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Paraplegia, A Rare Complication of Translumbar Aortography
THE .JOURNAL OF UROLOGY
Vol. 75, No. 2, February 1956 Printed in U.S.A.
PARAPLEGIA, A RARE COMPLICATION OF TRAN"SLUMBAR AORTOGRAPHY BENJAMIN S. ABESHOUSE
AND
ANTONIO T. TIONGSON
From the Department of Urology, Sinai Hospital, Baltimore, Jl!Id.
In recent years interest in translumbar aortography has increased considerably. The important diagnostic value and relative safety of this procedure are universally accepted and practiced. Because of its wide use one should expect to encounter some complications. In an editorial on arteriography published in the Journal of the American Medical Association, January 1952,1 the statement is made that the consensus of opinion is that translumbar aortography is safer and simpler than the method of retrograde catheterization of the femoral artery. However, one must realize that translumbar aortography is not without potential danger. Melick and his coworkers2 reviewed the present status of aortography and stressed three possible dangers attending this procedure, viz., 1) hern.orrhage from the puncture site in the aorta, 2) necrosis of the intestines resulting from inadvertent injection of the contrast directly into the superior mesenteric artery, and 3) sensitivity reactions to the contrast medium. Wagner and Price3 and Melick, Yarbrough and Boler4 reported fatalities due to necrosis of the intestines following the injection of 80 per cent sodium iodide i.nto the superior mesenteric artery at time of aortography. Gould and Willson (1954) 5 made an extensive review of the various complications of translumbar aortography and found the most common complication to be serious renal damage, which occurred in 14 cases. In 6 cases the contrast medium was injected directly i.nto one renal artery with resultant severe renal damage and no fatalities. In 8 cases, the contrast medium was injected into the aorta and bilateral renal shutdown occurred, which was fatal in 2 cases. The rnajority of the 8 patients had a high aortic obstruction and several had severe pre-existing renal damage. Josselson and Kaplan (1954) 6 subsequently reported a fatal case of anuriafollowing translumbar aortography with neo-iopax. The purpose of this paper is to report another case of the unusual complication of complete paraplegia following translumbar aortography. The literature contains very few reported cases, viz., 1) Antoni and Lindgren (1949), 7 2) Boyarsky (1954), 8 and 3) Baurys (1954). 9 Baurys stated that i\elson10 was Accepted for publication September 21, 1955. 1 Editorial on aortography. J. A. M.A., 148: 162, 1952. 2 Melick, W. F., Byrne, J.E. and Boler, T. D.: J. Urol., 67: 1019, 1952. 3 Wagner, F. B. and Price, A. D.: Surgery, 27: 621, 1950. 4 Melick, W. F., Yarbrough, C. P. and Boler, T. D.: .J. Urol., 66: 458, 1951. 5 Gould, D. M. and Willson, J. K.: Am. J. Med. Sci., 228: 586, 1954. 6 JosselROn, A. J. and Kaplan, A.H.: J. Urol., 72: 256, 1954. 7 Antoni, N. and Lindgren, E.: Acta Chir. Scandinav., 98: 230, 1949. 8 Boyarsky, S.: .J. A. M.A., 156: 509, 1954. 9 Baurys, W.: Urologist's Correspondence Club, Oct. 5, 1!)54; idem, Person:d communication. 10 Nelson: Quoted by Baurys, loc. cit. 348
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acquainted with two additional cases occurring in Europe and Canada respectively. The details in these 2 cases are lacking except that in both patients complete paraplegia developed and they survived. In the reported cases the chief symptoms of this complication are paraplegia with loss of reflexes (areflexia), loss of response to light and painful stimuli (anesthesia and analgesia), loss of response to heat and cold (thermanesthesia), and loss of bladder control. Antoni and Lindgren's patient was a 68-year-old man with arteriosclerosis and peripheral vascular occlusion. He died 3 months after the onset of gangrene of a leg that followed aortography with 70 per cent iodopyracet. Boyarsky's patient was a 63-year-old man with evidence of peripheral and retinal arteriosclerosis who complained of lower abdominal cramps due to an aneurysm of abdominal aorta. Paraplegia developed immediately after aortography with 70 per cent sodium acetrizoate (urokon sodium). The patient made a partial recovery from the paraplegia and 2 months later he was ambulatory with crutches, but had a partial spastic paresis of both lower extremities. He regained his control of urination and had no residual urine. Baurys's patient was a 68-year-old woman with a right renal cyst. Following translumbar aortography (type of contrast medium not mentioned), she experienced complete loss of motor power and pain perception, which persisted for 3 weeks without change when she died suddenly with a temperature of 103F of undetermined origin. Unfortunately, permission for autopsy was not granted. CASE REPORT
H. E., a 52-year-old white man, married, painter, was referred by Dr. Joseph Skloven. He was admitted to the urological service of the Sinai Hospital on October 25, 1953 complaining of pain in both loins of 2 weeks' duration. The pain was described as dull, gnawing, intermittent, and annoying. One week prior to admission a plain film of the abdomen was taken by his family physician, and the patient was told that he had a calcified mass in the left kidney region and a stone in the right kidney. Hospitalization and further study were advised. Past history disclosed treatment for lead poisoning in 1925 acquired as a result of his occupation as a painter. In 1926 he had an accident and sustained several fractured left ribs with left lung complications. He had no history of tuberculosis, syphilis, or allergic disease. Physical examination was essentially negative except for the presence of a firm, globular, nontender mass in the left lumbar region, which did not move during respiration. Blood pressure was 120 mm. Hg systolic and 80 mm. Hg diastolic. The hematocrit, red blood count, white blood count and differential count, blood sugar, blood urea, serologic test for syphilis, urinalysis, and electrocardiogram were within normal limits. On October 22, 1953, excretory urography revealed the right kidney to have a normal pattern, and the left kidney did not fill. There was a large calcified mass in the left retroperitoneal area, which was regarded as probably renal in
350
B. S. ABESHOUSE AND A. T. TIONGSON
Fm. 1. A, excretory urogram (15-minute film) showing normal right kidney and large calcified shadow in left renal area. B, aortogram showing normal blood supply of right kidney and displaced renal artery supplying left renal mass. Calcified mass 11ppears attached to kidney area.
