Carbon Monoxid Research Articles

Resuscitation from carbon monoxid asphyxia, from ether or alcohol intoxication, and from respiratory failure due to other causes

Resuscitation from carbon monoxid asphyxia, from ether or alcohol intoxication, and from respiratory failure due to other causes

EXSANGUINATION-TRANSFUSION

The treatment of the severe toxemias accompanying many of the diseases of childhood constitutes a problem of great difficulty. In those cases in which the toxemia arises from a suppurative focus, surgical drainage, by removing the source of the toxin, usually meets the requirements of the case. But in the majority of instances, the toxemia arises from a source which cannot be attacked surgically (for example the toxemia of severe superficial burns, of erysipelas, or of acute intestinal intoxication), and in such cases the problem of treatment assumes quite a different aspect. The method advanced in this paper for the treatment of such toxemias was suggested during the campaign of 1916 in France by observing two cases of soldiers suffering from severe carbon monoxid poisoning. They were treated by venesection, followed by blood transfusion, and made surprisingly rapid and complete recoveries. Apparently, the removal of a portion of the damaged

THE RELIEF OF INTRACRANIAL SYMPTOMS IN CARBON MONOXID ASPHYXIA

The growing menace of carbon monoxid as a source of hazard to mankind in various walks of life is beginning to find widespread appreciation.¹A danger that was formerly confined largely to poisoning with illuminating gas through accident or with suicidal intent has been greatly extended by the advent of the automobile, the exhaust gases of which contain carbon monoxid. Not only does asphyxiation from the gas occur with alarming frequency today, but there are signs that a subacute asphyxiation from the same cause may be far more common than has heretofore been supposed. The incipient symptoms include headache, fatigue, nausea and disturbances of temper. The precise causation is by no means entirely clear. In severe carbon monoxid asphyxiation, the chief damage is usually wrought on the central nervous system. This apparently selective action of the gas has led, as Haggard²has pointed out, to the belief that

MULTIPLE NEURITIS FOLLOWING CARBON MONOXID POISONING

In recent years, quite a number of contributions to the literature have appeared describing the changes in the central nervous system which result from carbon monoxid poison. The most constant of all these pathologic findings is bilateral softening of the globus pallidus. Cortical changes, while not nearly so common, have been described. 1 Multiple neuritis as a sequel to gas poisoning has been reported clinically, but satisfactory pathologic examination of the peripheral nerves is practically unknown. Starr, 2 Jelliffe and White, 3 Krantz, 4 Brissaud, 5 Lancereaux 6 and Glynn 7 have cited clinical cases of multiple neuritis secondary to carbon monoxid poisoning. Stewart 1 reported that the seventh and tenth nerves in a case of gas poisoning were intensely degenerated, this being especially true of the tenth. He did not examine nerves from the extremities. Claude and Lhermitte 8 tried to produce multiple neuritis in dogs by the use

CEREBRAL EDEMA AND HEADACHE FOLLOWING CARBON MONOXID ASPHYXIA

INTRODUCTION The purpose of this investigation has been to learn something of the physiologic mechanism causing a particular symptom: the headache suffered by persons exposed to carbon monoxid gas. Headache from this cause is extremely common among workers in special occupations: automobile repairing, blast furnace work, mining, etc., and with the increasing problem of motor exhaust gas in our city streets,1it becomes of especial interest to learn more exactly how the central nervous system is affected. This question is not only of clinical interest, but is of particular interest from a purely physiologic point of view. Carbon monoxid has been widely used by physiologists as an agent to produce anoxemia, and the laws governing its absorption and liberation from the blood have been carefully studied. By clinicians its action has been less well understood, but it has been thought by several authors to be directly toxic to nervous

