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The angiographic diagnosis of echinococcosis of the liver and spleen
Clin. RadioL (1971) 22, 466-471
THE ANGIOGRAPHIC DIAGNOSIS OF ECHINOCOCCOSIS OF THE LIVER AND SPLEEN IZHAK GARTI and VICTOR DEUTSCH
From the Departments of Diagnostic Radiology, Beilinson Hospital, Petach-Tikva, and Tel-Hashomer Government Hospital, Tel-Aviv University Medical School, Israel Selective visceral angiography is a useful, complementary method for the diagnosis of echinococcosis of the liver and spleen. The characteristic of the 'halo sign" provides information on the biological activity of the cyst. Angiography also provides the surgeon with important pre-operative information on the true size, number and localization of the cysts, the state of the surrounding parenchyma and the course of the blood vessels in the area. Tim diagnosis of echinococcosis or hydatid disease of the liver and spleen is based upon the history, physical and laboratory examinations, immunologic tests, radiographic and radioisotopic investigations. Unfortunately, all these investigations have only a varying degree of accuracy (Bonakdarpour, 1967; Morris et al., 1967; Garabedian et al., 1959). Radiological investigations play an important role in the diagnosis of hydatid cysts by demonstrating a round or oval calcified rim, or spotty calcified densities in the area of the liver or spleen, particularly in regions where hydatid disease is endemic. However, in the absence of calcifications, the radiological diagnosis of hydatid disease of the liver or spleen is difficult or even impossible. Moreover, if a calcified cyst is visualized on the plain film of the abdomen, additional non-calcified, biologically active cysts, can be missed: the calcifications may be localized in a daughter-cyst or multiple cysts may be present. The decision to operate on an asymptomatic calcified cyst is difficult without knowledge of the exact nature, true size and biological state of the cyst. Selective visceral angiography may provide important information: the purpose of this paper is to report on our observations. MATERIAL AND METHOD Our experience is based upon 22 cases of echinococcosis--18 in the liver and 4 in the spleen. In 20 patients the study was performed by selective coeliac and mesenteric angiography and in 2 patients by abdominal aortography. In 11 patients the indication for the angiographic examinations
was the presence of calcification, suspected to be due to echinocoecosis, on the plain films; in 7 patients the calcification was in the liver, and in 4 patients in the spleen. Seven patients were examined for unexplained hepatomegaly. Two other patients were examined because of the presence of abdominal masses, and another patient because of pains in the right hypochondrium and a positive Casoni test. In 18 patients the diagnosis of hydatid cyst was confirmed at operation. In 4 cases, diagnosed as inactive echinoeoccal cysts, it was decided that surgery was not indicated. PATHOLOGICAL FEATURES The fully developed hydatid cyst is lined by three layers. The innermost lining is a germinative membrane giving rise to scolices and daughtercysts. The middle layer is essentially a non-cellular laminated structure. These two layers belong to the parasite. The entire cyst is surrounded by an enveloping adventitia, which is derived from the host organ as a reaction to the parasite and consists of connective tissue rich in vasculature, giant cells and eosinophils. The hydatid cysts may be complicated by rupture into the neighbouring tissues or by infection. A certain proportion of cysts die after attaining considerable size; thereafter they become hyalinized. Eventually they calcify, complete calcification indicating quiescence (Manson-Bahr, 1950). The development of the hydatid cyst is, thus, a dynamic process which may show three different stages; (1) An active expansive stage; (2) A biological death stage and (3) Resultant complications.
466
THE ANGIOGRAPHIC
DIAGNOSIS
OF E C H I N O C O C C O S I S
OF T H E L I V E R A N D
FI~. IA-B
54 year-old female admitted with right hypochondrial pains. The physical examination did not reveal any abnormalities. The Casoni skin test was positive. The routine radiological examinations and the liver scan were negative. (A) Coeliac angiography, arterial phase: Stretching of the hepatic arteries and suggestion of a "halo" about to commence. (B) Hepatographic phase: A filling defect is surrounded by a "halo" (arrows) Comment: A negative liver scan does not exclude the presence of quite a large biologically active echinococcal cyst.
