Neuroradiology ventricular extravasation during cerebral angio graphy (8- 10, 13, 18). In this paper, we present a case of rupture of an intracranial aneurysm during carotid angiography a n d comment on the role of angiography a s a possible causative factor. To our knowledge, this will be the third such case in the literature. The classic picture of intraventricular h emorrhage as described by Sanders ( 15) a n d McDonald (12) consists of acute onset of persistent coma, symptoms of midbrain herniation, decerebration in ca ses o f long su rvival, m eningismus, early persi stent central regulation disorders, and death usually within 48 hours. This classic picture does not always occur as se veral nonlethal episodes of intraventricular hemorrhage have occurred in patients ex amined in our department during the past three years. Pia (14) classified intra ventricular bleeding into three morphologic types . The first is termed total hematocephaly in which the entire ventricular sy stem is filled with clot or hematoma. The second is partial hematocephaly in which blood masses fill circumscribed portions of the ventricular syst em , u sually a lateral ve n tricle , but rarely both lateral ventricles. Associated intracerebral hematoma is usually present in these types. In the third type, simply termed intraventricular hemorrhage , fr esh blood is present in the cerebrospinal fluid without eviden ce of a hematoma. Pia's classification h as prognostic significance in that the mortality rates were 100% with total hcma t ocephaly, 5(j% with parti al hematoceph aly and 14% with intraventricular hemorrhage. The great majority of survivors underwent surgical intervention . • Ventricular Opacification During Carotid . Angiography Secondary to Rupture of Intracranial Aneurysm Case Report l James S. Teal, M.D., Patrick J. Wade, M.D., R. Thomas Bergeron, M.D., Calvin L Rumbaugh, M.D., and Hervey D. Segall, M.D. ABSTRACT-Rupture of intracranial aneurysms during cer ebral angiography is a rare occurrence. A case of such a rupture with extravasation of cont ra st material into the cerebral v entricular system and ont o the floor of the middle cranial fossa is presented. The role of an giography a s a pos sible causat ive factor is discussed. I NDEX TE RMS: Aneurysm , intracranial > Brain , hemorrhage • Cerebral Angiography, complication s • Cerebral Blood Vessels , rupture· Meninges, hemorrhage Radiology 106: 581 -5 Q3, March 1973 the cerebral ventricles was deS scribed by Sanders into ( 15) in 1881, there have been two re I N CE HEMORRHi\.GE ports (5, 7) of an unequivocal nonoperative diagnosis i.e., demonstration of ex tr a v asatio n of cont ras t materi al into the ventricular system during cerebral angiography. These cases resulted fr om rupture of con genital aneurysms but others report rupture of congenital aneurysms with extra- Fi g. 1, A. Anteroposterior view of selective right internal carotid ar ter iogr am expo sed 1/ :2 second after initiation of injection demonst ra t es spont a neous op acifi cat ion of th e left ante ri or , middle and internal carotid arteries, small caliber of t he extr ad ural portion of the ri ght internal carotid arter y, small caliber of major intracranial vessels bilaterally, left middle cerebr al artery aneurysm , large lobulated aneur ysm near the bifurcation of the right internal carotid artery, elevat ion of the proximal ri ght middle cere br al artery, and ext r avasation of cont rast mater ial into the right lateral ventricle and ri ght middle cranial fossa . B. Anteroposterior vi ew exposed 1/2 second after F igure 1, A demonstrates incre ased extravasation into the right middle cranial fossa and increased opacificati on of the r ight lateral ventricle. C. Ant eropos ter ior view exposed 4 1 / " seconds after F igure 1, A showing opacification of essentially the entire ventricular system and extravasated contrast material in the right middle cranial fossa . I From the Departments of Neuroradiology (J. S. T. , R. T. B ., C. L . R. , H . D. S. ) and Ne ur osur ger y (P . J. \V.), Los Angeles CountyUniversity of Southern California Medical Center, Los An geles, Calif. Accepted in September 1972 . shan 581 JAMES S. TEAL AND OTHERS 582 ~) v March 1973 -, I "'," -;-) z- B Fi g. 2, A. Lateral view exposed simultaneously with F igure I , A showing th e same findin gs. B . Lateral v iew exposed simultaneously with Fig ure 1, B. No te identical findin gs. C. Lateral view exposed simultaneously wit h F igure 1, C revealing the same find ings and cont rast materi al in t he cervical subarachnoi d space (ar row) . CASE REPORT A 41-year-old Caucasian woman was transferred to Los Angeles County-University of Southern California Medical Center on July Ii, 1971 from an emergency hospital where she was taken after her car hit a utility pole. When first seen at the emergency hospital, she was alert and oriented but shortly afterwards suffered a grand mal seizure and was transferred to LAC/USC Medical Center. On arrival, she was agitated and delirious with bilateral, equally dilated, poorly reactive pupils; left hemiparesis; and a left central VII nerve palsy. Right carotid angiography was requested to confirm or exclude the presence of an epidural or subdural hematoma. Immediately following the injection of 10 ml of Conray at 125 PSI, the patient lapsed into a grand mal seizure with immediate coma. Examination of the biplane films (Figs. 1, and 2) revealed inadvertent cannulation of a spastic right internal carotid artery with visualization of spastic middle and anterior cerebral arteries bilaterally and supraclinoid left internal carotid artery. A large aneurysm of the left middle cerebral artery, a large ruptured aneurysm near the bifurcation of the right internal carotid