SARS COV-2 AS A RISK FOR ANGIOEDEMA

ABSTRACT

CASE This is a 41-year-old man who was admitted to the medical floor with mild COVID-19 symptoms without hypoxia. He had End Stage Renal Disease (ESRD) on Hemodialysis (HD), failed renal transplant, Hypertension and Schizophrenia. Patient had no relevant family history. Medications included Aspirin, Atorvastatin, Nifedipine, Benztropine, and Haloperidol. Patient had allergy to shellfish products. He tested positive a week prior to admission with mild cough no fever or hypoxia. As symptoms worsened, he presented to emergency department and was admitted because of his immunocompromised status. The night of admission, he developed wheezing and stridor, swelling of face and lips, and altered mental status. It was difficult to pass endotracheal tube due to swollen airways. Vital signs were stable except for a low oxygen saturation. Physical examination significant for stridor and swelling of the face and lips. Laboratory values were not significant. We reviewed and none of them was newly started or associated with risks of angioedema. He had no history of previous similar episodes. Patient was given anti-histamines and steroids with slight improvement. Flexible laryngoscopy was performed showing swollen epiglottis and aryepiglottic folds. He ended up getting a tracheostomy as he was regarded as a high risk to be liberated from intubation. IMPACT/DISCUSSION: Few other cases of COVID-associated angioedema have been reported in the literature, majority of the cases explained were in African American patients. The features of angioedema reported like the traditional angioedema, swelling of the face, lips and airways. This angioedema developed within 7 days of detection of COVID-19 in our case and >10 days in the previously reported cases. Angioedema develops due to increased levels of Bradykinin (BK) and its metabolites due to increased expression or decreased degradation. Angiotensin Converting Enzyme (ACE) with other enzymes prevent angioedema by degradation of BK and its metabolites . African Americans, have genetic susceptibility which leads to lower levels of other enzymes involved in the Bradykinin metabolism, thus ACE blockade put them at a higher risk of angioedema. The association of COVID-19 with ACE2 and its subsequent disruption of ACE activity is thought to be the reason behind the development of angioedema. Most of the published articles are either observational or sporadic case reports. More thorough study might help identify further mechanisms and if there is a direct true causal relationship between COVID-19 infection and angioedema or if it is the result of a “second hit,” as it was called by authors of another case that involved a Caucasian male with hypertension who has been using Lisinopril for years with no previously reported complaint. CONCLUSION: SARS CoV-2 should be suspected as cause for angioedema. Further studies needed to establish modalities for diagnosis, management and prevention in high-risk patients.