FIG. 2A--B
52 year-old female. In the routine plain film of the abdomen, a sraall amorphous calcification was seen in the splenic region. The Casoni skin test and Weinberg complement fixation tests were negative. The splenic scan revealed a fairly large avascular area. (g) Coeliac angiography, arteria[phase: Distortion of the splenic artery branches and early appearance of an incomplete "halo" (arrow). (B) Splenographic phase: A large filling defect is seen, surrounded completely be a "a "halo" (arrows). Comment: Angiography demonstrated the real size of a biologically active echinococcal cyst in the spleen.
SPLEEN
467
468
CLINICAL
RADIOLOGY
FIG. 3A-B 42 year-old female, admitted with right hypochondrial pain and hepatomegaly. Complement fixation test for hydatid disease was negative and liver function tests were normal. The liver scan showed a large spherical defect in the right lobe. No calcifications were detected on the plain radiograph of the abdomen. (A) Coeliac angiography, early arterial phase: Stretching of the right hepatic artery branches and incompletely stained "halo" are seen. (B) A large filling defect is surrounded completely by a "halo". Comment: A t laparatomy, a large hydatid cyst was found to have caused almost complete atrophy of the right lobe of the liver. This case demonstrates that the "halo-sign" may still be present when the surrounding parenchyma is almost completely destroyed.
RESULTS Sixteen out of the 22 cases examined were biologically active cysts and 6 were inactive. According to our observations, the angiographic findings varied with these different stages of the disease but were similar in both liver and spleen. In the active expansive stage, like in all benign expanding lesions, the large and medium-sized hepatic and splenic arteries and the intrahepatic portal vein branches showed stretching, elongation and displacement (Figs. 1, 2, 3 and 7). No pathological vessels were visible. In the arterial, capillary and porto-venous capillary phases, the cyst caused a filling defect. Concomitantly, a 2-3 ram. wide, dense 'halo-like' staining appeared around the cysts (Figs. 1, 2, 3 and 7). A 'halo' was observed in 13 out of 16 cases of biologically active cysts both in the liver and the spleen. In 6 of the latter, a partial calcification of the mother cysts--or of a daughter-cyst--was present, but the 'halo' surrounded the large mother cyst in all of them (Figs. 2 and 7). In the 3 cases of biologically active cysts which were not surrounded by a 'halo', either a large cyst compressed the portal vein, or the larger part of the cyst was located subcapsularly (Fig. 4). In the 6 cases with biologically inactive cysts, 4 were completely calcified dead cysts (Fig. 5). In these
latter cases, the size of the filling defect in the hepatographic or splenographic phase corresponded to the calcified area and no 'halo' was present. In 2 other biologically inactive cases, the hepatographic phase showed that the calcification in the liver was surrounded by an irregular polygonal filling defect (Fig. 6). The irregularity of the filling defect in these latter cases was caused by contraction due to fibrosis of the mother cyst and represented a dead cyst which had not yet calcified. In 2 out of the 22 cases investigated, the hydatid ruptured into the biliary ducts. One of these was also infected but selective coeliac angiography showed, nevertheless, a regular 'halo-sign' (Fig. 7). In the other case, the angiography was performed because of hepatic calcification, suspected to be due to echinococcosis. This case did not show any angiographic signs of biological activity and was presumed to be an old contracted hydatid cyst, an assumption which was proved to be correct when the patient was later operated on for hydrops of the gall-bladder. DISCUSSION The 'halo-sign' seen on visceral angiography in cases ofechinococcosis of the liver was first reported by McNulty (t968). It is supposed to be caused on the one hand by the pressure of the expanding cyst
TIlE A N G I O G R A P H I C
D I A G N O S I S OF E C H I N O C O C C O S I S
OF T H E L I V E R A N D S P L E E N
469
FIG. 4 A-B-C 50 year-old female, complained o f upper abdominal pains. The physical examination did not reveal any abnormalities. The Weinberg complement fixation test was negative. The splenic scan was normal. (A) Plain radiograph of the abdomen: Thin egg-shell type calcification located in the splenic area. (B) Coeliac angiography, early arterial phase: Splenomegaly without distortion of the intrasplenic artery branches. (c) Splenographic phase: Homogenous staining of the spleen. No "halo-sign" is visible. Comment: This case demonstrates the angiographic features of subcapsular echinococcosis.
