this exclusive theory. Here, then, we begin to touch an entirely different order of considerations, which must form the theme of the second part of our observations.

No suggestion was ever propounded in medicine more pregnant with future illumination than that of the increased destruction, in fever, of the nitrogenous tissues; and certainly no country has on the whole done so much to develop this important line of research as our own. The name of Parkes (which must always hold the first place) must be joined in this respect with those of Buchanan, Ringer, Squarey, and others who forced this topic on the consideration of the profession at a time when its true importance was very little perceived; and we may here notice with some regret, that the distinct precedence of the heightened urea-discharge to the rise of temperature, which is one of Senator's most important points, is not acknowledged by him as having been previously observed by Ringer. However, we have no wish to quarrel with an observer who has done so much, both in the way of personal observation and in collecting the experience of others respecting this exceedingly important topic of tissue-change in the febrile state. We must ask to be forgiven if we tax our readers' patience by a literal transcript of the numerous conclusions at which the author arrives.

"1. In the majority of diseases commencing with a high febrile temperature, there is no single and equable increase of tissue-exchange, but a disproportionately large destruction of albumen which leads to an increased urea-discharge.

"2. The increased formation and discharge of urea takes place from the commencement of the febrile process, and even before the beginning of the rise of temperature. This increased elimination amounts, on an average of the whole febrile period, to double what occurs in the absence of fever. The conditions are more unfavourable to the elimination of urea when formed in fever than in health.

"3. For this reason, and because albumen usually undergoes change also in other ways, the albuminous loss is yet greater than is represented by the urea, and is, in general, much more than doubled.

"4. The conditions for the discharge of carbonic acid are more favourable in pyrexia than in health: under propitious circumstances it is increased in the daytime by 30 or 40 per cent.; in the night it is probably, as in health, at a lower level than in the day. The formation of carbonic acid in fever is thus, at most, only increased by less than 30 or 40 per cent.

"5. It follows from this that the fevered organism is relatively poorer in nitrogenous constituents (albumen), but richer in non-nitrogenous and carbonaceous substances (fat).

The

"6. Of the nitrogenous constituents, those are most largely destroyed which are rich in potash and blood-pigment: for instance, the blood-corpuscles, and then the muscles. increased destruction of the red blood-cells, which are carriers of oxygen, produces fatty parenchymatous degenerations, just like those poisons which interfere with oxidation.

"7. Since the febrile organism cannot take up so much oxygen as a feverless organism similarly nourished, it also cannot furnish so many products of oxidation. But since the increased formation of urea has already used up larger quantities of oxygen, the other products of oxidation, such as carbonic acid, cannot be furnished in larger quantity.

"8. In the absence of oxidation, the only possible increase among the final products of tissue-exchange is that of the water, from synthesis and dishydration.

"9. The quantity of urine is generally regulated, in fever, by the supply of liquid; but it stands in a more unfavourable relation to the latter than in health, for a relatively smaller quantity of the fluid swallowed is discharged as urine than in the feverless state under similar circumstances.

"10. The quantity of watery evaporation is increased in fever, and to a greater degree than that of the expired carbonic acid; a relatively larger portion of the water drunk is therefore got rid of by evaporation.

11. The relation of the total water-discharge to the waterformation in fever, over and above the ordinary loss, is not yet distinctly made out. As happens in health, the water supply may be larger, yet water may be retained in the body. These varying relations of the supply and discharge of water are the principal causes of the fluctuations in body-weight in fever.

"12. The critical increase of urea-formation probably depends, not on incomplete oxidation of nitrogen, but on various other

causes.

"13. The waste of heat at the beginning of a fever is not increased, but diminished, during the shivering; at the height of the fever it is increased on the average, in the daytime to about 70 to 75 per cent., but considerably more at the critical defervescence.

"14. The greater part of the waste of heat depends, in pyrexia as in health, upon conduction and radiation; but in the critical defervescence upon evaporation.

"15. The excess of heat in the febrile organism cannot be explained by the tissue-destruction which is expressed by the final products-urea and carbonic acid.

"16. This excess has various causes, of which the following can, so far, be assigned with certainty:-(1) The consumption

of the tension-force which is available for work in the healthy organism; (2) the increase of heat in the pyrogenetic stage preceding the fever heat. Besides this, there are perhaps, in the increased conversion of albumen to urea, and in unknown processes connected with the formation of water, sources for the increased production of heat.

"17. The skin, in fever, has not lost its power to regulate the bodily temperature by its fluctuating contents of blood and heat; but its activity is diminished by the fact that, under the influence of the causes of fever, there is an abnormal excitability and stimulation of its vessels, whereby the latter, from the first development of fever, are either generally or locally contracted, and thus hinder the regulation of the heat-excess.

"18. The elevated temperature in fever is also favoured by the perverted relations between the abnormally increased formation and the less increased discharge of heat. In this way the discharge of heat may be always greater than normal at the height of fever, and occasionally even greater than the febrile heatformation. This perverted relation does not occur equally in every phase of the fever, and necessitates the occurrence of a pyrogenetic stage before every burst of fever heat, and an exactly opposite process in the stage of defervescence.

