_ (αιμα, blood, πτυω, I spit,) is now entirely restricted to bleeding from the lungs and lower air passages. It is a very rare complaint in the lower animals, but is sometimes seen in both horse and ox. In very plethoric subjects the overloaded circulatory organs give way in the delicate membrane, lining the ultimate bronchial tubes and the air cells. The exciting cause in such cases is usually some severe effort of draught, a violent gallop, or other unwonted exertion. It occurs in glanders from rupture of caseated pulmonary nodules. It does not appear to be so common in phthisis in the lower animals as in man, but one case occurred under the eye of the writer in which the bursting of a large tubercle in the lung of a cow involved the rupture of a considerable vessel with a fatal result. Pulmonary embolism and infarction, petechial fever, aneurism, ulcerated neoplasms, anthrax, and septicæmia are additional causes. Lastly hæmoptysis sometimes takes place in hæmorrhagic subjects without any appreciable rupture of vessels, the blood sweating from the surface of the bronchial mucous membrane.

Premonitory symptoms are sometimes noticed, such as dulness, and lassitude, loss of appetite, a frequent short cough, coldness of the limbs and surface, shivering, full, hard pulse, pulsation in the jugulars, tumultuous action of the heart, and unsteadiness of gait.

More commonly it comes on suddenly as the result of severe muscular strain or excitement. The blood flows from the nose, and rarely from the mouth in solipedes, but indiscriminately from both in other animals. It is bright red, clear, frothy, or mixed with mucus, and variable in amount. It is easily distinguished from nasal hæmorrhage, which is not frothy, and from bleeding from the stomach, which is clotted and blackened, with an acid odor from the presence of the gastric juice. The cough of hæmoptysis contrasts with the sneezing of epistaxis and the retching of hæmatemsis. The rattling cough increases the discharge, as does also a dependent position of the head. Besides the cough there is usually an anxious countenance, accelerated breathing and considerable lifting of the flank. When the loss is excessive there is weakness, giddiness, rolling of the eyes, and pallor of the visible mucous membranes.

The previous ill-health of the patient, the presence of tubercle as ascertained by auscultation and percussion, and the hæmorrhagic constitution as shown by occurrence of bleeding from other parts of the system will lessen the chances of a favorable termination. Sometimes, too, the flow is so profuse that the blood cannot be coughed up, and filling the bronchial tubes it destroys life suddenly by suffocation.

_Treatment._ When brought on by severe exertion absolute quiescence will usually check hæmoptysis. Keeping the head in an elevated position favors its arrest. The application of cold water to the head, neck and thorax, and the giving of iced water, strongly acidulated by vinegar or one of the mineral acids may sometimes be required. In threatening or obstinate cases one drachm of acetate of lead may be given thrice daily to check by its astringent effect on the vessels, and the addition of a drachm of opium is of great value in suppressing the cough. Ergot, tannin, matico, and oil of turpentine have each been employed with advantage, and when costiveness exists a saline laxative (one pound sulphate of soda) may be usefully resorted to. The patient should be kept in a cool, airy dwelling, and should rest for fifteen or twenty days after an attack.

PULMONARY APOPLEXY. HÆMORRHAGIC INFARCTION.

Different forms. Embolism with infarction. Embolism from arteritis.
Rupture of bloodvessel. Changes in color. Symptoms. Repair.

Hæmorrhage into the lungs may be: 1st. Petechial in infectious diseases. 2d. _interlobular_ as from ruptured vessels. 3d. _Infarction_ or apoplexy. _Infarction_ results from embolism of a branch of the pulmonary artery, which may in its turn be due to clots formed in a diseased heart or in the systemic veins and carried to the lungs in the blood stream. It may also result from inflammation of the inner coat of the pulmonary artery. A virtual stasis occurs beyond the embolism, and the blood filtering in through the anastomosing capillaries fills and blackens the affected lobule. With rupture of a considerable vessel the blood escapes _en masse_ and appears like black currant jelly. As it ages it becomes granular and changes to a yellow color, or it may form a necrotic mass enclosed in a cyst as in lung plague. The symptoms, apart from the absence of respiratory murmur and resonance, are not diagnostic. It may take months to undergo liquefaction and absorption. Iodide of potassium, bitters and stimulating diuretics may be given.

PNEUMONITIS; PNEUMONIA; INFLAMMATION OF THE LUNGS.

_Definition._ Inflammation of the spongy tissue of the lungs
uncomplicated by that of the bronchia or pleura.

