When considering a case of long continued abdominal disease, one is forcibly impressed withi the fact that a chronic lesion frequently manifests itself by periods of exacerbation alternating with periods of remission. Thus, although the lesion is chronic, the patient describes his troubles as occurring in attacks. This fact may confuse the examiner. The chronic indurated ulcer of the stomach acts in this way. Here the periods are long. Several weeks or often months of distress are followed by equal or longer periods of comparative comfort. In fact these quiescent periods are often considered a cure. These ulcers do heal and break out again in the same or another spot, as do ulcers of the leg. I have seen the scars of former ulceration in the stomach as well as in the intestine. A recent case illustrates this fact. In August, 1907, I opened an abdomen for a chronic indurated ulcer which was found as diagnosed. It was about one and a half inches in diameter and one-half inch in thickness, and located on the anterior wall of the stomach about three inches from the pylorus and near the greater curvature. The patient's condition was very weak and became alarming, so I closed the abdomen without doing any operation on the stomach. After three months he was well enough to go to work, but in March, 1908, a return of pain, vomiting of blood, etc., induced him to come again for operation. I then found a stellate scar at the site of the previous ulcer and a second indurate ulcer nearer the pylorus and the lesser curvature. At this time an apparently successful gastro-enterostomy was done.

Ulcers of the duodenum give their symptoms in definite, periodical attacks, lasting from a few days to several months, but during these periods the pain is daily or several times a day, three to five hours after eating. The fact that gallstones, although present continuously in the gallbladder, give symptoms in attacks is well known; these attacks being coincident with recurrent infections. It is less well known that gall stones impacted in the common duct also give symptoms in attacks, corresponding not to passage of the stone but rather to periods of complete obstruction, when a mucous membrane swollen by infection assists the stone in a total blocking of the duct.

It is hardly necessary to recall the fact that chronic inflammation of the appendix more frequently than otherwise gives evidence of its presence in attacks.

Chronic intestinal obstruction begins with periods of increasing constipation relieved at first by catharsis and later by vomiting, and only. when well advanced does the chronic lesion cause chronic symptoms.

Chronic tubercular peritonitis, although somewhat constant in its symptomatology, is yet characterized by exacerbations coincident with temporary increase of fluid or accumulations of intestinal gas behind bands of adhesions.

JOURNAL OF MEDICINE

In like manner do certain chronic kidney lesions and chronic inflammation of the Fallopian tubes manifest themselves chiefly in attacks.

The periodicity of the symptomatology of chronic inflammatory abdominal diseases is thus worthy of much consideration in arriving at a diagnosis.

The significance of vomiting is also worthy of study. While the various types of vomiting of reflex and toxic origin are well understood and do not cause confusion, vomiting in connection with epigastric pain is usually considered to indicate stomach lesion. Of course this is frequently true, as seen in chronic gastritis, cancer, ulcer, etc. Yet there are certain lesions of the digestive tract more or less remote from the stomach, that have vomiting as one of their chief symptoms. This is due to the presence of pyloric spasm which causes besides the vomiting, pain and perhaps a sense of resistance over the site of the pylorus. Occasionally also we see a case with spasm of the cardiac end of the stomach and pain in the thorax. In the light of recent operating-room pathology, pyloric spasm can not be regarded as a definite disease but rather as a symptom. Nor can it be regarded as indicative of gastric ulcer, for it is present with equal or greater frequency in duodenal ulcer, gall-stone disease, ulceration of the small intestine, and inflammations of the appendix and cecal region. This condition of pyloric spasm can be demonstrated on the operating table in connection with these diseases, and all gastric symptoms cease after the cure of lesion. Mayo has called attention to this fact, which can be confirmed by many a clinical history and should receive important consideration when making a diagnosis. His explanation is founded on embryology-in brief all of the intestinal tract derived from the primate mid gut and concerned in the absorption of food, when diseased in any part, appears to exercise some control in preventing food from reaching that part by spasmodic closure of the plyorus and vomiting.

