764

GENERAL
ANESTHESIA
CANADIAN JOURNAL
OF ANESTHESIA

Case report: Aggressive blood pressure management for carotid endarterectomy hyperperfusion
syndrome
[Présentation de cas : le traitement énergique de la tension artérielle pour le
syndrome d’hyperperfusion après une endartérectomie carotidienne]
James Scozzafava MD, Muhammad S. Hussain MD, Tom Yeo MD, Thomas Jeerakathil MD FRCPC,
Peter G. Brindley MD FRCPC

Purpose: Cerebral hyperperfusion syndrome (CHS) is a rare
but potentially devastating complication following cerebral
revascularization. Management of CHS requires aggressive
blood pressure control to prevent stroke and intracerebral
hemorrhage. This case report documents a severe case of CHS,
and outlines a successful outcome associated with aggressive
blood pressure control.
Clinical features: A 67-yr-old gentleman, nine days post left
carotid endarterectomy, required tracheal intubation and intensive care unit admission following seizures and acute right-sided
weakness. A computed tomography scan and magnetic resonance imaging revealed significant vasogenic edema in the left
middle cerebral artery territory, without evidence of infarction.
The history and radiographic findings suggested CHS. As such,
a systolic blood pressure target was set at 90–140 mmHg. This
blood pressure parameter was lower than typically targeted
following acute ischemic or hemorrhagic stroke. Rapid clinical
improvements were seen by day five, and tight blood pressure
control was maintained throughout. Repeat computed tomography and magnetic resonance imaging revealed improved
edema and no evidence of infarct or hemorrhage.
Conclusion: Cerebral hyperperfusion syndrome is believed
to occur following restoration of blood flow to a brain with
impaired autoregulation due to chronic hypoperfusion. Massive
brain edema and hemorrhage can result from higher pressures.
Clinicians should be aware of this potential complication following cerebral revascularization procedures, and the importance
of establishing blood pressure targets which are considerably
lower than for other patients with similar clinical presentations.

Objectif : Le syndrome d’hyperperfusion cérébrale (SHC) est
une complication rare, mais potentiellement dévastatrice après
la revascularisation cérébrale. Le traitement du SHC exige un
contrôle serré de la tension artérielle pour prévenir l’accident
vasculaire et l’hémorragie intracérébrale. Nous présentons un cas
sévère de SHC et l’heureux résultat associé au contrôle étroit de
la tension artérielle.
Éléments cliniques : Neuf jours après une endartérectomie de la
carotide gauche, un homme de 67 ans a dû être intubé et admis
à l’unité des soins intensifs pour convulsions et faiblesse au côté
droit. La tomodensitométrie et l’imagerie par résonance magnétique ont révélé un important œdème vasogénique dans le territoire
de l’artère cérébrale moyenne gauche, sans évidence d’infarctus.
Les antécédents et les résultats radiographiques étaient en faveur
d’un SHC. Une tension artérielle systolique cible a donc été fixée
à 90–140 mmHg. C’est une tension plus basse que celle qui est
généralement ciblée après un accident ischémique ou hémorragique aigu. De rapides améliorations cliniques ont été observées
au cinquième jour. Le contrôle étroit de la tension artérielle avait
été constamment maintenu. La reprise des examens d’imagerie a
montré une diminution de l’œdème et aucune évidence d’infarctus
ou d’hémorragie.
Conclusion : Le syndrome d’hyperperfusion cérébrale est connu
pour survenir à la suite de la restauration du débit sanguin dans
un cerveau où l’autorégulation est affectée par une hypoperfusion
chronique. Un œdème cérébral massif et une hémorragie peuvent
être causés par des pressions plus élevées. Les cliniciens doivent
connaître cette complication possible suivant la revascularisation
cérébrale et l’importance d’établir des tensions artérielles cibles
qui soient considérablement plus basses que pour d’autres patients
au tableau clinique similaire.

From the Divisions of Neurology and Critical Care Medicine, University of Alberta, Edmonton, Alberta, Canada.
Address correspondence to: Dr. Peter Brindley, Division of Critical Care Medicine, Unit 3C4, University of Alberta Hospital, Edmonton,
Alberta T6G 2B7, Canada. Phone: 780-407-7381; Fax: 780-407-6018; E-mail: peterbrindley@cha.ab.ca
Accepted for publication January 9, 2006.
Revision accepted February 2, 2006.
Competing interests: None declared.

