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44

Sex M

M

Diagnosis

History

Treatment and Results

Lumbo-sacral and Hamstring spasms (sacro-iliac) (sciatica)

Onset: cold 5 days ago followed by severe pain in Immediate relief after first ganglion treatment. back radiating down left leg. Walking with diffi- Walking without use of cane. Given treatment for culty. Using cane. 3 consecutive days. Walking improved but still has slight pain. Given treatment in 10 days following. Greatly relieved.

Lumbo-sacral spasm (sacro-iliac)

Pain in back, sacro-iliac region. Has had osteopath Given 3 ganglion treatments for 3 consecutive days. treatment. Has repeated recurrence, usually fol- Immediate relief after 1st treatment. Pain in back lowing colds. Has dry throat, repeated colds. relieved immediately following initial treatment. After 1 week, return visit, reported no recurrence ,,f back pain. Each treatment supplemented by intramuscular injections of Ironyl and Calcium Ascorbate.

The entire series of cases received injections of Ferrous adenylate (Ironyl) and Calcium ascorbate (Calscorbate) after each spheno-palatine ganglion treatment.

The injections were given intramuscularly in the gluteus, the calcium: on one side and the tronyl on the other.

R E F E R E N C E S 1. Blair, H. A.: Muscle Excitability. Biol. Symposia, Vol. l i e 2. Block, R. J. and Boiling, D.: Nutritional Opportunities with Amino Acids. J. Am. Dietetic Assn., Vol. 20, Sept. 1943. 3. Bozler, E.: Action Potentials and Conduction of Excitation in Muscle. Biol. Symposia, Vol. III. 4. Cannon, W. B. and Rosenblueth: Autonomic Neuro-Effector Systems. The Macmillan Company, 1937. 5. Eccles et al: Electric Potential Changes Accompanying NeuroMuscular Transmission. Biol. Symposia, Vol. III. 6. Fenn, W. O.: Muscle. Biol. Symposia, Vol. III. 7. Gordon and Sevringhaus: Vitamin Therapy in General Practise. The Year Book Publishers, 1942. 8. Hober, R.: Physical Chemistry of Cells and Tissues. Blakeston Co., 1945. 9. Meyerhoff, Otto: Significance of Oxidation for Muscular Contraction. Biol. Symposia, Vol. III. 10. Potter, V. R.: The Role of Vitamins in Energy Transformations. J. Am. Dietetic Assn., Vol. 19, No. 7, July 1943. 11. Rosenblueth, A.: Conduction in Smooth Muscle. Biol. Symposia, Vol. 11I. 12. Ruskin, S. L.: L Studies on Parallel Action of Vitamin C and Calcium. Am. J. Dig. Dis., 5:408, 1938; II. Studies in Calcium Metabolism: Further Contribution to Comparative Studies of Physico-Chemical Properties of Gluconate

and Cevitamate of Calcium and of Vitamin C. Ibid., 5:676, 1938; III. Mechanisms of Nephrosis in Sinusitis in Children. Acta. Paediatric 16, 249, 274, 33.; IV. Nucleic.Acid and Nucleotide Therapy in Nasal Diseases; Contributions to Study of Chemical Aspects of Nasal Diseases. Arch. Otol., 22:172, Aug. '35, V. Influence of Vitamin C on the Antihistamine Action of Various Drugs. Arch. Otol., 36:853-873, Dec. 1942. VI. Adenylic Acid in The Treatment of Agranulocytosis and Mucous Membrane Lesions. Am. J. Dig. Dis. VII. The Therapeutic Use of The Amino Acid. Histidine in Allergy and Shock. "Histidine as a Factor in Histamine Epinephrine Balance;" Am. J. Dig. Dis., Vol. II No. 7, July 1943. VIII. High Dosage Vitamin C in Allergy. Am. J. Dig. Dis., Vol. 12, No. 9, Sept. 1945. IX. The Role of the Coenzymes of the B Complex Vitamins and Amino Acids in Muscle Metabolism and Balanced Nutrition. Am. J. Dig. Dis., April, 1946. 13. Ruskin, S. L. and Jonnard, R.: Etudes Physical-Chemic. Compare due Gluconate, due Sel de Calcium et de La Vitamine C. Compt. Rend de Biol., 28:266-268, 1938. 14. Ruskin, S. L and Katz, E.: Therapeutic Action of Nucleotides; Treatment of Whole Blood Picture with Ferrous Adenylate. Ann. Int. Med., 9, 11, 36, 1549, 1560, May '36. 15. Wright, Samson: Applied Physiology. Oxford Univ. Press, 1941.

Physiological Derangements in Organic Disease of the Intestinal Tract B 3, SAMUEL STANDARD, M.D.** N E W YORK~ N. Y.

FUNCTION of the gastro-intestinal tract is priT HE marily the storage, conversion and absorption of food to meet the nutritional requirements of the animal organism. The immediate importance of organic disease of the tract may be measured by the extent and severity of interference with the maintenance of these nutritional requirements. In obstructive lesions the interference with transportation of its contents explains the clinical picture. In inflammatory lesions withont obstruction it often becomes difficult to account for the symptomatology purely on the basis of the organic lesion itself. The morbidity and often the critical fac*Presented before the New York Surgical Society, New York Academy of Medicine. "~From the Departments of Surgery and Physiology, New York University College of Medicine and the General Surgical Service, Montefiore Hospital. Submitted March 30, 1946.

tor in death may be, and often is, widely removed from the organic source, and can be accounted for only on a functional basis. The patient may die in uremia with normal kidneys, in convulsion with no cerebral damage, or may show a diffuse endocrinological breakdown with a normal set of endocrine glands. It becomes increasingly necessary to understand what the disease does as well as what the disease is. Neurologically the gastro-intestinal tract is an interdependent unit stimulated by the cranio-sacral and inhibited by the thoracico-lumt/ar autonomic fibers. In the normal the peristalsis setup in the colon immediately following a meal is responsible for the habit of defecation. The reflex vomiting seen in inflammatory intestinal lesions is an example in reverse of the same integration of function. One would expect to find functional involvement mediated through the autonomic

