Manual of Surgery by Alexis Thomson (golden son ebook .TXT) 📕

The irritation caused by infection with bacteria, on the other hand, is cumulative, as the organisms not only multiply in the tissues, but in addition produce chemical poisons (toxins) which aggravate the irritative effects. The resulting reaction is correspondingly progressive, and has as its primary object the expulsion of the irritant and the limitation of its action. If the natural protective effort is successful, the resulting tissue changes subserve the process of repair, but if the bacteria gain the upper hand in the struggle, the inflammatory reaction becomes more intense, certain of the tissue elements succumb, and the process for the time being is a destructive one. During the stage of bacterial inflammation, reparative processes are in abeyance, and it is only after the inflammation has been allayed, either by natural means or by the aid of the surgeon, that repair takes place.

In applying the antiseptic principle to the treatment of wounds, our main object is to exclude or to eliminate the bacterial factor, and so to prevent the inflammatory reaction going beyond the stage in which it is protective, and just in proportion as we succeed in attaining this object, do we favour the occurrence of ideal repair.

Sequence of Changes in Bacterial Inflammation.—As the form of inflammation with which we are most concerned is that due to the action of bacteria, in describing the process by which the protective influence of the inflammatory reaction is brought into play, we shall assume the presence of a bacterial irritant.

The introduction of a colony of micro-organisms is quickly followed by an accumulation of wandering cells, and proliferation of connective-tissue cells in the tissues at the site of infection. The various cells are attracted to the bacteria by a peculiar chemical or biological power known as chemotaxis, which seems to result from variations in the surface tension of different varieties of cells, probably caused by some substance produced by the micro-organisms. Changes in the blood vessels then ensue, the arteries becoming dilated and the rate of the current in them being for a time increased—active hyperæmia. Soon, however, the rate of the blood flow becomes slower than normal, and in course of time the current may cease (stasis), and the blood in the vessels may even coagulate (thrombosis). Coincidently with these changes in the vessels, the leucocytes in the blood of the inflamed part rapidly increase in number, and they become viscous and adhere to the vessel wall, where they may accumulate in large numbers. In course of time the leucocytes pass through the vessel wall—emigration of leucocytes—and move towards the seat of infection, giving rise to a marked degree of local leucocytosis. Through the openings by which the leucocytes have escaped from the vessels, red corpuscles may be passively extruded—diapedesis of red corpuscles. These processes are accompanied by changes in the endothelium of the vessel walls, which result in an increased formation of lymph, which transudes into the meshes of the connective tissue giving rise to an inflammatory œdema, or, if the inflammation is on a free surface, forming an inflammatory exudate. The quantity and characters of this exudate vary in different parts of the body, and according to the nature, virulence, and location of the organisms causing the inflammation. Thus it may be serous, as in some forms of synovitis; sero-fibrinous, as in certain varieties of peritonitis, the fibrin tending to limit the spread of the inflammation by forming adhesions; croupous, when it coagulates on a free surface and forms a false membrane, as in diphtheria; hæmorrhagic when mixed with blood; or purulent, when suppuration has occurred. The protective effects of the inflammatory reaction depend for the most part upon the transudation of lymph and the emigration of leucocytes. The lymph contains the opsonins which act on the bacteria and render them less able to resist the attack of the phagocytes, as well as the various protective antibodies which neutralise the toxins. The polymorph leucocytes are the principal agents in the process of phagocytosis (p. 22), and together with the other forms of phagocytes they ingest and destroy the bacteria.

If the attempt to repel the invading organisms is successful, the irritant effects are overcome, the inflammation is arrested, and resolution is said to take place.

Certain of the vascular and cellular changes are now utilised to restore the condition to the normal, and repair ensues after the manner already described. In certain situations, notably in tendon sheaths, in the cavities of joints, and in the interior of serous cavities, for example the pleura and peritoneum, the restoration to the normal is not perfect, adhesions forming between the opposing surfaces.

If, however, the reaction induced by the infection is insufficient to check the growth and spread of the organisms, or to inhibit their toxin production, local necrosis of tissue may take place, either in the form of suppuration or of gangrene, or the toxins absorbed into the circulation may produce blood-poisoning, which may even prove fatal.

Clinical Aspects of Inflammation.—It must clearly be understood that inflammation is not to be looked upon as a disease in itself, but rather as an evidence of some infective process going on in the tissues in which it occurs, and of an effort on the part of these tissues to overcome the invading organisms and their products. The chief danger to the patient lies, not in the reactive changes that constitute the inflammatory process, but in the fact that he is liable to be poisoned by the toxins of the bacteria at work in the inflamed area.