_Divisions._ This affection has been variously divided according to
_seat_, _nature_, and _complications_: thus:

_Single Pneumonia_: Affecting one lung: _right_ or _left_.

_Double Pneumonia_: Affecting both lungs.

_Lobar Pneumonia_: Affecting one lobe or by lobes.

_Lobular Pneumonia_: Affecting by lobules.

_Acute Pneumonia_: _Subacute Pneumonia._ _Chronic Pneumonia._

_Croupous or Fibrinous_: With fibrinous exudate.

_Catarrhal_: With exudate rich in cells and granules.

_Hæmorrhagic_: With extravasation of blood.

_Purulent_: Tending to pus: abscess.

_Necrotic_: Tending to gangrene: sequestra.

_Desquamative_: With great proliferation of alveolar epithelium.

_Interstitial_. _Interlobular_: Affecting mainly the interlobular
connective tissue.

_Hypostatic_: Dependent on gravitation of the blood.

_Metastatic_: Due to embolism.

_Parasitic_: Caused by parasites. Due to wounds or foreign bodies.

_Contagious_ and _Traumatic Pneumonia_.

Many of these are, however, but localizations of the same affection and others are manifestly microbian diseases which in the present state of pathology it is not always easy to early distinguish sufficiently for clinical and therapeutic purposes. For the sake of convenience therefore pneumonia will here be treated of generally, and under the headings devoted to etiology, pathology, therapeutics, etc., attention will be given to distinctions. Those pneumonias that are but pulmonary manifestations of other diseases—influenza, glanders, tuberculosis, strangles, contagious pneumo-enteritis, lung plague, septicæmia, pyæmia, swine plague, hog cholera, petechial fever, actinomycosis, and neoplasms will be considered under these respective headings.

ACUTE CROUPOUS PNEUMONIA. PNEUMONITIS IN THE HORSE.

Definition. Differentiation from acute vascular congestion.
Predisposing causes, age, sex, stabling, training, diet, impure air,
low health, previous lung disease, plethora, climate, season, exciting
causes, chill, fatigue, leucomaines, sudor, draughts, plunging in or
spraying with cold water, clipping, inhalation of irritant smoke, gas,
dust, drawing of food, irritating or insoluble drugs into the lungs,
neoplasms, parasites, contusions, fractured ribs, punctures,
contagion, plurality of germs, bacillus of Friedländer, micrococcus of
Talamon and Fränkel, diplococcus pneumoniæ equina of Schütz,
diplococcus pneumoniæ equina of Cadeac. Symptoms, chill, hyperthermia,
dullness on percussion and crepitation in the lower part of the lung,
reaction, congested mucosæ, accelerated labored breathing, excited
circulation, pulse oppressed, cough deep, patient statant, elbows
everted, nose protruded, nostrils dilated, approaching door or window,
pinched countenance, skin dry, harsh, adherent, partial sweats, loins
insensible, nasal discharge rusty, dependent part of lung largely
non-resonant, with peripheral crepitation. Blowing in abnormal
situation over hepatized lung. Decubitus, its significance. Course.
Results. Favorable indications in pulse, breathing, face, temperature,
appetite, decubitus, clearing of lung. Unfavorable indications in
breathing, pulse, fever, face, uneasy movements, pawing, cold limbs,
prostration, nervousness, weakness. Sabacuto Pneumonia. Terminations
of pneumonia, death, resolution, splenisation, abscess, gangrene, red
hepatisation, gray hepatisation, fibrinous consolidation. Lesions.
Congestion, exudation and cell growth, hepatization—red and gray,
deliquescence, abscess. Blood, loss of red globules, increase of
white, excess of fibrine, glandular swelling, pleurisy, degenerations
in other organs, laminitis, rheumatism. Treatment, adapted to strength
of subject and type of disease, hygienic, anti-rigor, antiphlogistic,
expectant, stimulant, antipyretic, febrifuge, sedative, moist
compresses, derivatives, laxatives. In subacute form tonics, heart
stimulants, febrifuge. In chronic cases add rich digestible diet, and
easy open air life.

This consists in inflammation of the spongy tissue of the lung involving mainly and primarily the walls of the alveoli and interlobular connective tissue with their respective trophic centres (nuclei). The acute congestion of excessive heart action and debilitated pulmonary capillaries described above, is primarily a disease of the bloodvessels which become over distended and may or may not lead to the inflammatory processes in their walls and the tissues adjacent. Pneumonia on the other hand is essentially inflammation of these tissues and nuclei, with exudation usually of a fibrinous material into their substance.

