The Causal Relation of Obstructed Car- 
diac Circulation to Lymph Stasis. 
BY 
SAMUEL C. BUSEY, M. 1)., 
0/ Washington, D. C. 
FROM 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES. 
Octohkr, 1885. Extracted from the 
American Journal of the Medical Sciences for October, 1885. 
THE CAUSAL RELATION OF OBSTRUCTED CARDIAC 
CIRCULATION TO LYMPH STASIS. 
By SAMUEL C. BUSEY, M.D., 
Of Washington, D. C. 
In my former contributions to the medical press,1 on the congenital 
and acquired forms of occlusion and dilatation of lymph channels, I col- 
lated a number of cases, previously published by different reporters, to 
illustrate the causes and special characteristics of these forms of disease. 
In a few of the cases it was evident that the existent lymphangiectasis 
was attributable to interruption of the blood vascular currents either 
through the heart or lungs. I referred incidentally to those reports, but 
the illustrative cases have not, as far as is known to me, been collected 
and arranged in a manner to distinctly exhibit the relation of cause and 
effect subsisting between obstructed cardiac circulation and lymphangiec- 
tasia. 
Before citing the cases relating to the direct proposition, it is necessary 
to refer to the predicate—that occlusion or stenosis of the thoracic duct, 
at or near its terminal extremity at the left subclavian vein, may, when 
the collateral circulation is not speedily and sufficiently established, pro- 
duce dilatation or rupture of some part of the lymph vascular apparatus. 
This can be shown both by the results of experimentation and by post- 
mortem reports. 
Morton* performed a number of experiments upon dogs by ligating the 
thoracic duct ; in some the “ receptaculum and in other the lacteals 
burst.” In every case there was extravasation of chyle. In Sir Astley 
Cooper’s3 experiments, when rupture occurred it took place at the recep- 
taculum ; and Dupuytren’s experiments upon horses were followed by 
nearly similar results. Cooper says it is not necessary to tie the duct. 
If the animal is fed with milk and the extremity of the duct is compressed 
1 New Orleans Med. and Surg. Jour.; and Congenital Occlusion and Dilatation of 
Lymph Channels. Win. Wood & Co., 1878, New York. 
2 Donald Monro, Essay on Dropsy and its Different Species, pp. 22, 23. 
* Medical Records and Researches, p. 100 et »eq. 2 
one-half hour afterwards, the receptaculum will rupture. Those and 
similar experiments prove that, under certain conditions involving an in- 
terruption or complete arrest of the current of the fluid through the tho- 
racic duct, the resultant distension and dilatation may prove sufficient to 
produce rupture, which may take place either in the receptaculum or in 
the lacteals. In those cases where rupture did not take place, the current 
of the fluid wras re-established through anastomosing branches. 
The clinical and post-mortem observations are even more conclusive. 
They connect directly the process of gradual occlusion of the duct by dis- 
ease with the concurrent development of a diffuse area of lymphangiec- 
tasis, which in some cases terminated in rupture and extravasation. 
Monro cites the case reported by Morton of “ hydrops ascites lactea” in 
which the rupture of the lacteals was occasioned by the compression of the 
thoracic duct near the subclavian vein by large indurated tumors. 
Morgagni’ refers to the cases of Valsalva and Santorino, in both of 
which there was considerable dilatation of the lacteal vessels produced by 
the pressure of an aneurismal tumor on the thoracic duct. In Valsalva’s 
case the aorta from the heart to the diaphragm was dilated, and “the lac- 
teal vessels presented the appearance of numerous white spots having a 
diversity of figure and magnitude.” 
In the body of a man who died after a large quantity of chylous liquor 
had been let out of his thorax, Bassius* discovered an orifice at or about 
the third dorsal vertebra from which the chylous material flowed as from 
a fountain. Below this orifice the thoracic duct w7as pervious. 
Cayley3 reports a case of obstructed thoracic duct and rupture of the 
receptaculum chyli. “ On post-mortem examination some yellow7 fluid 
was found in the peritoneal cavity, and the peritoneum in front of the 
spine was bulged forward by the effusion behind it of a large quantity of 
milk-looking fluid. The receptaculum was much dilated, and on its an- 
terior surface was a perforation two inches in length. The thoracic duct 
was immensely dilated throughout its course to its junction with the sub- 
clavian vein, where it suddenly became narrowed, and just at its mouth a 
fibrinous vegetation was attached to the lining membrane of the vein 
which completely occluded the opening of the duct. The narrowed part 
of the duct was blocked by a firm, yellow cylindrical coagulum.” 
