CONTENTdm
History of Nursing in Pacific Canada
Vancouver Medical Association
'Supplement' -- Title page
image/jpeg
EfSsHHi^SiffiSE ■■^— m SUPPLEMENT to the BULLETIN of the Vancouver Medical Association Papers read before the Vancouver Medical Association Summer School, held June 21st to 24th, 1938, and the Annual Meeting of the British Columbia Medical Association, held September 15 th to 17th, 1938. Published in collaboration with the B. C. Medical Association, February, 1939. SUPPLEMENT SECTION 1. Vancouver Medical Association Summer School, June, 1938 Index Page 5 Farquharson, R. F The Anaemias _>.«. " The Liver, diseases of 50 " Leukaemia L 6 6 " Lymph Glands, enlargement of 38 Hunter, Andrew Pregnancies and its toxaemias, chemical aspects 53 Sulphanilamide and related chemo-therpeutic agents 70 Ormsby, Oliver Mycotic infections (of the skin) . 9 " Precancerous dermatoses 44 Spurling, R. Glen Intractable pain ■ ', 22 Low back and leg pain from a neurological standpoint 37 Scalenus neurocirculatory compression 5 6 Walters, Waltman Obstructive Jaundice 30 Preparation of handicapped patients for surgical operations 40 Surgical treatment of the diabetic patient 60 Lesions of the stomach and duodenum 16 Note.—"Surgical and non-surgical treatment of Epilepsy," by Dr. R. Glen Spurling, which was given at the Summer School in 193 8, was published in the Bulletin, Vancouver Medical Association, v. 15, no. 1, p. 15. 99 99 99 >> SUPPLEMENT SECTION 2 British Columbia Medical Association Annual Meeting, 1938 Index of Medical Papers Bannick, E. J. Acute pancreatitis . . 75 .Sulphanilamide therapy 100 Bazin, A. T. .Cancer of the breast 84 Cancer of the colon and rectum . 93 Boyd, William Pathology of the gall-bladder I 77 Kilgore, A. R. Practical considerations in the handling of acute appendicitis and its complications 96 " Extra-abdominal diseases simulating the "acute appendix" 87 Lisser, Hans Chemical observations of the present status of gonadotropic and sex hormone therapy 102 " Indications for the proper use of thyroid substance 91 Masculinizing syndromes = 73 Mackenzie, K. A. Treatment of high blood pressure 78 Newburgh, L. H..~ New interpretations of diabetes mellitus in obese middle-aged persons. Cure by reduction in weight „~„„~„„~.„,,--_..—.-—..—~—~~~. 86 FOREWORD We present herewith the papers read before the Summer School of the Vancouver Medical Association at its 1938 meeting, and those read before the Annual Meeting of the B. C. Medical Association in September. We regret that this Supplement has been so long in making its appearance, but there have been some difficulties in assembling all the papers. The men who gave them are all very busy men, and of their kindness were willing to edit and amplify notes, and generally comb the hair and wash the face of their brain-child before sending it out on the stage for its public appearance. This has been very greatly appreciated, and of course it was not easy for them to do this in a hurry. But, especially in the case of certain papers, it has meant all the difference in the world. To take only one set of papers —those given by Dr. Walters of the Mayo Clinic—these were all very thoroughly revised and edited by the writer after he returned home, and the finished product shows the great care taken in doing this. The Mayo Clinic has ordered a great many reprints of each of these articles. Again, Dr. Kilgore went over his notes and made his papers fuller and more available to the readers. And others were good enough to do the same. Again we feel like expressing our admiration of the generosity and interest which these speakers show to us. They not only come here at considerable sacrifice of time and leisure; they not only give us excellent material ^well illustrated, concise and interesting to hear—but they grudge no trouble and pains to see that we have their offerings in good shape for publication. This makes their gift to us doubly useful. Our readers will, we believe, find considerable food for study in this Supplement and will derive much benefit therefrom. We believe that it is an excellent move on the part of the medical associations to make it possible, as they have done, for this matter to be put in the hands of every medical man in the province. It will do two good things: it will give the information and knowledge that these papers were designed to convey; and it will show men how important and necessary these scientific meetings are. They have a value that cannot be estimated—and it certainly does not all lie in the written papers. It is so much better to hear them; to see the slides and illustrations; to hear the explanations given as the speaker proceeds with his talk. We feel that the men who did attend will derive double benefit from this Supplement. To those who did not, we would say that only half the full benefit is theirs. It is better by far than nothing—but we can assure them that actual attendance more than repays any cost in time or money. It may be well to mention here that the second part of this volume is financed entirely by the B. C. Medical Association, and is part of their educational programme for their members in the province. SECTION ONE PAPERS READ AT THE VANCOUVER MEDICAL ASSOCIATION SUMMER SCHOOL, JUNE 21st to 24th, 1938 SPEAKERS: Dr. R. F. Farquharson, Associate Professor of Medicine, University of Toronto, Toronto, Ont. Dr. Andrew Hunter, Professor of Pathological Chemistry, University of Toronto, Toronto, Ont. Dr. Oliver S. Ormsby, Clinical Professor, Department of Dermatology, University of Chicago, Chicago, 111. Dr. R. Glen Spurling, Associate Professor of Surgery, Universit]y of Louisville, Louisville, Ky. Dr. Waltman Walters, Professor of Surgery, Mayo Clinic, Rochester, Minn. ANEMIAS By Dr. R. F. Farquharson. I wish to speak this morning on the anaemia of iron deficiency, its diagnosis and treatment. I am glad to say that this is one type of case that we cannot follow to post mortem very often. We deal here with the type of patient that does not die of the iron deficiency anaemia, but often suffers a great deal of ill-health from it. Iron has been used in the treatment of anaemia for centuries and has had its advantages and disadvantages in the therapy of anaemia. The reasons for this have been chiefly two: (1) the dose used has sometimes been insufficient, and (2) whereas iron is actually specific in the treatment of certain types, there are other types where it has no effect at all. Iron therapy suffered a serious set-back when experimental medicine came into play. The earliest surgeons produced an anaemia that was not due to an insufficient iron deficiency. They tried to cure these cases with iron, could not cure them with iron and said that iron was useless in the treatment of anaemia. Now, there are certain types which respond to iron and those which do not respond at all. This first slide shows the three main groups of anaemias. Most anaemias can be placed in one of these groups. It does not include them all but includes all the common groups. 1. Pernicious Ancemia.—A special anaemia that in this country is manifested as Addison's pernicious anaemia—when the bone marrow has not the specific substance to its red blood cells. It is cured by liver and by injecting this substance. It will be cured in only one way and it will be prevented in only one way, and it is no use giving iron to this class. 2. The iron-deficiency type—and this type occurs whenever the bone marrow has an insufficient amount of iron available for blood formation. This may come as a result of a prolonged insufficient intake of iron or may be due to loss of iron in haemorrhage. It may be aggravated by pregnancy. It is a very characteristic type. Now we have these two types where the anaemia results' because of a lack of building material, and if these materials are absent in any patient, this type will result. 3. This large group is really a secondary anaemia. The anaemia of iron deficiency is spoken of as a secondary type of anaemia and it is true that it is due to an insufficient amount of iron, but we come to this third group that is often confused with others, that is, anaemias that are secondary to other serious diseases. We may see it in far advanced carcinoma where the poisons inhibit bone marrow functions, and anaemia results. We see it also sometimes in far advanced tuberculosis, septicaemia, chronic osteomyelitis—all serious diseases. They give rise to a secondary anaemia. If you try to treat this type with iron you will not get very far.. The only way you can cure them is by curing the condition that causes the anaemia. I want to emphasize that if you have a patient with pernicious anaemia, you cure that patient by relieving the cause. Give that patient adequate potent liver extract. The other type of patient will be relieved by giving him iron if he has an iron deficiency, but if he has a serious disease elsewhere, then you won't cure that anaemia unless you treat the disease. These three types have characteristic blood pictures. In pernicious anaemia there are large, great big cells. In iron deficiency anaemia the cells are small and thin. This third group here is an anaemia in which the cells look much like normal cells. These people have a color index of about 1. The cells vary in size. This is a slide of my own blood taken in 1926 and it is essentially a normal smear. The red cells are fairly normal in size; no white cell is shown. I use this for comparison because in this next slide I am going to show you a pernicious anaemia in an acute relapse. This man is quite well today. He shows a typical picture of pernicious anaemia. You see here cells that are distinctly smaller than normal. Anyone not used to doing blood work should make a smear of his own blood and compare it with a picture of the blood of the patient he is studying. We go on now to a picture of an iron deficiency anaemia. Again the patient was under treatment in the Toronto General Hospital. This is an iron deficiency anaemia. The average size of the cells is smaller than normal, but scattered among these small, pale cells we do find some that are larger than normal. We always have the impression that here we are dealing with cells that are distinctly smaller than normal on the average. The [5] platelets are quite normal in number. The white cells may be a little increased or a little decreased. This girl had a fairly severe iron deficiency anaemia. Her haemoglobin was 22%. We see these small cells. This patient did well under iron therapy. She has relapsed several times because the factors that caused her iron deficiency anaemia have been still active. She has responded again and again to treatment with iron. I should like to discuss the changes occuring in our iron metabolism that lead to this type of anaemia. At birth the child has a store of iron in the liver and spleen and bone marrow that it has acquired from the mother. That store is sufficient to carry the child along for the first few months of life. In the first few months the haemoglobin falls to about 60%, but that is a normal physiological drop. The iron! that makes the haemoglobin must come from the blood as the child grows. The body is very careful of its iron supply, because even when we have a diet that is rich in iron, there is not much to come and go on; and if the body is wasteful of its iron supply, anaemia results. So the body husbands its supply of iron and if the diet is adequate in iron (foods especially rich in iron are meat and eggs) as growth occurs there is an abundance of iron and this makes haemoglobin for the expanding blood volume. But here, both in infancy and childhood, an iron deficiency will result because of insufficient intake. When we get to adult life, in women especially, another factor comes in and that is the factor of menstruation. Menstruation begins at a time when growth is active and causes a small amount of blood loss each month with a persistently small loss of iron and leads to an iron deficiency anaemia if the diet is poor. If there is excessive loss at the menstrual period, we are up against a different problem. This will lead to anaemia if the diet is bad. Any other loss of blood will also lead to anaemia, but it seems probable that much of the anaemia in women occurs because of this slightly increased loss of blood at the menstrual period. It does not occur in all women, but in women in a particular group. This group probably comprises 5 % of our population and these do not assimilate iron very well. They have an achlorhydria and many of them do not utilize iron very well and develop anaemia. If they get a mild anaemia their diet is apt to be worse and they increase their anaemia. Even in men we shall often find a loss of iron through haemorrhage from any cause— epistaxis, from the gastro-intestinal tract, etc.—from any type of chronic haemorrhage. This will sooner or later exhaust iron storage1 and anaemia will result. If the storage is exhausted and the diet contains less iron, and less iron is absorbed than is lost in haemorrhage, then anaemia will result and will be of this type, with small cells varying in size, pale, and will be relieved by iron therapy. Repeated pregnancies again aggravate this type of anaemia. So we have a type that occurs in infancy that corrects itself with ordinary diet, will not be very severe unless there is haemorrhage or unless, as a result of infection or other ill health, the child's diet is bad. The first time we are apt to see this in adolescence and is like the old-fashioned chlorosis. The great group that we are apt to see is the group that is called an idiopathic iron deficiency anaemia, or idiopathic hypochromic anaemia, and this particular type occurs in women as they approach middle age, in the late 3 0's and in the early 40's, and being often associated with other symptoms, menstrual difficulties, etc. I would just like to discuss these in greater detail for a moment or two. This idiopathic iron deficiency anaemia that we see so commonly in all sorts of women, occurs in people that tend to have a certain constitution and that constitution is associated with an achlorhydria, but it also tends to be associated with a rather highly strung, nervous background—a psychoneurotic constitution. These people are more nervous. They are apt to have an effort syndrome. They are apt to be short of breath on exertion. They are often worried. They have commonly had an iron deficiency anaemia in adolescence and carry it through their early adult life; they often have had repeated pregnancies and their anaemia tends to become worse. In the late 30's or early 40's we often see a change. The appearance of increased fatigue, of increased shortness of breath on exertion, of increased f aintness on exertion, are symptoms which occur. These symptoms become slowly worse and the patient goes and consults a doctor. The patient has often noticedl that there is a pigmentation on the skin, but this pigmentation is actually a different pigmentation than that found in pernicious anaemia. It tends to be most marked on the face and on the hands. Sometimes we see brown patches around the lips. Some of the patients will tell us that these are liver spots. Just what causes them is' hard to say. [6] We see this pigmentation on the exposed parts of the body, not over the whole body as in pernicious anaemia, and the patients have felt tired and their diet has not been adequate. They have been losing blood at the menstrual period and their anaemia has become worse. If this has been present for a long time^ certain characteristic results will occur. One of these is a difficulty in swallowing, which is associated with an atrophy. There will also be a smooth tongue with this difficulty in swallowing. Another characteristic is that the nails become flattened, brittle, and later may actually become hollowed out. This' is if the condition has been present for a long time. If we examine these people, we notice that they look worried and worn, commonly they are thin, though occasionally overweight. There are not any striking factors until we come to the examination of the heart. If the anaemia is severe the heart is inclined to be enlarged, and when we listen to it we are5 struck by the fact that.there are loud systolic murmurs. These will be diminished when the patient holds her breath, but the murmur remains. It is present when the anaemia is severe and it will clear up when the anaemia is relieved. Sometimes we give a wrong diagnosis of heart disease. The patient has been short of breath, has had swelling of the feet, etc., and the doctor hears this murmur and thinks maybe it is heart disease. His mistake may be made worse if he has taken the history a little carelessly and the patient has said that she has had pain over the heart. The pain is a dull, aching pain, pain the left of the praecordium. It is worse when ,they are lying down. It is so different from true angina, where the pain is a midline pain and is relieved by rest and made worse by exertion. But these other people have what we might call a nervous pain. You examine their abdomen and you commonly find that the spleen is palpable and is fairly firm. Again this sometimes leads to the doctor thinking that there is something funny. Here we have a palpable spleen, and they usually associate it with serious disease. But this will disappear under proper treatment. The liver may also be palpable. The nails will be seen to be curved in very severe cases. If you examine them you will find this difficulty in swallowing. The diagnosis is easy if you take the history, if you examine the blood and find the typical findings that I have described—a haemoglobin that is reduced far out of proportion with the red blood count; the cells are small and pale and the color index is low; the white count may not be very characteristic. You will recognize that it is an iron deficiency anaemia and that brings us to the treatment of this type of condition. The treatment of the anaemia is to give iron. You cannot give enough iron in food to relieve the condition quickly. You must treat them by giving them simple iron salts by mouth. You may use any of a number of iron salts. You can give reduced iron right after meals, in capsules, or you can give iron ammonium citrate three times a day, either during or right after meals. If you are using reduced iron or an iron ammonium citrate, they will give a good response. Most people can take iron in this form, but sometimes they are troubled with nausea, vomiting, cramps, etc. If you give a small dose you may get constipation, but if you give a large dose you will get cramps and diarrhoea. If you reduce the dose for a few days you will get a cure of these symptoms, but you don't need to do this. If you give ferrous salts you can give small doses. The ordinary Blaud's pill is the treatment usually given and your patients will do very well. The only disadvantage to these is th'at the pills will change if kept too long, so if we use Blaud's, it must be a fresh pill. We can use ferrous sulphate in capsules. You can get it at drug stores and give grs. iii or v three times a day. We shall get a very good response to the treatment with the iron. The response occurs within a few days. The haemoglobin starts to rise and rises steadily and is normal in a few months. The treatment is most satisfactory. I should like to emphasize the fact that the use of iron intramuscularly is not worthwhile. It can be given intra-muscularly, but if you do this you must give a good preparation. You would have to give one of these ampules intramuscularly twice a day to get the same results. The trouble has been that we have given srrtail doses once or twice a week. It doesn't work out. If this method is going to be used it must be given at least once a day, preferably twice, giving at least 100 grs. of iron sulphate. So it is more satisfactory to give the iron by mouth in capsules. If the patient does not like to take these capsules, give syrup of ferrous chloride. There is no need to give liver at all unless the same patient has both pernicious anaemia and iron deficiency anaemia. There is no need to add Vitamin [7] "B" to the diet. It is quite alright to give lots of Vitamin "B", but there is no need to do this. There is no need to give these patients a transfusion unless in an emergency. It is important to see to it that these patients get a good diet—important for their general health as much as for their anaemia. These women have often had a very fat diet and are not getting much meat and vegetables, so give them a well balanced ordinary diet. They need to have their daily regimen carefully supervised. They need to be in bed when their anaemia is very severe. Sometimes they are going about with a haemoglobin of only 20%. It is wise to keep them in bed until their haemoglobin is 60% or 70%, gradually increasing their activity in convalescence. Remember, these people have been ill for a long time, and if we are going to get them back to good health we should see that they have a long convalescence. See that they get lots of rest. Usually they are nervous people and need to be assured that they have no serious disease and that their anaemia can be relieved entirely. They need reassurance. They need to be told that they have not got cancer or heart disease or any of these serious disorders. Lastly, these people all must have a careful and most thorough examination to exclude any source of haemorrhage. Always be on your guard in treating any person with an iron deficiency anaemia to make sure that there is no lesion in the gastro-intestinal tract. If we can make sure of that, we can reassure the patient and let him carry on. If the haemoglobin has come up to normal, it is still wise to give iron in small amounts. Make sure that the iron balance is on the positive side. Sometimes we see these people when they are having very marked haemorrhage from fibroids of the uterus, etc., and we find that we can bring their haemoglobin quickly up to normal. About the anaemia of pregnancy—this is an iron deficiency anaemia. It is aggravated in pregnancy because: (1) In pregnancy the blood volume is increased and the haemoglobin falls. (2) In pregnancy, very commonly as1 a result of the nausea and vomiting early, the diet is often worse and the intake of iron is lower. ( 3 ) Iron is being transferred from the mother's diminished stores to the foetus and that is an added drain on the iron storage. The treatment is to give iron just the same way as I have described, to see that the patient gets a good diet, and she will carry through very well. There is no radical treatment necessary except in emergencies. Usually there is no need for transfusion and it is contra- indicated. The last group of iron deficiency anaemias is the one due to prolonged repeated haemorrhages. It is not associated with any trouble in the assimilation of iron. We see it not infrequently in people having repeated long haemorrhage from haemorrhoids, also from severe epistaxis. If we find this type of anaemia in men we know that there has been some haemorrhage, because when men have reached adult life they can carry on with a wonderfully small intake of iron if they have no haemorrhage. So we recognize that we are treating an anaemia, but we know that there is some haemorrhage behind it. Very commonly the cause is not obvious. They may have a polyp in the gastro-intestinal tract that is bleeding, and this is very difficult to find. They may have an ulcer that has been bleeding repeatedly. They may have cancer of the bowel that has come on slowly with little pain. This may be the cause of the anaemia—an anaemia that will still be relieved by iron therapy and they feel ever so much better after iron doses, but the danger is that we may be satisfied with their condition too quickly. The important thing is to look for a cause of haemorrhage and to treat this cause, as well as to treat this anaemia. We may have multiple causes of anaemia, and a person may have an iron deficiency anaemia, and that patient's bone marrow may also be inhibited as the result of a large carcinoma. Here we are dealing with a person with two diagnoses. We may have pernicious anaemia and iron deficiency anaemia associated together. Now I just want to show you this slide once more to emphasize the blood picture. This patient's haemoglobin rises quickly on response to iron and she repeatedly gets better of her anaemia after iron treatment. In this other slide you see the difference between that picture and the normal picture. Now, this patient never liked meat. For two or three years before she came in she had repeated haemorrhages at the menstrual period. She was treated with iron therapy and her haemoglobin shot right up. This patient is a very interesting case. She is fifty years of age; always a nervous woman, always short of breath on exertion, always tired. But there was a definite change two years ago. She began to be much more tired; she began to feel faint when she got up from her chair quickly; she had [8] difficulty in swallowing even liquid food. Six months before coming to hospital she began to have a real anginal pain. This was quickly relieved by having her rest for a few minutes. We thought she had a coronary disease, but under iron therapy her haemoglobin came up wonderfully; her pain disappeared; she could climb stairs without much shortness of breath. We examined her oesophagus and found quite a firm web at the upper end. We took an X-ray picture and we thought that perhaps this woman would have to have this web broken down, but it has been our experience that most of these people are relieved by iron therapy alone, so we gave her this therapy and she began to be able to eat more and more without any trouble in swallowing. This.next slide shows her oesophagus before treatment and after treatment. The obstruction is almost completely gone. She is feeling well; she has no anaemia but still has angina with very vigorous exercise. Her angina was due to coronary disease but was aggravated by anaemia. This man had had haemorrhoids for fifteen years with profuse bleeding. His haemoglobin was down to 22%. He had been taking a poor diet and had an iron deficiency anaemia. We put him on ferrous sulphate and his haemoglobin rose right away. Later we had his haemorrhoids treated and he was relieved. This next patient also had an iron deficiency anaemia from bleeding haemorrhoids. His haemorrhoids were injected in January. A month later his haemoglobin was at the same level. We started him on ferrous sulphate with prompt relief of the anaemia. This patient has had about twelve pregnancies in the previous twelve years. She had a poor diet and a fairly severe iron deficiency anaemia. We tried her on a preparation which contained bone marrow, liver, etc., but did not contain iron. Her haemoglobin stayed at the same level. Then we gave her iron and ammonium citrate and her haemoglobin rose rapidly. This next patient was a young woman of 34 who came to the General Hospital suffering from pernicious anaemia, but she had a long history that suggested that for many years she had an iron deficiency anaemia and the typical course of events could be judged from her history. She then had the development of the new disease—pernicious anaemia—and the picture of pernicious anaemia dominated the other. Her haemoglobin was between 10% and 20% but her red blood count was low as well. She was treated with iron and then liver extract intramuscularly and the red count and haemoglobin rose rapidly, although the haemoglobin stopped at 50%. Since then she has had further iron therapy and her count is much better. Her pernicious anaemia will have to be treated for the rest of her life, but the iron deficiency anaemia is now cured. This patient had carcinoma of the stomach but also had an iron deficiency anaemia. Her haemoglobin was 40%. On iron therapy her haemoglobin rose rapidly to 70%. It stayed there because she had a pernicious anaemia from carcinoma of the stomach. This iron deficiency anaemia will be entirely relieved by the administration of inorganic salts of iron by mouth. We must always be on the lookout for underlying haemorrhage as the cause of this anaemia and we must be particularly careful to see that there is no other cause of bleeding. ON SOME MYCOTIC INFECTIONS OF THE SKIN By Oliver S. Ormsby, M.D., Chicago, Illinois. The subjects chosen for discussion include ringworm of the hands and feet, ringworm of scalp and the group of yeast dermatoses. Ringworm of the Hands and Feet. This affection was practically unknown in the United States in 1916 when a report was made by Dr. Mitchell and the writer1, in which a group of sixty-five patients was studied, in all of whom fungi were demonstrated microscopically. This study included patients suffering with dyshidrosis and intertriginous eczema. Its importance is undoubtedly exaggerated in the popular mind. The chief criticism at present from our standpoint lies in the fact that practically every cutaneous affection occurring on the feet and hands is viewed by the layman as ringworm and so treated. Unfortunately, numerous physicians fall into the same error but to a smaller degree. On account of the popular demand for self-treatment, numerous proprietary articles are advertised and extensively sold, some of [9] which inflict much damage. We believe that it is essential that the diagnosis of ringworm be confirmed microscopically in every case before treatment for that affection is instituted, and this we have done since the beginning. Unfortunately, a large group of practitioners rely solely upon the clinical symptoms for a diagnosis. Clinical Description.—The affection was early described by Whitfield and Kaufman- Wolf. Each described three clinical types. First, acute vesiculo-bullous; second, chronic intertriginous, secondary to the first type; and, third, chronic hyperkeratotic. The initial lesion is a vesicle and this may be single or multiple, grouped or widely distributed. The vesicle is deep seated, slightly elevated or level with the surface and resembles a boiled sago grain imbedded in the epidermis. (This comparison is always made in so-called dyshidrosis.) The content of the vesicle is serous unless contaminated by secondary infection. As a rule the early vesicles are not surrounded by redness. After several days to a week the fluid is absorbed and a brown macule remains. After desiccation the roof of the vesicle becomes torn, exposing a red, smooth, shining surface surrounded by a collarette of scales. Sometimes the roof of the vesicle develops into a brown keratotic button 1 to 2 mm. in thickness in place of scaling. Beneath these keratotic lesions the usual red, shining surface is not found. In acute cases the vesicles may be grouped, become confluent and form bullae. In extensive bullous cases the patient may be incapacitated for weeks. At times well defined, shiny, red, circular areas develop in dry areas such as the centre of the palm or sole or on the arch of the foot. These patches may heal spontaneously or new vesicles may continue to form around the periphery. The grouped vesicles may develop into a dry or moist, well defined eczematous area. At the base of the fifth toe a fissure occupying both the interdigital and plantar area is commonly present. Occasionally similar fissures occur in the flexor folds of all the toes. In the keratotic variety, areas of keratoderma are formed, usually symmetrically and more often on the soles. When complicated by secondary infection there often is much swelling and oedema of the under surface of the toes and contiguous portion of the soles and the intertriginous surface of the toes. Under these circumstances much tenderness and pain is experienced. Ordinarily the subjective symptoms consist in itching, which may be moderate to severe, but is practically always present. In the widespread acute bullous cases, together with those complicated with secondary infection, sensitiveness and pain are characteristic. While in the major portion of cases the eruptive manifestations are limited to the feet and hands, occasionally well defined, scaling patches of dermatitis may occur over the trunk and limbs and in these the causative fungus can be found. Diagnosis.—The major portion of cases of dyshidrosis are examples of ringworm and also quite a proportion of those formerly classed as intertriginous eczema, together with a certain percentage of cases of localized keratoderma of the hands and feet. An immediate diagnosis can be made in practically all cases by a microscopic examination of the roof wall of the sago grain vesicle or of scales from the interdjigital spaces, as well' as from other scaling areas on the foot, using a 10% to 20% solution of sodium hydroxide. If the roof wall of the vesicle is used it is placed with its under surface upward, the cover slip is gently heated until the preparation boils. Examination with a medium powered lens reveals the fungus, which is seen as jointed mycelial filaments. Disorders from which it is to be distinguished are dyshidrosis, eczema, a resistant vesicular dermatitis of the palms and soles, a superficial vesicular eruption probably of infectious origin, an external irritant dermatitis, and a pustular eruption of the palms and soles described below. In none of these is the ringworm fungus found microscopically. Ringworm is readily distinguished from a pustular affection occurring on the palms and soles, described by Barber as pustular psoriasis, by Audry as an abortive form of acrodermatitis continue, and by Andrews, Birkman and Kelley as a recalcitrant pustular eruption of the palms and soles. This affection is characterized by an exfoliative type of dermatitis beginning in the centre of the palms, extending over the thenar and hypothenar eminences and at times covering the entire palm and palmar surface of the fingers. On the feet it occurs characteristically on the insteps, from which it may spread over the entire plantar surface. The interdigital areas, usually invaded by ringworm, are free. The early lesion is a small flat discrete pustule. Throughout the patch there are scattered pustules and crusts. These are more abundant at the margins. The course of the affection is charac- [10] terized by periods of activity and partial quiescence. During the former, severe burning sensations occur. The affection is resistant to treatment and a microscopic examination reveals no fungi. Absence of fungi in the vesicles or scales taken from the feet is important from a diagnostic standpoint. It is much less important from similar lesions taken from the palms. This is explained, as noted elsewhere, on the ground that in numerous cases of ringworm the palmar lesions are idle eruptions in which micro-organisms are rarely found. Etiology.