upon the host parenchyma, with resultant stasis, and on the other hand by the rich vasculature of the adventitia. The 'halo-sign' was encountered by us in the large majority o f cases of biologically active echinococcal cysts in the liver or in the spleen, and was not observed in the cases o f biologically dead cyst. Furthermore, we have not encountered a 'halo' in non-parasitic cysts o f the liver invesitgated by us by coeliac angiography; but we have observed it in a case of echinococcal cyst of the kidney. We therefore believe that the 'halo-sign' represents a characteristic, if not a pathognomonic sign of an echinococcal cyst in a parenchymatous organ and reflects the active biological stage of the disease. The 'halo-sign', in contrast to the calcification, also enabled us to evaluate the real size of the echinococcal cyst. As a matter o f fact, in the cases of biologically active cysts in which calcification was present, the latter was usually localized in a daughter-cyst, and the larger sized mother-cyst was recognized by the surrounding 'halo' (Figs. 1 and 2). However, the absence o f a 'halo-sign' is not a reliable proof that the cyst is biologically inactive; it was also absent when a larger part of the expanding cyst was located subcapsularly or when a large cyst compressed the portal vein. Infection or rupture of the hydatid cyst into the biliary tract did not alter the angiographic features in such a way as to affect recognition or suspicion o f these complications by means of this investigation (Fig. 1). However, it may be assumed that if the infection develops into a n abscess, the regular
'halo-sign' will disappear and be replaced by the irregular increased staining usually seen around an abscess. In these cases the differential diagnosis from primary pyogenic or amoebic abscess is probably impossible by angiography. In order not to confuse the 'halo-sign' with similar angiographic findings, it should be mentioned that in all abscesses of the liver, of parasitic or non-parasitic origin, we observed an increased staining of the 9arenchyma around the abscess. However, in contrast to the regular borders of the 'halo-sign', this increased density is broader and irregular, and its inner border is scalloped and ill-defined. Occasionally, richly vascularised malignant metastatic lesions of the liver may have a ring-like appearance, but these can easily be differentiated from the 'halo-sign'. The malignant lesions are fed by pathological vessels, are usually multiple and smaller than the 'halo' seen in echinococcosis. The staining of the gall-bladder wall during coeliac angiography may also cause a ring-like shadow, similar to the 'halo-sign', but the nature of this shadow can be determined by recognition of the feeding arteries of the gall-bladder (Deutsch, 1967) and if these are not visualised, intravenous cholangiography may solve the problem. Finally, the 'halo-sign' should not be confused with the angiographic staining of the fundus of the stomach which may be projected on the spleen or the left lobe of the liver.
470
CLINICAL
RADIOLOGY
FIG. 5 A-B 45 year-old male with upper abdominal pains. Physical, laboratory and routine barium studies were negative except for the presence of an amorphous area of calcification in the liver. (A) Coeliac angiography, arterialphase: No distortion of the hepatic arteries. (B) Hepatographic phase: Homogenous staining of the liver. No filling defect or "halo" is seen around the calcification. Comment: As there were no angiographic signs of activity, the case was considered as a biologically inactive cyst and surgical intervention was avoided.
FIG, 6 A--B 42 year-old female with abdominal pains. An amorphous calcification was found in the right lobe of the liver. (A) Coeliac angt'ography, early arterial phase: The right hepatic artery branches do not reach the periphery of the right lobe of the liver and are slightly distorted. The arrow indicates the calcification. (B) Hepatographic phase: A large filling defect with irregular polygonal contours is visualized, but no "halo" can be seen. Comment: The calcification is localized to a daughter-cyst. The irregular filling defect in the absence of a surrounding "halo" is caused by the contraction and fibrosis of the mother-cyst and represents an early sign of quiescence.
THE A N G I O G R A P H I C DIAGNOSIS OF ECI-IINOCOCCOSIS OF THE LIVER AND SPLEEN
471
FIG. 7 A--I~-C 42 year-old male with fever, hepatomegaly and jaundice. Plain radiograph of the abdomen showed small, amorphous area ofcalcification in the right lobe of the liver. (A) Coeliacangiography, arterialphase : Stretching ofthe hepatic arteries around the large mother-cyst. The arrow indicates a small calcified daughter-cyst. (B) Hepatographic phase: A large filling defect is surrounded by a "halo". (c) lntraoperative cholangiography: The dilated common bile duct shows filling defects caused by ruptured daughter-cysts. Comment: Angiography demonstrated the real size of the cyst, whereas the calcification was limited to a daughter-cyst. The presence of a surrounding "halo" indicated that the cyst was in an active stage. REFERENCES BONAKDARPOUR, A. (1967). Echinococcus Disease: Report of 112 cases from Ir0n and Review of 611 cases from United States. American Journal of Roentgenology, 99, 660-667. DEt~TSCH, V. (1967). Cholecysto-Angiography. American Journal of Roentgenology, 101, 608-616. GARABED~AN, A., MATOSStAN, M. & SmDAN, G. (1959). Correlative Study of Immunological Tests for Diagnosis of Hydatid Disease. American Journal Tropical Medicine, 8, 6%71.
