Chapter II: Part 2

=Temperature in disease.= Comparative temperatures should be taken at the same hours on successive days, bearing in mind that the morning temperature is usually slightly lower and the evening one slightly higher. Where possible both morning and evening temperature should be taken. With elevated temperature, repeat sooner to see that it is not transient. A transient rise of 1° to 2° is unimportant. A permanent rise of 2° or 3° indicates fever. A sudden additional rise of several degrees in the progress of fever is grave. A persistence of the high evening temperature to morning shows aggravation. A persistence of the low morning temperature to the evening bespeaks improvement. A sudden extreme fall to much below the normal (4° or 5°) indicates collapse. This is usually attended with other symptoms of extreme prostration and sinking. A sudden considerable fall to near the normal, without untoward attendant symptoms, may indicate a _crisis_ and a more or less speedy improvement may be hoped for. This sudden fall often attends the period of eruption of certain exanthemata, as cowpox, horsepox, sheeppox, aphthous epizootic, etc. A sudden extensive fall of temperature may result from some transient accidental cause, as a prolonged deep sleep, a hemorrhage, the relief of constipation, or of enuresis. A sudden rise may supervene on such suppressed function or other cause of nervous irritation or on toxin poisoning, but it does not persist more than twelve or twenty-four hours after the cessation of the morbific cause.

A rise of 10° or 12° above the normal standard is usually promptly fatal.

A continued high temperature indicates persistent disease, and a considerable rise during defervescence implies a relapse and in the absence of any error in diet or nursing is grave.

=Pulse.= Before the introduction of the clinical thermometer, the indications furnished by the pulse were held to be of the highest value. Though largely superseded by the usually more reliable thermometer, yet they should not be discarded, but employed as symptoms corroborative of the thermometric indications. In many cases the pulse will furnish criteria, when in the absence of fever, the heat of the body will tell of nothing amiss. This is especially true of diseases of the heart, the large blood vessels, and of the nervous system, and in cases of poisoning. For special indications furnished by the pulse, see diseases of the heart.

=Respirations.= The morbid activity or inactivity of the respiration, its modified rythm, the pathological significance of the altered breathing sounds and of the superadded sounds, the indications furnished by percussion, palpation, mensuration, succussion, sneezing, snorting, yawning, cough, moan, grunt, stertor, discharge, etc., afford material of inestimable value to the diagnostician. See under diseases of the chest.

=Skin Symptoms.= The erection of the hair of carnivora in rage or fear implies a profound nervous disturbance, and a similar erection (staring coat) in the larger herbivora especially, implies a corresponding nervous disorder, due however to a different cause. The pallor and coldness of (white) skin and extremities the retrocession of blood toward the internal organs, the contraction of the involuntary muscles of the hair bulbs, the sense of cold, and the actual shivering all come from the fundamental nervous disorder. The loss of lustre and gloss in the hair and the dryness, rigidity and mobility (mellowness) of the skin imply lack of nutrition. The mellow feeling of the skin under the pressure of the finger, soft and yielding by reason of the lax connection tissue and fatty layer in the thrifty animal, is in marked contrast with the dry, hard, tough, unyielding hide firmly adherent to the parts beneath (hidebound), which denotes the unhealthy or unthrifty animal, or from the thin, attenuated, mobile, bloodless skin of the debilitated subject, the victim of lung, liver, or intestinal worms. In sheep in parallel conditions there is a lack of _yolk_ in the wool, which is dry, lustreless and brittle and often flattened (clapped) on the skin. In fowls ruffling of the plumage indicates the nervous disorder and chill. The skin may be scurfy in conditions of low health or in connection with the presence of vegetable or animal parasites. Ringworm has excessive scurf, and tends usually to a circular form, and to complete shedding of the hair from the spots. The hairs split up before dropping. In acariasis there may be scurf, scab, abrasion and sore of many kinds, but the outline is not necessarily circular, nor strictly limited, isolated hairs remain even on the bare patches, and itching is extreme as shown by the movement of the body and especially of the lips or foot when the part is scratched.

The hair may be freely shed during convalescence from debilitating diseases, a condition that must not be confounded with the yearly shedding of the winter coat and the moulting of birds, which is a perfectly normal process. Yet even the spring shedding and the growth of the new coat makes a great drain on the system, and must always be taken into account as a probable cause of derangement of health.

The lesions of the skin in the different cutaneous affections must be remanded to the special chapter on skin diseases. The following however may be named as having a general bearing.

Emphysema may be due to a local wound, (elbow, trachea, rib); it may indicate black quarter, or it may occur subcutaneously in cattle without marked impairment of health.

Anasarca, from diseased blood, heart, liver or kidneys is denoted by swellings, often painless, or a general infiltration which pits on pressure. It often shows primarily in the lower parts of the hind limbs. Warty looking elevations must be carefully discriminated, having in mind primarily papilloma, tubercle (grapes), actinomycosis, condyloma (in dogs), cancer, melanosis. The secretions of the skin (sweat, sebum) may be suppressed, or in excess, producing at times a special odor, as in thrush and canker of the horse, cowpox and sheeppox, and rheumatism. Before death the cadaveric odor may be marked, and attracts crowds of flies to the victim.

=Facies.= The countenance may be expressive. Between the bright, full, clear, prominent eye of health, and the dull, sunken, lifeless, semi-closed eye of serious disease the contrast is extreme. The drooping lids (ptosis) may be paralytic and even unilateral, in which case drooping ear, and flaccid lips and alæ nasi complete the picture. With paralyzed lips there is usually drivelling of saliva, and dropping of half chewed morsels in the manger and stall. The eye may show dropsical lids in kidney or liver disease and in anæmic conditions like distomatosis in sheep. It may show the upper lid bent at an angle in recurrent ophthalmia of solipedes. The mucosa may be red in ophthalmia, yellow in jaundice, dusky brown in Southern cattle fever, anthrax, cerebral meningitis, and other fevers attended with destruction of red globules and liberation of their hæmatin. The pupils may be all but closed in internal ophthalmias, or widely dilated and irresponsive to light in amaurosis. The iris may lack its normal lustre or may be distorted or torn in various ways from adhesions. Opacities of the cornea, lens, or vitreous may be recognized.