origin (fig. 1, A). Barium enema and gastrointestinal series were not remarkable except for multiple small diverticula in the sigmoid. On October 29, 195:3, cystoscopy and retrograde pyelography were performed. There was a slight prominence of the posterior portion of the vesical neck due to median bar formation. The right ureteral orifice was normal in size, shape, and position, and was easily catheterized with a 6F ureteral catheter. The left orifice appeared as a faint dimpling and could not be catheterized. On November 2, 1952 translumbar aortography under 2 per cent pentothal anesthesia was carried out -with the patient in the prone position on the x-ray table. The usual No. 18 gauge long needle used for aortography was easily introduced into the aorta at the level of the second lumbar vertebra. A preliminary injection of 2 cc of 70 per cent urokon was made directly into the aorta as a sensitivity test with no reaction. During the injection of 30 cc of 70 per cent urokon, the patient had generalized convulsions, which were more marked in the lower extremities and trunk, and lasted about ten seconds. The configuration of the right renal vessels was normal. A smaller Yessel is seen partially filled and extending upward toward the region of the left kidney. This probably represented the left renal artery. There is no vascular pattern noted around or within the previously described cystic calcified mass. The remaining visualized aortic branches are grossly normal (fig. 1, B). The patient was returned to the ward in fairly good condition. AJter he had fully recovered from the anesthesia about six hours later, he was unable to move his lower extremities. Examination at this time revealed complete flaccid paralysis of both lower extremities ,vith loss of tendon reflexes at both knees and ankles.
RARE COI\IIPLIC_\TIO:\: OF THANSLUMBAR AORTOGHAPHY
The reaction to pain and temperature was absent below the level of the (-:ighth thoraeic vertebra_ The right foot could be slightly flexed and extended Sous::ition of vibration and positjon was good. The next morning Dr. Clinton Harrison, attending neurosurgeon, examined the patient and confirmed the aforementioned findings. His impressjon wa~ thrombosis of the anterior spinal artery or Rpasm of this artery following in_jec-tion of the contra,~t medium. l\!Ieehanical compression of the spinal cord war:: ruled out as there ·was no dynamic block on lumbar puncture done on No,·ember ±, 1953. The spinal fluid was clear and under normal pressure, the spinal fluid sugar was 68 mg. per cent and the total protein was 420 mg. per een1. ~:o evidence of vertebral fracture was present on the roentgcnograms of the spine. The patient was unable to void and an indwelling urethral catheter '18F Foley with 5 cc bag) was inserted and connected up to a McKenna tidal irrigation apparatus in order to de1'elop an automatic blaclde1·. He moved his bowels i11vol1mtarily in bed. He showed a gradual and progressive improvement for on November U, 19Ei3 the sensory levels of pain and temperature were equivocal at the level of the eighth thoracic vertebra and positive at the eleventh and twelfth t.bnraeic vertebrae. The response to tOLlCh and vibration continued good. D,,spii.t, good nursing care, a deeubLtus ulcer developed and the patient was placed on a Stryker frame. On December 12, 1953, he could flex his right knee slightly and move the right foot freely in any direction. The left toe could be mo1'cd io a lesser dPgree. Pain and temperature responses remained unchanged. Physiot.hernpy and massage were initiated in an effort to preserve aud improve Lhe muscles of his legs and baek. On December 18, Hl53, cystmnetric study revealed a mildly hypoto11ic bladder with fairly good bladder contractions and frequent uninhibitell contractions . Bladder sensation of fullness was absent_ The Foley catheter was nlmo\'Cd and he n1ided at intervals of four to five hours aided by simultaneous maimal comprestiion of the bladder. The residual urine was 40 cc. On March 8, 1954 the patient began to complain of pain in the chest and left hip, and the decubitus ulcer recurred. He became anorexic and lost weight. On April 18, roentgenographic study revealed metastar::es in the lungt:i, ribs, el!wi.cl1\ pelvic boDes, and lumbar vertebrae. His course was progressively downhill, and he expired un April 27, 19.54. of gcneralir.ed carcinomatosis. A potitrnortem examination was performed about two hours after cleai h. The positive findings included; 1) malignant Grawitz turnor of upper polo of left kidney, 2) metastases to adrenals, liver, periportal, periaortic, and iuguinal lymph nodes, left clavicle, ribs, vertebrae, and skull, ;3) encrusted ,·ystitis, 4) calcification of hydronephrotic left kidney, 5) coronary heart disease, f\) arterJoselernsic1, 7) pulmonary emphysema and atelectasis, 8) benign hypnrtwphy of the prostate. The spinal cord 1vas removed intact for further study. Careful study did not reveal any thrombor::is or occlusion of Lhe anterior :c;pinal arteries by tumor cells or organized blood clot. }fo,tologic:al examination of the spinal cord was rnadc by Dr. John YVagner,
