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Abdominal apoplexy
Abdominal Apoplexy Report of Two Cases and Review of the Literature LeROY J. KLEINSASSER, MD, Dallas, Texas
Spontaneous intra-abdominal bleeding r a r e l y occurs, but m a y be extensive and life-threatening. Even m o r e uncommon is r e t r o p e r i t o n e a l hemorrhage f r o m a b r a n c h of a splanchnic vessel. This has been called abdominal apoplexy, but the term is retire broadly used to encompass spontaneous inira-abdominal h e m o r r h a g e . Abdominal apoplexy has been so named because its n a t u r e and sponta~eity closely resemble those of its more common cerebral c o u n t e r p a r t , t I a r t l e y an(1 5IcKechnie [1] su~rgested the term, splanchnostaxis, f o r this condilion, but the t e r m has not gained acceptance. Barber [2! in 1909 is credited with the earliest reported case of abdominal apoplexy. D u r i n g labor, a t h i r t y - t w o y e a r old woman was delivered of a full term chi!d. Increasing abdominal distention developed and two (lays post I)artum, " t y m p a n i t e s " increased and she was explored. Dark blood was found but no bleeding site was detected. She recovered. and the surgeon surmised t h a t tile bleeding must b a r e c o m e from some vein in the pelvis. Although it is repeatedly reported t h a t F l o r e n c e 'rod I)ucuiP, g [13] were the first to describe the condition clearly, actually t h e i r case was a man with hemop e r i t o n e u m a f t e r a contusion of the kidney f r o m a fall, while drunk, a g a i n s t a bed made of a block of woo(l. It was postulated that t h e r e was a t e a r of the p o s t e r i o r peritoneum with bleeding into the peritoneal cavity. The patient had h e m a t u r i a and hemoperitoneum. The l a t t e r was substantiated by a p u n c t u r e of the cul-de-sac of Douglas by tile perineal route in a male. The p a t i e n t refused to undergo s u r g e r y and recovered. This p a t i e n t obviously did not have a spontaneous h e m o r r h a g e . The r e p o r t is not a b o u t " a y o a n g woman, eight months p r e g n a n t " with a r u p t u r e d b r a n c h of the s u p e r i o r mesenteric a r t e r y as r e p o r t e d in the lite r a t u r e [4]. The first case substantiated by p o s t m o r t e m examination w a s r e p o r t e d by S m i t h [5] in 1911. A thirty-five y e a r old woman, nine m o n t h s p r e g n a n t , had abdominal pain a f t e r some s t r e n u o u s activity. She died t w e n t y m i n u t e s a f t e r examination. PostFrom the Depa~ments of Surgery, Baylor University Medical Center and Presbyterian Hospital of Dallas, Dallas, Texas. Presented at the Twenty.Second Annual Meeting of the Southwestern Surgical Congress, Dallas, Texas, April 20-23, 1970. Volume 120, November 1970
m o r t e m study showed the tissues behind the gastrosplenic ligament " c o n s i d e r a b l y ecchymosed and torn up." As f a r as could be determined by dissection, "a b r a n c h of the splenic a r t e r y had given w a y j u s t before it got t,o the hilum." No a t h e r o m a was present in the vessel. T h e t e r m abdominal apoplexy was first coined by Green and P o w e r s [~] in 1931. Crile and Newe]l [6] in 1940 are credited with m a k i n g the first c o r r e c t p o s t o p e r a t i v e diagnosis of abdominal apoplexy. The bleeding point was not found, but it was assumed this was a b r a n c h of t h e celiac a r t e r y . The ease is suspect because it closely followed celiac ganglionectomy. My attention was directed to this condition by two patients successfully o p e r a t e d on ; the bleeding site was located and controlled with r e c o v e r y o f the patients. In most instances the diagnosis is m a d e a f t e r l a p a r o t o m y or at autopsy.
Case Reports CASE I. A forty-seven )'ear old woman (WBS) was admitted to Presbyterian Hospital of Dallas on February 11, 1968, with the sudden onset of abdominal pain and vomiting of twenty hours' duration. This became worse and she entered the Emergency Room in shock. The abdomen was silent, there was abdominal tenderness most marked in the right upper quadrant, and there was no muscle spasm. A vague aMominal mass was felt. Peh, ic examination gave negative results. Roentgenograms of the chest and abdomen were relatively within normal limits. No blood pressure was obtainable on admission, but rose to 90/60 mm Hg after she was given an intravenous infusion of Ringer's lactate solution. The hematocrit was 26 per cent. She was operated on as an emergency with a preoperative diagnosis of intraperitoneal bleeding. Laparotomy disclosed much intra- and retroperitoneal blood. The blood had extravasated widely to include the leaves of the mesentery of the bowel. I was called into consultation and continued the operative procedure. Tim aorta was first exposed to exclude the possibility of a leaking aneurysm, but the aorta proved to be normal. Further exploration revealed a mass posterior to the head of the pancreas. Th~ duodenum and head of the pancrea s were mobilized by the Kocher maneuver. A large clot was extracted from under the head of the pancreas and this was followed by a gushing hemorrhage which could be controlled by manual compression. The exposed bleeding 623
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vessel, the i n f e r i o r p a n c r e a t i c o d u o d e n a l a r t e r y , was ligated and sutured. I 2 n f o r t u n a t e l y . no specimen of the a r t e r y was obtainable. T h r e e d r a i n s w e r e i n s e r t e d and brought; out t h r o u g h a lateral stab wound in t h e upper p a r t of the abdomen and the midline incision closed. D u r i n g s u r g e r y she received 4 units o f blood and 4,500 ml of R i n g e r ' s l a c t a t e solution i n t r a v e n o u s l y . Nasog a s t r i c suction, i n t r a v e n o u s fluids, and a n t i b i o t i c s were employed postoperatively. T e m p e r a t u r e r e t u r n e d to normal. I n t e s t i n a l p e r i s t a l s i s developed on the f o u r t h day, t h e Levin tube was removed, anti she was fed. The s e r u m a m y l a s e rose to 815 u n i t s on the fifth (lay, but felt below 500 units by the eleventh clay. T h e h e m a t o c r i t rose to 35 p e r cent. T h e d r a i n s w e r e manipulated and finally removed on t h e eleventh postoperative day. She was d i s c h a r g e d on the t h i r t e e n t h day in excellent condition. She was s u b s e q u e n t l y r e a d m i t t e d to P r e s b y t e r i a n Hospital on A p r i l 28. t968 with a t r i m a l l e o l a r f r a c t u r e of the r i g h t ankle t r e a t e d by open reduction. She did well and was asyn',ptomatic from the a b d o m i n a l surgery. She was d i s c h a r g e d on May 4, 1968. She has h y p e r t e n s i o n and the blood p r e s s u r e was found to be 186'110 mm t t g on admission, f a l l i n g to 150/110 m m H g a f t e r bedrest. CASE lI. A sixty-five y e a r old w o m a n ( E P H ' ! was a d m i t t e d to Baylor U n i v e r s i t y Medical C e n t e r in Dallas as an e m e r g e n c y on N o v e m b e r 17, 1969 w i t h a t e n t a t i v e d i a g n o s i s of closed loop i n t e s t i n a l o b s t r u c t i o n . At 113 AM the previous clay she b e g a n to have l o w e r abdominal pain. The pain p e r s i s t e d with i n c r e a s i n g s e v e r i t y during the n i g h t w i t h i n t e r v a l s of d i s c o m f o r t l a s t i n g five to ten m i n u t e s . S h e experienced some n a u s e a and vomited. T h e pain w a s in the lower p a r t of t h e abdomen and s u p r a p u b i e area. In the past she had an appendectomy as welt as p a r t i a l g a s t r i c r e s e c t i o n and cholecystectomy in 1940. T e m p e r a t u r e was 98.2 ':~ F. pulse 106, and blood pressure 130,90 mm Hg. The abdomen was q u i e t and t e n d e r t h r o u g h o u t . T h e r e was left rectus muscle g u a r d i n g at the level of the umbilicus and t h e question of a mass b e n e a t h it t h o u g h t to be small bowel w i t h possibly v a s c u l a r i m p a i r m e n t . The h e m a t o e r i t w a s 40 per cent, w h i t e blood celt c o u n t 10,200 mm:L and t h e r e w e r e 82 p e r cent p o l y m o r p h o n u c l e a r n e u t r o p h i l s in t h e diff e r e n t i a l count. S u p i n e and u p r i g h t r o e n t g e n o g r a m s of the abdomen g a v e n e g a t i v e results. T h e l e f t psoas shadow was distinct, b u t the r i g h t one was n o t seen clearly. She was operated on as an e m e r g e n c y t h r o u g h a midline incision. T h e s u r g e o n found an e x t e n s i v e r e t r o p e r i t o n e a l h e m a t o m a . I was called in c o n s u l t a t i o n and continued the operation. F u r t h e r e x p l o r a t i o n revealed no a o r t i c a n e u r y s m , but disclosed a r u p t u r e d l e f t colic a r t e r y with a clot which had been o c c l u d i n g a slit app r o x i m a t e l y 1.5 em long in the a r t e r y , t h e source of h e m o r r h a g e . T h e involved a r t e r i a l s e g m e n t , 2 cm long, was resected and t h e vessel ligated. C o n s i d e r a b l e f r e e blood and r e t r o p e r i t o n e a l clot w e r e removed. Postope r a t i v e l y the p a t i e n t did well except f o r a t r a n s i e n t period o f psychosis. S h e was d i s c h a r g e d eleven days 624
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Fi£ure 1. ARe incidence. p o s t o p e r a t i v e l y and has done well. S u b s e q u e n t e x a m i n a tion has disclosed that she has h y p e r t e n s i o n witt~ a blood p r e s s u r e of 168'1 t0 mm Hg. Clinical
Material
