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Embolism and thrombosis of the abdominal aorta
EMBOLISM
AND
THROMBOSIS
OF THE
ABDOMINAL
UNUSUAL
CASES
REPORT OF THREE
AORTA
FRANKLIN W. FRY, M.D. HEMPSTEAD, N. Y.
T
HERE have appeared in the recent medical literature reports of approximately 135 cases of embolism and thrombosis of the abdominal aorta, of which 125 were ably abstracted by Rothstein,l in 1935. Of the 135 patients, only twenty survived, ten by virtue of the development of an adequate collateral circulation, as reported by Gull and Chvostek,*” Nunez,2b Derman and Dutkewitsch,3 van der Beek,” Bull,j and Rykert and Graham.$ One recovered spontaneously and two improved under treatment with alternating suction and pressure. 111 one case reported by Rothstein the patient recovered, probably because the embolus passed from the bifurcation of the aorta into the iliac artery. The remaining nine patients were relieved by embolectomy. Death was usually not long delayed, following close upon gangrene of one or both legs. In Hesse’s7series of forty-six cases,the duration of life after the onset of embolic symptoms was as follows: nine patients died within twenty-four hours, six more within forty-eight hours, a total of twenty-four within one week, a total of thirty-five in the first month, and the remaining eleven patients all died between the second and sixth month. In the three casespresented in this article death occurred from twelve months to five years after the initial embolic symptoms. In two of the three there was no evidence of gangrene, and the immediate cause of death was intercurrent disease. In contradistinction to embolism of the abdominal aorta, which is characterized by dramatic, sudden onset, as illustrated by Welch,s primary thrombosis of this artery may bc ushered in by slight, easily mistaken, or overlooked symptoms. In the majority of cases there is a primary embolus, followed by retrograde thrombosis of the involved artery. In these latter cases the classical sign of gangrene of an extremity may be late or entirely absent, depending on the speed of extension of the occluding thrombus up the vessel. Bull,” however, states that the presence or absence of gangrene depends upon whether the lumen is completely or partially occluded. To illustrate a marked degree of occlusion of the aorta with a minimum of symptoms of arterial obstruction, three casesof complete thrombosis of the abdominal aorta are presented in somedetail. REPORT
OF
CASES
1.-W. O., a 21.year-old grocer’s clerk, was admitted to the North Country Communities Hospital, Glen Cove, IA. I., on three occasions over a three-year period. CASE
Received
for
publication
Nov.
18,
1938.
He was first admitttvl April 2, 1933, with the history that two weeks prior to admission he had l~een forced to cease war, l- Irecause of tightness of the muscles of the left arm and of the calves of his legs. This condition was aggravated by exertion and wlieretl hy sitting or lying (10~~ hside from the pain, the patient had noted no aJ~norm:tlity in either arnts or legs. ‘l’wvr) (lays before admission he \vits awakened in the night with a severe pin in his upper abdomen which was :lssO?iilted with nituse:~ ;~nd I-onlitirlg. The pain and vomiting persisted the following day, and he wt I s ho~pitalizetl for this complaint. The family, past, ant1 persotral The patient histories were etrtirely negative. was a moderate user of tolracco. The examination r,n :~dmission ~~evcale~l that the Jmtient was a fairly wellnourished white man, not cyanotic or tlypneiv. The blood pressure in the right arm was M)/i8; in the left arm it could trot Iw measured. X:0 pulse was perceptilrle in the left amt. Whether or not there were pulsations in the femoral arterres was not ascertained. The heart ,\ountls \\ere normal. The abdomeii was scaphoid and showc~l no Jocalizetl tenderness or rigi(lit>-. liilaterxl costovertebral tenderness was present, more J)ronoun(~etl on the right side than on the left. The extremities were normxl. I~iLl~OKttOr~ E:xanlirlntioll.-‘l’lle urine was normal. The hemoglobin was 88 per cent, the erythrocyte count 4,5XJ,OtJt~, and the leucocyte count 9,500; 7.5 per cent of the leucocytcs were pal?-ltlorJ’hollucle:~r cells. The blood Wassermann reaction was negative. A roentgenologic examination of the chest failed to reveal any evidence of disease. Cholecystograms were reported as showing normal gall lrladder function. The patient remained in the hospital for eight days., during which time gradual improvement \ras noted. During the first three days of the hospital stay he continued to complain of vague abdomimtl pain. At no time were there any c*omplaints refernl~le to the legs, an11 no olrjective signs were found in the lowet extremities. The patient was next admitted to the hospital .Jan. 24, 1934, approximately ten months after his first admission, with the history that his legs had become too weak to permit him to CRI’L’) on his previous work as a grocer’s clerk. He had also noticed that they l)erame lminful on walking. The pain and weakHe complained that his feet ness had been noticed in lesser degree in the arms. became cold more easily, and that epicritic sensation in the feet was diminished. “Ace” bandages applied to the legs had caused intolerable pain. About seven months before this second admission, the Jmtient be,
FRY
:
EMBOLISM
ASD
THROMBOSIS
OF
ABDOMISAl~
AORTA
59
The patient was next seen in the hospital twenty-three months later, NOV. 21, 1035. He said that for the preceding four days he had been short of breath. A cough which had been present for approximately one week had become worse and productive of bloody sputum, and was associated with pain in the anterior portion of the left chest. Hospitalization was advised when a marked pericardial friction rub was heard by his physician. The interval history was otherwise negative except for the continued presence of intermittent claudication. There had been no diminution in cardiac reserve noted during the preceding two years. The physical examination on this admission showed a dyspneic, pale, acutely ill, thin young man. Slight cyanosis and orthopnea were present. The pupils were slightly irregular but reacted normally to light and in accommodation. Evidence of marked hypertrophy of the left side of the heart was found; the lower outermost point of the apical impulse was in the sixth intercostal space, 14 cm. from the midsternal line. At the apex of the heart a marked pericardial friction rub was heard and gallop rhythm was present. There were a rough systolic and a high pitched diastolic murmur both at the apex and base of the heart. The blood pressure in the right arm was 190/100, and in the left arm 144,000. The blood pressure could not be measured in either leg. The lungs were The liver was dull to percussion, and there were moist rales at both bases. palpable below the costal border. It was not tender. Through the thin abdominal wall no pulsation of the abdominal aorta could be felt. It was noted that the femoral pulse on the right side was cerv weak, u-hile no pulsation could be felt on the left. The extremities were otherwise normal. The electrocardiogram shoa-ed sinus tachycardia, right axis deviation, and an auriculoventrieular conduction time of .14 sec. The T wave was inverted in l,eads I and II, and varied in T,ead III. The precordial leads showed evidence of pericardial eflusion, with depression of the ST segments in precordial T,eads II1 and IV (met.hotl of Wilson, with the right arm 112~1 wire connected to the exploring electrode). Laboratory Examination.-On admission, the urine showed a very faint trace of albumin and three red blood cells to the high-power field. Red blood cells were not found on subsequent urine examinations, but granular casts appeared shortly before death. The hemoglobin was 63 per cent, the erythrocyte count 3,650,000, and the leucocyte count 9,000, of which ‘ii per cent were polymorphonuclear cells. The urea nitrogen content of the blood was $2 mg. per cent. The blood sugar and creatinine values were IX and 2.2 mg. per cent, respectively. The blood culture on several occasions was sterile. Roentgenologic examination of the chest at the time of admission showed a large pericardial effusion and soft, scattered pulmonrtry lesions suggesting lobulai pneumonia. The findings were more market1 in the central portion of the left lung. The patient’s condition grew stetrdily worse. The leucocytes gradually rose to 23,000, of which 84 per cent were polymorphonuclear cells. For the first fete days the pericardial effusion was the predominant lesion. The friction rub remainell for forty-eight hours. However, when fluids were forced the azotemia diminishctl, and within two weeks the pericardial eff’usion had disappeared. The gallop rhythm at the apex of the heart persisted. The veins of the neck remained diatendetl throughout the entire hospital stay. Five days after admission the patient developecl signs of fluid in the right sidfk of the client, and etlenm of the ankles which was more marked on the left title than on the right; the dyspnea and cyanosis increased, and the liver became palpable ten centimeters belo\v the costal border. The patient was fully digitalized without effect. The orthopnea became more marked and the edema of the legs increased. The patient lapsed into semicoma and expired sixteen days after admission. The total duration of the illness had been thirtythree months.
