Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 1767  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Resource Links
    Similar in PUBMED
    Article in PDF (747 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this Article
   Article Figures

 Article Access Statistics
    PDF Downloaded9    
    Comments [Add]    

Recommend this journal


Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 5  |  Page : 1444-1445

Unexplained and Unusual Cardiac Arrest Rhythm During Atlantoaxial Arthrodesis: Can Improper Positioning be the Facilitator?

Department of Anaesthesiology and Critical Care, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India

Date of Submission19-Jan-2018
Date of Decision21-Mar-2018
Date of Acceptance18-Nov-2019
Date of Web Publication30-Oct-2021

Correspondence Address:
Habib M R Karim
Department of Anaesthesiology and Critical Care, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.329556

Rights and Permissions

How to cite this article:
R Karim HM, Keshwani M, Panda CK. Unexplained and Unusual Cardiac Arrest Rhythm During Atlantoaxial Arthrodesis: Can Improper Positioning be the Facilitator?. Neurol India 2021;69:1444-5

How to cite this URL:
R Karim HM, Keshwani M, Panda CK. Unexplained and Unusual Cardiac Arrest Rhythm During Atlantoaxial Arthrodesis: Can Improper Positioning be the Facilitator?. Neurol India [serial online] 2021 [cited 2021 Dec 6];69:1444-5. Available from:


Cardiac arrest (CA) during neurosurgery has been relatively well-reported; bradycardia, asystole, ventricular tachycardia, or fibrillations are common rhythms described.[1] However, pulseless electrical activity (PEA) is probably reported.[1] CA reported during spine surgeries was mostly due to venous air embolism, screw, drain, etc., but due to improper positioning adjunctis, not yet reported.[1],[2],[3]

A 40-year-old, 66 kg, 160 cm gentleman presented with neck pain for one year, mild weakness of left upper limb for a few weeks along with complaints of a blackout with slight neck extension. Computerized tomography showed atlantoaxial dislocation (atlantodental interval 10.3 mm) with dense nearly reaching foramen magnum with spinal canal narrowing. No sub-axial canal stenosis/instability was noted. The preanesthetic assessment revealed new, uncontrolled diabetes mellitus (blood sugar 466 mg%, HbA1c 13%); started on insulin and was taken up for atlantoaxial arthrodesis after two weeks with blood sugar 128 mg%. Autonomic neuropathy features were absent. After obtaining consent and connecting standard monitoring, the trachea was intubated using awake fiberoptic technique. General anesthesia (GA) was induced on shifting trolley using an appropriate dose of Thiopentone and Vecuronium. Injection Morphine and Paracetamol were used for analgesia. GA was maintained using Nitrous Oxide, Oxygen (FiO2 45–50%), and Desflurane with targeted MACage of 1.1–1.2 with neuromuscular monitoring guided relaxant. Low flow anesthesia was used using Mindray-A7 workstation.

The patient was positioned in prone with head supported over horseshoe headrest with due precautions. Two pin skull traction was attached to 5-pound weight connected by a rope. Injection Dexmedetomidine 30 mcg was infused over 20 min with no cardiac adverse events, and was hemodynamically stable until the fourth hour of anesthesia. The surgeon was operating near the respective facet joint and was controlling venous bleeding. The facet joint was neither reduced nor any fixation device was inserted till then. Approximately 600 ml blood was lost till then (maximum allowable blood loss 1500 ml) with urine output of 400 ml. The patient was doing fine with the lowest blood pressure (BP) recorded 90/60 mmHg with a heart rate 68/min 5 min prior to the CA. Patient has already received 1600 ml crystalloid and another 200 ml bolus was given. Suddenly, it was noted that the EtCO2 trend was significantly reducing (reached 19 mmHg within a few breaths) despite unchanged ventilation. The multi-parameter monitor showed sinus tachycardia (118/min) and automatic monitoring failed to record BP. Plethysmography tracing was not right despite normal limb temperature and correctly placed probe. Immediately PEA was suspected; absent carotid pulse confirmed it. The surgeon was asked to withhold surgery, irrigate filed, pack immediately and resuscitation team was readied. Meanwhile, the patient was shifted to another trolley, positioned supine, negative carotid pulse reconfirmed and cardiopulmonary resuscitation started. Return of spontaneous circulation (ROSC) was noted within one min. Meanwhile, anesthetic agents were cut off, FiO2 increased to 100%. Then, it was decided to proceed for incision site closure as hemodynamics were stable. However, bradycardia (30/min) was noted when the patient was being made 70° prone. Adrenaline 1 mg was injected again and chest compression was started but rhythm reverted immediately. Arterial blood gas report showed normal gas and electrolytes. The chest was clear, heart sounds were normal, electrocardiogram and bedside echocardiography were within normal limit, and all 5 H and T were ruled out. Now, the patient was not maintaining hemodynamics. Triple lumen central venous catheter was inserted and infusion Noradrenaline 10 mcg/minute was started. The bilateral pupil was dilated and non-reactive and surgeon denied direct stimulation of the brain stem. However, an urgent CT head and neck was done which was apparently normal. Changing rhythm toward bradycardia was noted whenever patient's position was changed despite being on a hard collar and precautious moves. The patient was shifted to the critical care unit (CCU) and was put on a ventilator. Cardiac enzymes and serial electrocardiogram done in CCU were found to be normal. Hyperglycemia (246 mg%) was noted and the patient was started on insulin infusion and titrated. He was weaned off from the ventilator and successfully extubated the next morning. Noradrenaline was tapered off by next day and he was shifted to the ward on 3rd POD. Left upper limb power was found to be 3/5 which improved to 4/5 within 2 days. No other neurological disability was noted. The patient was anesthetized and operated after three months successfully, in a prone position with keeping the alignment horizontal.