The facial muscles may be flaccid and devoid of expression in palsy, and prostrating diseases; they may be firm, giving the bright, intelligent look of health; or they may be painfully drawn in the agonized expression of spasmodic colic or enteritis.

=Nasal Mucosa.= The pituita is bright red in sthenic fevers, simple acute coryza, strangles, laryngitis and inflammation of the larger bronchia. It assumes a violet hue in capillary bronchitis, pulmonary congestion, glanders, and petechial fever. Petechiæ appear in the last named affection, and in a number of bacteridian diseases, such as anthrax, swine plague, hog cholera, the red fever of swine etc.; a yellow tinge in shown in jaundice. Millet-like or pea-like nodules, or elevated patches, and ulcers show in glanders and may be felt by the fingers. In cattle hard millet-like nodules appear in a chronic coryza with hypertrophy of the mucosa. The orifice of the lachrymo-nasal duct, seen in the horse on the floor of the chamber at the friction of the mucosa with the skin of the false nostril and in ass and mule on the outer ala near the upper commissure, is sometimes plugged with inspissated mucus. Among other lesions of the nasal chamber may be named polypi—soft and calcareous,—thickening and obstruction in purpura hemorrhagica, osteoporosis and hypertrophy of bone, and parasites—pentastoma denticulata (in the horse and dog), and the larva of the œstrus (in sheep and buffalo). Disease of the upper molars and abscess of the fronto-maxillary sinus may be manifested by swelling beneath and on the inner side of the eye, fœtid discharge from the nose, and obstruction of the air current. Dullness on percussion will show the filling of the sinuses. These conditions must be carefully differentiated from actinomycosis, sarcoma and other morbid growths in the same situation.

Costiveness with fœtor and lack of the normal color in the stools may suggest _liver torpor_ or inflammation, while fatty stools may suggest pancreatic disease. The uneasy movements of colic, should lead to a careful investigation of the chylo-poietic organs (see digestive organs). Weakness of the hind parts, tenderness of the loins, and altered condition of the urinary discharge should demand a close enquiry into the state of the _kidneys_ and _bladder_. Satyriasis or nymphomania would suggest disease of the _generative organs_ or the nerve centres that preside over them. The same is true of impotence, sterility and abortion.

In eruptions on the skin (erythema, eczema, pustule, squama) a cause may be found in the local action of heat, friction, or other direct irritant, but in the absence of any such manifest cause, an enquiry should be made into the functions of sanguification, digestion, urination and the action of the liver. It may further suggest parasitism (ring worm, phthiriasis, fleas, acariasis, verminous disease, etc.)

Symptoms of _nervous disorder_ are too numerous to be here traced to local lesions. Motor paralysis of one limb may, however, suggest injury to its motor nerves, to the same side of the spinal cord, or of the opposite half of the cerebrum. Paraplegia almost always indicates injury to the cord. Sensory paralysis of one side may depend on disease of the opposite corpus striatum. The animal moves in a circle when a tumor (coenurus in sheep) exists in the roof of the lateral ventricle presumably pressing on the ganglia on its floor. An animal rolls on its axis when there is a lesion of the median cerebral peduncles, of the supero-external portion of these peduncles, of the posterior part of the encephalon, or of different parts of the hemisphere. Amaurosis suggests disease of the corpora quadrigeminia. Loss of coördination of muscular movement usually implies some lesion of the cerebellum. Vertigo may imply disease of the encephalon (congestion, anæmia, inflammation, dropsy, hæmorrhage, tumor, abscess); it may be disease of the internal ear; it may be digestive disorder connected often with cryptogamic poisoning; it may be heart disease with obstruction of the jugular veins; it may be parasites in the nasal sinuses; or it may be disease of the eye. Coma occurs in most congestions and pressures on the encephalon, and like vertigo in poisoning by alcohol, solanine, monoxide of carbon, etc. In acting on any ganglionic centre the agent may, according to its degree, operate positively or negatively, producing spasms, or paralysis as the case may be. As in the case of other visceral affections the specific diseases must be referred to for particular symptoms.

For the more precise points in diagnosis, including chemical, physical, electrical and instrumental methods, etc., the reader is referred to the special diseases.

PROGNOSIS.

Definition. Demands on the veterinarian, the question of economy.
Basis of Prognosis. Cause of the illness, internal or external, vital
or nonvital organ, enzootic, fatigue, infection, in one or two
symmetrical vital organs, regular or irregular in its course,
persistence, relapse, complications, effect of treatment, appetite,
temperature, pulse, breathing, youth, age, debility, previous disease,
breeding, climate, season.

Prognosis is a more complicated question for the veterinarian than for the physician. The latter must pronounce on the malady, whether it is likely to follow a regular or irregular course, whether it will last short or long, whether it will be curable or incurable, and if curable whether recovery would be complete or partial. For the veterinarian there is in addition the question of economy. The veterinary patient is, as a rule, of value, only if he can be rendered sound, and a partial recovery may be even worse than a fatal result, since the subject remains as a ruinous charge on his owner. The veterinarian must pronounce on the prompt and perfect curability of the case, on the outlay that will be requisite for treatment, on the depreciation which will be entailed on the patient, and whether, in certain lesions that do not harm the carcass, it would not be more judicious to butcher the subject. The physician is expected to do the best he can for life and health, and even a very imperfect recovery brings him a mead of gratitude. The veterinarian on the other hand must be an expert not only on disease, but on animal values, and if his treatment, however skillful it may be, results only in the prolonging of the life of an useless animal, the owner may charge him with imposing upon him an unnecessary outlay. The soundest judgment and highest skill are often necessary to secure the interests of an employer in such circumstances. In certain cases the recommendation to destroy is of much more value to the employer than the most skillful, and partially effective, curative treatment. On this basis, the reputation of a skillful man may be securely built. He can deceive no one if his prediction of recovery is not justified, while if he advises destruction and the patient recovers, he is at once discredited.

