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.
1 Des Plaies et de la Ligature des Veinse, Thèse, Paris, 1872.
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.
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
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.
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, 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 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
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.
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.
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.
8 Pathol. and Treat. of Phleg. Dolens, London, 1862; Med. Times and Gazette, Aug. 22, 1866.
9 Med. Times and Gazette, Jan. 14 and 18, 1859.
10 The Puerperal Diseases, New York, 1876.
Phlegmasia dolens occurs chiefly in the puerperal state, and affects chiefly 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
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. 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
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.
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 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.
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.
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.
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
15 Stocks, Med. Times and Gaz., April 22, 1876; Williams, Tr. Dublin Path. Soc'y, July, 1878.
The glandulæ concatenatæ of the neck are apt to be enlarged from the chronic engorgement. Watson mentions a case in which this added so much to the volume of the neck as to give a superficial resemblance to goitre.
Occlusion of the inferior vena cava produces, if life is continued, an immense dilatation of the veins of the abdomen and of the thighs. By compressing the abdominal veins it can be seen that the blood-current is reversed, flowing upward through vessels anastomosing with the intercostal and internal mammary veins. Internally, the circulation is carried on chiefly by the azygos, which may become as large as the normal cava.
There is usually, but not always,16 an extreme degree of ascites, together with anasarca of the lower half of the body. After a time, however, as the tributary circulation becomes established, the effusion will be reabsorbed.
16 Le Progrès Médical, May 26, 1877; Med. Record, July 28, 1877.
If the obstruction involves the portal vein, the ascites will be still more marked. In this case there is also enlargement of the spleen. When the cava is occluded above the point at which it receives the renal veins, congestion of the kidneys results, which in time produces interstitial change. Yet even here the establishment of the collateral circulation may be sufficiently prompt to avert the danger.
Anomalies of the cava are occasionally observed. Osler has reported a case in which the inferior cava was represented only by a fibrous cord. The condition was probably congenital.17 Greenfield mentions a case in which the descending cava was absent, both brachio-cephalic trunks passing into the heart by the coronary sinus.18
17 Journal of Anatomy and Physiology, April, 1879.
18 Med. Times and Gazette, April 22, 1876.
If the cause of the occlusion of either cava be not such as of itself to destroy life, the patient may get on with some degree of comfort for many years. The establishment of the collateral circulation sometimes keeps pace with the increasing obstruction, so that little or no ascites or oedema occurs.19
19 Turpin, "Obliteration Inf. Vena Cava," N. O. Med. and Surg. Journal, 1881, p. 575.
The TREATMENT of obstruction of either of the venæ cavæ can, as a rule, be only palliative. In the great majority of cases the cause is entirely beyond our reach. All violent muscular exertion, making an excessive demand upon the circulation, should be avoided. While the blood should not be impoverished, as that would favor dropsical effusions, the patient, on the other hand, should not be allowed to become plethoric through the influence of his enforced sedentary habits. The diet should therefore be light and digestible, and over-feeding should be carefully avoided. The occasional use of saline purgatives may be required. Dropsical accumulations may call for the administration of diuretics or drastic cathartics, and perhaps for tapping.
Occlusion of the vena portæ, by obstructing the return of the blood from the intestines, gives rise to rapid and abundant effusion into the abdominal cavity. As the gastric vein cannot empty itself, there is congestion of the stomach, often ending in hemorrhage, the blood being both vomited and passed by stool. The spleen also is enlarged by passive engorgement, its vein depending upon the portal for an outlet. This assemblage of symptoms renders the diagnosis almost positive.20 There is no enlargement of the liver unless the hepatic vein is also involved.
20 An interesting case is reported by A. A. Smith in the N.Y. Med. Journal, January, 1880.
Paget maintains that the occlusion of the principal vein of a limb may result in an increased growth of some of the tissues, especially of the muscles.
Degenerations.
Fatty degeneration is rarely observed in the veins, but it occasionally occurs in those which have long been subjected to excessive strain, which by compressing the nutrient vessels affects the nutrition of the walls.