CHRONIC CARBON MONOXID POISONING

The tragic results of acute carbon monoxid poisoning are so manifest, and the clinical aspects have been so thoroughly studied, that nothing will be said about this phase of the subject. Chronic carbon monoxid poisoning, on the other hand, although for a long time recognized, has not been given the attention it deserves by the medical profession; and, without a doubt, a considerable number of ailments and indispositions, not severe enough to be considered seriously, occur every year in a community that may be directly due to this ubiquitous gas, so characteristic of twentieth century civilization. The Ohio State Department of Health¹reported eighty-one cases of carbon monoxid asphyxiation, with thirty-four deaths, during the first ten weeks of the past winter. If this is true of carbon monoxid asphyxiation, how many are the cases of moderate and mild degrees of poisoning which are not reported or even suspected? That

THE TREATMENT OF CARBON MONOXID ASPHYXIA BY MEANS OF OXYGEN + CO2 INHALATION

At a meeting of the Commission on Resuscitation from Carbon Monoxid Asphyxia on Nov. 15, 1921, the writers were appointed a subcommittee to conduct investigations both in the field and in the laboratory on the treatment of carbon monoxid asphyxia by the inhalational method, to be here described. There is already available a considerable mass of theoretical knowledge and experimental material on which to base further advance along the line indicated. Recent investigations in this laboratory¹have confirmed the correctness of the view that carbon monoxid has no direct toxic action on the brain, or other organs or tissues of the body, except only the blood. It acts wholly through its combination with the hemoglobin or red coloring matter of the blood. When so combined, the hemoglobin is for the time deprived of the power to transport oxygen from the lungs to the tissues of the body. A condition

Effects of Carbon Monoxid upon the Eye

This paper gives a general survey of the subject and includes a graphic description of the subjective and general nutritional effects of carbon monoxid poisoning, by one of the victims; and incidentally throws light on the origin of a story of a haunted house. It gives an account of the ocular symptoms of such poisoning, revealing a distinct tendency of the poison to cause neuritis and especially to affect the optic nerve.

BLOOD VOLUME IN PERNICIOUS ANEMIA

Blood volume in pernicious anemia has been studied but little, and the results obtained have been at considerable variance. Of the literature concerning blood volume, only that portion bearing on pernicious anemia is considered in this paper. Various methods have been followed, such as the dye method of Keith, Rowntree and Geraghty, 1 the carbon monoxid method of Haldane and Smith 2 and those methods such as Quincke's 3 and Lindeman's, 4 based on the consideration of the red cells before and after transfusion. The dye method of Keith, Rowntree and Geraghty is based on the concentration in the blood of a dye injected intravenously which remains in the circulation for a long time. From this the plasma volume can be calculated and by the hematocrit readings the total blood volume determined. In three determinations made in cases of pernicious anemia they found the total volume in two to be decreased and in the

ACQUIRED DOUBLE ATHETOSIS

In 1916 I1reported several cases of a disorder occurring in one family, which seemed to me to belong to the group known as pseudosclerosis, probably a family form of a lesion of the lenticular nucleus, and in that paper I grouped the various disorders attributed to disease of the lenticular nucleus. These were the pseudosclerosis of Westphal and Strumpell, Huntington's chorea, Parkinson's disease, spastic pseudobulbar palsy with contractures and choreo-athetoid movemeunts of Oppenheim and Vogt, and Freund and Vogt, Oppenheim's dystonia musculorum deformans, and double athetosis. To this list I added von Bechterew's hemitonia apoplectica and certain forms of carbon monoxid poisoning, and I am inclined to add a certain form of paramyoclonus multiplex resulting from lethargic encephalitis. To the list might also be added arteriosclerotic muscular rigidity and certain forms of senile dementia, which Strumpell thinks belong to his amyostatic syndrome. He refers to a paper on