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system in segments of the intestinal tract anatomically remote from the organic lesion. Such a set of circumstances had been well established as operating in vascular organic lesions which, too, are autonomically innervated. Thromhophlebitis of the femoral vein induces edema, pain and ischaemia of the leg. It was thought that all of these could be explained on the basis of the blocked vein and adjacent lymphatics until Osehner and DeBakey (1) showed that by a para-vertebral block in the lumbar area all of these signs may disappear in twenty-four hours without in any way relieving the organic block that exists. It was then postulated that the signs were the result of a reflex vaso-spasm of the peripheral arterioles mediated through the thoracicolumbar autonomic chain. The organic lesion constituted the receptor organ for the reflex, the sympathetic fibers and chain, the afferent and efferent arcs, and the arteriolar musculature, the effector organ. Since then it has been shown that the ischaemia of an arterial thrombosis is only partly due to the organic block and in great part produced by the reflex vaso-spasm induced. Here, too, sympathetic block increases the blood supply to the limb without altering the organic thrombus in the main artery. The most dramatic example of this, published by Volpito (3), is the restoration of function in a hemiplegic extremity by stellate ganglion block on the side of a cerebral thromhosis or embolus proving that the cerebral ischaemia can be relieved by breaking the reflex arteriolar vaso spasm induced by the organic lesion. The same principle is involved in the improvement seen following autonomic cardiac denervation by alcohol or by surgical resection. Here too, the peripheral arteriolar spasm in the myocardium induced by the organic coronary thrombosis may be sufficiently relieved to increase the blood supply to the tissues not in the field of the actual infarct. Such autonomic denervation not only relieves pain but may actually increase myocardial vascularity. Many clinicians have been struck by the weight loss, anemia, hypoproteinemia and vitamin deficiencies of relatively mild intestinal lesions. An excellent example of this is the gastro-jejuno-colic fistula. It was once thought that the profound cachexia that often accompanies this lesion could be explained on the basis of food being transferred from the stomach, a non-absorbing organ, to the colon, another non-absorbing organ (except for water); the entire small intestine being side-tracked the patient absorbed nothing from the ingested food. Since then it has been established that the fistula is usually a small one, that little if any food finds its way into the colon directly from the stomach, that most of it does traverse the entire length of small intestine, and yet weight loss is profound. The inflammatory lesion at the fistula sets up an irritable focus which reflexly induces a hypelperistalsis in the small intestine of suOqcient intensity to carry food through it with such speed as to allow practically no time for absorption. A preliminary proximal colostomy side-tracks the infectious colonic contents away from

321

stomach and jejunum at the fistula. The acute inflammatory process subsides and though the fistula still exists, as proven later at operation, the reflex hyperperistalsis of small gut slows down sufficiently to allow adequate absorption. The improvement shown by these patients is often so marked that some refuse definitive surgery when it is later offered to them. Ulcerative colitis is known to be a most debilitating disease yet here too a lesion involving rectum and sigmoid with relative freedom of the remainder of the colon from organic disease will induce profound systemic effects. These can be attributed to the reflex effects upon the small intestine. Gastro-intestinal series demonstrate the speed with which the small intestine transports its contents from stomach to colon. Early in the disease the barium may be in the cecum in thirty minutes. True it is that water and minerals and proteins and blood are lost from the colonic mucosa. Yet with an intact small intestine one begins to wonder why replacement becomes impossible and one begins to understand why ileostomy fails to control the debility induced by the disease so long as the organic lesion continues Io constitute the irritable focus for a hyperperistalsis which prevents adequate absorption. The same principle may be applied to the relatively small lesions seen in regional ileitis. The diversity of surgical opinion on whether to resect or side-track the lesion rests on the differing responses of the organic lesion when it is defunctionalized. If the lesion heals by the side-tracking procedure no more surgery will be required. If it fails to heal, its reflex effects will continue to be a source of morhidity although it is anatomically no longer a factor. Tuberculous ileitis induces somewhat the same picture and needs to be dealt with in the same way. It is rare that a nutritional deficiency can be attributed to a single factor. Mackie (4, 5) has shown that usually the deficiencies are multiple. Once established the function of the small intestine may be variously disturbed. This part of the tract is emphasized because upon it, almost alone, falls the responsibility for adequate absorption and the maintenance of nutritional requirements. Early in nutritional deficiencies functional absorption is interfered with by hyperperistalsis; later actual organic pathology of the mucosa and myenteric plexuses have been demonstrated by Gordon. When this has occurred nutrition cannot be maintained even with slowing of propulsion of its contents. Thus a vicious cycle is set up. The functional derangement limits absorption which in turn induces a nutritional deficiency which further aggravates the already existing interference with proper absorption. Many disturbances related to chronic intestinal disease states have been emphasized in the recent literature. They include hypoproteinemia and vitamin deficiencies. To these completely reported by Golden and by Maekie may be added the rarer and more generalized manifestations such as hormonal deficiencies and resultant in-

322

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fantalism in the young, alterations in mineral metabolism particularly calcium loss and calculus formation, and production and maintenance of anemic states. The great importance of the maintenance of a constant and adequate protein content has been emphasized in both the medical and surgical clinical literature as well as in the preclinical fields of physiology and biochemistry. A survey of the biological defects that appear when the body is deprived of its most important building materials, either because of inadequate intake or excessive loss reveals a wide distribution of signs and symptoms. That these s i g n s m a y be attributed solely to the hypoproteinemia is questionable. Many of the intestinal changes have been reproduced in animals by simple plasmaphoresis, in the nephroses as demonstrated by Prendergrass (7) and with disorders of the liver; all three being associated with hypoproteinemia. The list of manifestations induced by hypoproteinemia is an impressive one, it includes water retention, calcium mobilization and depletion, alterations in liver function, in wound healing, in intestinal motility, in the production of anemia, and in multiple vitamin and hormonal deficiencies. The most important role of the plasma proteins is the maintenance of the constancy of the physical state of the plasma. In their absence or diminution the fluid bMance between the blood and the intercellular tissue spaces and serous cavities is disturbed. Water retension in hypoproteinemic states has long been recognized. The combined oncotic pressure of the 7 grams of protein per 100 cc. of blood is 30 ram. Hg. It is this force which keeps fluid within the vascular bed against the hydrostatic pressure tending to push it out. Elman (8) suggests that in speaking of protein deficiency it would more nearly present the chemical pattern to define it as "hypoalbumenia" rather than hypoproteinemia. The albumin molecule is about ~ the size of the globulin molecule and is the first to he lost and in most instances the only plasma protein lost. Note that in Case 1 the plasma protein fell from the normal (7 Gins. % with an A-G ratio of 4.5-2.5) to a total of 3.7 Gms. %. The inverted A-G ratio is due almost entirely to albumin loss with globulin practically unchanged. Each gram of albumin per 100 cc. of plasma exerts an oncotic pressure of 5.5 ram. Hg. each gram of globulin per 100 cc., a pressure 1.4 ram. Hg. From this it becomes plain that the albumin fraction is responsible for 85% of the total osmotic tension of the plasma proteins. With this in mind edema levels are reached because of an albuminemia in every instance. The loss of all the globulin from normal plasma would induce a fall in osmotic tension of lesser magnitude than the loss of one gram of albumin. This point deserves emphasis since albumin solutions are now available for parenteral use. A negative nitrogen balance is the rule in chronic ulcerative colitis with progressive breakdown of body protein. Unlike fat and carbohydrate there are no available stores or reservoirs of protein in the body. There are at least three causes for protein reduction in