60
THE
AMERICAN
HEART
The pertinent autopsy findings were as cavity 2,000 C.C. of bloody fluid were found right lung to the mediastinurn. Both lungs sizes.
follows: Upon opening the thoracic in the right pleural sac, pressing the were riddled with infarcts of various
The lining of t,he pericardium was smooth am1 glistening throughout, with no areas of roughening or inflammation. Fifty cubic centimeters of pericardial fluid were present. The heart weighecl 5(10 gm. The right auricle was normal. Enmeshed in the normal chordae of the tricuspid valve were found two large, extremely friable thrombi; the smaller one measuretl 1 cm., am1 the larger, ? cm., in diameter. The right ventricle and pulmonary valve were normal. Tht aortic valve was bicuspid, and the CUSPS were found to be thickened, producing :I hard, roughened, ragged, inelastic valve. At the tip of the larger (posterior) cusp t,here were very small, friable, well-organized vegetations. The wall of the left ventricle was markedly hypertrophied. The mitral valve and left auricle were normal. The liver weighed 1,735 gm., and the cut section of this organ showed chronic passive congestion. The gall bladder was large and distended; the walls were normal. A large, gray, friable thrombus was noticed at the junction of the hepatic vein and inferior vena cava. The spleen was small, shrunken, an11 of the fetal type. The pancreas was normal. The right kidney was large, of the fetal type, and weighed 217 gm.; this kidney was anomalous in that the main renal artery originated 2 cm. higher than The left kidney was small, weighing 70 gm.; on section, the left renal artery. the normal striations were lost, and the organ was of a darker hue than its fellow. The intercostal arteries, especially over the The arch of the aorta was normal. 1owTer half of the thorax, were slightly dilated. The thoracic aorta was not dilated, but showed more evidence of arteriosclerosis than is normal for a man Just below the diaphragm the aorta was occluded by an old, or21 years old. Between the apex of the thrombus ganized thrombus, covered with endothelium. One which was entirely patent, was found. and its base, the right renal artery, centimeter below this artery was the celiac axis, which was rompletely occluded by thrombus. Below the celiac axis was the left renal artery, which was found to l)e partially occluded. Immediately below the left renal artery the aorta shrank to a diameter of 2 cm. Both of the common iliac arteries were thrombosed in the aorta and iliac throughout their entire diameter (P’ig. 1 ). The thrombus A collateral circulation had vessels was identifietl as 0111 and well organized. Ibetween the tleep epigastric and internal pudendal been established, in part, arteries. Microscopic examination of the aortic cusps showed that the bicuspid condition as demonstrated by Bishop,9 was of congenital rather than inflammatory origin, the Weigert elastic fiber stain, using the technique of Lewis and et al., with Grant.lo Microscopic study of the aorta revealed severe sclerotic changes of the intima and media, with laminat,ed fibrinous thrombus filling the lumen. The lesions could not be identified by the pathologist as either syphilitic or rheumatic. CASE 2.--v. T., a housewife, 42 years of age, was admitted to the Nassau Hospital, Mineola, L. I., in November, 1937, following a cerebral achcident. The family history was negative. A history of rheumatic heart disease of two and a half was obtained. Eighteen months prior to admission she had had years ’ standing Five months later an embolus had an infarct of the lung, with a slow recovery. lodged in the left leg. This diagnosis was made because of coldness, pallor, and pain in the leg and foot, with inability to move the member. Within four months partial
FRY
function had only remaining
:
EMBOLISM
returned. symptoms.
ASD
Residual There
THROMBOSIS
OF
ABDOMISAJ,
AORTA
weakness and intermitt.ent elaudication was no involvement of the bladder.
61
were
the
Physical examination of the patient on admission showed a dyspneic and orthopThere was evidence of upper motor ncurone paralysis of neic middle-aged woman. the left side. The heart was enlarged; the lower outermost point of the apical impulse was felt outside the midclavicular line. There were a systolic and diastolic The ventricular rate wa!: murmur at the apex and a systolic murmur at the base. 100, the pulse rate 90. The blood pressure was 198/96. The spleen was not palpable. The liver was felt at the costal margin. The extremities were apparently normal. No discoloration was noted and the temperature of the legs was the same. There Whether or not femoral artery pulsations were present was not was no edema. ascertained.
Fig.
l.-Thrombosis
of the
abdominal
aorta
exten(ling
above
the
celiac
axis
(Case
1).