Since the days of Celsus (first century A.D.), heat, redness, swelling, and pain have been recognised as cardinal signs of inflammation, and to these may be added, interference with function in the inflamed part, and general constitutional disturbance. Variations in these signs and symptoms depend upon the acuteness of the condition, the nature of the causative organism and of the tissue attacked, the situation of the part in relation to the surface, and other factors.

The heat of the inflamed part is to be attributed to the increased quantity of blood present in it, and the more superficial the affected area the more readily is the local increase of temperature detected by the hand. This clinical point is best tested by placing the palm of the hand and fingers for a few seconds alternately over an uninflamed and an inflamed area, otherwise under similar conditions as to coverings and exposure. In this way even slight differences may be recognised.

Redness, similarly, is due to the increased afflux of blood to the inflamed part. The shade of colour varies with the stage of the inflammation, being lighter and brighter in the early, hyperæmic stages, and darker and duskier when the blood flow is slowed or when stasis has occurred and the oxygenation of the blood is defective. In the thrombotic stage the part may assume a purplish hue.

The swelling is partly due to the increased amount of blood in the affected part and to the accumulation of leucocytes and proliferated tissue cells, but chiefly to the exudate in the connective tissue—inflammatory œdema. The more open the structure of the tissue of the part, the greater is the amount of swelling—witness the marked degree of œdema that occurs in such parts as the scrotum or the eyelids.

Pain is a symptom seldom absent in inflammation. Tenderness—that is, pain elicited on pressure—is one of the most valuable diagnostic signs we possess, and is often present before pain is experienced by the patient. That the area of tenderness corresponds to the area of inflammation is almost an axiom of surgery. Pain and tenderness are due to the irritation of nerve filaments of the part, rendered all the more sensitive by the abnormal conditions of their blood supply. In inflammatory conditions of internal organs, for example the abdominal viscera, the pain is frequently referred to other parts, usually to an area supplied by branches from the same segment of the cord as that supplying the inflamed part.

For purposes of diagnosis, attention should be paid to the terms in which the patient describes his pain. For example, the pain caused by an inflammation of the skin is usually described as of a burning or itching character; that of inflammation in dense tissues like periosteum or bone, or in encapsuled organs, as dull, boring, or aching. When inflammation is passing on to suppuration the pain assumes a throbbing character, and as the pus reaches the surface, or “points,” as it is called, sharp, darting, or lancinating pains are experienced. Inflammation involving a nerve-trunk may cause a boring or a tingling pain; while the implication of a serous membrane such as the pleura or peritoneum gives rise to a pain of a sharp, stabbing character.

Interference with the function of the inflamed part is always present to a greater or less extent.

Constitutional Disturbances.—Under the term constitutional disturbances are included the presence of fever or elevation of temperature; certain changes in the pulse rate and the respiration; gastro-intestinal and urinary disturbances; and derangements of the central nervous system. These are all due to the absorption of toxins into the general circulation.

Temperature.—A marked rise of temperature is one of the most constant and important concomitants of acute inflammatory conditions, and the temperature chart forms a fairly reliable index of the state of the patient. The toxins interfere with the nerve-centres in the medulla that regulate the balance between the production and the loss of body heat.

Clinically the temperature is estimated by means of a self-registering thermometer placed, for from one to five minutes, in close contact with the skin in the axilla, or in the mouth. Sometimes the thermometer is inserted into the rectum, where, however, the temperature is normally ¾° F. higher than in the axilla.

In health the temperature of the body is maintained at a mean of about 98.4° F. (37° C.) by the heat-regulating mechanism. It varies from hour to hour even in health, reaching its maximum between four and eight in the evening, when it may rise to 99° F., and is at its lowest between four and six in the morning, when it may be about 97° F.

The temperature is more easily disturbed in children than in adults, and may become markedly elevated (104° or 105° F.) from comparatively slight causes; in the aged it is less liable to change, so that a rise to 103° or 104° F. is to be looked upon as indicating a high state of fever.

A sudden rise of temperature is usually associated with a feeling of chilliness down the back and in the limbs, which may be so marked that the patient shivers violently, while the skin becomes cold, pale, and shrivelled—cutis anserina. This is a nervous reaction due to a want of correspondence between the internal and the surface temperature of the body, and is known clinically as a rigor. When the temperature rises gradually the chill is usually slight and may be unobserved. Even during the cold stage, however, the internal temperature is already raised, and by the time the chill has passed off its maximum has been reached.

The pulse is always