E i g h t y - t h r e e cases have been selected f o r analysis, e i g h t y - o n e f r o m the l i t e r a t u r e [I.2.~-6t] and two from my o w n experience. A l t h o u g h o t h e r cases hav~:~ been tabulated, the i n f o r m a t i o n and d o c u m e n l a t i o n a r e so incomplete that the.',' are not acceptable for review. T h e r e w e r e f o r t y - s i x male and t h i r t y - s e v e n female subjects v a r y i n g in a g e f r o m two to e i g h t y - f o u r years w i t h the g r e a t e s t incidence in the fifty to fifty-nine y e a r range. ( F i g u r e 1.) The age was not stated in two reports. T h e illness usually began suddenly and c h a r a c t e r istiealiy was of b r i e f d u r a t i o n . In forty-five of t h e sixtyseven cases in which the d u r a t i o n of illness was recorded, t h e r e was a h i s t o r y of t w e n t y - f o u r hours or less p r i o r to admission a l t h o u g h e i g h t e e n had a h i s t o r y up to seve.n days. A b d o m i n a l pain was by f a r t h e first s y m p t o m o e e u r r f n g in s e v e n t y - f o u r of s e v e n t y - e i g h t eases in which t h e initial s y m p t o m is reported. Abdominal distention occurred as an initial s y m p t o m in two. back p a i n in one. and g a s t r i c d i s t r e s s in one. T h r e e p a t i e n t s died suddenly w i t h o u t p r e m o n i t o r y symptoms. The pain was generalized in t w e n t y - e i g h t , in t h e u p p e r part of the abdomen in t h i r t y - o n e (thin'teen of whom had e p i g a s t r i c p a i n ) , in the m i d p o r t i o n of t h e abdomen in t h r e e (in one of w h o m it: was described as p a r a u m b i l i c a l ) , and in the lower p a r t of the abdomen in twelve. F i f t y experienced abdominal t e n d e r n e s s of whom t h i r t y - t w o had g e n e r a l i z e d tenderness, t w e n t y n i n e showed a b d o m i n a l d i s t e n t i o n , fifteen had abdominal r i g i d i t y , and ten had muscle g u a r d i n g . T h i r t y - f o u r had some evidence of . hock d u r i n g t h e course of t h e i r illness. S i x t y - s i x w e r e o p e r a t e d on and seventeen w e r e n o t o p e r a t e d on. Of t h e s i x t y - s i x o p e r a t e d on, no p r e o p e r a t i v e d i a g n o s i s was g i v e n in t h i r t e e n cases. T h e m o s t frequent preoperative diagnoses were intraperitoneaI h e m o r r h a g e , acute i n t e s t i n a l o b s t r u c t i o n , r u p t u r e d peptic ulcer, appendicitis, m e s e n t e r i c thrombosis, and r u p t u r e d eetopic p r e g n a n c y . (Table I.) A t operation, all e m e r g e n c y , f r e e i n t r a p e r i t o n e a l blood was found in fifty-one, none in ten, and n o t s t a t e d in five. T h i r t y - n i n e had r e t r o p e r i t o n e a l bleeding, The
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o f Surl~e~'y
Abdominal Apoplexy
twenty-two showed no evidence of retroperitoneal bleeding, and the presence of bleeding was not stated in five. The amount of free blood varied to as much as 3 L. Of the sixty-six o~'Jerated on, twenty died (30.3 per cent) ; the bleeding source was found in thirty-five patients and thirty-two of these recovered. Three died !8.6 per cent}, one of a myocardial infarction. Of the twenty-five in whom the bleeding source was not found, eleven recovered and fourteen died (56 per cent). There were six in whom hematoma was present at the base of the mesentery. No vessel was ligated and three ~}f these patients died and three survived. Autopsy was performed in thirteen of the sixty-six patients operated on and the bleeding vessel was located in six and not found in seven. In four, no autopsy was permitted. Of the eight, y-O~ree collected cases, there were thirty-seven deaths, a mortality of 44.6 per cent. Of the seventeen patients not operated on, all died. The vessel responsible for bleeding in the eightylhree eases varied. I Table II.') The most common sources were the gastr;,c arteries in ten cases, the
TABLE I
Preoperative Diagnosis in Sixty-Six Operations
Diagnosis Intraperitoneal hemorrhage Acute intestinal obstruction Ruptured peptfc ulcer Appendicitis Mesenteric thrombosis Ruptured ectopic pregnancy Perforated stomach or acute pancreatitis Acute pancreatitis Ruptured aortic aneurysm Abdominal apoplexy Miscellaneous No preoperative diagnosis Total TABLE II
Number 11 7 6 6 5 4 3 2 2 2 5 13 66
Source of Bleeding Source of Bleeding
Celiac axis Splenic artery Hepatic a~ery Right gastric artery Left gastric artery Gastroduodenat artery Inferior pancreaticoduodenal Left gastroepiploic artery Superior mesenteric artery Middle colic artery Right colic artery Left colic artery Ileocolic artery Inferior mesenteric artery Appendix epiploic artery Renal artery Hematoma of mesentery Cul-de-sac and broad ligament U ndetermined Total
Volume 120, November 1970
Number 1 5 t 3 7 3
3 2 5 8
1 3 4 2 1 1 7 3 23 83
middle colic artery in eight, the splenic artery ir~ five. and the superior mescn ~ric artery in five. No source of bleeding was found in twenty-three and this group presented the highest mortality,
Comments
Although massive intra-abdominal hemorrhage w i t h o u t g r o s s a b d o m i n a l disease is r e f e r r e d to as s p o n t a n e o u s , it is unlikely t h a t this can o c c u r w i t h o u t an u n d e r l y i n g o r g a n i c lesion. H y p e r t e n s i o n w a s r~corded as being p r e s e n t in t h i r t y - t h r e e pat i e n t s (39.8 per cent) in the collected series a n d is c o n s i d e r e d a definite f a c t o r . In addition, since m a n y of the r e p o r t e d p a t i e n t s w e r e in shock w h e n first seen, it is likely the incidence of h y p e r t e n s i o n is h i g h e r . A l t h o u g h a r t e r i o s c l e r o s i s is s t r o n g l y implicated in the older patient, it c a n n o t a p p l y to the m u c h y o u n g e r p a t i e n t a n d did not exist as a c a u s e in m y second patient. T h e r e is a g r o w i n g b o d y of evidence t h a t this is likely due to an a n e u r y s m res u i t i n g f r o m a d e v e l o p m e n t a l d e f e c t in the a r t e r y . T h e c o n c e p t t h a t a n e u r y s m s in some cases m a y be due to c o n g e n i t a l o r d e v e l o p m e n t a l d e f e c t s w a s first s u g g e s t e d b y E p p i n g e r in 1887 [19]. F o r b u s [62] in 1930 d e m o n s t r a t e d t h e a s s o c i a t i o n of cerebral a n e u r y s m s w i t h a c h a r a c t e r i s t i c d e f e c t in the t u n i c a m e d i a of the a r t e r i a l wall at the a n g l e f o r m e d by the b r a n c h i n g of vessels. T h e d e f e c t consists of an i n t e r r u p t i o n in t h e m u s c u l a r coat at the p o i n t o f b i f u r c a t i o n of m e d i u m sized a r t e r i e s w h o s e a d v e n t i t i a and i n t i m a a r e intact. H e concluded these defects w e r e d e v e l o p m e n t a l in origin. S i n g l e and m u l t i p l e a n e u r y ~ m s h a v e been d e s c r i b e d in o t h e r a r t e r i e s , such as t h e splenic, hepatic, a n d renal, in w h i c h no i n f l a m m a t o r y or d e g e n e r a t i v e c h a n g e s could be found. Since s i m i l a r d e f e c t s occ u r in the s p l a n c h n i c vessels, it is p r o b a b l e that: some o f these a n e u r y s m s h a v e developed in association w i t h such defects, A l t h o u g h the d e f e c t i~ the m e d i a and i n t e r n a l elastic l a m i n a m a y be located e l s e w h e r e t h a n at the b i f u r c a t i o n ( b r a n c h ing) of vessels, o t h e r s [1g,22,52,62] h a v e subseq u e n l l y s u p p o r t e d this concept. T h e a s s o c i a t i o n o f c e r e b r a l m i t i a r y a n e u r y s m s a n d s p l a n c h n i c vessel i n w ) l v e m e n t in the s a m e p a t i e n t d e s c r i b e d by N e v i n a n d W i l l i a m s [ 19] f u r t h e r lends c r e d e n c e U~ this t h e o r y . H o w e v e r , G l y n n [64] believes t h a t ~he m o r e f r e q u e n t o c c u r r e n c e of a n e m - y s m s of the Circle o f "~Villis is m o r e likely related to differences in the t o p o g r a p h y o f the elastic tissue o f the vessels. In c e r e b r a l vessels a l m o s t the who]e of t h e Elastic tissue is c o n c e n t r a t e d in t h e i n t e r n a l elastic l a m h m a n d b y r e a s o n of this position is p r o b a b l y m~,re ~us-. ceptible to i n j u r y a n d dEgenEration t h a n if it w e r e m o r e w i d e l y d i s t r i b u t e d t h r o u g h the m e d i a anti ~
Kleinsasser
Figure 2. A, Verhoff elastic tissue stain showing the a b ru p t change from a relatively normal wall to the markedly thinned wall, There is toss of the internal elastic lamina and necrosis and inflammation of the markedly thinned media. There is
adventitia as in o t h e r vessels. It: has also been suggested t h a t an unrecognized acquired lesion m a y be causing degeneration of elastic tissue [65]. In the second ease r e p o r t e d by me, the a r t e r y a d j a c e n t to tile r u p t u r e d vessel was normal, and the p e r f o r a tion a p p a r e n t l y did not occur at the site of a r t e r i a l branching. However, tile histologie findings clearly indicate the u n d e r l y i n g lesion which involves tile media and the internal elastic ]amil{a. The histologic changes s t r o n g l y suggest tile r u p t u r e of a thrombosed a n e u r y s m . The internal elastic lamina and the media were deficient in most of the vessel. These changes n e v e r involved the e n t i r e circumference. The adventitia was intact except at the site of r u p t u r e . T h e thinned o u t e r media was focally necrotic and infiltrated by p o l y m o r p h o n u e l e a r leukoeytes. When present, the internal elastic lamina was wrinkled and slightly t h i c k e n e d ; the intima showed minimal fibrosis. The change f r o m the normal thickness to the thinned media was usually a b r u p t but sometimes gradual. Necrosis of the o u t e r media often extended a s h o r t distance into the a d j a c e n t wall. The blood clot proved to be a t h r o m b u s with a central lumen. ( F i g u r e 2A and B.)
