Read Ebook: Text book of veterinary medicine Volume 1 (of 5) by Law James

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HYPERAEMIA. 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 hyperaemia. Medicinal hyperaemia. Bacteridian hyperaemia. 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. Haemorrhage. 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.

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 mammae 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 anaemia, as from cold or chill, there is of necessity, an internal hyperaemia. 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 . In such cases those organs become congested in which there is some previous debility or disease of the blood vessels.

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, 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.

In making post mortem examinations mistakes may be made through the occurrence of changes after death. Thus a hvperaemia 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 hvperaemia 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.

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

INFLAMMATION. PHLOGOSIS. PHLEGMASIA.

Definitions. Relations to active hyperaemia. 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. Amoeboid 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 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 hyperaemia 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 hyperaemia 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 , is suggestive of the local heat of the inflamed part, just as fever indicates an elevation of the temperature of the body at large. Celsius enumerated the features of rubor, calor, dolor and tumor 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 , 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.

CHANGES IN THE TISSUE ELEMENTS.

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.

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 amoeboid 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.

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.

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

MICROBES, DIAPEDESIS AND PHAGOCYTOSIS.

But chemiotaxis may be exerted from within the bloodvessel as well as from without. Bouchard, Massart and Bordet have shown that a tube containing a culture of bacillus pyocyanus, introduced beneath the skin of a rabbit attracts in a few hours a great number of leucocytes. But if, immediately after its introduction, ten cubic centimetres of a sterilized culture of the same bacillus are injected into a vein, very few leucocytes enter the tube inserted under the skin. The chemiotaxis seems to operate in this case from within the blood, and the desires of the leucocytes are satisfied without leaving the vessel. It would seem that in such cases the migration and protective work of the leucocytes is best exerted at the outset of the illness and before the toxic products have been poured into the blood in any quantity, whereas in the advanced stages when the blood is charged with ptomaines and toxins migration and phagocytosis would be likely to be limited and ineffective. The same consideration would forbid the use of drugs that check migration in all cases of attacks by microbes for which leucocytes have a positive chemiotaxis.

Even with an abundant emigration of the leucocytes into the inflamed or invaded tissue, a number, greater or less, are usually destroyed by the bacterial poisons and pass into degeneration or liquefaction, as in the formation of pus, and yet the attacking germ may be overcome, destroyed and devoured by the rapidly increasing survivors. In general terms the migration of the cells is in inverse ratio to the susceptibility of the animal to the microbe or the disease which it causes.

The positive and negative chemiotaxis, which determine phagocytosis or prevent it, may be seen in the action of the leucocytes toward the germs of two diseases, to one of which the animal is susceptible and to the other of which it is not. Thus the leucocytes of the pigeon take in the bacillus anthracis and suffer nothing apparently, whereas the same white cells of the dove are repelled by the bacteria of fowl cholera which are not therefore found in their interior.

The leucocytes that migrate from the bloodvessels are in the main, the most numerous, form; the mononuclear leucocytes with horseshoe shaped nucleus also migrate but in much fewer numbers and are as a rule less occupied in phagocytosis. At the same time, these two forms may show each a preference for a particular microbe, the polynuclear cell sometimes devouring one which the mononuclear cell rejects, and the mononuclear cell taking in one which the polynuclear refuses.

The small round white cells and the eosinophile leucocytes take no prominent part in phagocytosis.

EXUDATION.

In inflamed vascular tissues one of the most important results is the exudation. This is not, however, a mere transudation of the liquid parts of the blood, as takes place in dropsy, but it is to a large extent a selective process determined apparently by the condition of the capillary walls, and the nature of the inflammation is stated according to the character of the exudate. The dropsical effusion contains little albumen, fibrine or cell forms, and does not coagulate. The inflammation exudate contains abundance of fibrine, cells and other solids and coagulates spontaneously in contact with inflamed tissue, or when removed from the body, by reason of the transforming leucocytes. Inflammatory exudate usually contains 6 to 8 per cent. of solids whereas the normal canine lymph contains 4 to 6. The exudate varies not only in different inflammations, but in successive stages of the same inflammation. The exudate may be mucous, serous, fibrinous or haemorrhagic.

These effusions are dangerous by reason of their interference with the functions of organs by pressure as with the dilatation of the lungs, the movements of the heart, the action of joints, or the integrity of the brain or spinal cord. When the causative disease has subsided they are usually speedily reabsorbed, the cells passing into the lymph vessels, or becoming degenerated, liquefied, and absorbed. Yet serous effusions often remain as permanent accumulations. For the blood staining of serous effusions and their clearing up, see under pleurisy.

Fibrinous inflammations are especially found in connection with inflamed fibrous tissues and in strong vigorous subjects.

RESULTS AND PRODUCTS OF INFLAMMATION.

As nearly all inflammations have significant exudations it is well to follow these in their subsequent progress through reabsorption and removal, development into new tissues, necrosis, suppuration and ulceration.

