ADD-ONS

Cerebral hyperperfusion syndrome (CHS)

Created 04/11/2021, last revision 05/11/2023

• Cerebral Hyperperfusion (reperfusion) Syndrome (CHS) can occur within hours to days after a revascularization procedure (most commonly carotid endarterectomy)
  
  • the peak incidence of CHS and hemorrhage after carotid endarterectomy (CEA) is  5-7 days, while it is 12-48 hours after carotid artery stenting (CAS)   [Ogasawara, 2007]
  • a longer delay (days to weeks) has also been reported
    
  • CHS after aortic stenosis surgery may lead to bilateral lesions
    
• diagnostic criteria include new-onset symptoms (headache, neurological deficit, and seizure) + evidence of hyperperfusion measured by TCD, MRI or SPECT
• incidence 1-14% (usually ∼ 7%)
  • CEA and CAS pose similar risks (Galyfos, 2017)
  • incidence seems to be higher in moyamoya surgery  (Hayashi, 2012)
• the cornerstone of prevention is strict perioperative blood pressure (BP) control (for at least 14-21 days)
• TCD should be available to identify patients with hyperperfusion

• the terms hyperperfusion (excessive flow/hyperemia) and reperfusion (flow normalization) are often used synonymously because both can cause cerebral injury with similar clinical presentation
• CHS results from a failure of cerebral blood flow autoregulation, leading to hyperemia
  • long-term hypoperfusion, seen in conditions like high-grade stenosis, is compensated by maximal peripheral vasodilation
  • the autoregulatory capacity is thus exhausted, and the blood vessels are unable to respond immediately with vasoconstriction when the perfusion pressure suddenly increases after successful CEA/CAS → tissue is therefore exposed to hyperemia
    
• hyperemia is usually defined as an increase in cerebral blood flow (CBF) >100% compared to the baseline   → Cerebral blood flow regulation
  • preoperative CBF value is usually unknown; the interhemispheric difference may be used (except in patients with contralateral stenosis)
    
  • the risk of CHS can also be estimated using TCCD/TCD – a 1.5- or 2-fold postoperative increase in mean MCA flow velocity compared to baseline may predict the occurrence of CHS   (Fujimoto, 2004)
  • symptomatic CHS was also reported with a CBF increase of < 50%; in such cases, the term reperfusion syndrome should be preferred (Karapanayiotides, 2004)
• reperfusion injury (typically after acute stroke therapy) is usually caused by rapid normalization of flow within the infarcted tissue
  • these patients have normal or only mildly increased CBF (20–44% above baseline)
  • however, true hyperperfusion syndrome may also develop in acute stroke patients   (Kneihsl, 2021)
• TCCD studies indicate that blood flow normalizes within one month after surgery; autoregulation is restored within approx. 6 weeks [Megee, 1992]

• reperfusion symptoms are increasingly recognized in many other organs following revascularization procedures, such as:
  • reperfusion arrhythmias
    
  • gastrointestinal injury after reperfusion, leading to decreased intestinal barrier function 
  • marked polyuria after angioplasty in patients with renovascular disease

• severe headache
  • worsening in the prone position
  • ipsilateral to the lesion side or diffuse
• impaired consciousness
• epileptic seizures (often focal)
• focal neurologic deficit (usually with ICH)

• timing of the procedure
  • benefit of CEA is greatest in the first 2 weeks following an ischemic event
  • in the case of large ischemia, however, some delay is advisable
• perioperative TCD/TCCD monitoring
  • enables early detection of hyperperfusion and the need for even more strict BP control
    
• strict blood pressure control
  • blood pressure reduction should be considered even in normotensive patients with hyperperfusion on TCD, as some may develop delayed hypertension.
  • the exact target value is unknown, and an individualized approach is advised (age, comorbidities, etc.)
  • blood pressure should preferably be lowered with drugs that do not increase CBF, such as labetalol and clonidine  (avoid ACE-I, CCB, and especially vasodilators)
• use of free-radical scavengers – further trials are needed

• rigorous blood pressure correction (ideally <120/80 mmHg) – it also serves as a preventive measure
  
• in the case of seizure activity, administer Anti Seizure Medication (ASM) – PHE, VPA, LEV → acute symptomatic seizures
• start antiedema therapy

• depends on timely recognition of hyperperfusion and adequate treatment of hypertension before cerebral edema or ICH develops
• the prognosis after ICH is poor (mortality of 36–63%, significant morbidity in the survivors)
• the prognosis of CHS in patients without ICH is much better, with low mortality