Calcification is less rare. It results in the formation of plates or rings which closely resemble bone in their structure. Such plates may not unfrequently be felt in old superficial varicose veins. Sometimes these formations project as spines into the lumen of the vessel, and, coagula forming about them, a thrombus is the result.21
21 See preceding reference.
Cancer of the veins is rare as a primary affection, but it is not uncommon when the vessel traverses a cancerous mass. The morbid process readily penetrates the thin wall of the vessel, and cancerous nodules form on the inside and become the starting-point of thrombi which are soon permeated and supplanted by the heterologous growth. This is sometimes moulded to the shape of the vein, and fills it for some distance in the form of a cylindrical plug. Fragments may be swept away in the blood-current and give rise to secondary cancer at the point of arrest in the liver or lungs. Virchow has described a case of primary sarcoma of the inferior cava.
The existence of syphilitic lesions in the veins has not been satisfactorily demonstrated. It is positively denied by some authorities, while certain appearances found in the veins, especially of new-born children, are attributed by other writers to syphilitic inheritance.
Phlebolithes.
Vein-stones are roundish, oval, or cylindrical bodies found in the veins or in pouches connected with the veins, or sometimes in the connective tissue adjacent to a vein. Their size varies from that of a hempseed to that of a nutmeg. Externally they are white, but when divided they are found of a yellowish color at the centre. There is generally a central cavity, around which are disposed concentric laminæ such as are observed in vesical calculi. Chemically, these bodies are composed of an animal substance in which are deposited phosphate and carbonate of lime, and sometimes magnesia. The inner part is hard and brittle, the outer softer and more earthy.
Usually, phlebolithes are found loose in the vein, but if large they may be firmly impacted in the vessel, causing complete obstruction. Sometimes the outer portion is of a gelatinous texture, from which a delicate mesh extends to the wall of the vein and becomes incorporated with it.
Frequently these concretions occupy sacs or diverticula connected with the vein. Occasionally these sacs become detached from the vessel and are absorbed and removed, and the stone, then entirely outside of the vein, becomes enveloped in a fibrous cyst formed from the surrounding connective tissue.
Some doubt exists as to the manner in which these concretions are formed, but the probability is that a small clot first forms in the vessel, and that around this, as a nucleus, successive layers are deposited from the plasma of the blood. These layers then undergo chalky transformation by the deposit within them of salts of lime and magnesia. These formations seem to be conditioned by a slow current in a dilated vein. Hence they are most frequently found in the enlarged pelvic veins of old people, and especially about the neck of the bladder in those suffering from prostatic enlargement. They are also found in the varicose veins of the extremities.
Except in superficial situations they are usually not recognized during life. They seldom produce discomfort, and therefore rarely call for treatment. When accessible they may be excised if requisite, the vein being secured above and below if not already permanently occluded.22
22 Rokitansky, Path. Anat., Philadelphia, 1858.
THE CAISSON DISEASE.1
BY ANDREW H. SMITH, M.D.
1 This article is mostly drawn from a report by the writer on The Effects of High Atmospheric Pressure, including the Caisson Disease, published in 1873 by the New York and Brooklyn Bridge Company.
Persons exposed for a considerable time to a greatly increased atmospheric pressure are liable, after the pressure is removed, to certain morbid effects which comprise what is known as the caisson disease. It is observed principally in those employed in submarine operations by the aid of compressed air, and who labor for hours together in what is termed by engineers a caisson. The pressure varies with the depth at which the work is carried on, and reaches sometimes fifty or more pounds to the square inch. The disease rarely if ever occurs when the pressure is less than fifteen pounds, and its severity is, other things being equal, in direct ratio to the increase in the density of the atmosphere.
SYMPTOMS.—These are, in the order of their frequency, intense neuralgic pain in one or more of the extremities, and sometimes in the trunk; epigastric pain; nausea and vomiting; more or less complete paralysis, which may be local or general; headache; vertigo; and coma.
The pain, which is often very severe, is usually paroxysmal, exacerbations and remissions occurring at short intervals. It may come on suddenly in its full severity, or it may be slight at first and rapidly increase until it becomes absolutely intolerable, "as if the flesh were being torn from the bones." The pain begins most frequently in the knees, extending rapidly to the legs and thighs, but the upper extremities may be first attacked. Sometimes the most severe pain is felt in the spine, and especially in the lumbar region. There is usually some tenderness with the pain, and a stiffness of the muscles of the affected limbs.
