The Trigemino-cardiac Reflex: Is Treatment With Atropine Still Justified?
Trigemino-cardiac reflex (TCR) is a well-established brainstem reflex1–3 that has practice implications (up to 90% prevalence in strabismus surgeries; influence on the functional outcome4). Latest research implies a strong correlation between the depth of anesthesia and TCR,5 underlining treatment with deeper narcosis instead of anticholinergic drugs.2 The aim of this study was to evaluate and review the standard treatment of TCR, with special reference to the depth of anesthesia.
A systematic literature review was performed from January 1995 to October 2015, using the terms “trigemino-cardiac reflex,” “trigeminal cardiac reflex,” and “oculocardiac reflex” in PubMed (MEDLINE) and EMABASE (OvidSP) databases. TCR was defined as a >10% decrease in heart rate or induced arrhythmia; inclusion criteria were the fulfillment of 2 major criteria (plausibility and reversibility)3 and availability of the exact cerebral state index (CSI)/bi-spectral index score (BIS) values and exact values of hemodynamic changes. Data extraction were made by 2 independent reviewers (κ>0.8).
Three of the 4 articles included reported a clinical prevalence of TCR during strabismus and neurosurgery.5–8 Because of strong differences (TCR-type, age, procedure, anesthesia), only 2 studies were included finally.6,7 The 144 patients included were divided into 2 groups: 1 with deeper anesthesia (CSI/BIS <50) (n=88) and 1 with light anesthesia (CSI/BIS>50) (n=56) (Tables 1 and 2). Anesthesia was maintained by volatile narcotics only (sevoflurane/desflurane). As in some clinics, it is still common to pretreat patients with anticholinergic drugs to lower their vagal potential and thereby the prevalence of TCR; 84 patients were premedicated with atropine i.m. 0.01 mg/kg.
There was a significantly lower prevalence of TCR in the CSI/BIS ≤50 group (22.7%) than in the CSI/BIS>50 group (67.9%) (χ2 [1, N=144]=28.976, P=7.3289E−8), demonstrating a 2.21 times higher risk for TCR under light anesthesia (Tables 1 and 2). The same significant difference was seen in patients with atropine pretreatment; the prevalence in the CSI/BIS ≤50 group was 21.4% and in the CSI/BIS>50 group 71.4% (χ2 [1, N=84]=19.788, P=9.0E−6).
In this analysis, we highlight light anesthesia as an independent risk factor for a higher prevalence of peripheral TCR and a significantly lower use of atropine as the treatment for bradycardia in deep anesthesia. We, therefore, recommend adequate depth of anesthesia to prevent the occurrence of TCR in high-risk procedures. We also recommend the following standard treatment of TCR: 1. immediately cease surgical manipulation; 2. reassess the depth of anesthesia; 3. administer anticholinergic drugs only in case of persistent asystole or repetitive TCR.