Laboratory Examinations.-The electrocardiogram showed auricular fibrillation. The urine was normal except for a faint trace of albumin and a few granular casts and leucocytes. The hemoglobin was 92 per cent and the erythrocyte count 5,360,OOO ; the leucocytes numbered 20,400, of which 78 per cent were polymorphonuclear cells. The blood culture was sterile on two occasions. The blood Wassermann reaction was negative. The third
patient hospital
remained in a state day with a rising
of semicoma ventricular
and delirium, dying on the twentyrate and body temperature. The
paralysis rcmainctl nn~~l~:tngfvl. Ku circ~ulatury c11an~w wr’c noted in the extremities throughout the entire 1)eriotl of hosl~italjz:Lti,,l1. At autopsy there wva.i :I zone of softening, 6 cm. iu diameter, in the right cerebral hemisphere, impinging on the lateral ventricle. The heart, showed a right ventricle three times the normal thickness, :I nlodrratrly thickened left rentri~~le, and an extremely stenotic mitral valve. On the* lmsterior leaflet of’ the mitral valve there were numerous, red, calcitic: granulations. There ,v:,.s an :/I lllerent thrombus in the left auricle. The aorta in the upper portion was normal for the age of the patient. &\t the level immediately lielow the ol,iyin of the renal arteries the lumen of the aorta was occluded by a soft, red, but arlherent, throtnbus. This thrombus became firmer and more tlenselj at.tachrd to the intinct of the aorta as the bifurcation was appro:K?lletl. At this level tile prowess WI?; well organized. The contents of the lumen were yellowish gray and appeared partly fibrous. The process continued uninterrupted into the common iliac arteries. The lungs showed diffuse congestion, but there was no evidence of pneumonia. The pleurae were covered by fibrous tissue; there was a small amount of fluid in both pleural spaces, from which the Type I pneumococcus was cultured. The spleen weighed 400 gm. and was grossly normal. The kidneys showed evidences of old infarction. The other organs were essentially normal. Microscopic examination of the heart failed to show typical Aschoff bodies. There were, however, numerous foci of dense fibrous tissue around the blood vessels of t,he heart muscle. Sections taken from that part of the aort:t wlliclt was completely thrombosed showed t.he lumen witlt ret1 thrombus adherent to tlie intima. Here the endothelium was deficient. The great part of the change Iay in the media, where there were diffuse engorgement and reduplication of the small vessels and widespread infiltration of these tissues by polymorphonurlear cells and phagocytes containing hemosiderin. The final diagnoses were rheumatic heart disease with mitral stenosis; mural thrombus of the left auricle; infarction of the right cerebrum; multiple old infarcts of the kidneys; acute fibrous and purulent pleuritis; diffuse mesaortitis; and endaortitis with thrombosis. The autopsy findings were a surprise. for thrombosis of the aorta in this case referable to the abdomen was not suspected because of the paucity of symptoms and legs. B., a Gyear-old nmn whore mother 11~1~1had hypertension, gave a CASE 3.-H. past history which was essentially negative except for rswssiw c.igarett,e smoking for many years. The present illness began tire years previously, when the patient noted :I sudden pain in the left leg which was localizetl to the foot and calf and was associated with coldness of that member. This condition kept the patient in bed for three months, during which time there was improvement with the use Thereafter the patient’s only symptoms had been interof Buerger’s exercises. mittent claudication and partial loss of epicritic sensation of the left leg until three years prior to admission, when he had a similar attack with gangrene and loss of a small portion of the medial side of the left great toe. The toe later regenerated completely. He was subsequently t,reated hy the Pavaex method, but Fifteen months earlier noticed no lessening of the intermittent claudication. 11c had hat1 coronary occlusion, recovery froul xlliclt was postponed by lobar plleumonia, the type :tnd sit.e of which were uuknoan to the patient. This ocr+lu*ion was folIowed by a ltilateral deep phlel)itis of the legs and 5 subsequent pulmonary embolus. Still later there occurred an attack characterized by severe abdominal distention and hiccough which was diagnosed as mesenteric thrombosis. All these events took place over a ten-month period, during which the patient
FRY
:
EMBOLISM
ASD
THRORlBOSIS
OIi‘
,~BDOMIS~~l,
AORTtY
63
However, during the was in a hospital in Canada practically the entire time. preceding four months he had been able to carry on his usual sedentary work as a writer, with no symptoms except intermittent claudication in both legs, worse an the left than on the right. There had been a loss of epicritic sensation in both feet. He had continued to smoke twenty to forty cigarettes a da) until his admission to the Naussau Hospital. Two weeks prior to admission, following a great deal of walking, he noticed early gangrene of the third, fourth, and fifth toes of the left foot. Examination on admission to the Nassau Hospital on March 22, 1038, showed a tall, spare, middle-aged man looking older than his years. The pupils were unequal, the right being larger than the left, but both reacted normally to light Examination of the eye grounds showed moderate arterioand in accommodation. The cervical veins were not distended. The sclerotic changes in the vessels. right, lung was normal, but a few moist Idles were heard at the base of the, I& lung. The heart was normal in size. The heart sounds ll-ere of fair quality at the apex and the base. There was a systolic murmur at the apex. The I~lootl pressure in both arms was 136/80. The blood pressure could not be measured in either leg. The cardiac mechanism was normal, and the rate was 110 beats a minute. Neither the liver nor spleen was felt. The abdominal aorta was palpable through the thin abdominal wall down to the level of the umbilicus, a-here There was marked sclerosis of the brachial and the pulsation abruptly ceased. radial arteries. There was a very poor femoral pulsation on the right side, but a fair pulsation of the left femoral artery was felt. No dorsalis pedis or posterior tibia1 pulsation was noted in either leg. There was dry gangrene of the left third, fourth, and fifth toes, with regional cellulitis extending to the ankle. The temperature of the legs was the same. The veins were prominent, but no varicosities were present. An electrocardiogram taken prior to admission showed changes typical of an old anterior wall infarction. Laljoratory Examination.-The specific gravity of the urine was 1.020; the urine contained no albumin or sugar. The blood Wassermann reaction was neg:ttive. The patient’s course in the hospital was characterized 1)~ slowly increasing dry gangrene of the entire left foot below the ankle, and by a sudden arterial occlusion in the right leg. This occlusion occurred seven days after admission, and resulted in a spreading dry gangrene of the right leg extending to midthigh. The patient was given the usual conservative treatment for gangrene, including alcohol by mouth, papaverine, tissue extract, generalized infrared light, and partially occlusive bandages to the leg. All treatment was to no avail. He became increasingly stuporous and “toxic” and had slight fever until the final week, when the temperature rose much higher. Death occurred suddenly eleven weeks after admission. The pertinent autopsy findings were as follows: External examination showed dry gangrene of the left leg below the ankle and of the right leg below mid-thigh. The lungs showed diffuse congestion. The heart weighed Bi.? gm. There was a definite increase in thicknfss of the wall of the left vcntrit*le. Moderatr generalized coronary sclerosis was present. The left descending coronary artery was found to he occluded and fibrosed by an old thrombus. At the apex of the left ventricle there was a large area of fibrosis, with an old, adherent, organized mural thromhus. There was no deformit,y of the valves. The heart, wax otherwise normal. The arch and thoracic portion of the aorta were normal, shoxing o,lly slight evidence of arteriosclerosis. There was no dilatation of the thoracic aorta and little increase in the diameter of the intercostal arteries. At the level of the
left renal artery the lumen of t,he aorta \q’as completeI>obstructed l)>- an organized thrombus, wit,h a svft, fresh extension into the superior mesenteric artery. The right renal artery ~vas patent, the left re11a1 artery l~artiall~occluded. The thrombus continue11 illto the common iliac arteries. The left iliac artery contained an old, white, organized thronlbw, and the right iliac arteq 1 was obliterated by a more recent, red, fllbrlnous thrornl)us (Fig. 2). There was very little evidence of collateral circulation. The upper pole of the left kidne?was scarred 1,~ a large infarct which showwl The right kidney \~‘:ts normal. various stages of healing. The liver and spleen were grossly normal. There was no evidence of Microscopic study of the ganization and no evidence was destroyed; the elastic Weigert stain.
