The morbid anatomy of pneumonokoniosis includes nearly all the

pathological processes incident to the pulmonary tissues. The bronchial

lesions are those of chronic bronchitis, with thickening of the

bronchial mucous membrane, associated with possible ulceration and

bronchial dilatations, forming bronchiectasic cavities. These cavities

are caused by combined softening of the bronchial tissues with traction

from without by the newly-formed fibrous tissue. The bronchial glands

may be enlarged to the size of walnuts, and are often perfectly black

and gritty on section. These enlarged glands may occasion, through

pressure, many changes in the pulmonary tissues. The effect of this

pressure is especially manifest in the lymphatic system. The

lymph-circulation is further crippled by the accumulation in the

lymph-channels of the inhaled inorganic materials. These interferences

with the lymph-circulation may be followed by exudation or lobular and

interlobular formation of tissue; secondary to these changes the

pressure upon the vesicles may cause local congestions, exudations, and

even hæmoptysis. By one or all of these processes the expansile power

and elasticity of the lung are slowly depreciated, emphysema develops,

intertwined with the lesions of acute, subacute, or chronic bronchitis,

fibroid phthisis, and atrophic emphysema. Nodules of cretaceous matter

can be recognized through the lungs, which are black in anthracosis or

gray in silicosis. These nodules occur from the size of a pin's head to

that of a pea, and are especially found in the lungs of glass-cutters,

sandstone-workers, and grinders. In these cases they consist in part of

iron and in part of stone. In sandstone-workers they are composed of

silica; the organ feels nodulated, very fibrous, and in some cases

actually gritty. The predominant form of pulmonary change is fibroid;

hardened districts of advanced cirrhosis occur measuring two inches and

upward in length and width, and in depth and thickness nearly as much.

These may be rounded, but are not separable from the adjacent

structures, the condensation of the tissues lessening without a

defining line. On section they appear tough and leathery, most

pronounced along the anterior edges of the lungs, and are apt to be

covered in by thickened pleura. If the nodules previously alluded to

are encysted, fibrous prolongations extend from these cysts into the

substance of the lung, the thickening of the lung being greatest in the

septa, on the pleural surfaces, and along the course of the bronchial

tubes. Sometimes subacute or chronic pleural processes coexist. The

caseous masses found in tubercular fibroid phthisis are infrequent in

pneumonokoniosis, but in the latter process the {458} pathological

changes may be identical with the ordinary forms of phthisis,

especially in those individuals who are predisposed to pulmonary

affections and those in whom the pathological processes are rapid.