MANSON-BAHR, P. (1950). Manson's Tropical Disease. Cassel & Co. Ltd., London, 13th Edition, 1080 pp. McNuLTY, J. G. (1968). Angiographic Manifestations of Hydatid Disease of the Liver. American Journal of Roentgenology, 102, 380-383. MORRIS, J., DOUST, B. ~; HANKS, T. (1967). The Roentgenologic and Radioisotopic Assessment of Hydatid Disease of the Liver. American Journal of Roentgenology, 101, 519-542.
NOTICE CHRISTIE HOSPITAL AND HOLT RADIUM INSTITUTE VISITORS' COURSES ONE week Visitors" Courses are held at the Christie Hospital twice a year, in November and May. These courses are primarily intended for visitors from this country and overseas who already have some knowledge of radiotherapy but who wish to see current methods and techniques being used in Manchester. They may be useful for D.M.R.T. and F.F.R. examination candidates but are not meant to be revision courses for either examination. During these courses there will be a full programme of talks, discussions and demonstrations by all the consultant radiotherapy staff of the hospital, which will include all the common varieties of disease treated by radiotherapy. The formal course will last five days beginning on the first Mondays in November and May. Visitors may, if they wish, remain for one further week to attend normal Out-patient, x-ray therapy, Radium Theatre and Mould Room work. No fee is asked for these courses but numbers will be limited. Prospective visitors are asked to write to Dr. E. C. Easson, Director of Radiotherapy, Christie Hospital, Withington, Manchester, 20, preferably at least one month in advance for further particulars.
THE ANGIOGRAPHIC DIAGNOSIS OF ECHINOCOCCOSIS OF THE LIVER AND SPLEEN IZHAK GARTI and VICTOR DEUTSCH
From the Departments of Diagnostic Radiology, Beilinson Hospital, Petach-Tikva, and Tel-Hashomer Government Hospital, Tel-Aviv University Medical School, Israel Selective visceral angiography is a useful, complementary method for the diagnosis of echinococcosis of the liver and spleen. The characteristic of the 'halo sign" provides information on the biological activity of the cyst. Angiography also provides the surgeon with important pre-operative information on the true size, number and localization of the cysts, the state of the surrounding parenchyma and the course of the blood vessels in the area. Tim diagnosis of echinococcosis or hydatid disease of the liver and spleen is based upon the history, physical and laboratory examinations, immunologic tests, radiographic and radioisotopic investigations. Unfortunately, all these investigations have only a varying degree of accuracy (Bonakdarpour, 1967; Morris et al., 1967; Garabedian et al., 1959). Radiological investigations play an important role in the diagnosis of hydatid cysts by demonstrating a round or oval calcified rim, or spotty calcified densities in the area of the liver or spleen, particularly in regions where hydatid disease is endemic. However, in the absence of calcifications, the radiological diagnosis of hydatid disease of the liver or spleen is difficult or even impossible. Moreover, if a calcified cyst is visualized on the plain film of the abdomen, additional non-calcified, biologically active cysts, can be missed: the calcifications may be localized in a daughter-cyst or multiple cysts may be present. The decision to operate on an asymptomatic calcified cyst is difficult without knowledge of the exact nature, true size and biological state of the cyst. Selective visceral angiography may provide important information: the purpose of this paper is to report on our observations. MATERIAL AND METHOD Our experience is based upon 22 cases of echinococcosis--18 in the liver and 4 in the spleen. In 20 patients the study was performed by selective coeliac and mesenteric angiography and in 2 patients by abdominal aortography. In 11 patients the indication for the angiographic examinations
was the presence of calcification, suspected to be due to echinocoecosis, on the plain films; in 7 patients the calcification was in the liver, and in 4 patients in the spleen. Seven patients were examined for unexplained hepatomegaly. Two other patients were examined because of the presence of abdominal masses, and another patient because of pains in the right hypochondrium and a positive Casoni test. In 18 patients the diagnosis of hydatid cyst was confirmed at operation. In 4 cases, diagnosed as inactive echinoeoccal cysts, it was decided that surgery was not indicated. PATHOLOGICAL FEATURES The fully developed hydatid cyst is lined by three layers. The innermost lining is a germinative membrane giving rise to scolices and daughtercysts. The middle layer is essentially a non-cellular laminated structure. These two layers belong to the parasite. The entire cyst is surrounded by an enveloping adventitia, which is derived from the host organ as a reaction to the parasite and consists of connective tissue rich in vasculature, giant cells and eosinophils. The hydatid cysts may be complicated by rupture into the neighbouring tissues or by infection. A certain proportion of cysts die after attaining considerable size; thereafter they become hyalinized. Eventually they calcify, complete calcification indicating quiescence (Manson-Bahr, 1950). The development of the hydatid cyst is, thus, a dynamic process which may show three different stages; (1) An active expansive stage; (2) A biological death stage and (3) Resultant complications.
