Anaphylaxis and Undiagnosed Aspirin Exacerbated Respiratory Disease in the Ambulatory Surgery Center: A Case Report

Severe bronchospasm and anaphylaxis are unanticipated emergencies that may occur in the ambulatory surgery setting. I present a case in which an asthmatic male with nasal congestion has anaphylaxis after induction, with severe bronchospasm as the primary manifestation. During the course of hospitalization, he was exposed to aspirin and a second episode of severe bronchospasm occurred. He was diagnosed with both anaphylaxis to an anesthetic medication and Aspirin Exacerbated Respiratory Disease, or Samter’s Triad.

Aspirin-Exacerbated Respiratory Disease: The Dentist’s Role in Recognition, Referral, and Management

Aspirin-exacerbated respiratory disease (AERD), also known as Samter’s triad, is characterized by aspirin intolerance, nasal polyps with recurrent rhinitis, and asthma. The components of AERD are frequently encountered in dental offices. This article reviews the screening and appropriate referral of patients who may have AERD. The implications of AERD on a patient’s daily life, as well as a brief overview of potential treatments, are followed by a case report of a 36-year-old female patient. In the case report, a 36-year-old female patient with a history of chronic sinusitis, asthma, and aspirin allergy presents to a dental office with no evidence of oral disease. The case then describes the referral process to Otorhinolaryngology (ENT) for further evaluation, the diagnosis of Samter’s triad, and subsequent treatment through endoscopic sinus (ESS) surgery to remove nasal polyps. The patient experienced relief of symptoms at the one-year postoperative follow-up. As dental providers often serve as a frequent point of contact for many patients—some of whom may see their dentists more regularly than their primary care providers—we are uniquely positioned to recognize signs and symptoms in the head and neck region that may indicate systemic disease.

Olfactory outcomes in the management of aspirin exacerbated respiratory disease related chronic rhinosinusitis

Patients with aspirin exacerbated respiratory disease(AERD)experience a severe and recalcitrant form of chronic rhinosinusitis with nasal polyposis(CRSwNP)and asthma,which are exacerbated by aspirin/NSAID ingestion.As compared with aspirin-tolerant CRSwNP,patients with AERD experience more severe olfactory dysfunction,which is one of the key contributors to the observed decrease in quality of life(QOL)in this disease.The objective of this paper is to review the published olfactory outcomes observed with various treatment modalities.

Pathogenesis of NSAID-induced reactions in aspirin-exacerbated respiratory disease

It is well-established that following ingestion of aspirin or any other inhibitor of cyclooxygenase-1, patients with Samter’s disease, or aspirin-exacerbated respiratory disease (AERD) develop the sudden onset of worsening respiratory clinical symptoms, which usually in-volves nasal congestion, rhinorrhea, wheezing and bronchospasm. Gastrointestinal distress, nausea, a pruritic rash and angioedema can also occasionally develop. However, the underlying pathologic mechanism that drives these clinical reactions remains elusive. Pretreatment with medications that inhibit the leukotriene pathway decreases the severity of clinical reactions, which points to the involvement of cysteinyl leukotrienes (cysLTs) in the pathogenesis of these aspirin-induced reactions. Furthermore, studies of aspirin challenges in carefully-phenotyped patients with AERD have confirmed that both proinflammatory lipid mediators, predominantly cysLTs and prostaglandin (PG) D 2, and the influx of effector cells to the respiratory tissue, contribute to symptom development during aspirin-induced reactions. Mast cells, which have been identified as the major cellular source of cysLTs and PGD 2, are likely to be major participants in the acute reactions, and are an attractive target for future pharmacotherapies in AERD. Although several recent studies support the role of platelets as inflammatory effector cells and as a source of cysLT overproduction in AERD, it is not yet clear whether platelet activation plays a direct role in the development of the aspirin-induced reactions. To further our understanding of the pathogenesis of aspirin-induced reactions in AERD, and to broaden the pharmacotherapeutic options available to these patients, additional investigations with targeted clinical trials will be required.

The importance of timely diagnosis of aspirin-exacerbated respiratory disease for patient health and safety

Backgroud:Aspirin-exacerbated respiratory disease(AERD)is a difficult-to-treat syndrome where timely diagnosis and initiation of disease-specific therapies are pertinent to improved patient outcomes.Objective:To characterize the most common timeline for development of the clinical triad[asthma,nasal polyposis,and reactions to nonsteroidal anti-inflammatory drugs(NSAIDs)],identify barriers to prompt diagnosis of AERD,and describe indications for an aspirin challenge to facilitate accurate diagnosis.Methods:Six hundred ninety-seven patients with diagnosed AERD and history of at least one sinus surgery to remove nasal polyps were identified in the Brigham and Women’s Hospital AERD registry.Patient reported age at disease onset of asthma,nasal polyposis,and age of first NSAID reaction were obtained from 2013 to 2019 at enrollment.Results:Of the 697 patients identified,diagnosis of asthma preceded diagnosis of nasal polyposis and first NSAID reaction,although there was considerable variability between patients.Conclusions:Prompt diagnosis of AERD is important for patient and provider education and improved care of this difficult-to-treat population of patients.Consider diagnostic aspirin challenge in patients without historical reactions to NSAIDs who have an otherwise compatible clinical history,specifically in patients who take daily low-dose aspirin,leukotriene modifiers,avoid NSAIDs,or who are severely symptomatic at baseline where it would be difficult to identify an acute worsening of symptoms.