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|LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 2 | Page : 606-609
Management of postoperative vasospasm following endoscopic endonasal surgery for craniopharyngioma: Report and review of literature
Varun Aggarwal1, Prakash Nair1, Pankaj Shivhare1, K Santhosh Kumar2, ER Jayadevan2, Suresh Nair1
1 Department of Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences, Trivandrum, Kerala, India
2 Department of IS and IR, Sree Chitra Tirunal Institute for Medical Sciences, Trivandrum, Kerala, India
|Date of Web Publication||13-May-2019|
Dr. Prakash Nair
Department of Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences, Trivandrum - 695 011, Kerala
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Aggarwal V, Nair P, Shivhare P, Kumar K S, Jayadevan E R, Nair S. Management of postoperative vasospasm following endoscopic endonasal surgery for craniopharyngioma: Report and review of literature. Neurol India 2019;67:606-9
|How to cite this URL:|
Aggarwal V, Nair P, Shivhare P, Kumar K S, Jayadevan E R, Nair S. Management of postoperative vasospasm following endoscopic endonasal surgery for craniopharyngioma: Report and review of literature. Neurol India [serial online] 2019 [cited 2021 Jan 26];67:606-9. Available from: https://www.neurologyindia.com/text.asp?2019/67/2/606/258043
Vasospasm is a major cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Vasospasm following surgical intervention in the suprasellar subarachnoid cisterns can also cause significant postoperative morbidity and mortality., Postoperative subarachnoid blood and its products are one of the most commonly implicated causes of vasospasm. However, vasospasm is also seen without SAH. The pathophysiology of vasospasm in this scenario is, however, poorly understood. We present a case of postoperative vasospasm 9 days following extended endoscopic endonasal (EEE) surgery for a suprasellar craniopharyngioma, which was reversed by an early endovascular therapy. A review the literature regarding this phenomenon is also presented.
A 41-year old female (non-smoker) patient presented with complaints of headache, amenorrhea, and deterioration of vision of 2 years duration. Clinical examination revealed bitemporal hemianopia and her hormonal studies showed panhypopituitarism. Magnetic resonance imaging (MRI) [Figure 1] showed a 4 × 4 × 1.2 cm mass with solid and cystic areas, extending from the sella into the third ventricle with compression of the optic chiasm, suggestive of a craniopharyngioma. She underwent an EEE excision of the tumor. During the procedure, the tumor was seen involving the pituitary gland and the stalk. The attachments to the anterior cerebral arteries, the anterior communicating artery (ACA), the internal carotid arteries (ICA) bilaterally, and to the wall of third ventricle were dissected meticulously. The resection was followed by skull base reconstruction using fat and fascia lata inlay and onlay pedicled nasoseptal flap based on the nasoseptal branch of the left sphenopalatine artery; the repair was reinforced by a tissue sealant. Contrast enhanced computed tomographic scan [Figure 2]a done following the surgery showed only a small amount of air in the basal cisterns, without any residual tumor or blood at the operative site. Her postoperative course was uneventful except for postoperative diabetes insipidus, (DI) which was managed by strictly monitoring volume status, free water by mouth, and vasopressin. On postoperative day 9, she developed sudden right-sided hemiparesis (upper limb 2/5 and lower limb 1/5) with motor aphasia, suggesting a stroke involving the left middle cerebral artery (MCA). An MRI [Figure 2]b and [Figure 2]c obtained immediately showed patchy areas of diffusion restriction along the vascular territory of the left MCA, and the CT angiogram [Figure 2]d showed vasospasm affecting the supraclinoid segment of the left ICA and the proximal segments of the left ACA and the left MCA. Digital subtraction angiography [Figure 2]e was performed immediately, which showed more than 50% diffuse smooth narrowing involving the supraclinoid left ICA, M1 segment of left middle cerebral artery, and A1 segment of left anterior cerebral artery. The right ICA, MCA, ACA, and posterior circulation vessels were normal. Cerebral circulation time was 3.5 s on the right side and 5 s on the left side.
|Figure 1: (a-c) CECT and contrast enhanced MRI showing a heterogeneously enhancing craniopharyngioma extending into the suprasellar cistern and the third ventricle; there is a large hyperintense cystic area within the lesion|
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|Figure 2: (a) Postoperative CT scan shows no residual lesion or blood in the operative cavity. A small amount of air can be seen. (b and c) Diffusion weighted images taken immediately following development of hemiparesis and aphasia showing ischemic changes in the left MCA territory. (d) CT angiogram taken immediately following development of hemiparesis and aphasia shows narrowing of the left supraclinoid ICA (blue arrow). (e) Lt ICA DSA (AP view) following development of hemiparesis and aphasia shows severe narrowing involving the supraclinoid ICA and proximal segments of anterior and middle cerebral arteries. (f) Lt ICA DSA (AP view) following intra-arterial milrinone infusion shows adequate opening of the narrowed segments|
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Through a right femoral arterial access, a vertebral glide catheter was taken up to the distal cervical segment of left ICA. Following this, milrinone was infused intra-arterially at the rate of 8 mg over 30 min. A total of 12 mg of milrinone was infused over 45 min to open the stenosed segments. Post milrinone angiogram [Figure 2]f showed complete opening of the MCA and ACA with mild residual spasm in the supraclinoid ICA. The cerebral circulation time on the affected side improved significantly from 5 s to 3.75 s. Following the procedure, the patient had clinical improvement in power in the right upper and lower limbs and resolution of aphasia. She remained on intravenous infusion of milrinone for 7 days following the procedure and developed no new deficits during the period, following which she was discharged. An MRI done 4 months following surgery showed no evidence of any residual tumor and small infarcts in the left MCA territory [Figure 3]a,[Figure 3]b,[Figure 3]c,[Figure 3]d. She remains asymptomatic 12 months following the surgery.