In anthracosis the lung is large and increased in weight; the surface

of the pleura has a bluish-black color, contrasting with the coal-black

color of the lungs, which are universally pigmented and contain nodules

of pigment. When only small quantities of pigment are present, it

presents the appearance of dark lines running between the lobules; on

section these are very hard and distinct, being about the size of a

millet-seed. They are universally distributed throughout the lung, and

in some places appear like small masses of charcoal. Upon squeezing the

organ a blackish fluid exudes which stains the hands, but the discharge

which is found lying in the bronchial tubes is often yellow and

muco-purulent, although the sputa during life is more or less

discolored. When the distribution of the discoloration of anthracosis

is investigated, it is found to closely correspond with the lymphatic

distribution of the lung, and the conclusion is probably well founded

that all other irritating particles pursue the same course through the

pulmonary tissues. When particles of coal or pigment enter the bronchi

with the air, they cannot pass through its mucous membrane, because the

basement membrane and fibrous coat underlying it present an obstacle to

their lodgment, whilst the cilia of the epithelium tend to prevent

their retention in the bronchi; they therefore enter the vesicles, and

may be found sticking to the walls. In this way the exemption of the

bronchi from pigmentation, even down to the smallest ramifications, can

be explained. The interlobular septa ate also the seat of great

pigmentation. The germinating epithelium elevates the cells slightly

above the surface, and in the interspaces between them the pigment

insinuates itself, and thus enters the underlying plasmatic or

lymphatic spaces; or the pigment may be incorporated into the

epithelial cells, which transfer it to the underlying lymph-space. Once

the pigment has found entrance to these lymphatic channels, it is

carried by them through the lymphatic vessels in the sheath surrounding

the bronchial tubes and the small branches of the pulmonary artery, and

in the interlobular septa to the bronchial glands. In this manner the

special distribution of the coloring matter in these situations is

explained. The special deposit around the small branches of the

pulmonary artery is owing to the double set of lymphatics, the

peribronchial and the perivascular, which form an anastomosis. The

perivascular set is the larger; consequently the pigment passes into

them more readily, forming the nodules. Pigment is also found in small

quantities around the bronchi, which can be accounted for by the

anastomosis of the lymphatics. The bluish-black appearance of the

pleura and the distribution of the pigment only in the deeper layers of

the visceral pleura are susceptible of a similar explanation, because

the deeper layers of the pleura contain lymphatic vessels which are

directly continuous by means of the lobular septa with the large

perivascular branches of the lymphatic system.

The consequences of the obstruction to the lymphatic and

pulmonary-artery circulation may be very serious. In grave cases the

lung breaks down, forming a gangrenous-like cavity, which differs from

an ordinary cavity in not being rounded; it is more like a gangrene or

slough. In a few cases the pathological appearances indicate phthisis,

chiefly interstitial, with formation of cavities; sometimes traces of

cavities are found which have cicatrized. More commonly oedema is

developed in the lung and the bronchial passages. As a consequence of

combined bronchial irritation from continuous inhalation of inorganic

particles, and the consequent oedema, a continuous germination and

shedding of the bronchial epithelium--a chronic bronchitis--associated

with emphysema, is maintained. The mechanical cause of this

bronchitis--more or less impediment to the vascular and lymphatic

circulations by the {459} pigment deposit--is capable of explaining the

persistence of various forms of bronchial processes in anthracosis and

in other forms of pneumonokoniosis after the patient has ceased working

in a dusty atmosphere.

SYMPTOMATOLOGY.--Pneumonokoniosis does not present a special

symptomatology. The course of the various morbid processes is insidious

and slowly progressive: the development of any of the forms of

pulmonary disease depends largely upon the degree of exposure to the

exciting causes, or the inherited tendencies, or the susceptibility to

influences liable to diminish general vitality or affect the personal

hygiene.

The earliest objective symptom of pulmonary lesion is cough, especially

recurrent in winter, accompanied by expectoration, which is whitish,

frothy, or stringy in character. Gradually the physical signs, taken

together with the symptoms, indicate the various forms of bronchitis,

acute, subacute, or chronic, sometimes associated with emphysema,

bronchorrhoea, or bronchial dilatation. In other cases the

symptomatology is that of asthma, either purely spasmodic or secondary

to emphysema or cardiac degeneration. In true anthracosis dyspnoea is a

marked symptom, and perhaps the accumulation of pigment may interfere

with the oxygenation of the blood, or dyspnoea may be due only to an

emphysematous pulmonary tissue. The sputa will be black so long as the

subject is working in an atmosphere loaded with pigment.

Fibroid phthisis is frequently associated with atrophic emphysema, and

the clinical history corresponds with that which is commonly observed

in these diseases. Hæmoptysis is rare, but if it occurs it suggests the

addition of some tubercular element; a purulent nummular sputa is a

suspicious sign of similar import. The symptoms and physical signs of

dry pleurisy are to be expected whenever any form of the phthisical

process supervenes. The cavities in the lungs are usually

bronchiectasic, unless tubercular phthisis occurs as a complication,

and the physical signs need no comment. Subacute and chronic laryngitis

with ulceration complicate certain cases, particularly those which have

inherited or acquired a tubercular tendency.

DIAGNOSIS.--The diagnosis involves a comparative examination of the

etiology and the physical signs.

PROGNOSIS.--The prognosis depends very largely upon the withdrawal of

the sufferer from an unhealthy environment. In each single case the

inherited tendencies, the personal constitution and habits, must be the

basis for an opinion upon the gravity of the pulmonary processes and

the possibilities of restoration to health. The progress of the disease

may be materially retarded or arrested by withdrawal from the

occupation involving the inspiration of dust, and restoration to

comparative health after years of invalidism is possible for these

victims of dusty avocations, even after serious damage has taken place

in the lung, if suitable hygienic conditions can be obtained.

TREATMENT.--The treatment of pneumonokoniosis divides itself into the

prophylactive and the curative. In works devoted to the hygiene of

occupation careful directions are given in reference to methods

designed to prevent the dust from entering the respiratory passages.