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ulcerative colitis. First, there is the direct loss from the ulcerated areas. Secondly there is the decreased a!)sorption in the small intestine clue, in the early stages, to hyperperistalsis with its speedy transit and evacuation of unassimilated contents. Later there is faulty absorption due to organic diseases of the mucosa. Thircily there is the increased caloric need due to hyperpyrexia and increased metabolic rate associated with anorexia which limits the actual intake. This combination of forces often reduces proteins to critical levels. Another effect of hypoproteinemia which is often considered an isolated occurrence, is calcium depletion. There are three chemical factors that determine calcium solubility in serum. 1. A portion (about 25%) held in solution by forces which ordinarily govern solubility in salt solution. 2. A larger portion (about 50%) which remains in solution by virtue of the retarded precipitation that is characteristic of supersaturated solutions of calcium carbonate and l)hosphate, perhaps as the result of the presence of the parathyroid hormone. 3. A portion (about 25%) held in solution by the serum proteins (Peters and Van Slyke ( 1 3 ) ) . With prelein breakdown as much as 2.5 mg. % calcium may be liberated. This may contribute to the frequency with which calculi are found in this and other similar debilitating diseases. The role of hypoproteinemia in wound healing and wound disruption has been experimentally and clinically confirmed. The not infrequent instances of edematous stomata following gastro-enterostomies have received attention because of the obstructive symptoms 1hey produce. The importance of adequate plasma protein values for the prevention of liver damage and for the restoration of normal liver lipids in fatty livers has been carefully worked out by Ravdin and his coworkers (14, 15, 16, 17). Vulnerability of the liver to damage by anaesthetic agents and anoxic states has been emphasized by the same investigators. This group was among the first to teach that adequate protein administration was a more important element in liver protection lhan adequate carbohydrate supply, with the additional warning that plasma protein will not be replaced by the ~,dministration of a high protein diet unless there is in addition a carbohydrate supply adequate for caloric needs. Only after the caloric need is met will ingested or injected proteins be utilized to replace tissue and plasma proteins. When tissue proteins are depleted the administered proteins will be utilized to replace tissue proteins first; serum proteins may remain low over a period of time. Elman's (8) studies have shown that the proportion of tissue protein depletion to plasma protein is of the order of thirty to one, i. e., for every gram reduction demonstrated in plasma proteins there has been a thirty gram loss in tissue proteins. This must be borne in mind in calculating quantitative replacement. Calculus Formation: The three cases reported in this paper all showed clinical calculus formation. Two of the cases showed both gall bladder and kidney

Jova. D. D. OCTOBER, 1946

DERANGEMENTS IN ORGANIC DtSE~SP, OV THE INTESTINAL TRACT

stones; one showed kidney stones. It is a summation of factors which is responsible for the formation of stones; the derangement including acceleratiou in both calcium mobilization and precipitation. Mobilization is increased by the decalcification of disuse seen in simple bed rest and demonstrated most dramatically in cast immobilization of fractured extremities. Secondly there is the release of calcium mentioned above in protein depletion. Thirdly in acidosis so frequently accompanying the debilitating gastro-intestinal diseases, bone decalcification is accelerated. Added to these sources of increased mobilization there is the factor of dehydration with increased concentration of body fluids which lead to precipitation of salts out of selution and the role played by Vitamin A deficiency in increased calcium precipitation. The role of Vitamin A deficiency in urinary calculus formation has been demonstrated experimentally and clinically. Osborne and Nedal (9) and Van Leersum (10) have demonstrated urolithiasis induced in -Vitamin A deficient rats. Higgins (11) has produced urinary calculi in Vitamin A deficient dogs. The stones produced consisted chiefly of calcium phosphate and carbonate. The widespread occurrence of urolithiasis in the orient is considered dependent upon Vitamin A deprivation. The mechanism appears to be celat-d to the known effect of Vitamin A deficiency in impairing epithelial structures and in promoting keratinization. McCamson (12) believes that desquamated keratinized epithelium from the urinary organs may provide the nucleus about which crystalline material is deposited. Eusterman's case of gastro-iejuno-colic fistlfla resulted in Vitamin A deficiency and night blindness, but he does not report stones in this case. Vitamin Deficiencies: Functional alteration in the small intestine due to Vitamin B deficiency in ulcerative colitis and other intestinal diseases associated with nutritional deficiencies have been described by Golden (6) and Mackie (5). Golden's description reads, "in the earlier less advanced stages the barium sulfate may pass rapidly through the jejunum reaching the lower part of the intestinal tract in a quarter of an hour and entering the caecum in less than a half hour . . . in the more advanced stages the movement of the barium sulfate is slowed. It may not reach the caecum in six hours or longer." He describes segmental puddling and retention of barium in the advanced stages. Ravdin points out teat the roentgen appearance of the small intestine in dogs with experimental hypoproteinemia is indistinguishable from that of dogs with Vitamin B deficiency. It has been suggested that these alterations seen in hypoproteinemia may be due to a reduced "acceptance" of vitamin B by hypoproteinemic tissue. As demonstrated in the appended case reports, the peripheral neuritis of Vitamin B deficiency may become so severe as to produce complete paralysis. The bilateral foot drop exhibited by this patient in the course of his illness is a dramatic example of this deficiency. It