PREDISPOSING CAUSES. =1.= =Age.= A very early age is nearly exempt, and from 6 years upward there are fewer cases relative to the equine population, variations that may be better accounted for by stabling, training and acquired immunity than by the mere fact of age. Of 237 cases, 2 were 3½ years; 32 were 4 years; 19 were 5 years; 131 were 6 to 11 years; 46 were over 11 years; and 7 of uncertain age (Trasbot). =2.= =Sex.= No visible effect. =3.= =Stabling, training, change of food.= While the young colt at pasture is practically immune, the period of stabling, transition to a dry and grain diet, and to the nervous excitement attendant on training and unwonted work as shown in the statistics of Percivall and Trasbot determine an enormous increase of cases. In a cavalry regiment Percivall found that 56.6 per cent. of all lung diseases occurred before the 5th year, and Trasbot found that at the Alfort Veterinary College 13.5 per cent. of all equine pneumonias occurred in the 4th year. =4.= =Hot Stables.= =Impure Air.= These two conditions usually coexist and prove potent causes especially in young horses brought from the fields. We cannot, however, separate this cause as usually observed from the action of pathogenic germs which are preserved and concentrated in such places. =5.= =Poor Health.= Debilitating diseases, insufficient and poor diet, overwork, exposure to cold draughts or darkness and any other cause which lowers the vitality predisposes. =6.= =A Previous Attack.= This usually leaves some structural or functional change which renders the lung more susceptible to a subsequent invasion. Against this must be placed the immunity which follows the contagious forms, but as this is usually exhausted in the course of six months it does not invalidate the position that the permanent impairment of pulmonary integrity is a predisposing cause. =7.= =Plethora.= Tending as this does to congestion it must be accepted also for the next pathological step—pneumonia. =8.= =Climate and Season.= This is notoriously an important factor. At Paris, Trasbot met with 237 cases in the nine months from October to June inclusive and but 8 cases in the summer months—July, August and September. In Great Britain, where the vicissitudes are less severe Percivall had in the cavalry horses in the seven months from October to April inclusive 146 cases = 20.85 Per month, and in the 5 months from May to September inclusive 62 cases = 12.4 per month.

_Exciting Causes._ Nearly all the above causes when acting with unusual force may become direct factors in causation. The effect of a sudden and extreme chill is especially to be feared. Even in cases that are unquestionably due to a microbe as the essential cause, the nervous disorder manifested in the chill, and the clogging of the pulmonary circulation in connection with the retrocession of blood from the surface of the body furnishes the opportunity for the colonization of the germ. The average horse at pasture will stand with impunity cold storms of rain, snow, and sleet, and transitions from a warm noonday sun to a cold night wind and dew and even frost, but under other conditions of the system, with the fatigue and fret and sudden changes of food and regimen attendant on domestication, or with any derangement of an important bodily function the _chill_ is often the manifest occasion of disturbance of the balance of health, and the supervention of pneumonia. =Fatigue=, a system charged with =leucomanies=, and a =free perspiration=, which is suddenly checked by exposure, at rest, to a =cold rain=, or =snow=, to a =draught between door and window=, to =immersion in the cold waters= of a river, or to =sponging with cold water= is quite liable to cause pneumonia. An unduly heavy winter coat, an individual peculiarity or determined by a cold environment in autumn often predisposes strongly to such dangerous chills, by the frequency and profuseness of the perspirations and general relaxation of the system. Clipping of such subjects is a true hygienic measure though it entails the need of extra care in blanketing. Again in the animal that has already suffered from disease of the respiratory organs these chills are more dangerous factors.

=Direct irritation= by inhalation of smoke and other products of combustion; or acrid or irritant gases or dust; by the drawing of food by aspiration into the lungs (as in paralysis of the larnyx or pharnyx, choking, apoplexy, vomiting, etc.); by pouring irritant or insoluble drugs (oil, lard) through the nose; by the pressure of neoplasms (actinomycosis, tubercle, glanders, cancer); or by the presence of parasites (strongylus, distomata, echinococci, linguatulas).

_Pneumonia_ from =Contusion= of the chest, fracture of a rib, or puncture or laceration of the lung is recognized.

