But this idiosyncrasy is by no means always an inherited one. It is

acquired as one of the results of profound disturbance of the nervous

system, such as is produced by moral causes, by temporary or recurrent

insanity, by wounds and injuries of the head, by the infectious

diseases, especially syphilis, enteric and typhus fever, and

small-pox, and by inflammations of the meninges.

What may be the precise mode of action of alcohol in the production of

its acute effects yet remains a matter of conjecture. It cannot be

doubted that its primary and direct action is upon the nervous system,

and that the circulation is secondarily but rapidly implicated. But it

is quite impossible to say, in the present state of knowledge, what

this action is. It has been suggested that certain chemical

modifications of alcohol in the blood, or of the blood itself in the

presence of alcohol, cause these phenomena; that aldehyde is the

active agent in their production; that the chemical changes by which

alcohol is transformed into aldehydes, acetic acid, and finally into

carbon dioxide, deprive the blood of the oxygen necessary for the

proper performance of the functions of the nervous system.

Unfortunately for these views, neither the presence of aldehydes in

the blood in acute alcoholism, nor these transformations themselves,

have yet been demonstrated, and a high degree of deoxygenation of the

blood is frequently observed in asphyxia, the inhalation of nitrous

oxide, etc., without the train of symptoms characteristic of the

condition now under consideration.

It is more than probable that varying conditions of the cerebral

circulation, secondary in themselves, have much to do in the causation

of certain symptoms. The experimental investigations of Bernard and

others have established the fact that during the period of excitement

there is actual congestion of the meninges. This condition is

transient, and reproduced after each repetition of the dose. After a

time, or if the dose at first be excessive, the congestion is

succeeded by anæmia.

PATHOLOGICAL ANATOMY.—Upon the examination of the bodies of persons

who have died by accident while drunk or in consequence of drunkenness

itself, deep congestion of the cerebral meninges, and especially of

the pia, has been almost constantly observed. In the pia effusions of

blood are occasionally encountered. The condition of the cerebral

{596} substance is not always the same. It is in a majority of the

cases more or less deeply congested, yet it presents in other

instances no appreciable departure from the normal state, and in a

smaller number still there is actual anæmia.

The sinuses and choroid plexuses are distended with dark blood; the

cerebro-spinal fluid is increased, and often tinged with blood; the

ventricles are distended with fluid, which not rarely has an alcoholic

odor. Occasionally the ventricles contain blood, and hemorrhage into

the substance of the brain has been observed.

The condition of the elementary nervous tissues after death from acute

alcoholism is not yet known.

The lungs are deeply congested, with small extravasations of blood

into their substance, and often œdematous. Congestion of the liver,

spleen, and kidneys in varying degrees of intensity is also seen. The

pancreas is usually deeply injected, occasionally the seat of large

extravasations of blood. The mucous membrane of the stomach is

invariably deeply injected when the alcohol has been introduced into

the organism in the ordinary manner. The observation of Caspar that

post-mortem decomposition takes place with diminished rapidity has

been denied by Lancereaux and others.

Other post-mortem conditions appear to be neither constant nor

characteristic. The stomach usually contains partially digested food

and alcohol. Lallemand, Perrin, and Du Roy observed, both during life

and after death, in the blood of animals subjected to experiments,

great numbers of minute glistening points, which upon microscopic

examination proved to be fat-globules. The same condition has been

observed in man, not only when death has taken place owing to acute

alcoholism, but also when it has occurred during the digestion of a

hearty meal without alcohol. The blood itself is often fluid and

dark-colored; the heart sometimes empty, sometimes containing a few

soft clots. Tardieu[22] states that in sudden death during drunkenness

pulmonary apoplexy and meningeal apoplexy, if not constant lesions,

are at least extremely frequent, and almost characteristic. Baer, on

the other hand, denies the occurrence of specific or characteristic

lesions.

[Footnote 22: “Observationes médicales sur l'Etát d'Ivresse,” _Annales

d'Hygiene publique et de Médecine légale_, tome xl.]