352
B. S. ABESHOUSE AND A. T. TIONGSON
consultant in neuropathology, Department of Laboratories. "Sections from the lower cervical, thoracic and thoracolumbar spinal cord were stained with hematoxylin and eosin. The nerve roots and meninges are apparently normal and without evidence of inflammatory change. In the cervicothoracic area, scattered fresh petechial hemorrhages and moderate congestive changes were found. The ventral horn cells in the thoracic and thoracolumbar areas are slightly reduced in number and showed pigmentary changes, particularly in the thoracic areas. The dorsal horn cells were also slightly reduced in number. "The most conspicuous lesion is an irregular sort of demyelination occupying principally the ventrolateral areas of the lateral funiculi and most of the ventral funiculus throughout all the section examined. A few irregular areas of demyelination are seen adjacent to the dorsal sulcus. The ventral areas of demyelination appear continuous with the ventral nerve roots, but in some sec-
Fm. 2. Photomicrographs. A, section of thoracic spinal cord showing areas of demyelination occupying principally ventrolateral areas of lateral funiculi and most of ventral funiculus. B, section (low power) of thoracolumbar portion of spinal cord showing presence of macrophages and dissolution of tissue in one lateral funiculus.
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353
tions this is not too clear. In one area in the midthoracic region, there is a focus in which almost complete dissolution of tissue is seen in one lateral funiculus. Macrophages are seen in this area, which would indicate that a cavity is in the process of formation. There is no intrinsic inflammatory activity. "The process of demyelination appears to be most intense in the thoracolumbar region where it involved the ventrolateral areas and to a lesser degree the gray matter of the ventral horns. The ventral nerve roots are affected with some slight possibility of the dorsal roots also being involved along with the sensory pathways in the lateral funiculi. One might synthesize, therefore, an irregularly segmented motor sensory syndrome with a predominantly lower motor neuron component along with a lateral and ventral spinothalamic syndrome, possibly of irregular distribution and of variable intensity. There is possibly some change in the dorsal column, which is difficult to detect and interpret. The etiology is not evident from the sections examined. There is no acute process, the duration of the lesion being measured certainly in terms of months or many weeks. Indeed a few small areas of gliosis seem to confirm the chronic nature of this process." DISCUSSION
The authors are of the opinion that the cause of the paraplegia in this case was the direct toxic action of the 70 per cent urokon (sodium acetrozoate) on the spinal cord. No definite thrombosis of the anterior spinal artery or its branches could be demonstrated. The pathological examination of the spinal cord revealed a process of demyelinization, which was more intense in the thoracolumbar region and principally involving the ventrolateral areas of the lateral funiculi and most of the ventral funiculus. The nutrient artery supplying this portion of the cord is the anterior spinal artery (i.e., anterior radicularis magna). The blood supply of the spinal cord has been studied by many investigators, particularly Kadyis.11 The latter demonstrated that the vascular supply of the spinal cord is predominantly of a transverse and segmental nature and that the anterior spinal artery does not exist as one continuous long-reaching blood vessel, but rather is composed of a series or chain of smaller arteries of shorter longitudinal extent. The spinal cord appears to be supplied by six to eight anterior radicular arteries. Their distribution is not symmetrical for there are usually one or two in the lumbar region, one in the lower thoracic region, none or one in the middle thoracic region, one or two in the lower cervical region and one in the upper cervical region. The largest artery is the one found in the lower thoracic or lumbar portion of the cord, which is designated as the "arterial radicularis magnae" by Kadyis. This artery measures 872 microns in diameter in the adult, is single, not symmetrical, and occurs on one side only, usually the left. It is most frequently found in the second lumbar segment, but may be found in any segment between the eighth thoracic and second lumbar. With the patient in the prone position and the direction of the needle pointing toward the ventral surface of the aorta, one can readily understand how a large 11
Kadyis: Quoted by Antoni and Lindgren, loc. cit.
