Unstable bradycardia induced by posterior nasal packing: a rare activation of the Trigeminocardiacreflex

Abstract

A woman in her 40s presented to the emergency department with epistaxis. Anterior nasal packing was unsuccessful in achieving haemostasis. After the exchange of devices and insertion of a posterior nasal pack, the patient developed a junctional rhythm and progressively unstable bradycardia. The rhythm and bradycardia immediately improved following the removal of the posterior nasal pack. This case describes a rare occurrence of Trigeminocardiac reflex (TCR), following an insertion of a posterior nasal pack. Only one other such case has been reported and published. This case highlights the importance of raising awareness of this rare reflex and the need for prompt removal of the triggering cause in such scenarios. TCR can induce a junctional rhythm, which progresses to unstable bradycardia and may lead to asystole in susceptible individuals. The removal of the stimulus resolves the reflex and can result in prompt resolution of the bradycardia and hypotension induced via the TCR.

Background

Epistaxis is a very common emergency department presentation, accounting for approximately 1.7 emergency department visits per 1000 population.¹ Posterior epistaxis accounts for a relatively small proportion of all epistaxis cases, with only 5% of cases reported to be due to posterior bleeds.² Epistaxis affects approximately 60% of people throughout their lifetime. Epistaxis can occur due to a number of both local and systemic causes; however, localised trauma is the most commonly described mechanism.³ The majority of cases are self-limited, and 65% of cases presenting to the emergency department are resolved with first-line measures.

Complications are unusual but include rebleeding, infection, sinusitis and a requirement for blood transfusion in severe cases.² Severe complications are rare.

In this case, we describe a rare complication of posterior nasal packing through inducing the Trigeminocardiac reflex (TCR), which can induce a junctional rhythm that can result in stable or unstable bradycardia. This complication is rare in peripheral procedures but can be life threatening without prompt intervention.

Case presentation

A woman in her 40s presented to the emergency department with a left nasal epistaxis. The bleeding had initially been intermittent and started the previous day; however, on the day of presentation to the emergency department, the patient’s bleeding had been prolonged and increased in volume. She was initially seen earlier that day in the emergency department and the haemostasis was achieved with the insertion of an anterior tranexamic acid-soaked nasal pack. The patient represented to the emergency department 8 hours later with a recurrence of bleeding.

Several years ago, the patient had been investigated for per vaginal bleeding; however, no coagulopathic issues were identified. The patient’s medical history was otherwise unremarkable. She was not taking any regular medications and had no known allergies. The patient herself worked in healthcare.

On her return to the emergency department, the patient was comfortable, but had clear haemorrhage from the left nostril. The degree of bleeding from an initial inspection was not initially concerning. Her vitals were stable: heart rate (HR) 82 beats per minute, blood pressure (BP) 167/105 mm Hg and oxygen saturation 100%. When she was initially assessed, no clear bleeding source could be identified, but ongoing haemorrhage was seen. An anterior inflatable epistaxis tamponade device was successfully inserted. The patient was reassessed 15 min later, and it was noted by the patient that she was experiencing a ‘trickling’ sensation at the back of her throat. At this point, it was considered that the bleeding source could be more posterior, and an extended nasal tamponade device would be required. The anterior inflatable epistaxis tamponade device was removed and replaced with a posterior inflatable epistaxis tamponade device. At the time of insertion, the patient was comfortable and successful cessation of haemorrhage was achieved. The insertion of the device was neither challenging nor technically difficult.

The patient’s observations were reviewed 5 min later by a senior nurse. At this point, the patient reported feeling lightheaded and was experiencing palpitations. Observations were repeated and her HR was noted to be 40 beats per minute. Immediate senior review was requested, vitals were obtained and cardiac monitoring was attached. The monitor demonstrated a junctional HR of 40 beats per minute with frequent premature ventricular contractions. The rate proceeded to rapidly drop over the following 1–2 min while initial care was given including intravenous access and a fluid bolus of 0.9% normal saline, and other measures such as dropping the head of the bed were instigated. The BP initially was maintained at approximately 124/70 mm Hg but dropped to a low of 67/40 mm Hg as the HR dropped below 35. The lowest HR noted was 28 beats per minute with a BP of 67/40 mm Hg. The patient was fully orientated throughout but appeared slightly drowsy with a Glasgow Coma Scale of 14.

Investigations

The ECG obtained during the incident is demonstrated in the attached figures. The junctional rhythm can be seen in figure 1, and the return of the p wave following the removal of the device is evident in figure 2.

Figure 1.

Junctional rhythm: heart rate 41 beats per minute.

Figure 2.

Post removal of posterior inflatable epistaxis tamponade device. Sinus rhythm with single premature ventricular contractions. Heart rate 51 beats per minute).

Differential diagnosis

It was established that some form of vagal stimulation must have occurred, given the combination of bradycardia and hypotension in an otherwise healthy individual with no previous cardiac history. The sudden resolution of the junctional rhythm following the removal of the posterior epistaxis tamponade device further reinforced this suspected mechanism.