466
THE ANGIOGRAPHIC
DIAGNOSIS
OF E C H I N O C O C C O S I S
OF T H E L I V E R A N D
FI~. IA-B
54 year-old female admitted with right hypochondrial pains. The physical examination did not reveal any abnormalities. The Casoni skin test was positive. The routine radiological examinations and the liver scan were negative. (A) Coeliac angiography, arterial phase: Stretching of the hepatic arteries and suggestion of a "halo" about to commence. (B) Hepatographic phase: A filling defect is surrounded by a "halo" (arrows) Comment: A negative liver scan does not exclude the presence of quite a large biologically active echinococcal cyst.
FIG. 2A--B
52 year-old female. In the routine plain film of the abdomen, a sraall amorphous calcification was seen in the splenic region. The Casoni skin test and Weinberg complement fixation tests were negative. The splenic scan revealed a fairly large avascular area. (g) Coeliac angiography, arteria[phase: Distortion of the splenic artery branches and early appearance of an incomplete "halo" (arrow). (B) Splenographic phase: A large filling defect is seen, surrounded completely be a "a "halo" (arrows). Comment: Angiography demonstrated the real size of a biologically active echinococcal cyst in the spleen.
SPLEEN
467
468
CLINICAL
RADIOLOGY
FIG. 3A-B 42 year-old female, admitted with right hypochondrial pain and hepatomegaly. Complement fixation test for hydatid disease was negative and liver function tests were normal. The liver scan showed a large spherical defect in the right lobe. No calcifications were detected on the plain radiograph of the abdomen. (A) Coeliac angiography, early arterial phase: Stretching of the right hepatic artery branches and incompletely stained "halo" are seen. (B) A large filling defect is surrounded completely by a "halo". Comment: A t laparatomy, a large hydatid cyst was found to have caused almost complete atrophy of the right lobe of the liver. This case demonstrates that the "halo-sign" may still be present when the surrounding parenchyma is almost completely destroyed.
