Chapter LVIII: Part 58

DIAGNOSIS.--The diagnosis is often uncertain. When not developing with extreme rapidity the symptoms are very similar to those caused by stenosis of the pulmonary artery, and in the suddenly fatal cases they are almost identical with rupture of the heart or rupture of a thoracic aneurism, or even angina pectoris. The history of an antecedent thrombus or of a disease of the heart which is likely to be accompanied by thrombus, together with the absence of physical signs, render a diagnosis many times probable.

PROGNOSIS.--To be regarded as of the gravest character.

TREATMENT.--In the rapid cases death occurs before anything can be attempted. In the less severe cases absolute rest must be enjoined, and free stimulation with brandy, ammonia, and ether attempted. It might be worth while to place the patient with the head lower than the body, to favor the flow of blood to the brain.

DISEASES OF THE SUPERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of both the superior and the inferior mesenteric arteries occurs. The former is the more frequent, though still a rare disease.

The symptoms are pain in the epigastric and lumbar regions, a globular pulsating tumor in the median line, the pulsation being accompanied by a bellows murmur. The tumor has been seen in at least one instance to be so large as to press on the renal arteries. Rupture is apt to take place with the signs of internal hemorrhage. The cause of the disease is the same as of aneurism elsewhere. Embolism is said to be a not infrequent precedent. The aneurism is seldom larger than a hen's egg, and is usually globular.

A positive DIAGNOSIS of the locality of the aneurism is not possible.

The TREATMENT must follow individual indications. Compression has been successful in a few instances.

Embolism.

Several cases where the superior mesenteric artery was found at autopsy to be completely occluded by coagulated fibrin were mentioned by Tiedemann in a work published in 1843. Virchow first described the characteristic {837} post-mortem appearances which follow this lesion in his _Gesammelte Abhandlungen_, and since then records of cases have been numerous.

CLINICAL HISTORY.--In by far the majority of cases there is an evident source for an embolus. Pain in the abdomen is the first symptom, and usually remains one of the most prominent throughout. At first it may be a dull aching just below the borders of the ribs, but soon there is superadded paroxysmal pain resembling colic, and which may at times even be relieved by pressure. The occurrence of this colic in cases where embolism might happen ought to put the physician on his guard for other symptoms; for, though insufficient in itself to establish a diagnosis of embolism, the presence of a colic resisting treatment in the course of cardiac disease justifies the suspicion that this may be the case. The pain is usually located near or above the umbilicus.

Intestinal hemorrhage occurs in nearly every case; death may take place before any change in color of the stools is observed or any blood appears at the anus, but on post-mortem examination blood is found in the intestine. The cause of this hemorrhage is the infarction of the intestine analogous to that which takes place in other organs supplied by end arteries, the superior mesenteric having been proved experimentally to be functionally such an artery, owing to its great length, the extent of tissue supplied by it, and the comparative smallness of the vessels with which it anastomoses on the borders of its territory. The collateral circulation is thus so long in being established that ample time is allowed for those disturbances of nutrition in the walls of the vessel which render them permeable and allow the blood to escape. In view of the hemorrhage certain other symptoms are readily accounted for, as, for example, pallor of the face and surface of the body, the considerable and rapid fall of the temperature, syncope, hæmatemesis, diarrhoea, and melæna. These two latter symptoms are important though inconstant. There is reason to believe that the first effect of the embolism is to paralyze the bowel and prevent peristaltic action. Diarrhoea is of frequent occurrence, and may be profuse, the stools remaining of their natural color; or fresh blood may be passed at first from the rectum, followed by the continuous passage of tar-like masses; or the stools may be of pulpy consistence, mixed with blood, or consisting of tarry blood. Lastly, profuse hemorrhage may take place in which the stools resemble tar-water. The character of the blood does not give any kind of clue to the locality of the lesion.

Vomiting is a frequent symptom, and may consist of altered blood of variable consistency. A fall in temperature can often be determined by the thermometer, especially after severe hemorrhage. Not rarely the temperature is normal or may be even increased, especially if secondary inflammation has set in.

Tension and tympanitic swelling of the abdomen may occur or fluid may be detected late in the case, these being evidence of peritonitis.

PATHOLOGY.--Before proceeding to consider the pathological changes occurring in embolism, a few words on the blood-supply of the intestine might perhaps render what follows clearer. The superior mesenteric artery supplies the whole of the small intestine except the first part of the duodenum; it also supplies the cæcum and the ascending and transverse colon. The inferior mesenteric supplies the descending and sigmoid flexure of the colon and the greater part of the rectum. The anastomoses are as follows: The pancreatico-duodenalis, a very small artery and a branch of the hepatic, anastomoses with the first branch of the superior mesenteric, also a very small artery and given off under cover of the pancreas. The middle colic artery anastomoses with a branch of the inferior mesenteric. Both these arteries are given off from the main trunks of the arteries.

The experiments of Litten in 1875 show that the superior mesenteric artery, {838} though not so anatomically, is functionally a terminal artery, the anastomosis not being developed with sufficient rapidity in case of extensive embolism to ensure the integrity of the circulation.

1. The result of sudden total closure by embolism of the trunk of this artery, therefore, is precisely like that of ligature of this artery in animals, and is first to produce sudden abdominal pain, attacks of colic, vomiting, uncontrollable intestinal hemorrhage, death. The intestine from the lower transverse portion of the duodenum to the middle of the transverse colon is found to be suffused, brown-red, blackish, or grayish. All the layers are swollen; innumerable capillary extravasations of small and great extent are seen, with venous hyperæmia and oedematous infiltration. In other words, there occurs necrosis with oedema and hemorrhage in all those portions of the intestines which are supplied by this artery.