_C_. ACUTE POISONING BY ALCOHOL IN LETHAL DOSES.—The symptoms are much

modified when overwhelming doses of strong alcohol are introduced into

the organism at once or in the course of a short time. Here alcohol

produces death as an acute poison. The cases may be arranged in two

groups:

1. _Corrosive Poisoning_.—These cases are very rare. They are caused

only by undiluted alcohol, and depend upon the action of this agent in

coagulating albumen and disorganizing the tissues with which it comes

in contact by its affinity for the water which they contain. Absolute

alcohol is a powerful corrosive poison. It produces intense

phlegmonous inflammation of the œsophagus and stomach, with erosion of

the mucous membrane, accompanied by vomiting, diarrhœa with bloody

stools, prostration, and stupor. Death occurs by heart-failure. Among

the direct effects of large doses somewhat less concentrated are acute

and subacute gastritis with characteristic symptoms.

{597} Percy[23] injected by means of an œsophageal tube 90 grammes of

absolute alcohol into the stomach of a dog. Death followed in the

course of eight hours in consequence of violent gastro-intestinal

inflammation with ulceration. Dujardin-Beaumetz and Andigie found the

gastric and intestinal mucous membrane of dogs poisoned by alcohol,

red, deeply injected, and “presenting at certain points a black

coloration due to effused blood.” This fact they regard as worthy of

note, because in their experiments the toxic agent was introduced, not

by the mouth, but hypodermically, and they explain it by the

supposition—which appears to me warrantable—that it is due to

elimination by the mucous glands. Hence the congestion, softening, and

hemorrhage.[24] These observers also found that the symptoms were more

acute and the lesions more marked when poisoning was caused by propyl,

butyl, or amyl alcohol than when it was produced by ethyl alcohol.

[Footnote 23: _An Experimental Inquiry concerning the Presence of

Alcohol in the Ventricles of the Brain after Poisoning by that Liquid,

together with Experiments illustrative of the Physiological Effects of

Alcohol_, London, 1839.]

[Footnote 24: Chatin and Gublier have emphasized the fact that certain

poisons introduced by intravenous injection or by absorption through

the respiratory tract are eliminated by the intestines, with the

production of the same local symptoms as when administered by the

mouth (_Bulletin de l'Académie de Médecine_, Séance du 6 Novembre,

1877).]

2. _Acute Narcotic Poisoning_.—Much more common are the cases in which

death is rapidly produced by excessive doses of ordinary diluted

alcohol taken at once or rapidly repeated. This happens under various

circumstances, as when a drunkard avails himself of some favorable

opportunity to gratify to the full a bestial appetite, or upon a wager

drinks a number of glasses of spirits in quick succession or a given

quantity down, or when a man already drunk is plied by his companions

for pure deviltry. Suicide by this means is, in the ordinary sense of

the term, rare, and murder still more so. The latter crime has, as a

rule, been committed upon infants and children. Blyth[25] estimates

the fatal dose of absolute alcohol, diluted in the form of ordinary

whiskey, gin, etc., at from one to two fluidounces for any child below

the age of ten or twelve years, and at from two and a half to five

ounces for an adult. In the instance recorded by Maschka[26] two

children, aged respectively nine and eight years, took partly by

persuasion, afterward by force, about one-eighth of a pint of spirits

of 67 per cent. strength—about 1.7 ounces of absolute alcohol. Both

vomited somewhat, then lay down. Stertorous breathing at once came on,

and they quickly died. Taylor relates a case in which a quantity of

brandy representing about two fluidounces of absolute alcohol produced

death in a child seven years old.

[Footnote 25: _Poisons, their Effects and Detection_, Am. ed., New

York, 1885.]

[Footnote 26: Cited by Blyth.]