CAN J ANESTH 2006 / 53: 8 / pp 764–768

Scozzafava et al.: CAROTID ENDARTERECTOMY HYPERPERFUSION SYNDROME

C

EREBRAL hyperperfusion syndrome
(CHS) is a serious complication of cerebral
vascular surgery. It typically occurs during
the first week following carotid endarterectomy (CEA) or carotid angioplasty, but can occur
as late as one month postrevascularization.1 While
the incidence varies, recent evidence suggests that the
incidence of CHS following CEA is as high as 3%.2–4
The rationale for intensive care unit (ICU) admission,
urgent investigations, and lower blood pressure (BP)
targets than targeted following acute stroke5,6 mean
that operating room and critical care staff need to be
familiar with CHS. We present a case of severe CHS
and successful outcome associated with aggressive BP
management. Patient consent was obtained prior to
writing this case report, in accordance with our institutional guidelines.
Case presentation
A 67-year-old gentleman with a past history of coronary artery disease, hyperlipidemia and hypertension
underwent an elective CEA for prevention of stroke.
Carotid disease was suspected due to neck bruits
during routine physical examination. Carotid ultrasonography and angiography confirmed 90% irregular
ulcerative stenosis of the left internal carotid artery,
and 99% stenosis of the right internal carotid artery.
A left CEA was planned to preserve the dominant
hemisphere, and because of collateral blood flow to
the right hemisphere via the anterior communicating
artery.
Carotid endarterectomy was performed uneventfully under general anesthesia, using a 3 × 5 Sundt
shunt (Integra Neurosciences, Plainsboro, NJ, USA)
between the left common carotid and distal internal
carotid artery, and a Vascutek patch (Vascutec USA
Inc., Ann Arbor, MI, USA) over the endarterectomy.
Doppler ultrasound confirmed normal flow pattern in
all vessels. Surgery was uneventful and the patient was
discharged home two days later, neurologically intact.
Medications at the time of discharge included clopidogrel 75 mg po daily, atorvastatin 80 mg po daily, and
metoprolol 100 mg po bid.
Nine days later, the patient was rushed to hospital
following two witnessed generalized seizures. After
administration of lorazepam and phenytoin, his trachea
was intubated, and he was transferred to the ICU. He
was afebrile, in normal sinus rhythm with a heart rate
between 60–100 beats·min–1, and a BP which fluctuated between 100/50 to 190/100 mmHg. His cardiac
examination was normal, but neurologically he had a
right facial droop, 3/5 right-sided arm and leg weakness, and brisker right-sided deep tendon reflexes.

765

FIGURE 1 Multiple areas of white matter hypodensity in
the left hemisphere.

FIGURE 2 T2 weighted (panel A) and fluid-attenuated
inversion recover y (FLAIR; panel B) magnetic resonance
imaging showing multiple areas of white matter hyperintensity, corresponding to the areas of hypodensity seen on
the initial computed tomography scan. Apparent diffusion
coefficient (ADC) map (panel C) also shows areas of hyperintensity, indicating changes are related to vasogenic edema
as opposed to infarction. After one week with aggressive
antihypertensive therapy, the repeat FLAIR magnetic resonance imaging shows improvement (panel D).

766

CANADIAN JOURNAL OF ANESTHESIA

TABLE Hemodynamic response during a continuous infusion of labetolol
Initial

Day 1

Day 2

Day 3

Day 4

Day 5

SBP (mmHg)
190
145
120
100
110
120
130
130
130
135
135
DBP (mmHg)
100
70
65
60
60
65
60
65
60
70
75
HR (beats·min–1)
70
70
70
110
90
70
60
60
70
60
60
Labetolol (mg·min–1)
---4
3
0
2
1
0
------------SBP = systolic blood pressure; DBP = diastolic blood pressure; HR = heart rate. Mean values of SBP, DBP and HR for each 12-hr period
following admission. Blood pressure was monitored through a radial arterial line. Twelve-hour averages for each parameter are listed, as
well as the average infusion rate of labetolol during the period of treatment.