—In our original study, which has been continuously confirmed, men were affected more often than women. The feet were affected much more frequently than the hands. Eczema marginatum not infrequently preceded the affection. Familial transmission occurs. Infection is more prevalent in warm weather, exacerbations occurring in the spring and autumn. Sporadic cases do occur during the winter months. These organisms may lie dormant in calluses, under or about the nail or even in the superficial layers of epidermis between the toes for long periods of time. From these points reinfection occurs when heat and moisture develop in the warm season. Common sources of infection are dressing rooms, runws^rs and shower baths in the athletic departments of schools and universities and in athletic and country clubs. Treatment.—The method of treatment depends on the type of eruption. When the affection on the feet is acute, accompanied by vesicles and bullae together with secondary infection, hot soaks with a 1:2000 solution of potassium permanganate used two or three times daily is efficient. In the interim between soaks, soothing ointments containing naf talan or ichthyol or both may be used. When the acute stages have subsided, an ointment containing salicylic acid and benzoic acid, originally recommended by Whitfield, is efficient. In our early work we used this or a 10 per cent chrysarobin ointment or suspension. These preparations cause exfoliation. When this is complete Hebra's unguentum diachylon alba may be employed at night with a drying dusting powder containing magnesium carbonate in the morning. This should be continued for several weeks, during which time the salicylic acid and benzoic acid ointment above mentioned should be continuously employed as a prophylactic measure around and beneath the nails and on calluses, if present. In the subacute and keratotic cases the keratolytic ointment is advisable from the beginning. In the chronic intertriginous type curettage employed when the leathery whitened mass has been softened hastens recovery. On the hands a zinc oxide and aqua calcis lotion is advisable in the vesicular cases, together with the keratolytic ointment suggested for the feet reduced 50 per cent. If the lesions consist only in dry scaling ones, the ointment will be sufficient. In certain cases injections of trichophytin may be required. These should be used with caution and the initial doses should be small and perhaps reserved for resistant and intractable cases. Prophylaxis.—Prevention on a large scale was practiced by Osborne and Hitchcock3 in the high schools of Buffalo. Through experimental work they demonstrated the efficiency of sodium hypochlorite as a preventive'measure. They recommend the employment of rubber pans approximately two feet square in which a one per cent solution of sodium hypochlorite be placed. These pans are placed in the shower rooms and the students immerse the feet in one as they go into the bath and into another as they come out. In the newer athletic departments, wells are built in the floor of the corridor passing from the dressing room to the shower baths through which th|e students pass. The disease in the high schools in Buffalo were reduced to a minimum through these measures. Sterilization of the shoes, socks and other articles of clothing together with rugs and carpets which have been in contact with the feet of an infected patient may be accomplished by formaldehyde fumigation. Ayres, Anderson and Youngblood4 recommended this method to be employed in the bedroom and bathroom of the affected individual. By the use of fumigation with a formaldehyde candle they demonstrated the effectiveness of this method. Individual prophylaxis in country clubs is promoted' by the use of wooden- soled sandals between the locker room and shower. Epidermophytids. These are eruptions produced by the local action of fungi brought to the skin by way of the blood stream from older foci, usually the feet. The fungi are immediately destroyed on account of the existing allergy. These eruptions occur, as a rule, in association with [11 ] ringworm of the feet. They may also be secondary to infection of the hands and in the crotch. The ringworm micro-organisms are rarely! present in these lesions as is shown by a microscopic examination. Ordinarily, these eruptions occur in association with acute and severe attacks of ringworm of the feet. The hands are the most common site of this eruption and the lesions may be superficial or deep and the accompanying inflammatory reaction is variable as to degree. Occasionally, a more widespread eruption occurs over the forearms, legs and elsewhere which may resemble pityriasis rosea or multiform erythema. Patches of dermatitis resembling ezcema occasionally occur and in rare instances the eruption may be of the general exfoliative dermatitis type. Microscopic examination of the secondary lesion reveals no micro-organism, while at the same time they may be demonstrated abundantly in the primary affection on the feet. Diagnosis.—Epidermophytids may be distinguished from eruptions they resemble by the location of the lesions and the accompanying ringworm infection present on the feet. The trichophyton reaction is positive and is a confirmatory finding. When the secondary eruption is eczematous, trichophyton is used by means of the patch method. Ringworm of the Scalp. Ringworm of the scalp in children has always presented a serious problem to school officers. Some years ago in London and Paris special ringworm schools were established for the education of this type of student. At that time it required on an average of three and a half years to eradicate the affection. Exclusion from school for this length of time would be serious. Since the advent of roentgen therapy the necessity for ringworm schools has been eliminated as has also the requirement for hospital beds. The affection can be treated as an ambulatory one and cleared up in a reasonable time. The common type in the scalp of children is that produced by the Microsporon audouini. It consists in partially bald areas of variable size in which there is a moderate amount of redness and scaling, together with broken stumps of hair, each one of which is surrounded with a white sheath which is found on microscopic examination to be spores of the causative fungi. The patches vary from the size of a small coin to an inch or more in diameter. There are practically no subjective symptoms. The affection is insignificant aside from the disfigurement and the knowledge of its presence. A second type is that known as the "black dot" or disseminated ringworm of Alder Smith, produced by trichphyton endothrix. In this there are numerous small bald areas. Each bald spot involves approximately one-half to a dozen hairs. Each area shows several dark points which indicate the broken stumps of hair, which in this case are level with the surface. This type is produced by the megalosporon endothrix. The third type is the kerion, usually produced by trichophyton ectothrix. This is a moist lesion resembling a flat carbuncle. It is variable in size up to as large around as a silver dollar. There are points throughout the surface from which fluid exudes. It is these points which suggest carbuncle. On palpation a sense of pseudofluctuation is present. The lesions never suppurate in the sense of forming an abscess. Incision into them, therefore, would be an error. Occasionally, an inflammatory reaction in these is marked and there may be accompanying regional adenopathy with elevation of temperature and constitutional symptoms. The hairs become thin over the surface of the lesion and in time all become exfoliated when resolution takes place. While there is usually one lesion, there may be several. This affection is commonly produced by the megalosporon ectothrix. This organism is one that is responsible for ringworm of the beard and other moist ringworms of the body. It is from the kerion that dissemination sometimes occurs, producing the secondary ringworm eruption which is known as the trichophytid. Diagnosis.—The common type of ringworm of the scalp is readily distinguished clinically from alopecia areata, in which the individual bald patches are completely denuded and shiny, whereas in ringworm the patch contains the broken stumps of hair. There may be short hairs in the margin of the patch of alopecia areata which resemble exclamation points. This exclamation point hair is diagnostic of alopecia areata and was originally pointed out by Crocker. The broken stumps of hair in the ringworm patch have lost their elasticity, which is shown when the finger is passed over the surface in that they do not return to their upright position in the same manner that normal hairs do. Finally, the removal of a [12] hair with its sheath and its examination microscopically reveals a mosaic of small spores surrounding it. In the black dot variety trichophyton endothrix is seen as a jointed mycelium lying entirely within the hair, and in kerion similar appearing fungi, trichophyton ectothrix, is seen both within and around the hair. Psoriasis and seborrheic dermatitis are readily distinguished by a lack of alopecia. Treatment.—When possible roentgen therapy should be employed. With the present methods of measurement of the rays the procedure is safe in the hands of an experienced operator. It is suggested that the scalp be blocked into areas so the surface exposure will be as nearly flat as possible. The dosage of the rays is designated as an epilating dose. Fourteen days after exposure the hairs fall and with them the fungi. The hairs are replaced in two months. If roentgen ray therapy is not available, the local application of iodine crystals in goose grease in the strength of 4 grams in 3 0 grams, vigorously and regularly applied, is efficient. Chrysarobin in the strength of 5 per cent is also valuable and should be employed until reaction occurs, after which a soothing ointment is used until the reaction subsides. Care must be exercised that chrysarobin does not get in the eyes of the patient. Other applications are less efficient but at times may be necessary, such as white precipitate and salicylic acid.. Paronychia. Mycotic paronychia presents a characteristic picture and occurs in two forms, acute and chronic. The acute form is quite generally distributed, but occurs frequently in workers in fruit canneries and other industrial labourers. The chronic form presents a characteristic picture described by McLeod as a "pad or bolster-like swelling of the nail wall, which on being squeezed emits a head of pus on the nail plate." This enlargement is most marked at the base of the nail and gradually tapers down on the sides toward the distal end of the nail plate. The degree of inflammation varies in different cases and there is usually an associated dystrophy of the nail plate, due to interference with the formation of the nail at the lunula. In acute cases, such as described by Kingery and Thienes, seen in workers in fruit canneries, there is much swelling and pain and often shedding of the nail. Monilial onychia resembles the ringworm type. In the chronic form transverse ridges Occur in the nail plate and it becomes opaque, thickened, discolored and brittle. Subungual keratoses are present beneath the lateral and distal portions of the plate, causing it to be raised from the bed. Perleche In this condition, there is an inflammatory reaction occurring at the angles of the mouth, usually in children. It is characterized by a thickening and whitening of the epithelium, together with fissures. The affection sometimes spreads toward the centre of the lip and over the glabrous skin in the immediate vicinity. The thickened epithelium, often likened to mother of pearl, is sometimes easily detached. Occasionally, a moderate degree of crusting occurs. The fissures are superficial and rarely bleed and ulceration does not occur. A scaling dermatitis of seborrhceic type sometimes occurs in the immediate vicinity. Erosio Interdigitalis. This type occurs on the web of the fingers, usually on the third and fourth interspace. It may occupy all of the interspaces and it sometimes occurs between the toes. It is characterized by a shiny red area, surrounded by a collarette of scales, or it may be represented by an accumulated mass of sodden moist whitened epidermis. Vesicles are usualh" absent, though points on the reddened area may indicate former vesiculation. This forrr of moniliasis is exceedingly difficult to eradicate. In addition to the erosio type of lesion, a vesicular and papulo-vesicular eruption occurs in the interdigital surfaces with occasional maceration and Assuring. Waterbed Mycosis. This form is characterized by the development of herpetic-like vesicles with red areolae, together with pustules. These develop in a continuous water bath or on areas of the skin where moist dressings are applied over a considerable period of time. A frequent site is the abdomen, following laparotomy where moist hot dressings have been employed. At times the inflammatory reaction becomes marked, in which case redness, edema, weeping and crusting occur. [13] Glabrous Skin Types. On the glabrous skin a mycotic dermatitis is characterized by variously sized, well- defined, circular, red, scaling patches. By fusion gyrate configurations are produced. Moist crusting patches, suggesting eczema, occasionally develop, while in widespread cases there occurs simply a dry dull red scaling dermatitis. Patches begin with vesicles or vesico- pustules, which rupture, leaving denuded red areas surrounded by rings of detached epidermis. These spread peripherally and by coalescence with others form the patches. By the development of new vesicles in the vicinity and their undergoing the above evolution, large areas become invaded. In the crotch and beneath the breasts and in other intertriginous regions, the bottom of the cleft is usually fissured, while the skin in the involved area is shiny, light to dark red, presents some moisture and has scale covered margins which are polycyclic in outline. When the ano-genital region is involved, varying degrees of itching occur for the relief of which scratching is practiced, which results in thickening, excoriations and Assuring of the skin. In the anal region the erosio type seen between the fingers is sometimes present. Patches of dermatitis characterized by redness and vesiculation, scaling and crusting, mav also be found on the dorsum of the hands and on the forearms. Involvement of these areas frequently occurs in association with paronychia seen in workers in fruit canneries. Dermatitis Seborrhoeica. The clinical description of this form of dermatitis will not be outlined, as it is familiar to all. The point of interest in this connection is the fact thkt a yeast-like organism, spore of Malassez or pityrosporon of Malassez, was cultivated by MacLeod and Dowling from all types of this affection and the disorder reproduced by experimental inoculation. In their work they found it necessary to inject the cultures intradermally or to rub them into lightly scarified areas, to reproduce the affection. Monilial Infection of Mucous Membrane. In addition to thrush, which has long been known to be of mycotic origin, other forms of stomatitis and glossitis occur. As there is no symptom complex characteristic of monilial infection, and as these organisms are sometimes found as saprophytes1 in such diseases as syphilis, some difficulty is encountered in recognizing these affections. On the lip and buccal mucosa and on the mucous membrane of the pharynx and larynx, grayish white membranous pellicles of varying dimensions are seen. These pellicles are translucent and usually easily detachable. They also occur on the tongue and gums. Occasionally there is apparently more thickening when the pellicles become more adherent, and when detached leave superficial erosions, thus presenting a clinical picture of leukoplakia. On the buccal mucosa Engman and Weiss early described a lesion which occurred as a glistening white mat of filiform projections situated on a white macerated base. On the tongue Zeisler described scroll-like patterns resembling geographic tongue. Robinson and Moss described an acute form in which the anterior surface of the tongue was red and the papillae were ©edematous and eroded; also a chronic form in which the papillae were absent, and the surface of the tongue presented a smooth or slippery appearance like wet, red rubber. Miller and Morrow described a deep form in which a gumma-like lesion developed in the soft palate in the tonsillar region. This lesion developed acutely and caused perforation of the soft palate. Etiology.—Cutaneous and mucous membrane mycotic infections may occur at any age from infancy on and in both sexes. Paronychia is at times an occupational affection induced by the cases described by Kingery and Thienes by contact with fruit juices in cannery workers, and by orange juice in cases described by Sutherland Campbell. It frequently occurs in women who handle sugar, such as those employed in confectionery factories, and in pastry cooks, and so on. Diabetes is occasionally a predisposing factor. In the eriosi type constant immersion of the hands in water, a condition imposed in washer- ' women, is effective, and constant wet dressings constitute the predisposing factor in the water bed type. Infection of the skin in infants frequently comes from oral and intestinal thrush and in adults not infrequently from the stools. The organism most frequently found [14] .:;■,-;■,'..*-.-:. :..^i:--;*.»-_., is monilia albicans (formerly oidium albicans). Cryptococci, pityrosporon of Malassez and other yeast-like organisms are also concerned in the production of these mycoses. Diagnosis.—The major portion of cases of mycotic infection of the skin due to monilia and related organisms usually present sufficiently characteristic symptoms for their recognition. A microscopic examination in all cases is essential. Scrapings from the lesions are mounted on a slide ina 10% to 25% solution of sodium hydroxide over which a cover slip is applied and gently heated. The organism shows plainly and presents the following characteristics with a medium high power objective. Mycelium and spore-like bodies are seen. The mycelia are more delicate and less refractile than those of ringworm. Septa are rarely demonstrable. Oval spore-like bodies with buds attached to the ends are also present. In young cultures the organism appears chiefly as round or oval cells, which multiply by budding. In old cultures hyphae develop. Treatment.—Oral thrush in infants responds well to swabbings with a 1 % solution of gentian violet, together with mild alkaline mouth washes. For superficial lesions of the mucous membranes of the mouth and vagina, a 3 % solution of gentian violet is efficient, using it as a swab twice daily. Alkaline mouth washes for the oral cavity and a douche containing a 1:2000 solution of potassium permanganate for the vagina facilitate recovery. For the deeper lesions on the oral mucosa surgical excision, roentgen rays and the internal use of potassium iodide may be necessary. Paronychia responds quickly to the local application of a 5% suspension of chrysarobin in chloroform. This is very efficient and was originally recommended by Morrow and Lee for the treatment of chronic paronychia before moniliasis had been recognized. In the erosio type, which is resistant, the parts are to be kept dry. The local application of chrysarobin in the strength of 5% to 10%, or tincture of iodine, is valuable. In the water bed type suspension of wet dressings, together with the application of a soothing lotion, such as the aqua calcis and zinc oxide lotion, together with a 10% naftalan, or 2% ichthyol ointment, soon relieves the condition. In the intertriginous type occurring especially beneath the breasts, and the crotch, painting with a 3 % solution of gentian violet is very efficient. When much inflammatory reaction is present, a preliminary treatment for several days may consist in soaking the parts twice daily with a hot solution of potassium permanganate in the strength of 1:2000, dressing the parts in the interim with an ointment containing 10 % naftalan. In perleche, Finnerud found the local application of an 8% solution of silver nitrate efficient. This application may be repeated at three or four-day intervals. Prophylaxis is necessary in this condition when occurring in epidemics and consists in the use of individual drinking cups and towels, and careful sterilization of the utensils used by the patients, and, also, avoidance of direct contact. BIBLIOGRAPHY. 1. Ormsby and Mitchell: Ringworm of the Hands and Feet. Jour. Amer. Med. Assoc, 72: 711, 1916. 2. Legge, Bonar and Templeton: Epidermomycosis at the University of California. Arch. Derm, and Syph., 27:12,1933. 3. Osborne and Hitchcock: The Prophylaxis of Ringworm of the Feet. Jour. Amer. Med. Assoc, 97: 453, 1931. 4. Ayres, Anderson and Youngblood: Fumigation as an Aid in the Control of Superficial Fungus Infection. Arch. Derm, and Syph., 24: 283, 1931. 5. Peck: Epidermophytosis of the Feet and Epidermophytids of the Hands. Arch. Derm, and Syph., 22: 40, 1930. 6. Jadassohn: Kor. Blatt, fur Schweizartze, p. 24, 1912. 7. Guth: Arch, fur Derm, und Syph., 118: 856, 1914. 8. Chable: Jadassohn's Clinic, Derm. Ztschr., 24: 20, 1917. [15] LESIONS OF THE STOMACH AND DUODENUM AND THEIR TREATMENT Waltman Walters, M.D., D.Sc, Division of Surgery, The Mayo Clinic, Rochester, Minnesota. In discussing lesions of the stomach and duodenum one too frequently refers to them as though they were similar structures. Such is not the case, however, and they differ widely not only in the reaction of their respective secretions, but also in the types of abnormal lesions which may develop in them. For example, the malignant lesions, carcinoma and sarcoma, involve the stomach but almost never involve the first portion of the duodenum. When a carcinomatous lesion develops in the duodenum it is usually either at the papilla of Vater, and hence really in the common duct rather than in the duodenum, or it is an extension of the carcinoma or sarcoma from the head of the pancreas into the wall of the duodenum. When malignant lesions occur in the stomach they may extend to the pylorus, but, almost without exception, they abruptly terminate at the duodenal wall. The similarity of the symptom complex associated with benign gastric ulcer and with benign duodenal ulcer has led to the thought that they are lesions of similar type. Not only do they differ from the standpoint of the tissue in which the ulceration occurs, but also from that of the variable pathologic nature of the lesions themselves and their response both to medical and surgical treatment. The primary ulcer which occurs in the first portion of the duodenum is never malignant, whereas that which occurs in the stomach has a 10 per cent chance of becoming malignant according to Stewart, and a 20 per cent chance according to Katsch. Benign Lesions of the Stomach. Ulcer.—When a patient presents a history suggesting benign ulceration, it is of first importance that a roentgenologic examination be made by a competent roentgenologist to determine the exact situation of the lesion. A gastric ulcer always should be regarded with the suspicion that it is an ulcerating carcinoma. This is particularly true of prepyloric lesions as well as of lesions on the greater curvature. At The Mayo Clinic, in dealing with gastric ulcers we proceed on the assumption that chronic ulcerating gastric lesions are malignant until they are proved to be benign. This has helped us in the early recognition and satisfactory removal of many small carcinomatous lesions of the stomach which, because of their temporary beneficial response to a medical regimen, otherwise might have been allowed to grow, under the erroneous impression that the lesions were benign. The treatment of gastric ulcer is dependent on several factors, among which are: (1) duration and type of symptoms; (2) healing of the lesion, or its failure to heal under a medical regimen carried out in scientific fashion; (3) presence or absence- of a crater, especially with respect to bleeding, and (4) presence or absence of pyloric obstruction. When the symptoms have been of short duration and the ulcer is small, every attempt should be made to induce healing by nonsurgical means. Such methods, of treatment have been commented on in detail by Eusterman4 5, Jordan7 8 and others. A favorable clinical response to such medical treatment consists of relief of pain, disappearance of blood from the stool and disappearance of the niche seen on roentgenologic examination. In most instances, these criteria can be assumed to be of immediate value in determining the ability of the lesion to respond to medical measures; however, a number of years ago the late Charles McVicar called attention to the fact that such a response is not confined to benign gastric ulcers but that it may occur as well in the treatment of small, ulcerating, malignant lesions of the stomach. Exact information should be obtained from the patient as to whether a medical regimen has been instituted previously, and evaluation should be made of the accuracy with which it was carried out and the results which followed its use. For if one or more attempts have been made to cause the lesion to heal by a carefully controlled medical regimen, but with recurrence of the ulcerating lesion, the lesion should be removed surgically. In the period during which our patients who have gastric ulcer are being kept under observation and medical treatment is being employed, even if the lesion appears to be healing satisfactorily, the patient is advised to undergo re-examination at intervals of three months for the first year, regardless of the presence or absence of symptoms, in order to determine that the ulcer has remained healed. If the ulcer recurs or if it fails to heal, [16] ■.»■-**;*•;.u\>.f- - i tSaia't'; surgical exploration is thought advisable. In a few cases, unfortunately, wherein response to the initial medical regimen seemingly was satisfactory, the patient failed to be impressed with the importance of repeated examinations either at the clinic or elsewhere, and returned later only to find that he had carcinoma of the stomach. Perforating gastric ulceration with crater.—The perforating gastric ulcer, with a crater more than 1.5 cm. in diameter, is not likely to respond to a medical regimen. These ulcers, for the most part situated on the lesser curvature, will be found to have penetrated into the gastrocolic omentum, whereas some situated on the posterior wall, in most cases near the lesser curvature, may penetrate into< the capsule of the pancreas. It might be inferred that this type of lesion is one in which malignant cells are most likely to be present. Although this may be the case, especially if the lesions have large craters, not infrequently the smaller ulcerating gastric lesions may be in a mass of highly malignant ulcerating carcinoma which already has involved the lymph nodes when the patient presents himself for examination or treatment. Gastric ulcers producing pyloric obstruction.—Ulcerating lesions of the stomach, either benign or malignant, if they occur on the lesser curvature, not infrequently produce so much disturbance of motility, as disclosed both by clinical and roentgenologic examination,, that only the presence of pyloric obstruction can be determined, and in some of these cases the lesion is suspected of being a duodenal ulcer. Particularly is this true if the patient has had an ulcer-like type of dyspepsia for a prolonged period. Fortunately, in cases of pyloric obstruction, surgical procedures are usually advised, the presence of a gastric lesion is recognized at operation and its appropriate treatment is carried out. The roentgenologist's diagnosis that an ulcerating lesion of the stomach is malignant is almost certain to be correct, particularly if the meniscus sign of Carman is seen in the course of roent- genoscopic examination. But the fact that an ulcer of the stomach is reported as being probably benign by the roentgenologist does not exclude the possibility that the lesion is carcinomatous. On many occasions at operation, with small gastric ulcerations readily visible and palpable, the fact that the lesion was carcinomatous was not recognizable until microscopic examination proved the fact. Other benign lesions of the stomach.—The other benign lesions of the stomach are fibromas, fibromyomas, leiomyomas, neurofibromas and polypoid adenomyomas. Although these benign tumours occur relatively infrequently, an incidence of 1.5 per cent of the cases of gastric lesions, they are lesions of considerable importance and should be removed surgically. The outstanding symptom which they produce is bleeding, which is usually of the weeping type and may escape the notice of the patient until the pallor of the skin or examination of the blood reveals the presence of a severe degree of anaemia. Seldom is the blood vomited, but occasionally the presence of tarry stools has been noted by the patient. The diagnosis of these lesions is made on fluoroscopic or gastroscopic examination and the skilled roentgenologist is able to demonstrate lesions of this type when they are thumbnail in size and not more than 1 cm. in diameter. Almost constantly, adenomatous polyps of the stomach are associated with a relative achlorhydria, thus leading one to suspect that they are malignant. Many of them are malignant, for in their early stages malignant cells may be found in the perforated polyp. The leiomyomas frequently degenerate, and Sworn and Cooper have reported that metastasis may occur. It is extremely important that early recognition of these tumours be made, not only to prevent the progressive anaemia which is likely to occur, but' also because some of them are malignant and many of them are likely to degenerate and become malignant. Before this happens, usually an excision of the portion of the gastric wall containing the lesion is all that is necessary, but if malignant cells are demonstrated in the stalk of the polyp, or in the polyp itself, if sessile in type, gastric resection should be performed. Polyps of the duodenum are exceedingly rare. They do occur, however, and may be the cause of bleeding. They may escape detection in palpating the first portion of the duodenum owing to the fact that the polyp has such a long pedicle that it extends into the second portion of the duodenum. Other benign surgical lesions of the stomach are tuberculosis and, in some cases, gastric syphilis. Tuberculosis is exceedingly rare and the diagnosis has been made in but seven [ 17] cases at The Mayo Clinic3. The diagnosis usually is not made preoperatively. Because gastric tuberculosis deforms the stomach in a manner similar to that of carcinoma, on roentgenographic examination the lesion is likely to be reported as being malignant. Usually tuberculosis can be found elsewhere in the patient's body. Treatment for these lesions is performance of partial gastrectomy. At operation, if there are tuberculous glands in the gastrocolic or gastrohepatic omentum, they can be removed with the portion of the stomach containing the tuberculosis. Syphilis of the stomach may produce digestive symptoms simulating malignant disease. The differential diagnosis usually is made by the roentgenologist, who is unable to palpate a tumour in spite of the fact that a large part of the stomach apparently is involved by the pathologic process. Such being the case, the absence of cachexia and presence of a normal blood count, together with serologic evidence of syphilis, will usually lead to a diagnosis of gastric syphilis. Some of these cases will respond to antisyphilitic treatment and healing of the multiple ulcerations of the stomach occurs without obstruction. In other cases, particularly when the ulcerations are confined to the lower third of the stomach, the healing process may result in fibrosis and obstruction, necessitating either resection of the involved portion of the stomach or the performance of gastro-enterostomy. I have used these methods of treatment of gastric syphilis, when indicated, with satisfactory results in each group. Malignant Lesions of the Stomach. The most frequent malignant tumour of the stomach is carcinoma. It is ninety-nine times more frequent than gastric sarcoma. The differential diagnosis usually cannot be made between these two lesions until the time of operation and frequently not until the pathologist examines the lesion microscopically. One of the characteristics of carcinoma of the stomach is that microscopic examination shows an extension of the growth to submucosal regions adjacent to the lesion. Such regions of extension may not be apparent on gross examination. This, together with the fact that in performing partial gastrectomy such avenues of extension are removed widely and, in addition, the gland-bearing avenues in the omentum along the lesser and greater curvatures of the stomach can be removed, would indicate that partial gastrectomy is the operation of choice rather than segmental resection of the portion of the stomach that contains the carcinoma. Extension of gastric carcinoma to the lymph nodes or by metastasis to the liver is erratic, for small gastric lesions may be of a high grade of malignancy and produce glandular involvement or hepatic metastasis, and huge lesions may be of a low grade of malignancy and produce no glandular involvement. Therefore, removal of the largest gastric carcinoma should always be attempted if sufficient uninvolved gastric tissue remains proximal to it for anastomosis with the intestine. The treatment of carcinoma as well as sarcoma of the stomach is essentially surgical and offers the greatest possibility not only of relief of the troublesome symptoms of obstruction, ulceration, haemorrhage and so forth, but, when the lesion is confined to the stomach or even when the adjacent glands are involved, removal of a large portion of the stomach and its adjacent gland-bearing omentum will give an incidence of five-year cures varying between 40 and 50 per cent if the glands are not involved, and 18 to 20 per cent if the glands are involved. Of the patients operated on, only about 40 to 50 per cent have removable lesions. In the period 1927-1936 at The Mayo Clinic, the incidence of resections has varied from 36.6 to 47.4 per cent. When the lesion is confined to the stomach, the surgeon must be willing to perform subtotal and, in a few cases, even total gastrectomy. The risk of subtotal gastrectomy is very little more than that of partial gastrectomy and for lesions of a comparable degree of malignancy the surgical results are comparable, for very large malignant lesions are frequently found to be of a low grade of malignancy. The great field for advancement lies in recognizing malignant gastric lesions in their early stages when they are small. This refers particularly to general acceptance of the hypothesis that 17 per cent of carcinomas of the stomach originate in chronic gastric ulcers (Stewart). Every ulcerating lesion of the stomach should be considered potentially malignant until it is proved otherwise, and even when the lesion is small, if it does not respond [18] promptly to a single course of medical therapy, it should, be removed. The same applies to the smaller polyps of the stomach, which in their early stages may be benign but which may later become malignant. It is a great triumph for the roentgenologist that he is able to demonstrate lesions of the stomach as small as 1 cm. in diameter in practically all cases, with an error of not more than 5 per cent; even this small error should'be lessened by gastroscopic examination. In following out these ideas in a group of 242 cases of malignant lesions of the stomach in which patients were operated on at the clinic in 193 6, partial gastrectomy, including subtotal gastrectomy, was performed in 109 cases, an operability of 45 per cent. The mortality rate in these 109 cases was 12.8 per cent. In sixty-seven so-called borderline cases of gastric ulcer in which the patient was operated on either because of the large size or perforating or hemorrhagic nature of the lesion, or because of failure of a small lesion to respond to a course iof medical treatment, the mortality rate was 2.9 per cent. Two deaths occurred in a series of thirty-eight cases in which partial gastrectomy was performed because of the large size or perforating or haemorrhagic nature of the lesion. In twenty-five cases in which the gastric ulcer was small and lent itself to segmental excision, and in which gastroenterostomy was performed, no deaths occurred. These results, it seems to me, refute the argument of a few that the risk of operation for gastric ulceration is greater than the chance that the lesion is malignant or may become so. Benign Ulcers of the Stomach and Duodenum. A primary duodenal ulcer, as has been said, never becomes malignant. Indications for operation in such cases are determined largely on the basis of whether or not complications such as perforation, obstruction and haemorrhage are present. Everyone is agreed that immediate surgical procedures are necessary when an intra-abdominal perforation of a duodenal or gastric ulcer occurs. When a duodenal ulcer has produced sufficient obstruction so that the patient's stomach is dilated with persisting gastric retention, the necessity for correcting this mechanical disturbance is well recognized. Repeated haemorrhages from a duodenal ulcer usually frighten the patient or the physician so that the patient is taken hastily to the surgeon or to the hospital. The statement that surgical treatment of lesions that would fall into these groups is advisable will find but few critics. On the other hand, the surgeon is very glad to refer to the medical man for treatment patients who have duodenal ulcer whose symptoms are mild and who have no complications. Particularly true is this if the patient is young and the symptoms have, been of but short duration. There are patients, however, who have a long history of chronic duodenal ulcer, who have obtained over many years periodic relief of their symptoms by adherence to a modified type of Sippy diet and who have become so tired of it that they are willing to go to almost any end to be relieved of their symptoms. In such cases I do not hesitate to/ advise a surgical procedure. Ty]pes of operation for gastric and duodenal ulcer.