This is partly accomplished by the use of masks or respirators, which

possess the obvious disadvantages of clumsiness and interference with

respiration. Various devices may be employed in different avocations to

prevent the generation of dust, but the most practical plans consist in

thoroughly ventilating the atmosphere, and thus preventing the dust

from reaching the artisan. Aside from these, the management of the

various pathological conditions must be based upon the general

principles which govern the treatment of pulmonary processes.

{460}

CANCER OF THE LUNGS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A malignant disease affecting the pulmonary tissues. (Vide

also MEDIASTINAL DISEASE.)

SYNONYMS.--_Fr._ Carcinome du poumon; _Ger._ Lungenkrebs.

ETIOLOGY.--Carcinomatous disease affecting the lung-tissue is

exceedingly rare as a primary process, and exhibits only a feeble

inclination to inoculate other portions of the body. In the majority of

cases the mediastinal glands are first affected, or it appears in the

lungs as secondary to disease elsewhere in the system. Metastasis is

probably effected by means of particles of living cellular material

which are transferred through the blood-vessels or lymphatics.

Cancer of the lung often reverses the rule that carcinoma occurs most

frequently in the female, Hasse, Kohler, and Cockle giving a majority

of cases among males. It has been met with in childhood and in extreme

old age, but is more common in the middle periods of life, from twenty

to sixty years.

PREDISPOSING AND EXCITING CAUSES.--The predisposing and exciting causes

of malignant pulmonary disease are involved in the obscurity that

surrounds the development of all neoplasms.

PATHOLOGICAL ANATOMY.--Clinically speaking, cancer in the pulmonary

tissues includes the scirrhous or encephaloid neoplasms. The colloid,

enchondromatous, or fibromatous growths have been recorded as possible

tumors, but possess only a pathological interest.

Malignant disease may commence in, or ultimately implicate, one or all

of the pulmonary tissues; secondary neoplasms have been experimentally

produced by lodgment in the lung of living cellular particles which

grew centrally by virtue of inherent cell-proliferation, independently

of changes produced in the surrounding tissues. Cancer of the lungs,

whether primary or secondary, usually originates near the roots of the

lungs, implicating the mucous and submucous membranes of the bronchi,

sometimes commencing in its small mucous follicles. The bronchial

passages and the lymph-channels become the viaducts along which the

growth proceeds in its march of invasion, involving most frequently the

posterior portion of the middle lobe. The apices of the lungs may be

implicated, but not primarily, as in tuberculosis. The mediastinal

lymphatics are originally involved in an unestimated number of cases,

or enlargement of these glands is coexistent with the development of

pulmonary cancer. The enlargement of the mediastinal glands is

sometimes moderate, but an enormous mass may be formed. (Vide

MEDIASTINAL TUMORS.)

Carcinoma is found in masses varying in size from a hempseed to an

orange or larger, and since its distribution follows the lymph-channels

in their circuitous route through the lung, we can account for the wide

distribution of the nodular masses of secondary cancer. The isolated

nodules present an {461} ovoid outline, sometimes situated near the

pleural surface, in contrast with the larger formations which affect

the roots of the lungs.

The primary malignant formation presents a single large mass of

infiltration, possibly associated with a few small nodules scattered

throughout the lungs; the right lung is conceded to be the most

frequently affected, but secondary cancer usually implicates both

organs.

Cancer in the parenchyma of the lung may diminish or occlude the lumen

of the bronchial tubes, or they may be filled with cancerous matter and

their walls perforated. The development of cancer along the

distribution of the bronchial passages shows us how readily chronic

bronchitis may occur as a complication and form a confusing element in

the diagnosis. The remaining pulmonary tissues may escape anatomical

change, or from pressure atrophic or hypertrophic emphysema or collapse

may ensue. These changes, together with the similarity to a fibroid

phthisical process which many cases suggest, must be borne in mind in

making a diagnosis. Pulmonary apoplexy, or even gangrene, is an

incident in some of the clinical pictures of this disease, and embolism

or thrombosis in other parts of the system may occur. The terminations

of intra-thoracic cancer vary in accordance with the history of these

growths elsewhere. Infiltration with blood or melanic deposition has

been noticed; evacuation of the new growth through the bronchi may

induce the development of cavities in the lungs, preceded or

accompanied by suppuration, ulceration, or gangrene. In addition,

hydro- or pyo-pneumothorax may occur by perforation or invasion of the

pulmonary pleura.

