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of the red amounting to one-eighth of the latter. Towards the end of this exacerbation pain and swelling also manifested themselves in the right axilla. Then, again, abatement of all symptoms ensued during four weeks, with exception of the swellings and a moderate degree of paleness. Sixteen weeks after the beginning of the illness-namely, in April, 1852, there was cough, and fresh pain in both axillary regions. In May, swelling of the lymphatic glands of the neck, quickly increasing, without much pain; paleness; loss of strength. In June, swelling also of inguinal glands, of the glands of the arm and legs; diarrhoea, alternating with constipation; adema of feet and face; glandular tumours of both axillæ and neck enormous; no perceptible swelling of spleen; layer of white globules, one-fourth of red. Second week of July: Great dyspnoea; extremities cold; radial pulse imperceptible; heart's impulse very weak; 13th, muttering delirium; coma. Death on 14th of July-i.e., less than eight months from the commencement of the disease. Post-mortem twenty hours after death.All the lymphatic glands of the body enormously enlarged, pale, moderately firm, exhibiting under the microscope the nuclear and cellular elements in an unusually developed degree; blood very pale; right heart filled almost entirely with a white coagulum, containing only few red elements; pulmonary arteries, up to their smaller ramification, filled with pale yellow coagula, some appearing drier and more firmly adhering to the walls than others. Spleen, eight ounces, tissue tense, rather pale; liver, four pounds and six ounces, very pale; all other organs normal, but highly anæmic; only the vessels of pia mater and the sinus of the head filled with pale blood and yellowish coagulum. The inflammatory character of the swellings was so great in this instance, that we considered it as a case of lymphatic adenitis; the alteration of the blood was so distinctly secondary that we hesitated in using the name leukæmia, as applying only to the secondary, not to the primary, affection. Regarding the course of leukæmia, Virchow says: "Little as we know at present of the origin of the disease of the organs, we may accurately survey the course and termination of the disease. As yet no well-proved case of cure is known." We may agree with this, as far as the developed cases of leukæmia are concerned, but further experience must show whether we may not be able to arrest the disease, while confined to the glandular or splenic affection, before the alteration of the blood has made much progress.

In another new article, On Colourless Blood-Globules, the author commences by considering three possibilities respecting their origin -1. Their formation in the blood itself; 2. Their introduction into the blood through the lymph and chyle; 3. Their being detached from the epithelium of the walls of the vessels. The first of these sources is limited to the division of the pre-existing cells; the third is regarded as unproved; but the lymph and chyle are conceived as conveying to the blood as well the developed, as also the undeveloped, globules, derived from the lymphatic glands, the spleen, and the connecting tissue. We cannot conclude our notice of this article in a

better manner than by giving Virchow's own words regarding the nature of these mysterious bodies:

"I therefore must still maintain the view which I have repeatedly brought forward, that the colourless blood-globules which we find circulating in the blood are simple cells, without a specific character, whose transformation into red globules cannot take place; that they therefore form a relatively superfluous constituent of the blood-a kind of excess, or waste. The transformation of lymph-globules into red blood-globules takes place much sooner, and it appears that if a certain cell, when passing into the blood, has transgressed that stage of development, it is unfit to undergo its specific coloured metamorphosis. It then circulates for some time, and perishes finally by retrogressive metamorphosis. Thus it may be easily conceived that the larger the number of colourless globules in the blood the smaller is the amount of red cells.” (p. 218.)

The fourth section, occupying one-half of the whole volume, contains the essays on Thrombosis and Embolia, and on Inflammation of Vessels and Septic Infection. (pp. 219-732.) These are also subjects on which our knowledge has been considerably enlarged, and in some respects corrected, by Virchow's labours. Many cases of obstruction of arteries and coagulation of blood within the vessels had been published, but insufficiently interpreted, when Paget's excellent memoirs, 'On Obstruction of the Pulmonary Arteries,' appeared in 1844 and 1845. Almost at the same time we received an essay by Bouchut, touching the spontaneous coagulation of blood in the vessels in cachectic states and in chronic diseases. To Virchow, however, the merit is due, not only of having explained that many of the cases of obstruction of the pulmonary arteries are the effect of the lodgment of fibrinous plugs, carried there from a distance, and having pointed out the places where, and the circumstances under which, the primary fibrinous coagula are formed, but to him also we must accord the priority in the question of the obturation of the systemic arteries in consequence of the detachment of solid substances from the valves of the left ventricle, &c. (1845.) Later we meet with the publications of Pioch, Meinel, Doederlein, Rühle, Kirkes, Tufnell, Klinger, Simpson, &c., some of which have evidently been written without the knowledge of our author's researches, as Pioch's de Gangrène partielle du Pied, attribué à un Caillot Détaché du Cœur ; and, above all, Kirkes' masterly essay 'On some of the Principal Effects resulting from the Detachment of Fibrinous Deposits from the Interior of the Heart, and their Mixture with the Circulating Blood.'+