The location of spontaneous pain is another point in the history that may be confusing. While epigastric pain is found in the various gastric diseases, functional and organic, yet by no means does epigastric pain always mean a gastric disease or, for that matter, even an abdominal disease. Umbilical pain is even more untrustworthy from the diagnostic standpoint.

The relation of pain to the ingestion of food, both in respect to the time after eating and in respect to the kind of diet that induces or from the patient's standpoint-produces the pain, is however of diagnostic importance. For example, pain in ulcer of the stomach near the pylorus comes within an hour after eating, and is relieved by a bland fluid such as milk; while pain in duodenal ulcer is at its height three or four hours after a meal, when the acid contents of the stomach and the spasm induced thereby and the accompanying gas reach the ulcerated area.

Pain in gall-stone disease is absolutely irregular as to time in relation to eating, and is neither increased nor decreased by variety or quantity of food. Pain in intestinal stenosis is greatly increased by bulky food with cellulose in abundance, and mitigated or even temporarily abolished by a scant nitrogenous diet. Pain in chronic tubercular peritonitis, or in chronic appendicitis with adhesion, is directly induced by various incompatible combinations of food that cause intestinal flatus. Pain in nephritic or vesical lesions is developed by exertion, by jolting, by over-indulgence in nitrogenous food, or alcoholic drinks.

Other examples might be mentioned where pain indicates with some clearness a definite chronic abdominal lesion; but it must never be forgotten that chronic constipation due to lack of exercise, scant ingestion of fluids, too concentrated a diet, ineffective enervation, or other physiological causes, gives a history of chronic abdominal pain and must be considered as a proof of a chronic surgical lesion. Chronic intestinal indigestion, that old diagnostic cover for so many types of intestinal disease, although it has been trimmed in many places by modern surgical effort is still the cause of more cases of chronic abdominal pain than the perusal of some modern writings would lead us to believe.

The neurasthenics are also subjects of abdominal pain and this pain so often mimics a definite lesion, or so modifies the picture when present in connection with actual abdominal disease, that it behooves us continually to be on our guard. Gastro-enterostomy is not the ideal treatment for neurasthenia.

Chronic abdominal pain may thus indicate a local surgical lesion, a general physiological disturbance of digestion within the province of medical and dietetic treatment, or a neurosis pure and simple, or any two or even three of the classes combined, and must therefore be carefully studied if its diagnostic value is to be correctly interpreted.

Another symptom, loss of weight, according to my observation is caused more frequently by restrictions of diet employed to cure abdominal distress, than by a diseased condition. Next in frequency it seems to be caused by those chronic inflammatory processes that interfere with digestion, the formation by restricting and physiological action of the bile and pancreatic secretion. Even less frequently is it caused by malignant disease. In fact, early malignant disease in the abdominal cavity acts chiefly as a mechanical agent in the production of symptoms and does. not produce symptoms of its own. A history of gas formation is frequently noted. While this may be a pure neurosis, or the result of chronic gastritis, or gastric atony, it is an early symptom of gastric and especially of duodenal ulcer, of chronic pancreatitis, of abdominal adhesions constricting the small intestine due to peritoneal tuberculosis or other low grade infections of the mesenteric glands, appendix, or pelvic organs.

The physical examination of a patient with chronic abdominal disease, without a definite tumor, is less important than a thoughtful consideration of the history. Some cases show a retracted abdomen indicative of starvation, some a distended abdomen showing a partial paresis of the intestine and tympanites. Such ascites can often be recognized by percussion and if not explained by hepatic or nephritic disease is suggestive of carcinoma or tuberculosis. An enteroptosis, general or partial, or a displaced kidney may be found.

