Your latest CEA patient – a left ICA embolic stroke with mild sensorimotor disturbance – deteriorates neurologically 2 days after the procedure – what is the differential?
We came up with the following reasons for late complications:
- Hyperperfusion syndrome
- Yet another stroke from a different source (the presumed etiology wasn’t correct)
- Hemodynamic instability because of restenosis or occlusion of the vessel
- Embolic complication after the fact (rare)
- Intracerebral hemorrhage into the original stroke
So how do you deal with that? Of course, you get the history and do a physical. But then?
- Ultrasound of the ICA – is it patent?
- TCD of the media on both sides: is there hyperperfusion (raised mean systolic velocity?) or hypoperfusion (e.g. distal stenosis) or occlusion of the MCA due to embolic stroke?
- CT: stroke? ICH? signs of hyperperfusion?
- EEG: PLEDs? Status?
If you cannot do emergency ultrasound turn the CT order into CT+CTA+CTP or – even better (and easier if the original procedure was done by your neuroradiologist) – MRI with PWI.
Next we talked about the hyperperfusion syndrome – or reperfusion syndrome (sounds better to me).
Here are the most important facts about it:
- Distinguish between hyperperfusion (raised CBF or – as surrogate marker – mean systolic velocity) and the hyperperfusion syndrome (headache, confusion, seizures, neurologic deterioration, in the worst case ICH)
- Pathophysiology: you need raised CBF (due e.g. to hypertension, often due to baroreflex disturbance) and autoregulatory failure, which leeds to endothelial damage and vasogenic, later cytotoxic edema, just as in PRES.
- Stent vs. TEA: Probably similar rates of hyperperfusion, but more ICHs with stents due to double platelet inhibition and balloon dilatation damage to the baroreflex. Thus in high risk patients (see below), you might think about balloon-free-stents (a recent hype)
- Predisposing factors are:
- Hypertension pre-procedure
- Blood pressure changes during the procedure
- Hypertension post-procedure
- Diabetes mellitus
- S/p contralateral CEA
- High grade stenosis (poststenotic hypotension) with or without
- Bad collaterals (incomplete Circulus Willisii)
- Volatile anesthetics?
- Perioperative stroke
- Symptomatic status
- Anticoagulation, platelet inhibition
- Impaired baroreflex [since this often coincides with impaired CO2 reactivity, many such patients have Cheyne-Stokes-respiration, so the latter might be a risk factor]
- Predictive numeric parameters
- MCA ipsilateral < 75% of contralateral side
- MCA normal, yet impaired autoregulation in acetazolamide test
- Low (< 40 mmHg) distal ICA pressure
- Cerebral transit time > 2,7sec (time for contrast from distal ICA to cortical veins)
- Impaired baroreflex (might be sensible to screen this)
- Diagnosis: Headache + Hyperperfusion. The most useful parameter apart from the above seems to be TCD about 2h after the procedure
- Epidemiology: roughly 1-2% of carotid revascularizations, about 0,5% bleed… Interestingly, stenting patients seem to develop hyperperfusion earlier (< 36h) than CEA patients (3-7d).
- Prevention: Statins preop might be an option (no real evidence yet, but some rationale and a recent retrospective study), RR < 140 mmHg, avoid predisposing factors, screen high risk patients with TCD 2h after the procedure
- Transfer to ICU, arterial line
- RR-goal < 100 mmHg (this is my personal recommendation, no evidence), using Urapidil/Labetalol or Clonidine, or even Dexmedetomidine, if delirium is bad. Next line agents would be Esmolol/Metoprolol. Enalapril iv might work, but could be dangerous. Dihydralazine, Ca antagonists, Nitro derivates should be avoided.
- If neurologic symptoms come up, consider Mannitol and steroids (again, no evidence)
References: There are many reviews on the topic, but not much has happened in the last two years.
- Neurologic complications after carotid revascularization. JNNP 2012
- Cerebral hyperperfusion syndrome after carotid intervention: a review. Cardiol review 2012