Epigastric pain occurs in a considerable proportion of the cases. It is often very severe, and if not relieved by treatment is liable to be followed by nausea and vomiting. The vomiting is usually limited to the ejection of the contents of the stomach, but it may persist, sometimes even after the pain has ceased. Vomiting accompanied by giddiness may occur without epigastric pain, and is then probably of cerebral origin. Paralysis, to a greater or less degree, occurs with considerable frequency, the percentage of cases increasing in proportion to the pressure of the atmosphere to which the patients have been exposed and the duration of the exposure. It affects most frequently the lower half of the body, but it may include the trunk or one or both arms. In rare cases an arm alone is affected.
The paralysis is of sensation as well as motion. It comes on soon after the invasion of the pains, but affords no relief from them. Thus, while pinching or pricking occasions no pain, the part may still be the seat of exquisite suffering. Paralysis may, however, occur in cases in which the pain is very slight or entirely absent. The paralysis varies in degree from a transient weakness of the limbs and slightly impaired sensation to complete loss of motion and sensation in the affected part. Even the minor degrees generally affect the bladder.
Symptoms of a transient character are often observed depending upon changes in the brain. They consist of headache, dizziness, double vision, incoherence of speech, and sometimes syncope. They usually pass off in a few hours. In fatal cases, however, coma is the usual forerunner of death.
The duration of the caisson disease is from three or four hours to six or eight days. When paralysis occurs it may continue for weeks, or it may pass off within twelve hours. The cases marked only by neuralgic pains do not generally last more than six to twelve hours, though some continue five or six days. Death occurs only in cases which are severe from the first and show symptoms of cerebral or spinal effusion.
MORBID ANATOMY.—The constant lesion in fatal cases of caisson disease is congestion of the brain or spinal cord. This congestion may be pretty evenly distributed or it may vary in intensity in different localities. This is especially true as regards the cord. It affects both the meninges and the substance of the brain or cord. In most cases there is more or less of serous effusion into the arachnoid. The tissues of the scalp and those surrounding the spinal column are sometimes engorged.
When sufficient time elapses before death the brain may be softened in spots. This is probably due to the occlusion of vessels by coagula formed during the primary congestion.
Congestions also occur in other localities, and especially in the solid abdominal viscera. The liver and spleen have been found engorged in nearly every case. Jaminet has found clots of blood in the kidneys.2 The mucous membrane of the stomach, intestines, and bladder is often injected and marked with patches of ecchymosis. The lungs in cases of true caisson disease, though occasionally found in a state resembling red hepatization, seldom present any other change than simple hypostatic congestion.
2 Physical Effects of Compressed Air, p. 20.
PATHOLOGY.—It is probable that the pathology of this disease is not entirely uniform in all cases. Doubtless the chief element in it is the congestions already described, and especially of the brain and spinal cord. The mechanism, therefore, of these congestions becomes a subject of paramount importance.
It was suggested by François3 that the morbid phenomena might be due to the liberation in the vessels of air which had been absorbed by the blood while under pressure, but which was set free again when the pressure was removed. This theory has been reasserted by Paul Bert,4 with this difference: that he claims that bubbles of nitrogen instead of air are the cause of the interruption of the circulation. These bubbles he has discovered after death in the vessels of the brain and cord. But he states that when the pressure does not exceed five atmospheres three minutes allowed for the restoration of the normal pressure will be found to prevent the formation of these globules of nitrogen. Now, we find the caisson disease occurring when the pressure does not exceed two atmospheres and when six to eight minutes are allowed for locking out.5 It would seem that under these conditions the gas should escape through the lungs as rapidly as it is disengaged from the blood. Moreover, we find that the attack often comes on several minutes or even hours after leaving the caisson. During this time any free nitrogen in the blood should be constantly becoming less by diffusion through the pulmonary membrane, and if enough were not present at first to cause obstruction, such an effect could scarcely take place at a later period.6
3 Annales d'Hygien publique et de Méd. legale, t. xiv., 1860.
4 Comptes Rendus, August, 1872, and February and March, 1873.
5 I.e. passing from the caisson into the open air through the lock, or antechamber, where the pressure is gradually reduced.