It is postulated t h a t the media became t h i n o r was deficient in p a r t of the c i r c u m f e r e n c e of the a r t e r y , and with dilatation of the vessel t h e r e w a s disruption of the intima and the internal elastic lamina f o r m i n g an a n e u r y s m which filled with clot and likely had a central lumen. Finally the external elastic lamina and a d v e n t i t i a gave way. T h e clot was extruded and h e m o r r h a g e ensued f r o m rupture of the a n e u r y s m . * 626
hemorrhage beneath the external elastic lamina with appearance of dissection beneath the n~edia, (Orip, itlal maf~nification X 100,) ~, a complete cross section of the thromhus demonstrating the smooth outer contour and central lumen. (Original magnification >~ 4.)
Necrotizing a r t e r i t i s associated with p e r i a r t e r itis nodosa [5x] m a y produce an anem-ysm which CiIll l'ttl)ttll'e ;t|1(t t)rodllce illlral)el'it(HlPal
hPmor-
rhage. Polyarteritis n(~s~ is an inflammatory disease of unknown c~ltlSe wilh segmental involvement of small and medium sized arteries. HistoloKieally the disruption of the media with cellular inliltation and later fibrosis involves all coats of the vessel and prcdisp(~ses 1o thrombosis and to aneurysm formation. It has been slated that lhe vessels of the gastrointestinal tract are involved in a maj o r i t y of cases and t h a t most often this involvement is near the mesenteric a t t a c h m e n t to the intestine and the j u n c t i o n s of medium sized vessels in the mesentery. I n t r a p e r i t o n e a t h e m o r r h a g e has been reported f r e q u e n t l y [57]. Spontaneous i n t r a p e r i t o n e a l h e m o r r h a g e m a y occur d u r i n g p r e g n a n c y or puerperiunL The maj o r i t y of r e p o r t s indicate t h a t i n t r a p e r i t o n e a l hemo r r h a g e d u r i n g p r e g n a n c y is most likely to originate in the spleen, splenic vessels, pelvic vessels, or varicosities [(;6]. Although it does not fulfill the exact c r i t e r i a f o r abdominal apoplexy, r u p t u r e of a sptenie a r t e r i a l a n e u r y s m is the best known source of such bleeding [67,63]. If this source is arterial, the site of r u p t u r e may a p p e a r normal s t r u c t u r a l l y or it m a y show a defective media or a n e u r y s m a l dilatation. Massive spontaneous intra-abdominat bleeding m a y be r e t r o p e r i t o n e a l , intraperitoneal, or both. Usually the bleeding originates in a splanchnic yes* These inte:'pretatio.~ts were made b y D r William K i n g s . Icy, Pathologist, Baylor University Medical Center, Dallas, Texas. The American Journal of Surgery
Abdominal Apoplexy
sel nnd is retrot)eritoneal. Occasionally the prosSlll'(~ ()I" btec'dinK will Iirodtlee. a teal" ill the l)eriloncum with nmre extensive hemorrhage. I f the bieedinK is r e t r o p e r i l o n e n l , the s i g n s m a y be lll;ISketI; }lowever, Wilell" tile b l e e d i n g o c c u r s directly inio tim peritoneal cavity, there will be signs iJI~t)eribuleal irritation. Tile sudden ollset of sevot'e alJ(lOlllilia] pain, often followed rapidly by shock anti tile sil,rl/S of ill(oriu/l bteedinT, is the c h i e f llOint in the diaKnosis. Peril.olmal tap [69] IllAy be }letl)ful ii~ col}firndnK tile diaKnosis of bleediilK if." bleediilK is not restricled to the retrol)eritoneal li Fell. ,'%it }l(;lllg}l select;ire meselll erie arteriogrAphy [?0] nliK}lt, be helpftl] ill Ioeaiizin7 tile b l e e d i n g site, survery ustlally cannot be postponed. A large part ill l.he dia.~nosis of a b d o n l i n a l a p o p l e x y d e p e n d s orl a hi.~rh illdex of stispieion. Tim t r e a t m e n t is s u r g i c a l 'lad e x p i o r a l i o n should l~e emv.hleled wiill the p a t i e n t ' s blood p r e s s u r e raised s,} It]at the b l e e d i n g s o u r c e call be fotlnd. 'lT}le e x l H o r a l h m is best p e r f o r m e d w i t h a knowle~ige o f tile a r t e r i e s m o s t e o m n l o n t y inwflved in this disease, l:f the bleed)ate point is not apparent, t h e r e should tm a c a r e f u l i n t r a p e r i t o n e a ] s e a r c h iliciudiilg the diatdn'aKm, i.}le Kastrollepntie o m e n {tlrli, lesser sac, sph,nic area, pelvis, And fhlally tile rci.l'olmritoneal area. A large portion of the retroperitoneal s p a c e can be e x p l o r e d by incising the p o s t e r i o r p e r i t o n e u m o v e r tile a o r t a , r e t r a c t i n g the l r a n s v e r s e colon s u p e r i o r l y and i;he small bowel to the r i g h t as well as mobilizillg the d u o d e n u m And the }lead of the p a n c r e a s 1)3, tile K o c h e r m a n e u v e r . Frc'qtleritly the b l e e d i n g will h a v e s t o p p e d , as a restilt of e i t h e r the fall ill blood p r e s s u r e o r the f o r m a t i . n o f a t h r o m b u s w h i c h will only t e m . p o r a r i l y cold.r-1 t h e bleeding. I t is i m p e r a t i v e thai the bleedinv site be f o u n d and t h e vessel tigated as i n d i c a t e d by this eolteeted series in which f a i h u ' e to find the s o u r c e resulted ill a m o r t a l i t y of 56 p e r cent in c o n t r a s t to a m o r t a l i t y of 8.6 p e r cent if the bleedillg source was follild. Ill v i e w of the p o t e n t i a l i t y f o r l i f e - t h r e A t e n i n g F,e m o r r h a ~ e , it is u r a e d t h a t sl)lanehnle Arterial a n e u r y s m s be reseeted p r o p h y l a c t i c a l l y r e g a r d l e s s of t h e size when d i s c o v e r e d d u r i n g v i s c e r a l angio~;r a t ) b y or at:, l a p a r o t o m y f o r a n y c a u s e .