To give a sound prognosis the practitioner must have a thorough knowledge of pathology, he must have acute powers of observation, and he must be quick to appreciate every point that makes for or against the patient in the particular case.

The _causes_ of the trouble must be carefully considered. Are they transient or permanent? Are they removable or irremovable? Are they external or internal? As a rule an internal cause is the more redoubtable. Some lesions are necessarily fatal, as a needle penetrating the heart or an attack of rabies or milk sickness. Is the cause an enzootic one? If so can the patient be removed from the locality? Is it a fatigue fever or an infectious one? Is it a simple inflammation or an infecting one? The latter are usually much more grave. In case of contagious disease, can its propogation be prevented? Is it of a fatal or non-fatal type? Is it situated in a tissue favorable to a fatal extension, (anthrax in lung) or in one unfavorable (anthrax in the tip of the tail)? Disease in a single vital organ like the heart is necessarily much more grave than in one of a symmetrical pair (kidneys, lungs) one of which can carry on the functions. The regular progress of the disease and especially an uninterrupted improvement, following on a critical perspiration or urination, is a good prognostic sign, whereas unevenness of temperature, pulse and respiration, with temporary aggravations of the general symptoms, should demand a less hopeful prognosis. The persistence of the malady is also an unfavorable indication. A relapse after partial recovery is a serious indication unless due to some obvious and easily removable cause, and unless the former convalescent condition is speedily restored on its removal. A complication is a serious indication whether it consists in an embolism, or new centre of the same disease, or the supervention of a second disease upon the first. The system has just so much more to contend with and the very supervention of the second focus or malady argues a special susceptibility, debility, or lessened power of resistance.

The prompt success or entire insuccess of treatment proves valuable.

The preservation of appetite, the slow, uniform descent of the temperature, and the improvement of pulse and breathing are among the most valuable indications.

Something may be deduced from the condition of the patient. If very young or old, debilitated by overwork, bad or insufficient food, previous disease, or any other cause, the prognosis is less hopeful, as it is also as a rule, during gestation, in the parturient state, or if abortion ensues. A hereditary predisposition to the malady in question is equally unfortunate.

Climate may be an important factor. Thus liver diseases are far more to be dreaded in a damp tropical or semi-tropical region, and rheumatism and catarrhal affections in winter and in cold northern localities. Acclimatization should also be considered. The bovine animal, raised on the Gulf Coast is likely to make a good recovery from Southern Cattle Fever while the northern beast would almost certainly die.

All in all the question of prognosis cannot always be judiciously decided at a first visit, and for the sake of his own reputation, it is well that the practitioner should give only a qualified opinion at first until he can certify himself as to the probable outcome of the disease.

PROPHYLAXIS. PROPHYLACTICS. PREVENTION.

A test of public sentiment. Soil. Water. Exposure. Buildings. Local
hygiene. Breeding. Diet. Work. Harness. Ventilation.

With advancing knowledge of veterinary medicine the subject of prophylaxis is steadily assuming a more important place, and especially in the classes of enzootic and epizootic diseases. Indeed for the fatal infectious diseases of animals one can fairly estimate the medical intelligence of the people by the extent to which therapeutic treatment is still allowed. With economy as the great central object of veterinary medicine, the problematical recovery of the few can never balance the assured preservation of the many. But this subject belongs to contagious diseases to which the reader is referred.

In enzootic affections, improvements in soil, water, exposure, buildings, and other local unhygienic conditions, are the final ends to be sought, according to the particular nature of the prevailing disease.

So in sporadic diseases the correction of faults in breeding, hygiene, diet, water, work, harness, exposure, buildings, ventilation, etc., are called for in different cases as will be noted under the individual diseases.

THERAPEUTICS. TREATMENT.

Definition. Mechanical and Medicinal Therapeutics. Adaptation to each
case of disease.

The ultimate object of all medicine is to prevent disease or when it cannot be prevented, to cure. The term therapeutics covers all measures applied with curative object. Therapeutics are naturally divided into =Mechanical= and =Medicinal=. To mechanical therapeutics pertains the whole domain of surgery. Medicinal therapeutics has to do especially with internal medicine. Each of them, however, encroaches more or less on the other. Modern surgery is essentially aseptic or antiseptic, and antisepsis is secured by medicinal agents. In medicine when cups are applied we adopt an essentially mechanical treatment. Both methods then must remain open to physician and surgeon. Another and no less important branch of treatment which is open to physician and surgeon alike is diet and general hygiene. The same care must be given to the use of these in the treatment of disease as in its prevention, and in many cases a judicious use of these may almost entirely obviate the necessity for medicine.

It would be useless to enter here into the subject of therapeutics. Suffice it to say that the choice of a system and of individual agents must be determined by the particular conditions of the case, its cause, and nature, the strength, vigor, and genus of the patient, the organ involved, the extent and stage of the disease, the existence of a relapse, or complication, and all other circumstances that would affect the action of the remedy. Specific statements must be made with the several diseases.

HYPERÆMIA. CONGESTION.