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should be mentioned that although this is obvious and easily demonstrable that other more subtle manifestations of Vitamin B deficiency exist and go unrecognized. Long before such complete paralysis occurs. milder symptoms such as heaviness of the lower extremities, calf muscle cramps, paraesthesias of the toes and fingers, burning of tile feet and pain in the legs appear. Vibratory sensation may be lost in the toes. Ankle jerks are diminished or absent. Kuee jerks may disappear and finally position sense of the toes becomes impaired. Calf muscle atrophy develops and foot drop follows. The medical complications of Vitamin B deficiency may be mentioned only in that a patient with ulcerative colitis and advanced Vitamin B deficiency constitutes a critical surgical risk if he shows evidence of an enlarged heart or a serous effusion and has had any history of circulatory collapse attributed to myocardial damage as the result of Vitamin B deficiency; the so called Beri-beri heart. The underlying mechanism by which vitamins function is not completely understood. The slowing or halting of cellular metabolism resulting from their deficiencies is recognized. Vitamin B1 is intimately concerned with the normal metabolism of carbohydrates. It acts as a carrier of oxygen and is necessary in the normal completion of carbohydrate oxidation. We may ply a Vitamin B1 deficient patient with a high carbohydrate diet to meet his caloric needs and wonder whv he fails to utilize it until his B1 deficiency is overcome. Until B1 deficiency is overcome the cells cannot utilize the carbohydrate offered, the caloric needs will not be met and administered proteins may fail to achieve cellular or plasma replacement. Vitamin A: Wilbur and Eusterman (18) report a case of night blindness in a patient with a gastrocolic fistula. Night blindness is due to a delay or failure of regeneration of visual purple in the retina which is in turn due to Vitamin A deficiency. Repair of the fistula resulted in complete recovery from the night blindness. The role of Vitamin A deficiency in calculus formation has been mentioned above. Hormonal Deficiency: Infantilism due to glandular hypofunction in nutritional deficiency states appears infrequently in the literature. It is described by Alpert (19) in a seventeen year old diabetic who before the insulin era was treated by a starvation diet; she showed advanced evidence of physical and sexual immaturity, One year after insulin became available, normal physical and sexual maturity were obtained. Langston (20) reports a seventeen year old boy with congenital hemolytic icterus, whose development was that of an eleven year old child. Splenectomy followed by anterior pituitary extract resulted in a dramatic development to normal physical stature. Benson and Bargen (21) reported a series of twelve cases of retarded sexual and somatic development occurring in ulcerative colitis. Davidson (22) has reported three cases of ulcerative colitis from the medical service at Montefiore Hospital. Twa of Davidson's three cases came to autopsy. Each

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showed that there was basophilic hyperplasia of the pituitary similar to that seen in Vitamin A and E deficient rats. In animals it implies a compensatory reaction to partial castration. In the human it may be interpreted as a secondary pituitary response to a subfunctioning testes. The pathological reports on the sex organs were identical in both cases. They read, "The testicles in each case were small and prepubertal. The tubules were small. There were no mitotic figures or any evidence of maturation. The interstitial cells were swollen with round vesicular nuclei and colorless cytoplasm." In the case presented tonight the patient was nineteen years old, showed all the signs of pluriglandular infantilism in the absence of breasts, absence of pubic hair and epiphyseal markings of a child of twdve. These pluriglandular manifestations represent evidences of hypofunction for which we have no laboratory tests. These glands reflect their metabolic derangement in alterations in physiological function resulting in the -,ounger age group in an underdevelopment such as described above. Hemoglobin and red cell formation: Ordinarily the restoration of hemoglobin and red blood cells is associated with iron ingestion or injection of liver extract or transfusions. It should be remembered that red cell formation requires proteins and in hypoproteinemic states red cell regeneration is markedly retarded. When anemia and hypoproteinemia coexist, hemoglobin production has precedence over plasma protein production (Robscheit-Robbins ( 2 3 ) ) . In nutritional deficiencies such as indicated above, replacement pre-operatively in a surgical case or as a main course of treatment in a medical case depends upon the ability of the intestinal tract to accept and absorb adequate diets. In any attempt to replace proteins it has been pointed out by Ravdin (14, 15, 16, 17) and others that unless an adequate caloric requirement in the form of carbohydrate is administered, protein will be utilized for energy rather than for replacement. Many of the failures in protein alimentation have arisen from this error in dietary management. No protein will be stored until the energy requirements have been fulfilled. Ravdin suggests a diet consisting of 75% carbohydrates, 20% protein and 5% fat in preparation for surgey in patients who are either obviously hypoproteinemic or in patients with gall bladder disease with increased lipids in the liver. Elman (8) suggests milk, skim milk, eggs, lean meat and soy beans as excellent sources of protein when these can be administered by the oral route. Where

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VOLUME 13 lO

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protein nourishment is difficult as it is in cases of ulcerative colitis there has been developed preparations of amino acids containing casein hydrolysates which can be taken by mouth or intravenously. In chronic hypoproteinemia due to malnutrition plasma transfusion which is of such inestimable value in acute protein deficiencies in hemorrhage, shock or burn may be a disappointment. This is to be expected since the plasma protein values represent only a measuring stick of body protein depletion and replacement. Each gram loss of plasma protein represents a 30 gin. loss in tissue protein. The replacement therefore requires a quantity of protein which would be impractical to supply through plasma transfusions. Hydrolized protein can be administered intravenously in 5% solution with 5% glucose. Such a solution supplies 50 grams of protein per 1000 co. In preparing nutritionally depleted patients for surgery some form of hydrolized amino acids should be added to the glucose and salt infusions. If the intestinal tract is available, one may administer by mouth 250 gms. of Amino Acids and 500 gins. of carbohydrate every twenty-four hours. If this is not tolerated, 500 gms. of dried milk per day will furnish 25 gins. of Nitrogen. For already existing vitamin deficiency Jolliffe (24) advises erring on the side of wasting the vitamin by massive dosage rather than giving a suboptimal amount. He suggests that vitamin supplements in addition to an adequate diet should include Vitamin A, 50,000 international units, ascorbic acid, 400-500 mg., Thiamine Chloride, 300-1000 mg., the first day and a maintenance of 50-200 mg. each day along with a source of the entire B complex included in Vegex, 20 gins. Brewer's yeast, 60 gms., aqueous liver extract, 30 grams. Start (25) adds riboflavine, 10 mg., nicotinic acid, 100 rag., Vitamin K, 2 mg. (in hemorrhagic states due to prothrombin deficiency). 111 these disease states the functional derangements are widespread. The underlying mechanisms are multiple. The signs and symptoms are diffusely distributed tln oughout the body as demonstrated in night blindness and foot drop. Yet the principles involved in their control are few. Rehydration, remineralization, protein and vitamin replacement and finally surgical removal of the organic etiological agent. Proper preparation is disappointingly slow and often incomplete as demonstrated in the cases presented. Yet any improvement makes surgery less hazardous. When the organic disease is removed the focus for reflex dysfunction of the organically uninvolved intestine is eliminated and the intrinsic compensatory mechanisms swiftly restore the constancy of the deranged ieternal environment to normal values.

R E F E R E N C E S 1. Ochsner, A. and DeBakey, M.: Arch. Surg., 40:208, 1940. 2. Idenr.: J. A. M. A., 114:117, 1940. 3. Volpito, P. P. and Risteen, W. A.: Anaesthesiology, 4:403, July 1943. 4. Mackie, T. T.: Med. CL N. A., 17:165, July 1933. 5. M~ackie, T. T.: J. A. M .A, .117:910, Sept. 13, 1941.

6. 7. 8. 9. 10. 11.