=Contagion.= The presence of a _contagium_ in pneumonia is today well established. Clinical observation had indicated this even before the discovery of a specific germ, but recent bacteriological investigations and the transmission of the disease by inoculation of artificial cultures have definitely settled the question. It does not follow that all cases are contagious, nor equally so, but the recognition of the contagious form satisfactorily explains the prevalence of the disease in one stable while an adjoining one escapes, and the eruption of new cases in a stable after an animal affected with the disease or convalescent from it has been introduced. It has been objected that many horses stand in the stable with pneumonia cases and escape, but so is it with glanders, cowpox, and many other affections. It merely argues an immunity in the case of some, and for the disease germ a very limited transmissibility through the air. The further objection that the existence of lesions in the lung before the onset of fever, excludes this from the list of infectious diseases, is untenable since many undeniably contagious diseases, like cutaneous anthrax, glanders, lung plague, cowpox, appear locally before any constitutional disturbance occurs, which later as the result of extensive local disease and the circulation of toxins in the blood. It places contagious pneumonia however in that long list of infectious diseases which develop first locally in the seat of infection and later become more or less generalized.

It must be admitted however that the germ of pneumonia is not the same for all cases of the disease and for all genera of animals. It must also be allowed that the same germ does not always maintain the same degree of virulence, and that it may even live for a time on the buccal mucosa of an animal belonging to a susceptible genus without any morbid result. In short we must recognize that different germs of pneumonia may become temporarily non-virulent or only slightly virulent, and remain pathologically quiescent, as for example during the summer months, to reassert itself later when the conditions become more favorable to its pathogenesis.

BACTERIOLOGY.

a. BACILLUS OF FRIEDLÄNDER. This is a short rod with rounded ends, often merely oval, occurring in pairs, or chains of four, and under given circumstances surrounded by a transparent gelatinous capsule. It is ærobic, nonmotile, does not liquefy gelatine, nor sporulate, and in gelatine stick cultures has a nail-like growth. This was found by Friedländer, Frobenius, Weichselbaum and Wolf in the pulmonary alveoli in a small proportion of cases of croupous pneumonia in man. The cultures, injected into the lungs of animals, killed one dog (out of five), six Guinea pigs (out of eleven), and thirty-two mice (all the injected). Lesions were intense congestion of the lungs, seropurulent pleural effusion, and enlarged spleen, while the bacillus swarmed in the blood and exudate.

MICROCOCCUS PNEUMONIÆ CROUPOSÆ. First found by Sternberg in his own saliva in health, and by Pasteur in the saliva of a rabid child. Afterward found in the great majority of lungs affected with croupous pneumonia in man, by Talamon, Salvioli, Sternberg, Fränkel, Weichselbaum, Netter, Gamalei, etc. Later it was found in meningitis, in ulcerative endocarditis, in arthritis, in otitis media, and in acute abscess in man.

It is a _spherical_ or _oval coccus_, arranged in pairs, in fours, or exceptionally in eights or tens. Lanceolate forms are the rule in the blood of animals, and circular in artificial cultures. It stains readily in aniline colors and by Gram’s method, grows in ordinary culture media, at 37° C. in the absence of free acid, and in gelatine stick cultures as small, white colonies along the line of culture, without liquefying the gelatine. It dies in ten minutes at 52° C. (Sternberg). Its virulence lessens in artificial cultures, but is restored by passing through the body of a susceptible animal.

Injection into the lungs or trachea of rabbits, mice, sheep and, less certainly, Guinea pigs, produced distinct fibrinous pneumonia filled with the microbe. In dogs, subcutaneously, it caused abscess, but in the lungs an acute fibrinous pneumonia which only exceptionally proved fatal, recovery usually taking place in ten to fifteen days.

Klemperer induced immunity, sometimes lasting six months, by intravenous injection of filtered cultures.

DIPLOCOCCUS PNEUMONIÆ EQUINA. First found by Schütz in the lungs of pneumonic horses in 1887. It is an oval coccus arranged usually in pairs or in threes or fours, and surrounded by a transparent envelope. It stains in aniline colors but not by Gram’s method. It is ærobic and grows in gelatine at ordinary temperature without liquefying it, and in stick cultures forms a line of small, white, separate colonies which do not coalesce by growth. Does not grow on the surface of the gelatine around the puncture. Line cultures on agar are in colonies like minute transparent droplets. In bouillon it develops long chains.

Inoculated on the rabbit, Guinea pig and mouse, it produced death with pneumonic affections (hæmorrhagic congestion or inflammation), but it failed to take in some of the rabbits and Guinea pigs. Chickens and pigs proved immune. Injected into the horse’s lung or as spray into the trachea it produced true croupous pneumonia. Fiedaler and others obtained similar results. Peter has found the fæces of pneumonic horses virulent, an important point in connection with disinfection.