Definition. Forms, active—arterial, passive—mechanical—venous.
Determination of blood. Causes of active congestion. Vaso-motor
nerves. Lesion of spinal cord; or of sympathetic nerve. Reflex
irritation. Central cause. Physiological hyperæmia. Medicinal
hyperæmia. Bacteridian (toxic) hyperæmia. Arterial obstruction.
Thrombus, tumor. Cold, chill. Removal of pressure. Cardiac
hypertrophy. Symptoms, bright red color, swelling, dropsy, migration
of cells. Rise of local temperature. Tenderness. Altered function.
Causes of passive congestion. Obstructions in the lungs, heart, veins.
Diminished force of circulation from age, debility, arterial disease,
distance from the heart, decubitus, vaso-motor disorder.
Gravitation—hypostatic congestion. Tumors. Paresis. Symptoms.
Cyanosis. Distended veins. Coldness. Transudation—watery. Hæmorrhage.
Thrombus. Hyperplasia. Atrophy. Postmortem lesions. Treatment. Remove
Cause. Correct injurious gravitation. Correct any fault in blood
pressure. Derivation. Constringe or support part. Massage.
Electricity. Improve general health.

_Definition._ An excess of blood in a part. It is distinguished from inflammation by the absence of that tissue reaction, which leads to or constitutes the special phenomenon of that morbid process.

Hyperæmia is divided into =active= or =arterial= and =passive=, =mechanical= or =venous=. A capillary form has also been described but usually capillary congestion is seen in both the arterial and venous types.

I. =Active= or =Arterial Determination of blood=. In this form the arteries are dilated under a direct nervous influence. _Causes._ In all the regular functions of the body, the flow of blood is under the direct control of the vaso-motor nerves which proceed from the spinal cord, through the branches of the sympathetic to be distributed with the blood vessels. The hard pulse of pleurisy is due to rigid contraction of the constrictor muscles under the action of the vaso-motor nerves, and the blush of shame is due to their relaxation. Some claim an active dilatation of the arterial muscular coats, others look more simply upon the dilatation as a mere yielding of the coats under the blood pressure, when the constrictor muscles are relaxed. This vaso-motor paresis may be induced: 1st, by any lesion of the spinal cord. 2d, by the cutting of a sympathetic trunk, that of the abdomen, for example, which leads to active congestion of the abdominal viscera, or the section of the cervical sympathetic which leads to watering of the eye, sweating, congestion, and scabbing on the corresponding half of the face. 3d, by reflex irritation through the sensory nerves, as in congestion through friction, heat or cold to the skin, or that resulting from excessive use of an organ such as the mammary gland. 4th, by causes acting directly through the brain as in emotional blushing or the facial congestion of violent rage.

Physiologically we see the operation of this nervous control in the congestion of the gums during dentition, of the salivary glands during mastication, of the stomach and bowels during digestion, of the womb during gestation, of the mammæ at parturition, and of erectile organs in copulation.

Medicinal agents act in the same way, opium or alcohol producing active dilatation, and belladonna and ergot causing active contraction of the arterial walls.

Bacteridian poisons act in the same way, tuberculin and a number of others causing active dilatation.

The obstruction of one artery by thrombus, tumor, or ligature, causes increased tension in the collateral branches coming off just above and an active congestion in the parts to which these are distributed. While this is directly due to increased local pressure, it is also an instance of the lack of balance between the blood pressure and the resistance of the vascular walls. In this case there is increase of pressure, in the other a diminished resistance.

If there is a superficial anæmia, as from cold or chill, there is of necessity, an internal hyperæmia. This contributes to the production of internal congestions and inflammations, though the seat of election of such inflammation is usually determined by the nervous sympathy between the part chilled and the deeper organ affected.

Another cause of congestion is the lessening of pressure by the parts surrounding the vessel. Thus in cupping, there is prompt cutaneous congestion, and a similar result occurs in pericardium, pleura, or peritoneum on the withdrawal of the liquid of hydropericardium, hydrothorax or ascites.

Another cause of congestion is found in hypertrophy of the heart and increased force of the blood flow (blood tension). In such cases those organs become congested in which there is some previous debility or disease of the blood vessels.

_Symptoms and results._ The symptoms are a bright vermillion redness, tension or swelling, heat and tenderness. Pulsation is stronger in the vessels leading into the part, secretions tend to increase but may give place to a serous effusion or hæmorrhage. The bright redness is attributed to the rapid circulation of the red globules which have not time to give up their oxygen to the tissues. It is sharply circumscribed where the affected arterioles have no free anastomosis with those of neighboring parts, diffuse where anastomosis is abundant, and when on the skin it is liable to rise in knots or buttons as in urticaria. When pressed the redness entirely disappears unlike the redness of inflammation.

The swelling may be due to the simple turgescence of the bloodvessels, but also often to transudation of serum as in and around the cow’s udder at parturition. The occasional migration of globules, and their escape through minute lacerations in the vascular walls add alike to color and turgescence.

The elevated temperature, (rising sometimes 3° C.) in the congested area, is attributed to the more active circulation, and Schiff prevented its appearance after section of the cervical sympathetic, by tying the carotid and vertebral arteries on the same side.

The tenderness of the congested parts varies inversely as the looseness of texture and the facility for swelling. It may be scarcely perceptible in the mammary region, and intense under the horn or hoof.

The functions in the congested organ are often seriously interfered with, secretions appearing in excess or entirely altered. When the congestion lasts it may cause hypertrophy, induration or hyperplasia, these are however rather sequels than lesions of the condition. Simple congestion is usually quite transient, and if prolonged, often merges into inflammation.

II. =Passive or Venous Congestion.= In this there is no excess of blood entering the part, but the regular supply is delayed in the veins by some obstruction, and these vessels and, later, the capillaries are gorged with black blood.

