Bradycardia and hypotension during laryngoscopy for intubation in maxillofacial trauma.

Sir,

Airway management in patients with facial trauma is usually challenging. Severe facial trauma often results in unstable tissues which can lead to bleeding, swelling, hematoma formation, and airway occlusion. Such patients may have an associated intracranial or cervical injury. Airway management in such cases is challenging and may be complicated with hemodynamic alterations.

A 54-year-old male patient was brought to our emergency department 6 h after an alleged history of road traffic accident. He was unconscious, irritable, producing inappropriate words but localizing pain response (GCS E2V3M5), heart rate 110/min, blood pressure 100/70 mmHg, respiratory rate 28/min, and oxygen saturation 95-97% on room air. Blood was continuously oozing into the oral cavity causing distress to the patient. Emergency endotracheal intubation was planned in emergency to prevent aspiration of blood and airway compromise.

We preoxygenated the patient with 100% oxygen using the Bains circuit. Due to lack of all the airway management apparatus in emergency and possibility of difficult airway, we administered injection (inj) glycopyrrolate 0.2 mg and propofol 100 mg followed by direct laryngoscopy. As the fracture segment of the mandible was falling down, laryngeal aperture was not visualized. An assistant was then asked to lift up the fractured segment of mandible forward and upward [Figure 1]. As soon as the mandible segments were lifted, there was sudden bradycardia (heart rate 36/min) with hypotension (blood pressure 66/38 mmHg). Laryngoscopy attempt was abandoned and inj. atropine 0.6 mg i.v. was administered. Following atropine administration, heart rate increased to 96/min and blood pressure 110/70 mmHg. After suctioning of oropharynx, we were able to intubate the trachea with 8.0 mm ID cuffed endotracheal tube orally. The patient was then shifted to radiology for necessary scans [Figure 2] and thereafter underwent emergency craniotomy, elevation of depressed fracture, duroplasty, evisceration (right eye), plating of maxilla, mandible, endoscopic cauterization of sphenopalatine artery, and tracheostomy. Intraoperatively the patient was stable.

Figure 1

Intubation procedure

Figure 2

Maxillofacial trauma

The possible causes of bradycardia and hypotension in our patient are hypoxic vagal stimulation, drugs, and laryngoscopy induced and stimulation of mandibular division of trigeminal nerve during dis-impaction, and lifting of the fractured segment of facial bones. Bradycardia during facial surgery has been described for different operations of the head and neck.[12] One of the causes of bradycardia considered was stimulation of structures innervated by the trigeminal nerve, known as the oculocardiac reflex. The terms trigeminocardiac and trigeminovagal reflex have been proposed to include the additional, nonocular sources of this reflex.[3] As there is no episode of hypoxia, bradycardia and hypotension during first attempt of laryngoscopy and association of the response immediately after lifting up of fractured segments of mandible, trigeminovagal reflex due to stimulation of the mandibular division of the trigeminal nerve may have been the most likely cause.[45]

We conclude that continuous and meticulous monitoring of the ECG and pulse waveform during intubation in maxillofacial trauma is of prime importance because of associated hemodynamic changes and by exercising extra vigilance during intubation, bradycardia, or asystole may be recognized immediately and managed effectively.