THE DETERMINATION OF HEMOGLOBIN BY THE ACID HEMATIN METHOD

In the course of a study of the blood in the anemias of infancy, certain discrepancies were encountered in the acid hematin method of determination of hemoglobin described by Sahli. 1 The study of the cause of these discrepancies has led to a modification of the method to produce accurate determinations comparable with those obtainable when a determination of hemoglobin by measuring its iron content, or by the carbon monoxid hemoglobin method, is made. These modifications consist in: first, the use of N/10 hydrochloric acid as the diluent of the acid hematin instead of water; and second, the employment of heat to bring the reaction of formation of the acid hematin to its endpoint of equilibrium more quickly than it occurs in the cold. Since the introduction of the acid hematin method by Sahli, various criticisms of it have been made. From the mechanical side these have been well summed up

A CONTRIBUTION TO THE HISTOPATHOLOGY OF EPIDEMIC ("LETHARGIC") ENCEPHALITIS

The various symptoms of epidemic (lethargic) encephalitis—somnolence, stupor with or without slight elevation of temperature, together with ocular and other cranial nerve paralyses, etc., may occur in many cerebral disorders. We may mention the hemorrhagic superior polioencephalitis of Wernicke, the cerebral form of poliomyelitis, the sickness caused by trypanosomiasis, syphilitic meningitis, paretic dementia, encephalitis caused by anthrax (Fulci1) or other infectious diseases, as tuberculosis, cerebrospinal meningitis and especially influenza. Here also belong cases of poisoning with carbon monoxid, sulphuric acid (Wernicke2) and meat and fish (botulism). Any of the types of encephalitis mentioned may so resemble the clinical picture and course of the epidemic (lethargic) form that they, undoubtedly, have been and are confounded with the latter. Especially striking is the clinical similarity between encephalitis and the sickness caused in man by theTrypanosoma gambiense, hence lethargic encephalitis is popularly called sleeping sickness. In

PITUITARY HEADACHES AND THEIR CURE

Headache as a symptom is well known to all. The patient who complains of it is too often given a cathartic and aspirin and dismissed without adequate study to determine its true etiology. He may then go elsewhere and return after he has developed more definite signs. I remember one patient who returned four days later with the complete picture of a tuberculous meningitis. Headache commonly presents itself to us as the symptom of some systemic disease, such as circulatory disturbance, especially hypertension, nephritis, anemia, an acute febrile disease, or poisoning by various toxic substances. These may be exogenous or endogenous; for example, lead, carbon monoxid, alcohol, or the toxins resulting from acidosis, diabetes, uremia, or from the gastro-intestinal tract. Syphilis is a frequent cause of headache. There are likewise local causes in disturbances of the cerebral circulation, a myositis of the occipitofrontalis muscle, periostitis or gumma of the cranium

CHANGES IN THE BRAIN IN GAS (CARBON MONOXID) POISONING

This subject is important for three reasons: Carbon monoxid is liberated by bursting shells and therefore is one of the gases responsible for mortality in the present war. Deaths, accidental and suicidal, from inhalation of illuminating gas are increasingly frequent in civil life.1Henderson2states that carbon monoxid causes more deaths than all other gases combined. There is a reason to believe that a higher carbon monoxid content in illuminating gas is in part responsible for this. Statistics of certain cities of Great Britain3indicate that the higher percentage of such deaths parallels the greater proportion of water gas used in the manufacture of a cheaper product. Carbon monoxid poisoning is of medicolegal significance. A history is not always available, and the characteristic cherry-red color of the blood and chemi- cal proof of carbon monoxid are aids to diagnosis only in the first few days after poisoning. Kolisko4in

THE BLOOD IN CARBON MONOXID POISONING

<h3>To the Editor:</h3> —In an excellent summary of the present knowledge of carbon monoxid poisoning (The Journal, Aug. 19, 1916, p. 580), Prof. Yandell Henderson of Yale University suggests that "asphyxial coma... indicates an intense acidosis." No data were offered to support this conclusion, nor have I, in a cursory examination of the literature, been able to find evidence on this point. Through the courtesy of Dr. Joseph Roby, I have recently had an opportunity of studying the blood of a person suffering from intense carbon monoxid poisoning. The patient was a country girl, aged 17 years, residing in a boarding house. She had just come to the city to attend school, and was not familiar with the operation of gas fixtures. One night, through some inadvertence, she left the gas cock partly open. When found, she was unconscious and pulseless. She was taken to the hospital, where stimulants were