_Causes._ 1st, Mechanical obstruction to the onward flow of blood, as in the case of disease of the lungs hindering the flow of blood from the right heart; disease of the right heart allowing a reflux of blood into the veins; or pressure by tumors or otherwise on the great or small venous trunks. If in the heart or lungs the whole systemic venous system becomes the seat of passive congestion; if in a single venous trunk then only the parts the venous radicles of which are tributary to this. We find examples of this in phlebitis, in compression by the swellings of strangles, in the result of a bandage or ligature tied round a limb at some distance from its extremity, and in the compression of the iliac veins by a gravid womb.

2d. Diminished force of the blood current in the veins, as from old age or great debility and especially from weakness of the heart’s action. Also from disease of the arterial coats which impairs their tonicity. The force being too weak to force the blood actively through the capillaries and veins, it becomes unduly charged with carbon dioxide and other products of tissue waste, so that nutrition suffers and the walls of the capillaries lose their vital force. This condition is aggravated in the hind limbs by the distance from the heart, and the dependent position, and in decubitus by the compression of the vessels of the limbs. Also by injuries to the vaso-motor nerve supply as œdema appeared in the hind limb after tying of the femoral vein in animals the abdominal sympathetic of which had been cut, but not in animals in which this nerve was left in its normal condition (Ranvier).

3d. Gravitation in weak states of the circulation must be looked upon as a cause of venous congestion. This is seen in the examples of hypostatic congestion and œdema seen in the lungs and other internal organs in low conditions and in the advanced stages of debilitating diseases, and in certain cases of stocking of the limbs in horses.

4th. Valvular insufficiency of the left heart and tumors or aneurisms interfering with circulation through the aorta, cause passive congestion of the pulmonary veins and œdema of the lung.

5th. Tumors and diseases of the liver determine passive congestion of the portal system and ascites.

6th. Passive congestion is very liable to take place in an organ the functions of which are impaired as in a paralyzed part. In this the hyperæmia may start in the capillaries and extend to the veins or even to the arteries.

_Symptoms and results._ If on a mucous membrane or white skin the color becomes dark red, or violet (cyanotic) with evident distension of the capillaries and veins, the latter of which may stand out as knots or cords, there is an appearance of swelling or enlargement and sometimes coldness of the part. Soon the watery part of the blood transudes in excess, constituting dropsy, with increased swelling and pitting on pressure. On the mucous surfaces it determines an abundant serous secretion. The color is deepened by the escape from the vessels of red globules as well as white. The transudation contains little albumen and only exceptionally fibrine. In connection with the marked deoxidation and high carbonization of the blood, the nutrition of the part is largely arrested together with the functions, secretory, motor or otherwise. The imperfectly nourished vessels may give way, leading to hæmorrhage, or nutrition may be definitely arrested producing moist gangrene or ulceration. Sometimes a thrombus is formed in a congested vein. The changes in the affected organs depend much on the degree and duration of the hyperæmia. If slight and lasting it causes permanent induration and thickening, from connective tissue hyperplasia as frequently seen in the hind limbs of the horse. In case of blood transudations the altered coloring matter gives the various shades of gray, brown or black. If long continued the organ may shrink and atrophy occur from defective nutrition and contraction of the fibrous hyperplasia.

In making post mortem examinations mistakes may be made through the occurrence of changes after death. Thus a hvperæmia which was quite considerable during life may virtually disappear through the contraction of the arterial and capillary coats forcing the blood on into the veins. A minute point of extravasation here and there may be the only macroscopic lesion left. Again a marked venous and capillary hvperæmia in a dependent part of the body or of an organ may be entirely due to hypostatic conditions, the blood having settled into the lowest part of the vessels since the death of the animal. To avoid this source of error one must always carefully note the position of the carcass after death. Under other circumstances the superficial veins and capillaries may fill up with blood through the occurrence of decomposition and the evolution of gases in the internal cavities, which empty the splanchnic and parietal vessels by compression.

_Treatment._ The general principles of treatment may be stated thus: 1st. Remove the cause of the hyperæmia if possible, especially any mechanical cause; 2d. Secure the influence of gravitation in favor of the return of blood to the heart; though not so available in animals as in man, it is of great value in congestions of the head, ears, tail, and to a less extent of other parts; 3d. Correct any fault of blood pressure, excess or deficiency, which may act so as to cause active or passive hyperæmia; 4th. Establish derivation by cupping, leeches, fomentations, pediluvia, sinapisms, etc.; 5th. Apply cold, astringents, bandages, to empty the hyperæmic vessels, or kneading, rubbing, or electricity, to hasten the flow of blood; 6th. To improve the quality of the blood and general health, in plethora by low diet, purgatives and diuretics, in anæmic or debilitated conditions by iron, bitters, nourishing food, fresh air, sunshine and exercise.

It is especially important to check passive congestion in febrile diseases, and mechanical congestion at an early stage of its progress (Roberts).

INFLAMMATION. PHLOGOSIS. PHLEGMASIA.

Definitions. Relations to active hyperæmia. Redness. Heat. Pain.
Swelling. Forms: in vascular tissues: in nonvascular. Changes in
tissue elements. Death of cells. Cloudy swelling. Granular
degeneration. Cell proliferation. Karyokinesis. Embryonic cells.
Amœboid functions. Migration of leucocytes. Red cells escaping.
Changes in innervation. Vaso-motor disorders. Fever. Changes in
circulation. Contraction of capillaries, dilatation, rapid flow, tardy
flow, stasis, oscillations, thrombus, collecting of white globules in
periphery of current, migration of leucocytes, blood plates, and red
globules, massing of red globules, exudation, softening of the
capillary walls, nutrient artery more rigid and transmits more blood,
heart contracts more forcibly, increase of fibrine, increase of waste
products. Buffy coat, physiological causes. Microbes. Ptomaines.
Toxins. Chemiotaxis. Phagocytosis. Polynuclear and mononuclear
leucocytes. Exudates, unlike dropsies. Mucous exudate. Serous exudate.
Fibrinous exudate. Blood exudations. Croupous exudation. Chyliform
exudate. Results and Products. Resolution. Delitescence. Metastasis.
New formations. Suppuration. Pus microbes. Pus. Healing by 1st
intention. Healing by 2nd intention, granulation. Granule corpuscles.
Interstitial neoplasia. Degenerations in lymph. Fatty degeneration,
melanotic. Softening. Ulceration. Gangrene.

