JRSM >
Volume 98, Number 10 >
Pp. 472-474
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The Vascular Unit, Worcestershire Royal Hospital, Worcester, UK
Correspondence to: Mr I K Nyamekye, c/o The Vein Clinic, BUPA South Bank Hospital, 139 Bath Road, Worcester WR5 3YB, UK E-mail: isaac.nyamekye{at}worcsacute.wmids.nhs.uk
Cerebral hyperperfusion syndrome, a serious complication of carotid endarterectomy, is easily missed when the patient presents as a medical emergency.
CASE HISTORIES
Case 1
A man of 74 on long-term antihypertensive therapy underwent endarterectomy
under general anaesthesia for symptomatic 490% left internal carotid artery
stenosis. The right internal carotid artery was occluded. Readings from his
arterial line showed mild postoperative hypertension that settled on his usual
antihypertensive medication (Figure
1). On discharge after 24 hours his systolic pressure was 150
mmHg. He was readmitted on the 'medical take' after 8 days
complaining of occipital headache, nausea, vomiting, and episodic right
hemiparesis. He had not been taking all his antihypertensive medication.
Systolic pressure was 180 mmHg and urgent carotid duplex showed a patent
endarterectomy site. CT of the brain showed a left intracerebral bleed
(Figure 2). Fifteen hours after
scanning he developed sudden dense right hemiplegia, dysphasia, and recurrent
seizures. He was medicated for seizures but no treatment was given for his
hypertension. Neurological function did not recover and he died of
complicating bronchopneumonia 32 days postoperatively.
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Case 2
A 78-year-old man, previously normotensive, underwent endarterectomy under
general anaesthesia for symptomatic 490% right internal carotid artery
stenosis. His left internal carotid artery was occluded. One dose of
nifedipine (5 mg sublingual) was administered for control of postoperative
hypertension in the recovery area. He was discharged after 24 hours on no
medication, with a systolic pressure of 140 mmHg
(Figure 1). He was readmitted
on the 'medical take' after 5 days with severe occipital headaches,
grand mal seizures and persistent left hemiparesis. Blood pressure was
persistently high (240 mmHg systolic) but no antihypertensive medication was
given, only repeated doses of diazepam. Following his chance recognition in
hospital by the vascular team, hyperperfusion syndrome was diagnosed. He was
transferred to the vascular high-dependency unit, where carotid duplex
scanning showed a patent carotid endarterectomy site. Aggressive treatment was
started with sublingual nifedipine, then glyceryl trinitrate infusion, and the
seizures and hemiparesis resolved completely within 60 minutes of normotension
being re-established. CT of the brain showed no acute changes. He was started
on bendrofluazide and phenytoin and discharged after five days with complete
neurological recovery. He remains well after 24 months.
| Box 1 Precautions against hyperperfusion syndrome Indications for emergency general practitioner referral to the vascular unit Recent carotid surgery (within weeks) and
Patient advice to contact our vascular unit after carotid surgery
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COMMENT
Post-carotid-endarterectomy cerebral hyperperfusion syndrome consists of headache and hypertension, with or without seizures and focal neurological signs, developing within days of successful carotid endarterectomy.1,2 Patients with this complication commonly have a poor outcome.3 When patients are admitted to medical rather than vascular units, the focus tends to be on control of seizures rather than hypertension.4
The timing of seizures and hemiparesis differed in our two patients but they had in common headache and hypertension. Headache after carotid endarterectomy should trigger clinical suspicion of hyperperfusion syndrome with urgent treatment of hypertension irrespective of seizures and neurological deficit. Scrupulous perioperative blood pressure management may be important in preventing the syndrome but good adherence to antihypertensive therapy is also necessary after discharge (in patient 1 this was poor). Patient 2 was not previously hypertensive, but nifedipine was required in the early postoperative period to establish normotension. We can only speculate whether tighter control of peri-admission blood pressure would have averted the hyperperfusion syndrome. High-grade stenosis (combined stenoses of 4190%), present in both patients, reduces cerebral perfusion reserve and has been linked to the syndrome.3 General rather than local anaesthesia may be another predisposing factor; the effect of carotid shunting on hyperperfusion syndrome is unknown. Changes in middle cerebral arterial flow have been implicated but were not measured in our cases.
In both patients hypertension developed after discharge, and a policy of checking blood pressure in the community within 48 hours of discharge might have signalled the onset of hyperperfusion syndrome. We are now assessing this management approach but the rarity of this complication will make any benefit difficult to establish. Patients are advised to contact our vascular high-dependency unit if they develop persistent headaches, nausea and vomiting or any new neurological symptoms (Box 1). Medical colleagues who see these patients as emergencies need to appreciate the relevance of the recent carotid endarterectomy and treat hypertension aggressively.4
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Case 1; 
case 2