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Effective management of cerebral vasospasm with balloon angioplasty after failed papaverine angioplasty
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Effective management of cerebral vasospasm with balloon angioplasty after failed papaverine angioplasty
M . K . M o r g a n * MD FRACS L.H.S. S e k h o n * MBBS PhD S.J. H a l c r o w * MBBS FRACS V. G r i n n e l l * MD W. Sorby* MBBS FRACR Departments
of Neurosurgery*
and
Radiology
t, Royal
North
Shore
Hospital,
St Leonards,
Australia.
A 37 year old male with symptomatic cerebral vasospasm complicating the rupture of a basilar tip aneurysm was initially treated with intra-arterial papaverine in conjunction with concomitant hypervolaemia and induced hypertension. However, the vasospasm was only moderately improved, with this effect lasting for less than 24 h. Following further administration of intra-arterial papaverine, without significant angiographic improvement, endovascular balloon dilatation of both vertebral arteries and basilar artery resulted in dramatic and sustained reversal of angiographic vasospasm. The patient's clinical condition improved dramatically after this procedure, progressing from an unconscious state requiring ventilatory support, to a Glasgow Coma Score of 15 in the absence of focal neurological signs (with the exception of a right oculomotor palsy), within 9 days. This case suggests that there may be a role for balloon dilatation angioplasty, in patients who have cerebral vasospasm refractory to treatment with intra-arterial papaverine. Journal of Clinical Neuroscience 1996, 3 (2): 162-165
© Pearson Professional 1996
Keywords: Aneurysm,Angioplasty, Papaverine, Subarachnoid haemorrhage, Vasospasm
Introduction
Case r e p o r t
Delayed ischaemic deficits as a consequence of cerebral vasospasm remain the leading treatable cause of disability after aneurysm rupture) Angioplasty is being reported, with increasing frequency, to be an effective treatment modality to reverse vasospasm, and is gaining acceptance as part of the standard m a n a g e m e n t armamentarium following subarachnoid haemorrhage. 2° The two most commonly reported methods of angioplasty are chemical, with intra-arterial papaverine, and mechanical, using balloon dilatation. Both methods are effective in selected cases in reversing the angiographic narrowing. Furthermore, when administered shortly after the onset of neurological deficits arising as a consequence of vasospasm, these manoeuvres have been shown to reverse neurological deficit. The first line m e t h o d of angioplasty at Royal North Shore Hospital has been intra-arterial papaverine, delivered either selectively through Tracker © catheterisation (Target Therapeutics, San Jose, CA, USA), or nonselectively, into the internal carotid or vertebral arteries? This case represents an example of a patient refractory to treatment by intra-arterial papaverine who subsequently responded to balloon angioplasty of the vertebro-basilar system. The merits of both forms of angioplasty are discussed.
A 37 year old male was admitted 2 days after sustaining a Grade II 1° subarachnoid haemorrhage from a basilar bifurcation aneurysm (Figs 1 & 2). On admission he had a Glasgow Coma Score of 15 with no neurological deficit and surgical repair was performed on the day of admission. Initial CT scanning demonstrating moderate
162
Fig. 1 Initial CT scan demonstrating the subarachnoid
haemorrhage resulting from the ruptured basilar tip aneurysm.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
Angioplasty for vasospasm
Case reports
Fig. 2 (A) AP and (B) lateral vertebral angiography at admission demonstrating a basilar tip aneurysm.
