Case Report Cerebral Hyperperfusion Syndrome following ...downloads.hindawi.com/journals/crivam/2013/207602.pdf · internal carotid artery. We discuss the risk and management of cerebral

Hindawi Publishing CorporationCase Reports in Vascular MedicineVolume 2013, Article ID 207602, 4 pageshttp://dx.doi.org/10.1155/2013/207602

Case ReportCerebral Hyperperfusion Syndrome followingProtected Carotid Artery Stenting

Rainer Knur

Department of Cardiology and Angiology, Allgemeines Krankenhaus Viersen, Hoserkirchweg 63, 47147 Viersen, Germany

Correspondence should be addressed to Rainer Knur; [email protected]

Received 2 May 2013; Accepted 26 June 2013

Academic Editors: K. A. Filis and N. Papanas

Copyright © 2013 Rainer Knur. This is an open access article distributed under the Creative Commons Attribution License, whichpermits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

The cerebral hyperperfusion syndrome is a very rare complication after revascularization of the carotid artery and accompaniedby postoperative or postinterventional hypertension in almost all patients. We report a case of a 77-year-old man who developeda complete aphasia and increased right-sided weakness following endovascular treatment of severe occlusive disease of the leftinternal carotid artery. We discuss the risk and management of cerebral hyperperfusion syndrome after carotid artery stenting.

1. Introduction

Neurological complications following carotid artery stenting(CAS) are usually ischemic in nature, due to embolization orocclusion of the carotid artery. However, in a small subsetof patients, cerebral hyperperfusion causes postinterven-tional neurological dysfunction, characterized by ipsilateralheadache, focal seizure activity, focal neurological deficit, andipsilateral intracerebral edema or hemorrhage. A high clinicalsuspicion and early diagnosis will allow early initiation oftherapy and preventing fatal brain swelling or bleeding inpatients with peri- and postinterventional cerebral hyperper-fusion syndrome (CHS).

2. Case Report

A 77-year-old man was referred for endovascular treatmentafter a transient ischemic attack with a right-sided facialand limb weakness. This episode occurred while the patientwas undergoing medical treatment consisting of 100mgacetylsalicylic acid and 75mg clopidogrel 4 weeks aftercoronary stenting of the left anterior descending artery.The patient had a history of hyperlipidemia, hypertension,and familiar disposition with coronary heart disease. Theneurological examination during the ischemic event revealeda mild right-sided hemiparesis. Brain CT and MRI showedno abnormalities. All hematological and biochemical tests

were normal, with a normal platelet count and coagulationscreen.

When assessed in our hospital, his blood pressure some-times jumped up to 180/100mmHg. Therefore, the anti-hypertensive medication consisting of 𝛽-blocker, diuretic,and AT1-antagonist was intensified. Another neurologicalexamination was normal. Color Doppler ultrasound showeda severe stenosis of the left internal carotid artery (ICA)with elevation of the peak systolic velocity at 3.9m/s andan end diastolic velocity of 1.4m/s (Figure 1). The patientgot a loading dose of 500mg ASS and 300mg clopidogreland underwent left carotid stenting the next day via afemoral approach under local anesthesia. The angiographyconfirmed 95% stenosis of the left ICA (Figure 2(a)). CASwasfrictionless performed with distal filter protection, pre- andpostdilation, and a self-expandable closed-cell design stent(Figure 2). The peri-interventional blood pressure variedbetween 140/85 to 160/95mmHg.The clinically stable patientwas transferred to the intermediate care unit for monitoring.

20minutes later the patient vomited, described ipsilateralheadache, and became very anxious. He then developed acomplete aphasia and increased right-sided weakness andbecame delirious. Blood pressure varied between 160/90 and200/110mmHg. Immediately color Doppler ultrasound ofthe CCA and ICA revealed a visibly patent vessel. Brainedema and bleeding could be excluded by an urgent cra-nial CT. Followup within 24 hours with cranial MRI and

2 Case Reports in Vascular Medicine

Figure 1: Color Doppler ultrasound of the left internal carotidartery (ICA). Severe stenosis of the left internal carotid artery withelevation of the peak systolic velocity at 3.9m/s and an end diastolicvelocity of 1.4m/s.

angiography showed totally normal findings.The patient wastransferred to the intensive care to control the hypertensionand to monitor the vital parameters. Under intensified treat-ment of the blood pressure with a 𝛽-blocker, diuretic, AT1-,and Ca-antagonist, and temporary intravenous application ofnitroglycerin and urapidil the neurological symptoms weretotally regressed within few days. The patient was dischargedafter 10 days from the hospital. Follow-up examinations after3 and 6 months were normal.