—My interest in the problem of whether or not gastric resection should be done for duodenal ulcer dates from that time in the early 1920's when Finsterer, visiting various surgical clinics in the United States, strongly advocated gastric resection as a routine method of treating duodenal ulcer in order to eliminate gastrojejunal ulceration. A similar viewpoint had been previously taken by Lorenz and Schur, two other Viennese surgeons. Although it had been the custom at the clinic as early as 190512 to perform partial gastrectomy in the treatment of largd, calloused gastric ulcers because of the possibility of the lesion being malignant, the more conservative procedures of gastroenterostomy or excision of the duodenal ulcer, with plastic operations involving the lower portion of the stomach and the duodenum, had been the surgical procedures of choice for patients who had duodenal ulcer and who had failed to obtain relief of symptoms on a medical regimen. Those who advocate partial gastrectomy for duodenal ulcer do so on the basis of the nresence of associated gastritis and the low incidence of recurring ulceration subsequently; however, the risk of partial gastrectomy for duodenal ulcer in the hands of those of considerable experience will vary from 3 to 9 per cent. To my way of thinking the only thing that partial gastrectomy does better than gastroenterostomy is to produce a greater reduc- [ 19] tion in gastric acidity in a greater number of cases. It is a matter of record that but 70 per cent of the patients obtain a relative achlorhydria; therefore there is no reason why the 3 0 per cent who fail to do so may not be as susceptible to recurring ulceration as those who have undergone gastroenterostomy. More interesting still is the fact that achlorhydria will in many cases develop after gastroenterostomy. After all, the crux of the matter, from the standpoint of recurrence, is whether or not the tissue resistance of the attached jejunum or duodenum has improved sufficiently so that, if free hydrochloric acid does remain in the gastric contents, recurring ulceration will not take place. It is generally recognized that gastroenterostomy carries a much lower surgical mortality rate than partial gastrectomy, and in our experience at the clinic, as well as is evidenced in reports from other surgical clinics, gastrojejunal ulcer appears in only about 3 or 4 per cent of the cases. We have not, therefore, been impressed with the necessity for the routine performance of partial gastrectomy for primary duodenal ulcer on a comparative basis of formation of gastrojejunal ulceration. In this connection it is worthwhile calling attention to the report of a collective investigation by the British Medical Association11 in 1928 into the subsequent histories of patients who had undergone gastroenterostomy in various parts of the British Empire during the period 1920 to 1924, inclusive. Quoting from this report: "Secondary gastrojejunal ulcer occurred in 2.8 per cent of 744 cases in which gastroenterostomy was performed for duodenal ulcer. . . . The postoperative mortality was 5 per cent. . . . The results of the operation were satisfactory in about 90 per cent of the cases." When one has a benign lesion of the stomach to remove, segmental resection of the portion of the stomach containing the lesion is satisfactory. If a gastric ulcer is present and is small in size, excision carries a] mortality rate as low as when gastroenterostomy is performed alone and the results are usually excellent. The perforating gastric ulcer with a crater more than 2 cm. in diameter is best treated by removal in the form of partial gastrectomy. During 1936, partial gastrectomy for benign and malignant-lesions of the stomach and duodenum was performed in 213 cases at The Mayo Clinic.17 Of these operations, 104 were for benign lesions,, with a mortality rate of 3.8 per cent. Of these 104 operations, in 33 cases the operation was primary partial gastrectomy performed for gastric ulcer. An additional five patients had undergone gastroenterostomy previously; in these five cases, therefore, in addition to partial gastrectomy, removal of the stoma and closure of the jejunal opening were carried out. In twenty-five cases in which ulcers were removed by local excision, combined with gastroenterostomy or destruction by cautery, no deaths occurred. On only two occasions in the last three years have I been satisfied to perform segmental resection of a portion of the stomach containing the ulcer without also performing gastroenterostomy. On both of these occasions the lesion was very large and was situated just below the esophageal-gastric junction. Both patients were large and obese, and partial gastrectomy would have been exceedingly difficult to perform and would have been attended by a high risk because neither patient was in good condition. On that account, excision of that portion of the gastric wall which contained the ulcer was carried out, with good results which have persisted to date in both cases. Good results have been obtained from the transgastric excision of certain large, perforating gastric ulcers situated high on the posterior wall of the stomach. The approach to the lesion is made through the anterior wall of the stomach. After excision of the lesion, the edges of the stomach are sutured together from the inside and, after closing the incision in the anterior wall of the stomach, a portion of the gastrocolic omentum is carried posterior to the stomach to serve as a patch over the region of the anastomosis. As has been indicated, whenever possible I prefer the operation of partial gastrectomy for accessible, large, perforating gastric ulcers. I use the Billroth I, the Polya, and the Polya-Balfour types of anastomosis; the choice of any one of these procedures depends on the situation of the ulcer, the mobility of the duodenum, the amount of fat in the transverse mesocolon and the accessibility of the avascular spaces in the transverse mesocolon. Partial gastrectomy can be applied in neraly all cases of gastric ulceration. [20] Gastric ulcers situated high on the lesser curvature and those situated high on the posterior wall of the stomach frequently are reported on the basis of roentgenologic examination as of questionable accessibility for surgical removal. Their high situation is likely to be considered an additional reason for continuation of medical treatment which has failed to cause healing of the ulcer previously. That all benign gastric lesions are accessible to surgical treatment is, therefore, a point which deserves emphasis. On several occasions, because of the perforating nature of the lesion and its attachment, particularly to the capsule of the pancreas, and because of contraction and fixation of the stomach in the vicinity of the lesion, the appearance has been that the lesion was highler than it really was. Removal of that portion of the lesser curvature which contains a gastric ulcer, as in the Billroth I or the Hoffmeister-Polya type of resection, enables the surgeon to preserve a sufficient amount of the body of the stomach and, particularly, the greater curvature, for its anastomosis with the duodenum or with the jejunum. The particular field of usefulness of the Billroth I type of anastomosis lies in the ability it gives the surgeon to remove perforating ulcers high on the lesser curvature without removing too much of the stomach itself. Sufficient mobility of the duodenum must be present, however, to allow attachment of it to the proximal segment of the stomach without tension. In my experience the Billroth I type of anastomosis following partial gastrectomy and partial duodenectomy for duodenal ulcer has not been as satisfactory as is the Polya type, and in a few of my cases duodenal ulcer has recurred. Apparently, however, results are different when the operation is performed for gastric ulcer and ulceration does not recur. In cases of gastric ulcer, study of the gastric acidity subsequent to operation discloses that relative achlorhydria is obtained in practically every instance16; this is contrary to the low occurrence of relative achlorhydria after the Billroth I type of anastomosis has been performed for duodenal ulcer, in which circumstance relative achlorhydria develops in but 2 5 per cent of the cases.18 In my experience, most cases of malfunctioning gastrojejunal anastomosis subsequent to both posterior gastroenterostomy and posterior Polya types of anastomosis following resection of the stomach have been the result of choosing to make the anastomosis posterior to the colon, through a very large, fatty transverse mesocolon. In such cases it would have been better to have chosen a longer loop of jejunum and to have made the anastomosis anterior to the transverse colon, as advocated by Balfour1 2, combining the operation with entero-anastomosis between the jejunal limbs. The operation of sleeve resection for gastric ulcer was performed more frequently years ago than it is at the present time. It is an operation of considerable usefulness in a selected group of cases. Such cases are those in which partial gastrectomy of the Billroth or Polya type does not seem indicated because of the mechanical difficulties entailed or because excision of the segment of the stomach containing the ulcer would not remove enough gastric tissue. In a study made of postoperative gastric acidity among patients who had had gastric ulcer and on whom different types of operations had been performed, the striking thing was the high frequency with which relative achlorhydria was the rule, provided that adequate drainage of the stomach had been obtained following operation. This was in contrast with the effect of similar types of operation performed for duodenal ulcer. REFERENCES. 1. Balfour, D. C.: Results of Gastro-Enterostomy for Ulcer of the Duodenum and Stomach. Ann. Surg., 92 : 558-562 (Oct.), 1930. 2. Balfour. D. C.: Factors of Significance in the Prognosis of Cancer of the Stomach. Ann. Surg., 105:733-740 (May), 1937. 3. Clagett, O. T., and Walters, Waltman: Tuberculosis of the Stomach. Arch. Surg. (In press.) 4. Eusterman, G. B.: Gastric and Duodenal Ulcers: Factors Essential to their Successful Medical Management. Wisconsin Med. Jour.. 34:473-477 (July), 1935. [21 ] 5. Eusterman, G. B.: Medical Treatment of Gastric Ulcer. In: Eusterman, G. B., and Balfour, D. C.: The Stomach and Duodenum. Philadelphia, W. B. Saunders Co., 1935, pp. 457-462. 6. Finsterer, H.: Die chirurgische Behandlung des Magen—und Zwolfflngerdarm— geschwiires und seiner Komplikationen. Ergebn. d. ges. Med., 15:431-566, 1931. 7. Jordan, Sara M.: The Present Status of Peptic Ulcer. New England Jour. Med., 203: 917-920 (Nov. 6), 1930. 8. Jordan, Sara M.: A Review of Gastric Ulcer Problem. Jour. Am. Med. Assn., 107:1451- 1456 (Oct. 31), 1936. 9. Katsch : Quoted by Hurst, A. F.: Carcinoma of the Stomach. Lancet, 2 : 1455 (Dec. 18), 1937. L0. Lorenz, Hans, and Schur, Heinrich: Unsers Erfahrungen fiber den Wert der Antrum- resektion bei der Behandlung des Ulcus pepticum. Arch, f. klin. Chir., 119: 239-276,1922. LI. Luff, A. P.: Collective Investigation into the After-History of Gastro-Enterostomy. Brit. Med. Jour., 2:1074-1078 (Dec. 7), 1929. L2. Mayo, W. J.: A Study of Gastric and Duodenal Ulcers with Especial Reference to Their Surgical Cure. Ann. Surg., 47:885-893 (June), 1903; Coll. Papers Mayo Clinic, 81-94, 1905-1909. L3. Stewart, M. J.: Quoted by Walton, Sir James: Carcinoma of the Stomach. Lancet, 1:1101-1107 (May 13), 1936. L4. Sworn, B. B., and Cooper, T. V.: Leioyoma of the Stomach. Lancet, 1:428-429 (Feb. 19), 1938. L5. Walters, Waltman: Carcinoma of the Stomach. Proc. Inter-State Postgraduate Med. Assemb. N. Amer., 1937. L6. Walters, Waltman: Should Gastric Resection Be Done for Duodenal Ulcer? Surgery, 2:759-768 (Nov.), 1937. L7. Walters, Waltman, and Gray, H. K.: Annual Report for 1936 of Surgery of the Stomach, Duodenum and Biliary Tract. Proc. Staff Meet. Mayo Clinic, 12 : 561-566 (Sept. 8), 1937. L8. Walters, Waltman, and Wolff, L. H.: (Unpublished data.) INTRACTABLE PAIN R. Glen Spurling, M.D. Surgical relief of intractable pain is one of the newer and more important developments in neurosurgery. It is not possible for me to define satisfactorily the term intractable pain. A pain that is unbearable to one individual may be quite tolerable to another. Therefore, each patient must be considered according to his own conception of the unbearable nature of his discomfort. Surgical treatment of intractable pain may be grouped under two general headings: First, where surgery is capable of removing the etiological factor, thus relieving the pain; second, where surgical procedures are designed to sever pain pathways without direct attack upon a known or unknown etiological factor. As specific examples in the former group we may cite pain associated with primary tumours of peripheral nerves, primary tumours of the spinal cord and intraspinal nerve roots, arm pain of which I spoke this morning, and low back and leg pain of which I shall speak tomorrow. In the second group, the pain may be of unknown etiology, like trigeminal neuralgia, or it may be associated with primary or metastatic growths of the spine, advanced malignancy of the pelvis and lower extremities. In either circumstance a direct surgical attack upon the cause would not be feasible. I shall not attempt to discuss all of the procedures which have been designed to relieve intractable pain. Many of them are still in a nebulous state of development; others are of questionable merit. I shall limit my discussion to those conditions producing intractable pain which in my own experience have responded satisfactorily to surgical efforts. Primary or Metastatic Malignancy.—The intense intractable pain associated with primary or metastatic malignancy is a problem with which we are all faced far too frequently. Routine administration of morphine in ever-increasing doses and at shorter intervals has proven unsatisfactory, because a dose sufficiently large to control pain must of necessity benumb mentality. Tolerance for the drug is acquired, as the disease may continue for [22] satwtmtmMM tm, ¥<*.*;« ; months or even years, and enormous doses may fail to afford even partial relief from suffering. For these and other reasons any surgical procedure which is effective in abolishing that pain, yet at the same time does not increase disability, should be a welcome therapeutic adjunct. Chordotomy, i.e., cutting the pain tracts within the spinal cord, answers just these requirements where the pain occurs below the level of the clavicles. Not until Spiller in 1911 demonstrated conclusively that in human beings the pain fibres pass upward in the cord in a definite tract was the solution of the problem placed finally upon a sound anatomical basis. Cutting the pain tracts within the spinal cord has now had sufficient trial to demonstrate its effectiveness and to justify its acceptance as a meritorious surgical procedure. It is, therefore, with the indications and contraindications for its use that I am now chiefly concerned. First, let me refresh your memory on the finer anatomy of the spinal cord. (Slides.) Indications and Contraindications to Chordotomy.—Of course, the pain tracts can be sectioned as high as the first cervical segment with relief of pain sensibility in the area on the opposite side of the body below the fifth cervical segment. However, the higher one performs chordotomy in the cervical cord the greater the risk of the procedure. Therefore, cutting the pain tracts higher than the fifth cervical segment, thus relieving pain below the first dorsal segment, is but seldom indicated. Chordotomy is a major procedure and, therefore, the general condition of the patient should be sufficiently good to justify the operative risk. Furthermore, the patient should have an ordinary life expectancy of six months or more. Age is not a factor providing his general physical condition answers the above requirements. The operation is always done under local anaesthesia; therefore, the operative risk should be small. Chordotomy will not relieve pain other than the type which is carried in the spinal thalamic tract; namely, a true root pain similar to that produced by painful stimuli. Pain of a burning character, itching, and other vague descriptive discomforts will not be favorably affected. After-effects.—Four ^segments below the level at which the chordotomy is done the opposite side of the body will be insensitive to painful stimuli. However, touch will be preserved and position sense and muscle, bone, and point sense will remain intact. Motor power of the leg should not be affected provided pyramidal tracts ha&ve been undamaged during the operative procedure. If both quadrants of the cord are cut at the same sitting there is usually retention of urine for several days to several weeks. This presumably is caused by the sudden elimination of painful stimulus which is initiated by bladder distention. If the operation is done in two stages this vesical disturbance is, as a rule, not observed. Other Conditions than Malignancy in which Chordotomy Is Useful.—Some of the most striking applications for chordotomy are in those cases with intractable pain from adhesions about the roots of the Cauda equina; amputation neuromas with causalgia, gunshot wounds of the peripheral nerves, etc. When the pain is limited to one leg the results of chordotomy are brilliant. Malignant Disease of the Face, Mouth and Throat.—Cases of inoperable malignancy about the face, gums, cheek or throat are eventually associated with intractable pain. In some instances the neoplastic growth is slow; consequently, years may elapse before death supervenes. Relief can be accomplished by section of the sensory nerve supply to the parts provided the disease is not too widely spread. When the growth is within the confines of the trigeminal distribution, section of the posterior roots of this nerve or alcohol injection or avulsions of peripheral roots may be sufficient. Where there is overlapping of the growth into the sensory distribution of the glossopharyngeal nerve, then posterior root section of the fifth and of the ninth cranial nerves accomplished through one cerebellar operative field is effective. If, in addition, when there is overlapping of the growth into the distribution of the higher cervical nerves, then rhizotomy, i.e., section of the sensory root of the cervical nerves, may be necessary in addition to the intracranial procedure. These operations may be quite formidable procedures, particularly when there is overlapping into one or more different sensory areas. Therefore, it is highly desirable for the patient's general condition to be such as to justify the procedure. [23 ] Subarachnoid Alcohol Injection for Intractable Pom.—I mention this procedure because of the frequency with which it is now being employed, yet my own experience with the method is sharply limited. I speak of it further to condemn its indiscriminate use. It is true that relief of pain may be obtained by the introduction of smalt amounts of alcohol into the subarachnoid space, yet the dangers inherent to the procedure are so great that its use as a substitute for chordotomy seems to me totally unjustified. I have personally observed paralysis of legs and incontinence of sphincters with or without recurrence of the original pain in enough cases to convince me that it is a dangerous procedure. In my opinion the only justification for its use is in those patients with advanced malignant disease in and around the pelvis, where life expectancy is so short that chordotomy is contra- indicated. Intractable Pain of Buerger's Disease. Pain is one of the earliest manifestations of thrombo-angeitis obliterans and continues to be the most disabling feature of the malady until gangrene and amputation supervene. In the early stages, intermittent claudication precipitated by exercise is of itself incapacitating. Later the excruciating leg pains which are constantly present irrespective of muscular activity are too well known to require further description. As early as 1858 Brown-Sequard stated: "In those cases of gangrene (in Buerger's disease) in which no obstruction has been found after death in the vessels of the dead part, it is extremely probable that a long persistent spasm of the blood vessels has existed." This early conception, now an established fact, pointed the way to a therapeutic measure which in properly selected cases has been the most important advance in the treatment of this disorder. Removal of the sympathetic tone to the vessels in the involved parts, thereby releasing the spasm of the vessels, has been practised successfully for a number of years. The first attempts to relieve the spasm was accomplished by removing vasomotor fibres peripheral to their ganglia (periarterial sympathectomy). This operation often gave satisfactory temporary results but the spasm soon recurred. Later, resection of the lumbar sympathetic trunk for disease in the lower extremities was proposed by Adson and his co-workers, and since then has been the method of choice in properly selected cases. Obviously, to treat this disorder successfully it is essential that We differentiate pre- operatively between arterial occlusions and arterial spasm. A number of tests have been proposed, but perhaps the simplest and most reliable one is spinal anaesthesia with procaine. The entire sympathetic mechanism is abolished in the anaesthetized zone, therefore, vasodilatation of all the arteries to their maximum degree occurs. The improvement in circulation can be measured accurately by the rise of skin temperature, by oscillatory readings, or by studying the capillary bed of the nails. The skin temperature response is, however, the most reliable and the simplest to perform. The rise of surface temperature (when the room temperature is constant) is, therefore, an accurate preoperative index of the amount of vasospasm present in each particular case and further indicates the probable improvement in circulation which may be accomplished by resection of the regional sympathetic ganglion. The symptomatic improvement from sympathectomy in properly selected cases is most gratifying; claudication disappears; small ulcers may heal and the feet stay warm and dry in all temperature environments. If the criteria for operation are not followed closely or if the surgeon compromises his position in the selection of cases for operation he is doomed to disappointments. However, sympathectomy does not cure the disease. It is purely palliative, and eventually, of course, the progressive occlusion of the arteries will occur and soft tissue changes result. This period of symptomatic relief is sufficiently long to more than justify the proceeding in all properly selected cases. Furthermore, when soft tissue changes supervene conservative amputations may be done with a better chance of stump healing than would have been the case if sympathectomy had not been resorted to. For those patients in whom sympathectomy is contraindicated much relief of the pain may be obtained by sectioning the peripheral sensory nerves. These procedures have given relief of pain in cases with ulceration and with advanced occlusive changes of the vessels. Section of the nerves not only interrupts pain impulses but usually brings about some release of peripheral spasm with appreciable warming of the part. [24] 'j-&aci**cM* iau :«>:-... Trigeminal Neuralgia: Tic Douloureux This violently painful state was described as early as the middle part of the 18th century, and statistics and figures indicate that the affliction has been known since the earliest civilization. In many respects the beginning of tic douloureux appears to be traceable to the teeth. The individual pains of an attack are like the agonizing stabs of a dying tooth pulp. However, no pathological changes have been discovered in either the peripheral nerves or the ganglion or the trigeminal root; therefore, the disease is still of unknown etiology. Usually the onset of the pain is abrupt, the first paroxysm being of painful severity and often likened to the darting of lightning into either the upper or lower jaw. Then there may be a considerable interval of freedom, after which the paroxysms come with increasing frequency. One division or other is always the starting point in each case. However, in the end, two or even all three divisions are likely to be involved. Although the intensity of suffering may diminish with time and the patient may have long intervals of comparative freedom, the disease continues to make life unendurable until relieved by death or surgical aid. Alcohol and drug addictions are not rare. Pain is often described as being like the stab of a knife or an electric shock and ending like an explosion in the face. The paroxysm may last from a few seconds to two or three minutes and then disappear as quickly as it came. The one characteristic invariable feature of tic douloureux is that between paroxysms the patient is comfortable. This feature clearly distinguishes true tic douloureux from the atypical neuralgias, and the importance of ascertaining this feature is essential in selecting cases for surgery. In true tic douloureux the pain does not leave the peripheral distribution of the trigeminal nerve. Any pain, whether it starts in this area or not, that radiates outside of this distribution is not tic douloureux. There is usually one spot on the face from which the paroxysm of pain may be initiated —the so-called trigger zone. If in the second division, the spot is usually about the lip or the nose; in the third division it is usually in the lower lip or gums, jaw^ or even the tongue. A blast of cold wind, applying water to the face or combing the hair may initiate an attack of pain. Usually the patient is free of pain in the early stages of the disease after he has gone to sleep. However, in the latter stages he may be awakened by paroxysms. The affliction is one of middle or late life, usually after the age of fifty. However, no age group is spared. In my series there has been one child of 15 with typical severe tic douloureux, and another of 17. Treatment.