Schütz found that 20 grammes of the culture, in an equal quantity of boiled water, injected into the horse’s trachea, produced a rise of temperature by two or three degrees, with rigors, cough, accelerated pulse, elevated temperature, dyspnœa and prostration, but that this subsided in a few hours. By repeating this every thirty-six hours, the fourth or fifth would fail to produce a reaction and the subject proved immune.

CADEAC’S DIPLOCOCCUS PNEUMONIÆ EQUINA. In the lungs of cases of contagious pleuro-pneumonia of the horse Cadeac found a round noncapsulated coccus appearing in pairs, or rarely in chains, and staining by Gram’s method. It grew slowly in bouillon and agar at 37° C., forming on the latter in twenty-four hours, a thick, whitish, oily drop, which, as it grew larger, assumed a silvery whiteness, and dried in the centre. In bouillon it precipitated a powdery sediment. The reaction of the culture medium was unchanged. It lost virulence rapidly in artificial cultures or by a heat of 50° C., and it died in ten minutes at a temperature of 60° C. Virulence was long retained when dried, or even in putrid material.

This proved infecting to the ass, rabbit and Guinea pig, while the cat and white rat proved immune. Intratracheal injection of the dog produced a transient pneumonia. The ass inoculated with the blood of the infected rabbit died in three days, with a hepatized lung, pleurisy, and swarms of the microbes in the lungs, blood and internal organs. Rabbits injected intravenously had enlarged spleen, reddish exudate in the serous cavities, urine stained with hæmoglobin, and lungs and kidneys congested. With intratracheal injections the lesions were exclusively pulmonary. The pulmonary lesions were less constant in the Guinea pig. Weakened virus caused pulmonary lesions only without septicæmia.

It has been suggested that this coccus is at least closely related to that of pneumo-enteritis of the horse.

_Symptoms._ The onset of pneumonia is not often seen by the veterinarian, who is called in only after the cough, loss of appetite, hurried breathing and rigor has revealed illness to the attendants. Hence perhaps chill and rise of temperature have been placed among the earliest symptoms. The symptoms are more violent in the racer, trotter and other nervous animals. Trasbot positively claims, that considerable pulmonary inflammation and even exudation have taken place before there is any chill or rise of temperature. This is especially the case in the heavy lymphatic races of draught horses, which often according to this author perform their usual work for days after inflammatory exudation has set in. A fair counterpart of this is found in lung plague of cattle and it would indicate that both start from a local infection, which gradually extends until the systemic derangement is induced. As usually seen, and especially when it follows exposure to severe cold, a staring coat or a shivering fit usher in the disease, the degree of the chill bearing some ratio to the coldness of the air and to the future severity of the malady. This may be accompanied by a small, dry cough, but without any other marked sign of lung disease. With the access of the hot stage the characteristic symptoms of lung disease are manifested, at first resembling those of _congested lungs_, but less severe than those given under that head. There is a distinct increase of the body temperature; the visible mucous membranes are suffused with a blush; the expired air feels hot upon the hand; the breathing, 30 to 40 per minute, is short and accompanied by much lifting of the flanks—(_labored_); the cough is deep as if coming from the depth of the chest, but not so hard nor so painful as in bronchitis; the legs are placed apart, the elbows turned out and the head protruded to facilitate breathing; the nose is turned to an open door or window if any such is available; the contraction of the muscles of the face, the dilated nostrils and the retracted angle of the mouth give an anxious expression to the countenance; the eyes are semi-closed; the pulse full but soft—(_oppressed_)—, beats from 48 to 70 per minute; the bowels are slightly costive, the urine scanty and high colored; the skin inelastic—_hidebound_—harsh and dry, though sweats may bedew it in parts; the loins insensible to pinching; and if there is any discharge from the nose it consists only in a reddish—_rusty_—colored mucus.