2. Closure of large branches by embolism gives rise to infarction of the portion of intestine concerned, followed by death. The symptoms differ only in intensity, if at all, from the preceding. A case has been seen where there was every reason to believe that embolism had occurred, and yet the patient recovered. (The patient, suffering from acute rheumatism complicated with peri- and endocarditis, suddenly developed profuse intestinal hemorrhage of tar-like color, which was repeated twice. Colic pains, tympanites, depression of the temperature of the body, followed. At the same time symptoms of embolism of various other arteries were present. Recovery took place after eight weeks.) This result of course depended on the subsequent perfection of the collateral circulation.

3. Closure of the smallest branches may produce the same kind of symptoms as the above, though less in degree. Limited portions of intestine have been found to be in a gangrenous condition from embolism of very minute branches, more especially when the embolus extended well into the artery. In place of gangrene of the intestine ulcers of the mucous membrane have been seen independent of typhoid fever or tuberculosis. Considerable stenosis has followed such ulcers.

The affected portion of intestine in embolism is found to contain a variable amount of blood mixed with the other contents of the gut. Peritonitis, dry and limited or general and accompanied by effusion, is the rule. The mesenteric glands are found enlarged and succulent, with perhaps here and there necrosed spots. Thrombosis of the corresponding veins is not uncommon. Large collections of blood under the peritoneum and in the mesentery have been observed. The color of the mucous membrane has been slaty, and a diphtheritic appearance has been observed.

DIAGNOSIS.--The following are the most important points in forming a diagnosis: 1. A source exists from which an embolus might be derived. 2. Profuse and even exhaustive intestinal hemorrhage sets in, which can neither be explained by primary disease of the intestinal walls nor by hindrance to the portal circulation. 3. There is a rapid and considerable fall of the temperature. 4. Pain in the abdomen comes on, which may resemble colic and be very severe. 5. Finally, tension and tympanitic swelling of the abdomen occur, and there may be fluid in the abdominal cavity. 6. Evidence of embolism of other arteries may have been obtained before the symptoms of embolism of the superior mesenteric artery come on, or such evidence may appear at the same time as the latter. 7. Palpation may reveal the presence of collections of blood between the folds of the mesentery.

PROGNOSIS.--The prognosis in embolism of the superior mesenteric artery, though not absolutely bad, is exceedingly grave. It must be borne in mind that the symptoms of occlusion of one of the large branches are similar to those where the main stem is involved, while the probabilities of recovery in the former are much greater, as already explained, from the shorter extent of {839} the anastomosis. There is evidence that recovery from the immediate effects of embolism may take place even where subsequent ulceration has been so great as to cause complete closure of the intestine through cicatrization. (A case is related by Parenski where the patient was operated on for stricture of the bowel, and only at the autopsy was it discovered that the stricture was due to cicatrization from ulceration caused by embolism of one of the branches of the superior mesenteric.) There are at least three cases of recovery on record where occlusion of the main stem was supposed to have taken place; but inasmuch as the situation of the embolus cannot be determined with certainty if the patient recovers, these cases are open to the suspicion that one or more of the larger branches only were occluded. The profuseness of the hemorrhage, though it may imperil the life of the patient from exhaustion, bears no constant relation to the gravity of the case. Copious and repeated hemorrhages per anum took place in cases of recovery, while in other fatal cases this symptom was entirely absent. Extreme fetor of the stools must be regarded as of evil omen, as it may be the evidence that gangrene of the bowel has taken place.

TREATMENT.--One of the first symptoms calling for relief is the colic, which is best met by morphia given subcutaneously or by suppository. For the hemorrhage ergot by the mouth and alum enemata have proved serviceable, or the application of ice to the abdomen. The lowering of the heart's action by sedatives is to be avoided when we remember that their use would lower the blood-pressure, and thus tend to retard the establishment of the collateral circulation.

Thrombosis.

The symptoms of thrombosis have not been determined apart from embolism, and it is doubtful if the affection proves fatal unless the extent of artery involved is very considerable or the formation of the thrombus is very rapid, for the anastomosis is gradually made compensatory. In either of the latter cases the symptoms are identical with embolism, and the pathological appearances are the same. With regard to treatment, general indications must be pursued.

Endarteritis.

This disease is met with, but it is usually slight and unaccompanied by symptoms.

DISEASES OF THE INFERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of this artery has been seen after death. The diagnosis could not be made, in all probability, during life. Pain might be a prominent symptom, though not necessarily, as many of the aneurisms of the abdomen are unattended by any symptoms. Rupture is not unlikely as a termination.

Embolism.

Embolism has been observed. Sudden pain in the abdomen comes on, followed by vomiting and diarrhoea. The patient looks miserably; the {840} belly is drawn in and painful on pressure almost exclusively in the left iliac region. Severe spontaneous colic-like pains continue, with occasional vomiting and diarrhoea. At first the stools are feculent and pap-like; then they begin to smell bad, and even stink. Red blood is passed. Soon there is a mixture of blood and slimy masses. Finally, the stools are slimy, blackish, almost tar-like, and have a terrible odor, and are passed with griping and tenesmus. Occasional vomiting still continues. The pulse becomes smaller and more frequent, and gradually irregular and intermittent. Soon collapse and death follow.

The predisposing and exciting causes are the same as in embolism of the superior mesenteric artery.

The duration is usually short, lasting from a few hours to three or four days. The termination is ordinarily fatal, though doubtless cases of recovery have occurred, as stated under Embolism of the Superior Mesenteric Artery, the size and position of the embolus not precluding the possibility of the establishment of collateral circulation.