Fig.
2.-Two
It is those in prising, and the abdominal bladder
stages
of
thronlhosis
gangrene or necrosis of the intestines. thromlnw at. the level of the renal artery showed orof reeanalization. The endothelial lining of the aorta layers were reduplicated, as demonstrated by the
of
akxlominnl
(Cme
3).
aorta
to the
level
of
the
renal
arteries
to compare the symptoms in these three cases with Rothstein’s series of seventy-two cases (Table I). It is surin view of the high extent of t,he thrombus in all three casts, organization present at the high level in two of these, that symptoms were not more marked and that spinal cord and symptoms were not present in any case. The symptoms
interesting
FRY :
EMBOLISM
AND
THROMBOSIS
OF
ABDOMIKAI.
65
AORTA
in all three cases were caused by slowly decreasing blood supply. It is interesting to note that in two of t.he cases the abdominal aorta was found to be abnormal before death. This observation alone served to indicate the high extent of the lesions. TABLE SYMPTOMATOLOGY
OF PARED
I
OCCLUSION OF THE AORTA IN ROTHSTEIX'S~ WITH THAT IN TIIE 3 CASES HERE REPORTED
A. MANIFESTATIONS EXTERMITIES
IN
LOWER
PER
1. Pain in legs 2. Loss of nulsation in arteries of lower extremities 2. Cyanosis or discoloration of lower extremities 4. Edema of lower extremities 5. IXsturbances in sensation of lower estremities 6. IXsturbances of muscle power of lower extremities 7. Preceding embolic phenomena in peripheral arteries of lower extremities 8. Intermittent limping 9. Disturbances in circulation beginning in one, and then in the other, extremity 10. Evidences of gangrene in lower extremities a. Involving only the right lower extremity b. Involving only the left lower eatremity c. One lower extremity (aide not noted) d. Involving both lower extremities B. MANIFESTATIOKS OF ABDOMINAL
1. 2. 3. 4. 5. Ii. 7.
CASES
Coar-
CASES
1
2
-3
44.4 40.3
t t
t 2
t +
22.2
0
0
t
ti.9 40.3
t t
0 t
0 t
30.0
t
t
+
-.“8
0
t
.I
2.8
t
t
t
lti.ti
t
t
t
67.0
0
0
t
12.5 19.4 1.4 2::.7
OF INVOLVEMENT ORGANS
Pain in the abdomen Pain in the back Loss of pulsation of abdominal aorta Incontinence of urine Retention of urine Incontinence of flatus Hemorrhage from anus and urethra Presence or absence of symptoms inclicxte~l
('EPI'T
70
PER
('EST
11.1 3.6 69 cj.9 2.8 4.3 x.?, by
+ or
+ 1
CASES 2
n
t t t 0 0 0 0
0 0 2 0 0 0 0
t t t 0 0 0 0
0.
The fundamental lesions in all of these cases were different, but all led to the same terminal condition in the aorta and iliac arteries. As is noticed from the description in the microscopic reports, the endothelial wall of the aorta around the thrombus was destroyed in all cases. It is impossible to differentiate primary infection of the arterial wall from nonspecific reaction in cases of complete obstruction of long duration. In Case 1, the congenitally bicuspid aortic valve with roughening and organized small vegetations may have been a nidus for small emboli. -“Jo doubt the cerebral signs in this case mere cmholic. The symptomatology and course in this case were essentially that of progressive thrombosis superimposed upon small rmholi. The long duration of life was l)ossihle only because of the anomalously high origin of the right renal
artery. In the second case, a mural thrombus in the fibrillating left auricle was t,he source of emholi. again with progressive superimposed thrombosis. In the third cast the etiology was atherosclerosis, and the case was somewhat simiIar to one reported by Rosenberg,ll et al. The use of the Weigert elastic stain was helpful in demonstrating the reduplication of the elastic fibers found in nthcrosclerosis.
Three eases of embolism and complete thrombosis of t,he abdominal aorta are reported ; the fundamental lesions were ctiologically different, but they all produced pract~ically identical gross and microscopic changes in the aorta. The patients survixed from one to five years after the onset of occlusive sympt,oms. Two of the t,hree patients showed no evidence of gangrenc in spite of the high level of the lesions. These cases are reported to demonstrate, in addition to the unusual and widespread lesions, the ability of the circulatory system to adapt itself t,o a gradually occluding process, and to emphasize the fact that estensivc pathologic changes may occur in thr large vessels of the body with only minor symptoms. REFERESCXS 1. Rothstein. Jacob L.: Embolism and Thrombosis of the Abdominal Aorta in Infancy and in Childhood, Am. J. Dis. Child. 49: 1.578, 1935. ?a. Gull and Chvostek: Wiener Med. Rhitter, p. 1513, 1881. Ph. Nunez: Gaz. Med. de la Habana II,’ p. 160,’ 18i9-80, quoted by Welch (reference 8). Zur Frage des vollstLndigen Ver3. Derman, 0. L., and Dutkewitsch, E. A.: sch1usse.s des unteren Teiles der Bauchaorta, Tirehow’s Arch. f. path. Anat. 274: 535, 1929-30. 4. van der Beek: Een gelal van thrombose ~-an de lunkaorta. Nederl. tiidschr. v. geneesk. 76: 433i, 1932. Hvad kan over 6000 Obduktioner lare os om embolia resn. gnngraena 5. Bull. P.: er’nbolica extremitatium? Norsk. maa. f. laenevidensk. 83: 1?3.-1922. in the Diagnosis, Prognosis and 6. Rykert, H., and Graham, I). : Some Problems Treatment of Acute Arterial Occlusion, AX. HEART J. 15: 395, 1938. i. Hesse, E.: Ueber die Embolie und Thrombose der Aorta abdominalis und ihre operative Behandlung, Arch. f. klin. Chir. 115: 812, 1921. 8. Welch, W.: Embolism and Thrombosis, In Albutt, I. C., and Rolleston, H. D.: System of Medicine, Sea Pork, vol. 6, p. 809, 1909, The Macmillan Company. 9. Bishop, Louis E’augeres, Bishop, Louis Faugeres, Jr., and Trubeck, Max: Aortic Stenosis of Inflammatory Origin With a Differential Study of the Acquired or Congenital Origin of a Bicuspid Aortie Valve, Bm. J. M. SC. 188: 506, 1934. 10. Lewis, T., and Grant, R. T.: Heart 10: 21, 1923. I I. Rosenberg, E. T., Keith, M. M., Wagener, H. P.: Diffuse Arterial Disease With Hypertension, Arch. Int. Med. 62: 461, 1938. ci
AND
THROMBOSIS
OF THE
ABDOMINAL
UNUSUAL
CASES
REPORT OF THREE
AORTA
FRANKLIN W. FRY, M.D. HEMPSTEAD, N. Y.