vessels responsitHe f a r hleedin~,'. 3. S i x t y - s i x cases in w|:ich Olmralion w a s tmr fol'tll(:d Iil'O SlllllIllal'izeit itleill(lillK t he pr(,oper:~tive diaKnoses. (ipcl'ative findings, and m o l ' i a l i t v . ,I. Tllere w e r e t h i r t y - s e v e n d e a t h s (.11.(i p v r c e n l ) in tim e i g h t y - t h r e e collected eases. O f s i x i y six p a t i e n t s o p e r a t e d ml, lweniy died (?,0.:{ per c e n t m m ' t a l i t y ) . I f the 1)teedinK source w a s o r e trolled, only t h r e e of t h i r t y - l w o died (g.6 p e r c e n t ) . T h e bleedin~e source w a s nut fmlnd in t w e n t y - f i v e and r . u r t e e n died (56 p e r c e n t ) . :3. It is n i a l l d a i o r y t h a t tile bleedin~ source. which m a y be i n t r a p e r i l o n e a l or r e t r ~ p e r i t o n e a l , tie located And oral rolled. 6. I t is til'ged t h a t All all?ttl'Vsnls l a w ) l y i n g the sl)lAtlehUie vessels be reseeted prol~llylaetieally. References 1. Hartley H, MacKechnie DM: A case of "sptanchnosta×is." Lancet 1: 289, 1934. 2. Barber MC- Intraabdomirlal hemordlage associated with labor. Btit M e d J 2: 203, 1909. 3. Florence and Ducuing: Contusion du rien. H~mopi}ritoine. Gu(~rison spontanee. Valeur diap_.nostique de la fonction exploratrice du cubde+sac de Douglas. Bull M~m Soc Chit Paris 39: 645, 1913. 4. Green WT, Powers JH: tntraabdominal apoplexy. Ann Surg 93: 1070, 193t. 5. Smith HBW: A fatal case of intraperito~mal hemorrhage from an unusual source. Brit M e d J 1: 83, 1911. 6. Crile G Jr, Newetl ET Jr: Abdominal apoplexy; spor~taneous rupture of a visceral vessel. JAMA 114: 1155,
1.940.
7, Churchman JW: Spontaneous intraperitoueal 8. 9. 10. 11.
12. 13. 14, 15, 16,
Summary
1. T w o eases of a b d o m i n a l Apoplexy s u c c e s s f u l l y n l a n a g e d a r e repro:ted w i t h the m i c r o s c o p i c findings in one ease i n t e r p r e t e d a s s h o w i n g an u n d e r lying lesion in the m e d i a And s t r o n g l y s u g g e s t i n g r u p t u r e of A t h r o m b o s e d a n e u r y s m . 2. E i g h t y - o n e collected eases a n d t w o f r o m m y e x p e r i e n c e a r e r e v i e w e d to i n d i c a t e the Age incidence, c h a r a c t e r i s t i c s y m p t o m s and findings, a n d Volume 120, November 1970
17,
18.
hemor-
rhage. A m e r J Med Sci 142: 825, 1911. Hilliard JW: Spontaneous hemorrhage into the peritoneal cavity in arteriosclerosis. Brit Med J 1: 231, 1918. Starcke G: Spontaneous rupture of gastrodllodel~al artery. Ugesk Laeg 85: 963, 1923. Cited by Green WT and Powers JH [4]. Budde M: Operativ Geheilte spontanruptur der Arteria gastroapiploica sinistrs. Munchen Med Wschr 72: 1383, 1925. Mourgue-Molines E, Cabanac E: Abondante h~,morrhal~ie intraperitoneale par infaretus de l'epiploon-~gastro-h~patique. Bull M ~ m Soc Nat Chit 59: 720, 1933. Matheson NM: Spontaneous retroperitoneal hemorrhage M e d Rec 140: 186, 1934. Thompson KW, Dunphy JE: Intra-abdominal apoplexy. Ann Surg 102: 1116, 1935. Buchbitlder JR, Greene El: Intraabdominal apoplexy. JAMA 105: 874, 1935. Moorehead MT, McLester JS: Abdominal apoplexy, fatal .intraperitoneal hemor,'hage due to spontaneous rupture of a visceral artery. JAMA 106: 373, 1936. Cutler CW Jr: Mesenteric apoplexy. Ann Surg 104: 144, 1936. Lewis EE: An unusual cause of mlernat hemorrhage. Lancet 230: 255, 1936. Bruce J: Massive sponta~eous inlrapeHtoneal hemor-
rhage (spontaneous hemopeHtop, e u n 0 , Lancet 232: 1451, 1937. 19. Nevin S, Williams D.+ The pathogenesL+, el multiple a n e u r i s m s , Lancel 233: 955, 1937, 20. Morton CB: h~tra.abdommal apoplexy. Arch Sur E 36: 723, t938. 21. Silverstone M: Mas.~,ive sr, o n l a ~ e o u s inlraDerito~,,at hemorrhage. Brit Med J I: 230, 1938. 62"#
Klemsasser 22, Lafferty CR, Pearson B: Intraperitoneal hemorrhage in essential hypertension. Amer J Surg 48: 460, 1940. 23. MacLeod D, Maurice T: Rupture of a branch of the splenic artery, associated with pregnancy, Lancet ] : 924, 1940. 24. Bunch GE, Madden LE: Abdominal arterial apoplexy. Southern Med J 34: 643, 1941. 25. Berk JE, Rothschild MS, Doane JC: Intraabdominal apoplexy. Arm Surg 113: 513, 1941. 26, Cushman GF, Kitgore AR: The syndrome of mesenteric or subperitoneal hemorrhage (abdominal apoplexy). Ann Sure 1].4: 672, 1941. 27. Doege PF, Gray JH: Abdominal apoplexy: report of two cases, Wisconsin Med J 42: 400, 1943. 28. Halprin H: Abdominal apoplexy: report of a case. US Naval Med Bull 41: 811, 1943. 29. Haugen Ah lntra-abdomJnat apoplexy. J Iowa Med Soc 34: 198, 1944. 30. Hawk GW, Homer HO: Spontaneous hemoperitoneum: report of a case. Guthrie CIin Bull 14: 19, 1944. 3 ] . Marks M, Freedlander SO: Spontaneous intra-abdominal hemorrhage. Ann Sure 121: 191, 1949, 32. Shallow TA, Herbut PA, Wagner FB Jr: Abdominal apo. plexy secondary to ruptured "congenital" a n e w rysm: multiple aneurysms of the inferior pancreaticoduodenal artery with rupture of one. Sur. gery 19: 177, 1946. 33. ]'anna JF: Abdominal apoplexy. Amer J Sure 73: 132, 1947. 34, Brewer AC. Marcus R: Massive spontaneous intraperitoneal hemorrhage. Brit J Sure 36: 198, 1948. 35. Lee AF: Intra-abdommat hemorrhage during pregnancy. Arner g Sure 74: 867, 1947. 36_ Gdlam J~E: Spontaneous rupture of the splenic artery. Brit J Sure 36: 203, 1948. 37. Woolf AL, Thumson HR: Spontaneous intra-abdominaf haemorrhage. Brit Meal g 1: 572, 1949. 38. Darling AP: Abdominal apoplexy: report of a case. Surgery 27: 911, 1950. 39. Becker WF: tntraabdominal apoplexy. New Orleans Med Sure J I 0 4 : 185, 1951. 40, Ross FP: "Abdominal a p o p l e x y " complicated by ruesenteric venous thrombosis: report of a case. Ann Sure I31: 592, 1950. 41. Le Souef JD: Intraabdominal hemorrhage during the later months of pregnancy, with reports on two cases. Med J Aust 2: 154, 1951. 42. Jurish~ca A J, Vaccaro JE: Abdominal apoplexy in a child. JAMA 150: 1115, 1952: 43. Wolskel HG: Extensive intraperitoneal hemorrhage of unknown o r i g i n Brit Med J 2: 704, 1952. 44. Zummo BP, Williams PC, Uznanski, M: Retroperitoneal hemorrhage complicating pregnancy, Sure Gynee Obstet 95: 512, 1952, 45. Wright CH. Mason VC, Pinton M: Spontaneous intraperitoneal hemorrhage. Amer J Sure 88: 645, 1954. 46. Kazmierski RH. Hellman LA: Abdominal apoplexy simulating acute appendicitis in a fourteen year old boy. A m e r "J Sure 87: 291. 1954. 47. B~rkitt R: Abdominal apoplexy due to spontaneous rupture of right gastric artery, BritMed J 1: 21~, 1956. 48. Manheimer LH: Massive intraperitoneal hemorrhage from appendix epiploica. New Eng J Meal 255: 570, 1956.