Computerize axial tomography (CT) of the head
(Figure 1) showed hypodensity throughout the left
hemisphere, predominantly involving the subcortical
white matter, with cortical involvement in the peripheral frontal, parietal and temporal lobes. Because CT
findings were inconsistent with typical stroke, urgent
magnetic resonance imaging and magnetic resonance
angiogram/venogram of the head and neck were
undertaken (Figure 2). The examinations showed
extensive vasogenic edema in the territory supplied
by the left middle cerebral artery. There was no acute
hemorrhage, and diffusion studies showed no infarction. The magnetic resonance angiogram confirmed a
widely patent left endarterectomy and intact collateral
circulation, whereas the magnetic resonance venogram was unremarkable.
The patient was admitted to neuro-ICU with the
diagnosis of acute CHS, and a plan to maintain strict
BP control with a target systolic pressure between
90–140 mmHg, as determined via right radial arterial pressure monitoring. Blood pressure control was
maintained using a labetolol infusion (2–8 mg·min–1
initially), and later as bolus doses of 10–20 mg iv
(hemodynamic response, Table). Concurrent oral
antihypertensive medications were started, including metoprolol 100 mg bid, ramipril 2.5 mg bid,
and hydrochlorothiazide 12.5 mg bid. The labatelol
infusion was weaned gradually over three days, while
avoiding antihypertensives with the potential for
vasodilation, such as nitroprusside, nitroglycerin and
hydralazine. On the second day following initiation
of therapy, transcranial Doppler showed no evidence
of microemboli, and the electroencephalogram was
normal. Daily electrocardiograms and cardiac enzymes
(CK, CKMB, troponin I) were negative for myocardial ischemia or infarction. Clopidogrel 75 mg·day–1
was re-initiated after a repeat CT head scan revealed
resolution of edema, and no hemorrhage.
In contrast to the typical course following ischemic
or hemorrhagic stroke, the patient improved rapidly.
He was fully awake within 48 hr of admission, at which

point his trachea was extubated. The fifth day following admission, the patient’s seizures had resolved and
he had no residual neurological deficits, at which point
he was transferred to the ward. On day seven, a repeat
magnetic resonance imaging with diffusion (Figure
2) showed evidence of significant improvement in
the vasogenic edema, and no restricted diffusion to
suggest infarction or hemorrhage. He was discharged
on the following oral medications: clopidogel 75 mg
daily, atorvastatin 80 mg daily, metoprolol 50 mg bid
and ramipril 5 mg bid. He was educated regarding
out-patient BP monitoring, with follow-up appointments to optimize vascular risk factors and BP.
Discussion
This case report describes a successful outcome following severe delayed CHS, and highlights the risk
factors, and as well as the goals of BP management
compared to patients with a typical stroke.
Carotid endarterectomy hyperperfusion syndrome
was first described by Spetzler et al. in 1978 as a rare
complication following surgical resection of arteriovenous malformations.7 Spetzler et al. theorized
that chronic cerebral vascular disease leads to loss of
cerebral autoregulation. Subsequent revascularization conferred higher intracerebral blood flow to
a vasculature bed less capable of compensating. As
such, surgical restoration of blood flow could result
in postoperative cerebral edema, stroke and intracerebral hemorrhage. Spetzler’s theory was expanded to
carotid revascularization in the 1980’s by Sundt et al.,
who described a triad of headaches, focal seizures, and
intracerebral hemorrhage post-CEA.8
Carotid endarterectomy hyperperfusion syndrome
has been reported following cerebral revascularization by carotid angioplasty and stenting. However,
due to the relative frequency of CEA, it remains the
most commonly associated intervention.9 Estimates of
incidence following CEA range from 0.4% to greater
than 3%.2,10–12 As with arteriovenous malformation
surgery, the etiology is believed to be supranormal