T
HERE have appeared in the recent medical literature reports of approximately 135 cases of embolism and thrombosis of the abdominal aorta, of which 125 were ably abstracted by Rothstein,l in 1935. Of the 135 patients, only twenty survived, ten by virtue of the development of an adequate collateral circulation, as reported by Gull and Chvostek,*” Nunez,2b Derman and Dutkewitsch,3 van der Beek,” Bull,j and Rykert and Graham.$ One recovered spontaneously and two improved under treatment with alternating suction and pressure. 111 one case reported by Rothstein the patient recovered, probably because the embolus passed from the bifurcation of the aorta into the iliac artery. The remaining nine patients were relieved by embolectomy. Death was usually not long delayed, following close upon gangrene of one or both legs. In Hesse’s7series of forty-six cases,the duration of life after the onset of embolic symptoms was as follows: nine patients died within twenty-four hours, six more within forty-eight hours, a total of twenty-four within one week, a total of thirty-five in the first month, and the remaining eleven patients all died between the second and sixth month. In the three casespresented in this article death occurred from twelve months to five years after the initial embolic symptoms. In two of the three there was no evidence of gangrene, and the immediate cause of death was intercurrent disease. In contradistinction to embolism of the abdominal aorta, which is characterized by dramatic, sudden onset, as illustrated by Welch,s primary thrombosis of this artery may bc ushered in by slight, easily mistaken, or overlooked symptoms. In the majority of cases there is a primary embolus, followed by retrograde thrombosis of the involved artery. In these latter cases the classical sign of gangrene of an extremity may be late or entirely absent, depending on the speed of extension of the occluding thrombus up the vessel. Bull,” however, states that the presence or absence of gangrene depends upon whether the lumen is completely or partially occluded. To illustrate a marked degree of occlusion of the aorta with a minimum of symptoms of arterial obstruction, three casesof complete thrombosis of the abdominal aorta are presented in somedetail. REPORT
OF
CASES
1.-W. O., a 21.year-old grocer’s clerk, was admitted to the North Country Communities Hospital, Glen Cove, IA. I., on three occasions over a three-year period. CASE
Received
for
publication
Nov.
18,
1938.
He was first admitttvl April 2, 1933, with the history that two weeks prior to admission he had l~een forced to cease war, l- Irecause of tightness of the muscles of the left arm and of the calves of his legs. This condition was aggravated by exertion and wlieretl hy sitting or lying (10~~ hside from the pain, the patient had noted no aJ~norm:tlity in either arnts or legs. ‘l’wvr) (lays before admission he \vits awakened in the night with a severe pin in his upper abdomen which was :lssO?iilted with nituse:~ ;~nd I-onlitirlg. The pain and vomiting persisted the following day, and he wt I s ho~pitalizetl for this complaint. The family, past, ant1 persotral The patient histories were etrtirely negative. was a moderate user of tolracco. The examination r,n :~dmission ~~evcale~l that the Jmtient was a fairly wellnourished white man, not cyanotic or tlypneiv. The blood pressure in the right arm was M)/i8; in the left arm it could trot Iw measured. X:0 pulse was perceptilrle in the left amt. Whether or not there were pulsations in the femoral arterres was not ascertained. The heart ,\ountls \\ere normal. The abdomeii was scaphoid and showc~l no Jocalizetl tenderness or rigi(lit>-. liilaterxl costovertebral tenderness was present, more J)ronoun(~etl on the right side than on the left. The extremities were normxl. I~iLl~OKttOr~ E:xanlirlntioll.-‘l’lle urine was normal. The hemoglobin was 88 per cent, the erythrocyte count 4,5XJ,OtJt~, and the leucocyte count 9,500; 7.5 per cent of the leucocytcs were pal?-ltlorJ’hollucle:~r cells. The blood Wassermann reaction was negative. A roentgenologic examination of the chest failed to reveal any evidence of disease. Cholecystograms were reported as showing normal gall lrladder function. The patient remained in the hospital for eight days., during which time gradual improvement \ras noted. During the first three days of the hospital stay he continued to complain of vague abdomimtl pain. At no time were there any c*omplaints refernl~le to the legs, an11 no olrjective signs were found in the lowet extremities. The patient was next admitted to the hospital .Jan. 24, 1934, approximately ten months after his first admission, with the history that his legs had become too weak to permit him to CRI’L’) on his previous work as a grocer’s clerk. He had also noticed that they l)erame lminful on walking. The pain and weakHe complained that his feet ness had been noticed in lesser degree in the arms. became cold more easily, and that epicritic sensation in the feet was diminished. “Ace” bandages applied to the legs had caused intolerable pain. About seven months before this second admission, the Jmtient be,
FRY
:
EMBOLISM
ASD
THROMBOSIS
OF
ABDOMISAl~
AORTA
59
The patient was next seen in the hospital twenty-three months later, NOV. 21, 1035. He said that for the preceding four days he had been short of breath. A cough which had been present for approximately one week had become worse and productive of bloody sputum, and was associated with pain in the anterior portion of the left chest. Hospitalization was advised when a marked pericardial friction rub was heard by his physician. The interval history was otherwise negative except for the continued presence of intermittent claudication. There had been no diminution in cardiac reserve noted during the preceding two years. The physical examination on this admission showed a dyspneic, pale, acutely ill, thin young man. Slight cyanosis and orthopnea were present. The pupils were slightly irregular but reacted normally to light and in accommodation. Evidence of marked hypertrophy of the left side of the heart was found; the lower outermost point of the apical impulse was in the sixth intercostal space, 14 cm. from the midsternal line. At the apex of the heart a marked pericardial friction rub was heard and gallop rhythm was present. There were a rough systolic and a high pitched diastolic murmur both at the apex and base of the heart. The blood pressure in the right arm was 190/100, and in the left arm 144,000. The blood pressure could not be measured in either leg. The lungs were The liver was dull to percussion, and there were moist rales at both bases. palpable below the costal border. It was not tender. Through the thin abdominal wall no pulsation of the abdominal aorta could be felt. It was noted that the femoral pulse on the right side was cerv weak, u-hile no pulsation could be felt on the left. The extremities were otherwise normal. The electrocardiogram shoa-ed sinus tachycardia, right axis deviation, and an auriculoventrieular conduction time of .14 sec. The T wave was inverted in l,eads I and II, and varied in T,ead III. The precordial leads showed evidence of pericardial eflusion, with depression of the ST segments in precordial T,eads II1 and IV (met.hotl of Wilson, with the right arm 112~1 wire connected to the exploring electrode). Laboratory Examination.-On admission, the urine showed a very faint trace of albumin and three red blood cells to the high-power field. Red blood cells were not found on subsequent urine examinations, but granular casts appeared shortly before death. The hemoglobin was 63 per cent, the erythrocyte count 3,650,000, and the leucocyte count 9,000, of which ‘ii per cent were polymorphonuclear cells. The urea nitrogen content of the blood was $2 mg. per cent. The blood sugar and creatinine values were IX and 2.2 mg. per cent, respectively. The blood culture on several occasions was sterile. Roentgenologic examination of the chest at the time of admission showed a large pericardial effusion and soft, scattered pulmonrtry lesions suggesting lobulai pneumonia. The findings were more market1 in the central portion of the left lung. The patient’s condition grew stetrdily worse. The leucocytes gradually rose to 23,000, of which 84 per cent were polymorphonuclear cells. For the first fete days the pericardial effusion was the predominant lesion. The friction rub remainell for forty-eight hours. However, when fluids were forced the azotemia diminishctl, and within two weeks the pericardial eff’usion had disappeared. The gallop rhythm at the apex of the heart persisted. The veins of the neck remained diatendetl throughout the entire hospital stay. Five days after admission the patient developecl signs of fluid in the right sidfk of the client, and etlenm of the ankles which was more marked on the left title than on the right; the dyspnea and cyanosis increased, and the liver became palpable ten centimeters belo\v the costal border. The patient was fully digitalized without effect. The orthopnea became more marked and the edema of the legs increased. The patient lapsed into semicoma and expired sixteen days after admission. The total duration of the illness had been thirtythree months.