~;~
49. Elits H, Griffiths PWW, Maclntyre A: Hemoperltoneum: a record of ! 2 9 consecuhve patients with notes on some unusual cases. Brit J Sure 45: 606, 1958. 50. Hahn GA: Rupture of the mid-colic artery (abdominal apoplexy) producing signs of pelvic hemorrhage, Amer J Obstet Gynec 66: 185, 1953. 51. Rauber G, Grosdidier J, Larcan A, Coxam B: Ruptures art~rielles successives spontan~es de localisations variees chez un sujet de 25 ans, Etude Anat Clin R~v M~.d Nancy 83: 594, 1958, Cited by Martorell, R [52 ]. 52. Martorell R: Spontaneous rupture of the superior ruesenteric artery. Ann Sur8 157: 292, 1963. 53. Crocco JA, Soscia JL: Rupture of a branch of the left gastric artery with massive intraperitoneal hemorrhage: report of a case. Amer J Dig Dis 8: 444, 1963, 54. Constantiner JP: Abdominal apoplexy. J tnt Coil Surg 41: 573, 1964. 55. Carter R, Gosney WG: Abdominal apoplexy; report of six cases and review of the literature. Amer J Sur E 3: 388, 1966. 56. Browne MK, Glasharl RW: Abdominal apoplexy. Brit J Surg 52: 362, 1965. 57. Woods AC Jr, Parry RG, Detmer DE: SuccesshH surEical t r e a t m e n t of massive abdominal hemorrhage due to periarteritis nodosa. Arch Surg 97: 541, ]968. 58, Akbarian M: Abdominal apt~plexy in polyarteritis nodosa: report of a case. Amer J Dig Dis 11: 63. 1966. 59. Cromier JM, Diebold J, Kalifat R, Florent J. Delarue J: Rupture arterielle spot,tahoe par dissection de l'art~re mesenterique inferieure. Presse Med 77: 971, 1969. 60. Dvorak A, Gazzaniga A: Dissecting aneurysm of the gastroduodenal artery: anatomic basis for the clinical syndrome of abdominal apoplexy. Ann Sure ]69: 425, 1969. 61. Garland EA: Spontaneous retroperitoneal hemorrhage simulating appendiceal abscess. J Indiana Med Ass 42: 903, 1949. 62. Forbus WD: On the origin of miliary aneurysms of the superficial cerebral arteries. Bull Johns Hopkins Hosp 47: 239, 1930. 63. Schuster NH: Familial hemorrhagic telangteetasia associated w~th multiple aneurysms of the splenic artery. J Path B act 44: 29, 1937. 64. Glynn LE: Medial defects in the Circle of Willis and their relation to aneurysm formation. J Path Bact 51: 213, 1940. 65. Richardson JC, Hyland HH: Intracrania{ aneurysmsc Medicine 20: 1, 1941. 66. Hanna WA, Myles TJM: Spontaneous intraperitonal hemorrhage during pregnancy: report of three cases. Brit Med J 1: 1024, 1964. 67. Sherlock SPY, Learmonth JR: Aneurysm of the splenic artery; with an account of an example complicating Gaucher's disease. Brit J Sure 30" 151, 1942. 68. Sherwin 8, Gordimer H: Aneurysm of the splenic artery: report of two cases. Ann Surg 131: 599, 1950. 69. Johnston CC: Diagnostic paracentesis in suspected intraabdominal hemorrhage. Ann Sure 111: 93, 1940. 70. Nusbaum M, Baurn S, Blakemore WS: Clinical experience with the diagnosis and management of gastrointestinal hemorrhage by selective mesenteric catheterization. Ann Surg 170: 506, 1969.
The American Journal of Surgery
Spontaneous intra-abdominal bleeding r a r e l y occurs, but m a y be extensive and life-threatening. Even m o r e uncommon is r e t r o p e r i t o n e a l hemorrhage f r o m a b r a n c h of a splanchnic vessel. This has been called abdominal apoplexy, but the term is retire broadly used to encompass spontaneous inira-abdominal h e m o r r h a g e . Abdominal apoplexy has been so named because its n a t u r e and sponta~eity closely resemble those of its more common cerebral c o u n t e r p a r t , t I a r t l e y an(1 5IcKechnie [1] su~rgested the term, splanchnostaxis, f o r this condilion, but the t e r m has not gained acceptance. Barber [2! in 1909 is credited with the earliest reported case of abdominal apoplexy. D u r i n g labor, a t h i r t y - t w o y e a r old woman was delivered of a full term chi!d. Increasing abdominal distention developed and two (lays post I)artum, " t y m p a n i t e s " increased and she was explored. Dark blood was found but no bleeding site was detected. She recovered. and the surgeon surmised t h a t tile bleeding must b a r e c o m e from some vein in the pelvis. Although it is repeatedly reported t h a t F l o r e n c e 'rod I)ucuiP, g [13] were the first to describe the condition clearly, actually t h e i r case was a man with hemop e r i t o n e u m a f t e r a contusion of the kidney f r o m a fall, while drunk, a g a i n s t a bed made of a block of woo(l. It was postulated that t h e r e was a t e a r of the p o s t e r i o r peritoneum with bleeding into the peritoneal cavity. The patient had h e m a t u r i a and hemoperitoneum. The l a t t e r was substantiated by a p u n c t u r e of the cul-de-sac of Douglas by tile perineal route in a male. The p a t i e n t refused to undergo s u r g e r y and recovered. This p a t i e n t obviously did not have a spontaneous h e m o r r h a g e . The r e p o r t is not a b o u t " a y o a n g woman, eight months p r e g n a n t " with a r u p t u r e d b r a n c h of the s u p e r i o r mesenteric a r t e r y as r e p o r t e d in the lite r a t u r e [4]. The first case substantiated by p o s t m o r t e m examination w a s r e p o r t e d by S m i t h [5] in 1911. A thirty-five y e a r old woman, nine m o n t h s p r e g n a n t , had abdominal pain a f t e r some s t r e n u o u s activity. She died t w e n t y m i n u t e s a f t e r examination. PostFrom the Depa~ments of Surgery, Baylor University Medical Center and Presbyterian Hospital of Dallas, Dallas, Texas. Presented at the Twenty.Second Annual Meeting of the Southwestern Surgical Congress, Dallas, Texas, April 20-23, 1970. Volume 120, November 1970
m o r t e m study showed the tissues behind the gastrosplenic ligament " c o n s i d e r a b l y ecchymosed and torn up." As f a r as could be determined by dissection, "a b r a n c h of the splenic a r t e r y had given w a y j u s t before it got t,o the hilum." No a t h e r o m a was present in the vessel. T h e t e r m abdominal apoplexy was first coined by Green and P o w e r s [~] in 1931. Crile and Newe]l [6] in 1940 are credited with m a k i n g the first c o r r e c t p o s t o p e r a t i v e diagnosis of abdominal apoplexy. The bleeding point was not found, but it was assumed this was a b r a n c h of t h e celiac a r t e r y . The ease is suspect because it closely followed celiac ganglionectomy. My attention was directed to this condition by two patients successfully o p e r a t e d on ; the bleeding site was located and controlled with r e c o v e r y o f the patients. In most instances the diagnosis is m a d e a f t e r l a p a r o t o m y or at autopsy.
Case Reports CASE I. A forty-seven )'ear old woman (WBS) was admitted to Presbyterian Hospital of Dallas on February 11, 1968, with the sudden onset of abdominal pain and vomiting of twenty hours' duration. This became worse and she entered the Emergency Room in shock. The abdomen was silent, there was abdominal tenderness most marked in the right upper quadrant, and there was no muscle spasm. A vague aMominal mass was felt. Peh, ic examination gave negative results. Roentgenograms of the chest and abdomen were relatively within normal limits. No blood pressure was obtainable on admission, but rose to 90/60 mm Hg after she was given an intravenous infusion of Ringer's lactate solution. The hematocrit was 26 per cent. She was operated on as an emergency with a preoperative diagnosis of intraperitoneal bleeding. Laparotomy disclosed much intra- and retroperitoneal blood. The blood had extravasated widely to include the leaves of the mesentery of the bowel. I was called into consultation and continued the operative procedure. Tim aorta was first exposed to exclude the possibility of a leaking aneurysm, but the aorta proved to be normal. Further exploration revealed a mass posterior to the head of the pancreas. Th~ duodenum and head of the pancrea s were mobilized by the Kocher maneuver. A large clot was extracted from under the head of the pancreas and this was followed by a gushing hemorrhage which could be controlled by manual compression. The exposed bleeding 623
Kleinsasser