The symptoms are uniformly the same. The period of excitement is

transient or absent altogether; occasionally the patient falls at once

to the ground while in the act of drinking or immediately thereafter;

complete coma, interrupted by shuddering convulsions, may terminate in

the course of a short time in death. If the fatal issue be delayed,

there are vomiting and involuntary discharges; the respiration becomes

slow, embarrassed, stertorous; the heart's action is feeble and

irregular, the pulse almost or wholly imperceptible; the temperature

rapidly falls several degrees: 90° F. has been observed. The pupils

are dilated; insensibility and muscular resolution are complete. The

face is bloated, cyanotic; the {598} surface bathed in a clammy sweat;

the mucous membrane of the mouth often swollen and blanched. Vomiting

is usual, but not constant, and there is occasionally thin mucous

diarrhœa, the stools being mixed with blood. If the patient survives

any considerable length of time, acute superficial gangrene of the

parts most exposed to pressure is liable to take place. Recovery is

rare; its possibility is, however, increased in proportion as the

subject is of vigorous constitution, previous sound health, beyond the

period of childhood, not yet approaching that of physiological

decadence, and as treatment is early instituted and carried out with

judgment.

The diagnosis is difficult, almost impossible, in the absence of

witnesses: it is rendered still more obscure by the fact that this, as

other forms of alcoholic coma, may be complicated by cerebral or

meningeal hemorrhage and by cerebral congestion, in themselves

fatal—lesions the onset of which may have been the cause of mental

aberration leading to the commission of impulsive alcoholic excesses.

The prognosis, in the highest degree unfavorable in all cases, is

rendered yet more so by the occurrence of intense cerebral and

pulmonary congestions.

The lesions found post-mortem are those of acute alcoholism, already

described. As this form of alcoholic poisoning frequently occurs in

the subjects of chronic alcoholism, the lesions of that condition are

often encountered, and must be distinguished from those due to the

lethal dose. Nor must we overlook the fact that in the action of

alcohol just described we have to do with a process differing from

ordinary acute alcoholism in degree rather than in kind—a

consideration which tends to simplify our notions of the pathology of

alcoholism in general.

II. Chronic Alcoholism.

The prolonged abuse of alcohol brings about a series of changes which

affect alike the organism at large and its various structures. The

changes thus brought to pass are of the most varied kind, and depend

upon individual differences too manifold and complex for enumeration

and classification. Among the more important of these individual

peculiarities are those which relate to temperament, constitution,

hereditary predisposition, occupation, social position, personal

habits, tendency to or already-existing disease of particular organs

and systems, and the like. The degree of the pathological change is

determined by the strength and quantity of alcohol consumed and the

duration of habitual excess. The human body is capable of adapting

itself to the habitual consumption of large quantities of alcohol,

just as to other directly acting agents of an injurious nature, such

as foul air, bad drinking-water, and unwholesome food, or even to the

action of substances dangerous to life, as opium or arsenic, and yet

presenting for a considerable time the appearance at least of health.

Degeneration of the tissues of the body and disorders of its functions

are nevertheless surely produced. These alterations are not the less

dangerous to health and life because they are insidious and remain for

a time latent. Furthermore, like the habit of which they are begotten,

they are progressive, and sooner or later declare themselves in open

disease.

{599} The condition, whether latent or manifest, that is produced by

prolonged habitual alcoholic excess is designated chronic

alcoholism.[27]

[Footnote 27: The writer, although fully aware of its imperfections,

regards the above definition of the term as more in accordance with

the present state of our knowledge of the subject, and therefore more

useful, than any other that he has been able to find. It is scarcely

necessary to repeat here that the restriction of the term chronic

alcoholism to accidental or occasional manifestations of a permanent

state is misleading and unscientific. The same criticism is applicable

to the attempt that has been made to establish this condition as a

substantive disease, chronic, progressive, and characterized

anatomically by inflammatory, sclerotic, and steatogenous processes.]

The symptoms of this condition, when fully established, differ within

wide ranges in kind and degree. They are the manifestations of

derangements of the viscera, of the nervous system, and of the mind.

Varying among themselves according as the stress of the pathological

action has fallen upon one organ or another, forming combinations at

once curious and inexplicable, developing quietly, without event,

almost imperceptibly at one time, breaking into the most furious

paroxysms at another, they present for our study perhaps the most

complex of chronic morbid conditions. The chronic alcoholism which is

latent is not, therefore, always without symptoms. They are, however,

often slight and escape observation, or when manifest they are not

infrequently ascribed to other causes; or, again, their etiological

relations being concealed or overlooked, they are exceedingly obscure

and puzzling. This is especially the case in the chronic alcoholism

produced by the secret tippling of otherwise respectable persons, and

especially women.