60
THE
AMERICAN
HEART
The pertinent autopsy findings were as cavity 2,000 C.C. of bloody fluid were found right lung to the mediastinurn. Both lungs sizes.
follows: Upon opening the thoracic in the right pleural sac, pressing the were riddled with infarcts of various
The lining of t,he pericardium was smooth am1 glistening throughout, with no areas of roughening or inflammation. Fifty cubic centimeters of pericardial fluid were present. The heart weighecl 5(10 gm. The right auricle was normal. Enmeshed in the normal chordae of the tricuspid valve were found two large, extremely friable thrombi; the smaller one measuretl 1 cm., am1 the larger, ? cm., in diameter. The right ventricle and pulmonary valve were normal. Tht aortic valve was bicuspid, and the CUSPS were found to be thickened, producing :I hard, roughened, ragged, inelastic valve. At the tip of the larger (posterior) cusp t,here were very small, friable, well-organized vegetations. The wall of the left ventricle was markedly hypertrophied. The mitral valve and left auricle were normal. The liver weighed 1,735 gm., and the cut section of this organ showed chronic passive congestion. The gall bladder was large and distended; the walls were normal. A large, gray, friable thrombus was noticed at the junction of the hepatic vein and inferior vena cava. The spleen was small, shrunken, an11 of the fetal type. The pancreas was normal. The right kidney was large, of the fetal type, and weighed 217 gm.; this kidney was anomalous in that the main renal artery originated 2 cm. higher than The left kidney was small, weighing 70 gm.; on section, the left renal artery. the normal striations were lost, and the organ was of a darker hue than its fellow. The intercostal arteries, especially over the The arch of the aorta was normal. 1owTer half of the thorax, were slightly dilated. The thoracic aorta was not dilated, but showed more evidence of arteriosclerosis than is normal for a man Just below the diaphragm the aorta was occluded by an old, or21 years old. Between the apex of the thrombus ganized thrombus, covered with endothelium. One which was entirely patent, was found. and its base, the right renal artery, centimeter below this artery was the celiac axis, which was rompletely occluded by thrombus. Below the celiac axis was the left renal artery, which was found to l)e partially occluded. Immediately below the left renal artery the aorta shrank to a diameter of 2 cm. Both of the common iliac arteries were thrombosed in the aorta and iliac throughout their entire diameter (P’ig. 1 ). The thrombus A collateral circulation had vessels was identifietl as 0111 and well organized. Ibetween the tleep epigastric and internal pudendal been established, in part, arteries. Microscopic examination of the aortic cusps showed that the bicuspid condition as demonstrated by Bishop,9 was of congenital rather than inflammatory origin, the Weigert elastic fiber stain, using the technique of Lewis and et al., with Grant.lo Microscopic study of the aorta revealed severe sclerotic changes of the intima and media, with laminat,ed fibrinous thrombus filling the lumen. The lesions could not be identified by the pathologist as either syphilitic or rheumatic. CASE 2.--v. T., a housewife, 42 years of age, was admitted to the Nassau Hospital, Mineola, L. I., in November, 1937, following a cerebral achcident. The family history was negative. A history of rheumatic heart disease of two and a half was obtained. Eighteen months prior to admission she had had years ’ standing Five months later an embolus had an infarct of the lung, with a slow recovery. lodged in the left leg. This diagnosis was made because of coldness, pallor, and pain in the leg and foot, with inability to move the member. Within four months partial
FRY
function had only remaining
:
EMBOLISM
returned. symptoms.
ASD
Residual There
THROMBOSIS
OF
ABDOMISAJ,
AORTA
weakness and intermitt.ent elaudication was no involvement of the bladder.
61
were
the
Physical examination of the patient on admission showed a dyspneic and orthopThere was evidence of upper motor ncurone paralysis of neic middle-aged woman. the left side. The heart was enlarged; the lower outermost point of the apical impulse was felt outside the midclavicular line. There were a systolic and diastolic The ventricular rate wa!: murmur at the apex and a systolic murmur at the base. 100, the pulse rate 90. The blood pressure was 198/96. The spleen was not palpable. The liver was felt at the costal margin. The extremities were apparently normal. No discoloration was noted and the temperature of the legs was the same. There Whether or not femoral artery pulsations were present was not was no edema. ascertained.
Fig.
l.-Thrombosis
of the
abdominal
aorta
exten(ling
above
the
celiac
axis
(Case
1).