Complications are varying degrees of peritonitis, evinced by tympanites, pain, and tenderness, either localized or diffused, and later by the occurrence of effusion. Sequelæ, when the disease is not immediately or rapidly fatal, are ulceration of the colon with subsequent cicatrization and contraction.

PATHOLOGY.--The mucous membrane of the descending colon, sigmoid flexure, and rectum is somewhat swollen, strongly reddened, and contains ecchymoses and extensive suffusions of blood; or the color may be blackish or slaty and the surface sloughy.

DIAGNOSIS.--The diagnosis can only be made by exclusion. The same points are to be carefully verified as in embolism of the superior mesenteric artery, only the pain and symptoms are in a different place, and the secondary peritonitis also begins on the left.

PROGNOSIS.--The prognosis is very grave, but recovery may take place, contractions or constrictions being left behind.

TREATMENT.--The treatment combines perfect rest, the exhibition of wine, opium, vegetable astringents, and the subcutaneous injection of morphia.

ANEURISM OF THE HEPATIC ARTERY.

The tumor varies in size from a hazelnut to a child's head, and is egg-shaped. Pain in the epigastrium and right hypochondrium or upper abdominal region is a characteristic symptom. At first the pain is not severe, and is occasional, recurring after a pause of several months' duration; later it becomes very severe and lasting. The abdomen is not tender to the touch or on pressure during the remissions from the attacks of pain, but after rupture of the aneurism, whether temporary or lasting, it is very severe. The abdomen is sometimes distended, at others not. The tumor, owing to its position, cannot be felt, nor can pulsation be detected, as the wall of the aneurism consists of connective tissue and blood-clot, and the stream of blood coming from a small artery is slow. In but a single case has increase in size of the spleen and liver been observed. The functions of the stomach and intestines remain normal in spite of the pain. The locality of aneurism of the hepatic artery is such as to readily cause temporary or lasting icterus--a phenomenon which occurs in perhaps two-thirds of the cases. Rupture, with the ordinary signs of internal hemorrhage, seems to be the usual termination. Inflammatory processes or fever does not follow hemorrhage into the abdomen. {841} If perforation occurs into the gall-bladder, a gall-duct, or the intestine, the hemorrhage may appear to be moderate. In such instances repeated discharges of blood may occur from the intestine, or at the same time may be thrown off from the stomach.

There is no means of determining how long aneurism of the hepatic artery may exist without giving any kind of sign of its presence. Judging from analogy, it is very probable that a considerable time may elapse before the disease is observed. Since pain in the abdomen is the first pathological indication, and rupture the last, we may measure the probable duration of the disease by these phenomena and also by the clinical course. This was not over ten days in two cases, and in three cases it was three to four months. Since aneurisms of the hepatic artery, even when they have reached their greatest dimensions, are not palpable, the pains which appear with them have in themselves no diagnostic worth. The same is true of the icterus which appears sooner or later. It is only after rupture has occurred that all the chances are so placed that a comprehensive estimate of them may be made and a diagnosis arrived at by exclusion. The fact that the function of the stomach remains unchanged in spite of rupture (hemorrhage), and the totally unchanged character of the blood-clots vomited, enable us to locate the situation of the hemorrhage as outside the stomach. If at the same time there is an alternate relation between the occurrence and disappearance of the icterus and the hemorrhage, the inference is admissible that the latter is located in the immediate vicinity of the gall-ducts. Other peculiarities of the blood-clots passed at stool are perhaps the imprints of the valvulæ conniventes of the jejunum.

The DIAGNOSIS of aneurism of the hepatic artery is usually impossible.

Aneurisms of the splenic, renal, and other abdominal arteries are recorded, but not in sufficient numbers to warrant a detailed description of them.

DISEASES OF THE COELIAC AXIS.

Aneurism.

Aneurism of the coeliac axis, when the tumor is large, is accompanied by very much the same symptoms as aneurism of the abdominal aorta. The disease is rather uncommon.

ETIOLOGY.--Syphilis, rheumatism, and advanced age play important parts in the etiology of this disease as predisposing causes of arterial degeneration. Many persons affected have been immoderate spirit-drinkers, which of itself does not directly tend to the disease, but does so indirectly, in that it encourages an early senescence of the tissues. In the same way any debilitating conditions may act as predisposing causes. Chronic endarteritis is most frequently found at the seat of the aneurism. Secondary or exciting causes are peculiarities of occupation, as those which are laborious and require much physical exertion and entail exposure to inclemencies of the weather.

SYMPTOMS.--Pulsation is usually the first symptom observed. It is felt in the epigastrium about two and a half inches below the ensiform cartilage, or even higher, and a little to the left of the median line; or it may be midway between the ensiform cartilage and the umbilicus, on the left. It is not unfrequently of a distensile character, and is unaffected by changes in the position of the patient. It is not synchronous with the cardiac systole, but follows in rapid succession to, and terminates with, the ventricular {842} diastole. A tumor, usually globular, is felt in the region of the pulsation. It is of variable size, from that of a hen's egg to a cricket-ball, or in case of false aneurism even much larger. The tumor is slightly tender; it moves with the diaphragm, and sometimes when it presses upon the pancreas ptyalism has been observed, which in one instance was increased by external pressure on the aneurism with the hands.

Another constant symptom is pain in the left side, extending from well up in the chest to the region of the hip, or located in the lower part of the chest alone, or perhaps in the epigastrium. This pain is either constant or excited by exertion, and paroxysmal in character.