6 In a private letter to the writer, T. Lauder Brunton suggests that a bubble of air might pass from a larger vessel, which it had only partially obstructed, into a smaller branch, which would be entirely occluded by it, or that additional nitrogen might be disengaged when the pressure was lessened by relaxation of vascular tension.
It is also very difficult to reconcile with Bert's theory the fact of the comparative immunity from danger which results from repeated exposures to the effects of compressed air. If the action were that of purely physical causes, habit could make no difference. The obstruction of the vessels, as described by Bert, is a condition of which the system could never become tolerant by frequency of repetition.
In the writer's view, the explanation is to be found in the changed conditions of the circulation, which result first from the increased pressure upon the surface, and then from the sudden removal of the pressure. While the subject is in the caisson the blood is driven from the peripheral vessels toward the interior of the body, where the pressure is less than at the surface.7 It is also forced from the more compressible tissues into the solid and resisting organs, such as the liver and kidneys; and lastly, it flows toward bony cavities, for the reason that their walls resist the effect of direct pressure, and equilibrium of pressure can be restored within them only by an afflux of blood. Thus the distribution of the blood is everywhere changed, and the size of the vessels is no longer determined by the muscular action of their walls, but by the amount of blood forced into them, the vital action which should regulate the circulation being entirely overpowered and set at naught by an overwhelming physical force operating from without. The vessels become merely passive tubes, distended in some places where they are protected from pressure, and compressed in others where the tissues about them are compressible. By this transfer of blood from one part to another the equilibrium of pressure is restored and the circulation goes on, though without any regard to the physiological demands of the different organs. There is no stasis anywhere so long as pressure and counter-pressure are equal, thus allowing fair play for the action of the heart.
7 This is shown by the marked pallor of the skin and the shrunken and wrinkled appearance of the hands.
If, now, the external pressure is suddenly removed, what will be the result? Vessels which have been compressed and almost emptied of blood will now offer new channels through which the blood can rush, and vessels overcrowded with blood, with their walls paralyzed by over-distension, will have the current within them slowed almost or quite to the point of stopping. The vessels of the brain and spinal cord, being within bony walls, where the direct pressure of the condensed air could not affect them, will be found the most distended and the most helpless to relieve themselves. They will get little aid from the vis a tergo of the circulation, for the blood will find easier courses by other ways, vascular tension being almost nil and the vaso-motor system out of use.
The longer the sojourn in the caisson has been, the more entirely passive the vessels will have become, and the longer will be the time they will require to resume their normal condition. At some points the circulation will be greatly slowed or entirely interrupted, and nerve-elements lying beyond and deprived of their blood-supply will express their want by pain or paralysis. Areas of stasis once formed will be likely to extend, and may thus affect nerve-elements which at first escaped. This would explain those cases in which the attack is deferred until some time after leaving the caisson.
It is readily conceivable that in persons beginning work when the pressure is slight and continuing day by day, as the pressure slowly increases the vessels should acquire the power of adaptation to the variations in the amount of their contents, since this is only an extension of the physiological principle which we see exemplified in all organs having an intermittent function.
The influence of the trophic system of nerves also, as the connecting link between central nerve-lesions and peripheral vascular disturbances, must not be forgotten in this connection. Suspension of function in trophic cells, either in the cerebral cortex or in the anterior horns of the cord, could easily be brought about by the action of the mechanical causes already described, and would result in areas of vaso-motor paralysis and consequent congestion at the termination of the corresponding nerve-fibres. The proneness of the large joints, and especially the knees, to be attacked is suggestive, in view of the like circumstance in chronic degeneration of the cord.
CAUSES.—The one essential cause without which the disease can never be developed is transition to the normal atmospheric pressure after a prolonged sojourn in a highly-condensed atmosphere. Hence we have to consider two elements, pressure and time, the danger in these cases being as the degree of pressure to which the person has been exposed multiplied by the duration of the exposure.
But inasmuch as a prolonged sojourn in the caisson does not in every case produce the disease (many of the men employed escaping it entirely), it follows that there must be concurrent causes which determine its development.
The first of these is a special predisposition. This is occasionally strongly marked, some persons being affected by a short exposure to a low pressure from which there would generally be experienced no inconvenience whatever.
