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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{at}cha.ab.ca
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Abstract |
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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.
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Case presentation |
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Carotid endarterectomy was performed uneventfully under general anesthesia, using a 3 x 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.
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.
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). 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.
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) 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 |
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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 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 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 hyper-tension, 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.
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Acknowledgments |
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Footnotes |
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Competing interests: None declared.
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References |
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2 Solomon RA, Loftus CM, Quest DO, Correll JW. Incidence and etiology of intracerebral hemorrhage following carotid endarterectomy. J Neurosurg 1986; 64: 29–34.[Medline]
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22 Powers WJ. Acute hypertension after stroke: the scientific basis for treatment decisions. Neurology 1993; 43: 461–7.
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