—There are now available four satisfactory methods of treatment: (1) alcohol injection of the peripheral branches of the nerve; (2) avulsion of peripheral roots; (3) alcohol injection of the gasserian ganglion; (4) intracranial section of the posterior roots of the nerve. Alcohol injection has been practiced for many years. The principle upon which this treatment is based depends upon placing within the nerve sheaths one or two cc. of absolute alcohol, thereby causing degeneration of the nerve fibres. The degeneration occurs from the point of injection peripheral to the sensory endings, leaving unaffected the cell bodies in Gasserian ganglion. Relief of pain is secured for just so long as it takes for the peripheral processes of the ganglionic cells to regenerate. If injection has been satisfactory, from six to twelve months are required for this regenerative process to be completed. Most patients, in my experience, demand preliminary injection in preference to the operative procedure. If the neuralgia is limited to the second or third division a preliminary injection is desirable for two reasons: first, that the patient becomes accustomed to numbness; secondly, if relief of pain is accomplished, it stamps the trouble as being true tic douloureux. It is significant, however, that most patients, after having had one alcohol injection, seldom demand another. The injection is extremely painful, for the needle must be inserted into the nerve directly while the patient is awake in order to produce a satisfactory anaesthesia. In addition, the apprehension incident to waiting for the pain to recur is usually sufficient to convince them that a permanent cure by operative procedure is to be preferred. Avulsion of the peripheral nerve fibres has been and continues to be a very satisfactory method of handling certain cases of tic douloureux. If the pain is limited to the second [25] . division, avulsion of the infraorbital nerve gives complete relief for months or even years. If in the first division, avulsion of the supraorbital nerve gives similarly satisfactory results. Avulsion of the third division of the nerve, however, is not feasible without leaving unsightly scars. In elderly patients who are poor operative risks I always prefer avulsion of peripheral nerves to the more formidable posterior root section. Alcohol injection of the Gasserian ganglion is in my experience a dangerous practice. It is difficult to control the spread of the alcohol, and if it seeps into the subarachnoid space it may do irreparable harm around the brain stem. Furthermore, corneal complications are very common following Gasserian ganglion injection. I would rate such injections as far more difficult and more hazardous than posterior root section and, certainly, the results are not in any way comparable in satisfaction. Posterior root section is the method of choice for permanent cure of tic douloureux. When the fibres between the Gasserian ganglion and the pons are severed, they do not regenerate. Therefore, avulsion of the whole sensory root produces complete anaesthesia to pain and touch in the distribution of the fifth nerve. The Operation has now been so refined that it is possible to section only those fibres to the involved area, leaving the ophthalmic fibres intact, unless there is a primary trigger point in this division. In this way the cornea is left sensitive and the danger of corneal complications is almost eliminated. The operation for the cure of tic douloureux is probably one of the most satisfactory and safest procedures in the whole field of surgery. In competent hands the mortality, even including the aged group, is less than one per cent. Tic douloureux in the distribution of the glossopharyngeal nerve instead of the trigeminal is a rare but interesting clinical entity. The typical paroxysmal pain occurs in one side of the throat instead of the face and the trigger zone can be demonstrated usually in the tonsillar fossa on the affected side. The patient with glossopharyngeal neuralgia is usually completely incapacitated by the disease, because each time swallowing is attempted a paroxysm of pain is initiated. A simple clinical test is sufficient to establish the diagnosis beyond reasonable doubt. The trigger zone is anaesthetized with cocaine, whereupon the patient can swallow without pain. Treatment consists of sectioning the glossopharyngeal nerve either intracranially or after its exit from the skull. Intracranial section affords permanent relief, while with peripheral avulsion the nerve may regenerate and the pain recur. Headache. When speaking of the relief of intractable pain I cannot refrain from discussing headache, especially from the neurosurgical standpoint. Headache, I suppose, is the most common pain to which the human race is subject. Its frequency is so great and its causes so many that to discuss this symptom adequately would involve the differential diagnosis of almost all neurological diseases. The seriousness of the symptom varies from the malignant headache of cerebral tumour to the benign psychogenic pressure pains. Therefore, a patient complaining of headache requires the most careful consideration of every physician, for to determine the etiology requires patience and often great skill. I know of nothing more discouraging or baffling than to have investigated carefully a patient with headaches and still be forced into the position of calling it "neurosis," "psychogenic," or whatever you wish to label it. Such a diagnosis is too insecure and so liable to be proven by the passage of time to be incorrect. It only takes a few mistakes of this type to make one respect this; symptom profoundly. Some types of headache, however, do have characteristic features. For instance, the pain of migraine is usually easily differentiated. The headaches of increased intracranial pressure have, as a rule, enough characteristics to be recognized. They usually occur in the morning on wakening. At first they may appear irregularly and transitorily, lasting only a few minutes. Gradually their occurrence increases in frequency and the pains may last from two to several hours before they disappear. They are commonly exaggerated by those things which increase intracranial tension—stooping over, coughing, straining, or sneezing. The headache may be described as dull but unrelenting, or it may be of a bursting nature. Periods of relief come frequently, or these relief periods may last for days, only to have the pain recur with renewed intensity. [26] As an example of the embarrassment which often follows the "neurosis" diagnosis I shall review the following case history: The following story was given by an unusually intelligent, understanding woman of 46 years. The facts are given in approximate chronological order, many of which are in the patient's own words. In 1912, she first consulted Dr. A. of Kentucky because of headaches at the top of her head and a nagging pain at the base of her skull. She was told that the symptom was nothing but "a woman's headache." Aspirin, bromides and a bitter liquid medicine were prescribed. From 1913 to 1916, she had two pregnancies, both of the deliveries occurring before the doctor arrived. The headaches continued. Many of the headaches during this time were attributed to "shock and torn nerves" caused by the calamitous method of child- bearing. (The patient states that it was not nerves that were torn!) In 1915 she consulted Dr. B. of Kentucky. Her complaints at this time were headaches and a small lump on the top of the head just back of the midline, which was quite sore to touch. Dr. B. told her that the lump was due to a bump of the head, in spite of the fact that she assured him it had been there for weeks. He told her "to forget it; it does not mean a thing.' In 1916 she consulted Dr. C, a personal friend, about the tender lump on her head and the severe headaches, and he told her "to forget it; some of us just have to be sore- headed." In 1917 the family moved to a gulf coast state. The headaches by this time would last all day long and the pain had shifted to the forehead and temples, as well as the back of the head. She consulted Dr. D. with these complaints, and he considered them to be due to worry and a general run-down condition. He advised sanitarium treatment. She went to a sanitarium in Chicago in 1917 and, as she expressed it, "I arrived there weak and dizzy from too many sedative drugs." Dr. E. examined her completely from the neck down, but never above the neck. She was placed on a regime of no meats, many nuts, much fruit, hydrotherapy treatment, and was told that these methods were the gateway to health. Her regime was rest, food, exercise, and baths, baths, baths. On one occasion the nurses left her in a tub of too hot water. She lost consciousness, slipped underneath the water, and was barely rescued from drowning by the nurse dragging her chin above the water. Dr. F., a famous surgeon of Chicago, was called. He repaired the tears made in childbirth. The surgeon assured her that these tears were responsible for the "shot nerves" and headaches. Before going to the operating room Dr. E., a Seventh-Day Adventist, knelt by her, praying for a safe deliverance from death, for a safe outcome from man's interference with God's handiwork—a cheerful little thought to carry to the operating table. She suffered with fewer headaches under this regime, but still the lump was there, sore as ever. Home again to the plantation in Mississippi in 1918. The "lump" was noticeably larger, growing upward and wider across. The gesture of the hand on the back of the head when entering a car became a habit. The headaches became throbbing affairs, the head throbbing against tightness of temples and forehead. Dr. G. of another southern state made a diagnosis of neuralgia and advised her to wear a thin woolen band over the forehead at night. He also prescribed shots of iron and strychnine for the headaches and many tablets which made her drowsy. There was little improvement. She was sent to Dr. H, an eminent neurologist. "Nerves," he said, "just nerves." He disdained to feel the lump on the head. He outlined a year's diet, medical baths, rest, sleep, exercise, etc. He gave her hormones and told her that unless she adhered strictly to his regime she might not have a year to live. In 1920 she consulted Dr. I., a country practitioner. By this time the pains were excruciating. Dr. I. prepared his hypodermic needle by a quick jab through the cloth of his trouser leg, followed by a lighted match under the needle to finish the sterilization. Many hypodermics of morphine were administered. She was told to take a teaspoon of laudanum every three hours and advised to apply heat over the affected area of the skull. This sequence of events continued, sometimes better, sometimes worse, until 1922, when she again went through a normal pregnancy. "Late in 1922 and the early part of 1923, it [27] was a marathon whether the headaches or I would go the longer—weeks, long stretches of dull, heavy pain, bursts of keen suffering, lasting perhaps an hour, back to the oppressive ache." For the first time, "the ugly implication 'neurotic' was applied to the case." In 1923 Dr. J. of Kentucky was consulted. A complete examination was done, all except the head. She was given migraine tablets, a diet and rest—the same advice she had been receiving for the past eleven years. In 1924 Dr. K. of Kentucky examined her for the same complaints and found evidence of infection about the base of the tonsils which had been removed twenty years ago. Later the same year she consulted Dr. L., who kept her under observation for approximately two years. At that time her complaints were headache, soreness in the top of her head and the perennial lump which was growing on the top of her head. Also, she was extremely nervous and had lost considerable weight. She told him that her head felt too large; that she had to turn the head on one side in order to sleep. She was given a thorough examination and told that she had pleurisy, and that there was some lung infection responsible for the pleurisy. She was then examined by Dr. M., who reported her lungs to be normal. He advised her "to go home, gather your courage; your lungs are in good condition; eat and sleep, and your headaches will take care of themselves." Relatives told her: "Your inheritance from your high-strung father's clan—rotten nerves." At this time she first noticed blurring of vision at times. Glasses were fitted by Dr. N. She told him that her eyes were "squeezed." Dr. O. in 1924 found bits of tonsils remaining, and a tonsillectomy was done. Later in the same year of 1924 Drs. P. and Q. advised a hysterectomy. This was done in the hopes that "her nerves would find peace." Again the effort proved futile in relieving the pain. In 1925 Dr. R. performed another tonsillectomy, the third time the tonsils had been removed. It was thought that the distress in the head might be caused by this chronic throat infection. In 1926 Dr. S., a nose and throat specialist, was consulted. The tonsils were again removed—the fourth time. After this operation she had not further tonsil trouble. Still the headaches continued, and the lump on her head was growing slowly. During 1927 she received treatment of her accessory sinuses by weekly irrigations by Dr. S. By this time the headaches had simmered down to a constant, dull throb which extended down the back of the neck. Sleepless nights were the rule because of the pain. She noticed that the veins were dilating about the eyes and over the forehead. They stood out prominently at times. The case was turned over to Dr. T., who directed her treatment for the next two or three years. The records all showed at the time she was referred to Dr. T. that her case was one of neurosis, perhaps secondary to an artificial menopause. After all the usual forms of treatment were tried in vain, an infra-red lamp was advised. After trying it for a few days, she states: "How I loathed, the Polyannaish glow of that lamp, and the steady heat always above my head—an aggravation to me." "The pain in the head seemed to pull the eyes with a band across me, the back towards the temples. The skin was too tight across the forehead—incessant ache at the base of the head." Dr. T. finally resorted to hypodermics of morphine in order to secure rest. The amount was steadily increased. A spinal puncture at this time was reported as being negative. The appetite was upset by the medication, and she gradually lost weight and strength. The morphine was finally discontinued because of the obnoxious symptoms which it produced, and the various barbitals were given with but little effect. When the morphine was discontinued and the barbitals started, she began to have fancies, dreams and hallucinations as if things were swirling about her. The children annoyed her. Finally, when her mental state became confused, she was taken to a private hospital, and after a few days she was transferred to the psychopathic ward of the City Hospital, where Dr. U. and Dr. V. observed her for ten days. During this time she was disoriented, full of delusions and hallucinations, and at times had to be restrained, all the time complaining bitterly of headache and begging them "to cut on her head to relieve the pain." She was finally transferred to a private sanitarium in an adjoining city, where Dr. W. and Dr. X. took charge of the case. Strange to relate, this patient remembers every detail of those periods of mental unrest even to her delusions and her hallucinations, and remem- [28 ] bers vividly every word spoken by the doctors and nurses who cared for her. She remained in this sanitarium for approximately two months when she grew stronger and was finally allowed to leave. Because of the blurring of her eyesight, she consulted Dr. Y. of a neighboring city in order to have glasses fitted. Early in 1927 she entered the nursing home under the care of Dr. Z. By this time her mental state was entirely normal, and she went to the convalescent home solely for the purpose of rest in order to be free of the noise and cares of her household. Later in 1927 she returned to a hospital in Kentucky under the care of Dr. U., again for treatment by psychiatric methods (her neurosis). Her sanity was vouched for by Dr. U. so that she might be admitted by the good Sisters to the hospital. At this time her eyes were examined by Dr. Alpha, an eye specialist. New glasses were fitted. Dr. U. advised that she be psycho-analyzed by Dr. Beta, the head of a large psychiatric clinic in the midwest. Arrangements were made that she be transferred westward to this clinic, and en route she stopped in St. Louis and visited Dr. Gamma, who had a basal metabolic test made, which proved to be negative. In Dr. Beta's sanitarium, his entire staff of eight physicians examined her at one time or another. She spent a year at the psychiatric clinic for psycho-analytic treatment. This was a year of extreme hardships in many respects; in other respects it was a time profitably spent. The expense of the analyst was great. The drain upon the family pocketbook reached the exhaustion stage early in the year. As an example of the privations which she underwent in order to continue treatment, she worked as a cashier in a cafeteria. The periodic attacks of unbearable headaches were occurring more frequently. On one occasion, while at work, the pain became unbearable. The eyesight became so blurred she could not see to make change. Things seemed to be moving farther and farther away from her. She slipped to the floor unconscious and five hours later regained consciousness in the hospital. The psycho-analysis proceeded satisfactorily and she succeeded in arriving at an understanding of herself which has been of lasting benefit. Of course this treatment in no way influenced the headaches or soreness in the top of her head and the gradual failing vision. Back home in 1929 after a year's absence. In the first few months after returning home she learned with bitter experience that like "damn Yankee" "damn neurotic" was one word. Her nearest relatives and closest friends behaved exactly as the analyst had prophesied. They let her severely alone—ostracism—"mental sickness, you know"— with uplifted eyebrows. In 1934, Dr. Delta, another eye specialist, was consulted. The vision was more blurred, blurred; it often faded. He again prescribed new glasses. From 1930 to 1932 the old story was repeated again and again: Severe bouts of headache followed by some relief, but always a dull, nagging pain; the lump on the top of her head gradually enlarging to either side of the midline, always sore to touch; eyesight none too good, at times fading out until she was unable to read. Occasional vomiting attack when the pain was at its height. In 1934 Dr. delta, another eye specialist, was consulted. The vision was more blurred. Sewing and reading were always followed by a worse headache. The eyes had sharp, needlelike pains in them. She began to see concentric circles of light, with jagged, shining white edges, outermost one of purplish blue, one white, inner one red—off and on, on and off, these flashes. Such visual hallucinations would last for from one-half hour to an hour. In 1933 the vision was more troublesome. The visual attacks became more frequent. On one occasion, while driving her car, her eyesight faded to the point where she could not distinguish between the green and red light at the intersection. She pulled to the curb waiting for the attack to pass. More nerves, underweight—cod liver oil before each meal, substantial diet and rest was the medical advice. The latter part of 1933 Dr. Epsilon made cultures of the stool and found an offending organism. Autogenous vaccines were made and given. Strange to relate, she was tem- prorarily improved with the vaccine therapy and shots of iron and strychnine—only for a few weeks, however, when the pains returned with rejuvenated vigor. One night in early 1934, during a bad bout of headache, Dr. Beta was called because of the absence from the city of Dr. T. She became irrational for several days, and when [29] she regained consciousness the headache was better. It was diagnosed as "just another headache." These attacks must have been extremely grave, inasmuch as on two occasions the doctors summoned the near relatives to her bedside. A few weeks later, in addition to the same headache, painful lump on the top of the head, failing vision and visual hallucinations, the right side of her face became numb. A conference of her doctors was called, and it was decided that this must be due to the novocain which had been injected around a tooth during an extraction a week previously. The face stayed numb, however. In 1934 a new eye specialist, Dr. Eta, in Lexington, where the patient now resided, was consulted. This visit was occasioned by double vision. One eye was pulled inward toward the nose. One side of the face was weak. Treatments of one sort or another were given with no benefit of symptoms. The pains of all varieties continued as before. The eyes were growing dimmer; the pains were more severe; the double vision persisted; the numbness of the face was the same. Walking became difficult because of the failing eyesight. Another visit to Dr. Delta with this statement: "It is like a film across my eyes since the paralysis began." He asked quickly, "Paralysis? Facial paralysis?" EtYes." He looked into the bottoms of the eyes and exclaimed, "With your permission, I should like to have you see a neurological surgeon." The patient remarked, "One more doctor to the list," without any show of interest. That was on the thirtieth of November, 1934. This story is not told with any thought of criticism of those men who have seen her and have given her careful, thoughtful service. Nor has she been embittered by her experiences; to the contrary, she speaks with gracious affection for those of her doctors with whom she became best acquainted. One of her expressions will perhaps best illustrate her character. When I first saw her, after having listened to a very small part of her history, I asked her to retire to the examining room. She said, "I warn you, you are wasting your time; I am just a damn neurotic." The first words she spoke following the operation were these: "Did you remove that lump?" When assured that it was removed, she said, "Thank God! I need no longer be called a neurotic." OBSTRUCTIVE JAUNDICE AND ITS SURGICAL J, TREATMENT § Waltman Walters, M.D., D.Sc, One of the most important things to be remembered in a discussion of lesions of the biliary tract is that the complicated lesions, with the exception of malignant lesions, begin for the most part fairly well localized to the gallbladder. It is when the gallbladder becomes obstructed, or when a stone formed in the gallbladder enters the common duct and produces obstruction, that the complications of acute cholecystitis and obstructive jaundice develop. Although formation of the biliary calculus in most instances is the relsult primarily of infection, many gallstones develop as a result not of infection but.of disturbed metabolic processes; such calculi are the cholesterol stones of pregnant women and the soft bile pigment stones of patients who have haemolytic icterus. Regardless of their mode of formation, if stones obstruct the gallbladder or the common duct, evidences of infection present themselves; for example, in cases of acute cholecystitis, invariably obstruction of the cystic duct is present and the cause of the obstruction usually is a gallstone. Infection in the common duct secondary to stone gives rise frequently to chills and intermittent fever, the so-called intermittent hepatic fever of Charcot. From the bacteriologic standpoint it is interesting that in a study of bile obtained from unobstructed gallbladders which were the site of cholecystitis, Thorsness was able to demonstrate the presence of organisms in the bile in but nine of fifty-nine oases, but organisms were found in the wall of the gallbladder in forty-five of seventy-five cases. When obstruction of the gallbladder or of the common bile duct occurs, however, organisms usually can be demonstrated in the contents of the obstructed viscus as well as in the wall. [30] For the past four years I have been culturing specimens of bile obtained from the common bile duct when it was opened and explored.16 In approximately 75 per cent of the cases, gram-negative bacilli of the colon group, alone or associated with streptococci or staphylococci, were present. These are the same organisms found in the urinary tract in association with such obstructing lesions as urinary calculi. The bacillary infections of the urinary tract have responded well to increase in acidity of the urine, brought about, first, by production of acidosis by using a high fat or a ketogenic diet; later, by using mandelic acid and ammonium chloride. The coccal types of urinary infection have responded to administration of arsenical products of a type similar to those used in the treatment of syphilis. Some of the urinary infections, particularly those caused by organisms of the genus Proteus, have been resistant to this type of chemotherapy but have responded to the judicious use of sulfanilamide. In the biliary tract, as in the urinary tract, adequate relief of obstruction is paramount in treatment and prolonged drainage usually causes the infection in the biliary passages to subside. However, as control of urinary infection has proved to be of great help in the prevention of recurring urinary infection, and has decreased the incidence of recurring renal calculi, it should be possible by chemotherapy to produce in the secretion of bile or its constituents changes which would assist in destroying the biliary infection; this too in spite of the fact that it is much more difficult to change the reaction of bile than that of urine. However, since the halogenated phthaleins are excreted in part through the biliary tract sufficiently well to outline the gallbladder, there is no reason why these substances might not serve as a base to which might be added an antiseptic radical which might affect the bacterial flora of the bile. This problem has been under study at the clinic for a considerable time. It is apparent, therefore, in evaluating the processes at work within the biliary tract, that therapeutic efforts should be directed toward an attack on the lesion, when it is localized to the gallbladder, rather than to wait until complications occur. The patient's clinical history and the results of physical examination form the basis of determining the situation of disease. These, with an understanding of the relative frequency of disease in various viscera, suffice in most cases to make a diagnosis. When, in addition, one has the benefit of such procedures as roentgenologic examination after introduction of barium as a contrast medium into the gastro-intestinal tract, direct observation of the interior of the peritoneal cavity by the peritoneoscope, inspection of the interior of the stomach or rectum by the gastroscope or proctoscope and direct examination of the interior of the urinary bladder by means of the cystoscope, the confirmation of the clinical diagnosis of lesions involving these structures usually is obtainable. The perfection of these procedures that serve as adjuncts to physical examination, however, has not been without some slight disadvantages. Unless one is constantly on the alert, one may depend too much on laboratory procedures in determining a diagnosis. This is particularly a danger when laboratory procedures fail to demonstrate the presence of the lesion, even though one may be present, and such failure may result from the so-called irreducible percentage of human error. By way of illustration, let us see how this error applies in recognition of lesions within the biliary tract. Every surgeon has operated on and removed diseased gallbladders containing stones after roentgenologic examination of the gallbladder has failed to reveal either the presence of stone or disease of the gallbladder, the operation being undertaken because the patient's clinical history was such that a clinical diagnosis of cholecystic disease seemed to be almost certainly correct. In some of these cases too much dependence had been placed previously on negative roentgenologic examination of the gallbladder and the patient had been denied operation until the presence of complications manifested, without question, the situation of the lesion. The error here was not that of the roentgenologist, because he accurately reported the results of roentgenologic examination, but was that of the clinician in failing to recognize the importance of the patient's history and in failing to recognize the fact that certain stones in the gallbladder are not opaque to roentgen rays. In similar manner, although roentgenologic examination of the gallbladder may reveal that it is not filling and emptying satisfactorily, and hence is the site of disease, it usually fails to determine the degree of pathologic change which is present. To put it in another way, roentgenologic examination may reveal what seems to be but a single opaque shadow of a stone, [31] whereas in addition there may be innumerable other stones which are not opaque to roentgen rays and their presence is not apparent until operation. The possibility in such a case, particularly if the symptoms are mild and if a shadow of a single stone of greater than average size has been seen, is that operation may be postponed because of the belief that the stone is too large to obstruct the cystic duct when, in reality, smaller not opaquqe stones already may be impacted in the cystic duct and subacute inflammation of the wall of the gallbladder may be present. This lends emphasis to the fact that the symptoms presented by patients who have lesions of the biliary tract may be out of proportion to the degree of pathologic change present. A subacutely inflamed gallbladder, distended with pus, may produce few symptoms in some cases, while in others a moderate degree of inflammation of the wall of the gallbladder may produce repeated and severe attacks of biliary colic. Biliary Lesions Producing Obstructive Jaundice. The most common causes of obstructive jaundice are stone in the common duct, stricture and tumours in the head of the pancreas, usually carcinoma. Whereas malignant and benign lesions of the duct may occur, these are extremely rare. In a study made in 1930, Marshall found that only four cases of benign tumour and forty-nine cases of primary carcinoma of the extrahepatic bile ducts had been seen in The Mayo Clinic in twenty years. Of primary importance to the patient with obstructive jaundice is whether the obstruction is owing to a nonsurgical lesion within the liver or to a surgical removable lesion in the bile ducts. In most instances, it is not difficult to distinguish between these two conditions. The patient with intrahepatic jaundice usually has had no pain, is in good condition considering the depth of the jaundice, or in very poor condition owing to the terminal stages of atrophy of hepatic cells. There is bile in his intestinal content, as can be determined most accurately by nonsurgical drainage with the Lyon tube. Patients with obstructive jaundice attributable to stones, in 86 per cent of cases will give definite histories of biliary pain or colic. In addition, the jaundice is variable; it usually appears immediately following the colic, and frequently is accompanied by chills and fever. In the presence of carcinoma of the head of the pancreas obstructing the common bile duct, and of stricture of the common bile duct, the element of pain is determined by the degree of obstruction and the amount of infection in the biliary passages. In a study of 275 operative cases of obstructive jaundice seen at the clinic, Weir and Partch found that 50 per cent of patients with carcinoma at the head of the pancreas and 5 0 per cent of patients with stricture had had pain associated with jaundice. Preoperative preparation.—A period of a few days' observation in the hospital prior to operation is, I believe, of definite advantage to the patient with obstructive jaundice. It gives an opportunity for a regimen of preoperative preparation to be carried out, and at the same time for the progress of the jaundice to be determined and for the condition of the patient in the presence of painless jaundice to be evaluated. Thus it is possible to determine the necessity of operation. It is well established that intravenous injections of d-glucose and of solutions of calcium chloride and blood transfusion are of definite value in the prevention of postoperative haemorrhage. The study of the degree of jaundice by the van den Bergh test gives accurate information concerning the progress of jaundice. The value of such knowledge is that it is unwise to operate on patients whose jaundice is increasing unless the condition of the patient forces such operative intervention. If the coagulation time is more than ten minutes, although this is not a contraindication to operation, it is usually an indication that considerable injury has been done to the hepatic cells, and this I believe to be the case if subcutaneous haemorrhages or petechiae are present. In such cases, in addition to the solutions of d-glucose and of 10 per cent calcium chloride, blood transfusion should be given prior to operation and should be repeated as often following operation as is necessary to control the bleeding. One patient, who had complete stricture of the common and hepatic bile ducts, was given seven transfusions in the ten days following operation, and one transfusion was given prior to operation. These transfusions saved her life, however, because on the second and third days following operation it seemed probable that the bleeding would not cease. The value of intravenous injections of solution of d-glucose, which usually is given in a concentration of 10 to 20 per cent, has been justly emphasized. Inter- [32] esting experiences at the clinic in the use of solution of d-glucose in these cases, beginning in 1921, have shown the efficacy of its use clinically. The early experimental work of Opie and Alford, of Mann and Magath and of others, called attention to its value. Since then, the interesting clinical and experimental studies by Radvin and his coworkers have borne out contentions concerning its value. Recently Butt, Snell and Osterberg have shown that putrefied fish meal contains a substance called "vitamin K" which will decrease the prothrombin time of the blood. The normal prothrombin time of the blood will be approximately 20 seconds. A prolongation beyond this point, as shown by Quick, Stanley-Brown and Bancroft, serves as a definite indication of the tendency to bleed. In several cases in which an increased prothrombin time was present the patient was bleeding but ceased to bleed with the decrease in the prothrombin time after the administration of vitamin K. Benign Obstructions of the Common Bile Duct. Stone.—Unfortunately, stones in the common bile duct are visualized but rarely in roentgenologic examination. In several hundred cases of stone of the common duct, I have seen but one in which stone was demonstrated roentgenographically. For diagnosis it is necessary to depend, therefore, on the patient's history of jaundice, of intermittent fever or of continuation of biliary colic after removal of a diseased gallbladder. If a stone in the common bile duct would always produce these symptoms, the diagnosis would not be difficult. Such is not the case, however. In a study of 219 cases in which, stones were removed from the common bile duct in 1936 and 1937 at The Mayo Clinic, Trueman found that in 35 per cent a history of jaundice and in 63 per cent a history of chills and fever had been absent. In addition, stones in the common bile duct, although they may fail to produce chills, fever, jaundice or colic, may give rise to pylorospasm, fullness after eating, nausea and, with the patient's precautionary restriction of diet, loss of weight. Associated duodenal spasm, which is probably a cause of the syndrome just described, will be discussed later. It seems obvious, therefore, that the way to prevent the entrance of stones into the common bile duct, and the way to prevent failure of recognition of their presence, either prior to or subsequent to operation on the gallbladder, is to remove the gallbladder before the stones have had a chance to enter the common duct; this, of course, is a very forceful argument in favor of early operation in cases'of cholelithiasis. In like fashion, it emphasizes the fact that stones may have entered the common bile duct from the gallbladder without giving evidence of their presence there prior to operation; their presence is recognized at operation by palpation or exploration of the interior of the enlarged common duct, which enlargement is always present when there are stones in the common duct. Noncalcareous biliary obstruction.—Stone in the common bile duct is not the only cause of biliary obstruction. Indeed, in approximately 10 per cent of cases in which there were benign lesions of the biliary tract and evidence of biliary obstruction, and in which I operated, the obstruction was found to be attributable to causes other than stone. In most of these cases the obstruction was the result of pancreatitis and associated cholangeitis secondary to the infection which existed in the gallbladder and which involved the pancreas and bile ducts not only as a result of lymphatic transmission but by extension through the walls of the ducts. Fortunately, the treatment in such cases is similar to that after removal of a stone of the common duct; namely, prolonged drainage of bile from the duct. Good results are obtained in such cases. Stricture of the common and hepatic ducts also will produce biliary obstruction. In addition, there is a small group of cases in which stone in the common bile duct, or stricture, or pancreatitis, or cholangeitis is not the cause of the patient's pain; the etiologic factor is spasm of the lower end of the duct, in the vicinity of the sphincter of Oddi. To cases which present this syndrome, Ivy, Mirizzi and others have given the name "biliary dyskinesia." Differential diagnosis of these lesions can be made only by surgical exploration of the common and hepatic ducts assisted by roentgenologic postoperative visualization of them and of their ability to empty properly after injection into them, through T-tubes, of such substances as lipiodol, brominol, or hippuran, and so forth, which are opaque to roentgen rays. Studies in biliary dyskinesia by three former Fellows of The Mayo Foundation, McGowan, Butsch and Knepper1, 5'17, not only have explained the physical and [33] physiological abnormalities associated with the colic-like attacks of pain but, in addition, have served as excellent examples of the benefits to be derived from clinical investigation. With the cooperation of some patients, exploration of whose common bile ducts had failed to reveal stones, stricture or pancreatitis, McGowan4, 5 studied biliary pressure by attaching a water-filled manometer to the T-tube that had been inserted into the common duct at the time of operaion. Working with Butsch and Gray, he found that attacks of spontaneous pain increased the biliary pressure from a normal of approximately 15 mm. of water to as much as 100 and 120 mm. of water. Kymographic tracings demonstrated this well. The investigators found that during these attacks morphine, given in average therapeutic doses of % grain (0.01 gm.), instead of relieving the pain accentuated it because the intraductal biliary pressure became increased. After using various antispasmodic substances, they found that amyl nitrite and nitroglycerin effectively decreased biliary pressure to normal and pain disappeared. In order to visualize what was taking place in the biliary tract during this experiment, lipoiodine, a substance opaque to roentgen rays, was used instead of water and the appearance of the biliary tract was noted at roentgenoscopic examination. With the onset of the increase in biliary pressure a spasm occurred in the lower end of the common bile duct in the vicinity of the sphincter of Oddi. With the increase in biliary pressure, marked filling of the intrahepatic biliary ducts was demonstrated. When the antispasmodic substances, amyl nitrite'and nitroglycerin, were administered, relief of spasm of the lower end of the common duct was noted, the opaque substance was seen to leave the common and hepatic ducts and enter the duodenum, biliary pressure decreased and pain was relieved. This was the first time that studies of biliary pressure in relation to pain, to the sphincter of Oddi and to the lower end of the common bile duct, had been made on patients. These studies not only explained the so-called postcholecystectomy colic following removal of stones and elimination of pancreatitis but also directed attention to the ineffectiveness of morphine in relieving the pain and called attention to the value of the antispasmodics, amyl nitrite and nitroglycerin, in such cases. Stricture of the common duct.