3. Discussion

In 1981, Sundt et al. [1] described a triad of complicationsthat included atypicalmigrainous phenomena, transient focalseizure activity, and intracerebral hemorrhage after CEA andused the term cerebral hyperperfusion syndrome (CHS).Thefirst report on CHS after CAS was published by Schoseret al. [2].They described a 59-year-old womanwith ipsilateralputaminal hemorrhage that was diagnosed on the 3rd dayafter CAS of a high-grade stenosis of the left ICA. Outcomein this case was not fatal. The patient recovered with a mildupper limb paresis. McCabe et al. [3] were the first to reportthe occurrence of fatal ICH soon after CAS. Only a few hoursafter the procedure, neurological symptoms occurredwithoutany prodromata (severe headache, nausea, and seizures)postulated by Sundt et al. [1] to be an obligate componentof CHS. CT of the brain revealed extensive ICH and thepatient died 18 days later. Abou-Chebl et al. [4] reported aretrospective single-center study on 450 patients who hadbeen treated with CAS. Three patients (0.67%) developedICH after the intervention. Further reports on results andcomplications after CAS have been published [5]. Nearly allreports onCHS after carotid revascularizations in general andCAS in particular have in common patients who had high-grade stenoses in the treated vessel.

CHS following surgical or endovascular treatment ofsevere carotid occlusive disease is thought to be theresult of impaired cerebral autoregulation, hypertension,

Table 1: Risk factors for CHS [6–8].

HypertensionHigh-grade stenosis with poor collateral flowDecreased CVRIncreased peak flow velocityContralateral carotid occlusion or high-grade stenosisRecent contralateral CAS or CEA within 3 monthsPeriprocedural ischemiaPresence of cerebral microangiopathyCAS: carotid artery stenting, CEA: carotid endarterectomy, CHS: cerebralhypertension syndrome, and CVR: cerebrovascular reactivity.

ischemia-reperfusion injury, oxygen-derived free radicals,baroreceptor-dysfunction, and intraprocedural ischemia [6].Chronic cerebral hypoperfusion due to critical stenosis leadsto production of vasodilatory substances. Autoregulatoryfailure results in the cerebral arterioles being maximallydilated over a long period of time, with subsequent loss oftheir ability to constrict when normal perfusion pressureis restored. The degree of microvascular dysautoregulationis proportional to the duration and severity of ischemiadetermined by the severity of ipsilateral stenosis and poorcollateral flow.

Hypertension plays an important role in the developmentof CHS. In the absence of cerebral autoregulation, cerebralblood flow is directly dependent on the systemic bloodpressure. The restoration of normal blood flow to chronicallyunderperfused brain can result in edema, capillary break-through, and perivascular and macroscopic hemorrhagesaggravated by peri- and postinterventional hypertension [6,7]. The risk factors for CHS after CAS are summarized inTable 1.

The classic clinical presentation includes ipsilateralheadache, seizures or focal neurological deficit, and ipsilateralintracerebral edema or hemorrhage. The diagnosis can bemade readily with color Doppler ultrasound of the carotidartery and especially with transcranial Doppler (TCD) ofthe middle cerebral artery [9]. An increase in peak bloodflow velocity of >100% is predictive of postinterventionalhyperperfusion. Diffusion weighted MRI or single photonemission computed tomography (SPECT) could also beperformed for diagnosis [10]. Angiography normally showsnormal findings.

The prognosis of CHS depends on timely recognitionof hyperperfusion and adequate treatment of hypertensionbefore cerebral edema or hemorrhage develops. The prog-nosis following intracerebral bleeding is very poor, withmortality over 50% and significant morbidity of 80% inthe survivors [4, 6]. The prognosis of CHS in patientswithout cerebral edema or hemorrhage is clearly betterespecially when they are identified and treated early.Themostimportant aspects in preventing and treating this syndromeare early identification, careful monitoring, and control ofblood pressure ideally in a high-dependency unit setting.In our special case, early diagnosis of CHS and immediateintensive medical treatment of blood pressure could preventdevastating cerebral edema or hemorrhage following CAS.