Inflammation has been variously defined as “perverted nutrition,” as a “protective reaction of the organism against irritant agents” and in other terms that express at once too much and too little, without actually defining the morbid process. Older definitions dealt with the manifest disorders of circulation, of innervation or of tissue change too often exalting the importance of one set of changes at the expense of another and thus giving in the main a one sided view of the morbid process.

Some modern bacteriologists are inclined to refuse the title to any morbid process that is not caused by the presence of microbes or their toxic products. To them the changes occurring in an aseptic wound or in a simple fracture in process of healing are purely reparatory and partake no more of the nature of inflammation than do the developmental changes in the growing embryo. While to a large extent true, this exclusive view implies exceptions, since if the chemical poisons derived from the bacteria can develop inflammation, the same must be admitted as possible for chemical irritants drawn from other sources.

As a matter of fact inflammation, occurring as it does in very different tissues, vascular and nonvascular, fibrous, cellular, parenchymatous, etc., and in connection with a great variety of irritants, must be held to include a large group of morbid processes, bearing to each other a strong family relationship and resemblance, and yet differing in many important details. Each irritant (heat, cold, electricity, chemical irritant, incised, punctured, lacerated or contused wound, rupture, fracture, foreign body, parasite, microbe, toxin, etc.,) has its own special character and mode of irritation; each tissue has its own special method of succumbing or reacting and its own amount of blood supply; and each system and organ has its own native or acquired power of resistance and reaction.

Inflammation agrees with active hyperæmia in the tendency to dilation of the vessels and an increased flow of blood to the part or if the irritated part is nonvascular like the cornea or articular cartilage, then to the parts adjacent. It differs, however, in the more active cell proliferation, and in the nature of the liquid transudation which is richer in albumen fibrine, cells and phosphates. Abstractly the inflamed part retains very active vital processes, trophic and exudative, but these, are largely changed from the normal and are, it is claimed, perverted, yet they preside over the processes of cell growth and decay, the removal of injured or useless tissue, and later, over the building up of new material, and repair of loss. Active hyperæmia on the other hand is mainly a circulatory disorder, and when it advances so as to determine changes in the cells and tissues it is held to have merged into inflammation.

The term inflammation (from inflammo, I set on fire), is suggestive of the local heat of the inflamed part, just as fever (febris) indicates an elevation of the temperature of the body at large. Celsius enumerated the features of rubor, calor, dolor and tumor (redness, heat, pain and swelling) which have come down to our own time as at least suggestive of inflammation. But any diagnosis, based on these alone, would be today woefully inadequate. Redness occurs in the transient blush, heat in the febrile state, though no inflammation can be recognized, pain is present in neuralgic and other nervous affections, and swelling in dropsy and tumor. On the other hand redness is entirely absent, for a time, after the outset of inflammation in nonvascular tissues (cornea, articular cartilage), the heat of the inflamed part may be actually lowered when there is much exudation around the capillary vessels and lessened flow of blood, pain may be absent in some circumscribed inflammations of the lungs, and swelling is not at first visible in the inflamed cornea or compact bony tissue. These phenomena which are so common in inflammation and, in general so characteristic of it, cannot therefore be accepted as infallible evidence of its existence, nor can their absence be held as absolutely implying its nonexistence.

=Forms of Inflammation.= This morbid process might be divided almost indefinitely according to the organ invaded, the cause, and type, yet it will be more convenient to deal with it generically and notice =inflammation in nonvascular and vascular tissues= respectively, and the different types of =granular degeneration=, =exudative inflammation= and =croupous inflammation=. It will be requisite further to notice an =acute= and a =chronic= type.

By dealing first with the changes in the anatomical elements of the tissues and in the innervation, we shall virtually cover the phenomena observed in nonvascular tissues, and later the changes in connection with the circulatory system will give the additional characteristics of inflammation in vascular tissues.

CHANGES IN THE TISSUE ELEMENTS.

=Death of cells and tissue.= By the application of an irritant (acid, heat, etc.,) a certain thickness of tissue with its enclosed cells is killed, and a thin layer of necrosis is usually produced. This does not constitute inflammation, but it acts as a foreign body, often septic, in producing inflammation in the parts adjacent.

=Cloudy Swelling, Granular Degeneration.= This may occur in the inflamed area surrounding the necrosed tissue in the seat of a burn or other injury, it is exceedingly common in the cells of inflamed parenchymatous tissue (liver, kidney), in the muscle of the heart, in the gastro-intestinal mucosa, in febrile affections and in poisoning with arsenic, phosphorus, or mineral acids. The gross appearance of the tissue is that of swelling, with a dull grayish color and a loss of its normal translucency. The cells of the affected organs are seen under the microscope to be filled with small albuminous granules which may be so abundant as to completely conceal the cell structure. The granules are insoluble in ether, but disappear under acetic acid. This condition of the cells is often associated with the exudative forms of inflammation.

