THE AMBULATORY PNEUMATIC SPLINT.— The attention of the profession is called to the advertisement of the Ambulatory Pneumatic Splint which appears on advertising page 32 of this issue of the News. No doubt every physician or surgeon has from time to time in his practice cases where this ingenious mechanical device constructed strictly upon scientific principles and endorsed by leading surgeons of this country, could be made use of to great advantage to their patients. It will be worth their while to look into this and to write for descriptive literature, special prices and to thoroughly understand one of the most recent advances made along surgical lines.

An Efficient Formula for Use in Rhinitis.


During the changeable spring weather it is no unusual matter for the physician to be called upon by his patients to treat their nasal troubles, among which the most common is, beyond all doubt, that catarrhal inflammation of the Schneiderian membrane, which is currently called rhinitis. It is that form which is not only annoying, but very often painful. Among the symptoms which may manifest themselves are pruritus as well as an aceompanying anosmia, both of which are exceedingly unpleasant to those so affected. There are many practitioners who begin treating such cases by at once cauterizing the mucosa with stick nitrate of silver, with chromic acid, with the acid nitrate of mercury or even with the galvano cautery.

These are methods which are but seldom indicated and should but rarely be employed, as the results of their use culminate in scars and a disagreeable condition of the nasal cavity with the constant formation of crusts.

Not long since I had occasion to see and examine some patients affected with such catarrhal rhinitis and the appearance presented was that of an angry-looking mucous membrane whose secretion was pronounced and inclined to become purulent. In all of these the patients were ordered to take appropriate tonic remedies and for local application the following was ordered to be applied three or four times daily: RIIvdrar. bichlor. Katharmon.

.. 5 vi. V. Sig.: t'ae four times daily in nose.

This acted like a charm and in a comparatively short time my patients reported themselves well. It would not be a bad idea to combine white liquid hydrastis with the above; but, above all, see that there is a liberal amount of katharmon, for that is the ingredient that does the work. Those colleagues who will employ the above formula will find it among the valuable ones they pos

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Published monthly at Austin, by THE TEXAS MEDICAL NEWS PUBLISHING

COMPANY. Subscription, $1.00 a year, in advance.

MATTHEW M. SMITH, M. D., Managing Editor.
JAMES M. LOVING, M. D., Assistant Editor.


T. J. BENNETT, M. D., Austin, J. W. MCLAUGHLIN, M. D., Galveston, E. D. OAPPS, M. D., Fort Worth, A. M. ELMORE, M. D., Dallas,

G. B. FOSQUE, M. D., Waco, R. W. KNOX, M. D., Houston,

WM. E. LUTER, M. D., San Antonio, H. A. BARR, M. D., Beaumont,

A. O. SCOTT, M. D., Temple.



No. 6.

Original Articles.

CONTRIBUTED EXCLUSIVELY TO THIS JOURNAL. The Management do not hold themselves responsible for the views of their corre spondents.

Written for The Texas Medical News.

Hepatic Therapeutics.


The treatment of the liver has to be considered from two standpoints, medicinal and hygienic. The medicinal treatment of the liver is but little understood, being confined to the use of a few drugs, the effects of which are irregular, owing to our being unable to distinguish the different pathologic conditions. Excluding the surgical diseases of the organ and those of the biliary passages, the pathology of hepatic disease can be summed up under the heading of cirrhosis, a condition which is always the result of an infection of toxemia. The hepatic cirrhoses are divided into two classes --those in which the lesions are simply a connective tissue growth,

* Original Lecturer on. Neurology and Psychiatry, and Lecturer on Physiologic Chemistry at the University of Maryland; Pathologist to the Maryland Asylum and Training School for Feeble Minded Children; late Pathologist to Mount Hope Retreat.

a simple sclerosis, and those in which the sclerotic changes are accompanied by lesions of the hepatic cell. Toxic cirrhosis may be due to an autointoxication or to a heterointoxication, the former being associated with digestive disturbances, gout, diabetes, etc., the latter exemplified by alcohol, lead or phosphorus poisoning; the one associated with hypertrophy, demonstrating the resistance and effort at compensation of the sick organ. Infectious diseases, as malaria, syphilis, etc., produce cirrhosis, usually affecting the biliary system, Hanot's hypertrophic cirrhosis being typical of this form. There are cirrhoses due to mechanical causes, as those associated with cardiac diseases.

Cirrhoses in which there is simply a growth of connective tissue do not long continue without affecting the liver cells, producing fatty, amyloid, or pigmentary degeneration, causing more or less grave derangement of cell function. During the progress of the disease they cause three modifications of function-exaggeration, diminution, and perversion. As a rule the exaggeration and perversion of function are transitory conditions; they are represented by hypertrophic toxic cirrhosis, the result of the resistance of the organ to the disease, but the overtaxed cells gradually succumb to the hyperfunction entailed, and hepatic insufficiency follows; the nature of the perversion or exaggeration controlling the precise form of insufficiency which results. Hepatic insufficiency may exist without demonstrable cell alteration; more often it is symptomatic of distinct lesions, but it means that the organ is unable to fulfill its normal functions. The functions of the liver may be divided into four groups:

(1) Circulatory. The liver destroys the erythrocytes, playing the part of a regulator to the composition of the blood. It holds iron in reserve, obtaining it from the destroyed cells and from the food.