To facilitate description, we shall consider the derangements of the

viscera, the nervous system, and the mind in regular order, according

to the scheme on p. 574. But the reader will observe that whatever may

be the prominence of particular symptoms or groups of symptoms in any

given case, all parts of the organism are involved, and that there is

no such thing as chronic alcoholism restricted to any particular

viscus or group of viscera, to the nervous system, or to the mind.

_A_. VISCERAL DERANGEMENTS.—There is nothing specific in the lesions

of chronic alcoholism. The chronic hyperæmia, steatosis, and sclerosis

induced by alcoholic excesses differ in no respect from those

conditions brought about by other causes. That which is specific is

the evolution of a series of morbid changes in the different

structures of the body under the influence of a common and

continuously acting cause. The digestive system is affected, as a

rule, long before the vascular or the nervous system.

1. _Local Disorders_.—_a_. Disorders of the Digestive System.—The

Mouth and Throat.—The action of insufficiently diluted alcohol upon

the mucous tissues is that of an irritant. The habitual repetition of

this action causes subacute or chronic catarrhal inflammation. The

condition of the tongue varies with that of the stomach. The mouth in

acute alcoholism is apt to be pasty and foul, the tongue slightly

swollen and coated with a more or less thick yellow fur; there is

often also an increase of saliva; in chronic alcoholism the tongue is

usually small, sometimes red, sometimes pale, often smooth from

atrophy of the papillæ, not rarely deeply fissured. In a word, the

condition of this organ is that seen in the various forms of subacute

or chronic gastritis. The salivary secretion is often notably

diminished, the sense of taste impaired. Relaxation of the throat and

{600} uvula and granular pharyngitis are common. Those who, whilst

leading a sedentary life, are inclined to the pleasures of the table

and a free indulgence in spirituous liquors often suffer from these

affections. Mackenzie[28] states that the worst cases of chronic

catarrh of the throat generally arise from the habitual abuse of the

stronger forms of alcohol. The associated influence of tobacco in the

causation of this group of affections is not to be disregarded.

[Footnote 28: _Diseases of the Pharynx, Larynx, and Trachea_, 1880.]

Lancereaux encountered ulceration of the œsophagus, and Bergeret a

case of narrowing of that organ, in chronic alcoholism.[29]

[Footnote 29: Peeters regards it as probable that the

connective-tissue hyperplasia and resulting stenosis seen in the

stomach as a result of the action of alcohol may also occur in the

œsophagus.]

The Stomach.—In addition to functional dyspepsia, which is scarcely

ever absent in chronic alcoholism, all forms of gastritis, from simple

erythematous inflammation of the mucous membrane to sclerosis and

suppurative inflammation of the stomach, are encountered. Armor[30]

assigns to the habit of spirit-drinking, especially to the habit of

taking alcohol undiluted on an empty stomach, a high place among the

causes of indigestion. He regards this habit as a prominent factor in

the production of chronic gastric catarrh—a condition very frequently

present in indigestion. This observer also regards the excessive use

of alcohol as the most frequent among the direct exciting causes of

gastric inflammation in this country, exclusive of acid or corrosive

poisons. Next to errors in diet as a cause of chronic gastritis he

places the immoderate use of alcohol, especially by persons whose

general health and digestive powers are below a healthy standard. The

primary lesions are vascular dilatation and hyperæmia. The mucous

membrane is discolored, red or bluish, in scattered patches of varying

size, with occasional ecchymoses of a bluish hue or spots of

pigmentation. These patches occupy more commonly the region of the

cardia and the lesser curvature. Vascular injection is conspicuous;

the veins are dilated, tortuous; the mucous glands hypertrophied; the

surface covered with thick, ropy, acid-smelling mucus. After a time

permanent changes in the mucous membrane are set up. It undergoes

atrophy or softening; or, again, it becomes hardened, thickened, and

contracted, its rugæ more prominent, its surface mammilated—sclerosis.