vessel, the i n f e r i o r p a n c r e a t i c o d u o d e n a l a r t e r y , was ligated and sutured. I 2 n f o r t u n a t e l y . no specimen of the a r t e r y was obtainable. T h r e e d r a i n s w e r e i n s e r t e d and brought; out t h r o u g h a lateral stab wound in t h e upper p a r t of the abdomen and the midline incision closed. D u r i n g s u r g e r y she received 4 units o f blood and 4,500 ml of R i n g e r ' s l a c t a t e solution i n t r a v e n o u s l y . Nasog a s t r i c suction, i n t r a v e n o u s fluids, and a n t i b i o t i c s were employed postoperatively. T e m p e r a t u r e r e t u r n e d to normal. I n t e s t i n a l p e r i s t a l s i s developed on the f o u r t h day, t h e Levin tube was removed, anti she was fed. The s e r u m a m y l a s e rose to 815 u n i t s on the fifth (lay, but felt below 500 units by the eleventh clay. T h e h e m a t o c r i t rose to 35 p e r cent. T h e d r a i n s w e r e manipulated and finally removed on t h e eleventh postoperative day. She was d i s c h a r g e d on the t h i r t e e n t h day in excellent condition. She was s u b s e q u e n t l y r e a d m i t t e d to P r e s b y t e r i a n Hospital on A p r i l 28. t968 with a t r i m a l l e o l a r f r a c t u r e of the r i g h t ankle t r e a t e d by open reduction. She did well and was asyn',ptomatic from the a b d o m i n a l surgery. She was d i s c h a r g e d on May 4, 1968. She has h y p e r t e n s i o n and the blood p r e s s u r e was found to be 186'110 mm t t g on admission, f a l l i n g to 150/110 m m H g a f t e r bedrest. CASE lI. A sixty-five y e a r old w o m a n ( E P H ' ! was a d m i t t e d to Baylor U n i v e r s i t y Medical C e n t e r in Dallas as an e m e r g e n c y on N o v e m b e r 17, 1969 w i t h a t e n t a t i v e d i a g n o s i s of closed loop i n t e s t i n a l o b s t r u c t i o n . At 113 AM the previous clay she b e g a n to have l o w e r abdominal pain. The pain p e r s i s t e d with i n c r e a s i n g s e v e r i t y during the n i g h t w i t h i n t e r v a l s of d i s c o m f o r t l a s t i n g five to ten m i n u t e s . S h e experienced some n a u s e a and vomited. T h e pain w a s in the lower p a r t of t h e abdomen and s u p r a p u b i e area. In the past she had an appendectomy as welt as p a r t i a l g a s t r i c r e s e c t i o n and cholecystectomy in 1940. T e m p e r a t u r e was 98.2 ':~ F. pulse 106, and blood pressure 130,90 mm Hg. The abdomen was q u i e t and t e n d e r t h r o u g h o u t . T h e r e was left rectus muscle g u a r d i n g at the level of the umbilicus and t h e question of a mass b e n e a t h it t h o u g h t to be small bowel w i t h possibly v a s c u l a r i m p a i r m e n t . The h e m a t o e r i t w a s 40 per cent, w h i t e blood celt c o u n t 10,200 mm:L and t h e r e w e r e 82 p e r cent p o l y m o r p h o n u c l e a r n e u t r o p h i l s in t h e diff e r e n t i a l count. S u p i n e and u p r i g h t r o e n t g e n o g r a m s of the abdomen g a v e n e g a t i v e results. T h e l e f t psoas shadow was distinct, b u t the r i g h t one was n o t seen clearly. She was operated on as an e m e r g e n c y t h r o u g h a midline incision. T h e s u r g e o n found an e x t e n s i v e r e t r o p e r i t o n e a l h e m a t o m a . I was called in c o n s u l t a t i o n and continued the operation. F u r t h e r e x p l o r a t i o n revealed no a o r t i c a n e u r y s m , but disclosed a r u p t u r e d l e f t colic a r t e r y with a clot which had been o c c l u d i n g a slit app r o x i m a t e l y 1.5 em long in the a r t e r y , t h e source of h e m o r r h a g e . T h e involved a r t e r i a l s e g m e n t , 2 cm long, was resected and t h e vessel ligated. C o n s i d e r a b l e f r e e blood and r e t r o p e r i t o n e a l clot w e r e removed. Postope r a t i v e l y the p a t i e n t did well except f o r a t r a n s i e n t period o f psychosis. S h e was d i s c h a r g e d eleven days 624
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Fi£ure 1. ARe incidence. p o s t o p e r a t i v e l y and has done well. S u b s e q u e n t e x a m i n a tion has disclosed that she has h y p e r t e n s i o n witt~ a blood p r e s s u r e of 168'1 t0 mm Hg. Clinical
Material
E i g h t y - t h r e e cases have been selected f o r analysis, e i g h t y - o n e f r o m the l i t e r a t u r e [I.2.~-6t] and two from my o w n experience. A l t h o u g h o t h e r cases hav~:~ been tabulated, the i n f o r m a t i o n and d o c u m e n l a t i o n a r e so incomplete that the.',' are not acceptable for review. T h e r e w e r e f o r t y - s i x male and t h i r t y - s e v e n female subjects v a r y i n g in a g e f r o m two to e i g h t y - f o u r years w i t h the g r e a t e s t incidence in the fifty to fifty-nine y e a r range. ( F i g u r e 1.) The age was not stated in two reports. T h e illness usually began suddenly and c h a r a c t e r istiealiy was of b r i e f d u r a t i o n . In forty-five of t h e sixtyseven cases in which the d u r a t i o n of illness was recorded, t h e r e was a h i s t o r y of t w e n t y - f o u r hours or less p r i o r to admission a l t h o u g h e i g h t e e n had a h i s t o r y up to seve.n days. A b d o m i n a l pain was by f a r t h e first s y m p t o m o e e u r r f n g in s e v e n t y - f o u r of s e v e n t y - e i g h t eases in which t h e initial s y m p t o m is reported. Abdominal distention occurred as an initial s y m p t o m in two. back p a i n in one. and g a s t r i c d i s t r e s s in one. T h r e e p a t i e n t s died suddenly w i t h o u t p r e m o n i t o r y symptoms. The pain was generalized in t w e n t y - e i g h t , in t h e u p p e r part of the abdomen in t h i r t y - o n e (thin'teen of whom had e p i g a s t r i c p a i n ) , in the m i d p o r t i o n of t h e abdomen in t h r e e (in one of w h o m it: was described as p a r a u m b i l i c a l ) , and in the lower p a r t of the abdomen in twelve. F i f t y experienced abdominal t e n d e r n e s s of whom t h i r t y - t w o had g e n e r a l i z e d tenderness, t w e n t y n i n e showed a b d o m i n a l d i s t e n t i o n , fifteen had abdominal r i g i d i t y , and ten had muscle g u a r d i n g . T h i r t y - f o u r had some evidence of . hock d u r i n g t h e course of t h e i r illness. S i x t y - s i x w e r e o p e r a t e d on and seventeen w e r e n o t o p e r a t e d on. Of t h e s i x t y - s i x o p e r a t e d on, no p r e o p e r a t i v e d i a g n o s i s was g i v e n in t h i r t e e n cases. T h e m o s t frequent preoperative diagnoses were intraperitoneaI h e m o r r h a g e , acute i n t e s t i n a l o b s t r u c t i o n , r u p t u r e d peptic ulcer, appendicitis, m e s e n t e r i c thrombosis, and r u p t u r e d eetopic p r e g n a n c y . (Table I.) A t operation, all e m e r g e n c y , f r e e i n t r a p e r i t o n e a l blood was found in fifty-one, none in ten, and n o t s t a t e d in five. T h i r t y - n i n e had r e t r o p e r i t o n e a l bleeding, The
American
Journal
o f Surl~e~'y
Abdominal Apoplexy
twenty-two showed no evidence of retroperitoneal bleeding, and the presence of bleeding was not stated in five. The amount of free blood varied to as much as 3 L. Of the sixty-six o~'Jerated on, twenty died (30.3 per cent) ; the bleeding source was found in thirty-five patients and thirty-two of these recovered. Three died !8.6 per cent}, one of a myocardial infarction. Of the twenty-five in whom the bleeding source was not found, eleven recovered and fourteen died (56 per cent). There were six in whom hematoma was present at the base of the mesentery. No vessel was ligated and three ~}f these patients died and three survived. Autopsy was performed in thirteen of the sixty-six patients operated on and the bleeding vessel was located in six and not found in seven. In four, no autopsy was permitted. Of the eight, y-O~ree collected cases, there were thirty-seven deaths, a mortality of 44.6 per cent. Of the seventeen patients not operated on, all died. The vessel responsible for bleeding in the eightylhree eases varied. I Table II.') The most common sources were the gastr;,c arteries in ten cases, the
TABLE I
Preoperative Diagnosis in Sixty-Six Operations
Diagnosis Intraperitoneal hemorrhage Acute intestinal obstruction Ruptured peptfc ulcer Appendicitis Mesenteric thrombosis Ruptured ectopic pregnancy Perforated stomach or acute pancreatitis Acute pancreatitis Ruptured aortic aneurysm Abdominal apoplexy Miscellaneous No preoperative diagnosis Total TABLE II
Number 11 7 6 6 5 4 3 2 2 2 5 13 66
Source of Bleeding Source of Bleeding
Celiac axis Splenic artery Hepatic a~ery Right gastric artery Left gastric artery Gastroduodenat artery Inferior pancreaticoduodenal Left gastroepiploic artery Superior mesenteric artery Middle colic artery Right colic artery Left colic artery Ileocolic artery Inferior mesenteric artery Appendix epiploic artery Renal artery Hematoma of mesentery Cul-de-sac and broad ligament U ndetermined Total
Volume 120, November 1970
Number 1 5 t 3 7 3
3 2 5 8
1 3 4 2 1 1 7 3 23 83
middle colic artery in eight, the splenic artery ir~ five. and the superior mescn ~ric artery in five. No source of bleeding was found in twenty-three and this group presented the highest mortality,
Comments
