Challenging Case:
Unexplained Fall in Near Infrared Spectroscopy (NIRS) Values During Carotid Artery Stenting

On Behalf of SNACC Trainee Engagement Committee

Siddharth Chavali, MD
Keshav Goyal, MD, DM
Jeyaseelan Nadarajah, MD

All India Institute of Medical Sciences
New Delhi, India

Eugenia Ayrian, MD
Siddharth Chavali, MD
 Keshav Goyal, MD,DM
Nadarajah, MD

Carotid artery stenosis is one of the most common causes of ischemic strokes and transient ischemic attacks.1 Various approaches such as medical, surgical and endovascular have been evaluated to reduce the neurological burden by reducing the degree of stenosis and potentially preventing further thromboembolism.

Near-infrared spectroscopy (NIRS) is used to monitor regional cerebral O2 saturation (rSO2). It allows noninvasive, continuous real-time assessment of changes in oxygen delivery in the frontal cortex. Previous studies have proven the utility of NIRS in predicting adverse sequelae following both carotid artery stenting, as well as carotid endarterectomy. We present the case of a patient who underwent carotid artery stenting under monitored anesthesia care (MAC), who had a sustained fall in bilateral NIRS values immediately after carotid artery stenting, which was not found to be significant clinically.

A 62-year-old right-handed male was scheduled to undergo a stenting procedure for critical stenosis of the left internal carotid artery (95%). He presented with a single episode of weakness in his right upper limb two weeks before admission, which was not associated with loss of consciousness, seizures or any other neurological signs. The weakness resolved spontaneously, and the patient had no weakness at the time of admission. His past medical history was significant for smoking, alcoholism, and hypertension, for which he was on irregular medication. His medications included aspirin, clopidogrel, amlodipine and atorvastatin. His routine preoperative evaluation was unremarkable. MR Imaging showed an MCA-ACA territory watershed infarct on the left side, with multiple acute infarcts in the subcortical and deep white matter tracts in the left frontoparietal region. Angiography showed a partly calcified plaque in the right ICA bulb causing 60% narrowing, with the rest of the right ICA, ECA and CCA showing normal course, caliber and contrast enhancement. On the left side, the left proximal ICA distal to the ICA bulb showed >95% narrowing. The right CCA showed multiple areas of narrowing and irregularity, causing approximately 35% narrowing.

He was subsequently scheduled for left-sided carotid artery stenting under monitored anesthesia care to enable better neurological assessment. Preoperative vitals were within normal limits. Monitoring included electrocardiography, pulse oximetry, noninvasive BP monitoring, and NIRS monitoring. Oxygen was administered at a flow of 2lpm via nasal prongs.

His baseline NIRS values were 59% on the left side, and 55% on the right side (Fig 1). Immediately following balloon angioplasty and stent deployment in the diseased vessel, values of NIRS started falling bilaterally, reaching a nadir of 38 %(L) and 39%(R), which was a deviation of 36% and 30% from baseline, respectively. During this period, there were no episodes of bradycardia. Systolic blood pressure fell from 150mmHg to 110mmHg immediately following stenting, but returned spontaneously to within 20% of baseline value within 5 minutes. The sudden fall in NIRS values prompted an immediate evaluation of the patient, who was comfortable throughout, and did not show any neurological signs. Imaging performed immediately showed no new areas of infarct, and there were no angiographic signs of any thromboembolic event. NIRS values continued to remain low, and the patient was shifted to the ICU for further management. Over the next 24 hours, the patient developed no new neurological signs, and was subsequently discharged on day five postprocedure.

This case presents multiple questions to the managing team:

  1. What are the anesthetic considerations for CAS?
  2. What are the complications anticipated during procedures such as CAS?
  3. What are the options for neuromonitoring during CAS?
  4. What is the utility of NIRS during CAS?
  5. What is to be done during an acute fall in NIRS values?

The goals of anesthesia for CAS are to maintain cerebral perfusion during manipulation of catheters in atherosclerotic cerebral vessels and temporary balloon occlusion, which are steps that carry a risk of ischemic or embolic stroke. The patient should lie still during the procedure and provide a reliable neurological examination, such as squeezing a toy during carotid occlusion. Drugs that should be kept ready include short-acting vasopressors and vasodilators to treat blood pressure fluctuations, and atropine to treat bradycardia. Some institutions administer atropine prophylactically, whereas others intervene only when bradycardia occurs with hemodynamic consequences. Respiratory complications are uncommon, and may be a result of a neurological event, mandating urgent airway management. The airway is accessible during CAS, allowing mask ventilation, LMA placement, or intubation.