Golden, R. J. A. M. A., 117:913, Sept. 13, 1941. Prendergrass, E. P. et ah Radiology, 26"651,, June 1936. Elman, R.: Med. Clin. N. A., March 1943. Osborne, T. B. and Nedel, L. B.: J. A. M. A., 69:32, 1917. Van Leersum, E. C.: J. Biol. Chem., 76:137, 1928. Higgins, C. C.: Jour. of Urology, 36:168, 1936.

JouR. D. D. OCTOBER, 1 9 4 6

DERANGEMENTS IN ORGANIC DISEASE OF THE INTESTINAL TRACT

12. McCamson, R.: Brit. Med. J., 1:717, 1927. I3. Peters and Van Slyke: Quant. Clin. Chem., Williams and Wilkins, Vol. I, p. 810, 1931. 14. Ravdin, et aI: J. A. M. A., 121:322, Jan. 30, 1943. 15. Ravdin, et at: J. A. M. A., 114:107, Jan. 13, 1940. 16. Ravdin, et al: Ann. Surg., 114:1018, Dec. 1941. 17. Ravdin, e t a l : S. G. O., 66:819, May 1938. 18. Wilbur, D. L. and Ensterman, G. B.: J. A. M. A., 102:364, Feb. 3, 1934. DISCUSSION

BY DR. ARTHUR

M. W R I G H T

T h e eases present~ed and the p a p e r r e a d this e v e n i n g a r e b o t h e x a m p l e s of the c h a n g i n g t h o u g h t in surgical practice and surgical teaching. These a r e p r e s e n t e d as physiological d e r a n g e m e n t s w i t h surgical t e c h n i q u e as a m e t h o d in our-th,erapeutie a r m a m e n t a r i u m . S u r g e r y was m e r e l y a m e a n s to an end. T h e r e was no stress laid on the t e c h n i q u e r e q u i r e d , the s u t u r e m a t e r i a l used or a n e w clamp for a special purpose. T h e p a p e r deals w i t h f u n d a m e n t a l concepts r a t h e r t h a n w i t h isolated details. T h e r e was a t i m e w h e n a s t u d e n t was t a u g h t the detailed s y m p t o m s of a disease w h i c h he t h e n had to label w i t h a name. He was t h e n t a u g h t to t r e a t this label. His e x c e l l e n c e as a student was t h e n m e a s u r e d b y the n u m b e r of such labels he could c o n j u r e up out of his m e m ory. T e a c h i n g t o d a y stresses the u n d e r l y i n g physiological d e r a n g e m e n t s responsible for t h e s y m p t o m s seen in the disease. The s t u d e n t thus becomes rich in p r i n c i p l e r a t h e r t h a n in fact. H e learns to b r i n g t o g e t h e r u n d e r one c o m m o n d e n o m i n a t o r v a r i o u s diseases t h a t h a v e no a p p a r e n t clinical s i m i l a r i t y b u t w h i c h s h a r e a c o m m o n p h y s i o logical dislocation. An e x a m p l e of the a d v a n t a g e of this t y p e of u n d e r s t a n d i n g of disease was illustrated in t h e cases presented. One n e e d o n l y h a v e a s t u d e n t u n d e r s t a n d t h a t h y p o p r o t e i n e m i a occurs in a disease and the r e a s o n for its occurrence. He k n o w s all of the s y m p t o m a t o l o g y t h a t follows h y p o p r o t e i n e m i a no m a t t e r h o w induced. He thus realizes the oneness of the origin of s y m p t o m a t o l o g y . T h e principles r e s p o n s i b l e for the s y m p t o m a t o l o g y hold u n i v e r s a l l y w i t h o u t r e g a r d to the body system involved. In this p a p e r it is d e m o n s t r a t e d t h a t the a u t o n o m i c a l l y i n n e r v a t e d gastrointestinal tract induces r e m o t e reflex f u n c t i o n a l d e r a n g e m e n t s in response to organic disease s i m i l a r to those found w i t h t h r o m b o - p h l e b i t i s or a r t e r i a l t h r o m b o s i s in the v a s c u l a r system. Tiae t r a i n i n g of a surgeon has c h a n g e d w i t h i n the r e l a t i v e l y r e c e n t past. P e r h a p s it is m o r e an amplification t h a n a change. T h e r e was a t i m e w h e n t h e professor of s u r g e r y had h e l d a similar position in a n a t o m y and a t r a i n i n g in a n a t o m y was considered t h e most i m p o r t a n t a p p r e n t i c e s h i p to surgery. T h e need of a k n o w l e d g e of a l t e r e d a n a t o m y in dis,ease states led to t h e additional t r a i n i n g in pathology. T o d a y the n e e d to u n d e r s t a n d the f u n c t i o n a l alterations associated w i t h a n a t o m i c a l disease brings t h e n e x t prec]inical science to t h e f o r e g r o u n d in the t r a i n i n g of a surgeon. The physiologist is n o w t a k i n g his p l a c e alongside the a n a t o m i s t and the pathologist, establishing the t r u t h of H a r v e y Cushing's definition of a surgeon. H e speaks of h i m as " t h a t m e d i c a l l y t r a i n e d artisan w~ call a surgeon." CAS~

I - - W . S., b o r n 1 9 0 7 .

In M a y of 1939, at the age of t h i r t y - t w o , he was adm i t t e d to a n o t h e r hospital in the city w i t h a history of m u c o u s diarrhea, w e i g h t loss, f a t i g u e and a b d o m i n a l pain. H e had a h i s t o r y of h a v i n g had f r e q u e n t b o w e l m o v e m e n t s for some ten y e a r s previously. H e had n e v e r noticed gross blood in t h e stool. His r e c e n t w e i g h t loss was t w e n t y pounds. A t t h a t hospital h e showed an a n e m i a of 2.9 million r e d .cells and 50,% Hgb. His stool was n e g a t i v e for amoeba, typhoid: d y s e n t e r y group or tuberculosis. It was B e n z i d i n e positive.