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B. S. ABESHOUSE AND A. T. TIONGSON
stream of highly concentrated medium injected under violent pressure could enter the arteriae radicularis magna and permit the direct toxic action of the drug upon the spinal cord. In this respect it is interesting to note that Hol and Skjervan12 have performed an interesting experimental study of the causes of spinal cord damage following aortography. They performed abdominal aortography in 18 rabbits by injecting the contrast medium (20 per cent diodrast) through a cannula inserted into the exposed left renal artery. They found that the repeated injections of this high concentration of the contrast medium into the abdominal aorta in rabbits gave rise to toxic damage to the spinal cord as a result of permeation of the spinal arteries by the contrast medium. Spasms and paralysis of the hind parts were encountered. The cord lesions occurred when the animals were injected in the supine position and not in the prone position. It is important to note that the technique and position of the animal employed were not the same as those used in translumbar aortography. There is no unanimity of opinion concerning the pathogenesis of paraplegia in translumbar aortography. Antoni and Lindgren maintained that the lesion was caused by compression of the aorta by the pillow placed beneath the abdomen, thereby supporting Steno's experiment (Niels Stensen 1638-1686) on compression of the abdominal aorta at the level of the renal arteries in rabbits producing motor and sensory paralysis of the lower part of the body. Boyarsky was the first to attribute the paraplegia to the toxic action of the contrast medium on the spinal cord, and the authors concur with this opinion. Hol and Skjervan have maintained that damage to the spinal cord following translumbar aortography may be expected theoretically under the following circumstances, singly or combined, viz., 1) supine position of the subject, 2) prolonged exposure to the contrast medium, 3) repeated injections of the contrast medium at short intervals, and 4) pre-existing weakness of the arteries of the spinal cord. They pointed out that with the patient in the supine position the high specific gravity of the contrast medium predisposes to the high concentration of the contrast medium with the dorsal arteries supplying the spinal cord. They maintained that this phenomenon is more likely to occur where aortography is performed by the method of retrograde catheterization of the femoral artery wherein filling of the dorsal branches of the aorta as well as the renal arteries occurs. We have failed to observe a single case of filling of the dorsal branches of aorta and the spinal arteries in more than 150 cases of retrograde aortographies. Hol and Skjervan also suggested the possible causative role of prolonged exposure to the contrast medium resulting from retardation of the bloodstream in cases of aortic coarctation, embolus or thrombus formation, reduced blood pressure, abdominal compression and possibly injections too violently performed in a proximal direction. Little consideration has been given to the likelihood of spinal cord damage being caused by localized ischemia resulting from transient or permanent vasospasm of the dorsal arteries supplying the spinal cord and induced by the velocity of the injection on the direct chemical action of the highly concentrated 12
Hol, R. and Skjervan, 0.: Acta. radiologica, 42: 276, 1954.
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355
contrast medium. According to Boyarsky, transient vascular spasm has been observed repeatedly following the use of organic iodides, but no case of permanent thrombosis has been reported although such cases have occurred following the use of inorganic (sodium) iodides. Goodwin and .Walter13 have successfully employed the intra-aortic injection of 3 to 6 cc of 1 per cent procaine immediately before injecting into the aorta 20 to 30 cc of the contrast medium in order to prevent the brief cramping pains in the abdomen and lower extremities, which are due to transient arterial spasm caused by the irritating effect of the organic iodide contrast medium. CONCLUSION
A rare complication of translumbar aortography characterized by sudden onset of paraplegia with areflexia, thermanesthesia, and loss of bladder and rectal control is reported. The complication occurred 6 hours after the injection of 70 per cent urokon sodium into the abdominal aorta. The procedure was done in the usual manner and all the customary precautions were employed. Although this is the fourth authentic case reported in the literature, the authors are inclined to believe that the true incidence of this complication is greater than these reports indicate. The authors believe that the cause of the paraplegia was the spinal cord changes produced by direct toxic action of the highly concentrated contrast medium which reached the spinal cord through the anterior spinal arteries and its collateral branches. The possible etiological role of a transient or permanent vasospasm or thrombosis of the spinal artery cannot be completely excluded despite the fact that no evidence of vasoconstriction or thrombosis was found in the pathological examination of the affected tissue. The authors reaffirm their belief that translumbar aortography is a relatively safe and simple procedure, but its use as a diagnostic procedure must always be carefully evaluated in any given case. The possible complications of this procedure must always be borne in mind.
