|Year : 2017 | Volume
| Issue : 1 | Page : 38-40
Hyperacute fatal intracerebral hemorrhage following carotid stenting
Sherief Sulaiman, Kader Muneer, Chakanalil Govindan Sajeev
Department of Cardiology, Government Medical College, Kozhikode, Kerala, India
|Date of Web Publication||8-Mar-2017|
Dr. Sherief Sulaiman
No. 30/1277D, Dream Land, Medical College (PO), Kozhikode - 673 008, Kerala
Source of Support: None, Conflict of Interest: None
We describe a case of fatal intracerebral hemorrhage (ICH) complicating carotid stenting. The manifestation is distinct from the well-known hyperperfusion syndrome. In our patient, neurologic deterioration appeared within 15 min of stenting, without any prodromal symptom. This early postprocedural complication is radiologically similar to hypertensive ICH and might have the same pathogenesis. Appropriate antihypertensive therapy might be beneficial in preventing this devastating complication.
Keywords: Carotid stenting, fatal intracerebral hemorrhage, hyperacute intracerebral hemorrhage, intracerebral hemorrhage
|How to cite this article:|
Sulaiman S, Muneer K, Sajeev CG. Hyperacute fatal intracerebral hemorrhage following carotid stenting. Heart India 2017;5:38-40
| Introduction|| |
Carotid revascularization procedures for symptomatic carotid stenosis include carotid artery stenting and carotid endarterectomy. A rare complication of any form of cervical revascularization is hyperperfusion syndrome (HPS), which usually manifests between 5th and 7th day of the procedure. Another distinct neurological complication involves early onset intracerebral hemorrhage (ICH), with rapid clinical deterioration and a fatal outcome. With only a few cases reported, the risk factors and pathogenesis of this complication remain elusive.
| Case Report|| |
A 72-year-old male with a history of long-standing diabetes and hypertension presented with multiple episodes of cerebrovascular transient ischemic attacks (TIAs) in the form of paresthesia involving right half of the body. The last episode of TIA was 6 weeks before presentation. The patient had inferior wall myocardial infarction 10 years before presentation. His electrocardiogram showed sinus rhythm with left axis deviation and poor R-wave progression in the precordial leads. Echocardiographic evaluation showed an ejection fraction of 56%. His blood sugars were well under control and renal parameters were within normal limits. He had undergone coronary angiogram a month before which revealed significant obstructive lesion in all three major epicardial coronaries and was planned for coronary artery bypass surgery. On evaluation, his carotid Doppler showed 90% stenosis of his left internal carotid artery (ICA). The patient was planned for elective stenting of left ICA. Preprocedural computed tomography (CT) brain did not show any infarct. The procedure was performed through femoral approach under local anesthesia. A bolus of 5000 IU of heparin was administered intravenously. Carotid angiogram revealed a short segment total occlusion near the origin of left ICA [Figure 1]. The lesion was crossed with Fielder FC wire and predilated serially with 2.0 mm × 15 mm Artimes balloon (BrosMed Medical Co., Ltd., China) followed by 4 mm × 15 mm High Trek balloon (Abbott vascular, US) at 8 atm pressure reaching a final diameter of 4 mm. Emboshield NAV6 (Abbott vascular, US) was used as distal protection device. The stenotic segment was stented with 6 mm × 40 mm × 8 mm Acculink carotid stent system (Abbott vascular, US). Post dilatation was done with 6 mm × 20 mm × 135 mm Viatrac 14 plus (Abbott vascular, US). There were no procedural complications. The vessel was completely recanalized and blood flow was reestablished [Figure 2]. The blood pressure was maintained at 150/80 mmHg. However, within 15 min of the procedure, the patient developed right-sided hemiplegia followed immediately by unresponsiveness. The blood pressure was then recorded 160/100 mmHg. A check carotid angiogram showed a patent stent and good blood flow. An unenhanced CT brain was performed which showed massive left-sided ICH involving basal ganglia and thalamus with extension into intra-axial cerebrospinal fluid spaces [Figure 3]. Despite intensives measures involving hyperventilation and antiedema measures, the patient expired 2 days after the procedure.
|Figure 1: Carotid angiogram showing total occlusion near the origin of left internal carotid artery (arrow)|
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|Figure 2: Fluoroscopic images following carotid angioplasty showing stent in the left internal carotid artery (arrow) (a) and final injection showing complete recanalization and good blood flow (b)|
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|Figure 3: Unenhanced computed tomography brain with 5 mm slices (done 30 min after the neurological complication) showing massive intracerebral hemorrhage involving left basal ganglia with ventricular extension|
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| Discussion|| |
Carotid stenting is commonly performed for symptomatic ICA stenosis. HPS is usually a delayed complication that presents with neurologic signs of intracranial hypertension such as ipsilateral frontotemporal or retro-orbital headache, nausea, and vomiting and is believed to be due to impaired cerebral autoregulation. ICH may or may not be present in classic type of HPS. HPS complicates about 1.45% of patients undergoing carotid stenting  whereas the overall rate of ICH (including HPS) following carotid stenting has been reported as 5%. However, the incidence of hyperacute ICH is much lower. In a single-center study, the incidence of hyperacute ICH following carotid stenting was reported as 0.22%. The onset of symptoms occurs within hours after the procedure and without any prodromal symptom, as in our case. In almost all the cases reported, the patients had high-grade stenosis (>90%) of ICA, and the outcome has been fatal. The cases have been reported following both right and left ICA stenting. Although ICH occurred in the ipsilateral basal ganglia in most of the cases, contralateral ICH was reported by Chamorro et al. In the cases reported, the timing of the procedure varied widely from 2 days to 5 months after the last symptom. The site of hemorrhage was not found to be related to previously infarcted area. In our patient, preprocedural imaging did not show any infarct. The risk factors proposed for hyperacute ICH include cerebral microangiopathy and insufficient intracranial collateralization. The pathogenesis of this early ICH might involve rupture of small perforating arteries in the basal ganglia. This could occur as a result of sudden exposure of hypoperfused areas to normalized perfusion pressure following recanalization of high-grade stenosis, analogous to hypertensive ICH where the sudden elevation of blood pressure leads to rupture of intracerebral microvasculature. Another possible explanation is the development of acute cerebral infarct following angioplasty with subsequent hemorrhage into the infarcted zone. This early complication characteristically mimics hypertensive ICH, and although sudden elevation of blood pressure has not been documented in all cases, careful blood pressure monitoring and antihypertensive treatment might prevent this complication in high-risk patients.
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[Figure 1], [Figure 2], [Figure 3]