Laboratory Examinations.-The electrocardiogram showed auricular fibrillation. The urine was normal except for a faint trace of albumin and a few granular casts and leucocytes. The hemoglobin was 92 per cent and the erythrocyte count 5,360,OOO ; the leucocytes numbered 20,400, of which 78 per cent were polymorphonuclear cells. The blood culture was sterile on two occasions. The blood Wassermann reaction was negative. The third
patient hospital
remained in a state day with a rising
of semicoma ventricular
and delirium, dying on the twentyrate and body temperature. The
paralysis rcmainctl nn~~l~:tngfvl. Ku circ~ulatury c11an~w wr’c noted in the extremities throughout the entire 1)eriotl of hosl~italjz:Lti,,l1. At autopsy there wva.i :I zone of softening, 6 cm. iu diameter, in the right cerebral hemisphere, impinging on the lateral ventricle. The heart, showed a right ventricle three times the normal thickness, :I nlodrratrly thickened left rentri~~le, and an extremely stenotic mitral valve. On the* lmsterior leaflet of’ the mitral valve there were numerous, red, calcitic: granulations. There ,v:,.s an :/I lllerent thrombus in the left auricle. The aorta in the upper portion was normal for the age of the patient. &\t the level immediately lielow the ol,iyin of the renal arteries the lumen of the aorta was occluded by a soft, red, but arlherent, throtnbus. This thrombus became firmer and more tlenselj at.tachrd to the intinct of the aorta as the bifurcation was appro:K?lletl. At this level tile prowess WI?; well organized. The contents of the lumen were yellowish gray and appeared partly fibrous. The process continued uninterrupted into the common iliac arteries. The lungs showed diffuse congestion, but there was no evidence of pneumonia. The pleurae were covered by fibrous tissue; there was a small amount of fluid in both pleural spaces, from which the Type I pneumococcus was cultured. The spleen weighed 400 gm. and was grossly normal. The kidneys showed evidences of old infarction. The other organs were essentially normal. Microscopic examination of the heart failed to show typical Aschoff bodies. There were, however, numerous foci of dense fibrous tissue around the blood vessels of t,he heart muscle. Sections taken from that part of the aort:t wlliclt was completely thrombosed showed t.he lumen witlt ret1 thrombus adherent to tlie intima. Here the endothelium was deficient. The great part of the change Iay in the media, where there were diffuse engorgement and reduplication of the small vessels and widespread infiltration of these tissues by polymorphonurlear cells and phagocytes containing hemosiderin. The final diagnoses were rheumatic heart disease with mitral stenosis; mural thrombus of the left auricle; infarction of the right cerebrum; multiple old infarcts of the kidneys; acute fibrous and purulent pleuritis; diffuse mesaortitis; and endaortitis with thrombosis. The autopsy findings were a surprise. for thrombosis of the aorta in this case referable to the abdomen was not suspected because of the paucity of symptoms and legs. B., a Gyear-old nmn whore mother 11~1~1had hypertension, gave a CASE 3.-H. past history which was essentially negative except for rswssiw c.igarett,e smoking for many years. The present illness began tire years previously, when the patient noted :I sudden pain in the left leg which was localizetl to the foot and calf and was associated with coldness of that member. This condition kept the patient in bed for three months, during which time there was improvement with the use Thereafter the patient’s only symptoms had been interof Buerger’s exercises. mittent claudication and partial loss of epicritic sensation of the left leg until three years prior to admission, when he had a similar attack with gangrene and loss of a small portion of the medial side of the left great toe. The toe later regenerated completely. He was subsequently t,reated hy the Pavaex method, but Fifteen months earlier noticed no lessening of the intermittent claudication. 11c had hat1 coronary occlusion, recovery froul xlliclt was postponed by lobar plleumonia, the type :tnd sit.e of which were uuknoan to the patient. This ocr+lu*ion was folIowed by a ltilateral deep phlel)itis of the legs and 5 subsequent pulmonary embolus. Still later there occurred an attack characterized by severe abdominal distention and hiccough which was diagnosed as mesenteric thrombosis. All these events took place over a ten-month period, during which the patient
FRY
:
EMBOLISM
ASD
THRORlBOSIS
OIi‘
,~BDOMIS~~l,
AORTtY
63
However, during the was in a hospital in Canada practically the entire time. preceding four months he had been able to carry on his usual sedentary work as a writer, with no symptoms except intermittent claudication in both legs, worse an the left than on the right. There had been a loss of epicritic sensation in both feet. He had continued to smoke twenty to forty cigarettes a da) until his admission to the Naussau Hospital. Two weeks prior to admission, following a great deal of walking, he noticed early gangrene of the third, fourth, and fifth toes of the left foot. Examination on admission to the Nassau Hospital on March 22, 1038, showed a tall, spare, middle-aged man looking older than his years. The pupils were unequal, the right being larger than the left, but both reacted normally to light Examination of the eye grounds showed moderate arterioand in accommodation. The cervical veins were not distended. The sclerotic changes in the vessels. right, lung was normal, but a few moist Idles were heard at the base of the, I& lung. The heart was normal in size. The heart sounds ll-ere of fair quality at the apex and the base. There was a systolic murmur at the apex. The I~lootl pressure in both arms was 136/80. The blood pressure could not be measured in either leg. The cardiac mechanism was normal, and the rate was 110 beats a minute. Neither the liver nor spleen was felt. The abdominal aorta was palpable through the thin abdominal wall down to the level of the umbilicus, a-here There was marked sclerosis of the brachial and the pulsation abruptly ceased. radial arteries. There was a very poor femoral pulsation on the right side, but a fair pulsation of the left femoral artery was felt. No dorsalis pedis or posterior tibia1 pulsation was noted in either leg. There was dry gangrene of the left third, fourth, and fifth toes, with regional cellulitis extending to the ankle. The temperature of the legs was the same. The veins were prominent, but no varicosities were present. An electrocardiogram taken prior to admission showed changes typical of an old anterior wall infarction. Laljoratory Examination.-The specific gravity of the urine was 1.020; the urine contained no albumin or sugar. The blood Wassermann reaction was neg:ttive. The patient’s course in the hospital was characterized 1)~ slowly increasing dry gangrene of the entire left foot below the ankle, and by a sudden arterial occlusion in the right leg. This occlusion occurred seven days after admission, and resulted in a spreading dry gangrene of the right leg extending to midthigh. The patient was given the usual conservative treatment for gangrene, including alcohol by mouth, papaverine, tissue extract, generalized infrared light, and partially occlusive bandages to the leg. All treatment was to no avail. He became increasingly stuporous and “toxic” and had slight fever until the final week, when the temperature rose much higher. Death occurred suddenly eleven weeks after admission. The pertinent autopsy findings were as follows: External examination showed dry gangrene of the left leg below the ankle and of the right leg below mid-thigh. The lungs showed diffuse congestion. The heart weighed Bi.? gm. There was a definite increase in thicknfss of the wall of the left vcntrit*le. Moderatr generalized coronary sclerosis was present. The left descending coronary artery was found to he occluded and fibrosed by an old thrombus. At the apex of the left ventricle there was a large area of fibrosis, with an old, adherent, organized mural thromhus. There was no deformit,y of the valves. The heart, wax otherwise normal. The arch and thoracic portion of the aorta were normal, shoxing o,lly slight evidence of arteriosclerosis. There was no dilatation of the thoracic aorta and little increase in the diameter of the intercostal arteries. At the level of the
left renal artery the lumen of t,he aorta \q’as completeI>obstructed l)>- an organized thrombus, wit,h a svft, fresh extension into the superior mesenteric artery. The right renal artery ~vas patent, the left re11a1 artery l~artiall~occluded. The thrombus continue11 illto the common iliac arteries. The left iliac artery contained an old, white, organized thronlbw, and the right iliac arteq 1 was obliterated by a more recent, red, fllbrlnous thrornl)us (Fig. 2). There was very little evidence of collateral circulation. The upper pole of the left kidne?was scarred 1,~ a large infarct which showwl The right kidney \~‘:ts normal. various stages of healing. The liver and spleen were grossly normal. There was no evidence of Microscopic study of the ganization and no evidence was destroyed; the elastic Weigert stain.