Virchow4 refers to the case he observed in a new-born calf, where in 
consequence of thrombosis of the external jugular vein the mouth of the 
thoracic duct was occluded, and nearly all the internal organs were dilated 
to the utmost with ectatic lymph-vessels filled with a slightly sanguinolent 
fluid. The intestines especially were covered with broad bead-like canals, 
1 17 Epistle, De Sedibus et Causis Morborum, 1761, Lib. ii. p. 152. 
2 Observationum Decade Secundum, Observatio Septima. 
3 Trans. Path. Soc. Lond., vol. xvii. p. 163, 18 6. 
4 Virchow, Archiv, vol. vii. p. 130. 3 
arranged so closely together that the intervening tissue could scarcely be 
recognized. 
Ormerod1 reports a case of chylous ascites from which on several 
different occasions large quantities of a milky fluid were removed. This 
fluid Drs. Wilks and Marcet proved to be chyle, mixed, more or less, 
with common serous peritoneal effusion. On post-mortem examination 
“ the left subclavian vein and its afferent vessels were found plugged with 
a light-colored, ragged clot, evidently of long standing. It was soft in 
the centre, and at one point was firmly adherent to the walls of the sub- 
clavian vein. In the abdomen and chest were also found numerous 
nodular masses consisting of an imperfectly fibrous structure.” 
Many other cases might be introduced in which dilatation of the thoracic 
duct, to a greater or less extent, was the result of partial or complete 
occlusion near its outlet, caused by the pressure of aneurismal or other 
tumors, or by disease of the coats of the duct; but such cases have rarely 
been associated with lymphangiectasia, other than cylindrical dilatation 
of the duct and enlargement of the receptaculum. In most of such eases 
the stenotic condition of the duct was compensated by the development 
of anastomosing branches through which the chyle and lymph channel 
connection with the venous system was preserved. 
The preceding citations of the experimental and clinical data establish, 
inferentially if not conclusively, the preliminary proposition, that retar- 
dation or arrest of the current of the fluid in the thoracic duct at or near 
its outlet into the subclavian vein may produce dilatation, distension, and 
rupture of lymphatic vessels, and consequent effusion of chyle and lymph 
into the serous avities. The remoteness of the effects from the obstacle 
interrupting the current of the fluid may depend upon various concomitant 
conditions, especially upon the anatomical integrity and the tensibility of 
the vascular walls. When the impediment to the flow of chyle and lymph 
occurs at or near its outlet the area of stasis and ectasis would necessarily 
depend upon the duration and extent of such obstacle ; and, hence, when 
the area of ectasia is extensive the manifest inference is that the cause 
has been one of gradual development and protracted duration. In the 
case of Bassius, dilatation and rupture were caused by impermeability of 
the distal extremity of the duct ; in Morton’s case the rupture of the 
lacteals was occasioned by the pressure of a tumor upon the duct near 
the subclavian vein. In Ormerod’s case of chylous ascites the interruption 
to the flow of the chyle was caused by the “ plugging of the left sub- 
clavian vein and its affluent branches with a light-colored, ragged clot, 
evidently of long standing.” The resistance to the flow of the contents 
of the thoracic duct must have been derived exclusively from the inter- 
rupted venous blood current. The heart was normal and the duct was 
1 Trans. Path. Soc. bond., vol. xix. p. 199, 1868. 4 
unobstructed. In Cayley’s case of obstructed thoracic duct and rupture 
of the receptaculum, two factors were in operation, interrupted blood- 
current, occasioned by the fibrinous vegetations attached to the intima of 
the subclavian vein, and the partial obliteration of the lumen of the duct 
near its terminus. In Virchow’s case of the new-born calf, the condition 
existing partially exemplifies the obstructing forces operating in the cases of 
Ormerod and Cayley. The mouth of the duct was occluded by a thrombosis 
of the external jugular. In addition to the slowing of the venous blood- 
current in the jugular and in the subclavian, produced by the projecting 
part of the thrombus, the exit of the fluid from the duct was also impeded. 
The occlusion of the mouth of the duct was probably inconstant and 
incomplete during life, nevertheless the area of lymphangiectasis was 
extensive, involving nearly all the internal organs. 