But the chief sign of local disease of a surgical nature is always local, or point tenderness. The right upper quadrant offers the most puzzling of diagnostic problems, for the organs liable to disease lie so closely together that the location of the tenderness seldom can be depended on to make a differential diagnosis. Taken in connection with the history of the development of the symptoms and the laboratory report of the examination of stomach contents and stools, the problem can often be solved. Tenderness due to nephritic, appendical, or tubal inflammation, or to lesions in other portions of the abdomen is usually discrete enough so that the organ at fault can be recognized. Not infrequently will the findings differ from day to day, depending upon the amount of food, gas, or feces present and it is wise to confirm by a second or third examination what seems to be clear on the first. Examination of the rectum and the lower sigmoid, by the tube and light with the patient in the kneechest position, will sometimes disclose a local lesion that has given symptoms of the general abdomen only, and no local ones.

The third leg of the tripod upon which the diagnosis must rest stands in the laboratory.

Here, as in the matter of the physical examination, it is wise to rely not on one but on several examinations. The presence of meat or fat in the diet, notwithstanding that care is used to avoid them, may be a source of error in examination of stools. Yet at the present time, it seems as if these examinations give more trustworthy information as far as the diagnosis of surgical lesions is concerned, than do examinations of stomach contents.

To distinguish between duodenal ulcer and certain obscure cases of gall-stone disease, the finding of occult blood in the stools is of prime importance. In pancreatic disease and in early carcinoma these examinations are of great value. Negative findings also enable one to differentiate between stenosis due to peritoneal conditions, and that due to lesions of the intestinal wall. The finding of gall-stones, although a matter of interest, seldom is much of a factor in determining the indications for surgical treatment.

Having reached a diagnosis with reasonable certainty, operation seems desirable in the following chronic abdominal conditions:

I. After several attacks of acute round ulcer of the stomach, although all urgent symptoms

have abated, a gastro-enterostomy will prevent other attacks with the chances of perforation to which this type of ulcer is especially liable.

2. In chronic indurated ulcer, a gastro-enterostomy with or without excision of the ulcer, depending on its location and size, will cure the ulcer and prevent a secondary carcinoma which follows this type of ulcer with amazing fre

quency.

3. In pyloric stenosis from adhesion, healed ulcer or early carcinoma, operation is satisfactory from the temporary standpoint at least, and if obstruction is benign the permanent results are especially good. Even in very weak patients the breaking up of the adhesions alone, which is attended by but slight risk, is often very useful.

4. In gall-stone disease, without jaundice, whenever a distended gall-bladder can be palpated. This means a cystic duct obstruction.

5. When after an attack of acute cholecystitis, tenderness remains on deep pressure over the gall-bladder. This means a chronic inflammation of the gall-bladder with cystic duct partly blocked by stone or adhesions, and sepsis still present.

6. In chronic jaundice of varying intensity, or after returning attacks in the absence of a distended gall-bladder. This means obstruction due to stone and infection still present.

7. In cases of chronic pancreatitis with or without gall-stones. Here the diagnosis rests on slight or pronounced tenderness in the epigastrium, gastric dyspepsia, chronic jaundice of moderate severity, sometimes a fullness or even an indistinct tumor, frequent bulky stools with offensive odor, light in color, greasy in appearance and usually the urinary Cammidge reaction.

8. In cases of partial intestinal stenosis. In those patients with a history of previous operations or peritoneal inflammation, adhesions will be found as the cause of the stenosis; with a history of chronic enteritis, or colitis, a stricture of the intestinal wall may be expected. Without any previous abdominal disease and a history of only a few weeks or months of increasing stenosis, carcinoma is the reasonable diagnosis.

In my experience, the presence of adhesions about the duodenum, the cecum, the Fallopian tubes, or more generally distributed, is a very frequent cause of abdominal distress of chronic type; relief of which by surgical procedure can be confidently expected.

9. After one attack of appendicitis, or even without such history, if tenderness is continually present on several examinations over the appendical area.

10. After two or more definite attacks of appendicitis, even in the absence of all local tender

JOURNAL OF MEDICINE

ADDRESS OF THE PRESIDENT OF THE THIRD DISTRICT BRANCH OF THE MEDICAL SOCIETY OF THE STATE OF NEW YORK.