Carcinoma of the pleura is usually secondary to its development in the

lung, but it may be communicated from a similar process in the mammary

gland by infection through the pectoral and intercostal muscles to the

parietal pleura. Carcinomatous formations on the pleura are small and

hard in scirrhous, but are larger in encephaloid, cancer. The minute

spots of early formation are found scattered over the pleura like drops

of wax. The thickened tissues, when they coalesce, undergo

degeneration, and may form plaques of cartilaginous hardness. Large

pleural growths may compress or nearly efface the lung, but are among

the curiosities of medical literature.

Neuralgia may be occasioned when nodules impinge upon the intercostal

nerves. Similar pressure is the cause of the pain in pulmonary cancer,

except that induced by the pressure of mediastinal enlargement. Chronic

pleural inflammation may be frequently developed by the new growth, and

the diseased lung may become adherent to the inner surface of the

sternum and ribs. The lung in other cases may be compressed or

retracted, uncovering the heart and rendering the chest-walls smaller.

The chest may be enlarged, especially if there is pleural effusion;

usually the contour is unchanged.

Pleural effusions are frequent in the history of this disease: they may

be passive, resulting from pressure on the azygos or hemiazygos veins,

preventing the return of the blood from the pleural veins, or from

mediastinal pressure. An inflammatory hydrothorax may be excited by the

deposit of cancerous material in the pleura; and it is possible for

these effusions to undergo purulent transformation or to become

hemorrhagic. A hemorrhagic effusion when grouped with other symptoms

may be considered an important evidence of malignant formation. The

further history of pleural effusions in this association is usually an

increase of such an amount as to necessitate removal by thoracentesis,

but reabsorption is possible.

SYMPTOMATOLOGY.--The interest of the clinical observer nucleates itself

around the symptomatology and diagnosis. The frequent negative results

of physical examination indubitably prove that its teachings alone are

insufficient for the purposes of diagnosis, so that any study of a case

would be partial which did not unite the evidence yielded by physical

signs with the general symptoms. The clinical evidences are more

definite when the {462} neoplasms are multiple and associated with some

mediastinal process than when single or absolutely primary growths. The

development of the disease is insidious. Gradually the facies and

general surface of a patient indicate the true nature of the malady by

the characteristic cachexia. Cough is an early symptom, unimportant

save that it cannot be assigned to any definite cause. It may be dry

and hard, attended only by expectoration of glairy mucus, or the sputa

may be purulent. Usually the amount is in ratio with the degree of

coexistent bronchitis. In the latter stages of the disease the sputa

may contain blood, resembling prune-juice or black-currant jelly, due

to erosion of some of the blood-vessels. In this stage of softening

cells characteristic of the new growth, with portions of the pulmonary

structure, may be found on microscopic examination of the sputa; the

appearance of the expectoration sometimes suggests fibrinous

bronchitis.

When there is elevation of temperature it may present a hectic type,

with night-sweats, which are stated by Walsh to be sometimes confined

to the affected side. The presence of an abnormal temperature-curve is

indicative of associated inflammation of the bronchial mucous membrane,

the development of a pleural process or of phthisis, especially the

fibroid form. The pulse becomes accelerated in ratio to the degree of

these inflammations and the failure of the sufferer's strength.

The new growth determines some mechanical symptoms cognate to all

intra-thoracic tumors, especially those which involve the mediastinum.

Lancinating pain would presumably be a constant symptom, but is, in

fact, infrequent, unless the growth or growths enlarge so as to cause

pressure on the nerve-trunks, in which event pain may become a

distressing symptom. Characteristic pains complicate those cases in

which the pleural tissues are involved in the morbid process. Dyspnoea

is a pressure-symptom of considerable import if other conditions

capable of producing it, especially uncomplicated emphysema, are

rigidly excluded. When the new formation is infiltrated throughout the

lungs, the growth may, as in miliary tubercle, impair the aërating

power of the lungs by diminishing their elasticity and increasing their

density. When, however, the process is local and restricted, the

dyspnoea may be due to irritation of the terminal filaments of the

vagus; this being a mixed nerve composed of accelerator and inhibitory

filaments, the balance of innervating power may be readily destroyed

and partial or incomplete respiratory effort follow. Dyspnoea may also

result from pleural adhesions or effusions, or may be secondary to

direct cardial or pericardial involvement in the cancerous process.