=Cell Proliferation and Change.= In the nonvascular organ attacked by inflammation the multiplication of tissue cells and their resumption of amœboid movements is a constant phenomenon. Virchow insisted on the fundamental relation of the cell to the morbid process, and Goodsir and Redfern showed the rapid increase of the cells of articular cartilage in attacks of arthritis. There is first a sensible increase of the nucleus of the cartilage cell which shows a more extended and deeper staining in carmine or aniline; then by a special method of division (karyokinesis) the cell and nucleus divide in two; by a similar process these divide in four and so on in regular order. Meanwhile the cartilaginous substance becomes softened and finally dissolves and disappears, leaving in the place a mass of closely aggregated cells.

In the nonvascular transparent cornea, the membrane of Descemet, the epithelium of serous membranes and in the epidermis a similar cell multiplication occurs, also in the lateral cartilages of the horse’s foot.

To follow the indirect cell division by karyokinesis, we must note the cell as a semi-solid mass, formed of protoplasm and nucleus, each having as its framework a network of exceedingly fine inter-crossing filaments, much finer in the nucleus than in the cell protoplasm. The nuclear filaments stain with hæmatoxylon and safranin and are called _chromatin_ threads. The intervening non-staining material is _achromatine_. The nucleus has a membranous envelope in two layers, of which the inner only stains. When about to divide two poles are formed in the cell protoplasm opposite to each other and near the nucleus the filaments concentrating to the poles. The chromatin threads in the nucleus thicken, become convoluted, split and multiply, and draw into their substance the chromatin layer of the envelope. Next the chromatin threads form long loops directed toward an achromatine centre or pole like a star, and this is followed by the progressive division of the star-shaped mass into two equal parts.

Finally they separate, together with the cell protoplasm, forming two daughter cells.

This cell proliferation under the action of an irritant is common to the vegetable kingdom in which galls, and tumors are formed in this way. It is a remarkable feature of these multiplying cells that they not only lose their power of developing the tissue in which they formerly lay, and have all their vital powers devoted to proliferation, but they acquire the amœboid power of their ancestors, the embryonic cells, which they further resemble in size. Indeed these cells are freely spoken of as embryonal cells, and the tissue formed by their massing together as embryonal tissue, and there is a widespread impression that they revert entirely to the form and characters of the embryonic cell. In some respects, however, they are unlike. The modified tissue cell of inflammation presents a nucleus of horseshoe outline, or after division of the nuclei they together retain this semi-circular outline; it has the power of actively digesting the adjacent tissues as the embryonic cells do not, and again it does not possess the power of differentiation into widely different tissues as does the early embryonic cell. It may be called a reversion, in the direction of the embryonic cell, however, since it reacquires a number of its functions.

=Migration of white blood cells.= This is another, and in vascular tissues the main source of the great cell accumulation in the inflamed tissue. This process was observed by Waller in 1846, but was given its true importance through the later observations of Cohnheim. The migration takes place through the walls of the capillaries and veins only, and the migrating cells are largely of the polynuclear variety of leucocytes. These remaining adherent to the inner wall of the blood vessel may be seen to have a small portion of their substance projected through the wall and appearing as a small buttonlike projection on the outer side. This gradually increases, while the remaining portion of the cell on the inner side of the wall correspondingly decreases until the whole cell is lodged in the tissue outside the vascular wall. The time occupied in passing through is very varied. It may be wholly accomplished in half a minute, and again hours may be required for the complete passage of a single leucocyte. The explanation of this migration has been sought in the supposed existence of stigmata (openings) in the vascular walls (Arnold), in the effect of the blood pressure within the inflamed vessels, in softening of the vascular walls and, in the contractility of the leucocyte which is strongly attracted by the pressure of certain bacteria and other irritants (chemiotaxis). The migrated leucocyte assumes in the tissues the same habit as the altered tissue nucleus. It multiplies rapidly, assists in the solution and removal of the inflamed tissue, contests the ground with infective microbes (phagocytosis), and subserves the purpose of assisting in building up new tissue, or of degenerations.

=Red Cells.= The red blood globules follow the active current in the centre of the blood vessel, yet a few of these also become adherent to the softened walls and pass through them (diapedesis). When stasis of blood takes place in the vessels, they become packed more closely with red globules which then pass outward into the tissues in much larger numbers.

=Changes in innervation.= As shown under hyperæmia the vaso-motor system of nerves exerts a potent influence on the circulation and is largely instrumental in bringing about circulatory disorders. The increase in the number and force of the contractions of the heart, and the rigid contraction of the walls of the arteries proceeding to an inflamed part, are distinctly the result of a reflex nervous action. The implication of the second eye when one has been violently inflamed from a mechanical injury is another example of this kind. The loss of power of the vaso-motor nerves is however even more characteristic. Experimentally the cutting of the cervical sympathetic or crushing of the superior cervical ganglion causes congestion and finally inflammation of the structures on that side of the head; the crushing of the semilunar ganglion similarly affects the abdominal viscera; and the cutting of the pelvic plexus, the structures of the hind leg. The contraction and dilatation of the inflamed capillaries is largely a nervous phenomenon. A certain number of irritants, like warm water, mustard, or ammonia cause contraction followed by dilatation of the capillaries, while others like dilute mineral acids, alkalies, chloroform, or sodium chloride and sugar in concentrated solution produce dilatation at once. Some poisons act variously on different parts, eucalyptol causing dilatation of the arteries and contraction of the veins, while corrosive sublimate causes contraction of the arteries and dilatation of the veins.

So with certain microbian toxins. Introduced into the general circulation they produce active congestion or inflammation in the seat of colonization of the microbe from which they were derived, as witnessed in the use of tuberculin or mallein. Finally the chill and febrile reaction which attends on extensive inflammation is essentially a nervous phenomena in its inception and progress.