SECOND ANNUAL MEETING, TROY, N. Y., OCT. 27, 1908. By HERMON C. GORDINIER, M.D. LADIES AND GENTLEMEN:

I

TAKE great pleasure in thanking all of you for the honor which you have bestowed in selecting me as your presiding officer at this the Second Meeting of the Third District Branch of the New York State Medical Society.

The address which I have prepared to present to you on this occasion is upon one of the numerous manifestations of that most common but interesting and important disease-arteriosclerosis. I refer to that variety of angiosclerosis of the extremities known as angina cruris, intermittent lameness, limping or claudication. The clinical manifestations of angiosclerosis of the vessels of the extremities are very variable and present themselves under five well defined clinical groups dependent upon the character, the location, and exact extent of the pathologic changes in the vessel walls. They are as follows: Intermittent claudication; symmetrical gangrene or Raynaud's disease; spontaneous or dry gangrene; erythromelalgia and arteriosclerotic neuritis, the latter condition being dependent upon pathologic changes in the walls of the vasa nervorum. Interesting as it would be to describe in detail the clinical manifestations of the various groups, above mentioned and to go into their differential diagnosis, it is my purpose to direct your attention only to intermittent claudication, a diseased condition which is not uncommon, is frequently overlooked, and whose clinical manifestations are clearly defined. If we are to judge from the scant references to this condition in our most recent text-books and from the few cases thus far recorded in American and English literature, intermittent claudication is extremely rare. Judging from the only references I can find in English literature, the disease has been until very recently completely overlooked in England. But two cases are recorded, one by Byron Bramwell in April, 1907, and the other by Parker Weber in January, 1908.

In America, however, cases have been recorded by Dana, Flinterman, Gordon, Hunt, Irish, Lovett, Patek, Putnam, Riesman, Talley, Walton and Paul, and J. C. White. I am convinced, however, that from the cases which I have seen during the past few years in private and consultation practice, that intermittent claudication is far more frequent than we are led to believe, but owing to the scant references to it, and the very meager description of it, in our best text-books and systems of medicine, it is perfectly evident that its clinical manifestations are almost unknown to the general practitioner, and hence it is very probable that many cases have been en

January, 1909

tirely overlooked. It is my opinion that intermittent limping is quite as common as is true angina pectoris.

Our attention was first directed to this symptom complex by the late Professor Charcot who in 1858 described his case and gave to the affection the name of claudication intermittente. He had thus early noted the remarkable resemblance between this affection in man and a similar condition observed in horses by veterinarians and called by them spring or string halt. Prof. Erb of Heidelberg, in 1898, published a most exhaustive and valuable monograph upon this subject and named the condition dysbasia angiosclerotica intermittens. Since then several important papers on this subject have appeared, more notably those of Higier, Goldflam, Idelsohn, Oppenheim, Walton and Paul, and Ramsay Hunt. Higier designated this affection myasthenia angiosclerotica and Walton and Paul called it angina cruris.

Etiology.-Intermittent claudication has been observed much more frequently in men than in women. Patek found that of 127 cases taken from the literature 120 occurred in men and 7 in women. Of the 10 cases I have observed, 8 occurred in men and two in women. Goldflam and Oppenheim emphasize the importance of the neurotic temperament as a condition favoring its production. I have observed one typical case in a very neurotic woman 35 years of age who had no objective vascular or cardiac disease. The disease is, however, most often met after middle life, at a time when vascular changes are most commonly observed. Hence all causes which favor the production of such changes such as the infectious diseases, alcohol, syphilis, diabetes mellitus, gout, lead, tobacco and exposure to cold and wet may also be productive of this disease. Erb from a very wide experience with this affection lays particular stress upon the excessive use of tobacco and exposure to cold in its production. Mechanical compression of the iliacs or femorals by a truss, aneurisms or other tumors are said to have produced this disease. Idelsohn found flat foot present in 10 of his 22 cases and believes that there is more than a casual relation between flat foot and intermittent claudication. In three of the cases which I have observed flat foot has been associated with well marked intermittent limping.