While the above conditions are favorable to the formation of pus, the process of suppuration must now be recognized as an infective process due to the propogation of bacteria . These or other bacteria are found in the pus of acute abscesses, and when absent in chronic abscesses are to be considered as having perished since the abscess was recent and active. Inoculation of a rabbit with an excess of the pus of an acute abscess produces general purulent infection and early death; from a medium dose an abscess is produced; while from a small dose there is no effect whatever. In the latter case the bacteria are overcome and devoured by the abundance of vitally potent white blood globules and tissue cells. This pus-forming action of these bacteria explains the great difference in results in wounds exposed to the air and those in the interior of the body and far removed from air and its floating bacteria. A broken bone, with no wound in the skin and little injury to parts around the fracture, is readily repaired without any formation of pus, if merely kept still and immovable; whereas a broken bone, continuous with a wound through the skin, always tends to form pus or become otherwise infected, and is extremely dangerous even to life. The tendency of every open sore is to form pus on its surface but this may be arrested and avoided by preventing the access of germs, or by a free use of disinfectants and a covering which shall arrest and filter out the germs. Similarly in an abscess, evacuation followed by the injection of disinfectants, without the formation of any perceptible permanent opening to the outer air, will put a stop to the pus-formation. The subjection of an inflamed part to the control of these pus-forming bacteria is dependent on the lowered vitality and power of resistance of the inflamed tissues, and of the white cells of their circulating blood. Healthy parts can successfully resist them, though they are constantly present in surrounding air and on objects, but in this as in all other cases, of bacterial infection, so soon as the tissue is injured, inflamed and lowered in its power of vital resistance, the pyogenic bacteria assail it successfully. Hence, too, the more abundant exudations of lymph, the centres of which are farthest removed from the healthy tissues and from nourishment, are the most prone to suppuration. That the germs can make their way to such deep-seated exudations in the substance of solid tissues is to be accounted for by their gradual advance through the inflamed and weakened structures from the adjacent skin or mucous membrane, or in some instances by reason of their presence in small numbers in the blood. It is further noteworthy that those animals in which suppuration does not occur readily are such as have a special power of resistance to some other organic poisons. Thus the hog, which is supposed to be proof against snake-bite, is also, to a large extent, proof against the pus-forming bacteria.

FEVER.

Definition. Symptomatic. Idiopathic. Symptoms. Contagion. Incubation. Premonitory symptoms. Chill, rigor. Reaction, hot stage. Defervescence. Crisis. Lysis. Natural temperature. Fever temperature. Retention of water in the system. Production of waste materials. Typhoid condition. High fever, low, hectic. Treatment in vigorous subject, in weak one. Regimen. Solipedes. Ruminants. Carnivora. Drink. Rest. Clothing. Air. General and local bleeding. Cupping. Warm baths, tepid, compresses, derivatives. Cold. Diaphoretics. Laxatives. Diuretics. Sedatives. Alkalies. Antipyretics. Stimulants. Tonic refrigerants. Tonics. In low fever. No depletion. Judicious elimination. Stimulants. Refrigerants. Antiseptics. Diet. Local treatment of inflammation. Cold. Astringents. Antiseptics. Warm applications. Stimulating embrocations. Blisters. Firing. Massage. Suppuration.

Of all extensive inflammations fever is the constant result and accompaniment, rising as the inflammation rises or extends, and subsiding as the inflammation subsides. It also occurs as a distinct affection, as in all the infectious diseases, as the result of a specific irritating poison in the system, and then is the manifestation of the disease, while a local inflammation may or may not be present as a special secondary feature of the malady or as an accidental complication.

TREATMENT OF INFLAMMATION AND FEVER.

Treatment will be guided very largely by the type of the attendant fever. If that is of a high type, with a hard, full, rapid pulse, bright red mucous membranes, a clear eye, and well sustained strength in a strong, vigorous animal, what is known as antiphlogistic treatment is admissible at the outset. But in many cases with a low type of fever, a weak, rapid pulse, pallid, yellow, or livid mucous membranes, a coated tongue, a dull or sunken eye, much depression and prostration, swaying on the limbs in walking, pendant head, ears, eyelids and lips, and varying and irregular temperature of the limbs, etc., such measures are forbidden from the first, and tonics and stimulants are demanded from the outset. Between the two extremes there are many grades, which demand a judiciously adjusted intermediate treatment. The general principles only of each characteristic form of treatment can be here formulated, it being understood that no two cases can be most advantageously treated in precisely the same way, but that according to its special grade each case will demand its own specific management applied according to the skill of the physician.

Similar good results are obtained from all remedies that induce surface warmth and vascularity and a free secretion from the skin.

When the preliminary stage has passed and the hot stage of the fever has set in, cooling and eliminating agents are especially called for.

In cases of infectious disease with poisoning by ptomaines and toxins the elimination of these by the bowels and kidneys is of the greatest importance.

In these cases of asthenic inflammation, as in the advanced and debilitated stages of sthenic inflammation, the diet should be as good as the patient can digest. Boiled oats, barley, or flaxseed, rich, well-boiled gruels, and beef-tea may frequently be resorted to with advantage.

DISEASES OF THE RESPIRATORY ORGANS.

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