Grayish-brown pigmentation, the remains of former

blood-extravasations, is seen at many points. Minute retention-cysts

are formed in consequence of the occlusion of the ducts of certain

glands. The submucous connective tissue and the muscular coat

occasionally undergo, in consequence of prolonged gastritis, local

hypertrophy.

[Footnote 30: See this _System of Medicine_, Vol. II. pp. 446, 464,

470.]

Acute suppurative inflammation of the stomach, with purulent

infiltration of, or the formation of abscesses in, the submucous

tissue, has been met with in drunkards. It is extremely rare, and

results from the violent irritant action of large doses of strong

alcohol in subjects debilitated by previous excesses.

Gastric ulcer is much more common. The abuse of alcohol is regarded as

an indirect cause of this lesion by the majority of writers. In the

present state of knowledge alcohol as usually taken can scarcely be

regarded as a direct cause of ulceration. Nevertheless, gastric ulcer

is relatively {601} common in alcoholic subjects. Leudet[31] found

gastric ulcer in 8 of 26 necropsies of drunkards. Baer and Lentz also

regard the abuse of alcohol as a very common cause of ulceration. The

ulcers are usually superficial, occupy by preference the neighborhood

of the cardia and the lesser curvature, and are apt to be multiple. In

these respects they differ from simple gastric ulcer. The latter

lesion is also probably as frequent, if indeed not more frequent, in

individuals dying of chronic alcoholism than in others.

[Footnote 31: _Clinique médicale de l'Hôtel Dieu à Rouen_, 1874.]

The view formerly entertained that alcohol was an important cause of

cancer of the stomach has been shown by Kubik, Magnus, Huss, Engel,

and others to be untenable. Carcinoma ventriculi is rarely associated

with chronic alcoholism.

The dimensions of the stomach are rarely normal. Dilatation is usually

present in the early stages, and in beer-drinkers throughout; in the

advanced course of alcoholism due to spirit-drinking the organ

undergoes, in consequence of changes secondary to prolonged

inflammation, more or less contraction, which is in many cases

irregular.

Dyspeptic symptoms are common: the appetite is variable, irregular,

and at length wholly lost. There is especially distaste for food in

the morning. This, together with the disordered state of the

secretions of the mouth and a feeling of nervous depression on rising,

leads to the disastrous habit of taking spirits early in the day.

Gastric digestion is performed with difficulty; it is accompanied by

sensations of distension and weight, by flatulence and acid

eructations. Heartburn is a common symptom. The drunkard is not rarely

tormented by an uneasy craving or sense of emptiness in the region of

the stomach, which he temporarily allays by nips and pick-me-ups and

morsels of highly-seasoned foods at odd times, with the result of

still further damage to his digestion and the complete loss of

appetite for wholesome food at regular hours. In the course of time

the characteristic morning sickness of drunkards is established. On

arising there is nausea, accompanied by vomiting—sometimes without

effort or pain, at others attended by distressing retching and

gagging. The matter vomited consists usually of viscid mucus, at first

transparent, then flaky, and at length, if the efforts be violent, of

a green or yellow color from the admixture of bile. These symptoms

ordinarily do not recur until the following day. In other cases

vomiting is more frequent, recurring at irregular periods during the

day, and not uncommonly an hour or two after the ingestion of food.

When gastric ulcer is present, portions of the vomited matter are

often dark and grumous like coffee-grounds or the settlings of

beef-tea, and are found upon microscopic examination to contain

blood-corpuscles. Actual hæmatemesis may also occur under these

circumstances, and be repeated from time to time. The quantity of

blood thrown up is frequently small; at times, however, it is

excessive, and occasionally so great as to cause death.

Common as are the evidences of gastric disturbance in chronic

alcoholism, they are far from being constant, and it is worthy of note

that in proportion to the number of the cases serious gastric

affections are, except in the later stages, relatively infrequent.

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