=Auscultation= and =percussion= complete the diagnosis. At the outset the inflamed portion of lung, usually near its lower part, conveys a _crepitating_ sound to the ear, but as consolidation extends the healthy murmur and the crepitating râle are alike suppressed over the whole extent of the hepatised portion around the margin of which a line of crepitation betrays the limit of the advancing inflammation. A similar line of crepitation encircles the hepatised mass even when the exuded products are being absorbed and when the lung is being cleared up and restored to its healthy state. Thus the advance of the inflammation, and the progress of recovery can be equally followed by the crepitation which, in the different circumstances, betokens active inflammation or active absorption. When both lungs are involved the posterior parts are chiefly implicated, while if the pneumonia is single it may attack the anterior, median or posterior part, or the entire lung may become consolidated. If hepatisation exists in the anterior part of the lung the thick fleshy shoulder will forbid any satisfactory examination, but if in the middle portion only, while the respiratory murmur is lost it will be replaced by a strong blowing sound (bronchial respiration) because the noise of the air rushing through the larger bronchial tubes to the posterior healthy part of the lung is conveyed with greater force to the ear through the consolidated lung tissue. This is audible from the lower third of the chest to the upper limit of hepatization. The respiratory murmur in the healthy lung is always louder than is natural.

=Percussion= confirms these results. Over the hepatised lung where no respiratory sound remains, a dull, dead sound only is brought out by the impulse of the fingers or closed fist, comparable to that obtained by percussion over the muscular masses of the shoulder or haunch, and forming a marked contrast to that obtained over the surrounding healthy lung. There is not that tenderness on pressure in the intercostal spaces which characterises pleurisy, but a sharp blow with the closed fist leads to wincing and usually grunting because of the concussion to which the diseased part is subjected. By increasing the force of such blows the deepest parts of the lungs may be tested, since in this way dullness due to consolidation of the deeper portions of the lungs may be detected even though the superficial investing parts are healthy.

The nature of the symptoms will vary according to the extent and character of the inflammation, from mild febrile reaction, with excited breathing and slight crepitation, to the more severe varieties in which the intensity of the symptoms are such as to threaten suffocation.

A marked feature of pneumonia in solipedes is that the patient obstinately stands in one position and never lies down so long as the severity of the inflammation lasts. The sharp crest on the lower border of his breast bone compels the horse to lie on his side, and since in this position the whole weight of the body has to be overcome in any full dilatation of the chest, he cannot retain the recumbent posture when any serious impediment to breathing exists. Hence it is that the fact of a horse suffering from pneumonia having lain down and remained so for some time is justly accepted as an indication of improvement.

_Progress and results of the disease._ The general symptoms above noted, remain with more or less intensity throughout. After the first flush of heat, on the occurrence of febrile reaction, the limbs become alternately hot and cold, and in this the general surface partakes to a less extent.

The tendency of pneumonia is to a crisis and recovery. Certain days have been supposed to be critical and on the whole the third, seventh, eleventh and fourteenth are those on which a favorable change is most probable.

Among the more _favorable indications_ are the manifest abatement of the high bodily temperature and febrile symptoms generally, the increasing ease and regularity of the breathing, the greater force, distinctness and slowness of the pulse, the permanent return of warmth to the limbs, the softer and more elastic feeling of the skin, the recovery of appetite, and above all, the turning of the nose from the open window or the retention of the recumbent position for a length of time. These symptoms will become more patent day by day, and the absorption of the effused products and the clearing up of the lung may be traced by the gradually decreasing area of dullness and of the circular line of crepitation as ascertained by percussion and auscultation.

If on the contrary the disease takes an _unfavorable_ turn, some such signs as the following will manifest it: Increasing rapidity and embarrassment of the breathing; smallness and indistinctness of the pulse, which is increased to perhaps 100 beats per minute; tumultuous heart’s action, the impulse of which is strongly felt behind the left elbow; a more laborious working of the flanks; frequent despondent looking toward the flanks; pawing with the fore feet, lying down, and as suddenly rising again; permanent coldness of the extremities; hanging head with great dullness and despondency of expression; dull, sunken, lusterless eye; hanging lower lip; leaden hue of the nasal mucous membrane; convulsive twitching of the muscles of the surface; reeling in gait, and extension of the crepitation over all the still pervious lung.

SUBACUTE PNEUMONIA. This term is employed to designate that subdued or milder form of the disease which sometimes arises spontaneously and at others follows the acute.

In this variety the characteristic symptoms may be much less marked and the disease is less easily recognized. There is some acceleration and quickness of pulse, lifting of the flanks and heat of the mouth and body generally. There are alternations of heat and cold of the surface and extremities, a rough, unthrifty coat, hidebound, a dull, listless moping manner and the same symptoms on auscultation and percussion as in the acute form.

The changes take place slowly but the disease may prove obstinate and is often followed by permanent alterations in the lungs. Rheumatic affections of the limbs, inflammation of the feet, and other diseases frequently supervene during the course of this form of the affection.