Part 53

ANGEIOMA. CIRCOID ANEURISM. ANEURISM BY ANASTOMOSIS. VENOUS TUMOR. NŒVUS.

These are forms of dilatation and elongation of the network of small arteries, or veins, and even of the intervening capillaries. In man these constitute the unsightly red patches and swellings that appear on the face and hands. In animals with dark skins and hairy covering they can only be recognized by the swelling, the feeling as of a bag of worms when the hand is passed over it, and by the rushing sound when auscultated. The trouble is usually subcutaneous and is essentially a surgical one. The most promising treatment is by persistent pressure, by electric current supplementing the pressure, by electro-puncture, and by injections of muriate of iron. When the nœvus is not too extensive a double thread drawn by a needle through beneath the tumor at short intervals, then cut and each point tied separately, so as to completely stop circulation is most effective.

PHLEBITIS.

Divisions, traumatic and idiopathic. Causes, punctures, defective blood supply in walls, debile coats, thrombus, infection, overstretching, injury or disease of serosa, irritants in blood, microbic infection. Lesions, exudation, cell growth, breaches in serosa. Adhesive phlebitis, desquamation, granulation, occlusion. Suppurative phlebitis, infection, pyæmia, erysipelas, metritis, ulceration, neoplasms, phlebolites. Symptoms, local, firm, corded, swollen vein, extends entad, venous congestion, dropsy, gangrene, diagnosis from lymphangitis. Fever, venous congestion in vicinity. Treatment, germicide, rest, cold, antiseptics, blisters.

Inflammation of veins as seen in the lower animals has usually been a sequel of bleeding and is hence a purely surgical lesion. Animals as well as man however are subject to idiopathic phlebitis which as affecting the deeper seated veins may be held to be a medical subject.

The causes of =idiopathic phlebitis= are varied. Injury to the walls like the punctures made in bleeding; if they result in the exposure of a raw, and above all an inflamed, surface to the blood, tends to the formation of a thrombus, and of local inflammation. Even the inflammation of the outer coat tends in the same way to thrombosis and phlebitis, and the experiment of Nicasse showed that the dissection of its sheath from a vein, thus robbing it of its vascular and nervous supply promptly induced coagulation of the blood in the denuded part. The debilitated or devitalized walls evidently give off fibrinogen and fibrine ferment in amount that is incompatible with the maintenance of fluidity. All other forms of direct injury to the veins, leading to disturbance of the endothelium or cell enlargement or exudation in the intima, will operate in the same manner. Sometimes as in puerperal phlebitis the inflammation extending from the adjacent tissue to the walls of the veins, determines thrombosis, and the invasion by pus microbes determines suppuration. Bruises, overstretching, pressure with overdistension, and the circulation in the blood of irritant matters may lead to changes in the wall, thrombus, and inflammation. Such irritants may be septic or other bacterial products, or they may arise from the colonization of bacteria on or in the venous coats with the same final result.

The lesions in the vein are often primarily of the nature of exudation and cell growth in the coat, without at first any change in the serosa or endothelium. Later the changes implicate those, thrombosis follows and one of various ulterior processes.

In =adhesive phlebitis= which is most frequent as the result of purely mechanical injury, the endothelium is desquamated and granulations from the denuded surface extend into the clot and finally occlude the vein. A recovery takes place by the organization of this new product and the contraction of the vessel into a simple fibrous cord.

In =suppurative phlebitis=, which occurs especially in connection with infection (erysipelas, metritis), the inflammation, though starting in the same way in the vascular coats, advances rapidly to suppuration, and the intima, lying in contact with the resulting thrombus may become itself the seat of the suppurating process. Cases of this kind are almost of necessity in the nature of an infection and the danger is greatly enhanced. Small abscesses formed in the vascular coats may burst into the vein and passing on with the blood produce general infection (pyæmia). Even when the pus enters the vein at a point covered by the thrombus, it may escape by the partial loosening of the clot from the serosa, or through the interior of a honey-combed coagulum and thus lead to general infection. This is especially liable to follow in erysipelas and metritis, in which the tendency as in the solid tissues is to diffuse suppuration without any investing limiting membrane. There are other forms of bacterial colonization of the vascular walls, of ulceration, and of the extension of morbid growths into or through the venous walls, producing inflammation more or less localized, and leading or not to general infection. The presence of phlebolites in the vein is a conceivable source of phlebitis, though no such case has been so far recorded.