Although massive intra-abdominal hemorrhage w i t h o u t g r o s s a b d o m i n a l disease is r e f e r r e d to as s p o n t a n e o u s , it is unlikely t h a t this can o c c u r w i t h o u t an u n d e r l y i n g o r g a n i c lesion. H y p e r t e n s i o n w a s r~corded as being p r e s e n t in t h i r t y - t h r e e pat i e n t s (39.8 per cent) in the collected series a n d is c o n s i d e r e d a definite f a c t o r . In addition, since m a n y of the r e p o r t e d p a t i e n t s w e r e in shock w h e n first seen, it is likely the incidence of h y p e r t e n s i o n is h i g h e r . A l t h o u g h a r t e r i o s c l e r o s i s is s t r o n g l y implicated in the older patient, it c a n n o t a p p l y to the m u c h y o u n g e r p a t i e n t a n d did not exist as a c a u s e in m y second patient. T h e r e is a g r o w i n g b o d y of evidence t h a t this is likely due to an a n e u r y s m res u i t i n g f r o m a d e v e l o p m e n t a l d e f e c t in the a r t e r y . T h e c o n c e p t t h a t a n e u r y s m s in some cases m a y be due to c o n g e n i t a l o r d e v e l o p m e n t a l d e f e c t s w a s first s u g g e s t e d b y E p p i n g e r in 1887 [19]. F o r b u s [62] in 1930 d e m o n s t r a t e d t h e a s s o c i a t i o n of cerebral a n e u r y s m s w i t h a c h a r a c t e r i s t i c d e f e c t in the t u n i c a m e d i a of the a r t e r i a l wall at the a n g l e f o r m e d by the b r a n c h i n g of vessels. T h e d e f e c t consists of an i n t e r r u p t i o n in t h e m u s c u l a r coat at the p o i n t o f b i f u r c a t i o n of m e d i u m sized a r t e r i e s w h o s e a d v e n t i t i a and i n t i m a a r e intact. H e concluded these defects w e r e d e v e l o p m e n t a l in origin. S i n g l e and m u l t i p l e a n e u r y ~ m s h a v e been d e s c r i b e d in o t h e r a r t e r i e s , such as t h e splenic, hepatic, a n d renal, in w h i c h no i n f l a m m a t o r y or d e g e n e r a t i v e c h a n g e s could be found. Since s i m i l a r d e f e c t s occ u r in the s p l a n c h n i c vessels, it is p r o b a b l e that: some o f these a n e u r y s m s h a v e developed in association w i t h such defects, A l t h o u g h the d e f e c t i~ the m e d i a and i n t e r n a l elastic l a m i n a m a y be located e l s e w h e r e t h a n at the b i f u r c a t i o n ( b r a n c h ing) of vessels, o t h e r s [1g,22,52,62] h a v e subseq u e n l l y s u p p o r t e d this concept. T h e a s s o c i a t i o n o f c e r e b r a l m i t i a r y a n e u r y s m s a n d s p l a n c h n i c vessel i n w ) l v e m e n t in the s a m e p a t i e n t d e s c r i b e d by N e v i n a n d W i l l i a m s [ 19] f u r t h e r lends c r e d e n c e U~ this t h e o r y . H o w e v e r , G l y n n [64] believes t h a t ~he m o r e f r e q u e n t o c c u r r e n c e of a n e m - y s m s of the Circle o f "~Villis is m o r e likely related to differences in the t o p o g r a p h y o f the elastic tissue o f the vessels. In c e r e b r a l vessels a l m o s t the who]e of t h e Elastic tissue is c o n c e n t r a t e d in t h e i n t e r n a l elastic l a m h m a n d b y r e a s o n of this position is p r o b a b l y m~,re ~us-. ceptible to i n j u r y a n d dEgenEration t h a n if it w e r e m o r e w i d e l y d i s t r i b u t e d t h r o u g h the m e d i a anti ~
Kleinsasser
Figure 2. A, Verhoff elastic tissue stain showing the a b ru p t change from a relatively normal wall to the markedly thinned wall, There is toss of the internal elastic lamina and necrosis and inflammation of the markedly thinned media. There is
adventitia as in o t h e r vessels. It: has also been suggested t h a t an unrecognized acquired lesion m a y be causing degeneration of elastic tissue [65]. In the second ease r e p o r t e d by me, the a r t e r y a d j a c e n t to tile r u p t u r e d vessel was normal, and the p e r f o r a tion a p p a r e n t l y did not occur at the site of a r t e r i a l branching. However, tile histologie findings clearly indicate the u n d e r l y i n g lesion which involves tile media and the internal elastic ]amil{a. The histologic changes s t r o n g l y suggest tile r u p t u r e of a thrombosed a n e u r y s m . The internal elastic lamina and the media were deficient in most of the vessel. These changes n e v e r involved the e n t i r e circumference. The adventitia was intact except at the site of r u p t u r e . T h e thinned o u t e r media was focally necrotic and infiltrated by p o l y m o r p h o n u e l e a r leukoeytes. When present, the internal elastic lamina was wrinkled and slightly t h i c k e n e d ; the intima showed minimal fibrosis. The change f r o m the normal thickness to the thinned media was usually a b r u p t but sometimes gradual. Necrosis of the o u t e r media often extended a s h o r t distance into the a d j a c e n t wall. The blood clot proved to be a t h r o m b u s with a central lumen. ( F i g u r e 2A and B.)
It is postulated t h a t the media became t h i n o r was deficient in p a r t of the c i r c u m f e r e n c e of the a r t e r y , and with dilatation of the vessel t h e r e w a s disruption of the intima and the internal elastic lamina f o r m i n g an a n e u r y s m which filled with clot and likely had a central lumen. Finally the external elastic lamina and a d v e n t i t i a gave way. T h e clot was extruded and h e m o r r h a g e ensued f r o m rupture of the a n e u r y s m . * 626
hemorrhage beneath the external elastic lamina with appearance of dissection beneath the n~edia, (Orip, itlal maf~nification X 100,) ~, a complete cross section of the thromhus demonstrating the smooth outer contour and central lumen. (Original magnification >~ 4.)
Necrotizing a r t e r i t i s associated with p e r i a r t e r itis nodosa [5x] m a y produce an anem-ysm which CiIll l'ttl)ttll'e ;t|1(t t)rodllce illlral)el'it(HlPal
hPmor-
rhage. Polyarteritis n(~
Abdominal Apoplexy
sel nnd is retrot)eritoneal. Occasionally the prosSlll'(~ ()I" btec'dinK will Iirodtlee. a teal" ill the l)eriloncum with nmre extensive hemorrhage. I f the bieedinK is r e t r o p e r i l o n e n l , the s i g n s m a y be lll;ISketI; }lowever, Wilell" tile b l e e d i n g o c c u r s directly inio tim peritoneal cavity, there will be signs iJI~t)eribuleal irritation. Tile sudden ollset of sevot'e alJ(lOlllilia] pain, often followed rapidly by shock anti tile sil,rl/S of ill(oriu/l bteedinT, is the c h i e f llOint in the diaKnosis. Peril.olmal tap [69] IllAy be }letl)ful ii~ col}firndnK tile diaKnosis of bleediilK if." bleediilK is not restricled to the retrol)eritoneal li Fell. ,'%it }l(;lllg}l select;ire meselll erie arteriogrAphy [?0] nliK}lt, be helpftl] ill Ioeaiizin7 tile b l e e d i n g site, survery ustlally cannot be postponed. A large part ill l.he dia.~nosis of a b d o n l i n a l a p o p l e x y d e p e n d s orl a hi.~rh illdex of stispieion. Tim t r e a t m e n t is s u r g i c a l 'lad e x p i o r a l i o n should l~e emv.hleled wiill the p a t i e n t ' s blood p r e s s u r e raised s,} It]at the b l e e d i n g s o u r c e call be fotlnd. 'lT}le e x l H o r a l h m is best p e r f o r m e d w i t h a knowle~ige o f tile a r t e r i e s m o s t e o m n l o n t y inwflved in this disease, l:f the bleed)ate point is not apparent, t h e r e should tm a c a r e f u l i n t r a p e r i t o n e a ] s e a r c h iliciudiilg the diatdn'aKm, i.}le Kastrollepntie o m e n {tlrli, lesser sac, sph,nic area, pelvis, And fhlally tile rci.l'olmritoneal area. A large portion of the retroperitoneal s p a c e can be e x p l o r e d by incising the p o s t e r i o r p e r i t o n e u m o v e r tile a o r t a , r e t r a c t i n g the l r a n s v e r s e colon s u p e r i o r l y and i;he small bowel to the r i g h t as well as mobilizillg the d u o d e n u m And the }lead of the p a n c r e a s 1)3, tile K o c h e r m a n e u v e r . Frc'qtleritly the b l e e d i n g will h a v e s t o p p e d , as a restilt of e i t h e r the fall ill blood p r e s s u r e o r the f o r m a t i . n o f a t h r o m b u s w h i c h will only t e m . p o r a r i l y cold.r-1 t h e bleeding. I t is i m p e r a t i v e thai the bleedinv site be f o u n d and t h e vessel tigated as i n d i c a t e d by this eolteeted series in which f a i h u ' e to find the s o u r c e resulted ill a m o r t a l i t y of 56 p e r cent in c o n t r a s t to a m o r t a l i t y of 8.6 p e r cent if the bleedillg source was follild. Ill v i e w of the p o t e n t i a l i t y f o r l i f e - t h r e A t e n i n g F,e m o r r h a ~ e , it is u r a e d t h a t sl)lanehnle Arterial a n e u r y s m s be reseeted p r o p h y l a c t i c a l l y r e g a r d l e s s of t h e size when d i s c o v e r e d d u r i n g v i s c e r a l angio~;r a t ) b y or at:, l a p a r o t o m y f o r a n y c a u s e .
