Carl Vernon Weller

The syndrome of abdominal aortic aneurysm rupturing into the gastrointestinal tract: Summary of the literature and case report

Abstract With the new case, which is reported in this paper, forty-one examples of rupture of an aneurysm of the abdominal aorta into some portion of the gastrointestinal tract are known to be available in the literature. In 71 per cent, rupture was into the third portion of the duodenum. The condition has been six times more frequent in men than in women. While the ages were widely distributed, the occurrence of eight cases between 27 and 32 years-of-age indicates the importance of this condition in relatively young patients. The resulting syndrome combines the features of abdominal aneurysm with those of profuse hemorrhage into the gastrointestinal tract. Hematemesis, often with abundant hemorrhage from the rectum, usually marks the onset of the terminal phase.

Pathogenesis of trichinous Myocarditis.

Several authors have recognized and described the histopathology of the parenchymatous lesions and accompanying myocarditis which are seen in the hearts of human cases of trichinosis dying in the fourth to eighth week of the disease. The importance of these lesions in the production of the circulatory failure, which is the cause of death in these cases, has been emphasized. 1 All who have had opportunity to study such material have noted the absence of encysted larvae in the heart muscle even though the skeletal muscles showed at the same time very many encysting and encysted organisms. Almost all of those who have searched sections prepared from such hearts have failed to find larvae present at all. Only Zenker 2 and Frothingham 3 saw them in the human heart, but Graham, 4 working with rats, described lesions similar to those in human cases and in addition found embryos associated with the inflammatory foci. This complete absence of encysted forms with but meager evidence even of the presence of larvae, has led to uncertainty as to the pathogenesis. Simmonds 5 concluded that the myocarditis was due to a toxin produced by the trichinae and brought to the heart in the circulating blood. In the present study, series of white rats were fed, in approximately known numbers, the larvae digested (McCoy 6 ) from trichinous meat. Animals were killed at appropriate intervals and both fresh, teased preparations and stained sections were made from their tissues. The myocardium showed alterative and exudative lesions in all respects comparable to those found in human hearts. Trichina embryos were found in these foci as early as 5 days after feeding and for some time thereafter.

Histological study of the testes of guinea pigs showing lead blastophthoria. Preliminary report

In an earlier report we have shown that the continued administration of small doses of lead produces a definite blastophthoric effect in male guinea pigs; and that the lead blastophthoria thus induced manifests itself in the offspring by a reduction of approximately twenty per cent, in the average birth weight, by an increased number of deaths in the first week of life and by a general retardation in development such that the offspring of lead-poisoned males often remain permanently underweight. The testes of these chronically lead-poisoned guinea pigs have now been examined in sufficient numbers to warrant a preliminary report. In a majority of the cases examined no histological differences can be detected between the testes of lead-poisoned guinea pigs and those of normal controls. Spermatogenesis appears to take place along normal lines and at a rate which seems not unlike that in normal pigs. This observation is in no degree incompatible with a state of true blastophthoria since it is to be expected that if fertilization takes place at all, the spermatozoa will show no great variation from the normal as far as their appearance is concerned. The reason for the inferiority of the offspring is to be sought rather in qualitative changes in the germ plasm. In a limited group of instances, in which the male guinea pigs became sterile during the administration of lead, histological examination of the testes shows a complete aspermatogenesis with marked atrophy and vacuolar degeneration of the germinal epithelium. There is an attempt at cell division which results in multinuclear giant cells, evidently comparable to spermatocytes, but division of the protoplasm appears to lag behind that of the nuclei and spermatids and spermatozoa are not produced.

Testicular changes in acute alcoholism in man and their relationship to blastophthoria

The blastophthoric effect of acute and chronic intoxications has been studied in the past chiefly by means of breeding experiments, in the course of which it has been shown that such agents as alcohol and lead can produce a definite blastophthoria without histologically demonstrable lesions in the germinal epithelium. By the same and other workers, it has been shown, however, that if the intoxication with these agents be increased, or if the subject be peculiarly susceptible, the germinal epithelium (male) may be made to exhibit degenerative changes, shown by atypical spermatogenesis or even by marked vacuolar degeneration and complete aspermatogenesis. It must be assumed as a working hypothesis that with any agent producing such demonstrable changes in the spermatogenetic process there is an earlier period in which spermatozoa showing less morphological deviation from the normal and capable of fertilizing are produced. Of great importance in this connection is the work of Widakowich 1 who has shown that the semen of syphilitics often contains increased numbers of atypical spermatozoa showing two, three or four heads; two, three or four tails, or combinations of such failures to divide. He notes also the occurrence of microcephalic and macrocephalic types. In human material it is almost impossible to determine the relative effects of chronic and of acute alcoholism; so that, while the earlier literature specifies in almost all cases that the changes found are those of chronic alcoholism, the more acute degenerative changes and disturbances in spermatogenesis that have been described may be chiefly due to the acute exacerbations. In investigation of this point five coroners autopsies were selected having in common the facts that death occurred in, or immediately after a period of severe alcoholic intoxication and that the testes did not show interstitial or vascular fibroid changes such as might be expected if a severe intoxication of any sort had been long operative.