Fig.
2.-Two
It is those in prising, and the abdominal bladder
stages
of
thronlhosis
gangrene or necrosis of the intestines. thromlnw at. the level of the renal artery showed orof reeanalization. The endothelial lining of the aorta layers were reduplicated, as demonstrated by the
of
akxlominnl
(Cme
3).
aorta
to the
level
of
the
renal
arteries
to compare the symptoms in these three cases with Rothstein’s series of seventy-two cases (Table I). It is surin view of the high extent of t,he thrombus in all three casts, organization present at the high level in two of these, that symptoms were not more marked and that spinal cord and symptoms were not present in any case. The symptoms
interesting
FRY :
EMBOLISM
AND
THROMBOSIS
OF
ABDOMIKAI.
65
AORTA
in all three cases were caused by slowly decreasing blood supply. It is interesting to note that in two of t.he cases the abdominal aorta was found to be abnormal before death. This observation alone served to indicate the high extent of the lesions. TABLE SYMPTOMATOLOGY
OF PARED
I
OCCLUSION OF THE AORTA IN ROTHSTEIX'S~ WITH THAT IN TIIE 3 CASES HERE REPORTED
A. MANIFESTATIONS EXTERMITIES
IN
LOWER
PER
1. Pain in legs 2. Loss of nulsation in arteries of lower extremities 2. Cyanosis or discoloration of lower extremities 4. Edema of lower extremities 5. IXsturbances in sensation of lower estremities 6. IXsturbances of muscle power of lower extremities 7. Preceding embolic phenomena in peripheral arteries of lower extremities 8. Intermittent limping 9. Disturbances in circulation beginning in one, and then in the other, extremity 10. Evidences of gangrene in lower extremities a. Involving only the right lower extremity b. Involving only the left lower eatremity c. One lower extremity (aide not noted) d. Involving both lower extremities B. MANIFESTATIOKS OF ABDOMINAL
1. 2. 3. 4. 5. Ii. 7.
CASES
Coar-
CASES
1
2
-3
44.4 40.3
t t
t 2
t +
22.2
0
0
t
ti.9 40.3
t t
0 t
0 t
30.0
t
t
+
-.“8
0
t
.I
2.8
t
t
t
lti.ti
t
t
t
67.0
0
0
t
12.5 19.4 1.4 2::.7
OF INVOLVEMENT ORGANS
Pain in the abdomen Pain in the back Loss of pulsation of abdominal aorta Incontinence of urine Retention of urine Incontinence of flatus Hemorrhage from anus and urethra Presence or absence of symptoms inclicxte~l
('EPI'T
70
PER
('EST
11.1 3.6 69 cj.9 2.8 4.3 x.?, by
+ or
+ 1
CASES 2
n
t t t 0 0 0 0
0 0 2 0 0 0 0
t t t 0 0 0 0
0.
The fundamental lesions in all of these cases were different, but all led to the same terminal condition in the aorta and iliac arteries. As is noticed from the description in the microscopic reports, the endothelial wall of the aorta around the thrombus was destroyed in all cases. It is impossible to differentiate primary infection of the arterial wall from nonspecific reaction in cases of complete obstruction of long duration. In Case 1, the congenitally bicuspid aortic valve with roughening and organized small vegetations may have been a nidus for small emboli. -“Jo doubt the cerebral signs in this case mere cmholic. The symptomatology and course in this case were essentially that of progressive thrombosis superimposed upon small rmholi. The long duration of life was l)ossihle only because of the anomalously high origin of the right renal
artery. In the second case, a mural thrombus in the fibrillating left auricle was t,he source of emholi. again with progressive superimposed thrombosis. In the third cast the etiology was atherosclerosis, and the case was somewhat simiIar to one reported by Rosenberg,ll et al. The use of the Weigert elastic stain was helpful in demonstrating the reduplication of the elastic fibers found in nthcrosclerosis.
Three eases of embolism and complete thrombosis of t,he abdominal aorta are reported ; the fundamental lesions were ctiologically different, but they all produced pract~ically identical gross and microscopic changes in the aorta. The patients survixed from one to five years after the onset of occlusive sympt,oms. Two of the t,hree patients showed no evidence of gangrenc in spite of the high level of the lesions. These cases are reported to demonstrate, in addition to the unusual and widespread lesions, the ability of the circulatory system to adapt itself t,o a gradually occluding process, and to emphasize the fact that estensivc pathologic changes may occur in thr large vessels of the body with only minor symptoms. REFERESCXS 1. Rothstein. Jacob L.: Embolism and Thrombosis of the Abdominal Aorta in Infancy and in Childhood, Am. J. Dis. Child. 49: 1.578, 1935. ?a. Gull and Chvostek: Wiener Med. Rhitter, p. 1513, 1881. Ph. Nunez: Gaz. Med. de la Habana II,’ p. 160,’ 18i9-80, quoted by Welch (reference 8). Zur Frage des vollstLndigen Ver3. Derman, 0. L., and Dutkewitsch, E. A.: sch1usse.s des unteren Teiles der Bauchaorta, Tirehow’s Arch. f. path. Anat. 274: 535, 1929-30. 4. van der Beek: Een gelal van thrombose ~-an de lunkaorta. Nederl. tiidschr. v. geneesk. 76: 433i, 1932. Hvad kan over 6000 Obduktioner lare os om embolia resn. gnngraena 5. Bull. P.: er’nbolica extremitatium? Norsk. maa. f. laenevidensk. 83: 1?3.-1922. in the Diagnosis, Prognosis and 6. Rykert, H., and Graham, I). : Some Problems Treatment of Acute Arterial Occlusion, AX. HEART J. 15: 395, 1938. i. Hesse, E.: Ueber die Embolie und Thrombose der Aorta abdominalis und ihre operative Behandlung, Arch. f. klin. Chir. 115: 812, 1921. 8. Welch, W.: Embolism and Thrombosis, In Albutt, I. C., and Rolleston, H. D.: System of Medicine, Sea Pork, vol. 6, p. 809, 1909, The Macmillan Company. 9. Bishop, Louis E’augeres, Bishop, Louis Faugeres, Jr., and Trubeck, Max: Aortic Stenosis of Inflammatory Origin With a Differential Study of the Acquired or Congenital Origin of a Bicuspid Aortie Valve, Bm. J. M. SC. 188: 506, 1934. 10. Lewis, T., and Grant, R. T.: Heart 10: 21, 1923. I I. Rosenberg, E. T., Keith, M. M., Wagener, H. P.: Diffuse Arterial Disease With Hypertension, Arch. Int. Med. 62: 461, 1938. ci