(2) Glycogenic. The liver forms and holds in reserve the glycogen, controlling the carbohydrate nutrition; it also controlls the proteid and fatty metabolic processes.

(3) Antitoxic function. The liver forms urea from ammonia, forms and destroys uric acid, forms the sulphoconjugations of the phenols; it arrests and modifies toxic substances, usually by oxidation, being the organ in which the most active oxidative processes occur.

(4) Biliary function. The liver forms a secretion—the bile, which may be considered both an excretion and secretion, as it contains the bile salta glycocholate and taurocholate of soda, which are necessary for intestinal digestion, while the bilirubin and other substances are excreted into the intestine for elimination.

Of these four groups of functions it is evident that one or more may be deficient, and to treat any case it is of importance to decide which function is insufficient. Physical examination gives little or no help in the differentiation. Antemortem examination of the bile is impossible except in cases of fistula, and it is to the urine and feces that we must look for the data necessary for a diagnosis. The following are the points to be examined to determine the nature of the hepatic insufficiency; alimentary glycosuria, hypoazoturia, ammonuria, hyperazoturia, urobilinuria, indicanuria, intermittent elimination of methylene blue, the oxidation of sulphur, the conjugate sulphates, uroerythrin, and hippuric acid. The feces should be examined for fat, bile pigments, and undigested proteid.

Alimentary glycosuria, first studied by Claude Bernard, followed by Robineau, Roger, Hanot, Gilbert, Reynaud, and others, as a pathologic condition, is usually tested by the administration of 200 grammes glucose or levulose syrup. Should the urine contain sugar, giving Fehling's reaction, the glycogenic function of the liver is affected. The value of this test as evidence of general hepatic insufficiency is disputed: Roger found the test positive only in 6 out of 10 cases of insufficiency, Surmount in 10 out of 15, Bierens and Haan in 18 out of 29, Reynaud and Olmer in 11 out of 30, Maury in 16 out of 53 cases. In atropic cirrhosis Valmont found the test positive in 1 out of 7 cases, Mehring in 2 out of 9, Fredrichs in 2 out of 19 cases of phosphorus poisoning. These figures show that in hepatic sufficiency the glycogenic function is impaired in about 40 per cent of the cases, and in atropic cirrhosis in about 16 per cent.

The test for urobilin in the urine is easy and should never be neglected. The filtered urine is heated with a little ammonia and a drop or two of zinc chloride added; if urobilin be present, green fluorescent coloration occurs. A more complicated test is to saturate the urine with ammonia sulphate and dissolve the precipitate in alcohol; a reddish-brown colored solution is obtained, which can be tested with ammonia and zinc chloride solutions or with the spectroscope. The latter can also be used with the fresh urine, but is too delicate, as small quantities are detected which are not pathologic. The question as to whether urobilin is formed in the intestine or in the liver is still a matter of dispute. Hayem says that urobilin is the pigment of the diseased liver, and stated emphatically that it is never found in the urine except in cases of hepatic insufficiency. Vires considers that clinically the presence of urobilin in the urine is definite proof of hepatic disease, and that it is of secondary importance where it is formed; he considers urobilin the pathologic and bilirubin the normal excretion of the liver.

Indican is found in small quantities in normal urine; in excess it is associated with hypochlorhydria, sometimes with hyperchlorhydria, with the presence of pus in any part of the body, in Asiatic cholera, cancer, typhus, and constipation; it is probably of intestinal origin, but the liver takes an active part in its formation. It is present in excess in most hepatic diseases, but it is not an absolute sign of hepatic insufficiency; it should be regarded as one of the toxins which produce the disease.

The elimination of methylene blue is a test which is difficult to carry out, at least in private practice; it consists in injecting 0.05 gramme of methylene blue in one-twentieth per cent solution and watching its elimination in the urine. Under normal conditions the coloration of the urine is regular, increasing to a maximum, and then diminishing. In patients suffering from hepatic disease the coloration is irregular, alternating in depth of color. In severe cases the coloration may be intermittent.

Hypoazoturia is the result of the failure of the liver to form urea from the carbonate and the carbamate of ammonia, consequently the proportion of the total nitrogen eliminated as urea is reduced and the ammonia increased. The methods for the quantitative estimation of urea and ammonia are complicated; Follin's method is best, but tedious for general practice. Under normal conditions the amount of nitrogen eliminated as urea should be about 82 to 95 per cent of the total nitrogen; in cirrhosis the percentage of urea nitrogen may be reduced to 75 or 79 per cent; in jaundice from 50 to 70 per cent, and in yellow atrophy from 40 to 60 per cent. The urea function of the liver can also be tested by injecting from 5 to 6 grammes of ammonium acetate into the buttocks; the ammonia is converted into urea under normal conditions, but is eliminated as ammonia if the hepatic function is impaired. A certain proportion of the sulphur is eliminated not fully oxidized to sulphate; if this proportion is increased it is evidence of imperfect hepatic function, the liver being the organ in which the most active oxidizing processes of the body are carried out. The proportion of neutral sulphur to total sulphur eliminated under normal conditions is from 10 to 12 per cent; in hepatic insufficiency it may be increased to 40 per cent. This is considered by many to be one of the most important of all tests for diagnosis.

Roger and Garnier introduced a solution of dihydrogen sulphide into the rectum; under normal conditions the gas is retained by the

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