Perhaps the most frequent exciting cause of the caisson disease is too rapid locking out. Indeed, it is altogether probable that if sufficient time were allowed for passing through the lock the disease would never occur. But what is sufficient time for one is too short for another; and all that can be done is to fix upon a duration for the process which shall be proportioned to the pressure, and as great as is consistent with the circumstances, and then to see that the rule is rigidly observed. At least five minutes should always be allowed for each additional atmosphere of pressure.
Newness to the Work.—Unquestionably, the liability to the caisson disease is greatest in those exposed for the first time to the influence of the compressed air. New hands are very apt indeed to suffer more or less during the first week. Those least affected are such as begin work when the pressure is comparatively slight, and continue without intermission as the pressure increases. It seems that the system after a time becomes adapted to the changed conditions, and is protected in a measure from their effects. Nevertheless, some serious cases occur among old hands, especially when for any reason their stay in the caisson is prolonged beyond the usual time, thus showing that their immunity is merely relative. A sudden increase of pressure also, even though very slight, is certain to develop new cases, men thoroughly inured to the work often being affected under such circumstances.
Fulness of Habit.—During the progress of the work on the East River Bridge in 1872 the writer, who had medical charge of the men, observed that among those taken sick there was a very marked preponderance of men of heavy build and with a tendency to corpulency. Of 39 men of this build, only 3 escaped illness, while of 53 lank and spare men 25 escaped. Of the 39 stout men, 8 were more or less paralyzed; of the 53 slender men, only 2 were paralyzed. The deaths, 3 in number, were all of heavy men.
These figures show unmistakably that a tendency to fulness of habit renders work in a compressed atmosphere much more hazardous. Persons of this build have more fluids in the body, the distribution of which is changed by the pressure in the manner before stated, and it is therefore not surprising that the effect upon them should be greater than upon lean and sinewy persons, whose bodies contain a minimum of fluid.
Severe Exertion immediately after Leaving the Caisson.—As at the moment of going out of the compressed air the system undergoes a violent reaction, it is manifestly unfitted to bear in addition a severe tax upon the muscular strength. Hence the ascent of a long flight of stairs immediately after leaving the air-lock is as wrong in theory as it has proved bad in practice. Triger, whose apparatus at Chalonnes was so arranged that the ascent of the ladder took place in the compressed air, the lock being placed at the top instead of the bottom of the shaft, found that the men ascended a distance of seventy feet without becoming in the least out of breath—making the ascent, in fact, more easily than if it had been in the open air.8
8 Comptes Rendus, t. xiii., 1841.
The Abuse of Alcohol.—Several writers have remarked that habitual drinkers are more likely to be affected than those who used spirits moderately or not at all. It is stated by the director of the work at Douchy9 that the attacks from which the men suffered were "almost always coincident with some excess committed in the interval of the shifts." It is easy to perceive that, as the disease is characterized by cerebral congestion, the abuse of alcohol, which has a tendency to produce the same result, would act as a predisposing cause.
9 Annales d'Hyg. pub. et de Méd. legale, 1854.
Entering the Caisson Fasting.—Jaminet insists very strongly upon the influence of this cause, and cites instances to prove his position. Several cases corroborative of his views occurred under the observation of the writer. One of the rules for the men working in the New York caisson prohibited entering the compressed air without having taken food, and in addition to this each new hand was especially cautioned as to the danger of disregarding this precaution, and the foremen were directed to use every effort to secure its observance. Yet, notwithstanding all this, a number of very severe attacks were found to be coincident with, if not dependent upon, violations of this rule. In these cases epigastric pain and retching were prominent symptoms.
TREATMENT.—The treatment of this disease will depend upon the severity of the case and the presence or absence of gastric symptoms or of paralysis. If we have to deal with the neuralgic pains only, the chief reliance must be upon anodynes administered with a liberal hand. Fortunately, the pain, though very severe while it lasts, is in most cases of short duration, the attack passing off usually in a few hours. It is therefore quite practicable to keep the patient under the influence of morphine during the whole time, and thus enable him to escape entirely all extreme suffering. But large doses will be required, the intense pain inducing a remarkable tolerance of the drug. Half a grain may be given at the outset, and a quarter of a grain every half hour afterward until relief is obtained. When employed hypodermically somewhat smaller doses may be used.
