Article, Neurology

Cerebral hyperperfusion syndrome: A rare postoperative complication of carotid endarterectomy

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American Journal of Emergency Medicine

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American Journal of Emergency Medicine 34 (2016) 2054.e1-2054.e2

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Cerebral hyperperfusion syndrome: A rare postoperative complication of carotid endarterectomy?


Acute Neurological deficits are common presentations to the emer- gency department. Cerebral hyperperfusion syndrome, a rare phenom- enon which can occur within one month following carotid surgical revascularization, may be challenging for the emergency physician to diagnose in the setting of an acute neurological presentation. Carotid ar- terial disease contributes 15-20% of ischemic Cerebrovascular accidents and surgical revascularization is the commonest intervention for preventing stroke in patients with significant carotid disease. However if the patient remains hypertensive postoperatively in the setting of sudden carotid reperfusion following revascularization, they are prone to cerebral hyperperfusion syndrome. Caused by increased, unregulated cerebral blood flow, cerebral hyperperfusion syndrome can result in ce- rebral edema and intracranial hemorrhage which may manifest in symptoms ranging from headaches, myoclonus, hemiparesis, seizures, reduced consciousness and potentially result in death. The most impor- tant facets in management of cerebral hyperperfusion syndrome in the emergency department is early recognition, prompt management and monitoring of hypertension (up to 81% of patients have severe hyper- tension at onset of neurological symptoms) and early imaging. We re- port a case of cerebral hyperperfusion syndrome in a woman who had ongoing Severe hypertension following carotid endarterectomy. Five days following surgery and after discharge, she presented to the emer- gency department with worsening right upper limb myoclonus, tremor, weakness and hypertonia. Initially treated with anticonvulstants with- out resolution of symptoms, prompt imaging and management of hy- pertension in the emergency department resulted in the correct diagnosis and complete resolution of symptoms without any perma- nent neurological deficits.

Carotid artery disease contributes 15-20% of ischemic cerebrovascular accidents (CVA) [1]. Carotid endarterectomy (CEA) remains the commonest surgical intervention for preventing stroke in patients with significant carotid artery disease [2]. A well-recognised cerebrovascular postoperative complication is ischemic CVA but rates of ischemia improve post endarterectomy [3]. However, intracerebral hemorrhage (ICH) rates increase following surgery, a devastating consequence of delayed diagno- sis of cerebral hyperperfusion syndrome (CHS) [3,4].

The pathophysiology of CHS is sudden carotid reperfusion resulting in increased, unregulated cerebral blood flow (CBF) [3,4]. Symptoms in- clude headaches, myoclonus, hemiparesis and seizures from cerebral hyperperfusion, edema and ICH which may cause reduced conscious- ness and death [3-5]. Early recognition of this syndrome prior to ICH

? Source(s) of support: None.

is crucial [4]. CHS must be considered in the relevant population pre- senting with neurological symptoms to institute urgent antihyperten- sive management and imaging [4].

A 68 year old female presented for elective left carotid endarterectomy (CEA) on background of multiple CVAs. An eversion endarterectomy was performed without intraoperative complications. She was transferred to ICU with postoperative orders for a systolic BP (SBP) between 100-

140 mmHg. On ICU admission, SBP was above 200 mmHg for 30 minutes peaking at 230 mmHg without cardiovascular or neurological deficits. Hypertension was treated in ICU with glyceryl trinitrate (GTN) and metoprolol infusions, remaining below 150mmg. She continued experiencing intermittent hypertensive episodes throughout the admis- sion but was discharged day three post CEA without abnormalities.

Two days post discharge, she presented to the ED of a regional hos- pital with persistent, worsening, uncontrollable right upper limb myoc- lonus and tremor without other neurological symptoms. Positive findings on examination included SBP 182 mmHg, hypertonia, myoclo- nus, tremors and weakness in her right upper limb. She was prescribed IV midazolam and phenytoin for query Focal seizures secondary to brain injury. Her vascular surgeon was contacted, advising urgent SBP reduc- tion to b 130 mmHg and urgent imaging for likely CHS. CT and MRI Head (Figure) revealed new left temporal hyperaemic changes with localised ischemia without hemorrhage. She was admitted to the ED, treated with a GTN infusion with strict BP monitoring. SBP improved with neu- rological deficits completely resolving prior to discharge the following day. She has not experienced neurological symptoms since discharge.