amounts of blood around the basilar trunk and no evidence of hydrocephalus. The operative procedure involved exposure of the aneurysm via a right pterional free bone flap craniotomy. Extradural dissection encompassed removal of bone forming the roof and lateral wall of the orbit, the anterior clinoid process, and the petrous bone medial to the line of the greater superficial petrosal nerve. Following dural opening, the Sylvian fissure was widely split and the crural cistern opened facilitating posterior retraction of the temporal pole. The tentorium was divided from its free edge to the superior petrosal sinus immediately lateral to the trigeminal nerve. The superior petrosal sinus was subsequently divided to incorporate the dural opening along the middle cranial fossa floor and the posterior fossa (adjacent to the previously resected petrosal bone). Tl~e trigeminal, oculomotor and abducent nerves on the right were then dissected for a short distance in the wall of the cavernous sinus allowing anterior retraction of the dura to expose the basilar trunk for proximal control. Dissection of the aneurysm neck followed and it was possible to secure the aneurysm with a straight Sundt Slim-Line aneurysm clip (Codman & Shurtleff, Inc., Randolph, MA, USA) without temporary clipping. The following day, the patient was well without neurological deficit, with the exception of a fight oculomotor nerve palsy. His postoperative management included an intravenous nimodipine infusion at 2 m g / h r with 1.7 m l / kg.hr of crystalloid solution, and his systolic blood pressure was maintained between 120 and 150 mmHg. The central venous pressure was maintained above 7 mmHg using intermittent infusions of colloid solution. Two days after surgery, and four days after subarachnoid haemorrhage, his level of consciousness deteriorated when he no longer obeyed commands. Cerebral CT scan demonstrated no evidence of hydrocephalus or infarction. A cerebral angiogram of the vertebrobasilar system at this time confirmed the suspicion ofvasospasm. During angiography he was infused with 60 mg and 48 mg of papaverine into the right and left vertebral artery respectively, until the narrowing was reversed. At this time his systolic blood pressure was increased to between 160 and 180 mmHg using further boluses of
colloid solution and concomitant inotrope therapy. With this treatment regime, the patient improved, but this improvement was not sustained. Within 94 h he was again unconscious, requiring venfilatory support. Repeat cerebral angiography demonstrated a return of the vasospasm, with even more profound narrowing (Fig. 3). A further 60 mg of intra-arterial papaverine was again administered, but with only a limited response (Fig. 4).
Fig. 3 Severevasospasmin the vertebrobasilar distribution demonstrated 24 h after a previous papaverine angiogram.
Fig. 4 Vertebral angiography following the administration of intra-arterial papaverine showing the limited response immediately prior to balloon angioplasty.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
163
Case reports
Fig. 5 Vertebral angiography immediately after balloon dilatation of both vertebral arteries and most of the basilar artery. Following this sequence the terminal basilar artery was dilated.
Fig. 6 Repeat vertebral angiography at 2 and 7 days after the balloon dilatation, confirming the durability and extent of the angiographic reversal of vasospasm
Because of this lack of response, a 3.5 m m Stealth angioplasty balloon (Target Therapeutics, Fremont, CA, USA) was inserted into each of the vertebral arteries and the basilar artery, inflated, and after 2 seconds, rapidly deflated, in o r d e r to restore normal arterial calibre (Fig. 5). Following the balloon angioplasty the patient began to make a gradual and steady improvement in conscious state, enabling extubation 36 h later. Although confused and with a persisting oculomotor palsy, he was without other neurological deficits at this time. Repeat cerebral angiography 2 and 7 days (Fig. 6) after the angioplasty confirmed the durability of the successful dilatation. He continued to improve neurologically over the next 2 weeks, and at discharge was free from any neurological deficit. Discussion
In this patient balloon angioplasty was more successful than arterial papaverine in achieving reversal o f cerebral vasospasm, both in terms of the degree of diameter enlargement and longevity of action. Both papaverine and balloon angioplasty have been used to reverse cerebral vasospasm arising as a
164
Angioplasty for vasospasm
consequence of subarachnoid haemorrhage. ~8 These studies have supported the efficacy of both procedures. The preferred m e t h o d o f neuroradiological interventional therapy for vasospasm in our unit has b e e n intraarterial papaverine, into the carotid or vertebral arteries, either non-selectively (as previously described) ,~or selectively via a Tracker © catheter. Between July 1992 and July 1994, 136 patients were surgically treated, after having sustained an aneurysmal subarachnoid haemorrhage. O f these, 36 subsequently u n d e r w e n t intra-arterial papaverine infusion. Whilst this treatment in general has been effective, there still remain cases in which the degree of dilatation is unremarkable, or where the duration of effect is less than 24 h ? The choice o f chemical angioplasty over balloon angioplasty in our unit has been influenced chiefly by the technical ease of administration and relatively low morbidity o f the f o r m e r treatment modality. The major c o n c e r n regarding balloon angioplasty is the threat of arterial rupture. O t h e r concerns raised include aneurysm clip disruption, failure o f the balloon to access distal parts of tortuous vessels in spasm, the r e q u i r e m e n t for vessel straightening during balloon inflation, and finally, the high level of technical expertise required for its application, s However, this case suggests that there is a role for balloon angioplasty in neurosurgical units where chemical angioplasty is the mainstay o f treatment for cerebral vasospasm. Balloon angioplasty should be considered when vasospasm affects angiographically accessible vessels, and papaverine is ineffective in achieving a satisfactory or sustainable dilatation. Furthermore, the use of either form of angioplasty should not be considered in isolation from the other regimens (induced hypertension, hypervolaemia etc.) important in managing cerebral vasospasm. Received31 August 1994 Accepted for publication 15 November1994
