Sinus Node Dysfunction Triggered by Tonsillar Abscess: Effects of Vagal Nerve Compression

Introduction

The palatine tonsils are bundles of lymphatic tissue located in the lateral oropharynx. Along with the adenoids, tubal tonsil, and lingual tonsil, they form Waldeyer’s ring, a collection of lymphoid organs that function as an essential part of the immune system [1]. To enhance understanding of how infections can lead to nerve compression, it is essential to elaborate on the anatomical relationship between Waldeyer’s ring and the pathways of the vagus nerve. Positioned in the pharynx, Waldeyer’s ring is closely aligned with the vagus nerve’s course through the neck, thorax, and abdomen. Hyperemia and edema of the Waldeyer’s tonsils can cause adjacent compression of the carotid sheath, which the vagus nerve traverses as it descends into the thoracic cavity [1]. Viral or bacterial infections can inflame the tonsils and cause swelling, restricting the airway. Tonsillitis often presents with pyrexia and a sore throat, but complications can include peritonsillar abscesses, tonsillar cellulitis, and obstructive sleep apnea [2]. If caused by streptococcal bacteria, rheumatic fever, scarlet fever, or acute glomerulonephritis may develop [3]. Viral etiologies are more common in patients under age 5 years, while group A beta-hemolytic streptococcus accounts for 5% to 15% of adults with pharyngitis and 15% to 30% of patients between the ages of 5 and 15 years [4].

While abscesses are a well-known complication of tonsillitis, this case report documents a rare secondary complication of vagal nerve compression induced by a tonsillar abscess, resulting in bradycardia and sinus node dysfunction (SND) [5]. When stimulated, the vagus nerve mediates the parasym-pathetic innervation of the sinoatrial node, with a potential mechanism of leading to the release of acetylcholine, which hyperpolarizes the sinoatrial node cells, thereby decreasing its pacemaker potential. In such situations, SND can arise from vagus nerve compression [6]. The tonsils’ proximity to the vagus nerve means any alteration in routine anatomy, such as a sizeable tonsillar mass or abscess, can exert pressure on the vagus nerve, leading to pathology [7].

A systematic review by Schmutzler et al highlighted the specific electrocardiogram changes, laboratory parameters, and symptoms associated with myocarditis subsequent to group A streptococcal pharyngitis and tonsillitis [8]; approximately 50% of the cases demonstrated ST-elevations, with fewer cases revealing T wave inversions and biphasic T waves [8]. The limited documentation of such cases underscores the significant gap in knowledge, calling for further research to effectively clarify this relationship and guide clinical interventions. Peritonsillar abscess prevalence varies by geography, age, and health status, typically affecting adolescents and young adults, while the incidence peaks in the second and third decades of life. A retrospective study at the Department of Otolaryngology, Regional Specialist Hospital in Radom, Poland (October 2003 to September 2013) found a higher burden among smokers; the study included 57.7% males and 42.3% females, with an average age of 31.0 years (range 5–78), and smokers represented 22.0% of the group.[9]

Case Report

A 59-year-old woman with a past medical history of asthma and a 15-month history of throat discomfort presented to the Emergency Department for evaluation and treatment of brady-cardia, palpitations, and recent voice changes. She previously underwent otolaryngology evaluation after being hospitalized for a shellfish allergy. During that evaluation, a computed tomography (CT) scan was significant for an enlarged right tonsil compared to the left. She was recommended to have a tonsillectomy but was unable to schedule the procedure. Additionally, she denied any previous biopsy. Upon presentation to the Emergency Department, she reported mild throat pain that radiated to the neck and ear, dysphagia to solids but not liquids, dysphonia that had progressively become hoarser over the last few months, rhinorrhea, and exertional dyspnea. She denied tobacco or recreational drug use, as well as a family history of heart disease. A through medication review on admission did not reveal prior use of negative chronotropic agents, including eyedrops or allergy medications.

On admission, her vital signs were temperature 37°C, blood pressure 119/66 mmHg, heart rate 47, respiratory rate 16, and oxygen saturation 100% on room air. Physical exam was significant for nasal congestion and a large right-sided peritonsillar mass with submental hard, non-tender, immobile lymphadenopathy. The patient was found to have an irregular heart rate without any cardiac murmurs upon auscultation and no prior history of arrhythmias. Laboratory test results demonstrated mild leukocytosis of 11.94k/uL without left shift. The electrocardiogram revealed sinus arrhythmia with a sinus pause of approximately 10 msec (Figure 1). The patient was given albuterol and ipratropium nebulizers as needed and pantoprazole 40 mg oral daily for acid suppression, and was administered dexamethasone 10 mg intravenous push once. She was admitted to the Medicine Department for continuous cardiac monitoring, exercise stress testing, thyroid function testing, and a CT of the head and neck.