Case Reports in Vascular Medicine 3

(a) (b) (c)

(d) (e) (f)

(g) (h)

Figure 2: Carotid angiogram demonstrating carotid artery stenting (CAS) with distal filter protection in a 77-year-old symptomatic patient.(a) Preprocedural angiogram showing a high-grade stenosis of the left internal carotid artery. (b)After the filter is positioned distal to the lesionthe stenosis is predilated with a 3mm balloon. (c)The self-expanding stent is deployed. (d) Stent after deployment. (e)The stent is postdilatedwith a 5mm balloon. (f) The final angiogram shows that the stented site is widely patent. (g), (h) Final angiogram of the intracranial vessels.

4 Case Reports in Vascular Medicine

4. Conclusion

CHS, which is characterized by ipsilateral headache, hyper-tension, seizures, and focal neurological deficits, is a rare butdevastating complication following carotid artery stenting.Hypertension is themost important risk factor.The diagnosiscan be confirmed quickly by TCD, DWI, or SPECT. Espe-cially peri- or postinterventional TCD monitoring should beavailable to identify patients with hyperperfusion who maybenefit from intensive blood pressure management ideally ina specialized intensive care unit.

Abbreviations

CAS: Carotid artery stentingCCA: Common carotid arteryCEA: Carotid endarterectomyCHS: Cerebral hyperperfusion syndromeCT: Computed tomographyCVR: Cerebrovascular reactivityDWI: Diffusion-weighted imagingICA: Internal carotid arteryICH: Intracerebral haemorrhageMRI: Magnetic resonance imagingSPECT: Single photon emission computed tomographyTCD: Transcranial Doppler.

Conflict of Interests

There is no conflict of interests existing.

References

[1] T. M. Sundt Jr., F. W. Sharbrough, and D. G. Piepgras, “Cor-relation of cerebral blood flow and electroencephalographicchanges during carotid endarterectomy. With results of surgeryand hemodynamics of cerebral ischemia,”Mayo Clinic Proceed-ings, vol. 56, no. 9, pp. 533–543, 1981.

[2] B. G. H. Schoser, C. Heesen, B. Eckert, and A. Thie, “Cerebralhyperperfusion injury after percutaneous transluminal angio-plasty of extracranial arteries,” Journal of Neurology, vol. 244,no. 2, pp. 101–104, 1997.

[3] D. J. H. McCabe, M. M. Brown, and A. Clifton, “Fatal cerebralreperfusion hemorrhage after carotid stenting,” Stroke, vol. 30,no. 11, pp. 2483–2486, 1999.

[4] A. Abou-Chebl, J. S. Yadav, J. P. Reginelli, C. Bajzer, D. Bhatt,and D. W. Krieger, “Intracranial hemorrhage and hyperperfu-sion syndrome following carotid artery stenting: risk factors,prevention, and treatment,” Journal of the American College ofCardiology, vol. 43, no. 9, pp. 1596–1601, 2004.

[5] J.-H. Buhk, L. Cepek, andM.Knauth, “Hyperacute intracerebralhemorrhage complicating carotid stenting should be distin-guished from hyperperfusion syndrome,” American Journal ofNeuroradiology, vol. 27, no. 7, pp. 1508–1513, 2006.

[6] V. Adhiyaman and S. Alexander, “Cerebral hyperperfusionsyndrome following carotid endarterectomy,”QJM, vol. 100, no.4, pp. 239–244, 2007.

[7] W. F. Morrish, S. Grahovac, A. Douen et al., “Intracranial hem-orrhage after stenting and angioplasty of extracranial carotid

stenosis,”American Journal of Neuroradiology, vol. 21, no. 10, pp.1911–1916, 2000.

[8] R. Gupta, A. Abou-Chebl, C. T. Bajzer, H. C. Schumacher, and J.S. Yadav, “Rate, predictors, and consequences of hemodynamicdepression after carotid artery stenting,” Journal of the AmericanCollege of Cardiology, vol. 47, no. 8, pp. 1538–1543, 2006.

[9] M. B. Sanchez-Arjona, G. Sanz-Fernandez, E. Franco-Macias,and A. Gil-Peralta, “Cerebral hemodynamic changes aftercarotid angioplasty and stenting,” American Journal of Neuro-radiology, vol. 28, pp. 640–644, 2007.

[10] Y. Kaku, S. I. Yoshimura, and J. Kokuzawa, “Factors predictiveof cerebral hyperperfusion after carotid angioplasty and stentplacement,” American Journal of Neuroradiology, vol. 25, pp.1403–1408, 2004.

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Case Report Cerebral Hyperperfusion Syndrome following ...downloads.hindawi.com/journals/crivam/2013/207602.pdf · internal carotid artery. We discuss the risk and management of cerebral