The field of atlantoaxial surgery is very near to the brainstem and both the anesthesiologist and surgeon remain concerned and vigilant throughout. However, CA during such surgery is relatively rare. PEA is characterized by the absence of a palpable pulse in an unconscious patient with an organized electric activity other than ventricular tachyarrhythmia on the electrocardiogram.[4] The common pathophysiology behind PEA is myocardial insult due to hypoxia or metabolic derangements.[4] But in this case, acidosis, hypovolaemia, metabolic derangements, and hypoxia were not there (PaO2 256 mmHg). Moreover, all 5 H and T were ruled out except mild hyperglycemia. There was also no direct stimulation of brainstem or dura by the surgeon.

Introspection in the case showed that the patient was responding adversely every time with the changing head position as found during shifting and suggested by blackout history. In this case, the head was supported by two pin skull traction on horseshoe headrest. However, the traction rope was not in horizontal alignment and was suspended using the fluid stand as shown in schematic representation [Figure 1]. This created a force whose vector was oblique and upward. The surgeon was controlling bleeding and used finger pressure (downward) with gauze. These two opposing forces most probably led the compression of the spinal canal and stimulation of brain stem leading to CA. Now the question arises, why PEA, not bradycardia and asystole? The stimulation of brain stem leads to vagus (parasympathetic) stimulation and most likely to cause bradycardia and arrest. Here, the happening or response might have been so fast that bradycardia episode (if any) would have been for a second or two and was missed, or it directly led to PEA. The study supports that even the parasympathetic nervous system can lead to primary PEA.[5] Moreover, PEA was initially thought to be rare as the presenting initial rhythm in CA; however, recent data shows an incidence of PEA arrests ranging from 19% to 23%.[6] Non-ischemic cardiac disorders and intracranial hemorrhage are also a significant cause of PEA.[7] Intracranial hemorrhage was ruled out by CT.
Figure 1: Illustrated schematic representation of the patient position and related forces acting on the surgical area

Click here to view

The case reiterates that positioning in atlantoaxial arthrodesis needs extra vigilance, especially in patients who have a preoperative history of a blackout with even slight extension.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Chowdhury T, Petropolis A, Cappellani RB. Cardiac emergencies in neurosurgical patients. Biomed Res Int 2015;2015:751320.  Back to cited text no. 1
Frenkel A, Binyamin Y, Brotfain E, Koyfman L, Roy-Shapira A, Shelef I, et al. A nearly lethal screw: An unusual cause of recurrent bradycardia and asystole episodes after fixation of the cervical spine. Case Rep Crit Care 2017;2017:3748930.  Back to cited text no. 2
Dumont TM, Stockwell DW, Horgan MA. Venous air embolism: an unusual complication of atlantoaxial arthrodesis: Case report. Spine 2010;35:E1238-40.  Back to cited text no. 3
Myerburg RJ, Halperin H, Egan DA, Boineau R, Chugh SS, Gillis AM, et al. Pulseless electric activity: Definition, causes, mechanisms, management, and research priorities for the next decade: Report from a National Heart, Lung, and Blood Institute workshop. Circulation 2013;128:2532-41.  Back to cited text no. 4
DeBehnke DJ. Effects of vagal tone on resuscitation from experimental electromechanical dissociation. Ann Emerg Med 1993;22:1789-94.  Back to cited text no. 5
Mader TJ, Nathanson BH, Millay S, Coute RA, Clapp M, McNally B, et al. Out-of-hospital cardiac arrest outcomes stratified by rhythm analysis. Resuscitation 2012;83:1358-62.  Back to cited text no. 6
Beun L, Yersin B, Osterwalder J, Carron PN. Pulseless electrical activity cardiac arrest: Time to amend the mnemonic “4H and 4T”? Swiss Med Wkly 2015;145:w14178.  Back to cited text no. 7


  [Figure 1]


Print this article  Email this article
Online since 20th March '04
Published by Wolters Kluwer - Medknow