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

BACKGROUND Compression of the vagus nerve by a pharyngeal mass is a well-documented condition that can result in sinus node dysfunction (SND). However, there is scarce literature on extrinsic vagal nerve compression from a tonsillar abscess. CASE REPORT A 59-year-old woman with a history of asthma and chronic throat discomfort presented to the Emergency Department with bradycardia, palpitations, and voice changes. Following a shellfish allergy hospitalization, an otolaryngology evaluation revealed an enlarged right tonsil, recommending tonsillectomy, but scheduling challenges persisted. The patient reported mild throat pain, dysphagia, hoarseness, rhinorrhea, and exertional dyspnea and was admitted for the evaluation of peritonsillar mass. She was found to be bradycardic with a heart rate of 47, with an electrocardiogram revealing SND. Albuterol and ipratropium nebulizers, as well as dexamethasone and pantoprazole, were initiated. With this treatment, the patient symptomatically improved with a new heart rate of 68. She was discharged with outpatient appointments, but was unfortunately lost to follow-up. CONCLUSIONS This case reveals sinus node dysfunction resulting from extrinsic vagal nerve compression by a tonsillar abscess. Pressure on the vagus nerve can trigger bradycardia and low blood pressure, possibly due to compensatory overfiring of afferent vagal nerve signals from local mass effect. Early recognition and antibiotic treatment are essential to prevent cardiac complications. Clinicians must remain vigilant for such extrinsic causes, particularly in patients with chronic sore throat and cardiac symptoms. Further research and case reports are needed to deepen our understanding of this rare yet significant association.

Severe Hyponatremia (96 mmol/L) Secondary to Primary Polydipsia and Pneumonia.

A 63-year-old man who presented to the hospital with altered mental status and decreased responsiveness was found to have severe symptomatic hyponatremia with a sodium level of 96 mmol/L and pneumonia. The patient was admitted to the medical intensive care unit for septic shock and acute severe hyponatremia. He was intubated for airway protection, and treated with 3% hypertonic saline bolus and antibiotics. After four days, sodium levels were corrected to 128 mmol/L, and the patient was extubated and downgraded to the medical floor. This case demonstrates one of the lowest recorded sodium lab values ever and the patient was successfully treated and discharged home with appropriate outpatient appointments.

Kawasaki Disease in a Young Adult: A Case Report and a Review of the Literature.

This case report describes a 21-year-old female who was diagnosed with Kawasaki disease (KD), a rare condition in adults. Careful clinical assessment, including the history of a recent upper respiratory tract infection and the physical findings of fever, sinus tachycardia, strawberry tongue, and skin peeling of the hands and feet, prompted further evaluation. Laboratory findings supported an inflammatory process, and multidisciplinary consultations led to the diagnosis of KD. Prompt treatment with acetylsalicylic acid and intravenous immunoglobulin resulted in rapid improvement and prevention of the severe complications associated with untreated KD, particularly in the cardiovascular system. This case emphasizes the importance of the high risk of suspicion and the need for a comprehensive evaluation in atypical presentations of KD in adults, where early recognition and management are crucial to prevent long-term sequelae such as coronary artery aneurysms and myocardial infarction.

Embolic Phenomena of Libman-Sacks Endocarditis and Antiphospholipid Syndrome.

Patients with systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS) are at high risk of developing arterial or venous thromboembolism and a state of systemic hypercoagulability. Libman-Sacks endocarditis (LSE) is a type of non-bacterial endocarditis usually seen in patients with systemic lupus erythematosus and antiphospholipid antibody syndrome. These vegetations dislodge easily and can cause profound neurological and systemic complications in the form of emboli. We describe one such case of a young woman with known SLE who presented with an acute middle cerebral artery (MCA) stroke and was found to have APS with extensive mitral valve vegetation, indicating Libman-Sacks endocarditis on echocardiography. Recognizing the increasing frequency of both APS and LSE in patients with SLE and screening patients, especially the younger population with SLE, for APS is vital. Furthermore, in those patients presenting with embolic events, echocardiography plays a key role as it can help expedite the diagnosis of LSE. Our case report also reiterates that warfarin, when compared to direct oral anticoagulants (DOAC), is superior in decreasing future embolic events.

Protein Phosphatase 2A as a Therapeutic Target in Pulmonary Diseases.

New disease targets and medicinal chemistry approaches are urgently needed to develop novel therapeutic strategies for treating pulmonary diseases. Emerging evidence suggests that reduced activity of protein phosphatase 2A (PP2A), a complex heterotrimeric enzyme that regulates dephosphorylation of serine and threonine residues from many proteins, is observed in multiple pulmonary diseases, including lung cancer, smoke-induced chronic obstructive pulmonary disease, alpha-1 antitrypsin deficiency, asthma, and idiopathic pulmonary fibrosis. Loss of PP2A responses is linked to many mechanisms associated with disease progressions, such as senescence, proliferation, inflammation, corticosteroid resistance, enhanced protease responses, and mRNA stability. Therefore, chemical restoration of PP2A may represent a novel treatment for these diseases. This review outlines the potential impact of reduced PP2A activity in pulmonary diseases, endogenous and exogenous inhibitors of PP2A, details the possible PP2A-dependent mechanisms observed in these conditions, and outlines potential therapeutic strategies for treatment. Substantial medicinal chemistry efforts are underway to develop therapeutics targeting PP2A activity. The development of specific activators of PP2A that selectively target PP2A holoenzymes could improve our understanding of the function of PP2A in pulmonary diseases. This may lead to the development of therapeutics for restoring normal PP2A responses within the lung.