100 W. Monument St., Baltimore 1, Md. (B. S. A.) 13
Goodwin, W. E. and Walter, R. C.: Angiography, 4: 410, 1953.
Vol. 75, No. 2, February 1956 Printed in U.S.A.
PARAPLEGIA, A RARE COMPLICATION OF TRAN"SLUMBAR AORTOGRAPHY BENJAMIN S. ABESHOUSE
AND
ANTONIO T. TIONGSON
From the Department of Urology, Sinai Hospital, Baltimore, Jl!Id.
In recent years interest in translumbar aortography has increased considerably. The important diagnostic value and relative safety of this procedure are universally accepted and practiced. Because of its wide use one should expect to encounter some complications. In an editorial on arteriography published in the Journal of the American Medical Association, January 1952,1 the statement is made that the consensus of opinion is that translumbar aortography is safer and simpler than the method of retrograde catheterization of the femoral artery. However, one must realize that translumbar aortography is not without potential danger. Melick and his coworkers2 reviewed the present status of aortography and stressed three possible dangers attending this procedure, viz., 1) hern.orrhage from the puncture site in the aorta, 2) necrosis of the intestines resulting from inadvertent injection of the contrast directly into the superior mesenteric artery, and 3) sensitivity reactions to the contrast medium. Wagner and Price3 and Melick, Yarbrough and Boler4 reported fatalities due to necrosis of the intestines following the injection of 80 per cent sodium iodide i.nto the superior mesenteric artery at time of aortography. Gould and Willson (1954) 5 made an extensive review of the various complications of translumbar aortography and found the most common complication to be serious renal damage, which occurred in 14 cases. In 6 cases the contrast medium was injected directly i.nto one renal artery with resultant severe renal damage and no fatalities. In 8 cases, the contrast medium was injected into the aorta and bilateral renal shutdown occurred, which was fatal in 2 cases. The rnajority of the 8 patients had a high aortic obstruction and several had severe pre-existing renal damage. Josselson and Kaplan (1954) 6 subsequently reported a fatal case of anuriafollowing translumbar aortography with neo-iopax. The purpose of this paper is to report another case of the unusual complication of complete paraplegia following translumbar aortography. The literature contains very few reported cases, viz., 1) Antoni and Lindgren (1949), 7 2) Boyarsky (1954), 8 and 3) Baurys (1954). 9 Baurys stated that i\elson10 was Accepted for publication September 21, 1955. 1 Editorial on aortography. J. A. M.A., 148: 162, 1952. 2 Melick, W. F., Byrne, J.E. and Boler, T. D.: J. Urol., 67: 1019, 1952. 3 Wagner, F. B. and Price, A. D.: Surgery, 27: 621, 1950. 4 Melick, W. F., Yarbrough, C. P. and Boler, T. D.: .J. Urol., 66: 458, 1951. 5 Gould, D. M. and Willson, J. K.: Am. J. Med. Sci., 228: 586, 1954. 6 JosselROn, A. J. and Kaplan, A.H.: J. Urol., 72: 256, 1954. 7 Antoni, N. and Lindgren, E.: Acta Chir. Scandinav., 98: 230, 1949. 8 Boyarsky, S.: .J. A. M.A., 156: 509, 1954. 9 Baurys, W.: Urologist's Correspondence Club, Oct. 5, 1!)54; idem, Person:d communication. 10 Nelson: Quoted by Baurys, loc. cit. 348
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349
acquainted with two additional cases occurring in Europe and Canada respectively. The details in these 2 cases are lacking except that in both patients complete paraplegia developed and they survived. In the reported cases the chief symptoms of this complication are paraplegia with loss of reflexes (areflexia), loss of response to light and painful stimuli (anesthesia and analgesia), loss of response to heat and cold (thermanesthesia), and loss of bladder control. Antoni and Lindgren's patient was a 68-year-old man with arteriosclerosis and peripheral vascular occlusion. He died 3 months after the onset of gangrene of a leg that followed aortography with 70 per cent iodopyracet. Boyarsky's patient was a 63-year-old man with evidence of peripheral and retinal arteriosclerosis who complained of lower abdominal cramps due to an aneurysm of abdominal aorta. Paraplegia developed immediately after aortography with 70 per cent sodium acetrizoate (urokon sodium). The patient made a partial recovery from the paraplegia and 2 months later he was ambulatory with crutches, but had a partial spastic paresis of both lower extremities. He regained his control of urination and had no residual urine. Baurys's patient was a 68-year-old woman with a right renal cyst. Following translumbar aortography (type of contrast medium not mentioned), she experienced complete loss of motor power and pain perception, which persisted for 3 weeks without change when she died suddenly with a temperature of 103F of undetermined origin. Unfortunately, permission for autopsy was not granted. CASE REPORT
H. E., a 52-year-old white man, married, painter, was referred by Dr. Joseph Skloven. He was admitted to the urological service of the Sinai Hospital on October 25, 1953 complaining of pain in both loins of 2 weeks' duration. The pain was described as dull, gnawing, intermittent, and annoying. One week prior to admission a plain film of the abdomen was taken by his family physician, and the patient was told that he had a calcified mass in the left kidney region and a stone in the right kidney. Hospitalization and further study were advised. Past history disclosed treatment for lead poisoning in 1925 acquired as a result of his occupation as a painter. In 1926 he had an accident and sustained several fractured left ribs with left lung complications. He had no history of tuberculosis, syphilis, or allergic disease. Physical examination was essentially negative except for the presence of a firm, globular, nontender mass in the left lumbar region, which did not move during respiration. Blood pressure was 120 mm. Hg systolic and 80 mm. Hg diastolic. The hematocrit, red blood count, white blood count and differential count, blood sugar, blood urea, serologic test for syphilis, urinalysis, and electrocardiogram were within normal limits. On October 22, 1953, excretory urography revealed the right kidney to have a normal pattern, and the left kidney did not fill. There was a large calcified mass in the left retroperitoneal area, which was regarded as probably renal in
350
B. S. ABESHOUSE AND A. T. TIONGSON
Fm. 1. A, excretory urogram (15-minute film) showing normal right kidney and large calcified shadow in left renal area. B, aortogram showing normal blood supply of right kidney and displaced renal artery supplying left renal mass. Calcified mass 11ppears attached to kidney area.