Correspondence and requests for offprints:
Associate ProfessorM. K. Morgan, Department of Neurosurgery Level 7, RoyalNorth Shore Hospital, St Leonards 2065, NSW, Australia Phone: 61-2--438-8756 Fax: 61-2-437-5172 References
1. Haley EC, Jr, Kassell NF, Torner JC. The international co-operative study on the timing of aneurysm surgery: the North American experience. Stroke 1992; 23: 205-14. 2. Higashida RT, Halbach VV, Cahan LD et al. Transluminal angioplasty for treatment of intracranial arterial vasospasm. J Neurosurg 1989; 71: 648-53. 3. Little N, Morgan MK, Grinnell V, Sorby W. Intra-arterial papaverine in the management of cerebral vasospasm following subarachnoid haemorrhage. J Clin Neuroscience 1994; 1: 47-51. 4. Brothers MF, Holgate RC. Intracranial angioplasty for treatment ofvasospasm after subarachnoid hemorrhage: technique and modifications to improve branch access. AJNRAmJ Neuroradiol 1990; 11: 239-47.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
Angioplasty for vasospasm
Case reports
5. DionJE, Duckwiler GR, Vifiuela F, Martin N, BentsonJ. Pre-operative micro-angioplasty of refractory vasospasm secondary to subarachnoid hemorrhage. Neuroradiology 1990; 32: 232-6. 6. Kaku Y, Yonekawa Y, Tsukahara T, Kazekawa K. Superselective intra-arterial infusion of papaverine for the treatment of cerebral vasospasm after subarachnoid haemorrhage.J Neurosurg 1992; 77: 842-7. 7. Kassell NF, Helm G, Simmons N, Phillips CD, Cail WS. Treatment of cerebral vasospasm with intra-arterial
papaverine. J Neurosurg 1992; 77: 848-52. 8. Russek HI, Zohman BL. Papaverine in cerebral angiospasm.JAMA 1948; 136: 930-2. 9. Newell DW, EskridgeJM, Mayberg MR, Grady MS, Winn HR. Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 1989; 71: 654-60. 10. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28: 14-9.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
165
, ~
0
®-;--
°
-..
r
~..
.
.
I1'1" ~ . .
.
. . . . . . . I'!r'l ! .- : . . . . . . . . . . .
.... -.....
Effective management of cerebral vasospasm with balloon angioplasty after failed papaverine angioplasty
M . K . M o r g a n * MD FRACS L.H.S. S e k h o n * MBBS PhD S.J. H a l c r o w * MBBS FRACS V. G r i n n e l l * MD W. Sorby* MBBS FRACR Departments
of Neurosurgery*
and
Radiology
t, Royal
North
Shore
Hospital,
St Leonards,
Australia.
A 37 year old male with symptomatic cerebral vasospasm complicating the rupture of a basilar tip aneurysm was initially treated with intra-arterial papaverine in conjunction with concomitant hypervolaemia and induced hypertension. However, the vasospasm was only moderately improved, with this effect lasting for less than 24 h. Following further administration of intra-arterial papaverine, without significant angiographic improvement, endovascular balloon dilatation of both vertebral arteries and basilar artery resulted in dramatic and sustained reversal of angiographic vasospasm. The patient's clinical condition improved dramatically after this procedure, progressing from an unconscious state requiring ventilatory support, to a Glasgow Coma Score of 15 in the absence of focal neurological signs (with the exception of a right oculomotor palsy), within 9 days. This case suggests that there may be a role for balloon dilatation angioplasty, in patients who have cerebral vasospasm refractory to treatment with intra-arterial papaverine. Journal of Clinical Neuroscience 1996, 3 (2): 162-165
© Pearson Professional 1996
Keywords: Aneurysm,Angioplasty, Papaverine, Subarachnoid haemorrhage, Vasospasm
Introduction
Case r e p o r t
Delayed ischaemic deficits as a consequence of cerebral vasospasm remain the leading treatable cause of disability after aneurysm rupture) Angioplasty is being reported, with increasing frequency, to be an effective treatment modality to reverse vasospasm, and is gaining acceptance as part of the standard m a n a g e m e n t armamentarium following subarachnoid haemorrhage. 2° The two most commonly reported methods of angioplasty are chemical, with intra-arterial papaverine, and mechanical, using balloon dilatation. Both methods are effective in selected cases in reversing the angiographic narrowing. Furthermore, when administered shortly after the onset of neurological deficits arising as a consequence of vasospasm, these manoeuvres have been shown to reverse neurological deficit. The first line m e t h o d of angioplasty at Royal North Shore Hospital has been intra-arterial papaverine, delivered either selectively through Tracker © catheterisation (Target Therapeutics, San Jose, CA, USA), or nonselectively, into the internal carotid or vertebral arteries? This case represents an example of a patient refractory to treatment by intra-arterial papaverine who subsequently responded to balloon angioplasty of the vertebro-basilar system. The merits of both forms of angioplasty are discussed.