Literature suggests that the incidence of medical complications following carotid endarterectomy (CEA) is about 10%, and even lesser for CAS.2 Medical complications following the procedure may be due to concurrent comorbidities such as HTN, DM, renal dysfunction or CAD, and proper preoperative evaluation and optimization may lead to a significant risk reduction. Special attention needs to be paid to optimization of preoperative HTN, since it is a major risk factor for development of neurological deficits following carotid revascularization procedures. In patients with uncontrolled HTN, postprocedural hypo as well as hypertension are more likely to occur. The anticipated complications during/after CAS are summarized below:

  1. Hypotension - postprocedural hypotension is common, usually resolves in 8-10 hours. More commonly seen with increasing age, history of previous myocardial dysfunction, or a history of recent stroke.
  2. Bradycardia - some degree of bradycardia is seen in up to 70% of patients during stent deployment and is due to carotid baroreceptor activation during balloon inflation. This usually resolves spontaneously, but may need treatment with atropine.
  3. Cerebral hyperperfusion - usually occurs after therapeutic procedure for a severely stenosed artery. This syndrome develops slowly, and manifests as headache, cerebral edema, or a new focal neurological deficit. Close monitoring, and careful control of BP to a SBP of 100-150mmHg after CAS leads to a significant risk reduction, since hyperperfusion tends to develop more rapidly following CAS than in CEA.
  4. Stroke - usually occurs due to distal embolization during stent deployment. Older patients, with complex lesions are at a greater risk. Periprocedural monitoring and the use of devices to prevent migration of emboli may help reduce risk.

Neurological injuries during CAS are typically due to ischemia caused by vasospasm or migration of emboli, and can be minimized if the insult is identified and treated immediately. Neurological examination of the awake patient is the gold standard of neuromonitoring in these cases. Baseline evaluations should be performed at the beginning of the procedure, and repeated every 15-20 minutes. Signs such as slurred speech, agitation, disorientation or loss of contralateral handgrip strength should prompt an urgent evaluation. Other options for monitoring an awake patient during CAS include non-invasive/invasive monitoring devices such as transcranial doppler, jugular venous oximetry and NIRS.

NIRS monitors use the principle of near infrared spectroscopy to detect changes in regional cerebral oxygen saturation via adhesive pads applied to the patient’s forehead. NIRS has been utilized with varying degrees of success to monitor patients undergoing both CEA as well as CAS. A study by Pedrini el al suggested that NIRS might be a reliable monitor during CEA under GA, using a cutoff of 25% or a cutoff of 20% for prolonged hypoperfusion.3 NIRS has also been used to predict the development of post CAS hyperperfusion syndrome, and a study by Matsumoto et al showed that an increase in rSO2 by greater than 10% 3 minutes after stenting was an excellent predictor of hyperperfusion syndrome.4 rSO2 values tend to be affected by transient bradycardia and hypotension in CAS, and hence changes in rSO2 need to be monitored continuously until heart rate and blood pressure are stabilized. In another study by Kakumoto et al, NIRS oximetry predicted occlusion intolerance during CAS with high sensitivity and acceptable specificity.5 The major limitation of monitoring NIRS are the multiple factors known to influence measured rSO2, namely: hematocrit, change in cerebral blood volume due to systemic and regional hemodynamics, blood oxygen transport, and tissue metabolism.

Falls in NIRS values should prompt management according to the following algorithm:

Management Algorithm
of Falls in NIRS Value


Since our patient was kept awake, and remained hemodynamically stable throughout the procedure without any major fluctuations in measured parameters, we were able to rule out any issues in oxygen delivery. Since the fall in rSO2 values persisted well beyond the stent deployment and subsequent balloon inflation, and failed to return to baseline even after pharmacologically increasing MAP, we concluded that the fall in rSO2 values was not related to changes in systemic BP. The patient remained neurologically intact throughout the period of fall in NIRS values, ruling out seizures as a cause for the fluctuations. We hypothesized that the initial NIRS values could be a reflection of the extensive network of pial collaterals and maximal cerebral vasodilatation that had developed secondary to the disease process to support the ischemic brain in the setting of critical stenosis. The fall in NIRS values immediately after stent deployment could have reflected the sudden increase in blood flow through the carotid artery, which immediately caused cessation of blood flow through the pial collateral vasculature and improved arteriolar tone and led to spuriously low values.

We maintain that although NIRS is an interesting tool, and provides a valuable, noninvasive means of neuromonitoring during CAS, its ability to reflect changes in cerebrovascular dynamics immediately following CAS remains unclear. Decision making should still be guided by neurological examination.


  1. Linfante I, Andreone V, Akkawi N, Wakhloo AK. Internal Carotid Artery Stenting in Patients over 80 Years of Age: Single-Center Experience and Review of the Literature. J Neuroimaging. 2009;19(2):158–63.
  2. Paciaroni Maurizio, Eliasziw Michael, Kappelle L. Jaap, Finan Jane W., Ferguson Gary G., Barnett Henry J. M. Medical Complications Associated With Carotid Endarterectomy. Stroke. 1999 Sep 1;30(9):1759–63.
  3. Pedrini L, Magnoni F, Sensi L, Pisano E, Ballestrazzi MS, Cirelli MR, et al. Is Near-Infrared Spectroscopy a Reliable Method to Evaluate Clamping Ischemia during Carotid Surgery? Stroke Res Treat. vol. 2012, Article ID 156975, 7 pages, 2012.
  4. Matsumoto S, Nakahara I, Higashi T, Iwamuro Y, Watanabe Y, Takahashi K, et al. Near-infrared spectroscopy in carotid artery stenting predicts cerebral hyperperfusion syndrome. Neurology. 2009 Apr 28; 72(17):1512–8.
  5. Kakumoto K, Harada K, Sankoda Y, Taniguchi S, Fukuyama K. Near-infrared spectroscopy cerebral oximetry as a predictor of neurological intolerance during carotid artery stenting with proximal protection. J Clin Neurosci Off J Neurosurg Soc Australas. 2018 Dec;58:89–93.

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