—If a stricture of the common bile duct exists, and there is sufficient normal duct above the stricture to allow anastomosis between this normal portion of the duct and the duodenum, a good result may be expected. It is necessary that accurate anastomosis and union of mucous membrane be effected between these two structures; otherwise obstruction will frequently recur at the site of the anastomosis. This procedure, for more than a quarter of a century, has given the best results in the treatment of stricture of the common bile duct of any type of direct anastomosis. Should the gallbladder be present, anastomosis between it and the stomach or duodenum can be made and satisfactory results can be expected, provided the stricture is distal to the entrance of the cystic duct into the common bile duct. However, the gallbladder usually is not present, because practically all strictures occur subsequently to cholecystectomy, because of injury to the duct. In some cases in which the stricture is localized and small in size, a section of the duct containing it can be removed readily, and end-to-end anastomosis can be made between the ends of the duct. I had occasion recently to use this method after I had removed a benign tumour (neuroma) about 1 cm. in diameter, involving the common and hepatic bile ducts. When the section of duct containing the tumour had been excised, the stump of the hepatic duct and the stump of the common bile duct were anastomosed over two small T-tubes. This was done October 11, 1930. In June, 193 5, the patient was presented at a staff meeting, having been free of biliary colic or jaundice for about two and a half years. Similarly, in another case, a stricture was excised, and excision was followed by this type of anastomosis because the stricture was in close proximity to the liver, because a very slight amount of duct remained above the point of stricture and because the stricture was distant from the duodenum, which was difficult to mobilize. The patient was well, without any further evidence of obstruction, when last heard from three and a half years following the operation. If the stricture involves the entire extrahepatic portion of the common and hepatic bile ducts, the establishment of an external biliary fistula, which two or three months later can be coned out and transplanted into the stomach or duodenum, has been followed by unexpectedly and unusually good results. Thirteen such cases have been reported in the literature, in seven of which the operation has been performed at the clinic. [34] -"-•»- • - .-r- - ~- ,'*tXm*» .&_..„ ] In 1937 my assistant, Dr. K. K. Nygaard, studied the results in a group of fifty-one patients on whom I had operated for stricture of the common and hepatic bile ducts from October, 1924, to January, 1937. The mortality rate in this series of cases was 13.7 per cent. Twenty-nine of these fifty-one cases were reported in 193 315. Of this group, 48 per cent of the patients were living and in good physical condition. Of the twenty-two patients operated on between 1933 to 1936 inclusive, 68.2 per cent were living and in good physical condition. It seems to me that the results of the operations are exceedingly good, especially when it is remembered that nine of the patients had complete strictures of the common duct and it was necessary first to establish an external biliary fistula and then transplant it into the stomach. Tumour of the head of the pancreas.—Obstructive jaundice which is the result of tumour at the head of the pancreas can be relieved by anastomosis between/ the distended gallbladder and the duodenum or stomach, the choice depending on the ease of anastomosis and freedom from tension. If the anastomosis is made with the stomach, the presence of bile in the stomach does not produce unusual symptoms. In cases of this type, the intense itching, which in most of these cases is the most constantly troublesome symptom, almost immediately disappears with the release of the obstruction. There is no doubt that some of these tumours at the head of the pancreas are the result of infection and that the relief of the obstruction by cholecystenterostomy gives permanent relief. In a study of 116 patients on whom cholecystenterostomy has been performed at the clinic, the course subsequent to operation would lead one to suspect that the pancreatic obstruction of the common bile duct, in 15 per cent of the cases (patients living longer than five years), might have been an inflammatory one, although one patient with a pancreatic carcinoma lived comfortably for almost four years. Even if a carcinomatous lesion is the cause of obstruction, the relief of the itching alone warrants the risk of the operation. Moynihan has made the statement that the incidence of suicide among such patients on account of the itching is as high as the operative risk. Noteworthy, also, is the fact that operation on such jaundiced patients allows thorough exploration of the biliary passages, and not infrequently a stone in the common bile duct is unexpectedly found as the cause of the obstruction. In a study made several years ago, Weir and Partch found that nineteen of 104 patients with stones in the common bile duct had painless onset of jaundice and that seventeen of these 104 patients had not had pain at any time. If jaundice is extreme, I believe that cholecystenterostomy can be done more safely in two stages than in one. In the first operation, the gallbladder is drained, and twelve or fourteen days later anastomosis between the gallbladder and the stomach or duodenum is effected. If the jaundice is not deep and the condition of the patient permits, there is no reason why cholecystenterostomy cannot be done in one stage. It has been my custom, when performing the operation in one stage, to make the anastomosis by suture, but when I have carried out the procedure in two stages I have found a small Murphy button to maintain a constant lumen and to prevent even its temporary closure by inflammation or oedema. The heavy end of the Murphy button always should be placed on the duodenal or gastric side of the line of anastomosis to Jessen the possibility of its dropping into the gallbladder. Cholecystenterostomy can be carried out with a fair margin of safety. Over a number of years the mortality rate in this deeply jaundiced group of patients has varied from 10 to 14 per cent. Complications.—The complications which occur following operations on patients with obstructive jaundice are haemorrhage and renal and hepatic insufficiency. Of great importance in lessening the incidence of postoperative haemorrhage is selection of the proper time for operating and the preoperative use of some means of assisting in coagulation of the blood. A successful outcome in such cases is absolutely dependent on the relief of the obstruction. When patients fail to recover following removal of stones from the common bile duct, it will be found that in most instances stones have been overlooked. Such overlooked stones can cause recurring obstruction, deepening jaundice with possible haemorrhage, and renal and hepatic insufficiency as terminal f eatures. The same necessity for complete relief of obstruction is involved in operating on patients with strictures and tumours at the head of the pancreas. On a few occasions I have seen patients, following [35] cholecystenterostomy for tumours at the head of the pancreas, almost lose their fives from temporary obstruction at the anastomosis owing to inflammation and oedema. The corollary of this is that if anastomosis is made by suture, the opening must be as large ass possible. In order to combat both renal and hepatic insufficiency I believe it is worth while to administer 10 per cent solution of d-glucose intravenously to jaundiced patients subsequent to operation, as often as such treatment is indicated. Our custom is to give 1000 cc. of 10 per cent d-glucose in physiologic saline solution once or twice a day. Should oedema develop owing to the increased amount of chloride administered, a 5 per cent solution is given intravenously without sodium chloride. Although d-glucose is of great value in these cases, blood transfusions are of greater value. I have seen several patients whose lives I am sure were saved by multiple blood transfusions following operations on the biliary tract. Not only was the bleeding stopped in some cases but the effect on the liver apparently was beneficial; indeed, so was the effect on all of the parenchymatous organs of the body. In view of the effectiveness of administration of vitamin K as a preoperative measure we have been using it also postoperatively, especially when the prothrombin time of the patient's blood was increased. REFERENCES : 1. Butsch, W. L., McGowan, J. M., and Walters, Waltman: Clinical Studies on the Influence of Certain Drugs in Relation to Biliary Pain and to the Variations in Intrabiliary Pressure. Surg., Gynec. and Obst., 63:451-456 (Oct.), 1936. 2. Butt, H. R. ,Snell, A. M., and Osterberg, A. E.: The Use of Vitamin K and Bile in Treatment of the Hemorrhagic Diathesis in Cases of Jaundice. Proc. Staff Meet. Mayo Clinic, 13:74-80 (Feb. 2), 1938. 3. Ivy, A. C;, and Sandblom, Philip: Biliarv Dyskinesia. Ann. Int. Med., 8 :115-122 (Aug.), 1934. 4. McGowan, J. M., Butsch, W. L., and Walters, Waltman: Pressure in the Common Bile Duct of Man: Its Relation to Pain Following Cholecystectomy. Jour. Am. Med. Assn., 106: 2227-2230 (June 27), 1936. 5. McGowan, J. M., Butsch, W. L., and Walters, Waltman: The Use of Glyceryl Trinitrate (Nitroglycerin) for the Control of Pain Following Cholecystectomy. Ann. Surg., 104: 1013-1018 (Dec), 1936. 6. Mann, F. C, and Maga.th, T. B.: Studies on the Physiology of the Liver. III. The Effect of Administration of Glucose in the Condition Following Total extirpation of the Liver. Arch. Int. Med., 30:171-181 (Aug.), 1922. 7. Marshall, J. M.: Primary Tumours of the Bile Ducts. (Unpublished thesis). 8. Mirizzi, P. L.: La Choleeystectomie sans Drainage (Choleeystectomie ideale). Paris, Masson et Cie, 1933, 105 pp. 9. Nygaard, K. K, Shelden, C. H., and Walters, Waltman: Strictures of the Bile Ducts: Results in Fifty-one Operative Cases. Proc. Staff Meet. Mavo Clinic, 12:25-30 (Jan. 13), 1937. 10. Opie, E. L., and Alford, L. B.: The Influence of Diet on Hepatic Necrosis and Toxicity of Chloroform. Jour. Am. Med. Assn., 62: 895-896 (March 21), 1914. 11. Quick, A. J., Stanley-Brown, Margaret, and Bancroft, F. W.: A study of the Coagulation Defect in Hemophilia and in Jaundice. Am. Jour. Med. Sc, 190: 501-511 (Oct.), 1935. 12. Ravdin, I. S., Riegel, Cecelia, and Morrison, J. L.: Coagulation of Blood. I. The Comparative Values of Calcium and Glucose as Agents for Decreasing the Clotting Time. Ann. Surg., 91:801-810 (June), 1930. 13. Thorsness, E. T.: Bacteriology of Cholecystitis: the Virulence and Spore Formation of Clostridium Welchii. Surg., Gynec. and Obst., 59: 752-755 (Nov.), 1934. 14. Trueman: (Unpublished data.) 15. Walters, Waltman: Resections of the Common and Hepatic Bile Ducts and Ampulla of Vater for Obstructing Lesions: Results in Thirty Cases. Surg., Gynec. and Obst., 56: 235-241-(Feb.), 1933. 16. Walters, Waltman: (Unpublished data.). 17. Walters, Waltman, McGowan, J. M., Butsch, W. L., and Knepper, P. A.: The Pathologic Physiology of the Common Bile Duct and Its Relation to Biliary Colic. Jour. Am. Med. Assn., 109:1591-1597 (Nov. 13), 1937. 18. Weir, J. F., and Partch, W. T.: The Relationship of Pain to Jaundice. Ann. Int. Med.. 4:1509-1520 (June), 1931; Abst. Proc. Staff Meet. Mayo Clinic, 6:120-122 (Feb. 25), 1931. [36] LOW BACK AND LEG PAIN FROM A NEUROLOGICAL STANDPOINT R. Glen Spurling, M.D. I am talking tonight on a subject that is of particular interest to me because of the recent developments in the field of treatment of low back pain. It has become a most lively topic of discussion in recent years. As a matter of fact, the two major neurological hospitals this year have devoted two days to the discussion of this subject. It is a new subject. We don't pretend to know all there is to know about it, but it opens up a new field that has been a very much neglected one in the past, and tonight I am going to try to present this subject to you as far as I am able. Pain in the lower back radiating into one or both legs is a common ailment. Investigation until recent years has been fixed upon extra-spinal causes—the sacro-iliac, joint, etc. Intra-spinal lesions were listed at the end of a differential diagnosis, particularly herniated nucleus. These lesions are far more common than have been generally supposed. There are three low back lesions causing low back pain and pain in the legs: 1. Neoplasms—which we have known about for many years; 2. Herniated nucleus; 3. Tearing with subsequent hypertrophy. What are some of the signs and symptoms of a low intra-spinal lesion? Low back pain is the characteristic and usually the constant finding in all of these cases. It may be severe in the beginning, only to disappear. At any rate, at the onset of one of these lesions there is usually backache. This backache has certain characteristics. The onset is usually typical in all cases. The patients usually state that while bending forward and picking up a heavy thing they feel something given in their back, or snap, and they have insufferable pain in the lower lumbar region. They find it difficult to straighten up and when they do the spine is rigid. The stiff back is manifested by a great spasm of the lumbar muscles. Upon examination of the back the whole spine is bent as a unit. There is usually tenderness on palpation or percussion over the vertebrae involved. Then there is a characteristic posture in most cases. There is usually tilting of the pelvis and there is usually scoliosis. I have seen patients with these lesions come in bent over and be walking in a semi-forward position. Others will walk in a very erect position with a stiff spine and their pelvis tilted, and one characteristic which is quite different from those suffering from bony disease is that the patients get no relief from the backache by lying down. This backache is different. If they get relief from lying down it is usually when they are in the face-down position. In addition to low back pain, there is leg pain in all these cases. This characteristically follows the nerve root which is most severely involved. That pain may be felt most in the thigh, in the calf of the leg or in the foot, depending upon which nerve root is most severely compressed. Another feature of these lesions is that anything that raises intraspinal pressure causes pain. This increased pressure causes the pain to be exaggerated. Another test is by compressing the greater veins and causing greater spinal pressure. I feel sure that that test cannot be positive in any extra-spinal lesion. Therefore, the lesion which is exaggerated by the test must be intra-spinal. Many patients have sensory findings. In the case of the fifth lumbar root the numbness' may be in the lateral aspect of the leg. A definite hypoassthesia may be demonstrated. Many patients do not have numbness. They just have pain. Then, again, patients who have large lesions of the lower spinal column have a lot of sensation or actually a subjective numbness—the inability to feel pain on the later aspect of the leg. This is an unusual story. In our series of 47 verified lesions of these types, more than half of them have demonstrated hypoaethesia in all the sacro-sensory roots. In addition, the patient may have a disturbance of his genital organs, in that he will have a sharp reduction in libido and sometimes complete loss of libido. This is usually seen in hypertrophy of the flavia. In addition to sensory subjective and objective findings, there are motor findings. There may be weakness in the legs. We have had patients with definite toe drop. On objective examination we can usually demonstrate some motor loss. There is weakness of the muscle —complete paralysis of those muscles. There was atrophy in the more advanced cases of [37] long standing, but in a fairly large number of our series we have seen fibrillation of the muscles with some atrophy of the cord. The saphenous may be involved. Now, about the pathology of these lesions. I shall not say much more about the neoplasms except to say that all the neoplasms are to be found in this region (slide). In our 47 cases we found 3 new growths that had the tran of symptoms that I have outlined ot you. The other two lesions would be worthy of description. (Slides were then shown, describing the various lesions. A movie was then shown of lipiodol injections and fluoroscopy in these cases.) Now, what about the treatment? As I indicated previously, I feel that every conservative means should be employed first before advising surgical interference, because I feel that some of the acute cases will heal without surgical intervention. The acute cases should be treated conservatively. Manipulation is very desirable in the hands of a skilled manipulator. If this fails, in the acute case, I think the patient should be put up in flexion in a cast for several weeks. However, the case that gets no relief from any of these must have something done. Then I would suggest lipiodol studies. Then if this corroborates the clinical examination, the lesion should be removed. This removal is simple enough after one is experienced. It means a laminectomy and excising the mass. It is better not to open the dura if the lesion can be found without doing this. Then the patient can be home on his fourteenth post-operative day and be back to work in a few weeks. It is not necessary to do a fusion if you don't do too mutilating an operation. What are the results? The results in our cases have been gratifying in the majority of cases. There have been some mistakes made, but most of the cases were treated successfully. In two of our cases especially we have had unsatisfactory results. That is about the story of the low backs as far as we know them. ENLARGEMENT OF THE SUPERFICIAL LYMPH GLANDS; § § DIAGNOSIS AND TREATMENT By Dr. R. F. Farquharson. I always feel a little apologetic when I talk on this subject. The diagnosis is commonly very easy. It is often extremely-difficult, and when it is difficult there is so little that any person can say, but tell how one can avoid making mistakes. I shall show slides of the general classification of the causes of superficial enlargement of the lymph glands. I should like to discuss the subject, first, from the point of view of local gland enlargement, and, second, from the things that give rise to general gland enlargement. The first cause, the perfectly obvious cause, is regional lymphadenitis. The diagnosis is almost always obvious and the treatment also. These glands are almost always discrete, usually small, always tender. The outline is seldom firm and definite. There is a little bit of peri-adenitis. We are all familiar with the type seen most commonly with Scarlet Fever, which may go on to suppuration. Streptococcic lymphadenitis with acute nephritis is now treated with sulphanilamide. To prevent the acidosis found in giving sulphanilamide we usually give sodium bicarbonate. These ordinary acute cases of lymphadenitis give us no trouble at all, but sometimes the subacute cases give us considerable trouble, for we sometimes have a secondary lymphadenitis existing after the primary lesion is gone. Tuberculosis lymphadenitis is probably the commonest cause of chronic lymph gland enlargement. It affects children and young adults particularly. It begins usually high in the neck and usually is found in persons drinking milk which has not been pasteurized. Its growth is very insidious. These glands are very tender and there is usually a certain amount of inflammatory oedema about the gland that makes them less easily defined. These glands tend to become matted together, tend to enlarge, sometimes go on to suppuration. They may gradually resolve and disappear entirely or become smaller or become calcified. The diagnosis is easy in a typical case. The treatment of tuberculous lymphadenitis is like the treatment of tuberculosis anywhere else; that is, rest and a good, well-balanced diet. If it is a very small lesion and not very acute, you can let the patient up and around for awhile, but when the lesion is sharply localized it should be excised, but commonly that is not possible because of its position. The type of tuberculous lesion most difficult to [38] diagnose is the one which begins low in the neck, low in the clavicle, sometimes in the axilla. It is usually a low grade infection and may be confused with Hodgkin's Disease. The differential diagnosis from Hodgkin's is sometimes impossible. Occasionally we see multiple tuberculous lymph glands high and low in the neck. This is a rare form but sometimes it is present and sometimes both tuberculosis and Hodgkin's occur together. I should now like to discuss the diagnosis of Hodgkin's Disease. We must regard it just as we regard leukaemia—as a disease which shows very different degrees of acuteness. It is commonly called a granuloma and considered to be infectious, but many consider it to be malignant. It is very hard to say which is right. As the disease progresses there are areas of necrosis and there follows also fibrosis. The ordinary chronic case of Hodgkin's is a slow growing lesion. It tends to begin as a local disease and the glands are firm and elastic and not tender. By the time the patient first notices them, he begins to have some of the generalized symptoms of the disease. He begins to feel tired, to lose weight, often has a fever. There is sometimes, among the early symptoms, an itchiness of the skin and this sometimes precedes the enlargement of the lymph glands. When there is this itchiness of the skin it is quite common to find that this skin of the palms of the hands is a little bit thicker than normal, not infiltrated but with a peculiar cuticular oedema. The glands increase in size, become matted together a little bit and become distinctly hard, and the lymph glands spread from one region to the adjacent regions. It is almost always an asymmetrical enlargement. These patients finally go to a doctor and on that story of the general malaise and the local enlargement of the glands that are not painful, one makes a pretty definite diagnosis of Hodgkin's Disease. After that we should take a piece of tissue out and have it examined by the pathologist. We must be sure not to mistake this diagnosis for tuberculous lymphadenitis. If there is itching, or if the spleen is palpable, the diagnosis is much easier. When we send a lymph gland to the pathologist we should recognize clearly that the pathologist can't make a definite diagnosis on the pathology alone, but we should give him the history of the case. Now, in Hodgkin's there is no definite blood picture. As the disease continues the white count rises but the blood picture is not diagnostic. Having confirmed the diagnosis, we advise X-ray treatment in our chronic cases. We find the glands melt away very rapidly and if only they would stay that way, that treatment would be wonderfully satisfactory. The patient feels ever so much better. If we start this treatment in the earliest stages, we may get it before there is anaemia from the Hodgkin's. A girl of 26 had obviously a typical picture of Hodgkin's. She had been feeling miserable for about six months. When you took her history further, however, one found that fourteen years before she had gone to the Mayo Clinic because of enlarged glands in the left supraclavicular region. Treatment was given at that time and the patient remained well until a few months before we saw her—fourteen years of almost complete! freedom from symptoms. The ordinary course is to have great improvement in the symptoms for twelve months to two years. Eventually, however, the glands come back and increase. They may then invade the bone marrow. This may be relieved by X-ray therapy, but not in the late stages. I would like to differentiate between chronic Hodgkin's and acute Hodgkin's. This acute form of the disease may be associated with very slight lymph gland enlargement, but tends to be generalized instead of local. The spleen is also involved and very commonly there is high fever, sometimes up to 101 ° or 102°, with a very definite irregularity. This slide shows you a very typical picture of the temperatures taken of a patient with acute Hodgkin's Disease. When you examined the patient carefully you could feel a few glands in every area. He had a palpable spleen and an anaemia. He died after nine months of the disease. This was an anaemia secondary to the Hodgkin's and could not be relieved except by relieving the primary disease. Hodgkin's is almost always grouped with lymphosarcoma because they say there is such a small differentiation that it isn't worthwhile making a difference. Lymphosarcoma is a malignant disease of the lymph glands. It begins in the mucous membranes of the lymphoid tissue. The enlargement is very similar to that of Hodgkin's. One of the commonest sites is the supraclavicular region. In Hodgkin's we have the general malaise [39] coming early. In tne otner disease, however, the first thing complained of is either the appearance of the gland, the appearance of a mass, if it is in the abdomen, or the local symptoms, the pressure symptoms if it is in the mediastinal glandp. Lymphosarcoma tends to remain local for a long time, later being widely generalized. This is a slide illustrating a typical case of acute mediastinal lymphosarcoma. It was a.very typical case. He was given X-ray treatment and we got a most most rapid disappearance of the sarcomatous lesion. He was very much better and thought he was cured; but the improvement was only temporary. He was treated in October and died in February. Now we come to the lesions of secondary carcinoma. Sometimes the primary site is difficult to determine. In other cases it is easy to determine. I should like to go on to the discussion of the causes of generalized lymph gland enlargement. I have seen a case of German measles where an enlargement came out a week before the rash appeared. Syphilis is often spoken of as a common cause of lymph gland enlargement, and if one were to act on that belief, one would make a lot of mistakes. If there is a tendency for the lymph glands to be enlarged up the back of the neck and if this enlargement persists or six months or longer, we should always think of syphilis. Late syphilis very seldom gives rise to lymph gland enlargement. It is a rare thing to see chronic enlargement of the lymph glands from syphilis. I had one patient with a diagnosis of Hodgkin's. She had syphilis. She had not had an obvious primary sore. Her Wasserman was positive. We took out the gland for interest and our pathologist had not had another example of a gland to examine histologically that was secondary to a primary sore and he would not have been able to make a diagnosis if we had not given him the history. Infectious mononucleosis affects chiefly children and young adults. It is a disease of unknown etiology and has an extremely variable course. It is a very slowly progressive condition and the most prominent local symptoms are found in the throat. After a few days, or even up to a month, there is a gradual enlargement of the lymph glands, first up in the neck, then in the axilla, often in the groin; the spleen is commonly palpable. This disease behaves just like an infection and will get better just like an infection. When we find a count increased to 15,000 it is extremely important that we do not make the serious mistake of diagnosing this as an acute lymphoid leukaemia or acute Hodgkin's Disease, which are fatal conditions. Sometimes this disease lasts over a long period of time, but usually does not last longer than a month or so. The differentiation is made first in the onset. In infectious mononucleosis the onset is of much shorter duration than the other diseases named. If we are not sure of the diagnosis we should refain from making a diagnosis of the fatal conditions until we are absolutely sure. I am not going to talk at any great length about Leukaemia, as I shall be talking about it on Friday morning. There is no disesae that gives such widespread generalized lymph gland enlargement as that in chronic lymphoid leukaemia. In closing, I want to reiterate that mostly these cases of lymph gland enlargement are easy to diagnose, but if they are not easy to diagnose, then they are very difficult indeed, and we must be very careful not to mistake the condition for something else. PREPARATION OF HANDICAPPED PATIENTS FOR SURGICAL OPERATIONS Waltman Walters, M.D., D.Sc, Surgical lesions which have a more disturbing influence than usual on the physiologic activities of the body are those associated with obstruction, infection and haemorrhage. Usually the condition of a patient can be greatly improved and the surgical risk involved can be lessened to a large extent by the employment of certain therapeutic measures during a period of two or three days prior to operation. There are, in addition, many patients past the meridian of life who may have associated changes in such parenchymatous organs as the heart, kidneys and lungs. Recognition of the disturbance of these parenchymatous organs is important prior to operation, not only because such information is an index of what the possible risk of a surgical procedure may be in such cases but also because, frequently, improvement in function can be accomplished by appropriate treatment. [40] Examples of such are the control of auricular fibrillation by the administration of digitalis, the relief of cardiac decompensation by rest in bed, the intravenous use of solutions of d-glucose and the use of transfusions of blood to compensate for hepatic dysfunction and the use of local or spinal anaesthesia in the treatment of certain types of pulmonary lesions. Obstruction. Because of the intimate relationship which exists physiologically between the gastrointestinal, the biliary and the urinary tracts, obstructing lesions of one tract frequently have an associated effect on the others. Striking examples are the toxaemia of dehydration and the associated hepatic and renal insufficiencies occurring in cases of biliary and renal obstruction and infection. For the sake of brevity, I will limit my remarks, for the most part, to the pathologic changes which lend themselves to improvement prior to the performance of surgical procedures. Gastro-intestinal tract.—The most frequent obstructing lesions of the gastro-intestinal tract occur in the stomach and colon, although the frequency with which an adynamic ileus is associated with many intra-abdominal lesions and renal lesions as well must not be forgotten. The pylorus and the duodenum are the sites of obstructing lesions which may be caused by carcinoma, ulcer, and, occasionally, polyps. In these cases, the stomach will retain food for many hours beyond the normal and depletion of fluids, blood and chlorides of the tissues may occur owing to vomiting of gastric secretions. In such cases, the performance of gastric lav*age is advisable twice daily until the stomach is clean; a liquid diet which may pass beyond the point of obstruction is given and the restoration of an adequate fluid balance as well as a normal chloride level can be obtained by intravenous and subcutaneous injections of physiologic solutions of sodium chloride and intravenous injections of solutions of d-glucose. It is our custom, in such cases, to give a liter of 10 per cent d-glucose in physiologic solution of sodium chloride two or three times a day. In cases of obstruction of the small intestine, the patient suffers a greater loss of fluid, because of vomiting, than occurs in cases of duodenal or pyloric obstruction. Thus, in cases of obstruction of the small intestine, a duodenal tube is passed through the nares and is allowed to remain in place for a period of a few hours. This will sufficiently deflate the small intestine when suction is applied, so that, after fluids and chlorides have been replaced intravenously, operation on the obstructed intestine becomes less difficult and the patient's condition will have been improved to the extent that the risk of operation has been considerably lessened. The majority of obstructing tumours of the large intestine occur in the descending part of the colon, particularly in the region of the sigmoid flexure. In such cases, frequent enemas will occasionally relieve the colonic stasis existing proximal to the tumour; if not, the performance of a caecostomy or a colostomy is in order. As a preliminary step to the removal of the lesion, performance of the latter type of operation is always advisable. Biliary tract.