A 37 year old male was admitted 2 days after sustaining a Grade II 1° subarachnoid haemorrhage from a basilar bifurcation aneurysm (Figs 1 & 2). On admission he had a Glasgow Coma Score of 15 with no neurological deficit and surgical repair was performed on the day of admission. Initial CT scanning demonstrating moderate
162
Fig. 1 Initial CT scan demonstrating the subarachnoid
haemorrhage resulting from the ruptured basilar tip aneurysm.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
Angioplasty for vasospasm
Case reports
Fig. 2 (A) AP and (B) lateral vertebral angiography at admission demonstrating a basilar tip aneurysm.
amounts of blood around the basilar trunk and no evidence of hydrocephalus. The operative procedure involved exposure of the aneurysm via a right pterional free bone flap craniotomy. Extradural dissection encompassed removal of bone forming the roof and lateral wall of the orbit, the anterior clinoid process, and the petrous bone medial to the line of the greater superficial petrosal nerve. Following dural opening, the Sylvian fissure was widely split and the crural cistern opened facilitating posterior retraction of the temporal pole. The tentorium was divided from its free edge to the superior petrosal sinus immediately lateral to the trigeminal nerve. The superior petrosal sinus was subsequently divided to incorporate the dural opening along the middle cranial fossa floor and the posterior fossa (adjacent to the previously resected petrosal bone). Tl~e trigeminal, oculomotor and abducent nerves on the right were then dissected for a short distance in the wall of the cavernous sinus allowing anterior retraction of the dura to expose the basilar trunk for proximal control. Dissection of the aneurysm neck followed and it was possible to secure the aneurysm with a straight Sundt Slim-Line aneurysm clip (Codman & Shurtleff, Inc., Randolph, MA, USA) without temporary clipping. The following day, the patient was well without neurological deficit, with the exception of a fight oculomotor nerve palsy. His postoperative management included an intravenous nimodipine infusion at 2 m g / h r with 1.7 m l / kg.hr of crystalloid solution, and his systolic blood pressure was maintained between 120 and 150 mmHg. The central venous pressure was maintained above 7 mmHg using intermittent infusions of colloid solution. Two days after surgery, and four days after subarachnoid haemorrhage, his level of consciousness deteriorated when he no longer obeyed commands. Cerebral CT scan demonstrated no evidence of hydrocephalus or infarction. A cerebral angiogram of the vertebrobasilar system at this time confirmed the suspicion ofvasospasm. During angiography he was infused with 60 mg and 48 mg of papaverine into the right and left vertebral artery respectively, until the narrowing was reversed. At this time his systolic blood pressure was increased to between 160 and 180 mmHg using further boluses of
colloid solution and concomitant inotrope therapy. With this treatment regime, the patient improved, but this improvement was not sustained. Within 94 h he was again unconscious, requiring venfilatory support. Repeat cerebral angiography demonstrated a return of the vasospasm, with even more profound narrowing (Fig. 3). A further 60 mg of intra-arterial papaverine was again administered, but with only a limited response (Fig. 4).
Fig. 3 Severevasospasmin the vertebrobasilar distribution demonstrated 24 h after a previous papaverine angiogram.
Fig. 4 Vertebral angiography following the administration of intra-arterial papaverine showing the limited response immediately prior to balloon angioplasty.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
163
Case reports
Fig. 5 Vertebral angiography immediately after balloon dilatation of both vertebral arteries and most of the basilar artery. Following this sequence the terminal basilar artery was dilated.