with extravasation of media into the lateral ventricle and the floor of the right middle cranial fossa, and an avascular right temporal lobe mass, indicating recent intracerebral bleeding, were demonstrated. Within three seconds of injection, the entire ventricular system was visualized: contrast material had passed into the cervical subarachnoid space. The patient never regained consciousness and died 71.5 hours later. DISCUSSION Based on the limited studies of Greitz (6) and Bakay and Sweet (2), most cerebral angiographers, including ourselves, feel that no significant increase in intracarotid pressure occurs during carotid angiography. Greitz's results were primarily based on 4-ml injections and Bakay and Sweet's on 10-12 ml, with injection times of 2-3 seconds. Neither of these are comparable to the routine situation in our department where lO-ml common carotid artery and 1i-8 ml internal carotid Vol. 106 VENTRICULAR OPACIFICATION SECONDARY TO RUPTURE OF INTRACRANIAL ANEURYSM artery injections are routinely done in 1.0-1.5 seconds utilizing Taveras Picker, Turner MDT and Viamonte-Hobbs injectors. We feel that the volumes and injection times utilized in our department are probably comparable to those of most neuroradiology departments. Lin et at. (11) reported that slight elevation (5-25 mm Hg) of intracarotid systolic pressure occurred in 7 of 12 patients during retrograde brachial injections of 45 ml by hand and at 225 and 625 PSI by pressure injector. This at least suggests that slight elevation of intracarotid pressure may occur during carotid angiography. During selective vertebral angiography utilizing forceful hand injections of 5-6 ml of contrast material and small catheters with tips at the level of the 6th cervical vertebra, there is an extremely high incidence of retrograde filling of the opposite vertebral artery. This can logically be explained only in terms of a transient increase in intravertebral artery pressure. A similar change in the internal carotid artery is certainly not inconceivable. Additional evidence which suggests that elevation of intracarotid pressure may occur during carotid angiography is the increased incidence of transient opacification of the basilar and contralateral proximal anterior cerebral arteries during selective internal carotid angiography compared to common carotid angiography. The elasticity of arteries and the large total volume of the arterial system accounts for most, if not all, of the stability of the intraluminal pressure following forceful injections of relatively small volumes of solutions. In view of the seemingly conflicting reports of Greitz, and Bakay and Sweet in comparison with Lin and associates, we feel that additional investigations of this phenomenon based on statistically valid numbers of patients in various age groups are warranted. An exhaustive investigation at this time may be quite difficult, but with significant' improvement in strain gage transducers, as recently advocated by Deck et at. (3), it may be possible in the near future. In the case presented here, a significant increase of intracarotid pressure during angiography probably occurred but this was a special case with associated pathologic vascular physiology and cannot be compared to the studies of Greitz, and Bakay and Sweet. The peculiar circumstances here were an inadvertent selective internal carotid artery injection of 10 ml of contrast material into a markedly spastic internal carotid artery with associated spasm of the anterior and middle cerebral arteries. These conditions contributed to what we feel represented a wedge injection into a relatively inelastic, spastic arterial tree producing a significant increase in intra-arterial pressure with resultant aneurysmal rupture and spontaneous visualization of the opposite middle cerebral and supraclinoid internal carotid arteries. The magnitude of rupture into the right lateral ventricle was such that, within three seconds of injection, the entire ventricular system and a portion of the cervical subarachnoid space were opacified. The intraluminal pressure required to produce such a forceful rupture is unknown to us, but Turner (17) states that wedged forceful hand injections of 3-4 ml of contrast material into abnormal pulmonary arteries produces intraluminal pressures of greater than 800 mm Hg. It is, therefore, not inconceivable that the intracarotid pressure in our patient approached or even exceeded the 250-500 mm Hg range. The aneurysmal rupture presented here was likely iatrogenic in nature, but its occurrence could have been prevented only by a preliminary low-volume, low-pressure test injection for needle placement and subsequent recognition of the 583 Neuroradiology marked spasm of the internal carotid artery. It has not been our policy to routinely perform such test injections in approximately 1,500 carotid angiographies per year. Carotid angiography was performed in this patient to confirm or exclude the presence of an epidural or subdural hematoma and not for evaluation of subarachnoid hemorrhage. In view of subsequent findings, the initial presenting clinical picture can best be explained by subarachnoid hemorrhage and intracerebral hematoma formation secondary to spontaneous aneurysmal bleeding. Radiographic demonstration of the rupture of congenital aneurysm implies a grave prognosis. All cases (5, 7, 8-10, 13) known to us, with a single exception (18), ended in death shortly thereafter, but in view of the rare occurrence of this phenomenon, the benefits of indicated cerebral angiography far outweigh this possible hazard. . ACKNOWLEDGMENT: The authors wish to thank Barbara Chapman for her assistance in manuscript preparation. 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