Pathology. Our knowledge of the pathology of intermittent claudication is based upon the study of the autopsies of Charcot, Elzholtz, Magrez and Erb, together with the arterial changes observed in the amputated limbs removed from cases suffering with this affection. Charcot from a study of his cases believed that the symptoms were due to arterial changes localized to the proximal trunks, such as the abdominal aorta, iliacs and femoral arteries, while Erb on the other hand, holds that the symptoms are dependent upon changes in the distal arteries of the extremities. The most constant change found in these cases was an obliterative arteritis of

the vessels of the extremities which results in a gradual narrowing of the lumen of the vessels with a consequent ischemia of the parts beyond. In a later stage as the caliber of the vessels becomes narrower and the nutrition of the muscles and nerves suffer, muscular atrophy and arteriosclerotic neuritis may come on. Lastly, spontaneous or dry gangrene often occurs as a late event which may necessitate amputation and is often a forerunner of death.

Symptomatology.-There are five clinical characteristics which stamp intermittent claudication as a perfectly distinct clinical entity and which also serve to make the diagnosis of it very clear. They are in the order of their import as follows:

First. The intermittent character of the symptoms. Second-The absence of the symptoms while the limbs are at rest.

Third. The development of painful limping on exertion.

Fourth. The disappearance of all symptoms after a period of rest, to be repeated again on exertion, and,

Fifth. The absence in most cases, especially during the attack, of pulsation of the posterior tibial and dorsalis pedis arteries.

Altogether the most striking and interesting feature of this affection is the intermittent character of all the symptoms. The patient while at rest is perfectly comfortable, and is able to move his limbs freely and in a natural manner. He experiences no paresthesia, heaviness, pain or cramp in the limbs and they do not feel weak. On attempting to walk any distance, however, say a few blocks, or especially if he attempts to climb a hill or walk rapidly up-stairs, he notices the appearance of numbness, tingling and weakness in his limbs, to be followed quickly by heaviness, great pain, cramps, stiffness and a disordered limping gait; all of which symptoms increase as he attempts to proceed, when his limbs feel as if they were becoming rigidly fixed, and if he attempts to go further, they feel as if they would become paralyzed and he would fall to the ground in a heap, "abasia." Hence he is enforced to rest either in the sitting or recumbent posture for a brief period, perhaps a halfhour or more, when all the above described symptoms gradually disappear and he again feels perfectly well and is able to go on. If, however, he attempts to walk again at his usual rate of speed and continues far enough, all the symptoms recur but with greater severity.

The objective symptoms during the attacks while somewhat variable are quite characteristic. The limbs usually feel cold, are often cyanotic and swollen or white and ashen. Sometimes they are red and deeply congested, and the patient complains during the attack of a burning pain in them. If the arteries of the feet are palpated, they either do not pulsate or pulsate very feebly. In a few instances no changes in the pulsation

of the arteries of the feet were observed. Bramwell has recently reported such a case and in one of my patients afflicted with this disease no palpable change could be observed in them.

Intermittent claudication is most often observed in both lower limbs, although it may only be confined to one. This symptom complex, however, is not necessarily confined to the lower extremities. Several observers have recorded cases of a similar character involving one or both arms, with changes in the vessels of the wrist exactly like those observed in the feet. I have observed two such cases, one involving the left arm and one recently seen in consultation with Dr. Irish who has kindly permitted me to record it, involving the right upper extremity. In both of these cases one could feel but very feeble pulsations in the vessels of the wrist.

Vascular changes with intermittent symptoms identical in nature to those of intermittent claudication have been observed in the brain, retina, kidneys, and intestines. Doubtless, all of you are familiar with the sudden but evanescent symptoms associated with cerebral arteriosclerosis, probably induced by spasm of the blood vessels of the brain, similar in every respect to intermittent claudication such as temporary blindness, unilateral, bilateral, or hemiopic in effect; aphasia, monoplegia or hemiplegia and partial or complete, unilateral sensory defects. And lastly it is very probable that true angina pectoris is a disease which is in every respect similar to angina cruris.