—Preoperative management of such cases depends on the cause of the obstruction and whether or not jaundice is present, for the greatest chance for improvement of the condition of a patient by proper preoperative treatment exists in cases of jaundice, particularly if the jaundice has been intermittent in character. In such cases, when the jaundice has been associated with pain, the possibility that the biliary obstruction is owing to the presence of a stone should be recognized and, if the patient's condition can be kept reasonably normal, the possibilities are that the stone may loosen and the jaundice subside, making the patient a much better risk for surgical procedures. In such cases, duodenal drainage is helpful. By introducing a tube through the nares into the duodenum and then irrigating with warm solutions of magnesium sulphate, relaxation of the shpincter of Oddi will occur and a flow of bile into the duodenum will be promoted. This procedure has been valuable in decreasing the concentration of bile in the blood more rapidly that otherwise would occur. In such cases, if the patient is deeply jaundiced, failure to obtain bile in the duodenal contents is indicative of the! presence of malignant obstruction. Yesterday, in discussing obstructive jaundice, I emphasized the value of administering large amounts of fluids, solutions of d-glucose, calcium, blood transfusions and vitamin K preoperatively when the patient is deeply jaundiced. That such methods of preparation have reduced the mortality, particularly that from postoperative haemorrhage and hepatic insufficiency, is evidenced by the fact that of 209 jaundiced patients operated on at The [41 ] Mayo Clinic in 19 3 62 but two died from haemorrhage. This is in contrast to a very high incidence of haemorrhage as a cause of death of jaundiced patients operated on prior to the introduction of these methods of preparation in 1921. Furthermore, the extent to which jaundiced patients can be operated on is evidenced by the fact that I recall but one jaundiced patient whom I have seen in two years on whom it was thought inadvisable to carry out a surgical exploration. Many of these patients had varying degrees of cirrhosis associated with biliary obstruction and some had hepatic decompensation with ascites; yet, for the most part, they not only survived the operation with relief of the obstruction but also their hepatic function improved. Urinary tract.—Urinary obstructions which produce the greatest disturbances are those which occur suddenly and are almost complete. I have particularly in mind urinary obstruction as the result of stones passing from the pelvis of the kidney into the ureter and acute retention of urine within the bladder as a result of prostatic obstruction. In the latter condition, the bladder can be emptied by catheterization. However, the bladder should not be allowed to empty itself completely at one time. After a stone obstructs the ureter it is occasionally several hours before the patient is brought to the surgeon. In such cases, although the immediate removal of the stone is frequently advisable if renal infection is present, I have found it advantageous in some cases to relieve the obstruction by passing a ureteral catheter through the bladder by means of the cystoscope to a point beyond the site of the obstruction in the ureter, allowing the kidney to empty, jhe infection to subside and the patient's general condition to improve. Thus, the surgical procedure may be carried out at a time when the kidney or ureter is not distended, inflamed or surrounded by inflammation. If the stone is in the lower part of the ureter andl a catheter cannot be passed beyond the stone, it is frequently safer to introduce a tube into the renal pelvis by surgical means, and thus relieve the obstruction. This will allow the inflammation about the stone to subside so that the removal of the stone can be accomplished when the patient is not ill from the obstruction and infection. Infection. In most instances, particularly in the biliary and urinary tracts, infection is secondary to obstruction and, with relief of the obstruction, infection usually subsides spontaneously unless such relief has been too long delayed and intrahepatic infection has occurred or cortical abscesses have developed in the obstructed kidney. In some such cases a bacteriaemia or septicaemia may have developed. When the infection is renal in origin and provided that the opposite kidney is normal, the infected kidney had best be removed without delay. In some cases chemotherapy, intravenous injections of mercurochrome (7 to 10 cc. of a 1 per cent solution), blood transfusions and, more recently, the oral administration of sulfanilamide have accomplished remarkable results as regards control of infection. When using sulfanilamide, it is our custom to give 60 grains (4 gm.) daily for about two days and then reduce the dose to 40 grains (2.6 gm.) for the next four or five days. Haemorrhage. Secondary anaemia is usually the result of loss of blood caused by malignant lesions, although the most frequent cause of bleeding from the stomach or duodenum is a duodenal ulcer. Frequently, however, gastric polyps cause bleeding and produce severe secondary anaemia. In all of these cases, it is our custom to give a transfusion of blood preliminary to operation if the concentration of haemoglobin is less than 40 per cent (Dare) and the number of erythrocytes is less than 3,000,000 per cubic millimeter of blood. Although the idea generally held is that the presence of active bleeding from duodenal ulcer is a contraindication to the giving of a transfusion of blood, I believe that, if administered slowly by the drop method and if sufficiently large amounts are given, it may be life-saving to such patients. One such patient recently received 4 Yz liters of blood over a period of three days, at the end of which time it was possible to perform a successful partial gastrectomy. Blood transfusions, too, have a very important place as a measure preliminary to operation on debilitated, elderly patients and particularly those who have idiopathic types of secondary anaemia. The frequency with which blood transfusions have been generally used has, I am afraid, subtracted the element of fear that a possible serious reaction might occur. This possibility should never be forgotten, for reactions still do occur following blood [42] transfusions and some of them are serious. It is not necessary, I am sure, to emphasize the need for carefully determining the blood group of the donor and the recipient and, whenever possible before giving the transfusion, of carefully matching the blood to be sure that haemolysis will not take place. The first 5 0 cc. of blood should be given extremely slowly. If the patient shows evidence of a reaction, such as a chill, a sensation of tightness in the chest and difficulty in breathing, the transfusion should be discontinued immediately. I have been hesitant, too, about advising transfusion for patients who I have known from actual experience have previously had a reaction to a transfusion. It is an interesting fact that when reactions have occurred they have usually occurred among those patients who had blood of group II. Doan, Curtis and Wiseman reported the occurrence of haemolytic crises in some such cases, the fatal outcome of which was prevented by the immediate performance of splenectomy. Cardiac Efficiency. The most serious cardiac lesions menacing a patient's recovery from an essential operative procedure are bundle branch block and recent coronary thrombosis. For patients who have bundle branch block, postponement of surgical procedures indefinitely should be considered. For patients who have recently had coronary thrombosis, every effort should be made to postpone the surgical procedure for a period of several months. With the exception of these two lesions, any other patient, regardless of the cardiac lesion present, will usually withstand a short and properly performed surgical procedure without too great risk, if the patient has been able to be up and about and doing his own work without having developed cyanosis, oedema of the legs or other signs of cardiac decompensation. When signs of decompensation are present, frequently a period of rest in bed and the judicious use of digitalis and sedatives will allow the heart to regain its tone and permit the performance of a surgical procedure with relative safety. It is advisable among patients who have any type of cardiac lesion that an electrocardiogram be taken prior to operation to determine the type of lesion present. If auricular fibrillation exists, it can be controlled by the administration of digitalis. If coronary disease is demonstrable in the absence of a history of coronary thrombosis, an essential surgical procedure should not be denied, if the patient is otherwise in good condition. The inf requency with which f atalities occur owing to coronary thrombosis among patients who have coronary disease and who have had operations performed at the clinic is emphasized by the fact that Willius stated that in the twenty-odd years that he has been at the clinic, of all of the patients who had coronary disease and who were operated on, he could recall less than ten who had died owing to coronary thrombosis. Renal Function. It is the custom at the clinic, in the treatment of all patients having surgical lesions of the gastro-intestinal, biliary and urinary tracts, to estimate renal function by a study of the concentration of urea of the blood. Its elevation may be the result of renal damage or may be owing to the toxaemia of dehydration. I have previously discussed the methods of controlling the toxaemia of dehydration by the oral administration of fluids when the patient can take them, and by the subcutaneous administration of physiologic saline solutions and the intravenous injection of solutions of physiologic sodium chloride and d-glucose. In a few cases in which severe acidosis has been present, 250 to 500 cc. of a 5 per cent solution of sodium bicarbonate has been administered intravenously with beneficial effects. General Considerations. It is, I believe, generally accepted by clinicians and surgeons that, in many instances, the presence of a diseased organ was recognized because of the employment of a routine method of examination. This, I believe, is a very important point to emphasize. I have previously emphasized the importance of a physical examination, routine urinalysis and determination of the cellular and chemical condition of the blood, particularly the concentration of urea in the blood. The presence of sugar in the urine may be unsuspected by the patient, and in such patients frequently serious difficulties arise owing to the occurrence of acidosis subsequent to operation. Because they have a mild degree of diabetes which does not express itself clinically, such patients may not be carefully watched after [43 ] operation. This type of case represents a group of patients in which the mortality rate associated with operation is likely to be.high, owing directly or indirectly to the presence of diabetes. One patient, a man aged seventy-one years, had such a mild degree of diabetes that it had been necessary for him to restrict carbohydrates only qualitatively for twenty- three years. The concentration of blood sugar was never more than would be considered in the higher limits of normal; yet, on the night following the operation (ileosigmoid- ostomy) the concentration of blood sugar rose to 425 mg. per 100 cc. of blood. If the routine management of that case had not revealed the presence of the hyperglycaemia and if insulin had not been given, a fatal outcome might have occurred. We will have more to say of this tomorrow in discussing the surgical treatment of the diabetic patient. Generally speaking, with the exception of patients suffering from conditions which constitute acute surgical emergencies, there are few surgical patients who are not benefitted by a day or two of observation in the hospital before operation. When the patient's lesion is similar to any of those which have been described, the surgeon not only can direct his attention toward securing organic compensation by employing adequate therapy but also he has a better opportunity to evaluate the condition of the patient. At the same time, if conditions are such that the need for operation is urgent, or if further useful information regarding the patient's physical condition cannot be obtained, or if by delaying operation longer further advantages cannot accrue to the patient, operation should be undertaken without delay in order that valuable time may be saved. REFERENCES. 1. Doan, C. A., Curtis, G. M., and Wiseman, B. K.: The Hsemolytopoietic Equilibrium and Emergency Splenectomy. Jour. Am. Med. Assn., 105:1567-1573 (Nov. 16), 1935. 2. Walters, Waltman: Discussion. Ann. Surg., 106:750-751 (Oct.), 1937; Tr. South. Surg., 55: 269-270, 1937. 3. Willius, F. A.: Personal communication to the author. PRECANCEROUS DERMATOSES By Oliver S. Ormsby, M.D. Cancer develops in the skin secondarily to several conditions. To those who define precancerous as a condition not malignant in itself, but one which invariably leads to malignancy, there are no precancerous conditions or dermatoses. If, however, the definition is broadened to include affections which may undergo malginant transformation, several affections or pathologic conditions must be considered. The most important are the keratoses. The chief ones are senile, arsenical, tar, paraffin and Roentgen ray keratoses and leukoplakia. Carcinomata sometimes develop on the keratoses found in Darier's disease (keratosis follicularis). The precancerous dermatosis of Bowen is probably a distinct type of epithelioma, though much confusion exists as to its limitations. Carcinoma is a prominent feature in xeroderma pigmentosum and malignant growths not infrequently develop in or from pigmented moles. In persons much exposed to the sun's rays and all-weather conditions, such as sailors, farmers, mountaineers, and so on, a presenile dystrophy characterized by atrophy, pigmentations, telangiectases and keratoses occurs which not infrequently terminates in multiple epitheliomata. Whether or not Paget's disease is malignant in the stage of dermatitis is still a debated question, but there is no doubt about the fact that it should be so viewed and treated. The association of kraurosis vulvae and carcinoma is well known and malignant transformation is of great importance in this disease. Epitheliomata develop occasionally in lupus vulgaris, lupus erythematosus, psoriasis and scleroderma; also, in old scars, particularly those following burns; also, on cutaneous horns and callosities, in wens, dermoid cysts, ulcers and fistulae. The most important form of keratosis terminating in cancer and the one to which the term precancerous is appropriate is the senile keratoma of Besnier. In a paper on circumscribed hyperkeratosis presented at the International Congress of 1896 in London, [44] —-.„ _*._«•, m.'nm, , . . .„. ^*fj*a.?*;! Dubreuilh1 gave a clear description of the affection and adopted Besnier's title. Eller and Ryan consider this term a misnomer and prefer the term senile keratoses. These lesions are seen in people past middle life, more often after the age of 60, and chiefly on exposed surfaces. They occur more often in men than in women and in those exposed to the sun and changing weather conditions. The common regions affected are the forehead, temple, the upper part of the cheeks, the nose, the dorsal surfaces of the hands, the sides of the neck and the ears. They are occasionally! seen elsewhere. The lesions are pinhead to dime size, moderately elevated, slightly greasy or more often dry and hard, firmly adherent, yellowish brown or black crusts, which when forcibly removed present numerous horny spines on the under surface which have projected into the dilated mouths of the underlying follicles. The skin beneath is uneven, moist and red, bleeds readily and is sometimes superficially ulcerated. They commonly present no intlammatory symptoms, but as they are changing their type into true epitheliomata some inflammatory reaction may be noted. The course is variable. They may remain for years without change. Some are gradually transformed into epitheliomatous ulcers which gradually enlarge, while others become more elevated and wart-like and present the clinical characteristics of the papillomatous epithelioma. The senile fiat wart—Verruca Seborrheica—Seborrhceic keratoses resemble senile keratoma, but the clinical and histologic distinction is usually readily made. The lesions of verruca seborrhceica occur usually around and past middle life and are found chiefly on the back over the shoulders, on the chest, on the abdomen at the waistline and occasionally on the face and neck. They are flat, moderately elevated, oval or round, pea to small coin sizes, gray, yellow, brown or black, and present a soft granular surface. The friable greasy crust is easily removed, revealing a red granular or slightly papillomatous base. They may be accompanied by itching which at times may be severe. Unlike the senile keratoses, these lesions rarely undergo malignant transformation. Occasionally, their surface is smooth when they resemble non-hairy pigmented moles. This type has been designated nevoid keratoses. In addition to the typical verruca seborrhceica above described there occurs a hyperkeratotic seborrhceic keratosis in the form of scaling pigmented patches which closely resemble senile keratoses. In theses the scales are waxy and the skin is thickened, sometimes slightly verrucous, and thir color is yellow- brown to brownish-black, and they are found on the face, scalp and upper portion of the trunk in elderly people. These not infrequently undergo malignant transformation. Hookey summarizes the changes as follows: Keratoma semilis is characterized by hyperkeratosis, irregular acanthosis, with dyskeratotic phenomena and secondary inflammatory reaction. Verruca senilis is characterized by hyperkeratosis, irregular acanthosis with the formation of an epithelial network, absence of dyskeratosis, a mild inflammatory reaction and usually increased pigmentation. The chief points of distinction clinically between the two are, first, the location. Senile keratoses occur chiefly on the forehead, upper portion of the sides of the face, on the ears, sides of the neck, and on the dorsum of the hands. The lesions are hard, firmly adherent crusts with horny spines on the undersurface which fit into the open mouths of follicles beneath. The surface beneath the crust is moist red and bleeds easily and is sometimes superficially ulcerated. The seborrhceic keratoses select the trunk front and back, the abdomen, and, less often, the face and neck. These lesions are soft and granular and easily removed, revealing a soft granular or slightly papillomatous base. The senile keratoses often undergo malignant transformation and are therefore a precancerous condition, whereas the seborrhceic keratoses rarely undergo this change and are not considered precancerous. Treatment of Keratosis Senilis.—The lesions may be removed by softening with a keratolytic ointment (salicylic acid) for a few days, then curetting the surface, after which refrigeration with carbon dioxide snow is satisfactory, or trichloracetic acid may be applied in place of the snow. Diathermy or electric coagulation are also used. If malignant change is already progressing, one or the other of the last two methods or surgical excision is preferable. Treatment of Seborrhceic Keratoses—Sebaceous warts.—Their removal is necessary only for cosmetic purposes as a rule. When numerous and large and limited to the trunk, [45] complete removal is not necessary. They may be reduced in size and made less conspicuous by the use of an ointment containing salicylic acid and sulphur in the strength of three and five per cent respectively. If complete removal is desired, they may be curetted and frozen with carbon dioxide snow or trichloracetic acid applied. Roentgen rays are also efficient. Up Keratoses.—Keratoses occur quite commonly on the lips, especially the lower. They often are small round or oval lesions and moderately elevated. At times they are linear and may cover one-half of the surface of the Up in the form of a narrow band. They occur usually in men around middle life and older, although they are not infrequently seen at an earlier age. They are persistent and often undergo malignant ulceration. They should always be viewed as having dangerous potentialities and thoroughly removed as early as possible. Leukoplakia.—This affection as seen in the mouth occurs as whitened areas of varying size and diverse outline. There may be one or several patches situated on the surface of the tongue, beneath the tongue, on the buccal mucosa, particularly behind the commissures and over the area opposite the molars, on the gums, lips and the hard palate. At times the affection occurs profusely over a large portion of the buccal cavity. The patches are white or greyish white, thickened in varying degrees, often rough. Erosions occur in patches when the superficial covering is shed. At times the patch becomes verrucous, fissured and vegetating. It is not known in what proportion malignancy develops. The affection occurs in both the syphilitic and the non-syphilitic. The chief affection from which it is to be distinguished is lichen planus. In the latter affection the white areas are linear-and striate on the buccal mucosa and consist of white papules on the tongue. The presence of cutaneous lesions of .Hehen planus is a valuable diagnostic point. Occasionally a syphilitic interstitial glossitis with atrophy is associated with leukoplakia. The use of tobacco both by smoking and chewing is often an etiologic factor. Treatment.—Cessation of the use of local irritants is first indicated, the first one being tobacco. Hot and cold substances, condiments and vinegar are to be avoided. Electro- desiccation, the electric cautery or radium are the most efficient methods of direct removal. In extensive quiescent cases, palliative treatment is recommended. Partial removal is likely to induce malignant change. Kraurosis Vulvae.—This affection occurs usually in women of advanced age or at the menopause, or in younger women, in whom this condition has been produced through surgical removal of the uterus or ovaries. It is essentially a sclerosing atrophy of the mucocutaneous structures of the vulva. It is characterized at its height by the complete or almost complete disappearance of the labia minora, the frenulum, and the clitoris, with flattening and reduction in the volume of the labia majora, together with rigidity of all the vulvar tissues and atresia of the vaginal orifice. The color of the retracted tissues may be whitish, yellowish, reddish, or bluish. A characteristic glistening appearance, seeming as though varnished, may be present. The affection is usually preceded by intense itching, which may persist, though in some late cases there is loss of cutaneous sensibility. Taussig states that 75 per cent occur at the menopause and that the balance have some disturbance of ovarian function. Leukoplakia may occur as a complication, in which case malignancy often follows. This condition is to be distinguished from simple leukoplakia of this region which is similar to that seen in the mouth and from pruritus with lichenification (neurodermatitis) which produces a whitish thickening of the vulva. When the last condition is present the usual picture of neurodermatitis is apt to be seen extending over the pubes and down over the inner aspects of the thighs. The treatment of the condition is surgical. Taussig8 believes that the incidence of cancer can be reduced 50 per cent by complete vulvectomy for leukoplakic vulvitis. Precancerous dermatosis of Bowen .—In 1912 Bowen recorded two cases of chronic atypical epithelial proliferation with unique clinical characteristics. In his cases the lesions occurred in well defined patches. The early lesion was a firm pale red papule covered with a thickened horny layer of a cornified crust. Beneath the crust the surface was papillomatous. By enlargement of the papule, lenticular or rounded nodular [46] lesions were formed which were discrete or grouped and confluent. The lesions at the margins of the patch had an annual or serpiginous outline. The patches increased in size by the formation of new lesions at the periphery. The clinical appearance suggested a late nodular syphiloderm. Diagnosis.—The affection is to be distinguished from extra-mammary Paget's disease and superficial epitheliomatosis. The localization of the lesions described by Bowen, with their papular and nodular character with a serpiginous configuration makes the clinical distinction from the red scaling patches seen in the first-named affections. Treatment.—Surgical removal is recommended. Pigmented Moles.—The most dangerous type of lesion is the flat slatey or blue-black mole. These not uncommonly are- seen near the eye and on the feet. These sometimes undergo malignant transformation without apparent traumatism. As a rule, however, chronic irritation, trauma, application of caustics or incomplete surgical removal is the immediate cause of malignant change. As a rule the large brown, flat or elevated, hairy or free from hair moles are not a menace unless irritated. In quite a number of generalized fatal cases of malignant melanoma seen by me, all have followed incomplete surgical removal or cauterization (usually with an acid) of a pigmented mole. As a rule the malignant metastatic tumours are classed as nevo-carcinoma or malignant melanoma. Nomland11 described multiple basal cell, pigmented epitheliomata developing on basal cell pigmented nevi. Erythroplasia of Queyrat.—This is a rare form of precancerosis originally described by Darier and Fournier as a precancerous condition. It occurs on the glans, the prepuce and on the vulva, as well as on the buccal mucosa, including the tongue, cheeks or lips. The lesions are well defined areas with brilliant red velvety surfaces. The condition progresses slowly and indefinitely and it is resistant to local treatment. The cause is unknown, though it is often associated with syphilis. Conditions from which it has to be distinguished are superficial epithelioma, tuberculosis and syphilis. The characteristic histologic changes consist in marked acanthosis with some cellular infiltration in the upper cutis. Occasionally dyskeratotic changes, such as seen in Bowen's disease, occur. Carcinoma always follows unless it is totally destroyed in its early stages. Keratosis follicularis (Darier's disease).—This is a classical keratotic affection first described by Morrow12. It was early studied intensively on account of peculiar round bodies found on microscopic examination which were believed to be parasites (psoro- sperms). Bowen described these bodies, in his histologic examination of White's original case, as epithelial cells which had undergone an anomalous cornification. The disease occurs at all ages, not infrequently beginning in infancy, and is seen also in the elderly. Males are attacked more often than females and heredity is a factor in its production. Trimble15, for example, recorded five cases in three generations. The disease is characterized by an eruption beginning as papules which soon become crust-covered and by coalescence produce papillomatous vegetating and tumour-like growths. The eruption is usually most extensive on the trunk, especially in the axillary and inguinal regions and around the neck. It also occurs on the head and extremities. The vegetating and papillomatous lesions are found chiefly in the axillary and genital regions and behind the ears. Seborrhceic crusting occurs in the scalp. The early lesion is essentially a follicular keratosis. The essential pathologic lesion is a hyperkeratosis of the follicles which are filled with horny material. The round bodies are found between the prickle cells of the rete malpighii. The disease is among the uncommon affections, though numerous examples have been seen all over the world. Wende16 recorded the first example of malignant transformation seen in the affection. Its treatment is unsatisfactory. Amelioration of the symptoms may be effected with the use of keratolytic ointments and Roentgen therapy. The prognosis as to recovery from the distorder is unfavorable, but as to a serious termination it is good, aside from the possibility of malignant transformation. Paget's Disease.—This affection as seen on the nipple was first described by Paget17 in 1874. Extra-mammary cases were reported many years later. Hartzell18 was an early reporter in this country. [47] The nipple cases usually occur on the breasts of women, though a number of examples have occurred in men. On the nipple the process is characterized by redness and scaling which later becomes more marked, and the redness deepens and the surface becomes granulating and exudes a clear viscid secretion forming crusts, and is accompanied by sensations of heat and burning and itching of varying intensity. The inflammatory area is well defined, and as time progresses the process extends deeply, forming a circumscribed infiltration of the skin, which on palpation suggests a large-sized coin or button in the substance of the areola and surrounding parts. The nipple becomes flattened or retracted. Sooner or later carcinomatous infiltration occurs in the substance of the breast. The course of the disease is usually slow and no attempt at healing of the eczematous process on the nipple occurs. Extra-mammary cases have been seen on the penis, scrotum, buttocks, vulva, perineum, in the axillae and numerous other situations. The clinical symptoms are those seen on the nipple. It is likely that the major portion of those reported on the trunk are examples of superficial epitheliomatosis which is usually of the basal cell type. His to pathology.—The characteristic histologic changes consist of cedema and hypertrophy of the epidermis, in which peculiar cells are found, together with an inflammatory cellular infiltration in the corium. There is marked hypertrophy of the rete with down growth of its pegs into the corium. Peculiar double-contoured cells of large size are found1 in varying numbers. These cells are vacuolated, round or irregular in shape and often contain two or three nuclei which show varying changes as to form, size and location. The Paget cells resemble the dyskeratotic cells found in Bowen's disease, but they have no intercellular bridges. They were formerly considered by Darier to be coccidia or psoro- sperms, but it is now known that they are cellular degenerations. A cellular infiltration consisting of leukocytes, small connective tissue, plasma and a few mast cells is found in the corium, together with dilation of the blood/ vessels and in the areas of infiltration the collagen and elastin are more or less destroyed. The retraction of the nipple is due to sclerosis occurring around the mammary ducts, the latter being involved in malignant infiltration early in the process in some cases. The subsequent carcinoma may develop either from these ducts or glands beneath or be derived from the surface epithelium. The histology of the extra-mammary cases corresponds to the above in most particulars. In some cases the cellular exudate is less pronounced. The presence of the "Paget cell" and other characteristics identify the condition histologically. Montgomery19 believes that most of the cases reported as extra-mammary Paget's disease, particularly those of the scrotum, perineum and penis, were histologically frank squamous cell epithelioma showing individual cell keratinization, while those of other parts of the body histologically were basal cell epithelioma, Bowen's disease or metastatic carcinoma. Diagnosis.—Paget's disease of the breast is distinguished from eczema by its intractable character, localization to the nipple area, its deeper infiltration shown clinically by a f eeling of hardness revealed by palpation and, finally, by its accompanying malignant growth in the substance of the breast. The reported extra-mammary cases on the trunk are practically indistinguishable from superficial epitheliomatosis in its crusted type. Treatment.—Paget's disease of the breast requires surgical extirpation. Complete removal of the breast and accompanying glands is recommended. The extra-mammary type may be excised or treated with radium or Roentgen rays. Xeroderma Pigmentosum is a rare disease which begins in childhood and is characterized by hyperpigmentation, atrophic areas, telangeictases, warty and malignant growths. This disease was first described by Kaposi in 1870. The eruption occurs largely on exposed surfaces and these include the face, neck, upper chest and the hands and forearms. Other areas are occasionally invaded. Sunburn has initiated the process in several instances. It is distinctly a family disease, being present in two or more members as a rule. The earliest symptom may be an erythema or dermatitis. Following this, or independent of it, freckle-like lesions develop. These become numerous and are of variable size and present different shades of yellow and brown. Interspersed between these lesions, variously sized whitish atrophic areas or cicatriform patches develop. [48] Telangiectases and small angiomata are common. Flat or convex warty growths also develop and these resemble senile keratoses. They are pea sized or larger and are scattered among the pigmented and telangiectatic lesions. A.t a later date malignant growths appear and various forms occur, the chief of which is carcinoma. Ectropion is common with its associated photophobia and lacrimation. This often causes ulceration on the face. Keratitis is common and nodules and opacities occur in the cornea, causing obstruction of vision. The progress of the disease is usually slow, though death from marasmus may occur within a few months. Malignant transformation usually occurs after many years and results in a fatal termination. A striking thing about the affection is its resemblance to the changes seen in the senile skin. Aside from the fact that it is a family affection and apparently is the result of the action of the sun's rays on a peculiarly sensitive skin, nothing is known of its cause. Pathology.—All the changes seen microscopically are closely simulated in sailors' skin and in chronic roentgen ray dermatitis. The malignant growths most often seen are basal cell epitheliomata. In addition, melano-epitheliomata, tricho-epitheliomata, round, spindle and giant cell sarcomata endotheliomata, peritheliomata and angiosarcomata have been described, as well as fibromata and angiomata. A detailed histologic description of the disease and its sequels will not be outlined here. Diagnosis.—Xeroderma pigmentosum presents such striking symptoms that it is readily recognized. The early date of onset in most cases, the limitation of symptoms to exposed surfaces, together with the combination of pigmented lesions, telangiectases, atrophic spots and areas, associated with the peculiar photophobia and lacrimation, are only seen in this affection. Treatment.—This is unsatisfactory. Life may be prolonged, however, by preventing exposure to the rays of the sun. The general hygienic care is important. The malignant growths respond well to radium and Roentgen rays. Surgery is often indicated. Prognosis.