The experimental production of a relative immunity to the cerebral manifestations of lead poisoning

When guinea pigs are poisoned with lead in the form of commercial white lead administered by mouth in capsules, with a daily dosage of about 300 mg. per kilo of animal, convulsions result on about the fourth day. These convulsions are highly characteristic, being epileptiform in character and exhibiting both clonic and tonic phases. Such animals may die in the first, or in subsequent convulsions, or, if the administration of lead be stopped, they may recover. If a resting period of sufficient length be allowed after the cessation of convulsions, the survivors will be found to have acquired a partial immunity in respect to the cerebral manifestations of lead poisoning, so that they may be given a larger number of doses of the same size as those first used without producing convulsions. If this process be repeated, the amount of lead which can be administered without producing convulsions may be greatly increased. A limited number of animals thus prepared have reached a point at which four times the usual convulsion-producing dosage has been given without convulsions resulting. During each of the longer periods of administration the usual loss of weight, cachexia and muscular weakness develop, indicating that whatever immunity is produced is against a local action of lead and not against its general toxic effect. There has been noted a marked individual variation in the ability of animals to develop this relative immunity, and in certain instances death has occurred unexpectedly in animals well along in the course of lead administration. The experimental evidence thus obtained is in accord with the belief of some of the older writers upon lead encephalopathy, that the manifestations of this condition are more apt to be shown by those relatively new to a particular lead hazard than by those who have been long exposed to lead, Clinically, there are found numerous exceptions to this rule, although our experimental results indicate that it is founded upon a scientific basis.

The experimental production of lead gangrene in guinea pigs

Kazda 1 has reported three clinical cases of gangrene of the feet in relatively young typesetters. These he believes to be the first clinical observations of lead gangrene. Similar experimental results have been obtained by us in guinea pigs which have received large amounts of white lead by mouth. In this animal there can be produced a dry gangrene of the ears. The extreme margin of the pinna becomes slightly shrunken with a hyperemic zone proximal to the border. The margin to a varying depth becomes necrotic, drys down and is finally cast off, leaving an irregular margin which is somewhat thickened. The condition is usually bilaterally symmetrical. This result has been obtained only in those animals which have received an unusually large amount of lead, such as is made possible by the method described in the preceding communication. That it has not been observed hitherto is apparently due to the fact that it has been impossible to administer a sufficient amount of lead without killing the animal through lead convulsions. The induction of a partial immunity makes this possible.

The toxic action of dichlorethylsulphide (“mustard gas”)

The investigations recorded in these two papers are founded upon numerous series of animal experimentations and also clinical observations of human mustard gassing. 1. Local Action: Skin.—Dichlorethylsulphide (“mustard gas”), in liquid or in vapor form, even in very low concentrations, is an escharotic poison for the animal tissues (skin, conjunctivæ, cornea, mucous membranes of respiratory and gastrointestinal tracts) with which it comes in direct contact. The degree of the injury is proportionate to the concentration of the gas, the time of exposure, individual susceptibility, and local physical conditions, such as moisture, sweating, warmth, pressure and friction. The escharotic action is, for the greater part, painless, the anesthetic effect being especially notable upon the skin; while upon the mucous membranes its action may be more irritant, probably chiefly reflex in character. The cutaneous surfaces most susceptible are those with thinner, more delicate skin, well supplied with sweat glands and hair follicles, where sweat may collect, and which are exposed to friction or pressure, such as the axillæ, flexor surfaces, genitals, inner surface of arms and corresponding surface of trunk, inner surfaces of thighs, between the fingers, etc. There is a penetration of the gas into the sweat and sebaceous glands, and a re-solution of mustard gas vapor into the sweat or sebum occurs. The injuries are particularly striking in their insidious, slowly progressive development, becoming first apparent only some hours after the exposure. Upon human skin the lesion appears as a hyperemia, followed by vesication, eschar formation, sloughing and slow healing, with more or less pigmentation. Depilation may occur; in severe cases the eschar may extend entirely through the corium into the subcutaneous tissues. Secondary infection and gangrene of the eschars occur invariably in cases not properly treated. Milder lesions may show only the earlier stages of hyperemia, vesication or pigmentation. In general the injuries may be classed as burns of first, second or third degree.