The force exerted upon the contents of the thoracic duct by the'passing 
current of the blood in the subclavian vein is nothing more ,.than an 
illustration of (he hydraulic principle of Venturi ; that is, if tf stream of 
water is made to flow through a tube, into which another opens and com- 
municates at its distal end with a reservoir of water, a current will be 
established in the second tube and continue as long as the straam flows 
through the first tube, or any fluid remains in the reservoir of second. 
The anatomical junction of the thoracic duct with the venous system is 
peculiarly favorable to the maximum development of this principle, for 
the near affluence of the internal jugular, and the downward inclination 
of the duct to the subclavian, contribute to the enhancement of the effect 
upon the current of chyle. Out of this principle of Venturi must 
grow the converse, that any retardation of, or obstacle to, the current of 
blood in the subclavian vein, either from diminution of its lumen or from 
regurgitant heart affections, must slow the movement of the chyle in the 
duct and in its tributaries. 
The influence of partial obliteration or stenosis of the thoracic duct at 
or near its termination in the causation of dilatation or rupture of some 
part of the lymph vascular system cannot be doubted. The evidences of 
experimentation must be accepted as conclusive. The effects of stenosis 
produced by the gradual encroachment from disease of the duct or of 
surrounding and contiguous tissues and structures have been shown by 
the clinical and post-mortem citations. In this latter class of cases the 
ectasia is gradual in its development and more extensive in its field. In 
those cases where the lymphangiectasis was consequent upon the slowing 
or interruption of the venous blood-current in the left subclavian vein, the 
relation of cause and effect seems equally well established. It remains 
now to show that such diseases of the heart as slow, impede, or stagnate 
the venous blood-current in the left subclavian or innominate vein, may 
also produce lymph-stasis. Petters1 reports a case of lymphangiectasis in 
1 Vierteljahrschrift fur die Practische Heilkunde, vol. xiv. p. 141, 1861. 5 
which were found upon the visceral peritoneum “ numerous cysts from 
the size of peas to that of filberts, some colored bright, and containing 
serum. Upon the small intestines numerous lenticular protuberances, 
transparent, and filled with wine-yellow fluid. . . The glands of the 
right inguinal region were transformed into cysts of small walnut size, 
filled with wine-yellow fluid. From the inner wall of these cysts extended 
dilated lymph-vessels of crow-quill size, which connected the cysts with 
each other, so that a dilated vas efferens and afferens could be seen in 
each cyst. Upon puncture a yellowish fluid spouted from these cysts in a 
jet of several inches. The lymph-vessels and cysts formed a mass which 
it was difficult to unravel. The lymph-vessels in the vicinity and the 
thoracic duct were greatly dilated. 
“ The heart occupied the entire anterior thoracic cavity. The enor- 
mous enlargement of the heart included the entire right side of the organ, 
so that the left ventricle with the auricle formed only an appendix. The 
muscular tissue of the left ventricle, which would not contain a hen’s egg, 
was thin and flaccid. The left venous orifice, by the growing together of 
the apices of the bicuspid valves, was changed into a small crescentic 
opening, barely admitting the point of the little finger. The latter was 
callous and inclosing here and there a bony plate. Right ventricle largely 
dilated, with thinned walls. Columnae carneae of both ventricles very 
slender and tendinous. Right auricle as large as a child’s head, its walls 
here and there formed of a thin layer of pericardium. Apertures of 
coronary vein gaping finger wide. Aortic valve competent. Right 
venous orifice contracted.” 
This autopsy discloses a stenosis of the left venous orifice, and a 
moderate contraction of the right ventricular opening. Petters concluded 
that the stasis of lymph, followed by great dilatation of the lymph-vessels 
and glands, was caused by the organic disease of the heart. It cannot 
be doubted that the interruption of the current of blood by the narrowing 
of the orifices and dilatation of the right side of the heart retarded the 
movement of the column of fluid in the lymph-vessels. This influence, 
first demonstrating itself upon the movement of the contents of the 
thoracic duct, causing distension and dilatation of the trunkal vessels, 
was transmitted backward, or rather produced stasis of lymph in remote 
vessels. The lenticular eminences, filled with a transparent fluid, grouped 
together on the mucous surface of the small intestines, were, probably, 
ampullar dilatations of terminal lymph-spaces, and the bodies described 
as cysts on the peritoneum were of like histological nature. Concerning 
the nature of the gland implication there can be no doubt. The case 
exemplifies the three varieties of lymphatic telangiectasis made by Lebert, 
in its lenticular eminences, cyst-like bodies, and transformed glands. 