CHS is an uncommon but major consequence following interven- tional reperfusion of carotid artery disease [4]. The critical period of CHS is one month post carotid reperfusion [3]. Long term carotid artery stenosis leads to Cerebral hypoperfusion and subsequent compensatory vasodilation of intracranial vessels [4]. However, as chronic vasodilation becomes less vasoreactive over time, sudden reperfusion leads to a pe- riod of increased CBF with ongoing dysfunctional autoregulation [3]. This postoperative period of autoregulatory dysfunction makes CEA pa- tients vulnerable to CHS [3].

The most important implication of CHS is early diagnosis to prevent unregulated cerebral hyperperfusion resulting in ICH [3]. Reducing postoperative periods of hypertension plays a crucial role in both reduc- ing the risk of developing CHS and treating CHS [2,3]. In this case, there were periods of significant hypertension postoperatively and on re- admission. Studies revealed up to 81% of patients had severe hyperten- sion at onset of CHS/ICH with largest cumulative frequency above SBP 150 mmHg [3]. Not only is postoperative BP a modifiable risk factor of CHS, rapid achievement of normotension in CHS, rather than anticon- vulsants, can resolve symptoms, cerebral edema and prevent progres- sion to ICH [2,3,4].

0735-6757/(C) 2016

2054.e2 M. Guirgis, K. Sieunarine / American Journal of Emergency Medicine 34 (2016) 2054.e12054.e2

Image of FigureThis case highlights a rare syndrome where early recognition in ED of the neurological presentations with recent cerebral reperfusion is crucial as urgent imaging and prompt aggressive Antihypertensive treatment in a monitored setting are required [4,5]. Otherwise, this time critical syndrome may progress to irreversible neurological deficit or death whilst being treated as a general or focal neurological disorder without appropriate attention placed on hypertension management.


Authors only.

Mina Guirgis, MBBS? Kishore Sieunarine

Department of Surgery, Joondalup Health Campus, Australia

?Corresponding author. Joondalup Health Campus, Grand Boulevard & Shenton Avenue, Joondalup, Western Australia, 6027. Tel.: +61 08 9400

9400, +61 412315375; fax: +61 08 9386 9866

E-mail address: [email protected]


  1. Chaturvedi S, Bruno A, Feasby T, Holloway R, Benavente O, Cohen SN, et al. Carotid endarterectomy-An evidence based review. Neurology 2005;65:794-801.
  2. Adhiyaman V, Alexander S. Cerebral hyperperfusion syndrome following carotid end-

    arterectomy. QJM 2007;100:239-44.

    Bouri S, Thapar A, Shalhoub J, Jayasooriya G, Fernando A, Franklin IJ, et al. Hyperten- sion and the post-carotid endarterectomy cerebral hyperperfusion syndrome. Eur J Vasc Endovasc Surg 2011;41:229-37.

  3. Moulakakis KG, Mylonas SN, Sfyroeras GS, Andrikopoulos V. Hyperperfusion syn- drome after carotid revascularization. J Vasc Surg 2009;49:1060-8.
  4. Schaafsma A, Veen LVD, Vos JPM. Three cases of hyperperfusion syndrome identified by daily transcranial Doppler investigation after carotid surgery. Eur J Vasc Endovasc Surg 2002;23:17-22.

    Figure. (a) Computed tomography scan of the brain during cerebral hyperperfusion syn- drome (CHS) revealed serpiginous type low density changes in the left temporal region (centrum semiovale) consistent with hyperemic changes with associated ischemia.

    (b) Magnetic resonance Axial FLAIR brain imaging following CHS revealed confluent high-signal intensity in the left temporal region corresponding to the low density CT find- ings in the same territory, suggestive of hyperemic and Ischemic changes.