RESULTS Sixteen out of the 22 cases examined were biologically active cysts and 6 were inactive. According to our observations, the angiographic findings varied with these different stages of the disease but were similar in both liver and spleen. In the active expansive stage, like in all benign expanding lesions, the large and medium-sized hepatic and splenic arteries and the intrahepatic portal vein branches showed stretching, elongation and displacement (Figs. 1, 2, 3 and 7). No pathological vessels were visible. In the arterial, capillary and porto-venous capillary phases, the cyst caused a filling defect. Concomitantly, a 2-3 ram. wide, dense 'halo-like' staining appeared around the cysts (Figs. 1, 2, 3 and 7). A 'halo' was observed in 13 out of 16 cases of biologically active cysts both in the liver and the spleen. In 6 of the latter, a partial calcification of the mother cysts--or of a daughter-cyst--was present, but the 'halo' surrounded the large mother cyst in all of them (Figs. 2 and 7). In the 3 cases of biologically active cysts which were not surrounded by a 'halo', either a large cyst compressed the portal vein, or the larger part of the cyst was located subcapsularly (Fig. 4). In the 6 cases with biologically inactive cysts, 4 were completely calcified dead cysts (Fig. 5). In these
latter cases, the size of the filling defect in the hepatographic or splenographic phase corresponded to the calcified area and no 'halo' was present. In 2 other biologically inactive cases, the hepatographic phase showed that the calcification in the liver was surrounded by an irregular polygonal filling defect (Fig. 6). The irregularity of the filling defect in these latter cases was caused by contraction due to fibrosis of the mother cyst and represented a dead cyst which had not yet calcified. In 2 out of the 22 cases investigated, the hydatid ruptured into the biliary ducts. One of these was also infected but selective coeliac angiography showed, nevertheless, a regular 'halo-sign' (Fig. 7). In the other case, the angiography was performed because of hepatic calcification, suspected to be due to echinococcosis. This case did not show any angiographic signs of biological activity and was presumed to be an old contracted hydatid cyst, an assumption which was proved to be correct when the patient was later operated on for hydrops of the gall-bladder. DISCUSSION The 'halo-sign' seen on visceral angiography in cases ofechinococcosis of the liver was first reported by McNulty (t968). It is supposed to be caused on the one hand by the pressure of the expanding cyst
TIlE A N G I O G R A P H I C
D I A G N O S I S OF E C H I N O C O C C O S I S
OF T H E L I V E R A N D S P L E E N
469
FIG. 4 A-B-C 50 year-old female, complained o f upper abdominal pains. The physical examination did not reveal any abnormalities. The Weinberg complement fixation test was negative. The splenic scan was normal. (A) Plain radiograph of the abdomen: Thin egg-shell type calcification located in the splenic area. (B) Coeliac angiography, early arterial phase: Splenomegaly without distortion of the intrasplenic artery branches. (c) Splenographic phase: Homogenous staining of the spleen. No "halo-sign" is visible. Comment: This case demonstrates the angiographic features of subcapsular echinococcosis.
upon the host parenchyma, with resultant stasis, and on the other hand by the rich vasculature of the adventitia. The 'halo-sign' was encountered by us in the large majority o f cases of biologically active echinococcal cysts in the liver or in the spleen, and was not observed in the cases o f biologically dead cyst. Furthermore, we have not encountered a 'halo' in non-parasitic cysts o f the liver invesitgated by us by coeliac angiography; but we have observed it in a case of echinococcal cyst of the kidney. We therefore believe that the 'halo-sign' represents a characteristic, if not a pathognomonic sign of an echinococcal cyst in a parenchymatous organ and reflects the active biological stage of the disease. The 'halo-sign', in contrast to the calcification, also enabled us to evaluate the real size of the echinococcal cyst. As a matter o f fact, in the cases of biologically active cysts in which calcification was present, the latter was usually localized in a daughter-cyst, and the larger sized mother-cyst was recognized by the surrounding 'halo' (Figs. 1 and 2). However, the absence o f a 'halo-sign' is not a reliable proof that the cyst is biologically inactive; it was also absent when a larger part of the expanding cyst was located subcapsularly or when a large cyst compressed the portal vein. Infection or rupture of the hydatid cyst into the biliary tract did not alter the angiographic features in such a way as to affect recognition or suspicion o f these complications by means of this investigation (Fig. 1). However, it may be assumed that if the infection develops into a n abscess, the regular
'halo-sign' will disappear and be replaced by the irregular increased staining usually seen around an abscess. In these cases the differential diagnosis from primary pyogenic or amoebic abscess is probably impossible by angiography. In order not to confuse the 'halo-sign' with similar angiographic findings, it should be mentioned that in all abscesses of the liver, of parasitic or non-parasitic origin, we observed an increased staining of the 9arenchyma around the abscess. However, in contrast to the regular borders of the 'halo-sign', this increased density is broader and irregular, and its inner border is scalloped and ill-defined. Occasionally, richly vascularised malignant metastatic lesions of the liver may have a ring-like appearance, but these can easily be differentiated from the 'halo-sign'. The malignant lesions are fed by pathological vessels, are usually multiple and smaller than the 'halo' seen in echinococcosis. The staining of the gall-bladder wall during coeliac angiography may also cause a ring-like shadow, similar to the 'halo-sign', but the nature of this shadow can be determined by recognition of the feeding arteries of the gall-bladder (Deutsch, 1967) and if these are not visualised, intravenous cholangiography may solve the problem. Finally, the 'halo-sign' should not be confused with the angiographic staining of the fundus of the stomach which may be projected on the spleen or the left lobe of the liver.