In some instances the very best results are obtained from hypodermic injections of atropine at the seat of pain, but in other cases they fail to procure relief, and, upon the whole, atropine is inferior to morphine.
Jaminet, regarding the affection as wholly the result of exhaustion, relies entirely upon stimulants and concentrated nourishment, ignoring the aid of anodynes altogether. It is difficult to see the reason for this, even admitting to the fullest extent his theory of the disease, for nothing can be more exhausting than the intolerable pain which characterizes this affection, and nothing could act more promptly as a restorative than an efficient anodyne.
Starting from the theory already given as to the mode in which the disease is produced, the writer was led to the idea that benefit would be derived from the use of an agent that would induce contraction of the capillaries, and thus correct the want of tone which was considered to lie at the foundation of the difficulty. For this purpose ergot was employed, with the belief that it would be useful, first, by contracting the vessels of the brain and spinal cord and relieving their congested state; and, secondly, by restoring tone to the superficial vessels, and thus imparting vigor to the circulation.
An extended trial warrants him in saying that the results justified the theory. In his hands, though not always successful, ergot was certainly very useful in a considerable number of cases. He has seen very severe pain completely relieved within half an hour after the administration of a drachm of the fluid extract. In other instances unsteadiness of the limbs, which seemed about to usher in paralysis, yielded promptly to one or two doses. A teaspoonful of the fluid extract may be given, and the dose repeated in half or three-quarters of an hour, unless the pain is relieved.
Frictions, with or without stimulating liniments, are very generally resorted to, and seem sometimes to give momentary relief, but it appears to be rather by occupying the attention of the patient than by any action occasioned in the part. In some instances, when the pain is confined to a particular locality, having the part immersed in hot water will afford temporary relief. But the use of the general hot bath is not advised, as it is unsafe to increase the already existing relaxation of the vessels. In several of Jaminet's cases paralysis came on while in the hot bath. In two of the writer's cases cold was applied to the spine, with apparent benefit in each.
Epigastric pain is almost always relieved at once by the use of an alcoholic stimulant with ginger, as employed by Jaminet.
Vomiting is best treated with sinapisms to the epigastrium and swallowing small bits of ice.
When paralysis occurs it is to be treated on general principles. Cups or leeches, with douches and frictions to the spine, may be useful; and, if the case be protracted, the use of strychnine may be called for. Electricity may be of service in preserving the nutrition of the muscles. The bladder will almost certainly be involved, requiring the constant use of the catheter.
The cerebral symptoms which occasionally occur are, with the exception of coma, so transient in their nature as to call for no special treatment. Coma, when it takes place, is to be managed according to the circumstances of the case, as when proceeding from other causes. If accompanied by a full, strong pulse, venesection may be expedient.
There remains to be considered a plan of treatment originally suggested by Pol, and carried out to some extent by Foley—viz. returning the patient at once into the compressed air. Foley says, as the result of his experience, "A true specific is returning to the caisson, through which means all such accidents (pains, vertigo, etc.) speedily disappear. It is to be resorted to unhesitatingly in all threatening cases, and the pressure should be admitted rapidly." But the means of access to the caisson are usually such that it would be difficult to remove a patient into it, even if he could be comfortably cared for while there or if his presence would not interfere with the work. It would therefore be desirable to have facilities for employing compressed air at some point above ground which would be easily accessible.
Of course the secondary effects which arise in protracted cases would not be capable of direct relief by simply reproducing the physical conditions existing in the caisson. The most that might be hoped for in such cases would be that the pressure might result in giving a new impulse to the circulation in the congested part, and thus favor resolution.
Reasoning from his view of the pathology of the disease, Bert has proposed the inhalation of oxygen in order to displace the free nitrogen from the blood by diffusion. Experiments upon animals demonstrated that the sounds produced in the heart by the presence of free nitrogen speedily disappeared when the animal was made to inhale oxygen, the nitrogen diffusing into this gas much more readily than into common air. But, though immediate death was averted by this expedient, paralysis nevertheless occurred, and the post-mortem examination showed the presence of bubbles of nitrogen in the vessels of the cord.