325

19. Alpert, E., Translated by R. W. B. Ellis, London, M. Hopkinson, 1933.

20. Langston, W. Smith: Med. J., 28:316, 1935. 21. Benson, R. E. and Bargen, J. A.: Gastroenterology, 1:147, Feb. 1943. 22. Davidson, S.: Arch. Int. Med., 64:1187, Dec. 1939. 23. Robscheit- Robbins, F. S.: Federation Proc., 1:219, 1942. 24. Jolliffe, N.: Bull. N. Y. Acad. Med., July, 1934, p. 469. 25. Starr, P.: Int. Abstr. Surg., 74:309, A~ril 1942. In J u l y , 1939, at that hospital he had a p o l y p r e m o v e d f r o m the rectum, and a double b a r r e l ileostomy p e r f o r m e d for an established diagnosis of u l c e r a t i v e colitis. He showed some i m p r o v e m e n t , gained weight, and felt g e n e r a l l y b e t t e r f o l l o w i n g this procedure. In October, 1939, he had a history suggesting left n e phrolithiasis w h i c h subsided spontaneously. I n April, 1940, he was r e a d m i t t e d to t h e hospital for a p e r i r e c t a l abscess at t h e site of t h e r e m o v a l of the rectal polyp w h i c h had n e v e r healed. This was incised and d r a i n e d b u t failed to heal. T h i s a n a l lesion c o n t i n u e d w i t h a d v a n c i n g s e v e r i t y t h r o u g h o u t his illness. A f t e r this b r i e f i m p r o v e m e n t his s y m p t o m s r e t u r n e d w i t h i n c r e a s i n g severity. H e lost w e i g h t and s t r e n g t h and on October 7, 1940, was a d m i t t e d to Montefiore H o s pital bedridden, c o m p l a i n i n g of e x q u i s i t e p a i n in t h e anus and a b d o m i n a l cramps. H e h a d b e c o m e an addict d e m a n d i n g m o r p h i n e for relief and r e q u i r i n g one q u a r t e r g r a i n of m o r p h i n e six times a d a y f o r relief. P h y s i c a l ~ x a m i n a t i o n r e v e a l e d a cachectic m a l e (Fig. 1A)., ( w e i g h t s e v e n t y - e i g h t p o u n d s f r o m an original w e i g h t at the start of his illness of one h u n d r e d a n d f o r t y nine) psychically demoralized, a b e e f y red t o n g u e and ulcerations at the angles of t h e mouth, characteristic of a d v a n c e d v i t a m i n B deficiency. H e h a d a d r a i n i n g ileostomy, w i t h an a d j a c e n t a b d o m i n a l w a l l abscess, a sloughing p e r i n e u m , an anal r e g i o n in w h i c h t h e t e r m i n a l anus had sloughed a w a y w i t h the r e c t a l opening in the h o l l o w of the s a c r u m s o m e t w o inches a b o v e the s k i n m a r g i n . T h e r e was a profuse b l o o d y p u r u l e n t discharge f r o m the rectal stoma. L a b o r a t o r y data s h o w e d a p r o f o u n d a n e m i a : 2.9 M. Hgb. 53%. His blood u r e a was 10.7 m g m . %. His w h i t e blood count v a r i e d f r o m t w e l v e to t w e n t y t h o u s a n d w i t h a h i g h p o l y differential. His total p r o t e i n v a r i e d b e t w e e n f o u r and five g r a m s % w i t h n o A. G. reversal. H e did not d e v e l o p n u t r i t i o n a l edema. He was put on a h i g h caloric, high v i t a m i n diet w i t h r e p e a t e d transfusions and infusions of glucose and sa]ine. Massive v i t a m i n t h e r a p y was t r i e d g i v i n g t h e whol, e v i t a m i n B c o m p l e x w i t h riboflavin and nicotinic acid. F o r a t i m e he r e c e i v e d 50 mgm. of n i c o t i n i c acid e v e r y h o u r for t e n hours a d a y for a period of five days C h e m o t h e r apy was g i v e n in the f o r m of sulfaguanidin~ t h r o u g h the distal i l e o s t o m y loop. T h e patient s h o w e d little i m p r o v e m e n t u n d e r this t r e a t m e n t . On M a y 12, 1941, t h e first stage colectomy was p e r f o r m e d t h r o u g h a t r a n s v e r s e incision. T h e colon was r e m o v e d f r o m t h e i l e u m to t h e sigmoid (Fig. 2). T h e distal sigmoid b e i n g left out on the a b d o m i n a l w a l l as a m u c o u s fistula. His p o s t - o p e r a t i v e course was s t o r m y for the first week. H e t h e n b e g a n to s h o w slew i m p r o v e m e n t . On N o v e m b e r 3, 1941, the p e r i n e a l sloughing w o u n d m e a s u r e d some six inches by t h r o e inches in d i a m e t e r and t h e t e r m i n a l r e c t u m was at th~ a p e x of this w o u n d d r a i n i n g a bloody p u r u l e n t discharge. On N o v e m b e r 11, 1941, an a b d o m e n - p e r i n e a l resection was performed removing the remainder of the involved colon. O n June 22, 1942, the patient had an attack of calculous cholecystitis with jaundice which subsided spontaneously. In May, 1942, a skin graft to the perineum faded to take, and the w o u n d was permitted to granulate in spontaneously. O n November 18, 1942, all wounds had healed. The

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A

B

"Nv~s

lo

C

Fig. I, Case 1 - - A. November, 1941, one week after complete colectomy. Weight 85 pounds (preoperative weight 70 pounds). B. November, 1942, one year after colectomy. Weight 154 pounds. C. Demonstrates 3" protruding ileostomy which falls into bag and spares skin irritation of ileal contents.

patient had gained s e v e n t y pounds in w e i g h t back to his original one h u n d r e d and f o r t y - e i g h t pounds (Fig. 1B and C). H e was left w i t h a d r a i n i n g i l e o s t o m y for which he w e a r s a bag and was discharged f r o m the hospital on N o v e m b e r 21, 1942. This case is p r e s e n t e d as one of a d v a n c e d u l c e r a t i v e colitis w h i c h failed to r e s p o n d to i l e o s t o m y and did not s h o w significant i m p r o v e m e n t until t h e entire colon was r e m o v e d . C o l e c t o m y was f o l l o w e d by ,prompt and p r o gressive i m p r o v e m e n t . E x c e p t for the u n a v o i d a b l e ileost o m y t h e p a t i e n t ' s p h y s i c a l h e a l t h has b e e n restored a l m o s t to its original state. This case is p r e s e n t e d as one of a d v a n c e d u l c e r a t i v e colitis w h i c h failed to respond to m e d i c a l t r e a t m e n t or ileostomy and w h i c h showed f u n c t i o n a l r e c o v e r y f o l l o w i n g r e m o v a l of t h e organic p a t h o l o g y b y c m n p l e t e colectomy. He demonstrages a n u t r i t i o n a l deficiency w i t h clinical u r i n a r y and gall b l a d d e r stones. N e i t h e r of these w e r e p r o v e n surgically. C A S E I I - - K. S., b o r n 1920.

Fig. II, Case I - - Colon from terminal ileum to sigmoid; first stage of colectomy. Note complete mucosal destruction with pseudo-polyposis.