origin (fig. 1, A). Barium enema and gastrointestinal series were not remarkable except for multiple small diverticula in the sigmoid. On October 29, 195:3, cystoscopy and retrograde pyelography were performed. There was a slight prominence of the posterior portion of the vesical neck due to median bar formation. The right ureteral orifice was normal in size, shape, and position, and was easily catheterized with a 6F ureteral catheter. The left orifice appeared as a faint dimpling and could not be catheterized. On November 2, 1952 translumbar aortography under 2 per cent pentothal anesthesia was carried out -with the patient in the prone position on the x-ray table. The usual No. 18 gauge long needle used for aortography was easily introduced into the aorta at the level of the second lumbar vertebra. A preliminary injection of 2 cc of 70 per cent urokon was made directly into the aorta as a sensitivity test with no reaction. During the injection of 30 cc of 70 per cent urokon, the patient had generalized convulsions, which were more marked in the lower extremities and trunk, and lasted about ten seconds. The configuration of the right renal vessels was normal. A smaller Yessel is seen partially filled and extending upward toward the region of the left kidney. This probably represented the left renal artery. There is no vascular pattern noted around or within the previously described cystic calcified mass. The remaining visualized aortic branches are grossly normal (fig. 1, B). The patient was returned to the ward in fairly good condition. AJter he had fully recovered from the anesthesia about six hours later, he was unable to move his lower extremities. Examination at this time revealed complete flaccid paralysis of both lower extremities ,vith loss of tendon reflexes at both knees and ankles.
RARE COI\IIPLIC_\TIO:\: OF THANSLUMBAR AORTOGHAPHY
The reaction to pain and temperature was absent below the level of the (-:ighth thoraeic vertebra_ The right foot could be slightly flexed and extended Sous::ition of vibration and positjon was good. The next morning Dr. Clinton Harrison, attending neurosurgeon, examined the patient and confirmed the aforementioned findings. His impressjon wa~ thrombosis of the anterior spinal artery or Rpasm of this artery following in_jec-tion of the contra,~t medium. l\!Ieehanical compression of the spinal cord war:: ruled out as there ·was no dynamic block on lumbar puncture done on No,·ember ±, 1953. The spinal fluid was clear and under normal pressure, the spinal fluid sugar was 68 mg. per cent and the total protein was 420 mg. per een1. ~:o evidence of vertebral fracture was present on the roentgcnograms of the spine. The patient was unable to void and an indwelling urethral catheter '18F Foley with 5 cc bag) was inserted and connected up to a McKenna tidal irrigation apparatus in order to de1'elop an automatic blaclde1·. He moved his bowels i11vol1mtarily in bed. He showed a gradual and progressive improvement for on November U, 19Ei3 the sensory levels of pain and temperature were equivocal at the level of the eighth thoracic vertebra and positive at the eleventh and twelfth t.bnraeic vertebrae. The response to tOLlCh and vibration continued good. D,,spii.t, good nursing care, a deeubLtus ulcer developed and the patient was placed on a Stryker frame. On December 12, 1953, he could flex his right knee slightly and move the right foot freely in any direction. The left toe could be mo1'cd io a lesser dPgree. Pain and temperature responses remained unchanged. Physiot.hernpy and massage were initiated in an effort to preserve aud improve Lhe muscles of his legs and baek. On December 18, Hl53, cystmnetric study revealed a mildly hypoto11ic bladder with fairly good bladder contractions and frequent uninhibitell contractions . Bladder sensation of fullness was absent_ The Foley catheter was nlmo\'Cd and he n1ided at intervals of four to five hours aided by simultaneous maimal comprestiion of the bladder. The residual urine was 40 cc. On March 8, 1954 the patient began to complain of pain in the chest and left hip, and the decubitus ulcer recurred. He became anorexic and lost weight. On April 18, roentgenographic study revealed metastar::es in the lungt:i, ribs, el!wi.cl1\ pelvic boDes, and lumbar vertebrae. His course was progressively downhill, and he expired un April 27, 19.54. of gcneralir.ed carcinomatosis. A potitrnortem examination was performed about two hours after cleai h. The positive findings included; 1) malignant Grawitz turnor of upper polo of left kidney, 2) metastases to adrenals, liver, periportal, periaortic, and iuguinal lymph nodes, left clavicle, ribs, vertebrae, and skull, ;3) encrusted ,·ystitis, 4) calcification of hydronephrotic left kidney, 5) coronary heart disease, f\) arterJoselernsic1, 7) pulmonary emphysema and atelectasis, 8) benign hypnrtwphy of the prostate. The spinal cord 1vas removed intact for further study. Careful study did not reveal any thrombor::is or occlusion of Lhe anterior :c;pinal arteries by tumor cells or organized blood clot. }fo,tologic:al examination of the spinal cord was rnadc by Dr. John YVagner,