Stress echocardiography was negative for arrhythmias or chest pain and demonstrated chronotropic competence, with the patient meeting the target heart rate goal (Figure 2). The CT revealed an edematous appearance of the anterior soft palate and uvula with tonsillar enlargement (Figure 3). The tonsillar enlargement was determined to be a chronic infection and was not superimposed with an acute infection, therefore not requiring antibacterial treatment. Otolaryngology was consulted, and it was recommended that no surgical or procedural interventions, such as abscess drainage, be performed at this time. Continuous telemetry monitoring demonstrated irregular rhythm with sinus pauses throughout the hospitalization, which required electrophysiology outpatient clinic follow-up. The patient’s shortness of breath improved with the nebulizer treatment. She achieved symptomatic and clinical improvement with the steroid treatment, leading to reduced peri-abscess edema and inflammation and likely decompression of the vagus nerve. The patient’s repeat electrocardiogram revealed normal sinus rhythm with the heart rate improving to 68. She remained symptom-free from palpitations and chest pain throughout the hospitalization. The patient followed up in the outpatient ENT, allergy, and immunology clinics 1 week after hospital discharge and noted symptomatic improvement. She denied all symptoms, including chest pain, at these visits.

Discussion

The various forms of primary and secondary SND have been extensively documented [10]. Our focus in this report is on the occurrence of SND due to compression of the vagal nerve by a tonsillar abscess, which has not been well-reported in the past. Tachycardia in the setting of complete vagal nerve transection is well described. However, a theorized mechanism for bradycardia observed in this case could be compensatory overfiring of an afferent vagal nerve signal from irritation of the nerve secondary to a local mass effect. The vagal nerve provides parasympathetic innervation to the sinus node, located in the superior right atrium, and is the natural pacemaker of the human heart. Pressure stimulation (though cervical spine instability or abnormal masses in the parapharyngeal space) of the vagus nerve has been known to induce bradycardia and low blood pressure [11]. It is also important to be aware that other potential factors, such as structural cardiac changes, electrolyte disturbances, and medications, can also lead to bradyarrhythmias [11].

Tumors arising from the vagus nerve or cervical masses that compress or infiltrate the nerve can lead to uncommon symptoms like SND, cardiac arrhythmia, dysphagia, and hiccups. Therefore, significant diagnostic delays may occur, and patients may undergo unnecessary examinations [12]. Lesions within the parapharyngeal space have been linked to reflex cardiovascular syncope through pressure exerted on the vagus nerve. However, tumors of the parapharyngeal space are rare, with neurogenic tumors being the most common [13]. Neurilemomas (also known as schwannomas or neuromas) account for 55% of these tumors [14]. Approximately half of reported parapharyngeal schwannomas arise from the vagus nerve. Neoplasms of the vagus nerve include paragangliomas (50%), schwannomas (31%), neurofibromas (14%), and neurofibrosarcomas (6%) [14]. Our patient presented with tonsillitis, which eventually progressed to abscess formation.

The most common complications of peritonsillar abscesses are descending mediastinitis, para-and retro-pharyngeal abscess, necrotizing fasciitis, and Lemierre’s syndrome. Other notable complications include mediastinitis, epiglottitis, and airway obstruction [15]. This case report is exceptional in that the patient presented with SND related to vagus nerve compression, a complication not typically seen in peritonsillar abscesses. With treatment of the tonsillitis, the patient’s bradycardia improved, suggesting that the tonsillar abscess was directly linked to the cardiogenic symptoms. Our literature review revealed that the underlying mechanism through which these peritonsillar abscesses can affect the vagus nerve has not been adequately studied, and the identification of SND due to vagal nerve compression as a rare symptom of abscess formed by tonsillitis can help spur further research into this condition. A notable limitation of the report is the failure to address the immobile lymphadenopathy, which could suggest potential malignancy and confound the etiology of bradyarrhythmia. Furthermore, broader investigations, such as pulmonary function tests for the evaluation of dyspnea, could have enhanced the comprehensiveness of the findings.

Conclusions

Compression of the vagus nerve by a significant mass or abnormality in the oropharyngeal wall can lead to excessive vagal nerve activation, resulting in bradycardia and, potentially, SND. While tumors of the parapharyngeal space or the vagus nerve have been linked to these cardiac symptoms, the present case demonstrates that a tonsillar abscess arising from bacterial tonsillitis can also induce SND through vagal nerve compression. Further research is needed into the mechanism of this complication and the effectiveness of antibiotic treatment of tonsillar abscess in treating related vagal nerve compression.