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In his first publication, On the Obturation of the Pulmonary Artery,‡ Virchow distinguishes primary and secondary obturation. In the primary form the obstruction commences in the artery, the alteration of the parenchyma being the consequence; in the secondary form. the alteration of the parenchyma causes the obstruction. Many cases of obliteration of branches of the pulmonary artery in tuberculosis and pneumonia are attributed to the secondary obturation, but a large

• Gazette Médicale. Août, 1847.

† Med.-Chir. Trans., 1852. Froriep's Neue Notizen, No. 794. 1846.

number of obturations are of a primary nature, and concerning these Virchow long since said:

"These plugs have been formed in some part of the vascular system, situated in the circulation anterior to the lungs-i.e., either in the veins or in the right side of the heart; and have been carried by the blood into the pulmonary artery." (p. 224.)

In proof of this, he adduces: 1. That plugs are met with in the venous system. 2. The plugs fill, when fresh, the whole lumen of the artery; they adhere only loosely to the walls, which exhibit no alteration; when old they adhere only to one side of the vessel. 3. The plugs do not usually commence from the capillaries, but extend only to the division of a larger branch, riding frequently on the bifurcation. 4. The age and condition of the plug are in general similar to those formed in the plug of the veins. 5. The thrombus of the vein, in which the blood is coagulated, extends some distance beyond the inosculation into the larger vein, which is still capable of carrying on the circulation. This prolongation of the plug takes place in the direction towards the heart, along the wall of the vein, where the plugged branch enters; thus the circumstances are given which are most favourable to the softening of the plug, a part of which may then break off and be carried away by the stream of the blood. This view gains strength by the irregular step-like appearance of the termination of the prolongated venous plug.

Further Researches concerning the Obturation of the Pulmonary Artery and its Consequences.-The author's experiments on animals show that the venous stream of blood is able to carry off bodies of greater specific gravity than the venous blood through the right heart into the pulmonary artery; that the contact of these bodies with the internal surface of the heart does not cause any marked symptoms; that the plugs either ride on bifurcations or pass some distance into a branch; a consecutive coagulation of blood takes place before the plug, and another coagulation around it, if any space is left between its edges and the walls; but the walls of the artery behind the plug collapse if the lumen is completely obturated by the plug. The view of Rokitansky and older French pathologists regarding the spontaneous coagulation of the blood in the pulmonary arteries, in consequence of the admixture of products of inflammation to the blood, is rejected. Due justice is done to Paget's merits on this subject, but his hypothesis, that the presence of urea in the blood may increase the adhesion between blood vessels and blood, and thus lead to spontaneous coagulation in the pulmonary arteries, is considered as still unproved. Retardation (or complete stoppage) of the circulation appears to be the principal condition favouring the coagulation of the blood within the vessels, while relative or absolute increase of fibrin is considered as of secondary importance. Retardation to such a degree as to lead to spontaneous coagulation is, however, almost only met with in the venous system-very rarely in the arteries either of the body or of the lungs; it is therefore, also, à priori, not likely that we should meet with spontaneous coagulation in the pulmonary arteries.

This first appeared in Traube's Beiträge zur Experiment. Pathologie und Physiologie, Heft 2. Berl. 1846.

"The eases of obstruction of the arteries of the body by fibrinous plugs, cannot (he then already said) be adduced in proof of the just-refuted hypothesis, as they are likewise to be explained by blocking up through substances transported there from the left ventricle."

In order to elucidate the consequence of the mere obturation without complication, Virchow performed a series of experiments on dogs, which he relates under the following heads:-a, Introduction of animal substances into the jugular vein (fibrinous coagula, plugs taken from veins, pieces of muscle). b, Of pieces of the pith from the elder tree. c, Pieces of caoutchouc.