—In the major portion of cases the outlook is grave. With careful treatment life may be prolonged several years. Arsenical Keratoses develop in people who have taken the drug over long periods of time for the relief of cutaneous dermatoses, such as psoriases, and dermatitis herpetiformis. They are usually associated with pigmentation. Multiple epitheliomata not infrequently develop on these keratoses. In one case observed by the writer more than a dozen epitheliomata, both superficial and deep, developed among hundreds of keratoses and hyperpig- mented lesions. The malignant transformation occurred chiefly on the hands, limbs and scrotum. Keratoses occurring in tar and paraffin workers are often associated with acneform lesions and areas of dermatitis, together with scars, the previous site of epitheliomatous ulceration that healed spontaneously. Cancer from tar is an industrial reportable disease in England. Chimney sweep soot cancer, usually occurring on the scrotum, is only of historic and scientific interest here, as it has been seen chiefly in England and only rarely at present. Roentgen ray keratoses occur in chronic radiodermatitis and, unfortunately, are seen quite often. They occur in the skin of unprotected operators most often, but occasionally in others. They are usually associated with areas of atrophy and telangiectasia and not infrequently undergo malignant transformation. Electrodesiccation, endothermy or excision are recommended for the removal of these keratoses. It is not necessary here to discuss farther the malignant growths occurring in the various dermatoses mentioned earlier in this paper other than to say that cancer thus developing is usually of the prickle cell type and is therefore capable of early metastasis, and requires immediate and complete operative removal by surgical procedure. BIBLIOGRAPHY. 1. Dubreuilh: Annales 1896, xiii, p.- 1158. 2. Hartzell: Jour. Cut. Dis., 1903, xxi, p. 393. 3. Fordyce: Trans., xvii, Internat. Cong, of Med., London, 1913—Sec. xii, part 1, p. 4. 4. Freudenthal: Arch, of Derm, and Syph., 1926., vol. 152, p. 504. [49] Eller and Ryan: Arch. Derm, and Syph., 1930, xxii, p. 1043. Hookey: Ibid, 1931, xxiii, p. 946. Montgomery and Dorfell: Arch. Derm, and Syph., 1932, clxvi, p. 286. Taussig: Arch. Derm, and Syph., 1930, xxi, p. 431. Montgomery, Counseller and Craig: Ibid, 1934, xxx, p. 80—Kraurosis, Leukoplakia and Pruritis Vulvae. For an admirable discussion of this subject, see this article. Bowen: Jour. Cut. Dis., 19192, xxx, p. 241. Nomland: Arch. Derm, and Syph., 1932, xxi, p. 1002. Morrow: Ibid, 1886, iv, p. 257. Darier—Annals, 1889, x, p. 547. "White: Jour. Cut. Dis., vii, p. 201, and Ibid, 1890, viii, p. 13. Trimble: Jour. Amer. Med. Assoc, 1912, lix, p. 604. "Wende: Jour. Cut. Dis., 1908, xxvi, p. 531. Paget: St. Bartholomew's Hosp. Reports, 1874, p. 87. Hartzell: Jour. Cut. Dis., 1910, xxviii, p. 379.9 Montgomery: Archiv. Derm, and Syph., 1929, xx, p. 339. DISEASES OF THE LIVER By Dr. R. F. Farquharson. The reserve of the liver is so great that there may be very extensive disease of that organ with much destruction before there are any symptoms. Conversely, there is no test of the liver that will detect very early disease. Some of the functions of the liver are obvious and some of them very difficult to demonstrate and concerning them there is nothing known. We are all familiar with the functions of the liver. Its function with regard to metabolism is of great importance both theoretically and practically, and the practical importance lies in the fact that very great strain is placed on the liver. It is extremely important in any liver disease to give a diet that is high in carbohydrates and one low in fat and protein. The function of the liver with regard to the storage of several substances is important but difficult to measure. The function with regard to the control of haemorrhage I shall speak of later. The symptoms that we get depend upon the acuteness and diffuseness of the disease. There is always jaundice. There is always loss of appetite, and a marked loss of appetite is probably the most constant single symptom that accompanies jaundice and commonly precedes it, when it is acute. We also find nausea and vomiting, and sometimes the patient complains of pain due to a pylorospasm. This is often confusing. With acute disease of the liver there is commonly itchiness of the skin, and this itchiness is an interesting thing. It may come in catarrhal jaundice; is much more apt to occur where jaundice persists for some time. It is very severe in many cases of obstructive jaundice. When we find this itchiness there is a peculiar appearance of the skin, not unlike the appearance in Hodgkin's Disease. There seems to be an oedema of the skin and the itchiness is difficult to relieve. When there is very severe disease of the liver there are mental effects present. With regard to the symptoms of haemorrhage that is found in many types of jaundice and in some types of liver disease without jaundice—this does not occur very often with catarrhal jaundice. It does occur in people with acute yellow atrophy. It occurs most commonly in the condition of obstructive jaundice, particularly when due to stone, and most when there has been some cholangitis and long-continued jaundice. This haemorrhage tends to come after operating, not at the time of operation but about the fifth or sixth day after it. It may be from the site of the wound, but may be from anywhere in the body, showing that it is not a local but a generalized condition. There may be haemorrhage from the nose, into the gums, etc., and this haemorrhage is shown to be related to a reduction in the prothrombin of the blood and is similar to the experimental disease of chicks when placed on a diet insufficient in Vitamin "K". This Vitamin "K" is found in dried spinach, putrefied fish ,etc. It will be very interesting to carry on further research and to find out what are its limitations. Vitamin "K" is a fat soluble vitamin. Whether it is discharged in the presence of continued jaundice, where there are other toxic factors, will remain to be seen. So much for the type of symptoms in acute diseases of the liver. [50] These are very different from chronic diseases of the liver. The liver may be gradually destroyed with replacement by fibrous tissue with very few symptoms. The early signs may be the finding of a large liver; the development of ascites; haemorrhage from oesophageal varices; or there may be vague, gastro-intestinal symptoms and general ill health. Because of the tremendous reserve of the liver and because of the poor results of liver function tests, our diagnosis depends almost entirely on the history that we get from the patients, and on our examination. Our treatment consists in reducing to the greatest degree the load that is placed on the liver by the metabolism of our bodies. First I shall discuss the acute diseases of the liver that are associated with jaundice. Jaundice is due to the presence of bilirubin, which is due to the breaking down of haemoglobin. It always gives a negative direct Vandenbergh. It does not pass into the urine even if there is definite jaundice. This bilirubin circulates in the blood, comes to the liver and is extruded into the body. It passes into the urine.and on into the bowel. If the liver is particularly damaged, it passes into the urine and the finding of an excessive amount in the urine is a helpful sign in diagnosing liver diseases. We may get jaundice from an increase in the blood destruction, but that is a relatively rare type of jaundice. We may get jaundice when there is any type of disease of the liver. When there is toxic disease of the liver we get jaundice. In the next slide I would like to give a very brief classification of jaundice. 1. Jaundice due to haem. icterus. Disease is relieved by splenectomy. 2. Constitutional hyperilirubinaemia (mild icterus). Secondary mild or latent jaundice (toxic). We see this in almost every case of pneumonia; also in typhoid fever. It does not require any special treatment, except to treat the primary condition. Gross jaundice—due to disease of liver parenchyma. Obstructive jaundice—obstruction of common bile duct or hepatic ducts. These last two conditions can be easily differentiated at most times, but at other times it is extremely difficult to do this. The recognition of the two types is of the utmost importance. In the first case we must not have any surgical interference whatsoever, but in the second type it is so important to have early surgical interference that we want to recognize it as clearly and as early as possible. The important thing in making the differentiation is the theory of the patient and the examination. One test which helps a little is the tolerance test. (A slide was then shown of the various parenchymatous diseases which give rise to jaundice.) Table. JAUNDICE. Disease of Liver Parenchyma. (Catarrhal Jaundice. C. Passive Congestion. Hepatitis \Epidemic Jaundice. _ ll . ,^r ., . . ^Acute. W7-^:i> T»:„Q.,oa D. Necrosis (Yellow Atrophy )-)C u '-1 $i I Weil s Disease. v r -^(Subacute. E. Biliary Cirrhosis (Chronic Hepatitis). 3. 4. 5. A. B. To xic. Glucose and saline intravenously should be given only if patients are unable to take proper diet by mouth. They should not be allowed to become constipated. Sometimes there is no trouble in having them sleep; sometimes they want to sleep all the time. It is very important to see that they get plenty of rest. The itchiness is usually very Hard to control. Sometimes we have to come down to the use of sedatives tosget them to sleep. We can use bromides without any danger. Sometimes a combination of bromide and codeine is helpful. We should avoid Nembutal. If the patient has acute necrosis and haemorrhage and we have a supply of Vitamin "K" in hand, we can try it and should try it. If not, we should try transfusion of blood for these cases with haemorrhage. Give them milk in their diet, but it has been my experience that transfusion has been wonderful. A few years ago I had a case of biliary jaundice. She came into the hospital pregnant and with haemorrhage everywhere, but only a slight jaundice. She was transfused at once and immediately after that her haemorrhage stopped. She had to be transfused several times before delivery and at time of delivery she acted very well. [51 ] Sometimes we get jaundice from passive congestion. This is a very rare but very serious disease. Any of these conditions, even the passive congestion, may give rise to a terminal necrosis that may be either acute or subacute. We may have jaundice also in biliary cirrhosis. The ones of this group that are going to be difficult to differentiate from obstructive jaundice are those cases of catarrhal jaundice that come on very gradually with very little general disturbance. They are not common, but tend to come on in older people. Here the tolerance test is a good thing to use. If we could tie off the common bile duct without injuring the surrounding tissues, that jaundice would come on so insidiously that the patient would not think that there was anything wrong with him until he was very severely jaudiced. The nearest we get to that is in cancer of the head of the pancreas or its related structures. It is true that sometimes cancer of the head of the pancreas is very large and gives rise to the symptoms of cancer. There is quite a big cancer before there is obstruction. Sometimes, the cancer being small, and there being no destruction of the duodenum, there is obstructive jaundice without any other symptoms, and these people frequently are going about at their work when some person notices that they are jaundiced. Very soon they get the symptoms of liver insufficiency, which shows that there is obstruction to the common bile duct. What are we going to do if we make a diagnosis of this particular type of cancer? We make the diagnosis on its insidious onset, usually painless. We shall almost always be right in our diagnosis. We cannot do anything for the patient medically. If we don't operate, all we can do is to make the patient as comfortable as possible. The chief thing to alleviate is the terrible itching. The diagnosis is confirmed almost always by the finding of a great big gall bladder. We can make a communication . between the distended gall bladder and stomach, or duodenum, and if we do that, providing the patient is not suffering too much from symptoms of cancer itself, we shall see a remarkable alleviation of the symptoms. The itchiness goes almost immediately, the other symptoms clear up gradually and the jaundice clears up in a few weeks. However, on the average, all these patients will be dead within a year. To go on to the commoner type of obstruction—stone in the common bile duct with cholangitis. It is very unusual to find jaundice in this type of case if they have not had pain before. If we get a clear-cut history of pain, followed by jaundice, associated with fever, that is pathognomonic. Almost always there will be a history of preceding attacks of mild jaundice before there is a severe jaundice. If we have repeated attacks there is no difficulty about the diagnosis at all. The time when the diagnosis is difficult is when we cannot get the former history of attacks of pain and the jaundice has come on rather insidiously. What are we going to do for these people? There is no medical treatment except to prepare them for operation. If we are going to operate, we must operate on them at the right time. It is important that we operate on them when they are free from their jaundice; so we treat them for this jaundiced condition first of all. What if they are persistently jaundiced and the jaundice is severe? If we are reasonably sure of the diagnosis we should advise operation immediately. Stricture of the common bile duct comes almost always in people who have had an earlier operation on the gall bladder or in the common bile duct, and it is of the utmost importance that we recognize this possibility and that we don't tell the patient or his friends that the results will be 100% sure. The danger of damage at this operation is great in these cases. The danger of not finding the stone is present. So we must tell the patient or his friends just what the situation is. People that have a stone in the common bile duct almost always continue to have trouble, and it is usually much safer to operate on them than not to operate. Foreign body in the common bile duct will cause jaundice. Carcinoma also will give severe jaundice. As to chronic disease of the liver: Portal cirrhosis is the most typical example of chronic disease of the liver. Sometimes there is a history of alcohol consumption. The disease comes on gradually and gives few symptoms until the liver is tremendously changed, and if we happen to examine the patient before the development of symptoms, we shall find that the liver is enlarged and very hard. We may feel that hard liver and that hard spleen on a routine examination when the patient has no symptoms whatsoever, and we shall see that patient later with the characteristic symptoms of portal cirrhosis: (1) the appearance of ascites; (2) (or it may be the first symptom) hemorrhage, from the stomach or from [52] the dilated varices of the oesophagus; (3) most commonly the first symptom is just a feeling of lack of well being and malaise; (4) if there is a history of prolonged use of alcohol in large quantities, we have something to go on in our treatment. In any case, there is not much we can do for the disease, but we can see to it that the patient gets as much rest as possible. If the patient has been taking alcohol in large quantities, he must be told to keep away from it altogether. We can regulate, eliminate all toxins. We can see to it that diet is properly regulated; that they don't take a great deal of water and that they cut down on salt. If ascites is present, in spite of the reduction of the fluid intake and salt, we may try the diuretic treatment. Sometimes we have to resort to tapping. Sometimes we will tap the patient many times and they can carry on for a while longer. There is no operation that is of any value. Now for some of the causes of gross enlargement of the liver. Cancer is obvious. Syphilis of the liver tends to give rise to a great big liver that is grossly irregular. We can give them mercury and bismuth and iodide. The patient won't be cured but his symptoms will be relieved. Arsenical jaundice occurs in some people being treated with arsenic, for treatment of syphilis. Another cause of grossly enlarged liver is myocardial failure. Hodgkin's Disease in the late stages commonly gives rise to a very enlarged liver; also Leukaemia. CHEMICAL ASPECTS OF PREGNANCY AND • Wlf' ITS TOXEMIAS By Dr. Andrew Hunter. I need not say anything to emphasize the importance of the so-called toxaemias of pregnancy. Enormous labour has been spent in order to find a cause for these toxaemias with very little results. After I have discussed the chemical aspects I shall simply have to end up by saying that these really throw practically no light at all upon the origin of these conditions, but it is perfectly obvious that if we are to attempt to find anything about this condition we must know something about the chemical aspects of a normal pregnancy. To take things in their logical sequence, the first thing that might arise is whether there is any difference in the total metabolism in pregnancy. There is no peculiar metabolism. The metabolism of the pregnant woman amounts to the sum total of the metabolism of the pregnant woman and the foetus. The normal adult organism is in a state of nitrogen equilibrium—nitrogenous metabolism. In the pregnant female that is no longer the case. It is necessary that the combined organisms should be in positive nitrogen balance. The combined maternal and foetal organisms should be taking in more than they are giving out. That is found to be the state of affairs in pregnancy in the human female almost from the beginning of the pregnancy. As the pregnancy progresses, the extent of nitrogen becomes greater and greater. Here is a slide showing a table of nitrogen amounts as the foetus grows. In a perfectly conducted pregnancy the woman adds to her own original content of nitrogen. The mother gains nitrogen and stores up a very considerable quantity. This is in preparation for subsequent lactation. This is the state of affairs in the human organism. In some of the lower animals this is not the case. In the dog and in the cow it has been found that at the beginning of pregnancy the nitrogen balance suddenly becomes negative. During the early pregnancy in these animals the foetus is growing, not from the food supply taken in by the mother, but is taken in at the expense of the maternal organism. That is called the negative phase. In the human individual, in the pregnant woman, if her food is properly attended to, that negative phase never appears, but it does appear in some of the lower animals. What is the reason? It may have some bearing upon the physiological vomiting which occurs so commonly in early pregnancy. In the lower animals we have taking place a rapid growth of the ovum, which attacks the uterine wall, breaking it down by means of powerful enzymes. It is possible that although this negative phase does not occur in the human female there may be, nevertheless, something approaching it and that possibly in this may be found the cause for physiological vomiting. In the dog and other animals, the balance changes from negative to positive at about the time when the placenta becomes [53 ] finally completely formed and that corresponds to the time at which physiological vomiting disappears in humans. If we enquire into the details of nitrogen metabolism in pregnancy we must first look at the urine and at the blood for the indication of any possible peculiarities. As far as the urine is concerned there are no peculiarities to be noted. There is, as a rule, proportionately less urea excreted. There is more ammonia, but these conditions are not peculiar to pregnancy. They are encountered in any condition in which there is taking place any synthesis of protein material, as in convalescence from any serious disease. This is only to be expected. If we look at the blood, here is a slide showing the non-protein- nitrogen of the blood. In the normal pregnancy, here we see the average figures. Here we see the figures for non-pregnant women. In pregnancy the whole organism is keyed up to the saving of protein. The urea is diminished in amount. The uric acid tends on the whole to be increased. Just what the explanation is, we cannot say, but it does tend to increase in most cases. What about carbohydrates and fat? Is there any peculiarity there? There is nothing peculiar. The blood sugar in pregnancy is just the same as in the non-pregnant. The sugar tolerance curve obtained after giving a dose of 100 gm. of glucose has exactly the normal shape and the only respect in which there is any deviation from the normal is that sometimes there is a little glycosuria following a large dose of glucose. It is supposed that this may be due to certain degree of hepatic insufficiency. It is found that the glycogen content of the liver is apt to be less in the pregnant state. With regard to fat metabolism, it is not surprising to learn that there is, even in a perfectly normal pregnancy, a slight tendency to ketosis. The pregnant individual develops ketosis more readily than the nonpregnant. There is nothing abnormal in this tendency. It is just the sequence of a slight degree of hepatic impairment. Now, does the blood show any further peculiarities beyond what is shown on this slide? In the first place, there is a slight increase in the! volume of the blood in normal pregnancy, taking place in the latter months. That increase is almost entirely due to an increase in the volume of plasma. There is a certain amount of hydration taking place and this is not a mere addition of water to the plasma. The total salt content falls but the chloride remains normal. The serum proteins are reduced in concentration. Here is a slide showing the plasma volume throughout pregnancy. These changes in plasma volume may have an effect on oedema. The question next is about acid-base balance. We find a peculiar situation. The bicarbonate of the blood is found to be below the normal. It is reduced quite distinctly. It is reduced 10% or more. Parallel with that reduction takes place a reduction in the free carbonic acid. The ratio of the two remains normal and the PH. of the blood remains normal. This is the condition of non-gaseous acidosis. There is no over-production of acids in a normal pregnancy to account for this. The explanation of this can be illustrated best by this slide. The total base has fallen, as you will see in this slide. The bicarbonate is reduced because the total volume is reduced. Here we have a very distinct fall in the total base. This is very difficult to explain and no satisfactory explanation has been given. It is a very remarkable phenomenon. The behaviour of certain hormones and certain enzymes comes into discussion here. Two of the sex hormones in particular are the Prolan and the Estrin, which is normally produced in the ovary. This chart shows the amount of Prolan which is excreted during pregnancy. Within ten days after the onset of pregnancy, Prolan begins to appear in the urine. The excretion begins very early and this is what is used to determine pregnancy by the Ascheim-Zondek test. I mention this because some authorities have sought to find some connection between the early and late toxaemias and the behaviour of this or other hormones. The Estrin content rises from the beginning of pregnancy more steadily, but does not rise so high. It has been said by some that there is an association between pernicious vomiting, one of the early toxaemias, and an abnormally high concentration of Prolan in the urine. On the other hand, certain American observers have found no such connection whatsoever, so there you are. We don't know what to think about this at present. It does seem that the possibility of a connection here should be investigated. It is a very interesting phenomenon. With regard to late toxaemias, it has been stated that in r 541 the toxaemias we don't find the Prolan coming down quite so far as it does in the normal pregnancies, but that again has not yet been confirmed and these observers are just at the stage of collecting information on the question. They may possibly find some clue ultimately to the origin of the toxaemias. This slide is simply a summary of what I have been saying. One other point is this. Certain enzymes appear during normal pregnancy. They are ones which are capable of digesting placenta. The plancental proteins are abnormal ones and they get spread throughout the organism sometimes; form an embolus, perhaps. This may get digested, and it sometimes thought that this is the actual source of the toxaemias. Whether this is so or not is by no means certain, but, at any rate, in order to protect itself against this, the organism establishes enzymes as a protection. So much for normal pregnancy. Now to pass to the toxaemias. Classification of Toxaemias. I. Minor manifestations—pruritus, neuritis. II. Early toxaemias—hyperemesis gravidarum. III. Late toxaemias—albuminuria; nephritic toxaemia; pre-eclampsia; eclampsia. With regard to early toxaemias. The biochemical findings in this condition (hyperemesis gravidarum) are summarized in this slide. They are not very helpful and don't show anything specific. They are simply the natural consequence of the vomiting. All the findings stated here are simply the consequence of these events. Blood—Hypoglycaemia. High serum protein. Slight rise of N.P.N. Acidosis common. Urine—High ammonia. Ketonuria. The above table shows the biochemical findings in pernicious vomiting. There is nothing characteristic in the urine. This is a slide showing to what extreme the overproduction of ammonia may appear to go. It was thought at one time that this ammonia . co-efficient in pernicious vomiting might be of great use in diagnosis, but in actual practice that hardly proves to be the case because it is nothing peculiar to hyperemesis gravidarum. It may be the result of vomiting from any cause in any individual, but is already, as it were, at the edge with respect to the production of ketone urine. I had a case of a pregnant woman who had severe vomiting as a consequence of a gastric ulcer. In that case the ammonia co-efficient rose almost as high as this. In this early toxaemia the biochemical studies show nothing that is specific and nothing that is particularly helpful. With regard to the late toxaemias. An enormous amount of work has been done on the chemistry of the late toxaemias. Very frequently the work has been done on a few cases only and is of very doubtful value. The largest series of cases that I have come across is that reported by the Medical Research Council of Great Britain, through Dr. Cruikshank and others at the Royal Maternity Hospital in Glasgow. There were about 40 cases of normal women and a similar number each of albuminuria, pre-eclampsia and eclampsia. This slide shows the normal cases and the others, by comparison. A rise in the uric acid of the blood almost invariably is a result of any one of the toxaemias and the more severe the condition is, the greater is the rise. These other apparent changes are of very doubtful significance. A case of toxaemia may have a perfectly normal N.P.N, of the blood. Similarly with the urea, which just about runs parallel with the N.P.N. The uric acid is a little more consistent. A rise in uric acid appears to be a pretty regular feature of all the toxaemias. Even in eclampsia, however, it may be within normal limits so that even this is not one to be relied upon altogether. The general conclusions reached by the Medical Research Council on these findings were these: That the variations were so great that it would be very difficult to diagnose the type of toxaemia from the chemical findings alone. Such changes as do reveal themselves are all in the nature of an exaggeration in the peculiarities of the blood and urine in normal pregnancies. The most obvious changes in the blood are most obvious in eclampsia. We find that in the blood there is very often an accumulation of lactic acid. This might be due to the severe damage to the liver. Sometimes we find an increase in the ketone acids of the blood. This may be the result of starvation resulting from vomiting. With regard to the proteins of the blood: Here is another chart showing the plasma protein concentration in pregnancy, both in the normal cases and in the toxaemias. [55] The last point I can illustrate is the effect of eclampsia upon the acid-base balance. The result is a very decided acidosis, a very extreme acidosis which, in some cases, results in a fatal termination. This slide shows the acid-base balance in the non-pregnant, in nomal pregnancies and in toxaemias of pregnancy. Now, that concludes what I have to show with regard to the biochemical changes in the toxaemias. We find in the toxaemias of all kinds, biochemical changes which do not seem to reveal the causes for these toxaemias. Nor do they help in differentiating different types of toxaemias. The only positive statement is that when you are dealing with a nephritic toxaemia, then an N.P.N, of about 40 is of the gravest possible prognostic import. The treatment of these cases will have to be directed, not to the treatment of any of these biochemical changes, but to the relief of the symptoms and from other principles altogether than those which can be furnished by these particular laboratory observations. SCALENUS NEUROCIRCULATORY COMPRESSION R. Glen Spurling, M.D. Attention was first called to the importance of the scalenus anticus muscle in the cervical rib syndrome by John B. Murphy1 in 1905. Apparently he did not fully appreciate the therapeutic value of his observation, for he did not suggest cutting the muscle as a step in treatment of this anomaly. Adson and Coffey2 were the first to propose sectioning the scalenus anticus muscle for the relief of symptoms produced by supernumerary ribs. Their contribution has stood the test of time and is now the accepted procedure for treatment of this disorder. That the symptoms of cervical rib do occur in patients in whom no . supernumerary rib can be demonstrated is a matter of common clinical experience. Naff- ziger3, however, recognizing the possibility that these symptoms occurring in the absence of a cervical rib might be a definite clinical entity, sectioned the anterior scalenus muscle in a number of his patients and obtained complete relief of symptoms. He considered the symptoms to be due to compression of the artery and plexus between the scalenus muscle muscle and the first rib and called it the "scalenus syndrome." Naffziger told many of his neurosurgical colleagues of his observation, talked before medical meetings, but did not publish his observations upon the subject until January, 1937. Ochsner, Gaze and DeBakey4 in the meanwhile, though giving full credit to Naffziger as the originator of the idea, read before the Southern Surgical Association in 193 5 the only complete, authoritative treatise on the subject. The data which I shall present is assembled from thirty-four cases of scalenus compression without cervical rib treated surgically. We have suggested the name scalenus compression instead of scalenus syndrome because we feel it describes more accurately the underlying pathological anatomy. Anatomy of the Scalenus Angle. The scalenus anticus muscle passes downward and slightly lateralward beneath the clavicle to be inserted into the scalene tubercle of the first rib. The phrenic nerve courses across this muscle from its lateral border above to its medial border below, leaving the medial edge of the muscle near its insertion to pass into the root of the neck. The angle made by the muscle and the portion of the first rib lateral to it is an acute one due to the downward direction of the first rib. The subclavian vein emerges from the thorax to pass over the first rib medial to the insertion of the scalenus anticus muscle. The subclavian artery, however, passes beneath the muscle to emerge in the vertex of the angle described above before passing over the first rib. The brachial plexus lies in the scalenus angle immediately lateral to the subclavian artery. The first thoracic and eighth cervical nerves pass slightly downward, deepest in the angle, and over the first rib to bend rather sharply in coursing to the arm. The seventh, sixth and fifth cervical nerves have a more downward course in inverse order, do not pass as deeply into the scalenus angle, and do not have to change their direction so markedly because of their already downward direction. It may be of importance that the subclavian arteries vary in the height at which they take their origin and [ 56 ] in the height to which they ascend in the neck before passing into the scalenus angle. Variations include the piercing of the scalenus anticus muscle by the subclavian artery, or a separate slip from the muscle may pass posterior to the artery. The subclavian artery may be accompanied by the subclavian vein, or the normal position may be reversed. The separation of the subclavian artery from its accompanying, vein is a situation which finds no analogy elsewhere in the human body. It seems reasonable to assume that earlier in the evolutionary development the subclavian artery and vein were together, but that as the scalenus angle developed, the subclavian vein became constricted and collateral veins developed superficial to the muscle; the subclavian vein now represents these collaterals. Incidence. Scalenus neurocirculatory compression is a relatively common clinical entity. In a period of two years we have seen thirty-four cases which were confirmed by their response to surgical treatment. As the diagnostic criteria become more generally known, there will be an increasing number of cases recognized. Our cases were equally divided between the sexes. Age was apparently not a factor; the youngest patient was 17 years of age, the oldest 67 years. In eighteen cases the right side alone was involved, in thirteen the left, and in three both sides. The occupations were so varied that no correlation could be made. Symptoms and Signs. As would be expected, the symptoms of scalenus neurocirculatory compression are those of cervical rib, showing the same variability. The symptoms referable to direct involvement of the brachial plexus are of the most diagnostic importance. Usually the medial cord of the plexus is involved alone, or most severely. Thus the pain, paresthesias, and various degrees of sensory impairment are most apt to affect the ulnar distribution (or the dermatomes of C8 and Dl), and, if present in the median and radial distributions also, will be most severe in the ulnar. Correspondingly, the small muscles of the hands, the flexors of the fourth and fifth digits, the flexors