ILLUMINATING-GAS POISONING

I. THE EFFECT OF FORMALDEHYD ON TESTS FOR CARBON MONOXID IN THE BLOOD In an examination of the blood from the body of a man in which post-mortem showed evidences of poisoning with illuminating gas (especially a brilliant red color of the muscles and blood), the question arose whether formaldehyd, used in embalming the body four days previously, would in any way modify or inhibit the various reactions ordinarily used to demonstrate the presence of carbon monoxid hemoglobin. A careful study of the literature failed to reveal any previous note on this subject, which may well be one of practical interest, especially in cases of a medicolegal nature. The following preparations were studied by the spectroscope and by means of various chemical tests, which will be discussed individually: (1) the blood of the body examined post mortem after formaldehyd embalming; (2) normal blood; (3) normal blood containing formaldehyd solution; (4)

STUDIES ON WATER-DRINKING

Considerable investigating has been done on the influence of copious water ingestion on the chlorid excretion of fasting animals. The work of Forster 2 is often quoted in this connection. In one instance this investigator increased the urinary chlorid output from 0.175 gm. to 0.992 gm. by causing a dog to ingest 3 liters of water on the eighth day of the fast. This is the most pronounced increase in the chlorid excretion yet reported as following the ingestion of large volumes of water. From a series of investigations on dogs in which different animals were subjected to the influence of external hemorrhage or to the influence of poisoning by phosphorus or by carbon monoxid Kast 3 later came to the conclusion that there was a very close relationship between increased protein catabolism and the augmented chlorin output accompanying such catabolism. Inasmuch as the procedure of Kast rendered his

THE DANGERS OF THE DOMESTIC USE OF ILLUMINATING GAS AND THE MEANS OF AVOIDING THEM.

The employment of illuminating gas manufactured from coal is about a century old. The original method, exclusively in vogue for many years, was by destructive distillation of soft coal. The operation is simple: The coal is heated strongly in a closed vessel, and the gases produced are cooled, purified and distributed. The impurities of the crude gas are numerous, but of only few types. Ammonium compounds and sulphur compounds are the most objectionable, and much attention has been given to devising methods for their removal, which in well-operated works is satisfactorily accomplished. The purified gas as conducted into the storage tanks consists principally of hydrogen and hydrocarbons, among the latter being methane, ethene and benzene. Some carbon monoxid is also present. Laboratory experiment and clinical experience have shown that gas made in this manner has not very high toxic qualities. The hydrocarbons and hydrogen are rather negative than positive. They

THE GLYCOSURIC SYMPTOM OF DISEASE AND ITS MEDICINAL TREATMENT.

An unusual amount of grape sugar in the urine is by no means an absolute indication of the presence of diabetes mellitus; it may be concomitant with, or sequential to, various other transitory, as well as chronic, anomalies. Thus glycosuria in its alimentary form e saccharo may be induced in the presence of various traumatic and non-traumatic neuroses; of alcoholism; of Graves' disease; of gastrointestinal disorders, as hyperacidity; of hepatic affections, etc. Glycosuria, mostly of the spontaneous transitory type, may appear after injury and extirpation of less important organs; after ether and chloroform anesthesia; after administration of drugs and chemicals like phloridzin, mercuric bichlorid, chloral, morphin, strychnin, amyl nitrite, curare, thyroid preparations, adrenalin, etc.; after inhalation of carbon monoxid; after the excessive use of tobacco; during the luetic process, and during or after infectious diseases. Generally speaking, non-diabetic glycosurias are the result of intoxications, that is, of slight or graver