Fig. 6 Repeat vertebral angiography at 2 and 7 days after the balloon dilatation, confirming the durability and extent of the angiographic reversal of vasospasm
Because of this lack of response, a 3.5 m m Stealth angioplasty balloon (Target Therapeutics, Fremont, CA, USA) was inserted into each of the vertebral arteries and the basilar artery, inflated, and after 2 seconds, rapidly deflated, in o r d e r to restore normal arterial calibre (Fig. 5). Following the balloon angioplasty the patient began to make a gradual and steady improvement in conscious state, enabling extubation 36 h later. Although confused and with a persisting oculomotor palsy, he was without other neurological deficits at this time. Repeat cerebral angiography 2 and 7 days (Fig. 6) after the angioplasty confirmed the durability of the successful dilatation. He continued to improve neurologically over the next 2 weeks, and at discharge was free from any neurological deficit. Discussion
In this patient balloon angioplasty was more successful than arterial papaverine in achieving reversal o f cerebral vasospasm, both in terms of the degree of diameter enlargement and longevity of action. Both papaverine and balloon angioplasty have been used to reverse cerebral vasospasm arising as a
164
Angioplasty for vasospasm
consequence of subarachnoid haemorrhage. ~8 These studies have supported the efficacy of both procedures. The preferred m e t h o d o f neuroradiological interventional therapy for vasospasm in our unit has b e e n intraarterial papaverine, into the carotid or vertebral arteries, either non-selectively (as previously described) ,~or selectively via a Tracker © catheter. Between July 1992 and July 1994, 136 patients were surgically treated, after having sustained an aneurysmal subarachnoid haemorrhage. O f these, 36 subsequently u n d e r w e n t intra-arterial papaverine infusion. Whilst this treatment in general has been effective, there still remain cases in which the degree of dilatation is unremarkable, or where the duration of effect is less than 24 h ? The choice o f chemical angioplasty over balloon angioplasty in our unit has been influenced chiefly by the technical ease of administration and relatively low morbidity o f the f o r m e r treatment modality. The major c o n c e r n regarding balloon angioplasty is the threat of arterial rupture. O t h e r concerns raised include aneurysm clip disruption, failure o f the balloon to access distal parts of tortuous vessels in spasm, the r e q u i r e m e n t for vessel straightening during balloon inflation, and finally, the high level of technical expertise required for its application, s However, this case suggests that there is a role for balloon angioplasty in neurosurgical units where chemical angioplasty is the mainstay o f treatment for cerebral vasospasm. Balloon angioplasty should be considered when vasospasm affects angiographically accessible vessels, and papaverine is ineffective in achieving a satisfactory or sustainable dilatation. Furthermore, the use of either form of angioplasty should not be considered in isolation from the other regimens (induced hypertension, hypervolaemia etc.) important in managing cerebral vasospasm. Received31 August 1994 Accepted for publication 15 November1994
Correspondence and requests for offprints:
Associate ProfessorM. K. Morgan, Department of Neurosurgery Level 7, RoyalNorth Shore Hospital, St Leonards 2065, NSW, Australia Phone: 61-2--438-8756 Fax: 61-2-437-5172 References
1. Haley EC, Jr, Kassell NF, Torner JC. The international co-operative study on the timing of aneurysm surgery: the North American experience. Stroke 1992; 23: 205-14. 2. Higashida RT, Halbach VV, Cahan LD et al. Transluminal angioplasty for treatment of intracranial arterial vasospasm. J Neurosurg 1989; 71: 648-53. 3. Little N, Morgan MK, Grinnell V, Sorby W. Intra-arterial papaverine in the management of cerebral vasospasm following subarachnoid haemorrhage. J Clin Neuroscience 1994; 1: 47-51. 4. Brothers MF, Holgate RC. Intracranial angioplasty for treatment ofvasospasm after subarachnoid hemorrhage: technique and modifications to improve branch access. AJNRAmJ Neuroradiol 1990; 11: 239-47.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
Angioplasty for vasospasm
Case reports
5. DionJE, Duckwiler GR, Vifiuela F, Martin N, BentsonJ. Pre-operative micro-angioplasty of refractory vasospasm secondary to subarachnoid hemorrhage. Neuroradiology 1990; 32: 232-6. 6. Kaku Y, Yonekawa Y, Tsukahara T, Kazekawa K. Superselective intra-arterial infusion of papaverine for the treatment of cerebral vasospasm after subarachnoid haemorrhage.J Neurosurg 1992; 77: 842-7. 7. Kassell NF, Helm G, Simmons N, Phillips CD, Cail WS. Treatment of cerebral vasospasm with intra-arterial
papaverine. J Neurosurg 1992; 77: 848-52. 8. Russek HI, Zohman BL. Papaverine in cerebral angiospasm.JAMA 1948; 136: 930-2. 9. Newell DW, EskridgeJM, Mayberg MR, Grady MS, Winn HR. Angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. J Neurosurg 1989; 71: 654-60. 10. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28: 14-9.
J. Clin. Neuroscience Volume 3 Number 2 April 1996
165