Scozzafava et al.: CAROTID ENDARTERECTOMY HYPERPERFUSION SYNDROME

postoperative cerebral perfusion pressure in a previously hypoperfused brain. Preoperatively, chronic
hypoperfusion distal to the high-grade stenosis results
in chronic arterial dilatation and impaired autoregulation. Surgical correction elevates perfusion pressure,
but impaired autoregulation prevents protective reflex
vasoconstriction.
Early stroke following CEA has been reported in
0.9 to 7% of patients. Hingorani et al. reviewed 444
consecutive CEA patients and found the incidence
of stroke within 30 days to be just over 1%.3 Two
of these five strokes were believed to be the result
of hyperperfusion syndromes. This led Hingorani to
conclude that CHS may be under-recognized.
Seizures following CEA are uncommon, but cerebral edema in CHS increases the risk. Nielsen and
Naylor reported the incidence of seizures after CEA to
be from 0.8% to 3%, and associated with subsequent
stroke and hemorrhage. The incidence was greater in
patients with labile hypertension, bilateral carotid disease and poor collateral circulation.13,14 These authors
concluded that postoperative seizures, in the absence
of infarction or hemorrhage, should increase suspicion
of CHS.
When suspected on clinical grounds, the diagnosis
of CHS should be confirmed by urgent radiological
investigation. Unfortunately, CT lacks the sensitivity
and specificity to delineate CHS from arterial and
venous infarcts. Therefore, urgent perfusion magnetic resonance imaging is recommended. In regards
to carotid imaging, transcranial Doppler ultrasound
detects early hemodynamic changes in arterial flow
velocity, but may not be sufficiently sensitive in CHS.15
Prompt magnetic resonance angiography or four-vessel cerebral angiography may be required. Prompt
cerebral angiography also remains the best means of
detecting correctable lesions within the carotid artery.
Findlay has shown that this invasive approach is not
associated with increased morbidity or mortality.16
The most catastrophic event secondary to CHS is
intracerebral hemorrhage, and the progression from
hyperperfusion to hemorrhage significantly worsens
prognosis. The Mayo Clinic reviewed 2,362 consecutive CEAs and found that intracerebral hemorrhage
occurred in 14 (0.6%) of patients within two weeks
of surgery.17 Other reports have listed the incidence
of hemorrhage associated with CHS to be as high as
1.2%.18,19 Intracerebral hemorrhages were fatal in 60%
of cases, and associated with severe morbidity in 25%.
Risk factors were similar to those for postoperative
seizure and stroke and included advanced age, labile
hypertension, high-grade stenosis, and poor collateral
flow.20 Because of the concern of hemorrhage, many

767

neurologists and intensivists are cautious about reinstituting anti-platelet therapy following CHS. However,
given that thromboembolism remains the most common cause of stroke in patients with carotid disease,
anti-platelet therapy is likely safe and warranted, following clinical and radiological improvement.
Following routine CEA many centres recommend
short-term ICU admission because of potential complications including hemorrhage at the surgical site,
and resultant cardiac instability. However, there is a
lack of controlled studies to justify routine ICU admission. In fact, O'Brien and Ricotta concluded that only
a few patients benefited, and recommended ICU
admission be based on risk factors including advanced
age, coronary artery disease, poorly controlled hypertension, and high-grade carotid stenosis.21 Because of
the significant risk of stroke and hemorrhage, and the
presumed need for tight BP control, there is a stronger argument to expedite ICU admission for those
suspected of CHS.
Given the putative mechanism for CHS, experts
have suggested maintaining systolic BP between 90–
140 mmHg.5,15,16,18 Of note, however, this recommendation is based upon a physiologic rationale, rather than
data from randomized controlled trials. Furthermore,
uncertainty remains regarding optimal BP management
in acute ischemic and hemorrhagic stroke. In acute
stroke, lower BP may reduce edema and hemorrhagic
complications. However, aggressive BP reduction could
decrease perfusion which could expand the area of
infarction.22 This has resulted in liberal BP parameters
in acute stroke. However, narrower parameters may be
necessary in CHS compared to stroke, because most
stroke patients are assumed to have intact auto regulation. In contrast, CHS patients likely cannot tolerate
high perfusion pressure. This key difference is essential
to understand the aggressive lowering of BP in CHS.
Furthermore, vasodilating antihypertensive medications are avoided because of the potential to aggravate
pre-existing cerebral vasodilation.
Rigorous randomized controlled trials are required
to determine the optimal hemodynamic treatment
parameters and duration of therapy in patients with
CHS. Case reports/case series offer a measure of
current best evidence. Our experience highlights
clinical risk factors and a diagnostic approach to CHS.
Aggressive targeting, and maintenance of a relatively
low systemic BP in a critical care setting were associated with a favourable outcome in a patient with CHS.
Acknowledgement
Thanks to Dr. J Max Findlay for helpful editing suggestions.

768

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