352
B. S. ABESHOUSE AND A. T. TIONGSON
consultant in neuropathology, Department of Laboratories. "Sections from the lower cervical, thoracic and thoracolumbar spinal cord were stained with hematoxylin and eosin. The nerve roots and meninges are apparently normal and without evidence of inflammatory change. In the cervicothoracic area, scattered fresh petechial hemorrhages and moderate congestive changes were found. The ventral horn cells in the thoracic and thoracolumbar areas are slightly reduced in number and showed pigmentary changes, particularly in the thoracic areas. The dorsal horn cells were also slightly reduced in number. "The most conspicuous lesion is an irregular sort of demyelination occupying principally the ventrolateral areas of the lateral funiculi and most of the ventral funiculus throughout all the section examined. A few irregular areas of demyelination are seen adjacent to the dorsal sulcus. The ventral areas of demyelination appear continuous with the ventral nerve roots, but in some sec-
Fm. 2. Photomicrographs. A, section of thoracic spinal cord showing areas of demyelination occupying principally ventrolateral areas of lateral funiculi and most of ventral funiculus. B, section (low power) of thoracolumbar portion of spinal cord showing presence of macrophages and dissolution of tissue in one lateral funiculus.
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tions this is not too clear. In one area in the midthoracic region, there is a focus in which almost complete dissolution of tissue is seen in one lateral funiculus. Macrophages are seen in this area, which would indicate that a cavity is in the process of formation. There is no intrinsic inflammatory activity. "The process of demyelination appears to be most intense in the thoracolumbar region where it involved the ventrolateral areas and to a lesser degree the gray matter of the ventral horns. The ventral nerve roots are affected with some slight possibility of the dorsal roots also being involved along with the sensory pathways in the lateral funiculi. One might synthesize, therefore, an irregularly segmented motor sensory syndrome with a predominantly lower motor neuron component along with a lateral and ventral spinothalamic syndrome, possibly of irregular distribution and of variable intensity. There is possibly some change in the dorsal column, which is difficult to detect and interpret. The etiology is not evident from the sections examined. There is no acute process, the duration of the lesion being measured certainly in terms of months or many weeks. Indeed a few small areas of gliosis seem to confirm the chronic nature of this process." DISCUSSION
The authors are of the opinion that the cause of the paraplegia in this case was the direct toxic action of the 70 per cent urokon (sodium acetrozoate) on the spinal cord. No definite thrombosis of the anterior spinal artery or its branches could be demonstrated. The pathological examination of the spinal cord revealed a process of demyelinization, which was more intense in the thoracolumbar region and principally involving the ventrolateral areas of the lateral funiculi and most of the ventral funiculus. The nutrient artery supplying this portion of the cord is the anterior spinal artery (i.e., anterior radicularis magna). The blood supply of the spinal cord has been studied by many investigators, particularly Kadyis.11 The latter demonstrated that the vascular supply of the spinal cord is predominantly of a transverse and segmental nature and that the anterior spinal artery does not exist as one continuous long-reaching blood vessel, but rather is composed of a series or chain of smaller arteries of shorter longitudinal extent. The spinal cord appears to be supplied by six to eight anterior radicular arteries. Their distribution is not symmetrical for there are usually one or two in the lumbar region, one in the lower thoracic region, none or one in the middle thoracic region, one or two in the lower cervical region and one in the upper cervical region. The largest artery is the one found in the lower thoracic or lumbar portion of the cord, which is designated as the "arterial radicularis magnae" by Kadyis. This artery measures 872 microns in diameter in the adult, is single, not symmetrical, and occurs on one side only, usually the left. It is most frequently found in the second lumbar segment, but may be found in any segment between the eighth thoracic and second lumbar. With the patient in the prone position and the direction of the needle pointing toward the ventral surface of the aorta, one can readily understand how a large 11
Kadyis: Quoted by Antoni and Lindgren, loc. cit.