Palpitation or increased pulse-rate may be referred to irritation of

the vagi, or to some of the foregoing pathological processes.

Kindred to these symptoms are the changes in the voice, which sometimes

undergoes frequent variations due to irritation or pressure on the

trachea or on the branches of the pneumogastric nerve, especially when

mediastinal disease is present. Aphonia, huskiness, a bass voice, or

high treble, one or all, may be constant or alternating harbingers of

the concealed mischief. The laryngoscope will inform one whether there

is direct involvement of the larynx with morbid growth. Dysphagia is to

be expected if the new formation involves the regions through which the

oesophagus passes, and a sacculated pouch may be formed above the

compressed spot. Changes of posture may increase or diminish the

pressure, and thus the dysphagia or dyspnoea may at times be more

pronounced than at others. Dysphagia may also be due to swelling of the

oesophagus near the location of pressure. Reflex irritation of the

sympathetic ganglia may induce pupillary contractions in one or both

eyes: this symptom is chiefly present when the mediastinum is involved.

The physical signs contingent on pulmonary cancer include those

ordinarily indicative of bronchitis with or without atrophic emphysema,

simple pleural effusion, or chronic pleurisy with retraction. By

inspection a study {463} should be made of the contour of the thorax,

the respiratory movement, and displacements of the intra-thoracic

viscera. The thorax may appear enlarged, either from the new formation

or from associated pleural effusions. It is often retracted, owing to

the atrophic changes, and collapse brought about by the new formation

or induced by pleural adhesions. The movements of the chest, unless

there is a pleural complication, possess no distinctive character in

this disease. Displacements of the heart or trachea may be expected on

mechanical principles if there is mediastinal disease. General

inspection may detect in the clubbed fingers evidences of venous

obstruction, and sometimes an asphyxial hue of the upper portion of the

body. Nearly always a general emaciation with anxious expression

exists, and a tawny or lemon-hued skin indicative of the cancerous

cachexia.

By palpation of the substernal or supra-clavicular spaces one may reach

masses of painless, movable, glandular enlargement, but these may be

easily overlooked unless a careful study be pursued. Circumscribed

swellings of the thoracic walls may be detected, though not often, and

the glands of the axillæ and neck may enlarge. Palpation may also

reveal an inequality in volume between the radial pulses, but not so

commonly as in purely mediastinal tumors or in aneurisms. Percussion

and auscultation are negative or yield an area of dulness or flatness

with restricted or absent respiratory murmur. When there is a single

large growth the boundaries of these signs are local. If the tumors are

diffused the respiratory murmur varies. In tiers of lung it is feeble

or absent; elsewhere it is harsh, puerile, or bronchial. Chiefly

remarkable is the fact that the character of the respiratory murmur

cannot be harmonized with any other pulmonary states when the entire

clinical evidence is taken. Vocal resonance corresponds with the

respiratory murmur according to accepted laws. When there is pressure

on the principal bronchus on one or both sides, one can detect either a

snoring, increased bronchial respiration, or else, if the pressure

decidedly narrows the calibre of the bronchus, the breathing becomes

feeble or wheezing. Expiration may be prolonged and sonorous in

character, with or without râles. The pressure is rarely equal on the

two sides. The vocal resonance in these cases is ringing and brazen.

Mensuration corroborates inspection. Pleural effusion from whatever

cause is revealed by the ordinary signs. Enlargement of the bronchial

glands, either primary or coexistent with the development of cancer in

the lung, reveals itself by pressure-symptoms proportionate in their

severity to the degree of bronchial enlargement. Pain, laryngeal

irritation, differences in the radical pulses, tumor if the enlargement

is anterior, one or all, may be present. The aorta itself may be

compressed by the enlarged glands; and by the narrowing of its lumen

thrill, and even systolic, murmur can appear, making a differential

diagnosis from aortic aneurism very difficult. (Vide MEDIASTINAL

TUMORS.) Embolism and thrombosis, with the ordinary symptoms, may

complicate the course of pulmonary cancer and obscure the diagnosis.

A system of practical medicine. By American authors. Vol. 3 · 第 70 / 161 段