The symptoms in localized cases of simple adhesive phlebitis may be purely local. The vein if within reach may be felt like a firm, rounded cord, which extends in a direction from the heart. If there are no free anastomosis with neighboring veins on the distal side of the thrombus, venous congestion and dropsy of the tissues ensue, and in some cases moist gangrene. When, however, such anastomosis is abundant these peripheral symptoms may be absent, especially if the affected vein returns blood from a higher level than the heart, and then the symptoms are confined to the vein and its immediate surroundings. From lymphangitis which shows similar hard cords, it is distinguished by the absence of an extended network of diseased vessels, by the lack of a diffuse, doughy swelling, and by the fact that the adjacent lymph glands remain free from inflammation, pain and swelling. In the more extended cases there is fever, which may be of a very high type and may merge into pyæmia. In deep-seated cases it may be difficult to identify the disease, but it may be suspected if in the course of erysipelas or metritis there is a sudden increase of fever with pain and swelling, and distension of veins leading into the part.

The treatment of idiopathic phlebitis is largely that of the particular infecting disease on which it depends. In simple cases due to trauma absolute rest and the application of ice and antiseptic solutions, or where these cannot be applied, the use of antiseptics internally, will be indicated. Hyposulphite of soda and sulphide of calcium are especially indicated. From the early days of veterinary medicine, flying blisters of Spanish flies, over the inflamed vein or veins have proved very successful, and under the lead of Nonat the same was in 1858 and since adopted with gratifying success in the human subject. Abscesses formed in accessible situations should be promptly opened and treated antiseptically, and swelling of the affected part should be checked by elevated position, or if that is impossible, by a smoothly applied bandage. Rubbing and active movement are dangerous, as tending to detach clots which float off to start new emboli and inflammations in the lungs.

VARICOSE VEINS. DILATED VEINS WITH ALTERED WALLS.

Rare in animals. Angioma Varix. Superficial. Deep. Causes, obstructed circulation, compression, congestion. Symptoms, enlargement, elongation, tortuosity of veins, stiffness, lameness, complications. Treatment, compression, coagulants, cauterization, ligature.

Varix is not so common in the lower animals as in man, and is generally observed in the superficial veins, so that it comes under the domain of surgery. In the form of angioma, which affects the veins, there is extensive dilatation and elongation, but it involves a large group of connecting and anastomosing veins, whereas varix usually affects but one or a few connecting vessels. In the horse the most common seat of varix is in the saphena vein, as it passes obliquely over the inner side of the hock. Less frequently it appears on the flank or other superficial part. In cattle the mammary veins are the most frequent seat. Varices, however, occur also in deep-seated veins and in connection with normal venous plexuses, as in the buccal, palatal, and peneal. Anatomically they may be simple fusiform dilatations, as in the saphena; dilated, elongated and tortuous, branching trunks, as in the mammary veins; or dilated veins with thickened walls and pouch-like dilatations.

Causes. There is usually some obstruction to the circulation through the affected vessel, it may be by pressure by a tumor, or a constrained position, obliteration by a phlebitis and thrombus, extension of inflammation from adjacent organs, increased blood pressure by gravitation, or from diseased heart or lungs. Whether from the extension of contiguous inflammation, from external pressure, or from blood tension, the morbid process has much in common; the circulation and nutrition in the vascular walls are interfered with, degenerations set in (softening, fatty, connective tissue), which predispose to dilatation under the blood pressure. The pouch-like dilatations of the jugular consequent on bleeding, are essentially traumatic. The impaired innervation which lessens the resistance of the vascular walls is not to be forgotten. Varix of the saphena is usually an attendant or sequel of tibio-tarsal synovitis, and is the result of combined pressure and congestion. Mammary varices are manifestly connected with the congestion and exudations which affect the udder and environment at the time of parturition, or with a casual mammitis.