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stream of highly concentrated medium injected under violent pressure could enter the arteriae radicularis magna and permit the direct toxic action of the drug upon the spinal cord. In this respect it is interesting to note that Hol and Skjervan12 have performed an interesting experimental study of the causes of spinal cord damage following aortography. They performed abdominal aortography in 18 rabbits by injecting the contrast medium (20 per cent diodrast) through a cannula inserted into the exposed left renal artery. They found that the repeated injections of this high concentration of the contrast medium into the abdominal aorta in rabbits gave rise to toxic damage to the spinal cord as a result of permeation of the spinal arteries by the contrast medium. Spasms and paralysis of the hind parts were encountered. The cord lesions occurred when the animals were injected in the supine position and not in the prone position. It is important to note that the technique and position of the animal employed were not the same as those used in translumbar aortography. There is no unanimity of opinion concerning the pathogenesis of paraplegia in translumbar aortography. Antoni and Lindgren maintained that the lesion was caused by compression of the aorta by the pillow placed beneath the abdomen, thereby supporting Steno's experiment (Niels Stensen 1638-1686) on compression of the abdominal aorta at the level of the renal arteries in rabbits producing motor and sensory paralysis of the lower part of the body. Boyarsky was the first to attribute the paraplegia to the toxic action of the contrast medium on the spinal cord, and the authors concur with this opinion. Hol and Skjervan have maintained that damage to the spinal cord following translumbar aortography may be expected theoretically under the following circumstances, singly or combined, viz., 1) supine position of the subject, 2) prolonged exposure to the contrast medium, 3) repeated injections of the contrast medium at short intervals, and 4) pre-existing weakness of the arteries of the spinal cord. They pointed out that with the patient in the supine position the high specific gravity of the contrast medium predisposes to the high concentration of the contrast medium with the dorsal arteries supplying the spinal cord. They maintained that this phenomenon is more likely to occur where aortography is performed by the method of retrograde catheterization of the femoral artery wherein filling of the dorsal branches of the aorta as well as the renal arteries occurs. We have failed to observe a single case of filling of the dorsal branches of aorta and the spinal arteries in more than 150 cases of retrograde aortographies. Hol and Skjervan also suggested the possible causative role of prolonged exposure to the contrast medium resulting from retardation of the bloodstream in cases of aortic coarctation, embolus or thrombus formation, reduced blood pressure, abdominal compression and possibly injections too violently performed in a proximal direction. Little consideration has been given to the likelihood of spinal cord damage being caused by localized ischemia resulting from transient or permanent vasospasm of the dorsal arteries supplying the spinal cord and induced by the velocity of the injection on the direct chemical action of the highly concentrated 12
Hol, R. and Skjervan, 0.: Acta. radiologica, 42: 276, 1954.
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contrast medium. According to Boyarsky, transient vascular spasm has been observed repeatedly following the use of organic iodides, but no case of permanent thrombosis has been reported although such cases have occurred following the use of inorganic (sodium) iodides. Goodwin and .Walter13 have successfully employed the intra-aortic injection of 3 to 6 cc of 1 per cent procaine immediately before injecting into the aorta 20 to 30 cc of the contrast medium in order to prevent the brief cramping pains in the abdomen and lower extremities, which are due to transient arterial spasm caused by the irritating effect of the organic iodide contrast medium. CONCLUSION
A rare complication of translumbar aortography characterized by sudden onset of paraplegia with areflexia, thermanesthesia, and loss of bladder and rectal control is reported. The complication occurred 6 hours after the injection of 70 per cent urokon sodium into the abdominal aorta. The procedure was done in the usual manner and all the customary precautions were employed. Although this is the fourth authentic case reported in the literature, the authors are inclined to believe that the true incidence of this complication is greater than these reports indicate. The authors believe that the cause of the paraplegia was the spinal cord changes produced by direct toxic action of the highly concentrated contrast medium which reached the spinal cord through the anterior spinal arteries and its collateral branches. The possible etiological role of a transient or permanent vasospasm or thrombosis of the spinal artery cannot be completely excluded despite the fact that no evidence of vasoconstriction or thrombosis was found in the pathological examination of the affected tissue. The authors reaffirm their belief that translumbar aortography is a relatively safe and simple procedure, but its use as a diagnostic procedure must always be carefully evaluated in any given case. The possible complications of this procedure must always be borne in mind.
100 W. Monument St., Baltimore 1, Md. (B. S. A.) 13
Goodwin, W. E. and Walter, R. C.: Angiography, 4: 410, 1953.