Flatness on percussion over the tumor of varying extent is observed in many cases, and a systolic bruit, perhaps of a whistling character, is heard.

The usual termination of aneurism of the coeliac axis is rupture with internal hemorrhage. The symptoms of this accident do not differ from those of the same occurrence in abdominal and thoracic aneurism, and are likewise usually fatal.

PATHOLOGY.--Strain doubtless forms an important factor in the production of this aneurism in an artery previously weakened by disease of its coats. The tumor is frequently a false aneurism, and has for walls connective tissue and the neighboring organs. When it is of large size, on account of its position it sometimes presses upon the pancreas or vertebræ, and produces absorption with consecutive symptoms. In the former case ptyalism has been observed, which perhaps may have been due to reflex action through the coeliac plexus and pneumogastric nerve, the reflex centre being the medulla oblongata with the facial origin. The wall of the aneurism is usually thin, and in some cases it has given way, leading to the formation of so-called false aneurism. Not infrequently the wall is atheromatous. The size of the aneurism varies greatly, though it is never larger than the two fists.

DIAGNOSIS.--This aneurism is apt to be confounded with aortic aneurism, and can only at times be distinguished from it by its locality and small size.

PROGNOSIS.--This must be grave if a diagnosis is made, for the ultimate result is usually rupture and hemorrhage.

TREATMENT.--The general principles recommended in treating abdominal aneurism should be followed out. It is but rarely the case that compression is admissible, and then the distal pressure is to be used. Rest and diet form the most reliable means of treatment at our command.

{843}

DISEASES OF THE VEINS.

BY ANDREW H. SMITH, M.D.

The principal affections to which the veins are liable are the following: Inflammation (phlebitis), acute and chronic; Dilatation; Narrowing or obliteration; Degeneration; Concretions.

Inflammation.

Idiopathic phlebitis occurs for the most part under one of three conditions: First, as a simple primary inflammation of the tissues composing the walls of the vessel; second, as a participation in an inflamed or diseased condition of surrounding structures; third, as the result of the absorption of poisonous material into the blood.

Like any other structure of the body, the veins are liable to inflammation as a purely local affection. It is nevertheless true that, in the acute form, this inflammation is most likely to occur in connection with certain conditions of the system which seem to act as predisposing causes, although the connection between them and the local phlebitis is not apparent. Thus it occurs (perhaps associated with more or less of lymphangitis) in the puerperal state, in phthisis, in heart disease, and in other conditions of general depression. I have met with it, for example, during recovery from pneumonia after typhoid fever and after suffocative laryngitis. Under these circumstances it constitutes the chief element in the affection known as phlegmasia dolens. Now, none of the above conditions implies, so far as is known, any source of irritation to the venous structures, much less to a limited portion of the venous system; and the only explanation of their association with phlebitis seems to be in the assumption that these conditions favor coagulation of the blood, and that, in these cases, the formation of a clot precedes the local inflammatory process. The location of this clot is probably determined by anatomical conditions.

In other cases, however, the process evidently begins in the wall of the vessel, and the formation of the thrombus is secondary. Any change which interferes with the smoothness of the inner coat, whether by loss of endothelium or by producing inequalities of the surface, will very certainly determine the deposition of fibrin and the formation of a coagulum. The glossy smoothness of the intima seems to require the most perfect nutrition of the subjacent tissues for its maintenance, and its loss produces an immediate slowing and ultimate stoppage of the blood-current. This is admirably shown by the experiments of Nicasse,[1] which demonstrate that simply denuding a portion of a vein, and thus cutting off its vascular and nervous supply, induces almost immediately the formation of a thrombus coextensive with the denuded portion.

[Footnote 1: _Des Plaies et de la Ligature des Veinse_, Thèse, Paris, 1872.]

{844} Inflammation affecting the inner coat of a vein and extending along its surface, as in the case of a serous membrane, probably never occurs. The picture of phlebitis formerly drawn, and which embraced the exudation of false membrane or the formation of pus upon the inner surface of a vein, the pus in the latter case floating off with the blood and constituting pyæmia, the formation of a clot being a later and unimportant event, has little or no resemblance to what actually occurs.

The observations upon which these assumptions were based were erroneous, as shown by Virchow, in that the staining of the intima by absorption of coloring matter from the blood was mistaken for inflammatory redness, and changes in the clot itself were confounded with exudation and suppuration. Indeed, when we reflect that the intima is not vascular, we should scarcely expect from it anything analogous to serous inflammation. The only acute process to which it appears liable is an erosion or crumbling away under the same conditions which determine, in the middle or outer coats, increased vascularity, exudation, and the formation of pus.

Thus, from some general condition favoring the coagulation of the blood we may have a thrombus formed, followed by secondary inflammation of the wall of the vessel, or, without such general condition, we may have inflammatory changes, commencing in the outer or middle coat and causing the secondary formation of a thrombus. In either case the clot shuts off the affected portion of the vein from the general circulation. Changes take place in the clot which are more properly considered under the head of thrombosis, and by which it is ultimately removed. Exudation takes place into and between the tunics which form the venous wall, the latter becoming thickened and comparatively rigid, so that when the vein is cut across its lumen remains open like that of an artery.

Sometimes pus is formed between the different coats, constituting small mural abscesses; sometimes the intima crumbles away and exposes the middle coat, which suppurates on its inner surface, and the pus mingles with the débris of the clot. In this way a larger abscess is formed, bounded by the wall of the vein and by a partly-organized coagulum on either side. These coagula sometimes break down, and fragments from them, infected by the pus and its contained micrococci, are swept on in the current of the blood until they find a lodgment, where the process begins anew, and whence it may be propagated in like manner to other and more distant parts.[2] It is only to the condition above described that the term suppurative phlebitis can properly be applied.