At the conclusion of this report, Petters refers to the case of an old 
female “ suffering with stenosis of the left venous orifices of the heart,” 6 
upon whose right arm he found several semi-solid tumors, situated imme- 
diately under a fatless cutis, which he regarded as dilated lymph-glands. 
T. Granger Stewart1 reports a case of “ dilatation of the lacteals,” 
associated with an hypertrophied and fatty heart, with diseased aortic 
valves and dilated auriculo-ventricular orifices. In this case the stasis of 
chyle occurred in the intestinal villi, producing dilatation of the central 
lacteal vessels of the villi, and arresting the further absorption of the 
chyle. To the incompetency of the aortic and auriculo-ventricular valves 
was added fatty degeneration of the heart. Here enfeebled action of the 
organ and regurgitation were co-operating factors in slowing the move- 
ment of the chyle. 
In Rokitansky’s* case of chylous ascites, there was dilatation of the 
heart, “ with thickening and shortening of the mitral valves.” The 
cardiac affection not only interrupted the flow of chyle in the thoracic 
duct, but caused a stasis of cbyle in the lacteals and mesenteric glands; 
of lymph in the subpleural lymphatics ; and an effusion of a milk-like 
fluid into the pleural and peritoneal cavities. 
In Hughes’s3 case of abdominal effusion of a chylous fluid, supposed to 
have resulted from the pressure of mesenteric tumors, “ the heart was 
thin, pale, weak, and flabby,” and numerous “ lacteals—large, tortuous, 
varicose, and distended, some with milk and others with a clear fluid”— 
were observed in all parts of the mesentery. The case was complicated 
with abdominal tumors, “ consisting of several agglomerated mesenteric 
glands,” believed to have been cancerous ; but from a number of the 
enlarged glands “a cream-like fluid exuded,” and hence it is not improb- 
able that the morbid condition of the glands and lacteals was due to 
stasis of chyle and lymph, caused by the disease of the heart. 
In this connection the case of mitral and tricuspid insufficiency, with 
granular liver, ascites, anasarca, and thrombosis, reported by Oppolzer,4 
is interesting. The inferior and superior venae cavoe were occupied at 
their outlets with pale, yellow, soft coagula. From the superior, the clot 
extended with a jagged end into the auricle, and continued into the right 
subclavian, as well as into the right internal jugular as far as he foramen 
lacerum. The left innominate and the terminus of the left subc avian 
were obliterated. The thoracic duct was plugged at its termination by a 
pale-red, fibrous coagulum. Its walls were thickened, and its lumen, 
from the receptaculum to the occluding thrombus, was greatly dilated. 
The regurgitation of blood into the thoracic duct was caused by the 
obstruction to its entrance into the heart. 
There is another class of cases of lymphangiectasis associated with 
1 Edinburgh Med. Journ., vol. ix. p. 448, 1863. 
2 Path. Anat., Bd. ii. s. 388; also Ziemsscn’s Cylco., vol. vi. p. 531. 
3 Guy’6 Hospital Reports, vol. vi. p. 297, 1841. 
4 Allgemeine Wiener Medicinisch. Zeitung, p. 149, 1861. 7 
symptoms of cardiac disease, but the direct connection of the lymph- 
stasis with an affection of the heart was not proven by a post-mortem 
examination. The following, reported by Cholmeley,1 is an example of 
this class :— 
This was a case of great enlargement of the right lower extremity, with 
an intermitting How of a milky fluid from behind the ankle. The lymph- 
atic engorgement began at the age of three years, and continuously in- 
creased during the succeeding six years, when it had involved the whole 
leg up to the groin. “ The pulse was normal as to frequency and rhythm, 
and of fair volume and force; but all over the heart there was a soft, 
blowing, systolic murmur, which was loudest at the junction of the second 
left costal cartilage with the sternum.” 
The child was “short, stout, and generally healthy-looking, with a good 
bright-red color in the cheeks and lips, but was easily affected by cold, 
and then complained of a want of breath and a feeling of tightness in the 
chest ; and at such times the complexion assumed a markedly livid tint; 
respiration became somewhat labored and noisy, the extremities cold, and 
the nails dark-blue.” 