I n March, 1937, at the age of 17, t h e p a t i e n t w a s a d m i t t e d to a hospital in N e w Y o r k w i t h a diagnosis of s u b a c u t e appendicitis. She h a d l~een a "sick]y" child for s e v e r a l y e a r s b e f o r e but h a d had no a c u t e illness. H e r complaints at that t i m e w e r e a b d o m i n a l pain, some d i a r r h e a and vomiti1~g. She h a d b e e n m e n s t r u a t i n g scantily for t h r e e years. M e n s t r u a t i o n stopped at this t i m e and has not r e t u r n e d . L a p a r o t ~ m y at this t i m e r e v e a l e d a diffuse intestinal tuberculosis. A section of o m e n t u m and a l y m p h gland w e r e r e m o v e d at this time,

JouR. D. D. OCTOBER, 1 9 4 6

DERANGEMENTS IN ORGANIC DISEASE OF TIlE INTESTINAL TRACT

both of which were pathologically demonstrated as being tuberculous. No further surgery was done at this time. Ten days later the patient was reopened and an il,eotransverse colostomy was performed on the right side of the transverse colon. Following this operation she developed multiple abdominal fecal fistulae which persisted. Her symptoms of diarrhea, abdominal pain and occasional distension and vomiting continued. A chest plate at this time showed a minimal, inactive tuberculosis of the left upper lobe. She was sent to a sanatorium for treatment for six months. The x - r a y appearance of this lesion has not changed and has remained quiescent through these years.

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On April 26, 1940, eighty centimeters of small intestine were resected and an ileotransverse colostomy performed at the distal end of the transverse colon. The ileal stump entering the caecum was closed thus sidetracking the ileum, caecum and adjacent colon and the fistulae leading from them to the intestinal wall. The post-operative course was stormy for two weeks, requiring multiple transfusions and infusions to maintain water balance. Macroscopic examination and miscroscopic examination of the removed specimen were reported as showing tuberculosis. A lymph node attached to the sl~ecimen showed typical tubercules and areas of caseation. Following this procedure the abdominal wall inflam-

Fig. Ill, Case 2 - - A. April, 1940, before operation, weight 50 pounds. Note absent breasts and pubic hair of infantilism. Age 19, appeared to be 12-13 years old. B. November, 1940, eight months postoperative. Weight 104 pounds. Note development of breasts and pubic hair, general maturity of face and body. On J a n u a r y 17, 1938, she was admitted to Montefiore Hospital. She was bedridden, emaciated, weighed fifty pounds, showed all the signs of pluriglandular infantilism (Fig. I l I ) with absence of breasts and pubic hair. Her epiphysea] markings were those of a child of twelve (Figs. IV and V). Her abdomen showed multiple fecal fistulae draining small intestinal contents. A note by the physio-therapy department at this time r e m a r k e d " T h e patient is learning to walk." She showed carious degenerated teeth (Fig. VI). In March of 1940 she was seen by the surgical service and since the pulmonary disease was considered minimal and inactive and the patient was a hopeless invalid with the abdominal pathology that existed, surgery was decided upon.

marion subsided with the reduction in fecal flow and on March 17, 1941, a resection of the terminal ileum, caecum, ascending colon and transverse colon to the distal ileotransv,erse colostomy was performed. The abdominal wall containing the fecal fistulae was removed in one mass with the intestine. The post-operative course was smooth f,911owing lhis procedure. The pathological report on this specimen which had been exposed to infection by the fecal fistula was reported as nonspecific granuloma of the intestine. Before going to the surgical service she was treated by diet, .iron, vitamins.:, cortate, estrogenic substances, pituitary and ovarian products, liver extracts and multiple transfusions but show,ed no improvement on this care. Following the second procedure i m p r o v e m e n t was p r o -

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Fig. IV, Case 2 - - A. Anteroposterior view showing epiphyses of child of 12 (patient 19 years old) March, 1938.

Fig. V, Case 2 - - A. Lateral view showing epiphyses of child of 12 (patient 19 years old) March, 1938. gressive and eight months after the second procedure her w e i g h t h a d r i s e n to o n e h u n d r e d a n d f o u r p o u n d s (a g a i n of fifty p o u n d s ) . T h e r e w a s o b v i o u s d i s a p p e a r a n c e of t h e signs of i n f a n t i l i s m . P u b i c h a i r r e a p p e a r e d , b r e a s t d e v e l o p m e n t w a s n o t e d (Fig. I I I B ) a n d e x c e p t f o r a n c c c a s i o n a l d i a r r h e a l stool p a t i e n t h a d n o c o m p l a i n t s . T h i s p a t i e n t d e v e l o p e d calculi i n b o t h t h e k i d n e y a n d t h e gall b l a d d e r . I n J u n e , 1940 ( b e t w e e n t h e first a n d second intestinal operations), the patient developed an obstructive infection in the right kidney for which a p y e l o l i t h o t o m y w a s p e r f o r m e d . I n A u g u s t of 1943 t h e patient developed an acute obstructive calculous cholecystitis f o r w h i c h a c h o l e c y s t o s t o m y w a s p e r f o r m e d w i t h r e m o v a l of stones. T h i s p a t i e n t is p r e s e n t e d as a case of n u t r i t i o n a l d e ficiency s h o w i n g : 1. P l u r i g l a n d u l a r i n f a n t i l i s m a n d 2. P r o v e n c a l c u l o u s f o r m a t i o n in t h e k i d n e y a n d t h e gall b l a d d e r . 3. F u n c t i o n a l r e c o v e r y f o l l o w i n g c o m p l e t e r e m o v a l of the organic pathology. CASE III D

A . K., b o r n 1910.

Oct., 1938. O n s e t a t t h e a g e of 28 w i t h a b d o m i n a l c r a m p s , d i a r r h e a , b l o o d a n d p u s i n ~tools. W e a k n e s s , loss of aplaetite, w e i g h t loss a n d f e v e r . J a n . , 1939. A d m i t t e d to a h o s p i t a l w h e r e x - r a y a n d s i g m o i d o s c o p y s h o w e d t h e l e s i o n of u l c e r a t i v e colitis. Ileostomy was performed with no improvement. Weight loss f r o m 215 t o 145 (70 p o u n d s ) . A n e m i a w i t h h a e m o g l o b i n of 44% a n d o n e r e p o r t of 25%. Fig. IV, Case 2 - - B. Showing adult fused epiphyses December, 1943.

JouR. D. D.