|Figure 3: (a and b) Postoperative MRI, 4 months following surgery shows no residual tumor. (c and d) MR diffusion weighted images, 4 months following the surgery show small infarcts in the left MCA territory|
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Vasospasm without SAH following surgical intervention in the suprasellar subarachnoid cisterns is uncommon, poorly understood, and often recognized late. There is no clearly defined protocol of management in this scenario. Most published reports of vasospasm following transsphenoidal surgery pertain to pituitary tumors.,,
Eseonu while reviewing literature on the occurrence of vasospasm following transsphenoidal surgery for pituitary adenomas noted that of all the patients who developed vasospasm and delayed cerebral ischemia (DCI) following surgery, postoperative SAH was seen in 84.6% patients. They also noted a mortality of 30% in the cases reviewed. Vasospasm following surgery for suprasellar craniopharyngioma has been described earlier, with most reporting postoperative SAH demonstrated by CT scan immediately following surgery or in a delayed fashion.,,, Blood in the subarachnoid cisterns and its degradation products such as methhemoglobin and oxyhemoglobin are the most often implicated causes of vasospasm.
Postoperative vasospasm without any SAH following transsphenoidal surgery has been reported previously., However, in the absence of blood in the subarachnoid cisterns, other factors such as direct arterial trauma, hypothalamic injuries, meningitis, a hypovolemic state, and hypocortisolism need to be considered. Chemical meningitis and irritation of vessel walls by the contents of cystic tumors like a craniopharyngioma have also been observed. An instance of vasospasm in the preoperative period has also been observed following spontaneous rupture of a craniopharyngioma cyst. In our case, the tumor had a very small cystic part, which was related to the third ventricle. There was no vascular injury during the procedure. Vasospasm was also seen in the left MCA, which was anatomically distant from the lesion. The wall of the cyst and tumor fragments, dissected off the wall of the third ventricle could have resulted in manipulation of the hypothalamus. Hypothalamic injury, especially of the median eminence, has been shown as a contributory factor to vasospasm. However, the patient was extubated uneventfully and remained neurologically intact till the ischemic episode, which was reversible with vasodilators. Finally, following surgery, the skull base defect was reconstructed with fascia lata and fat. There have been suggestions that fat used for skull base repair could lead to vasospasm by causing aseptic meningitis. The products of lipid metabolism have also been shown to cause vasospasm in canine basilar arteries; however, we have no means to ascertain which of these factors actually caused the vasospasm. It is rather more likely that one or more factors in tandem resulted in vasospasm in this scenario.
An optimum management of postoperative vasospasm without SAH is not supported by large clinical studies. In the view of our experience and from other instances in literature, we feel that an urgent MRI to rule cerebral ischemia and to assess the cerebral vasculature are essential. Patients with radiological signs of ischemia and evidence of vasospasm on an MRI or CT angiogram may benefit from endovascular therapy. Chemical angioplasty results in immediate reversal of vasospasm and improvement in neurological deficits. Ratanaprasatporn has also reported a case of pituitary necrosis and vasospasm following transcranial surgery for a craniopharyngioma, which was treated with intra-arterial nicardipine resulting in improvement in neurological deficits. Our patient was managed with euvolemia and induced hypertension using dopamine and milrinone for 7 days following endovascular therapy. While hypertension, hypervolemia, and hemodilution have been long held as the cornerstones of managing vasospasm, hypervolemia does not shown improvement in outcomes nor does it reduce the incidence of DCI, while contributing to other complications such as fluid overload, congestive heart failure (CCF), and pulmonary edema (PE)., This is especially pertinent in cases like ours where management of DI requires careful correction of free water loss., Volume depletion can, in turn, lead to cerebral hypoperfusion, whereas an over enthusiastic replacement can lead to congestive cardiac failure, pulmonary edema, and hyponatremia. Nimodipine can be tried, as it improves clinical outcome in aneurysmal SAH, despite the lack of evidence in this situation.
To the best of our knowledge, this is a rare case of angiographically proven vasospasm in a clinically symptomatic patient without SAH following an EEE resection of a craniopharyngioma where endovascular therapy was successfully used to reverse vasospasm and the clinical signs of ischemia. We report this case and its management to highlight the importance of recognizing vasospasm as a cause of clinical deterioration in patients undergoing EEE for craniopharyngiomas.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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