The clinical history does not, in the absence of a post-mortem examina- 
tion, positively establish any connection between the lymph-stasis which 
first appeared near the ankle, and the disturbed cardiac circulation ; but 
such an hypothesis cannot be excluded. The remoteness and limitation 
of the area of lymphatic engorgement cannot be accepted as negative con- 
ditions disproving it. Retardation of the venous current near the heart, 
and consequent repletion and distension of the thoracic duct and recep- 
taculum, would assuredly offer resistance to the movement of the lymph 
in affluent vessels. The assumption that the engorgement could have been 
due to devastated inguinal glands, or occluded lymph-vessels in the ab- 
dominal cavity, is discredited by the appearance of the intumescence first 
about the ankle, and its gradual and continuous extension upward; 
whereas, if either of those conditions had existed, the lymph-stasis would 
have begun at the locality of such obstruction and extended in the reverse 
direction. Lymphatic engorgement does not follow the law of symmetry, 
and its limitation to one lower extremity may be ascribed to any one or 
more of the variety of circumstances, such as the varying tensibility, loca- 
tion, distribution, or the anastomosing connections of the lymph vascular 
system of the lower extremities. 
The explanation of this relation of cause and effect between cardiac dis- 
turbances and lymph-stasis must, in a general way, be sought in the vary- 
ing conditions of blood-pressure. A potential, if not the predominant 
factor concerned in the locomotion of the lymph is the difference between 
the arterial and venous blood-pressure ; the greater this difference the 
more rapid the movement of the lymph. In a normal condition of the 
1 Trane. Clin. Soc. Lend., vol. ii. p. 116, 1869. 8 
heart, venous orifices, and great afferent and efferent vessels, the blood- 
pressure in the innominate veins and their affluent branches, during dias- 
tole, is at its minimum—represented in comparison with the pressure at 
the aortic summit, as nil; so that, whatever may be the potentiality of 
the difference between the arterial and venous blood-pressure as a force 
in promoting the locomotion of the chyle and lymph, it is at its maximum 
when the venous blood-current is flowing most easily and rapidly into the 
right auricle. Therefore, it must follow that any disease of the heart, or 
any condition of its affluent veins which retards, impedes, or obstructs the 
free and rapid flow of the venous blood into the right auricle and through 
the tricuspid orifice, will slacken, interrupt, and obstruct the movement 
of the chyle and lymph in the thoracic duct and its tributary vessels. 
This conclusion is not derived merely through inductive reasoning, but is 
illustrated and verified by clinical observation and post-mortem appear- 
ances. 
The chief function (Kiiss) of the right auricle is to facilitate the flow of 
the venous blood by allowing itself to be filled, thereby lessening the blood- 
pressure in the affluent veins. During its contraction reflux is prevented 
by the fulness of the veins and by the elasticity of the ventricular walls. 
If these functions are disturbed and changed by disease of the walls of 
these cavities, reflux may take place, with increased blood-pressure in the 
affluent veins, lessening of difference between the arterial and venous 
blood-pressure, and consequent slowing of the lymphatic current. 
If, as claimed by some, the circulation of the lymph is due mainly to 
transudation and endosmosis taking place at the periphery, increased 
pressure in the venous system would be equally, if not more effective in 
the causation of disturbances of the intermediate plasmatic circulation. 
The inquiry is not, however, into the causes of lymph-stasis and ectasis, 
but relates to the influence of cardiac disease in the production of these 
affections of the lymphatic system. 
In conclusion I append the following quotations :— 
“ Obstructive engorgement of the great veins extends also to the thoracic (luct. 
When the subclavian vein is tilled to distension, the flow of chyle and lymph 
must encounter a resistance equal to that opposed to the current of any other 
vessel which empties into the subclavian. Nay, if lymph be the source of the 
fibrin in the blood, we see, upon simple physical grounds, why the blood of em- 
physematous patients is poor in fibrin, why the venous crasis presents hyperinosis 
and increase of fibrin. Restricted afflux of chyle must, moreover, prejudice 
nutrition both of the blood and of the entire organism. It is one of several causes 
which contribute to the general emaciation and to the premature marasmus of 
emphysematous persons; perhaps, too, it may account for the lack of albumen in 
the serum of the blood, which produces a tendency to the establishment of drop- 
sical symptoms.”1 
“ The inadequate emptying of the thoracic duct into the left subclavian vein, 
over-distended with blood, will, in cases of pulmonary emphysema, lead to im- 
poverishment of the blood in so far as concerns such elements as are derived from 
the lymph, the colorless blood-corpuscles, fibrin, and albumen.”* 
1 Nierneyer, Text-Book of Practical Mediciue, vol. i. p. 120. 
2 Hertz, Ziemsseu’s Cyclop., vol. v. p. 382. TH E MEDICAL NEWS. 
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