an example of physiological antagonism as that between atropia and physostigma shows that the toxic influence of a morbific agent may be directly opposed by a physiological antidote, and that recovery may be produced by influencing the abnormal conditions themselves, in such a manner as to cause their return to a normal state."

July, 1873.

ON SOME FORMS OF PHTHISIS PULMONALIS AND THEIR SPECIAL TREATMENT.

By H. NANKIVELL, M.D. Edin.

I SHALL endeavour to lay before you, as succinctly as may be, the chief points of practical importance in relation to phthisis pulmonalis, which have been brought to the front-I cannot say settled-by the recent investigations of German and English pathologists. And I shall also endeavour to indicate the importance of these views in their bearing on the prognosis and treatment, whether specific or hygienic, of that scourge of our race, consumption.

As you will see by the outline of the paper, which you already possess, I propose to discuss, first, the etiology and relationship of non-tubercular and tubercular phthisis. And I must guard these terms from being misunderstood, by saying that I intend by the first term that form of phthisis which is primarily not tubercular, but arises from an inflammatory process set up in the alveoli by the presence of some other exciting cause than tubercle; and by the second term I indicate that form of phthisis which is to all appearance of primary tubercular origin, or which is developed as a secondary complication in the course of a previously pneumonic phthisis.

Professor Niemeyer may be looked upon as the apostle of the following views, but his work has been based on and seconded by the labours of Cohnheim, Rindfleisch, Waldenburg, and others. Of late an able paper by Dr. Wilson Fox has thrown doubt on the soundness of these pathological theories; but seeing that they bear the test of clinical practice, which is the best of all tests, we cannot do better than accept them, and leave to histologists the attempt, in which I doubt not they will succeed, of reconciling microscopical appearances with clinical facts.

A. Etiology of Non-tubercular Phthisis.

In a very large proportion of cases which we recognise under the term "pulmonary phthisis," the starting-point of the diseased condition is catarrhal pneumonia. Granted a certain amount of chronicity to this morbid process, and we pass by imperceptible degrees from what may be termed incipient phthisis to the establishment of a true first stage.

Catarrhal pneumonia may be set up in several ways, of which the following are the most frequent:

(1) In the course of a bronchitis affecting the smaller bronchi, and characterised by the secretion of tough mucus, a small bronchus becomes plugged, and atelectasis of the lobule which is dependent on it for its supply of air occurs. The current of blood is thereupon obstructed, œdema sets in, and splenization is established: a condition of things most favourable for the supervention of catarrhal inflammation.

(2) Or else the bronchial catarrh insidiously extends itself to the alveoli, and an alveolar catarrh is set up throughout a certain number of lobules. An effusion occurs of a viscid character, rich in cells, which proliferate actively, and distend the alveoli: expectoration is also rendered more difficult, or even impossible, from the simultaneous obstruction of the bronchi.

These two causes are the most general and important, but catarrhal pneumonia may be set up also in the following ways:

(3) After an attack of homoptysis: the whole of the effused blood is not expectorated, a portion having been drawn into the alveoli during acts of inspiration. It there acts as a foreign body: the air-cells become inflamed, and a catarrh is set up.

(4) Hyperæmia of the lungs, brought about by sudden, violent, or long-sustained exertion, has in many instances of persons engaged in usually sedentary occupation proved the starting-point of catarrhal pneumonia, either directly, or indirectly through hæmoptysis.

(5) The irritating presence of such foreign bodies as coal, iron, or stone dust must also be included in this list. We have thus rapidly traced up the conditions named catarrhal pneumonia from their different causations, and have arrived at this point: one or more lobules, imper

vious to the air, blocked with an ever-multiplying secretion, for which there is but little chance of escape; the lung tissue proper becoming in turn compressed and devitalized. This point we must consider as the borderland between incipient and established phthisis; it is the limit of the absolute curability of phthisis. The secretion may alter and be partly absorbed or partly expectorated, and the lung tissue may in course of time resume its normal condition; or else a further stage of the disease is reached, termed CASEATION which consists of a peculiar fatty degeneration of the diseased tissues, and of the effusion which they contain; by this change the individuality of all the tissues involved is lost, with the exception of the elastic tissue and the large arteries. This process is then one of destruction, but preceding it, simultaneously with it, or following it, a process of conservation is in many cases established by a proliferation of the peri-bronchial and peri-vascular fibrous sheaths. The relative proportions maintained between these two processes continually varies: when caseation is in excess, we find "softening" occurring and the second stage of phthisis developing; when fibrosis is in excess, we get a chronic first stage and a tendency to cure by INDURATION; the caseous masses become encapsulated, and gradually shrink up with slight if any ulceration.

SOFTENING consists in the addition of fluid to the caseous solids, and then in a communication being established between them and the external air, by means of which the expectoration of the degenerated and semifluid tissues is brought about. This process may continue until the cheesy material has been excavated; or it may be arrested, and remain chronic for many years.

CASE I.-Four years ago a chronic case of softening was seen by me at Bournemouth: both apices were undergoing this process, and had been in a similar condition for six or eight years: occasionally small abscesses formed and burst, but no permanent cavity was established. This patient, when last I heard of him, was enjoying fair health at the Cape.

Softening is usually followed, however, by the establishment of the third stage, viz., an open cavity. Here we may hope for a third point of departure towards cure, viz., by cicatrization. A pyogenic membrane is formed to line the cavity, the surrounding tissues are protected

from the more irritating effect of exposure to air, and contraction of the cavity commences, and may under careful management continue. The opposite alternative is the continuous enlargement of the cavity by inflammation and softening of the neighbouring tissue; or else by the deposit of true tubercle in these tissues, or generally throughout the lung.

We must not overlook the fact that croupous pneumonia may eventuate in abscess of the lung, and that from the time that a cavity is thus formed, the case practically becomes a third stage of phthisis: with this important distinction, that there is generally but one single lesion in the lung, and that a cavity succeeding croupous pneumonia has a great tendency to heal.

B. Tubercular Phthisis.

We will now pass to the discussion of true tubercular phthisis, ie., destruction of lung-tissue accompanied with the deposition of what is commonly known as miliary tubercle.

This deposit is found either as an apparently primary occurrence in the disease termed acute miliary tuberculosis, and here it exists in the disseminated form; or as a secondary complication arising in sequence to some caseous degeneration; and here it may assume, according to its intensity, either a disseminated or a localised form.

Some late observers have gone so far as to say that it is never of primary occurrence: that when it exists it does so in direct sequence to some previous point of caseation, either in lung, gland, or pleura; that where this point of caseous degeneration is apparently wanting, it has undergone such an amount of absorption or withering in the course of the disease as to be to all intents unrecognisable. These possibly extreme views receive support from the fact that the inoculation of animals with caseous matter induces miliary tuberculosis; and that too even in the case of Rodentia, a class which is particularly free from that disease.

If we carefully weigh these facts, and consider how seldom tuberculosis is to be found without the pre-deposition of caseous matter, and how frequently the inoculation of caseous matter has induced a crop of tubercle, we must acknowledge that the relation existing between these two conditions is generally one of cause and effect. We may