[Footnote 2: Ziegler, _Path. Anatomie_, Jena, 1881, p. 429.]

But, instead of a suppurative process taking place, the endothelium may be thrown off and replaced by minute vegetations of the character of granulation-tissue, which, penetrating into and blending with the clot, may temporarily or permanently occlude the vein, and the contraction which follows may ultimately leave only a fibrous cord to represent the vessel.[3]

[Footnote 3: Leroux, _Gaz. méd. de Paris_, 28 Juin, 1879.]

This process is designated adhesive phlebitis, and is one of frequent occurrence and very important in its results. It takes place in connection with suppurative phlebitis, and by closing the vessel on either side of the suppurating portion serves to prevent the pus from mingling with the general circulation.[4] By its action the largest veins, including the venæ cavæ, are occluded, and extensive and important changes in the circulation are brought about.

[Footnote 4: While this is true of a pus-cavity forming within a vein, an abscess originating outside of a vein or between the layers of the venous wall may open into the vessel at a point not protected by a clot, and the pus mingling with the blood will constitute veritable pyæmia.]

The second condition under which phlebitis occurs is that in which a vein, {845} coursing through an inflamed or diseased structure, becomes itself inflamed. This takes place most frequently in phlegmonous erysipelas and in diffused inflammation of the cellular tissue, but it may be the result of any inflammation in the neighborhood of a vein. Under these circumstances the external layer of the venous wall is first affected, and the others subsequently. Only a portion of the circumference of the vessel may be involved, and the wall may bulge inward considerably without necessitating the formation of a thrombus (Virchow). But if the nutrition of the walls is seriously impaired, the intima becomes roughened by the loss of its endothelium, the blood-current is slowed by the increased friction thus caused, and, the uneven surface favoring at the same time the adhesion of fibrin, a clot is formed, and the course thereafter is the same as when the vessel is primarily affected.

Suppuration may also take place between the vein and its sheath, and extend for a considerable distance along the vessel. The walls participate secondarily, and the vein becomes occluded as before described.

In the third class of cases, those depending upon toxic infection, the inflammation is caused by the irritation of some poisonous material circulating in the blood. The phlebitis is therefore secondary, and is to a great degree overshadowed by the general condition which accompanies it. Aside from instances in which there is a direct inoculation of a poisonous material--as, for example, the venom of a serpent--the conditions merge into those which come under the designations pyæmia and septicæmia--diseases which were formerly confounded with phlebitis, but which are now recognized as distinct from, though often coexisting with, it.

If in acute phlebitis the inflammation does not result in the formation of pus, the vein may recover its normal condition, or the walls may remain thickened and the lumen contracted, but still pervious, or it may be entirely occluded. Suppuration, however, always results in complete and permanent closure of the vein.

The symptoms of acute phlebitis are chiefly such as indicate obstruction of the vein. When a large vein, situated in one of the extremities, is the seat of the affection, there are usually severe pain of a tensive character and decided tenderness on pressure. The limb swells, sometimes to a very considerable extent, and becomes stiff and unwieldy. If a superficial vein, such as the long saphena, is affected, there will be subcutaneous oedema and pitting; but when the vessel lies beneath a firm, tense fascia, this will limit the swelling, and the limb will be hard and brawny, while the tension will greatly aggravate the pain.

When the vein is sufficiently near the surface it may be felt at the affected part as a hard cord, usually more or less knotted. The skin over it may be discolored, presenting a red or somewhat coppery hue and a streaked or mottled appearance, or the pressure from the effused serum may empty the capillaries of blood and render the skin pale and shining.

The temperature of the limb may be elevated, normal, or subnormal. In the outset, under the influence of the inflammation, there is usually increased heat, but as the tension from the oedema interferes more and more with the circulation, the temperature falls, and the limb may become colder than its fellow.

Inflammation of a limited portion of a vein may not be attended by any notable symptoms, the collateral circulation being quickly established, and the effects of the obstruction thus obviated, while, at the same time, the local symptoms are masked by the morbid conditions in the surrounding tissues which give rise to the phlebitis.

The constitutional symptoms accompanying phlebitis are those of inflammatory fever, the grade of which will depend upon the extent and severity of the inflammation. When a considerable length of vein is involved, as {846} may be the case in the form of phlebitis already referred to, which progresses along the sheath of the vessel, the irritation of the general system may be great, especially if pus is formed, when hectic or even typhoid symptoms are not uncommon.

The differential diagnosis of phlebitis in its local appearances requires only its distinction from lymphangitis. The latter disease is more abrupt in its invasion, depends almost always upon some wound or injury with which the local symptoms are directly connected, is more diffuse, affecting a network of vessels rather than a single one, and is invariably accompanied by engorgement of the lymphatic glands to which the affected vessels lead, as, in the case of the extremities, the axillary or inguinal glands.

In complicated cases the occurrence of phlebitis may not be marked by any distinctive symptoms. It may be suspected if, in the course of erysipelas, diffuse cellulitis, etc. in the neighborhood of an important vein there is a somewhat sudden increase of pain and swelling, and if an enlargement of the tributary cutaneous veins is soon observed.

The treatment of phlebitis consists in complete rest, in the use of such constitutional means as may be necessary to allay the irritation of the system, and locally in the application of leeches and warm fomentations. If, on the other hand, the local temperature is very high, the use of ice may be indicated.