=Changes in the circulation.= The usual changes in the bloodvessels of the inflamed part may be thus succinctly stated: 1. Contraction of the capillary vessels of the affected part and hastening of the current of blood through them. 2. The succeeding dilatation of the capillaries and the slowing of the blood stream, which still flows uniformly throughout the diseased tissue. 3. The flow of blood becomes irregular, at points tardy, and at others oscillating or even recoiling between the pulse beats when it has been forced into a vessel already blocked by coagulum. 4. In the still pervious vessels the red blood globules occupy the centre of the vessel where the current is rapid, while the white globules roll slowly along the inner surface of the walls where the current is slow and become adherent to the walls and stationary, while the general current rolls on. This is a direct abstraction of the white globules from the circulating blood and greatly favors the coagulation of the blood in the capillaries. The blood plates equally collect in the periphery of the vessel and escape. 5. The adherent white globules migrate in large numbers through the capillary and venous walls into the tissues. The red globules migrate to a less extent at first. 6. Small coagula form in the affected capillaries, forming minute red points which cannot be pressed out by the finger. 7. The red globules in the area of stagnation back of these capillary emboli adhere to each other by their flat surfaces and form rolls which pack into the vessel and are enveloped in a fibrinous clot. 8. The liquid part of the blood rapidly exudes into the tissues leaving the red globules relatively much more abundant in the liquid which remains inside the vessel. 9. The walls of the capillaries become softened and allow a readier transudation of liquor sanguineous, and escape of the globules through the walls of the vessels. 10. The arteries leading to the inflamed part have their muscular coats more rigid and unyielding and transmit much more blood than the corresponding artery leading to the healthy part. 11. The heart is equally roused to more rapid and often more forcible contractions, which modify the pulse both in number and rhythm. 12. The circulating blood is found to have received a great increase in the fibrine formers, the fibrine in the shed blood amounting to 6, 8, or 10 parts per 1000 in place of 3 parts as is normal. The contraction of this causes a depression on the surface of the clot. 13. The red globules become viscous and adhere together by their flat surfaces to form rolls, which precipitate much more rapidly than single globules and leave the coagulated blood with a straw-colored upper stratum (buffy coat). 14. Increase of waste products, urea, uric acid, hippuric acid, etc.

Other changes in the blood are alleged, like lessening of the albumen, as balancing the increase of fibrine, and lipæmia, but the constancy of these in all cases of inflammation is uncertain.

By way of comment and explanation of the above changes in the circulation the following may be advanced: The primary contraction of the capillaries is by no means a necessary condition of inflammation, and contractions and dilatations within certain limits occur in health and as a purely physiological act. The dilatation of the capillaries and the increased flow of blood to the part are related to each other as in part cause and effect, yet both are due to a reflex act from the seat of irritation which inhibits contraction in the capillaries and determines a more rigid contraction in the walls of the arteries running to the part. A rigid inelastic vessel of the same calibre and under the same pressure transmits more liquid than the one with elastic walls. The movement of the white globules to the walls of the vessel depends in part on their levity, light bodies passing into the outer slow moving layer, which is less dense, from the central stream where the force and density are greater. The epithelial cells of the intima undergo cloudy swelling and are often detached, allowing the readier migration of the globules through the openings of the lymphatics and the softened and friable walls. When the capillaries are blocked the pressure necessarily increases on the arterial side, favoring laceration of the friable walls and the escape of minute masses of blood. The formation of the buffy coat is characteristic of the normal equine blood; in inflammation it becomes more abundant. In the other genera a buffy coat apart from inflammation may be shown in: (a) anæmia or oligocythæmia in which the blood is deficient in red globules; (b) in plethora in which there is an excess of blood solids; (c) in pregnancy in which there is an excess of white and small red globules; (d) in violent exertion or over-excitement, in which the blood has circulated with extraordinary rapidity. The all-sufficiency of the tissue cells in determining inflammation may be deduced from the following experiment. A ligature is tied around a frog’s thigh so tightly as to arrest circulation, and the leg amputated above the ligature; mustard is then applied to the web of the foot and a blister rises precisely as though circulation continued.

MICROBES, DIAPEDESIS AND PHAGOCYTOSIS.

The rôle of =microbes= in inflammation is much greater than was formerly supposed. It is now demonstrated that a large class of inflammations are directly caused by the colonization of microbes in the tissue and by the local irritation caused by their ptomaines and toxins. We must also admit the direct action of the latter on the heat producing and vaso-motor nervous centres, as a factor more or less potent in different cases in the causation and maintenance of inflammation. No less important is the relation of the microbe to the migration of the globules and the subsequent results of the inflammation. This influence microbes share with certain chemical agents. Migration may be greatly checked even in inflamed parts by the hypodermic or intravenous injection of sulphate of quinia, eucalyptol, salicylic acid, or iodoform. Some have thought these acted by a chemiotactic attraction, but quinia is otherwise found to repel the leucocytes. Their action on the leucocytes or capillary walls is problematic.

=Chemiotaxis= is that power by which a microbe or any element attracts or repels the leucocytes. When it attracts the chemiotaxis is said to be positive, when it repels it is negative. Among negative chemiotactic agents are quinia, solutions of sodium chloride (10%), and potassium salts, lactic acid, alcohol (10%), chloroform, glycerine, jequirity, and bile. To some agents, (creatine, creatinine, allantoin, peptone, phlorydzine,) leucocytes are indifferent. To gluten, wheat casein, pea legumin and the great majority of pathogenic microbes, leucocytes are positively attracted. As microbes exercise a great influence in producing local inflammation, so they are important factors in procuring an abundant emigration of leucocytes. Some of the most fatal of microbian diseases, like fowl cholera, repel leucocytes, and the benefit of their defensive work is to a large extent lost. The toxins of the chemiotactic microbe filtered from the bacteria exert the same influence as the living bacteria, as shown by Gabritchevski, Massart and Bordet.