The symptoms in superficial vessels are visible enlargement, and often elongation and tortuous direction of the vein or veins, with or without tenderness. Deep-seated varicosities may be attended by stiffness of the part and a halting in progression with or without pain on pressure. These cases may recover spontaneously as the result of adhesive phlebitis, or they may develop phlebolites, suppuration, inflammation, ulceration and hæmorrhage.

Treatment. Superficial varices have been treated by compression, cauterization, coagulating injections, and ligature. It is not often that interference is demanded but in such cases, pressure with elastic bandage having failed, ligature with antiseptic precautions is indicated.

PHLEBOLITES. CALCAREOUS BODIES IN THE VEINS.

Nature. Location. Mode of formation. Calcareous plates in two inner coats. Phlebotomy. Altered sanguification. Treatment. Extraction.

Calcareous bodies have been repeatedly found in the veins of man and several observations of the same kind have been made in the horse. Spooner found them in the abdominal veins and Simmonds in the jugular. Much difference of opinion has existed as to the mode of formation of these bodies whether by calcareous deposit in a coagulum or by degeneration of a neoplasm in the vascular wall. Andral held the latter opinion, and Tiedemann and Cruveilhier found the bodies connected to the inner coat of the vein by a fine membrane. Morton’s cut of one of Simmonds’ specimens (Calculus Concretions) shows a structure in successive layers having their centre at one end, evidently corresponding to a former connection by pedicle. Cornil and Ranvier says “sometimes there are seen in chronic varices, calcareous incrustations in the form of plates, nodules or spheres with concentric layers ... calcareous infiltration is seen in the form of spheres or phlebolites in the varicose diverticula. An extensive calcareous induration several centimetres in length, is also sometimes observed, the vein being transformed into a calcareous tube with the ramifications also varicose.

The calcareous plates of the vein are developed in the fibrous and internal portion of the middle coat. At the beginning they consist of granules deposited in the fasciculi of the connective tissue or between them; these soon unite and form transparent plates with granular striæ.”

Phlebolites in the jugular suggest a connection with the pouch-like dilatations, and transformations in the vascular walls that have been subjected to phlebotomy. It is probable however that there is usually a morbid condition of sanguification and nutrition which predisposes to their formation. In Simmonds’ case the jugular was impervious below the bodies, there was hepatitis and arthritis of the fetlock joint.

When recognized during life these may be extracted with due antiseptic precautions. If the vein can be dispensed with it may be ligatured above and below, if not an attempt may be made to preserve it, extracting through a clean cut longitudinal incision and securing as perfect coaptation of the edges of the wound as possible.

HÆMORRHAGE.

Arterial, venous and capillary hæmorrhage belong almost exclusively to the domain of surgery. Internal hæmorrhages will be considered in connection with the organs in which they take place.

HÆMOPHILIA.

Definition. Causes, lack of plasticity of the blood, thin walls, blood tension, cardiac erethism, hypertrophy and neurosis. Sex. Heredity through the female. Treatment, depletive, styptic, astringent. Transfusion.

This is a constitutional infirmity, usually hereditary and characterized by the occurrence of profuse and continuous bleeding as the result of otherwise insignificant injuries or even apart from any recognizable lesion. It has been attributed to a slow coagulation of the blood, but at the start of a hæmorrhage the blood is rich in corpuscles and coagulates firmly. It has also been ascribed to extreme tenuity of the vascular walls, but this has only been met with in a certain proportion of the cases. Another potent factor is a permanent over-filling of the bloodvessels (Immermann, Delafield, Prudden). The same writers attach importance to cardiac erethism, cardiac hypertrophy, and certain neurotic influences which temporarily increase the habitually congestive diathesis. In man the majority of victims have been males, perhaps because most subject to traumatisms. On the contrary the hereditary transmission is mainly through the female members of the family. The families are very prolific, a condition counterbalanced by the death of the majority of the victims at an early age. Among the lower animals it has been observed in horses consequent on castration (Siedamgrotzky, Kohne, Friedberger and Fröhner), setoning (Kohne, Dieckerhoff), and an ulcer of the leg (Kohne).