Nonat, in cases of commencing phlebitis from venesection, tried the use of flying blisters over the part affected. Obtaining good results, he extended the treatment to phlebitis following typhoid fever, etc., and the morbid phenomena were at once arrested.[5]

[Footnote 5: _Gaz. des Hôp._, No. 86 (_Med. Times and Gaz._, Aug. 7, 1858).]

Much disturbance of the parts, either in examining them or in the use of frictions, etc., is to be avoided, as there are not a few instances on record in which portions of thrombi have been detached in this way, and, floating off in the current of the blood, have resulted in pulmonary and even cardiac embolism, the latter causing immediate death.[6] The tendency to oedema will be lessened by placing the affected part in a position that will favor the return of the blood by the collateral circulation.

[Footnote 6: _Lyon Médicale_, June 18, 1876 (_N.Y. Med. Rec._, Sept. 2, 1876).]

As an internal remedy the calcium sulphide is worthy of trial.[7] The administration of ammonia is thought to lessen the tendency to the formation of coagula and to promote their absorption if already formed. Abscesses occurring in superficial localities should be promptly opened, antiseptic precautions being observed. The strength of the patient should be maintained by every possible means, the danger of an extension of the mischief being proportioned to the lowering of the vital forces.

[Footnote 7: "Report of N.Y. Therapeutical Society," _N.Y. Med. Journ._, June, 1882.]

As already stated, acute phlebitis plays a very important part in the affection known as phlegmasia alba dolens or white leg. Indeed, many writers consider that it is the only essential factor in the affection. This view is strongly insisted upon by Hervieux, but the researches of Mackenzie,[8] Simpson,[9] Barker,[10] and others have shown that something more than phlebitis is embraced in the disease. Tilbury Fox claims that there is an association of lymphangitis with the phlebitis. At all events, whatever may be the exact pathology of the affection, it appears to be certain that an abnormal condition of the blood, favoring the formation of coagula in the veins, is an essential prerequisite.

[Footnote 8: _Pathol. and Treat. of Phleg. Dolens_, London, 1862; _Med. Times and Gazette_, Aug. 22, 1866.]

[Footnote 9: _Med. Times and Gazette_, Jan. 14 and 18, 1859.]

[Footnote 10: _The Puerperal Diseases_, New York, 1876.]

Phlegmasia dolens occurs chiefly in the puerperal state, and affects chiefly {847} the lower extremities; but it may affect males and non-puerperal females, and may be seated in the arms as well as the legs. Outside of the puerperal state it is met with in conditions of depressed vitality, as during convalescence from acute disease, and in those suffering from phthisis, cancer, and other cachexiæ. When one of these conditions is present a degree of venous obstruction--from pressure, for example--which would ordinarily cause merely a slight amount of oedema may result in an adhesive or even suppurative phlebitis, and the associated phenomena which form the disease in question.[11]

[Footnote 11: Murchison, _Med. Times and Gaz._, May 23, 1863, reports the case of a man recovering from typhus in whom phlegmasia dolens resulted from the pressure of a diverticulum from the bladder upon the right iliac vein.]

The preponderance of cases, however, occurring from the second to the fourth week after delivery indicates a special condition present at that time tending to produce the disease. Some cases, doubtless, are due to the cause suggested by Lee--viz. the formation of clots in the uterine veins, and the growing out of these thrombi through the hypogastric and into the iliac and femoral veins. But that this is not the only or the usual cause is proved by numerous autopsies in which no evidence of thrombosis has been found in the uterine veins. Still, the puerperal period is very generally one of vital depression, in which hyperinosis and inopexia are presumably present. To this is added another source of irritation, in the loading of the blood with the material absorbed from the uterus in the rapid reduction of its bulk which is taking place.

It is not improbable also that small amounts of decomposing blood, and even clots, may be retained in the uterine sinuses, and ultimately be forced suddenly on into the venous circulation by the pressure resulting from the shrinking of the tissues by which they are surrounded. This would explain the suddenness with which symptoms of toxæmia or embolism often occur.

The principal difference between phlegmasia dolens and simple obstructive crural phlebitis is in the degree rather than the character of the symptoms.

When, in a healthy animal, phlebitis of the crural vein is set up artificially, causing complete obstruction, there is but little pain, and only a comparatively slight effusion into the cellular tissue, and the limb pits readily. In phlegmasia dolens, on the other hand, the pain may be very severe and the oedema very great, and the limb is stiff, hard, tense, and shining, and pits only with firm and continued pressure (Barker). Moreover, crural phlebitis may occur and prove fatal without causing phlegmasia dolens.

These facts have perhaps been allowed undue weight in the argument for non-identity. It would seem that we have only to admit a depraved condition of the blood favoring thrombosis and secondary phlebitis, and disposing to more abundant effusion of a more plastic character as the result of the obstruction, and all the distinctive phenomena of phlegmasia dolens are covered. The experiment has never been tried of producing phlebitis artificially in a subject, with the blood-condition predisposing to white leg, in order to determine whether this condition would follow; but clinically it has more than once been demonstrated that in such a subject phlegmasia dolens may result from simple pressure upon the iliac vein.

The fact, too, that the disease occurs three times in four on the left side, where the iliac vein is pressed upon by the rectum and by the iliac artery, is not to be forgotten in this connection. If lymphangitis were a necessary factor in the disease, pressure upon the vein would not have such a marked causative influence.