• TCR—a parasympathetic response would explain the constellation of symptoms and the sudden resolution following the removal of the stimulus.

• Arrhythmia—no cardiac history and would not explain the sudden resolution following the removal of the stimulus.

• Haemorrhage from an alternative site—would explain hypotension but not bradycardia; bloods revealed no coagulopathy. The patient suddenly recovered following the removal of the device.

• Septic shock—no source of infection. The device was only put in 5 min prior so it would not allow time for toxic shock syndrome to develop.

Treatment

Given the sudden change in vitals so soon following the application of the posterior epistaxis tamponade device, the reviewing doctor decided to remove the posterior inflatable epistaxis tamponade device prior to the administration of drugs such as atropine. On the removal of the device within 20 s, a resolution of the junctional rhythm was noted, and the reoccurrence of p waves was appreciated. No medication was administered, and the HR and BP steadily improved over the subsequent 5 min. The patient’s drowsiness resolved in addition to her symptoms of ‘lightheadedness’ and palpitations (figure 3).

Figure 3.

Timeline of events.

The sudden decrease in BP invertedly resulted in haemostasis of the epistaxis. The patient was kept on monitoring for further 6 hours in the emergency department but was well throughout this observational period. Bloods performed during this time demonstrated normal platelet counts and a normal coagulation panel including prothrombin time and activated partial thromboplastin time. She was discharged the following morning with advice that she should alert healthcare professionals in the future of this reaction should she have a recurrence of her epistaxis.

Outcome and follow-up

The patient was well during the observational period following the unstable bradycardic event in the department. The patient was discharged after 6 hours of observation with a follow-up for a 24-hour BP monitor given her initial hypertension noted on arrival. The patient was advised to inform healthcare workers in the future of this event should she have further epistaxis or require any future nasal surgical procedures.

Discussion

The unstable bradycardia was suspected to be due to a rare complication reported following nasal packing or nasal interventions called the TCR. The TCR was first described in 1970 by Kratschmer and had previously been referred to as the Kratschmer reflex.⁴ A more recent description of TCR has been defined by a drop in HR and mean arterial BP of more than 20%.⁵ Various subtypes of TCR have been described: central, peripheral and ganglion subtypes.⁶

The TCR appears to be activated through stimulation of any nerve ending of the trigeminal nerve. After activation of these sensory fibres, an afferent signal is transmitted to the sensory nucleus of the trigeminal nerve. The method through which this activation appears to cause bradycardia appears to be through the close connection of afferent and efferent pathways of the trigeminal nerve, with the efferent premotor neurons which are in close proximity to the dorsal motor nucleus of the vagal neurons, located in the nucleus ambiguous. The activation of this pathway in some individuals appears to result in parasympathetic vagal neuron activation which results in a bradycardic response.⁷ This relation between these afferent and efferent pathways is located within the brainstem. The type of reflex subtype described in this case appears to be a peripheral activation of the TCR, which is primarily related to the spinal nucleus of the trigeminal nerve of the Kölker-Fuse nucleus.

The activation of the TCR can result in potentially life-threatening bradycardia and hypotension due to hyperstimulation of the parasympathetic nervous system. This can progress to asystole and death.⁸ Stimulation of this response from nasal packing appears to be extremely rare, with only one published case report identified during the literature review. In this case, the response unfortunately resulted in a patient’s death.⁸ The patient experienced extreme bradycardia and hypotension 15 min after posterior nasal packing, which progressed to asystole. Despite active resuscitation measures, Return of spontaneous circulation was not achieved. Interestingly, this case also reported the use of posterior nasal packing which was not removed. This raises the possibility that a refractory asystole episode may have ensued without the removal of the nasal packing. The TCR response has been reported in 10%–18% of neurosurgical procedures; however, activation of the TCR peripherally resulting in unstable bradycardia appears to be extremely rare.⁹ There is evidence from animal studies which suggests that posterior nasal stimulation may be more sensitive than anterior stimulation in inducing the TCR, which may explain why the initial anterior nasal packing for our patient did not stimulate a response.

The high prevalence of epistaxis in the general population means that this is a common emergency department presentation. Nasal packing to achieve haemostasis is a frequent procedure with some notable complications. Despite the case we described demonstrating a seemingly very rare complication, it is extremely important that providers are aware of this potentially fatal reflex and the importance of prompt removal of nasal packing in scenarios where a patient experiences bradycardia and hypotension. From the cases described in the literature, prompt removal of packing appears to result in rapid correction of bradycardia.

Learning points.

• Activation of the Trigeminocardiac reflex is a very rare complication of posterior nasal packing.

• In cases where sudden unexplained bradycardia occurs following the application of nasal packing, the packing should be promptly removed to reverse the possible parasympathetic activation induced from the nasal packing.

• After any adverse episode, the event should be explained to the patient, and they should be advised to inform healthcare providers of such a reaction.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).