The results of these experiments show, that up to a certain period the consecutive alterations are similar in all cases of obturation, but that important differences are seen in the later development. In all cases we observe, first, coagulation of blood in the vessel round the plug, as already mentioned; later, inflammation of the coats of the artery, manifested by changes in the wall itself, without exudation into the cavity of the vessel. From this point great differences commence, no further alterations being witnessed after the intromission of the caoutchouc plugs, while the substances under a and b cause violent pneumonia, terminating either in suppuration or necrosis, pleuritis with extravasation into the parenchyma of the pleura, and abundant serous and hæmorrhagic effusion into the cavity, with predominant tendency to ichorous metamorphosis; the pleura over the affected part of the lung became necrotic, and by bursting, led to pneumothorax. The whole series of these phenomena developed itself in one case within less than five days.

We may infer from these results that the local affections following the obturation depend only to a small degree on the plugging up itself, but much more on the chemical and mechanical nature of the plug. The circumstance that the pulmonary tissue, after the complete obturation of the artery of an entire lobe, remains unaltered, corroborates the view that the bronchial artery is the nutritive vessel of the lung. Virchow's experiments further show the formation of a distinct collateral circulation through the bronchial and intercostal arteries after the obturation of the pulmonary artery. A very important experiment, in which a large number of pieces of muscle was introduced, exhibits the occurrence of death with all the symptoms of asphyxia, the heart having been found in the diastolic state. The ingestion of air acts likewise by the impediment it originates to the circulation through the lungs. Here, too, the heart is found in the diastolic state, as, in the whole, the most different forms of asphyxia produce paralysis of the heart, which again appears to be the effect of the regurgitation of the blood into the coronary arteries, through its accumulation in the right ventricle. The tetanic stretching of the voluntary muscles, the retardation of the respiration, the dilatation of the pupils, the protrusion of the eyes, &c., are the immediate consequences. Some of the author's experiments exhibit also very clearly the subsequent metamorphosis of the thrombi: 1, the organization, by vascularization and canaliculization; 2, the formation of detritus by simple softening or putrid deliquescence.

Regarding the secondary disturbances in man, the author shows that here, too, the greatest differences are met with, according to the size and nature of the obturating substance. Smaller obstructions remain probably without any urgent symptoms, as Paget had already mentioned; the fibrinous plugs become in general organized into cellular tissue, which sometimes contains vessels (usually also pigment), and adheres to the internal surface of the vessel. Sometimes they undergo the sinus-like degeneration. Larger thrombi exhibit symptoms that may at first more or less resemble syncope, but later assume the character of asphyxia. Thus we find in Case 8 the occurrence of several attacks marked by feelings of anxiety, by oppression, moaning, feeble pulse, coldness of the extremities, cold perspiration, at last death, with stretching of limbs, turning of eyes, jerking motion of thorax, and sighing.

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On Acute Arteritis (pp. 380-450). In this chapter Virchow examines the results of the observations and experiments of other observers (Sasse, Bouillaud, Rigot and Trousseau, and Gendrin), from which no positive inferences can be drawn, and then relates thirteen experiments of his own, made on dogs. From these the author concludes: 1. That no exudation takes place on the free surface of the interior membrane of arteries. 2. That two circumstances may have led to an erroneous, opposite view on the subject-namely, the overlooking of the small collateral branches by which blood is conveyed into the empty artery, and the rupture of the internal membrane by which exudations collected between the coats may enter into the cavity of the vessels. 3. That necrosis of the arterial coats causes coagulation of the blood in the affected part. 4. Chemical and mechanical irritation causes inflammation of the external and middle layers of the coats of vessels. The alterations of the internal membrane are of a secondary and passive nature. 5. The phenomena of inflammation of the external and middle layers are entirely analogous to the common phenomena of parenchymatous inflammations. The fibrinous coagula in the cavity of arteries are therefore not to be considered as the products of exudation from the lining membrane, but as caused by coagulation of the blood. These coagulations may be considered under three heads: a, those only attached to the wall, and thus effecting a diminution of the lumen, occasioned either by local retardation of the circulation, or by roughness of the wall, or by a combination of both circumstances; b, locally obturating coagula, induced either by the preceding variety, through further coagulation of the blood, or by coarctation of the lumen, acting like a ligature, or by plugs detached from another point and carried by the circulation to the place of obturation. The proof for the embolic nature of an arterial obturation may be found in the locality of the coagulum, in the multiplicity of the coagula, in the co-existence of analogous bodies in the centre of the obturating coagulum, and on distant points of the arterial system, in the suddenness of the appearance of the phenomena, and in their constancy, in the condition of the arterial walls, and in the conformation of the secondary coagula round the embolus. A * Archiv f. Path. Anat. und Phys., Band i. p. 272.

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