of the remaining digits, and the flexors of the arm, are usually involved in approximately this order before the extensions are affected. Pain was present in all except four cases. In addition to the pain which occurred in the area supplied by the brachial plexus, it was occasionally present in the deltoid region, in the supraclavicular fossa, in the neck, or localized to the region of the seventh cervical spine. It is entirely possible that degrees of compression of the artery which do not affect the circulation enough to be detected may cause pain through the afferent nerves from the artery. The corollary of this may also be true in some instances—that is to say, the circulation of the upper extremity may be affected by involvement of the vasomotor nerves in the brachial plexus without any arterial compression. Numbness or hypcesthesia occurred in all of our cases. The ulnar distribution was chiefly affected although several cases showed impairment of the median distribution and two showed impairment of sensation primarily in the radial distribution. Muscular weakness of some degree was present in every case, although in two cases it was so slight that it was considered questionable. The weakness had been noted by the patient in most, but not all, instances before motor power was tested. Usually the flexors of the fingers were affected along with the intrinsic muscles of the hands. In two unilateral cases and in one bilateral case definite atrophy of the intrinsic muscles of the hands was noted. The pulse was diminished in one case and barely perceptible in another. In the latter case the blood pressure could not be obtained on the affected side and the extremity was cool and pale purple in color. One case with a normal pulse had a cool, cedematous hand, but this case was complicated by a definite arthritis. By having the patient turn the head toward the involved side and take a deep breath, the radial pulse was obliterated or considerably diminished in all except three cases. It was possible to obliterate the pulse by pressure over the scalenus anticus muscle in every instance. Often slight pressure was sufficient. It must be borne in mind that the pulse can be obliterated in this way in many normal individuals. r 57 n Scalenus tenderness was a very constant finding and of great help diagnostically. Pressure was made over the scalenus muscle just above the clavicle, and the two sides compared in their sensitivity to pressure. In most of the cases this manoeuvre caused, in addition, radiation of tingling or pain down the arm, usually in the ulnar distribution. Pathology. At operation it was noted that in some cases the scalenus anticus muscle was large and very tight. Beneath it there frequently appeared to be tough, fibrous bands which may, at times, have been a thick posterior capsule of the muscle. In addition, there were in some instances bands passing beneath the subclavian artery and attaching to the first rib. These may have represented variations in the scalenus anticus muscle or bands passing from the transverse process of the seventh cervical vertebra to the first rib, similar embryologically to cervical rib. Specimens of the scalenus anticus muscle were submitted to microscopic examination in all of the earlier cases. There was arteriosclerosis of the small arteries in four cases and moderate fibrosis in two, but these findings were not considered to be of great significance. Etiology. Many explanations have been put forward to explain why, in cases of known cervical rib, many have symptoms only late in life, and many never have any indication of brachial plexus involvement. The shoulder girdle is situated higher in youth, gradually descending as age progresses, thereby forcing the brachial plexus farther into the scalenus angle. The shoulder on the dominant (usually right) side drops lower in adults than on the other side, predisposing to brachial plexus involvement on this side. We feel that the mechanism which brings on symptoms in cases of scalenus neurocirculatory compression is much the same as in cases of true cervical rib. In our unilateral cases, eleven involved the right side and six the left, a right-sided predominance as in cervical rib. However, our cases were divided equally between the sexes, although symptoms from cervical rib predominate in women due to the fact that their posture allows the shoulder girdle to drop lower than in men. Definite trauma has precipitated symptoms in five of our cases, and in two additional cases, both women, the unaccustomed throwing of a soft ball initiated symptoms. The role of trauma is so important that two cases are presented to illustrate more fully the relationship. I. B., a white male, age 17 years, was perfectly well until January 7, 1937, when, while carrying a 7 5-pound cake of ice on his back, he felt as though something gave way in his right shoulder. This was accompanied by no severe pain, nor did any severe pain occur later. In about two hours his right upper extremity became weak, cold and numb. Examination one week later revealed the following positive findings: Definite tenderness on pressure over the right scalenus anticus muscle; diminished pulse at right wrist, diminished still further by turning the head to the right and taking a deep breath, and obliterated by pressure over the right scalenus anticus muscle; paresis of the entire right upper extremity; profound ulnar hypaesthesia and slight median hypaesthesia. Two weeks after he was first seen the symptoms were still further advanced, so section of the right scalenus anticus muscle was performed under local procain anaesthesia. Immediately after the muscle and bands beneath were divided, the patient felt an improvement in the numbness of his hand and arm. The motor weakness rapidly cleared up during the following week and the patient has remained free of symptoms. He is playing football five months after the operation. W. A. R., a white male physician, age 31 years, sustained a rather severe injury to his neck and left shoulder region while playing football in 1924. Since then he has had vague pains in this area. In 1929 there was transient ulnar numbness, and from time to time some weakness of the left arm. On May 8, 1936, the patient wrenched his neck when the car in which he was riding went over a bump, throwing him against the roof. Severe aching pain in the left shoulder persisted for 36 hours and was followed by progressive weakness in the left hand and numbness in the ulnar side of the left hand and arm. Examination revealed extreme tenderness over the left scalenus anticus muscle. Pressure here or depression of the shoulder caused tingling paraesthesia down the ulnar distribution. The circumference of the left forearm was 2 cm. less than of the right. There was [58] marked weakness of the left grip, and to a less extent of the whole left arm. Roentgenologic examination was negative for cervical rib. Two weeks later a further progression of symptoms wa.« noted; so the scalenus anticus muscle was sectioned. There was a fibrous band beneath it, constricting the subclavian artery. There was immediate improvement in the motor power of the left hand; the numbness disappeared, and the patient has remained completely free of symptoms. • Treatment. We have seen a number of cases of scalenus neurocirculatory compression with the symptoms so mild that surgery was not suggested. Relief has been obtained by using a figure-of-eight bandage about the shoulders or by elevating the elbow by means of a sling. Nocturnal symptoms have frequently been prevented by having the patient sleep with the affected arm above the head. Relief by these measures is of diagnostic aid. Probably many of these mild cases will have to be operated upon later. We have operated only on those cases in which symptoms were disabling to a moderate or severe degree. The bilateral cases should be operated on one side at a time because of the inevitable phrenic paralysis or paresis following anterior scalenotomy. In instances where it was not even necessary to retract the phrenic nerve, paralysis has occurred just the same. It is possible that the springing apart of the taut muscle fibres after cutting makes sufficient traction upon the nerve to impair its function. The phrenic paralysis has been found to clear up in about six weeks. Operative Technique. An incision four cm. long is made two cm. above the clavicle, parallel with it, overlapping the lateral edge of the sternocleidomastoid muscle. It is usually possible to avoid the external jugular vein. The platysma is divided and the clavicular portion of the sternocleidomastoid muscle retracted medially. Ordinarily the posterior belly of the omohyoid muscle can be retracted; if not, it is cut. The deep fascia is divided, being careful to identify the transverse cervical vessels or other large vessels which may be present. Thus the scalenus anticus muscle is exposed. At the level of this incision the phrenic nerve, as a rule, courses along the medial edge of the muscle. A small portion of the muscle beneath the phrenic nerve is separated with it in order to protect it and is then either retracted or allowed to retract medially. Usually the interior jugular vein is exposed medially, appearing beneath the sternocleidomastoid muscle. The scalenus anticus muscle is separated from the deeper structures by placing a smooth retractor beneath it. It is sectional piecemeal. Care is taken to cut completely the tendinous posterior covering of the muscle and any fibrous bands passing beneath it. Palpation within the wound frequently reveals the presence of bands which cannot be seen. In this way part of the brachial plexus is exposed and usually the subclavian artery, although at times the latter can only be palpated behind the clavicle. After careful haemostasis a small rubber tissue drain is left in the dead space and the deep fascia, superficial fascia, and skin are closed with separate rows of interrupted silk sutures. The drain is removed after 12 to 24 hours. Prognosis and Results The immediate result of operation has been uniformly good. Many recovered normal sensation and relief from pain on the operating table while others required several days or weeks. Improvement in motor power was equally prompt in some instances, slower in others. One of the bilateral cases in which there was an excellent result died three months later following an appendectomy. Two cases could not be traced for a late follow-up. Of the remaining 31 cases, all are without symptoms except three. One has annoying paraesthesias in the ulnar nerve distribution, but his pain, weakness and hypaesthesia have cleared up. In the second case there is occasionally a tired feeling in the operated side, with some guarding of this arm, but the patient works regularly and is free from pain. The third case was complicated by arthritis of the hand and shoulder. The ulnar hypaesthesia and weakness of the hand have disappeared. The pain in the shoulder has improved somewhat, but is still disabling. [59] Discussion. That trauma about the neck or shoulder does cause compression within the scalenus angle naturally opens up many interesting speculations. Probably some patients who have been considered to have had torn brachial plexuses or avulsed roots of the plexus from direct trauma to the arm or shoulder may have nothing more than scalenus compression. We have seen two such cases not included in this report—one of them several weeks after the injury and one almost a year after—who had the usual signs of scalenus compression. Both, however, had complete peripheral nerve lesions. Section of the scalenus anticus muscle improved the circulation but did not improve the paralysis. In both cases the plexus was demonstrated not to have been torn. Also, some of the brachial birth palsies, particularly those which do not have an accompanying Horner's syndrome, may be due to this lesion. So far we have had no opportunity to observe new-born infants of this type. "Neuritis" is one of the more frequent ailments. If we eliminate from consideration those cases of frank polyneuritis of infection, chemical, deficiency, or toxic origin, we find in most instances pain and disability limited to one arm or one leg. When pathology in the joints is ruled out, such pain in the arm and shoulder is commonly termed "brachial neuritis" and in the leg "sciatica." It is unnecessary for us to review the unsatisfactory methods of treatment which have been available for these chronic cases of "neuritis" in the past. Fortunately, in recent years a better understanding of the underlying causes of a painful arm or leg has come about, especially in the latter case. Nowadays the patient with sciatic pain is properly studied from the point of view of mechanical compression of the nerve or its component roots. In most of the chronic cases one is able to demonstrate a lesion within or of the spine, or in the course of the sciatic nerve. Once the cause is found, treatment can be directed at the cause rather than at the symptom. In cases with arm pain, our knowledge is in a more nebulous state. After arthritis of the shoulder joint, diseases of the bursae about the shoulder, and cervical ribs have been eliminated, we have formerly often been forced to conclude that the patient suffered with "neuritis" of unknown etiology. A more general appreciation of the signs and symptoms of compression within the scalenus angle will without doubt clarify many of the cases of unexplained brachial neuritis. From our experience we feel that it is probably one of the most common causes of the painful arm and shoulder. BIBLIOGRAPHY. 1. Murphy, John B.: A Case of Cervical Rib with Symptoms Resembling Subclavian Aneurysm. Annals of Surgery, 41:399, March, 1905. 2. Adson, A. "W., and Coffey, J. R.: Cervical Rib. Annals of Surgery, 85: 839, 1927. 3. Naffziger, Howard: Salenus Syndrome. Surg., Gynec. and Obst., January, 1937. 4. Ochsner, A., Gage, M., and Debakey, M.: Scalenus Anticus (Naffziger) Syndrome. Am. Jour. Surg., 28:669,695, June, 193 5. SURGICAL TREATMENT OF THE DIABETIC PATIENT Waltman Walters, M.D., Sc.D., Division of Surgery and Edwin J. Kepler, M.D., Division of Medicine, Little more than a decade ago, as Joslin tells us, "there were few diabetic patients and their life was short and firmly bound with chains of acidosis and undernutrition. Today there are many diabetics because they five longer and insulin has set them free." He estimated that every third person who had diahetes and probably "every other diabetic at some time during the course of his disease needs the surgeon and will not seek him in vain, provided he secures the cooperation of accurate and interested technicians, faithful nurses, and doctors conversant with diabetes." Operating on patients with this disease formerly involved a hazard which few surgeons were willing to accept. The rates of mortality encountered varied from 18 to 46 per cent, and although this was due in some degree to operating mostly for emergencies as a measure of last resort, it was largely attributable to the lack of effective means for preventing the [60]. development of acidosis. The hazard in these cases is still serious but may be overcome by employing skilful surgery, the best possible anaesthesia, and modern methods of controlling acidosis. Trauma to tissue, shock from loss of blood, and prolonged anaesthesia are poorly borne especially in diabetes; neglect of these patients before and after operation often leads to dangerous acidosis. The attendance of physicians and nurses who possess special experience in diabetes is desirable, and closest cooperation between surgeon and physician is imperative. Every case in which operation must be performed in the presence of diabetes is a potential case of coma, and should be treated accordingly. That judicious treatment of diabetes with insulin has increased the span of life of the diabetic is well recognized. As a result, more diabetics have reached the older age groups and hence are subject not only to the degenerative cardiovascular lesions1 commonly found in older diabetic patients, but also to such surgical lesions as tumours, obstruction and infections which afflict nondiabetics of comparable age. Because of this larger number of diabetics in the older age groups on whom serious surgical procedures will of necessity have to be performed, there will in all probability be an increase in the surgical mortality in years to come. Time of Operation. In the presence of surgical emergencies nothing is to be gained by delaying operation; indeed, when a curable infection exists, delay may be actually harmful. This applies especially to amputations of the extremities for rapidly spreading gangrene with infection and to acute appendicitis, pelvic abscesses, mastoiditis, and other inflammatory processes. Acute infection favors the development of resistance to insulin and its removal is therefore the primary consideration. Under such circumstances the operation is not delayed until control of glycosuria has been obtained. The patient is given an injection of 1000 cc. of physiologic saline solution intravenously, a preliminary dose of insulin (the exact amount will depend on the severity of the diabetes, the age of the patient, and other factors), and the operation is then performed without further delay. On the other hand, when a surgical lesion is not infected, or when an existing infection is chronic, and has little or no influence on metabolism, there is no such excuse for haste, andj time should be taken to secure the most favorable conditions before operating. The aims are complete freedom from acidosis, a sugar-free urine, and adequate reserves of glycogen, fluids and salts. When the diabetes is uncontrolled and complicated by acidosis, marked dehydration results, and this, in turn, adds to the risks of surgical shock. Water is lost in the course of operations on patients who do not have diabetes, especially when general anaesthesia is used. Newburgh and Lashmen computed the amount of water lost to be as much as 6 or 7 liters and attributed much postoperative shock to the resulting deficiency of fluid. Attention Before Operation The routine procedure at The Mayo Clinic has been as follows: The patient is observed in the hospital for two or more days while a measured diet is prescribed and sufficient insulin is used to clear the urine of sugar and to free it of ketone bodies. The diet for these patients is made somewhat richer in carbohydrate to provide extra glucose for storage as glycogen, but we have not found it necessary, except in operations on the biliary tract, to resort to the very high allowances of carbohydrate such as have been recommended by various clinics. The use of d-glucose solutions is particularly valuable as a preoperative and postoperative measure in the case of jaundiced patients and those in whom there is reason to suspect some degree of hepatic insufficiency. None of our preoperative diets has contained more than 170 gm. of carbohydrate. If dehydration is apparent, fluids are given by rectum or by vein. In cases of those with milder diabetes, on the morning of operation both breakfast and insulin are withheld. Patients with very severe diabetes under control with regular insulin are given one-half to two-thirds of the usual dose of insulin even though breakfast is withheld. Patients who are taking protamine zinc insulin are given one-half to two-thirds of the usual dose, but supplementary regular insulin is usually not given immediately prior to the operation. In the preoperative and postoperative treatment of diabetic patients who have surgical complications, and in the treatment of diabetic acidosis, protamine zinc insulin has proved to be of value. Situations not infrequently arise in which, although the immediate use of insulin will be contraindicated, the status of the patient will be such that several hours [61] later the immediate use of insulin will be imperative. For example, the urine of one of our surgical patients who had severe diabetes was sugar free at 10 p.m. Six hours later well marked diabetic acidosis had developed. In situations of this kind protamine zinc insulin can be used to marked advantage. For example, diabetic patients prior to an operation may have a normal concentration of blood sugar so that one would hesitate to give a dose of regular insulin. Several hours later the need for insulin may be urgent. Protamine zinc insulin can be given with comparative safety prior to the operation, for by the time the protamine zinc insulin begins to work the need for it will have arisen. Any glycosuria that may appear after the operation is treated with regular insulin. The daily use of protamine zinc insulin, supplemented, if necessary, with regular insulin, is continued throughout the postoperative period until the patient is back on his usual diet and dosage of insulin. When this programme is followed, there is very little danger that the disease will get out of hand during the immediate postoperative period, although, following tonsillectomy in two of our cases of severe diabetes in which treatment was with the foregoing preoperative and postoperative programme, severe acidosis and incipient coma developed. The Anaesthesia and Operation The choice of anaesthetic depends on the surgical indications. General anaesthetics are poorly borne in diabetes. They may produce some degree of hyperglycaemia and acidosis in normal persons, and postoperative vomiting and unavoidable starvation intensify this. Anaesthetic methods and agents in the order of preference are local, regional and spinal; ethylene; cyclopropane; nitrous oxide; the intravenous anaesthetics (pentothal sodium), and lastly, ether. However, when ether can be expected to provide better relaxation and therefore to expedite and shorten time of operation or to reduce the degree of surgical trauma, it may be preferred. In some clinics an intravenous injection of insulin and d-glucose is given during the course of operation. We have not found this necessary. The most important single factor is that the surgical procedure should be carried to completion with accuracy and celerity. A minimum of trauma and a minimum of anaesthetic time are crucial. Attention After Operation As soon as the patient has returned to his bed he is treated with insulin and injections of fluid. Saline solutions are preferred to solutions of d-glucose, because d-glucose, given parenterally, escapes the glycogen barrier of the liver and is in part excreted in the urine. This vitiates urinalysis as the gauge to the amount of insulin needed. Sugar is usually in high concentration in the blood of diabetic patients, and for a time at least it seems unnecessary to provide additional sugar. The dose of insulin must be judged at first from periodic determinations of blood sugar. Later, when excretion of urine begins, each specimen of urine, as it is voided, is immediately analyzed for sugar, iand thesej analyses enable a reasonably accurate appraisal of the demand for insulin. It is well to remember that the time of action of regular insulin is shortened by anaesthesia, infection, and surgical trauma, and that the intervals between injections must be shortened. One injection every six hours is required, but no absolute rule about this is safe. The amount required will have to be determined largely by one's previous experience with the particular patient and by frequent analyses of the blood and urine for sugar. Oral feeding is started as early as possible, usually after twenty-four hours. At first fruit juices alone are given, or ginger ale, or 10 per cent solutions of d-glucose. Later a more liberal diet is gradually resumed. The danger of overdosing with insulin should be constantly in mind. We attribute one of our fatalities to insulin shock. The patient went into shock four hours after operation, and, although he was restored to consciousness, fatal bronchial pneumonia developed and may have been precipitated by the period of apncea that accompanied the severe insulin reaction. The physician in charge of these patients must be trained to recognize quickly any evidence of metabolic abnormality. Acidosis threatens on the one hand, hypoglycemia from overuse of insulin on the other. It is probably safer 'to err on the side of too little control than too much, at least for the first day or two after operation, and until the patient can begin to cooperate effectively. Slight glycosuria will do little harm; an attack of insulin coma has much more serious consequences. [62] Surgical Risk. The risk of operating on patients with diabetes is definitely increased as compared to that of operating on patients of the same age who have diseases of comparable seriousness but uncomplicated by diabetes. In our experience, immediately after the introduction of insulin there was a sharp decline in the operative mortality rate among diabetic patients in spite of the fact that the benefits of operation were extended to patients with severe diabetes who previously would not have beeni operated on with any degree of confidence. In fact, shortly after the introduction of insulin no patient was declined for operation simply because he had severe diabetes. The selection of patients for operation was made on the basis of exactly the same indications as those that obtained for patients who were not afflicted with diabetes. From 1921 to 1932, 1028 major and 1058 minor surgical procedures* were performed at The Mayo Clinic on diabetic patients. The deaths numbered sixty-nine, a mortality rate of 3.3 per cent. Since this time there has been a gradual increase in the mortality rate, which has increased from 4.5 per cent in 193 5 and 5.1 per cent in 1936 to 6.2 per cent in 1937, while at the same time the surgical mortality rate for nondiabetic patients has progressively decreased. The reasons for this were the magnitude of the surgical procedures, many of which were resections of the colon and stomach for malignant disease (which in the case of nondiabetic patients carries an average mortality rate of approximately 10 per cent), and the advanced age of the patients as a result of insulin replacement therapy. The increase is not the result of inability to control the manifest metabolic abnormalities of diabetes, namely, the glycosuria, ketonuria, "and dehydration. Nevertheless, the debilitating effect of prolonged diabetes on the cardiovascular and renal systems, especially of older patients, has played a very important role. Considerable light on the subject can be obtained from a review of our statistics for 1937. In that year 1171 diabetic patients were examined at the clinic; of this number 761 were new patients. There were 354 surgical operations (173 major and 181 minor), performed on 28 5 patients. Twenty- two patients died, three of them following minor surgical procedures (1.6 per cent) and nineteen following major surgical operations (10.9 per cent). Among these major surgical procedures in which death occurred were the following: three gastric resections for carcinoma, one gastro-enterostomy, one transfrontal craniotomy and decompression with removal of a tumour, one cerebral decompression, one resection of the colon for carcinoma, one bilateral ureterosigmoidostomy, one ileocolostomy, one Mikulicz resection of the colon for carcinoma, one resection of strangulated bowel, one choledochoduodenostomy for stricture of the common bile duct with fistula, and one vaginal hysterectomy. Of the twenty-two patients who died, eighteen were more than fifty years of age; none was less than forty. Their average age was 5 8.7 years. Eleven of them had mild diabetes and were not taking insulin; only five could be classified as having severe diabetes. Eleven had diabetes more than five years. The causes of death included those usually encountered after surgical procedures, such as pulmonary embolism, bronchopneumonia * The classification of the operations of this series into major and minor groups is in accordance with the procedure of The Mayo Clinic for classification of all operations. Multiple procedures on separate dates are counted as separate operations; multiple procedures on the same date are counted as one operation and listed under the principal procedure. This means that many operations, listed as single operations, are in fact multiple operations. The major operations include: the procedures in which a body cavity (pleura, peritoneum, joint, eyeball) is, entered by a knife; operations on the thyroid gland, hernia and prostate gland; resection of a cataract and iridectomy; ventriculogram; open operation for fracture: manipulative reduction of fracture of hip, spine or .pelvis; all amputations of arms, legs, hands, feet, fingers or toes, and incision of carbuncles. The minor operations include: aspiration of all kinds; operation on the eye in which the eyeball is not entered; tonsillectomy and adenoidectomy; encephalogram;; manipulative reduction of fractures of extremities; resections primarily done for purposes of biopsy; hsemorrhoidectomy; endoscopy of all kinds, except transurethral prostatic resection; drainage of all abscesses except carbuncles; transfusions of blood, and treatment of varicose veins by multiple injections at separate dates (one minor operation). Reapplication of casts, removal of drainage tubes, removal of sutures, other surgical dressing, and intravenous injection of fluids and drugs are not listed as operations. [63] and parotitis, but there were three deaths from coronary disease and three from renal insufficiency (27.3 per cent of the deaths). In only one instance was the death intimately and directly related to the diabetes. In this instance marked resistance to insulin developed following tonsillectomy. The glycosuria eventually was controlled, but death resulted from bronchopneumonia. Although these figures were obtained only from the year 1937, they are typical of what has occurred during the last few years. It is apparent that the mortality occurs chiefly among older patients with relatively mild diabetes (often of long standing) who undergo operations of the magnitude of gastric or colonic resections for carcinoma, removal of common duct stones in the presence of jaundice and cholangitis, or operations for advanced lesions (frequently malignant) of the kidney and bladder. Given adequate preoperative and postoperative care, the younger patient with severe diabetes tolerates surgical procedures with very little additional risk because of bis diabetes. Healing of Wounds. The healing of surgical incisions is delayed when treatment of diabetes is inadequate; not otherwise. A former Fellow in The Mayo Foundation, Bennett, studied surgical wounds in dogs made diabetic by pancreatectomy. The pancreas was removed under ether anaesthesia. The animals were supported with insulin and a suitable regimen until they had recovered completely. Then insulin was withheld, and when the ensuing diabetic state was developed, abdominal incisions were made under local anaesthesia. As compared to the behaviour in identical wounds, in healthy animals used as controls, the healing of these wounds was abnormal. The tissues were cedematous, deposit of fibrin was delayed, and the amount of fibrin was restricted. The cellular reaction was excessive and the exuded cells appeared to be of the so-called toxic type. New blood vessels were slow to form, and more thrombosis than normal was noted in preformed vessels. On the other hand, healing proceeded perfectly normally when the diabetes was well controlled. The delayed healing of the extremities of diabetic patients who have undergone amputations for gangrene is attributable to atherosclerotic obstruction to the peripheral circulation. Gangrene. Some years ago Allan and Kintner reviewed our experiences at the clinic with the serious complication of gangrene. The lesson to be drawn is obvious: either operate early and operate high, or treat the lesion medically and avoid tail surgery. This1 old rule has guided us through the last decade to a mortality rate in diabetic gangrene that is comparatively very low. When we deviated from it, as we did occasionally, we had reason to regret it. Primary amputation through the foot for removal of gangrenous toes was performed in fifteen cases. Higher amputation was necessary in 3 3 per cent of these. The ultimate outcome was fatal in 20 per cent of cases. By contrjast, in seventy-one cases of gangrene of the toes or foot, in which primary amputation was through the leg, a secondary operation was required in only four cases, and the ultimate outcome was fatal in only 7 per cent. Attempts to save feet by amputation of toes, by open drainage, and by other procedures unquestionably are hazardous. The fifteen cases chosen for such attempts were suitable by all ordinary criteria: the gangrene was limited to the toes, the pulsation of the dorsalis pedis and posterior tibial arteries was fair, the extremity was Warm, and there was no great difference in blanching or reddening on elevating or lowering the leg. Yet the mortality rate in this group almost equals that observed in sixty-seven cases in which medical treatment alone was provided. Once amputation is decided on it should be done below the knee, provided pulsation is good in the popliteal artery; above the knee if pulsation is inadequate. A well-fitting artificial leg, or even a wooden peg, is to be considered an asset in the fight of the danger of imperfect healing of wounds after amputation. These observations do not apply to perforating ulcers, other sores, and other chronic infections of the feet which are not accompanied by massive necrosis of tissue or obvious impairment of circulation. In such cases the leg usually can be saved. When infeotion is 'superimposed on arteriosclerosis, and if it is clearly advancing and reaches the ankle, high amputation is desirable and should be done without delay. The medical care for infected extremities, with or without gangrene, is as follows: absolute rest in bed is enforced; the foot is slightly elevated above the horizontal; glycosuria [64] "
@en ; edm:hasType "Periodicals"@en ; dcterms:identifier "W1 .VA625"@en, "W1_VA625_1938_06Supp"@en ; edm:isShownAt "10.14288/1.0214557"@en ; dcterms:language "English"@en ; edm:provider "Vancouver : University of British Columbia Library"@en ; dcterms:publisher "Vancouver, B.C. : McBeath Spedding Limited"@en ; dcterms:rights "Images provided for research and reference use only. Permission to publish, copy, or otherwise use these images must be obtained from the Digitization Centre: http://digitize.library.ubc.ca/"@en ; dcterms:source "Original Format: University of British Columbia. Library. Woodward Library Memorial Room. W1 .VA625"@en ; dcterms:subject "Medicine--Periodicals"@en ; dcterms:title "The Vancouver Medical Association Bulletin: June Supplement, 1938"@en ; dcterms:type "Text"@en .