The symptoms of phlegmasia dolens may be gathered from the preceding remarks, together with the description of the symptoms of acute phlebitis. {848} It is to be noted, however, in addition, that the majority of cases are ushered in by one or more chills, and that the progress of the case is usually marked by a tendency to profuse perspirations. In the puerperal woman lactation is generally very much interfered with or entirely suspended. "The lochial discharges seem, in very many cases, to be very little influenced by the onset and progress of this disease, but in others they have been observed to become very fetid and offensive" (Barker).

The tendency of this affection is to terminate by resolution. The hardness diminishes before the size of the leg becomes less, and with this diminution of tension the muscles regain their power. Gradually the oedema subsides, and the knotted cords which indicated the course of the affected veins disappear. If all goes well, the limb is restored in the course of three or four weeks apparently to its normal condition. Yet even in these cases the affected vein probably remains entirely obliterated, the circulation being carried on by the subsidiary vessels.

But in many cases the recovery is only partial, and for months or years the limb remains larger than its fellow, the superficial veins are enlarged, and the skin congested and of a dusky hue. Long standing or walking causes increased oedema, and there is a disposition to eczema and ulceration above the ankle.

What was said in regard to the treatment of phlebitis is applicable to that of phlegmasia dolens. As the tension subsides the application of a roller bandage will hasten the return of the limb to its normal size. But care must be taken that it is not tight enough to still further impede the already obstructed circulation. At a later period the support of an elastic stocking may be required. Constipation is to be avoided, especially in those cases in which the left lower extremity is affected, as the pressure of the loaded rectum interferes with the return circulation.

Chronic phlebitis is usually the sequel of an acute attack or else is developed in a vein already varicose. The coats of the vessel become thickened and hardened by interlamellar development of nucleated fibrous tissue, so that the walls become more or less rigid. This thickening may be partly at the expense of the lumen of the vein, thus reducing its calibre, or it may be entirely excentric. The vasa vasorum are sometimes developed in chronically-inflamed veins to a remarkable extent. Quincke states that they may attain the size of cuticular veins.[12]

[Footnote 12: _Ziemssen's Cyclopædia_, art. "Dis. of the Veins."]

Except in the case of superficial veins, in which the vessel may be felt as a hard cord, the affection cannot be recognized during life. It may be assumed to exist when the symptoms of acute phlebitis continue in a less degree, or when tenderness, without other active symptoms, is found along the course of a vein. Under these circumstances there are apt to be acute attacks of pain and swelling from the operation of slight causes, the attacks subsiding, but the chronic condition remaining through the intervals.

The treatment looks to the avoidance or removal of the causes which tend to produce acute exacerbations. Rest is of the first importance. In chronic inflammation of a superficial vein the local use of iodine or of the ointment of iodide of lead will be of service. A succession of flying blisters along the course of the vein may be employed with advantage. When there is chronic enlargement of the limb the persistent administration of potassium iodide may be useful in promoting the absorption of effused material. After the subsidence of all inflammatory action massage may be resorted to.

{849} Dilatation of the Veins.

This condition results either from undue pressure of the blood within the veins or from impaired resistance of their walls. The former condition is found in certain forms of heart disease affecting the right chambers; on the distal side of an obstruction in a vein; when collateral veins are required to carry on the circulation, the natural channel being narrowed or obliterated; and in the veins of a limb when the position is such, a great portion of the time, that the blood is forced to mount against gravity.

The second condition, that of diminished resistance of the walls, is found in enfeebled constitutions and in the degeneracy of tissue incident to advancing age. A familiar example is furnished by the enlargement of the veins on the back of the hand in old persons.

Excessive dilatation of the veins which go to make up the superior cava often results from insufficiency of the tricuspid valve. When this insufficiency exists a proportionate part of the systolic energy is expended in driving the blood back into the systemic venous circulation, and the superior cava, from the nearer correspondence of the axis of its opening with the axis of the auriculo-ventricular opening, receives the larger share. Hence with every contraction of the ventricle a direct distending force is exerted upon this vessel and its branches which they are not fitted anatomically to resist. In such cases the distended veins may reach an enormous size, and are seen to pulsate synchronously with the arteries. The distension is greatest in the neck, but affects also the veins of the chest and of the upper extremities.

Whenever a vein is obstructed, either by some process taking place within it or by pressure from without, the distal portion is more or less dilated. Examples of this are seen in the closure of veins from phlebitis and by the pressure of abdominal tumors or the gravid uterus.

Under like conditions the tributary veins also, being forced to carry more than the normal amount of blood, become enlarged. This we see constantly in the dilated veins of the abdomen when the internal vessels are pressed upon by large dropsical effusions.

The term caput Medusæ is applied to a collection of enlarged veins radiating from a common centre or arranged in the form of a corona. Such collections often occur on a small scale above the ankles, but under some conditions they assume vast proportions. When there is obstruction of the inferior cava a great mat or pad of dilated, convoluted veins may form on the abdomen or thighs. Some of these veins may be as large as the little finger.

In the erect posture the veins of the lower extremities are subject to a distending force proportioned to the height of the column of blood which they have to sustain. For short periods at a time the resistance of the walls is ordinarily sufficient to bear this pressure without yielding, but in persons whose occupation requires them to stand a considerable portion of each day, and especially in those past middle life, there is a gradual giving way, which results in increasing not only the diameter but the length of the vein.