"19. The pyrogenetic stage is most strongly expressed in the febrile shivering, the defervescent stage in the crisis; the same processes occur, however, only less stormily, in every kind of development and decline of the fever, and are also expressed, though more weakly, during the febrile stage in the fluctuation of increase and diminution of the waste of heat.

"20. The absence or presence of sweat does not depend on the febrile process in itself, but on the nature of the febrile disease, or on peculiar causes, and has no relation to the regulation of heat. It is probable that in many febrile diseases the necessary stimuli to perspiration are absent, or are hindered in their operation; while in other diseases, and at the occurrence of the critical sweat, the opposite conditions prevail."

Such are the conclusions at which Senator arrives; and the reader, whether he be inclined to accept them all or not, will confess that they offer a broad and most suggestive view of the pyrexial state. Perhaps the most valuable service that they render is the light which they throw on the possible independence of the pyrexial temperature of positive destruction of tissue. Senator states very strongly that the tissue-destruction (as evidenced by urea and carbonic acid discharges) is not sufficient to account for the amount of fever heat. We assent entirely to the statement, and we shall only render it more important if we put in a preliminary caveat, to the effect that

Senator decidedly underrates the normal amount of urea discharge, and that the "doubled or trebled" rate of urea-discharge which he mentions as occurring in pyrexia does not mean, as might be supposed, the discharge of 1,000 or 1,500 grains of urea in twenty-four hours by an adult suffering from fever. On the other hand it must be remembered, as Senator himself points out, that the urea is not the full measure even of the albuminous destruction; and that, further, there is all the destruction of fatty tissues (frequently so striking and extensive) to be considered as a source of heat-production. The best proof, however, that tissue-destruction is not the only source, nay, that it may even hardly be a source at all, of febrile heat-excess, is to be found in such cases as those related in the March number of this journal1 (and which appear to be not so very uncommon), in which a very high pyrexia is accompanied by a quite low urea-discharge, and an absence of any considerable emaciation either of the muscular or of the fatty tissues.

It is most important that attention should be drawn to a cause of febrile heat which, though not overlooked by Senator, is ignored by most writers, and unquestionably is never thought of by the majority of practitioners. We refer to that removal of the tendency for force to become latent which takes place when, as in pyrexia, the usual quiet building up of tissue comes to a sudden end. In ordinary tissue-building a large amount of force becomes latent; in fever that same force is set free under the form of heat. If we add to this the collection of heat within the body in the early febrile stages (when there is little or no heat-waste), and the obscure chemical processes connected with water-formation, we have enough to account for a large heat-production, even independently of the destruction of nitrogenous and fatty tissues.

It is very surprising to us that Senator should have been content with such feeble and insufficient trials of the action of alcohol in pyrexia, considering the pointed way in which he describes the destruction of tissues which accompanies that state. The chief reason perhaps is,. that his febrile experiences seem to have lain more in the direction of relapsing fever than in any other. It seems very plain that there is no more important duty now incumbent on pathologists and physicians than to try every possible means by which we may strike at the root of that excessive combustion of tissues which (in any fever which is below the degree of imminently dangerous hyperpyrexia) is one of the phenomena that we have most to dread. We shall hope to see this able observer entering with great zeal upon a line of inquiry which he is so amply qualified to carry out with solid results.

1 "On Tissue-destruction in the Febrile state.". By Dr. Anstie.

Clinic of the Month.

Discussion on Cancer.-The chief subjects of clinical interest in the journals of the present month have been the discussion on pyæmia in the Clinical Society, and the discussion on cancer in the Pathological Society. The latter discussion was opened by Mr. Campbell de Morgan. Mr. De Morgan defines cancer to be a malignant growth, consisting of a delicate fibroid stroma, containing within its meshes aggregated but not coherent cell-elements-cells, nuclei, or granules-generally nonuniform, though often similar to natural cell-elements. He limits the term "cancer" to those forms of disease which are specialised as medullary cancer, scirrhus, epithelioma, and rodent cancer; and in regard to its origin, the view he is disposed to hold is that, though essentially local, there is in some, and perhaps in all cases, a predisposition to the disease, which may possibly be distributed through the system, but which more probably has its seat in some among the tissues of the body. He therefore questions the evidence of there being any special disease in the blood which either alone produces cancer or co-operates with tissue specially fitted for the development of the disease. He adduces as arguments against the constitutional or blood-contamination theory, the good health of the patients previously to the discovery of a cancerous tumour; the possibility of its non-return after removal; the recovery of wounds and other lesions in those actually suffering from cancer; the occasional wasting away of a cancerous tumour; and its tendency to attack women. Mr. Simon remarked that, looking on the one hand at the hereditariness of cancer, and on the other at the insusceptibility of bodies generally to the inoculation of cancer, it is necessary to assume that a certain specific predisposition is required. In addition, he thinks we must recognise that the essence of the disease is the development in some one spot of a specific impregnative influence; but whether this local infection is a local neo-genesis, or is a contagium ab extrá, is a question on which it is not safe to speculate. Mr. Hutchinson followed the same line of argument, and con