A Case of Trauma-Related Angioedema of the Airway in a Patient on an Angiotensin Receptor Blocker.

BACKGROUND Angioedema is non-pitting edema that occurs in the deep layers of the skin and subcutaneous tissue due to vascular leakage of plasma resulting from 1 of 2 major pathophysiological processes: mast cell-mediated angioedema and bradykinin-mediated angioedema. While it is a well-recognized adverse reaction of angiotensin-converting enzyme inhibitors, the association of angioedema with angiotensin receptor blockers is relatively less studied. Direct local trauma, although rarely, has been suggested to induce angioedema under certain conditions. We present a unique case of direct, local, trauma-related angioedema in a patient on an angiotensin receptor blocker. CASE REPORT The patient, an 83-year-old woman on telmisartan for hypertension, hit her neck against the edge of a chair during a fall. Shortly thereafter, she developed progressive airway compromise due to airway angioedema, as noted on direct laryngoscopy. A contrast CT scan of the neck also noted edema of the periglottic and supraglottic regions. She required intravenous corticosteroid administration and intubation in the emergency room and was successfully extubated 3 days after admission. She had no prior history of angioedema or allergy. We hypothesize that increased levels of circulatory bradykinin in the setting of telmisartan, combined with a local release of bradykinin from trauma, was the main pathophysiologic cause of the angioedema. CONCLUSIONS This case report highlights the rare and often forgotten adverse reaction of angioedema with use of angiotensin receptor blockers and confirms the finding of local trauma as a possible trigger.

Severe Lactic Acidosis Due to Acute Intoxication by Emtricitabine/Tenofovir Alafenamide.

A 46-year-old female with a history of generalized anxiety disorder was admitted after intentional ingestion of an unknown amount of emtricitabine/tenofovir alafenamide (Descovy®) in a suicidal attempt. Patient was emergently intubated secondary to severe agitation and inability to protect airways. Patient developed severe lactic acidosis early in the admission, secondary as to a possible mitochondrial toxicity. Failed attempts to fluid resuscitation with Lactate Ringer®, eventually warranted to start the patient on norepinephrine infusion. Metabolic acidosis remained refractory to bicarbonate bolus and infusion. Hypothermia and hypoglycemia were corrected. Despite the initial approach, the patient remained acidotic, and the nephrology was consulted for emergent continuous renal replacement therapy (CRRT). After three days of intensive care unit stay and CRRT, the patient improved and was successfully decannulated. Her metabolic profile also showed remarkable improvement and the metabolic lactic acidosis resolved. The previous formulation of tenofovir with disoproxil fumarate is associated with severe lactic acidosis due to inhibition of mammalian mitochondrial DNA polymerase. Risk factors include liver cirrhosis, chronic kidney disease, hepatitis B and C coinfection, and metformin use. The new pharmaceutical formulation of tenofovir with alafenamide (TAF) has caused a significant decrease in the incidence of lactic acidosis. However, its real incidence and the usual plasma level to induce toxicity and mitochondrial dysfunction are unknown. The aim of this report is to highlight the risk of severe lactic acidosis with the use of TAF.

Weil's Disease in an HIV-Infected Patient.

Leptospirosis is a zoonosis caused by the spirochete Leptospira. Most cases of leptospirosis are mild to moderate and self-limited. The course of disease, however, may be complicated by multiorgan dysfunction with liver and kidney failure causing Weil's disease. Leptospirosis is also rare among HIV-infected patients. We report a case of an HIV-infected patient with Weil's disease.