Mesentric vascular thrombosis with report of a case. ALFRED M. WEDD.. The effect of a meal upon the titratable alkali of the blood. ROGER S. HUBBARD. The history of epilepsy. J. FRANCIS WARD.. Mohammedan Medicine. J. A. SANDERS. The blood picture as a help in the diagnosis of glioma with hemorrhage. D. C. WILSON.. A clinic illustrating blood dyscrasias. Edited by W. S. THOMAS Index for volume 13, 1927... 97 100 105 109 117 121 126 133 Beginning January, 1928, The CLIFTON MEDIcal Bulletin will be published in January, April, July and October, instead of March, June, September and December. MESENTERIC VASCULAR OCCLUSION, WITH REPORT OF A CASE ALFRED M. WEDD, M.D. Although it cannot be considered a rarity, mesenteric vascular occlusion is seen so infrequently that each example presents some interesting and instructive phase. In 1920 Ross (1) reported that only two cases were seen in thirty thousand surgical admissions to the Lankenau Hospital. Three years later Brady (2) stated that records of about 500 cases of mesenteric thrombosis and embolism were to be found in the literature. There have been numerous case reports since that paper, dealing for the most part with instances of recovery after operation. The consensus of opinion regarding the diagnosis of mesenteric occlusion can be summarized by a quotation from the paper of Brady: "Although some writers apparently believe there is a clinical picture which is diagnostic of mesenteric vascular occlusion I have been compelled from a study of our cases to agree with those that maintain that the picture is indistinguishable from that of acute intestinal obstruction due to causes other than mesenteric thrombosis." It is interesting to note that Cope (3) in his monograph on the diagnosis of the "acute abdomen" does not list mesenteric vascular occlusion. The example here reported is of interest primarily for the orderly sequence of events which made the diagnosis possible before operation. The source of embolism in this instance is particularly worthy of emphasis. The patient, a man of 52 years, was admitted to the clinic on July 31, 1927. He had suffered from acute rheumatic fever in early life and had his last attack at 22 years of age. Later he had had typhoid fever, acute meningitis and malaria. He found that his activities were greatly restricted when he tried to live at a high altitude. His general health had been good until an attack of influenza in 1922, following which his life had been that of a cardiac invalid with repeated attacks of congestive heart failure. The patient came here to convalesce from an acute illness which had followed exposure in rainy weather and had kept him in bed for nearly five months. When examined on August first, the patient's nutrition was good and save for the sallow skin his general appearance was The quite normal. The principal abnormal findings were the presence of a right hydrothorax, which had been first recognized eight weeks before, and mitral stenosis. The heart rate was 74 and the blood pressure 94 mm., systolic and 69 mm., diastolic. He was not cyanotic and there was no edema of the extremities. Neither the liver nor the spleen showed enlargement. The finger nails presented no clubbing. urine was normal. On August second, 1300 cubic centimeters of clear, straw-colored fluid were removed from the right pleural cavity. Following this the patient was able to lie down flat at night and had no dyspnoea or palpitation, symptoms which had been troublesome for some time. On the morning of August fifth before breakfast, just after a copious bowel movement, while still sitting on a commode at the bedside, the patient suddenly experienced severe abdominal pain. This was first felt in the epigastrium but soon became diffuse throughout the lower abdomen. The nurse observed that he was cyanotic and perspired freely. He was nauseated and vomited a small quantity of watery fluid. When examined fifteen minutes after the onset of pain the skin was dry but rather cold. There was no cyanosis. The blood pressure was 130 mm., systolic, 66 mm., diastolic. The heart rate was 76. The facial expression was anxious but the pain was well borne. Any shock that had been present passed off rapidly and the skin of the extremities soon became warm. Three hours after the onset of pain the significant findings were severe abdominal pain referred to the left of the umbilicus, not relieved by morphine, leucocytosis without fever, and the soft abdomen with absence of peristalsis. The cellular changes in the blood are given in Table 1. Late in the afternoon peristalsis was heard but not at any subsequent examination. A urine specimen of 200 cubic centimeters voided during the afternoon contained 1.28 grams of sugar, albumin two plus and many hyaline and a few granular casts. At the end of twelve hours the pain was less severe. The abdomen was still soft and without any localized tenderness or rigidity. The maximum leucocytosis recorded was then observed. During the night projectile vomiting occurred once. Nothing was expelled from the bowels. The following morning there was tenderness along the course of the descending colon and in the lower abdomen generally. There was slight rigidity in the upper mid abdomen and in the region of the gall bladder. The circulation was well maintained. Morphine was still required for pain. By noon signs of peritoneal involvement was more marked, the abdomen having become generally rigid. It may be noted in the chart (Fig. 1) that there was no significant rise in temperature until thirty hours after the onset of pain. At this time laparotomy was performed by Dr. C. W. Webb. On opening the abdomen in the mid line a small amount of dark colored fluid of fetid odor was found. About 40 inches of small intestine were seen to be cyanotic and part of this was already gangrenous. The mesentery was congested. It was necessary to remove about four feet of bowel, following which an end to end anastomosis was made. Several small irregularly distributed dark colored patches were observed in loops of intestines. beyond the point of resection, but it was hoped that they would be taken care of by collateral circulation. The operation was well borne and the next day the patient's condition was fair. However, it was soon apparent that an overwhelming peritonitis had developed and this resulted in death on the morning of August eighth. Necropsy was performed at once. In the heart, the mitral valve showed high grade stenosis; the left auricle was moderately dilated and in the left auricular appendage was a friable thrombus 8 mm. in diameter. The superior mesenteric artery was completely occluded immediately below the first branch. The embolus was similar in color and consistency to the mass in the left auricle. Cephalad to the embolus was a thrombus mass about 15 mm. in length. The remaining bowel, save for the duodenum and upper portion of the jejunum, was dark green in color and the coils were matted together. The sources of embolism which may give rise to mesenteric occlusion that are mentioned in the literature comprise endocarditis, atheroma of the aorta, and aneurysm. Under the term endocarditis may be included two types of lesions; (a) subacute bacterial endocarditis, with its masses of large, friable vegetations from which fragments may be broken off, and (b) chronic endocarditis, a healed lesion clinically known as chronic valvular disease of the heart. Not infrequently a healed valvular lesion is accompanied by the formation of calcified placques at the ring margin and these placques may break off and form emboli. In Brady's list of cases are several in which mural thrombi in the heart gave rise to mesenteric embolism but in these cases "acute abdomen" was not considered and the mesenteric lesion was found at autopsy. There had been a striking want of emphasis in the literature concerning the rôle of mural thrombosis in the heart, and yet this constitutes a very frequent source of embolism. In Table 2 are given six examples that have recently come to autopsy in this. clinic. The list includes three types of heart disease in which mural thrombi may be anticipated; (1) lesions associated with long standing dilatation of the auricles, typically mitral stenosis; (2) infarction of the heart following occlusion of a large coronary vessel; (3) intraventricular thrombosis resulting from scar formation consequent on |