470
CLINICAL
RADIOLOGY
FIG. 5 A-B 45 year-old male with upper abdominal pains. Physical, laboratory and routine barium studies were negative except for the presence of an amorphous area of calcification in the liver. (A) Coeliac angiography, arterialphase: No distortion of the hepatic arteries. (B) Hepatographic phase: Homogenous staining of the liver. No filling defect or "halo" is seen around the calcification. Comment: As there were no angiographic signs of activity, the case was considered as a biologically inactive cyst and surgical intervention was avoided.
FIG, 6 A--B 42 year-old female with abdominal pains. An amorphous calcification was found in the right lobe of the liver. (A) Coeliac angt'ography, early arterial phase: The right hepatic artery branches do not reach the periphery of the right lobe of the liver and are slightly distorted. The arrow indicates the calcification. (B) Hepatographic phase: A large filling defect with irregular polygonal contours is visualized, but no "halo" can be seen. Comment: The calcification is localized to a daughter-cyst. The irregular filling defect in the absence of a surrounding "halo" is caused by the contraction and fibrosis of the mother-cyst and represents an early sign of quiescence.
THE A N G I O G R A P H I C DIAGNOSIS OF ECI-IINOCOCCOSIS OF THE LIVER AND SPLEEN
471
FIG. 7 A--I~-C 42 year-old male with fever, hepatomegaly and jaundice. Plain radiograph of the abdomen showed small, amorphous area ofcalcification in the right lobe of the liver. (A) Coeliacangiography, arterialphase : Stretching ofthe hepatic arteries around the large mother-cyst. The arrow indicates a small calcified daughter-cyst. (B) Hepatographic phase: A large filling defect is surrounded by a "halo". (c) lntraoperative cholangiography: The dilated common bile duct shows filling defects caused by ruptured daughter-cysts. Comment: Angiography demonstrated the real size of the cyst, whereas the calcification was limited to a daughter-cyst. The presence of a surrounding "halo" indicated that the cyst was in an active stage. REFERENCES BONAKDARPOUR, A. (1967). Echinococcus Disease: Report of 112 cases from Ir0n and Review of 611 cases from United States. American Journal of Roentgenology, 99, 660-667. DEt~TSCH, V. (1967). Cholecysto-Angiography. American Journal of Roentgenology, 101, 608-616. GARABED~AN, A., MATOSStAN, M. & SmDAN, G. (1959). Correlative Study of Immunological Tests for Diagnosis of Hydatid Disease. American Journal Tropical Medicine, 8, 6%71.
MANSON-BAHR, P. (1950). Manson's Tropical Disease. Cassel & Co. Ltd., London, 13th Edition, 1080 pp. McNuLTY, J. G. (1968). Angiographic Manifestations of Hydatid Disease of the Liver. American Journal of Roentgenology, 102, 380-383. MORRIS, J., DOUST, B. ~; HANKS, T. (1967). The Roentgenologic and Radioisotopic Assessment of Hydatid Disease of the Liver. American Journal of Roentgenology, 101, 519-542.
NOTICE CHRISTIE HOSPITAL AND HOLT RADIUM INSTITUTE VISITORS' COURSES ONE week Visitors" Courses are held at the Christie Hospital twice a year, in November and May. These courses are primarily intended for visitors from this country and overseas who already have some knowledge of radiotherapy but who wish to see current methods and techniques being used in Manchester. They may be useful for D.M.R.T. and F.F.R. examination candidates but are not meant to be revision courses for either examination. During these courses there will be a full programme of talks, discussions and demonstrations by all the consultant radiotherapy staff of the hospital, which will include all the common varieties of disease treated by radiotherapy. The formal course will last five days beginning on the first Mondays in November and May. Visitors may, if they wish, remain for one further week to attend normal Out-patient, x-ray therapy, Radium Theatre and Mould Room work. No fee is asked for these courses but numbers will be limited. Prospective visitors are asked to write to Dr. E. C. Easson, Director of Radiotherapy, Christie Hospital, Withington, Manchester, 20, preferably at least one month in advance for further particulars.