The dilatation takes place irregularly, being greater at one point than at another, and in one place affecting the entire circumference of the vessel, while in another it produces a bulging on one side or even a pouch or diverticulum. Especially just above the valves in the veins of the lower extremities, where the diameter is naturally a little greater, the larger area gives rise to greater pressure, and more marked dilatation results. Their breadth remaining the same, the valves are no longer able to reach across the vein, and the circulation is deprived of the aid which it is their office to give. Instead of the column of blood being divided into a number of portions, each resting upon the valve beneath it, there is now a continuous column which exerts its full static pressure. Dilatation is thenceforth doubly rapid, and at the same {850} time the vein is stretched longitudinally and becomes tortuous, thus adding another impediment to the circulation. The nutrient vessels ramifying in the venous walls are pressed upon, and the nutrition of the several tunica is impaired. From this arises fatty or calcareous degeneration. Under these combined influences the walls often become so thinned that rupture takes place. But it is rare that the blood is effused into the tissues surrounding the vein, for the overlying integument or mucous membrane, atrophied from the pressure of the vein beneath, usually gives way at the same time, affording a means of escape. Even bone is not capable of resisting the continuous pressure of an enlarged vein, but may be absorbed in the same way as in the case of arterial aneurism (Bristowe).

Sometimes the dilated vein becomes thicker instead of thinner by addition to the outer tunic; probably the result of a slow inflammatory process, to which, as already stated, varicose veins are peculiarly liable.

The slow circulation, especially in pouched and tortuous veins, favors the formation of coagula which frequently close up the vein entirely, thus bringing about a spontaneous cure. Independently of this, there is a disposition to recovery when the cause is removed, and the vessel may, under favorable circumstances, regain its normal condition. If, however, the valves have atrophied, as they are apt to do after their efficiency has ceased, entire recovery is impossible.

Oedema is apt to occur in connection with dilated veins if the impediment to the circulation is considerable. Chronic ulcers of the legs, accompanied by eczema, are a very common result of a varicose condition of the superficial veins of the lower limbs; and a permanent cure can seldom be effected unless the varicose condition is first removed.

Dilatation of the hemorrhoidal veins is an important factor in hemorrhoids. But it is far from constituting the disease, as was formerly supposed, the tumors being largely made up of dilated capillaries and hypertrophied connective tissue. Indeed, in some of the worst forms of piles it is not possible to find any evidence of varicose veins in the extruded mass.

In most cases, however, these varices are present, and may be distinguished as smooth blue or purple nodules. When a hypodermic needle is thrust into one of these, the point is felt to be in a free cavity, which immediately becomes filled with a solid coagulum when a few drops of a weak solution of carbolic acid are injected--an operation which usually effects a cure.

Obstruction of the portal circulation predisposes to hemorrhoids; hence they are a frequent attendant upon diseases of the liver. The habitual presence of fecal accumulations in the rectum, pressing upon the veins, operates directly to impede the return circulation, while the straining at stool which accompanies this condition greatly aggravates the difficulty.

The TREATMENT of external varicose veins belongs properly to the province of surgery. When the dilatation can be traced to changes occurring in any of the internal organs, treatment should be directed to removing the cause or mitigating its effects. A constipated habit should be corrected and the hepatic circulation be promoted.

The presence of ascites will call for the use of diuretics or purgatives or of the aspirator. In cases having a cardiac origin much good may often be accomplished, for a time, by the judicious use of digitalis.

In all cases advantage is to be taken of position to aid the circulation as far as possible.

In the case of superficial veins the application of moderate and evenly-distributed pressure is of much service.

{851} Narrowing of a Vein.

This condition may occur as the result of inflammation which has stopped short of occlusion.

Under the name of hypovenosity has been described a condition of the saphenous system in which there is a deficiency in the number and size of the veins. The outlines of the limb (bone, muscle, etc.) are effaced, the skin is dusky, the limb brawny, and there are no veins visible. The motion of the limb is painful and difficult. There is degeneration of the superficial veins, collateral dilatation of the deep veins, and ultimately atrophy of the muscles.

Exercise, frictions, and hot applications are to be employed. Rest and bandaging as a mode of treatment aggravate the disease.[13] The affection is of rare occurrence.

[Footnote 13: J. Gay, _Lancet_, Nov., 1871.]

Occlusion of Veins.

Venous occlusion results very frequently from adhesive phlebitis. It is also brought about by the presence of cancerous or other tumors. The complete arrest of the current of blood through a vein rarely produces the serious results which may occur from a like obstruction of an artery. The aggregate diameter of the venous system is much greater than that of the arterial, and the venous walls are much thinner and more distensible. Hence an adequate collateral circulation is more readily established. In a healthy individual and in a healthy condition of the part simple occlusion of a vein produces only a moderate oedema of the tissues on the distal side of the obstruction. In unhealthy conditions, however, as already pointed out in discussing phlegmasia dolens, very serious results may follow.

Occlusion of either the superior or the inferior vena cava is of not very rare occurrence. It may be the result of pressure from a cancerous or other growth,[14] which is the most frequent cause, or in the case of the inferior cava it may be brought about by a thrombus gradually extending upward in one of the iliac veins until it reaches the bifurcation, when a thrombus in the other iliac is occasioned by the partial obstruction of its entrance into the cava. These united thrombi then extend upward into the cava, producing complete occlusion. This is an occasional event in phlegmasia dolens.

[Footnote 14: Watson describes a case arising from pressure from hydatids of the liver.]

Occlusion of the superior cava is less frequent than that of the ascending. It is nearly always the result of pressure from an intra-thoracic tumor, and its symptoms are more or less masked by those directly referable to the growth. There are, however, great dilatation of the veins and oedema of the tissues of the head and neck and of the upper part of the thorax. These symptoms in a case in which there are physical signs of a substernal growth would afford a strong presumption of obstruction of the cava.[15]

[Footnote 15: Stocks, _Med. Times and Gaz._, April 22, 1876; Williams, _Tr. Dublin Path. Soc'y_, July, 1878.]