The symptoms of intermittent claudication are due to the sudden but intermittent withdrawal of blood from the tissues of the affected limbs during activity, the result of a sudden narrowing of the caliber of the blood vessels (from vasomotor spasm) beyond that which is normal to the parts while at rest. It is perfectly evident that in this condition during rest the blood supply though feeble is ample for the requirements of the tissues, but during activity, owing to the increased metabolic changes occurring in the tissues, especially in the muscles, the blood supply being further diminished by sudden vascular spasm, is insufficient for the extra demands put upon the tissues, and hence are induced the symptoms, weakness, numbness, pain, spasm, and limping which are so characteristic of this disease.

"Ramsay Hunt well expresses it when he states that there are three factors in the production of this disease. First one constant and organic in nature angiosclerosis, narrowing the caliber of the blood vessels; and Two-factors functional and inconstant; the tendency to vasomotor spasm, and the increased demand put upon the circulation during activity."

Diagnosis.-The diagnosis of intermittent claudication will in most instances be perfectly simple if one will bear in mind the five cardinal points so characteristic of this disease and mentioned in detail under the head of Symptomatology, namely; the intermittency of all the symp

toms, the absence of the symptoms while the limbs are at rest, the development of numbness, cramp, weakness and painful limping on exertion; the disappearance of the symptoms after a brief period of enforced rest and the absence of or enfeeblement of the pulse in the dorsalis pedis and posterior tibial arteries.

Prognosis. Owing to the organic factor angiosclerosis, in the production of most cases of this disease, the prognosis is unfavorable. Many of the cases improve, however, under appropriate treatment and a few of the early neurotic cases without objective arterial changes get well, or are so far restored that they are able to walk in a normal manner. This has been the result in the case of mine referred to under the head of etiology, of a Jewess thirty-five years of age, without objective arterial changes but with the characteristic intermittent limping and other associated symptoms, who has so far improved that she can walk perfectly for a mile. or two without the slightest discomfort or occurrence of any of the symptoms of this disease. I may state that she was seen during the height of her disease by Dr. Putnam of Boston who concurred in the correctness of the diagnosis.

Treatment.-The treatment of this condition may be summed up as follows: Restriction of exercise, short of bringing on the attack, or absolute rest in bed; saline baths; gentle massage and electricity, particularly the D'Arsonval current, which relieves pain and produces vasomotor dilatation; vasomotordilators, especially nitroglycerin and sodium nitrite together with small doses of potassium or sodium nitrite and general tonics, particularly the glycerophosphates, arsenic and strychnia. Tobacco and alcoholic stimulants should be prohibited. The condition of flat foot should be carefully corrected; if a syphilitic infection is suspected a systematic and thorough course of mercury and the iodids should be given.

THE HOSPITAL AS A TEACHING
INSTITUTION.

Moreover trustees may overlook one important advantage of a teaching hospital. Who will be least slovenly and careless in his duties, he who prescribes in the solitude of the sick chamber and operates with two or three assistants only, or he whose every movement is eagerly watched by hundreds of eyes, alert to detect every false step, the omission of an important clinical laboratory investigation, the neglect of the careful examination of the back as well as of the front of the chest, the failure to detect any important physical sign or symptom? Who will be most certain to keep up with the progress of medical science, he who works alone with no one to discover his ignorance; or he who is surrounded by a lot of bright young fellows who have read the last Lancet or the newest Annals of Surgery, and can trip him up if he is not abreast of the times? I always feel at the Jefferson Hospital as if I were on the run with a pack of lively dogs at my heels. I cannot afford to have the youngsters familiar with operations, means of investigation or newer methods of treatment of which I am ignorant. I must perforce study, read, catalogue and remember, or give place to others who will. Students are the best whip and spur I know.-W. W. Keen.