CHAP XV. Watson saw him with Mr. Brown and myself at the end of May; and Dr. Blakiston being in London for a day or two, favoured us with a visit. There was a doubt whether some malignant formation or deposit occupied the right lung; the age of the patient and rapid progress of the case somewhat favouring this supposition. Treatment of a supporting kind was directed; but, in spite of all our efforts, the patient daily lost strength, and died exhausted, with symptoms of effusion into the pleura, on June 12, 1860, being within six months of the time of the earliest symptoms. Post-mortem examination 36 hours after death (with the assistance of Mr. Brown):-About 4 quarts of fluid in the pleuræ, chiefly the right; right lung pressed upwards and backwards; no adhesions excepting at apex of left lung; right lung dark, solid, hard, non-crepitant upper two-thirds ; this portion was infiltrated with granular tubercle commencing to soften; a small cavity existed at the posterior part of the apex; the deposit appeared to be a form of tubercle with an exudation of inflammatory products of a white fibrinous appearance; under the microscope there was a large amount of fat and tubercle corpuscles; left lung at its apex was slightly infiltrated with the same; heart large, flabby, dilated, valves and lining membrane of vessels healthy; the femoral vessels healthy; liver enlarged, very hard, studded with yellow granular deposit. Dr. Lionel Beale, and my colleague Dr. Scott Alison, agreed with me that the deposit in the lung was tubercle, modified by inflammatory action. This was a very rapid case, ending within six months. When examined in January, he had no signs of consolidation of the lung, and only the symptoms of bronchitis. The invasion of tubercle was inflammatory, and the consolidation such as, if placed at the base instead of at the apex of the lung, would certainly have passed for a pneumonia during life, accompanied as it was by a rusty-coloured expectoration. The postmortem appearances and microscopical evidence left no doubt as to its being tubercle. The invasion was acute and expended itself. The pulse was latterly tranquil, the pulmonary symptoms quite in abeyance. The anasarca was accounted for by the disease of the liver. The cause of the gangrenous ulcer was not very evident, and we were not able to explore the vascular system sufficiently to clear up this point. As regards the tubercular disease, the case illustrates many features of rapid senile phthisis. CHAP. XV. pht. 2. Chas. M., æt. 63. Cough for 10 years; slight difficult Chronic expectoration; dyspnea; no hæmopty. ; digestion impaired; dulness and marked humid crepitus for some inches right apex; much improved by sedatives and counter-irritation. Thos. P., æt. 52, bricklayer. Winter cough and dyspnoea 4 Phthisis years; hæmopty. some years ago; difficult frothy expec- chitis. toration; no fever; much out of flesh; decubitus on left; Dilated sinking and fixity under both cavicles; dry bronchial râles bronchus. both sides; tubular respiration and voice right apex. He improved on mist. scillæ c. lobelia, pil. conii c. morphia, and was under treatment 18 months with the same physical signs. The diagnosis appeared at the time to lie between dilated bronchus and tubercular deposit with bronchitis. with bron mation of July 1855.-Robert D., æt. 56, clerk. Ill 5 months; dry Acute forcough in Feb.; slight hæmoptysis twice 6 weeks ago; cavity. moderate but increasing expectoration, yellow, easy, chiefly at night; had sweats and much fever in Feb. ; none now; app. good; b. reg.; weight 10 st. 23lb.; dulness, immobility, flattening, gurgling for 3 inches apex right. Improved on oil. January 1857.