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ACUTE TUBERCULOSIS—SCROFULOUS PNEUMONIA. 3

merable miliary tubercles are scattered throughout the pulmonary tissue, and these are the obvious cause of the intractability of the case. They break out simultaneously, like the eruption of an exanthem, and by their numbers and bulk induce such an amount of obstruction and congestion in the lungs, as to destroy life before there is time for any considerable degeneration or softening to take place. This acute tuberculosis is the worst and most surely and rapidly fatal form of consumption.

The second form of acute consumption begins with pneumonia in one or both lungs. The patient, generally a young subject, is of consumptive family, and may have previously had cough and occasional haemoptysis. The fever attendant on the inflammation may not be very high at first, and the expectoration by no means so viscid and rusty, nor the crepitation so fine and even, as in simple inflammation of the lungs. But the symptoms are more persistent. The pulse and respiration remain frequent. The heat of the body, particularly of the chest, continues remarkably high, almost burning the ear of the auscultator as he examines the back. But this intense heat is alternated with occasional chills and profuse sweats at night. The cough continues distressing, and the expectoration becomes opaque, purulent, and clotty; the flesh wastes, and the strength ebbs away; and if the appetite does not return, the progress of consumption and decay is rapid. Auscultation reveals the steps of the destructive process in the lung. The affected part, or the whole side, or part of both sides, becomes dull on percussion, only varied with the cracked-pot note from the gurgling within; the loud tubular sounds are replaced by coarse crepitation, in parts amounting to gurgling; and the diffused bronchophony is modified into detached islands of voice, loud and pectoriloquous, or into the snuffling or whispering sounds equally characteristic of a cavity. This form of galloping consumption may also prove fatal in a few weeks; and the lungs are found after death in a state of consolidation little more dense than the hepatisation of pneumonia, but their red is mottled with grey and yellow patches of tuberculous or aplastic matter, and excavated in various parts into numerous small cavities communicating with the bronchial tubes, and containing more or less of the same compound matter which was expectorated during life, consisting of mucus, pus, degenerating epithelium and exudation-matter, with disintegrated fragments of lungtissue. This form of acute phthisis, although generally rapidly fatal, is not universally so. When not too extensive, it may sometimes be arrested and brought to a chronic state; and the chance of this result will very much depend on the recovery of the appetite, and the power of the stomach to bear strong nutriment, tonics, and, above all, cod-liver oil.

And in a large majority of the cases of consumption the destructive element is still less extensive and less active, and its progress is much more slow; and we have both time and means to resist its inroads and to fortify the system against its operation to a greater or less extent. In the greater number of instances the disease begins with the symptoms of common cold, often referred to the throat as much as to the chest;" and there is, in truth, more or less of bronchial irritation and inflammation attendant on the development of the disease, and recurring with renewed intensity at the time of its increased activity. Often the disorder is mistaken for a common cold, until either its remarkable persistence, or the occurrence of haemoptysis, of night sweats, of loss of flesh, or of some other uncommon symptom, gives intimation of its more serious nature. Then it is found that, in addition to the signs of bronchial catarrh, there are some of the signs of consolidation of the lungs, generally near

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an apex; slight dulness or raised tone of the stroke-sound at or below a clavicle, or at or above a scapula; a tubular character in the breath-sound and voice; an undue intensity or duration of the sounds of expiration, or a weakness or absolute obstruction of the inspiration; and sometimes the various slight degrees of crepitus substituted for the proper breath-sound; and various other signs which it is unnecessary here to detail. These signs, however, are the indications of incipient pulmonary consumption—that is, of a disease which tends, sooner or later, to injure and destroy the structure of the lung, and to deteriorate and waste the flesh and blood of the whole body. And the progress of this work of injury and destruction is marked by signs of increased density and diminished motion of parts of the lungs; by more of the moist crepitus, from augmented humidity,in and around the consolidations; and eventually by signs of excavation at one or more points, which announce the removal of the diseased tissue.

The progress of this disease may vary infinitely in time and in extent. The more extensive the mischief, generally the more rapid will be its progress, which goes on in the worst cases, uninterrupted by any check or pause, attended by the distressing train of symptoms—harassing cough, opaque clotty expectoration, increasing shortness of breath, burning fever alternated with profuse sweats and chills, rapid loss of flesh and strength and colour, sometimes diarrhoea, and aphthous mouth ; and terminates in death in a few months.

But in other cases, and these are by far the most common, the destructive lesions are less extensive, and their progress is more slow and intermittent, and often seems in great degree to depend on occasional attacks from cold or other external causes, in the absence of which the disease may be quiescent or stationary, and may not destroy life for years.

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Powerless as medicine is in the overwhelming and rapid types of the disease, it has yet considerable influence over these milder forms; and the following pages will give some evidence that under careful treatment life may be prolonged for many years in comfort and usefulness, and in not very few cases the disease is so permanently arrested, that it may be called cured.

It may well be questioned whether a disease which presents such striking differences in form, intensity, and result, can be truly one and the same disease; and there seems to be a growing disposition among modern pathologists to supersede the comprehensive terms consumption and tubercle by others more specifically applicable to definite forms of the disease. But while I fully participate in the objections to include all forms of phthisis under the head of tubercle, and have long insisted on the origin of many cases in inflammation, I still maintain that all the varieties of phthisical lesion are identified by their common consumptive nature; and the following pages will supply numerous proofs that all are characterised by a tendency to degeneration and decay. It will be shown that all are due to the presence of various kinds of phthinoplasm,1 a withering or decaying modification of the proper plasma or formative material of the body; and although for clinical purposes it is useful to note their differences, an'd group them accordingly, yet we hold it to be most important, in relation to pathology and treatment, to consider them as varieties of one common malady—Pulmonary Consumption.

1 I have found it necessary to coin this word, phthinoplasm (from </>9lu, or tpBlvui, ' I waste or decay '—whence also 'phthisis'—and nKiana), to give expression to one of the leading ideas of this book, and to avoid the common use of the word tubercle, which is quite inapplicable to many kinds of degenerative formation which cause pulmonary consumption. I trust that the utility of the term will reconcile the reader to its novelty.

CHAPTER II.

PATHOLOGY OF PULMONARY CONSUMPTION.

Pathology of Pulmonary ConsumptionViews of Laennec criticised, and compared with those of Andral, Cruveilhier, Alison, and AbercrombieOriginal Conclusions of the AuthorConsumption produced by defective Vitality and Organisation of the Plasma resulting from Inflammation or Malnutrition.

The term 'pulmonary consumption' was restricted by Laennec to the wasting disease produced by the presence and progress of tubercles in the lungs. These tubercles he described as existing in the form of grey granulations, or miliary tubercles (of Bayle), yellow tubercles, and tuberculous infiltration, which might be either grey or yellow. But he held that the yellow is only a more advanced stage of the grey, and that the yellow tubercle tends to change further from the crude hard state to that of softening and ultimate excavation. He entirely denied the inflammatory origin of tubercles; and in classing them among 'accidental productions' he associated them with cancer and other formations, which have been subsequently denominated growths, although he was well aware of the generic difference between them in regard to both structure and history.

These views of Laennec, characterising pulmonary consumption as an essentially tuberculous disease, and repudiating the previously prevalent notion, that it might arise from inflammation, were adopted by Louis, and by most writers in this country, with very little qualification.

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