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329

7.5 gms. (normal 17 gms.) and red blood count of 3.3 million. Advanced evidence of vitamin B deficiency despite vigorous treatment was seen in loss of vibratory sense, absent ankle jerks and bilateral foot drop so patient was unable to walk, exquisite tenderness and calf atrophy. Feet had been immobilized in molded plaster splints to escape contractures due to foot drop. Abdominal examination showed a draining ileostomy with multiple intestinal fistulae about the ileostomy and multiple peri-anal fistulae from rectal lesion. X - r a y and sigmoidoscopy showed involvement of entire colon and rectum. May 23, 1940. First stage of colectomy was done through a transverse incision through which the colon from terminal ileum to sigmoid was removed (Fig. VII), leaving the distal sigmoid out of the wound. The first post-operative week was a stormy one. Fluid balance was preserved with infusions and transfusions. I m p r o v e m e n t was slow but progressive. Weight rose to 182 pounds (some 40 pounds gain). Total protein rose to 7.7 gms. % with an A / G ratio of 4.5/3.2 and edema disappeared. All the signs of vitamin B deficiency disappear,ed foot drop was relieved and patient was able to walk. Hgb. rose to 88%. A year was allowed to elapse, but pus and blood continued to be discharged b y rectum and sigrnoidostomy, the perianal fistulae remained uncontrolled and there were recurrent bouts of fever. Sigmoidoscopy showed involvement to anus. May 1, 1941. A one stage combined abdomino-perineal resection was done removing the remaining colon and rectum. Recovery from this was uneventful. The wounds

Fig. V, Case 2 - - B. Showing adult fused epiphyses, December, 1943. Aug., Medical fusions, 200 rag.

1939. Admitted to Montefiore Hospital on the Service, w h e r e despite high protein diet, intransfusi.~ns, whole yeast, thiamin chloride 100a day, nicotinic acid 500 rag. a day, iron, cortate,

Fig. VI, Case 2---Degenerated upper teeth due to nutritional deficiency. riboflavin, sulfanilylguanidine, and local care, the patient showed progressive deterioration. May 11, 1940. First seen by Surgical Service. Examination showed m a r k e d evidence of weight loss despite a diffuse edema of lags and trunk due to hypoproteinemia of 3.7 gms. % with a ~ reversed albumin globulin ratio, A / G ratio being 1.5/2.2. An anemia showing an hgb. of

Fig. VII, Case 3 - - Colo~ from terminal ilium to sigmoid; first stage of colectomy. Note mucosal destruction. healed well, the perineal wound continued to hax~e a slight, but foul discharge. The ileostomy functioned well, semi-solid fecal material discharged frown it. A prolapse of four inches let it fa].l into the bag sparing the skin from erosion. Nov. 5, 1941. Because prolapse has become six inches

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long, this was revised and mesentery sutured to prevent prolapse. At the same time the posterior wound was reopened and packed with sulfathiazol. Dec., 1943. Patient has a blood count of 4.3 million, Hgb. 88%, normaI total protein and A/G ratio, now weighs 215 pounds, is in good health. The pathology was reported as granuloma of colon at first resection and ulcerative colitis in the second. In January, 1939, at another hospital the patient had hematuria and cystoscopy at that time revealed a hemorrhagic cystitis, biopsy of which was repor~d as chronic granulation tissue.

VOLUME 13 NUMBER 10

In January, 1940, at Montefiore Hospital the patient developed an attack of left renal colic with typical pain distribution and hematuria. On F e b r u a r y 16, 1940, he passed a 2 ram. yellow brown calculus in the urine. This patient is presented as showing a nutritional deficiency due to ulcerative colitis which resulted in: 1. Peripheral neuritis with foot drop due to Vitamin B deficiency. 2. Massive oedema due to hypoprotein~mia, and 3. Proven urinary calculus. 4. Complete recovery followed removal of the organic pathology.

Proctalgias and Allied Non-Inflammatory Perianal Dyscrasias."Coccygodynia Proctalgia Fugax, Neurogenic Pruritus Ani. By E M I L G R A N E T , M.D. NEW YORK~ N. Y.

ANO-RECTALSYNDROMES to be discussed are not T HEinfrequently seen in practice and are of interest because each poses problems in etiology, pathological physiology and treatment, the satisfactory solution of which in most cases eludes us. Commonly, pain or discomfort in the perianal region or rectum is due to conditions associated with inflammation or infection. These lesions include: 1. Acute Abscesses - - Perianal, Perirectal, Ischiorectal, Supra-levator, Cryptitis, Pilonidal 2. Fistulae 3. Acute and Chronic Fissures 4. Acute Thrombotic Hemorrhoids 5. Specific Chronic Infection - - Perianal Tuberculosis, Gonorrhea, Syphilis, Lymphogranuloma Venercum 6. Ulcerative Colitis - - Idiopathic, Dysenteric, Amebic, Chronic Hypertrophic Proctitis. Neoplasms, benign or malignant, involving the anus, rectum, or pelvis, are obvious causes of perianal pain or discomfort. COCCYGODYNIA The pain in this syndrome centers about the coccyx, frequently radiating up the rectum, laterally to the gluteal region, and occasionally down the back of the thighs. The characteristic pain is severe, continuous, throbbing, and is commonly brought on by prolonged sitting. Trauma resulting from falls on the sacrocoecygeal region or following parturition, or even after ano-rectal surgery is considered the chief etiologic factor of onset in this syndrome. Lesions of the coccvx itself following trauma are infrequent as demonstrated by Duncan (1). H e found that in patients with coccygodynia studied at the New York Orthopedic Hospital, fracture of the coccyx was found in only 4% and dislocation in 2% of 262 patients. Submitted April 10, 1946.

The usual symptomatic treatment with sedation, physical therapy, strapping, injection of analgesics about the coccyx, and even coccygectomy have too frequently given little or no relief to the patient. Thiele (2) as a result of careful observation over a period of years believes that the pain in this condition results from tonic spasm of the pelvic muscles which insert into the lateral margins of the coccyx. He reports that as early as 1859, Sir J. Y. Simpson described this mechanism by calling attention to the fact that, "when the coccyx or the coccygeal joints have heen injured, or when the surrounding tissues were the seat of inflammation, any contraction of the muscles attached to the coccyx would excite the characteristic pain of coccygodynia." Thiele demonstrated the definite relationship between the syndrome of coccygodynia and tonic spasm of the levator ani and coccygeal muscles, and in some cases of the piriformis. In 53 patients with coccygodynia personally treated by this author, the physical findings were described as follows: "On digital rectal examination with the patient in the Sims' position, spasm of the levator and coccygeus is easily detected by latero-posterior pressure, the spastic muscles being felt stretched from their origin at the arcus tendineus or ischial spine to the side of the coccyx and the lower part of the sacrum." Piriformis spasm is difficult to detect because the distance of this muscle from the anus makes palpation uncertain. My personal experience with 12 patients from the Proctological Clinic at the New York Hospital and 8 patients seen in the naval service afloat and ashore, all of whom suffered with coccygeal pain, completely confirms Thiele's findings. However, an added finding, to my knowledge not previously described, was found in about half of the cases seen. This was the presence of well-developed bursae which on finger palpation were found in the lateral pelvis situated between the pubococcygeus and the ileo-coccygeus portions of the levator