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Heparin-induced thrombocytopenia is an immune-mediated reaction to heparin and heparin analogs, which results in an acquired hypercoagulability syndrome resulting in paradoxical arterial and venous thrombosis leading to thrombocytopenia. Organs with high vascularity, such as the adrenal glands, are at an increased risk of injury in heparin-induced thrombocytopenia due to thrombus formation in the adrenal vein causing adrenal insufficiency. The standard of treatment remains discontinuation of heparin and heparin analogs and starting corticosteroids and non-heparin antithrombotic therapy such as argatroban.

A 28-year-old woman presented with sudden onset dyspnoea, left-sided chest pain and dry cough for 3 days. She was a non-smoker. Her blood pressure was 90/60 mm Hg; respiratory rate, 20 breaths/min; finger pulse oximetry, 95% on 10 L/min; supplemental oxygen via non-rebreather mask and heart rate, 100 bpm. On chest auscultation, air entry was absent bilaterally. Initial chest X-ray showed ‘bilateral’ pneumothoraces, left more than right (figure 1). Tube thoracotomy was performed on the left pleural space, with complete resolution of left pneumothorax and partial resolution of right pneumothorax. Contrast-enhanced CT of chest revealed anterior …

Catamenial or cyclical anaphylaxis is a complex clinical syndrome with poorly reported incidence and prevalence in the literature review. The underlying mechanism is still a myth although a few proposed hypotheses are stated. Early recognition of these symptoms will bring optimal treatment and prevent unnecessary intubation and complications. Here, we present a 48-year-old woman without significant medical and family history with recurrent angioedema in the setting of catamenial anaphylaxis or cyclical anaphylaxis in the setting of progesterone hypersensitivity.