—James M., labourer, æt. 61. No pre- Chronic disposition; cough for 10 years in winter, constant last 2 cavity years; no hæmoptysis; morning expectoration abundant, thick, easy; is slightly out of flesh; app. poor; b. regular; no fever; dulness, gurgling, subclav.; bronchial resp. and voice posteriorly right. Improved on sedatives with counter-irritation. Frank R., tea-dealer, æt. 76 (looks 66). No predisp. to Inherited phth. His father died at 76, mother at 87, his aunt at 97. longevity. Signs at Has suffered from dyspnoea for 10 or 12 years; nights broken base. by this distress; cough moderate; expectoration slight; app. good; bowels regular; dulness and very marked crepitation over anterior inferior portion of left lung; decubitus on right. СНАР. Strumous phthisis; cavity; æt. 50. Chronic slow phthisis with bron chitis. Diffused tubercle, æt. 59. Rob. A., æt. 50, clerk, height 6 feet 3 inches. No predisposition; suppuration of cervical glands 18 months ago; cough ever since; thick white expectoration; no hæmopty.; fistula in ano, operation years ago, but discharge remains; tongue very red, cracked; nausea; night-sweats; dulness, coarse crepitus, nearly pectoriloquy right apex; occasional click on cough, left. Got rapidly worse, the gastric symptoms increasing in severity. Thos. S., æt. 62, lodge-keeper in Kensington Gardens. Winter cough for 3 years; slight, difficult, frothy expectoration; no hæmoptysis; no loss of flesh; app. good; bowels irregular; percussion note low throughout both sides; coarse crepitation and much resonance of voice supraclav. only, right. Was doing well at the end of 12 months (the fourth year). Thos. H., æt. 59, labourer. Ill 1 year with cough and expectoration; occasl. hæmopty. with relief; night-cough; cold sweats; loss of flesh; walks from Norwood to the hospital; dulness, flattening, crepitation moist diffused over left. Improved much on oil and sedatives, with iodine solution externally. Prognostics of Phthisis in the Aged. 1. Phthisis occurring in advanced life is commonly slow. Gradual emaciation is generally the earliest symptom. 2. The more advanced the age, the more likely s it that the form of the disease will be the laten in development, and the chronic in form. 3. Acute phthisis may arise in age, and either terminate in rapid and extensive deposit, or in localised and massed deposit in the apex which forms a cavity. 4. A quiet pulse is one of the most favourable of the good symptoms. A permanently accelerated pulse indicates extensive and advancing deposit in the aged. 5. A long-continued and progressive emaciation is a bad symptom, even while the pulmonary symptoms are moderate. 6. The complications common to phthisis in the ordinary form (diarrhoea, laryngitis, profuse hæmoptysis) are not ordinarily present in the tuberculosis of advanced life. Their absence does not imply safety, although their presence is of evil import. 7. Old deposits in the lung, the result of low inflammatory action, often at the base, commonly break up in old age, and assume the tubercular form. These cases are often very slow. 8. The disease may be confined to one lung in the aged, and yet prove fatal; a fact which, as it is the reverse of the ordinary events of phthisis, should be borne in mind in offering a prognosis. XV. CHAP. The rheu matic diathesis a cause of phthisis. CHAPTER XVI. RHEUMATISM, GOUT, DISEASE OF THE HEART. In the section on the premonitory stage of phthisis, the rheumatic and gouty constitution was considered as a causative agent in the production of tubercle. In many instances rheumatism is the direct forerunner of phthisis, and in very many the two affections are associated in the same individual, attacks of rheumatism or gout occurring in the course of ordinary consumption. The tubercular and the rheumatic diatheses are doubtless very intimately allied. The hereditary influences may be the same in both. Rheumatic parents often have phthisical children, or one child of such parentage will exhibit the rheumatic, and another the tubercular affection. That rheumatism is frequently propagated by descent is undoubted, and with such hereditary antecedents it is not uncommon to see strumous affections in earlier, and pulmonary in later life, while some of the children may only have the muscular form of rheumatism, or the acute attack on joints. Some again may have cardiac disease without Rheuma- preceding rheumatism. In the course of phthisis rheumatic affections are frequent, oftentimes alternating with the more active chest symptoms, and for the time suspending the progress of the lung disease. tism in the course of phthisis. Its character. The rheumatic attacks in phthisis are not of the extreme severity which we witness in uncomplicated rheumatism. Acute inflammatory affections of |