vessels responsitHe f a r hleedin~,'. 3. S i x t y - s i x cases in w|:ich Olmralion w a s tmr fol'tll(:d Iil'O SlllllIllal'izeit itleill(lillK t he pr(,oper:~tive diaKnoses. (ipcl'ative findings, and m o l ' i a l i t v . ,I. Tllere w e r e t h i r t y - s e v e n d e a t h s (.11.(i p v r c e n l ) in tim e i g h t y - t h r e e collected eases. O f s i x i y six p a t i e n t s o p e r a t e d ml, lweniy died (?,0.:{ per c e n t m m ' t a l i t y ) . I f the 1)teedinK source w a s o r e trolled, only t h r e e of t h i r t y - l w o died (g.6 p e r c e n t ) . T h e bleedin~e source w a s nut fmlnd in t w e n t y - f i v e and r . u r t e e n died (56 p e r c e n t ) . :3. It is n i a l l d a i o r y t h a t tile bleedin~ source. which m a y be i n t r a p e r i l o n e a l or r e t r ~ p e r i t o n e a l , tie located And oral rolled. 6. I t is til'ged t h a t All all?ttl'Vsnls l a w ) l y i n g the sl)lAtlehUie vessels be reseeted prol~llylaetieally. References 1. Hartley H, MacKechnie DM: A case of "sptanchnosta×is." Lancet 1: 289, 1934. 2. Barber MC- Intraabdomirlal hemordlage associated with labor. Btit M e d J 2: 203, 1909. 3. Florence and Ducuing: Contusion du rien. H~mopi}ritoine. Gu(~rison spontanee. Valeur diap_.nostique de la fonction exploratrice du cubde+sac de Douglas. Bull M~m Soc Chit Paris 39: 645, 1913. 4. Green WT, Powers JH: tntraabdominal apoplexy. Ann Surg 93: 1070, 193t. 5. Smith HBW: A fatal case of intraperito~mal hemorrhage from an unusual source. Brit M e d J 1: 83, 1911. 6. Crile G Jr, Newetl ET Jr: Abdominal apoplexy; spor~taneous rupture of a visceral vessel. JAMA 114: 1155,
1.940.
7, Churchman JW: Spontaneous intraperitoueal 8. 9. 10. 11.
12. 13. 14, 15, 16,
Summary
1. T w o eases of a b d o m i n a l Apoplexy s u c c e s s f u l l y n l a n a g e d a r e repro:ted w i t h the m i c r o s c o p i c findings in one ease i n t e r p r e t e d a s s h o w i n g an u n d e r lying lesion in the m e d i a And s t r o n g l y s u g g e s t i n g r u p t u r e of A t h r o m b o s e d a n e u r y s m . 2. E i g h t y - o n e collected eases a n d t w o f r o m m y e x p e r i e n c e a r e r e v i e w e d to i n d i c a t e the Age incidence, c h a r a c t e r i s t i c s y m p t o m s and findings, a n d Volume 120, November 1970
17,
18.
hemor-
rhage. A m e r J Med Sci 142: 825, 1911. Hilliard JW: Spontaneous hemorrhage into the peritoneal cavity in arteriosclerosis. Brit Med J 1: 231, 1918. Starcke G: Spontaneous rupture of gastrodllodel~al artery. Ugesk Laeg 85: 963, 1923. Cited by Green WT and Powers JH [4]. Budde M: Operativ Geheilte spontanruptur der Arteria gastroapiploica sinistrs. Munchen Med Wschr 72: 1383, 1925. Mourgue-Molines E, Cabanac E: Abondante h~,morrhal~ie intraperitoneale par infaretus de l'epiploon-~gastro-h~patique. Bull M ~ m Soc Nat Chit 59: 720, 1933. Matheson NM: Spontaneous retroperitoneal hemorrhage M e d Rec 140: 186, 1934. Thompson KW, Dunphy JE: Intra-abdominal apoplexy. Ann Surg 102: 1116, 1935. Buchbitlder JR, Greene El: Intraabdominal apoplexy. JAMA 105: 874, 1935. Moorehead MT, McLester JS: Abdominal apoplexy, fatal .intraperitoneal hemor,'hage due to spontaneous rupture of a visceral artery. JAMA 106: 373, 1936. Cutler CW Jr: Mesenteric apoplexy. Ann Surg 104: 144, 1936. Lewis EE: An unusual cause of mlernat hemorrhage. Lancet 230: 255, 1936. Bruce J: Massive sponta~eous inlrapeHtoneal hemor-
rhage (spontaneous hemopeHtop, e u n 0 , Lancet 232: 1451, 1937. 19. Nevin S, Williams D.+ The pathogenesL+, el multiple a n e u r i s m s , Lancel 233: 955, 1937, 20. Morton CB: h~tra.abdommal apoplexy. Arch Sur E 36: 723, t938. 21. Silverstone M: Mas.~,ive sr, o n l a ~ e o u s inlraDerito~,,at hemorrhage. Brit Med J I: 230, 1938. 62"#
Klemsasser 22, Lafferty CR, Pearson B: Intraperitoneal hemorrhage in essential hypertension. Amer J Surg 48: 460, 1940. 23. MacLeod D, Maurice T: Rupture of a branch of the splenic artery, associated with pregnancy, Lancet ] : 924, 1940. 24. Bunch GE, Madden LE: Abdominal arterial apoplexy. Southern Med J 34: 643, 1941. 25. Berk JE, Rothschild MS, Doane JC: Intraabdominal apoplexy. Arm Surg 113: 513, 1941. 26, Cushman GF, Kitgore AR: The syndrome of mesenteric or subperitoneal hemorrhage (abdominal apoplexy). Ann Sure 1].4: 672, 1941. 27. Doege PF, Gray JH: Abdominal apoplexy: report of two cases, Wisconsin Med J 42: 400, 1943. 28. Halprin H: Abdominal apoplexy: report of a case. US Naval Med Bull 41: 811, 1943. 29. Haugen Ah lntra-abdomJnat apoplexy. J Iowa Med Soc 34: 198, 1944. 30. Hawk GW, Homer HO: Spontaneous hemoperitoneum: report of a case. Guthrie CIin Bull 14: 19, 1944. 3 ] . Marks M, Freedlander SO: Spontaneous intra-abdominal hemorrhage. Ann Sure 121: 191, 1949, 32. Shallow TA, Herbut PA, Wagner FB Jr: Abdominal apo. plexy secondary to ruptured "congenital" a n e w rysm: multiple aneurysms of the inferior pancreaticoduodenal artery with rupture of one. Sur. gery 19: 177, 1946. 33. ]'anna JF: Abdominal apoplexy. Amer J Sure 73: 132, 1947. 34, Brewer AC. Marcus R: Massive spontaneous intraperitoneal hemorrhage. Brit J Sure 36: 198, 1948. 35. Lee AF: Intra-abdommat hemorrhage during pregnancy. Arner g Sure 74: 867, 1947. 36_ Gdlam J~E: Spontaneous rupture of the splenic artery. Brit J Sure 36: 203, 1948. 37. Woolf AL, Thumson HR: Spontaneous intra-abdominaf haemorrhage. Brit Meal g 1: 572, 1949. 38. Darling AP: Abdominal apoplexy: report of a case. Surgery 27: 911, 1950. 39. Becker WF: tntraabdominal apoplexy. New Orleans Med Sure J I 0 4 : 185, 1951. 40, Ross FP: "Abdominal a p o p l e x y " complicated by ruesenteric venous thrombosis: report of a case. Ann Sure I31: 592, 1950. 41. Le Souef JD: Intraabdominal hemorrhage during the later months of pregnancy, with reports on two cases. Med J Aust 2: 154, 1951. 42. Jurish~ca A J, Vaccaro JE: Abdominal apoplexy in a child. JAMA 150: 1115, 1952: 43. Wolskel HG: Extensive intraperitoneal hemorrhage of unknown o r i g i n Brit Med J 2: 704, 1952. 44. Zummo BP, Williams PC, Uznanski, M: Retroperitoneal hemorrhage complicating pregnancy, Sure Gynee Obstet 95: 512, 1952, 45. Wright CH. Mason VC, Pinton M: Spontaneous intraperitoneal hemorrhage. Amer J Sure 88: 645, 1954. 46. Kazmierski RH. Hellman LA: Abdominal apoplexy simulating acute appendicitis in a fourteen year old boy. A m e r "J Sure 87: 291. 1954. 47. B~rkitt R: Abdominal apoplexy due to spontaneous rupture of right gastric artery, BritMed J 1: 21~, 1956. 48. Manheimer LH: Massive intraperitoneal hemorrhage from appendix epiploica. New Eng J Meal 255: 570, 1956.
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