Acute-Onset Achalasia Following a Recent COVID-19 Infection: A Case Report

Abstract

Achalasia is a rare esophageal motility disorder that leads to dysphagia, regurgitation, and several other symptoms. While the etiology of achalasia is not completely understood, studies have suggested an immune reaction to viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as a potential cause. Here, we present a case report of a previously healthy 38-year-old male who presented to the emergency room with severe shortness of breath, recurrent vomiting, and dry cough, that had progressively worsened over five days. The patient was diagnosed with coronavirus disease 2019 (COVID-19), and a chest CT also revealed prominent features of achalasia with a markedly dilated esophagus and areas of narrowing at the distal esophagus. The initial management of the patient included IV fluids, antibiotics, anticholinergics, and corticosteroid inhalers which improved his symptoms. This case report highlights the importance of considering the acute-onset of achalasia in COVID-19 patients and the need for further research on the potential association between SARS-CoV-2 and achalasia.

SARS‐CoV‐2, periodontal pathogens, and host factors: The trinity of oral post‐acute sequelae of COVID‐19

“…To our knowledge, however, the oral‐coronavirus connection is unique due to the increased mortality risk and extended multiple tissue morbidity through PASC. Multiple studies have reported increased risk for respiratory, oesophageal‐intestinal, cardiovascular, renal, and neurologic‐brain disorders in COVID‐19 patients 25–30 . We propose that periopathogen‐derived metabolites and enzymes depress the host oral mucosal resistance and extend the initial oral infection systemically.…”

“…Multiple studies have reported increased risk for respiratory, oesophageal-intestinal, cardiovascular, renal, and neurologic-brain disorders in COVID-19 patients. [25][26][27][28][29][30] We propose that periopathogen-derived metabolites and enzymes depress the host oral mucosal resistance and extend the initial oral infection systemically. Further, PD pathogen-driven attenuation of host oral mucosal immunity targets the microbiome organization and perpetuates the survival of selective pathogens.…”