The use of intravenous thrombolytic agents has revolutionised the treatment of acute myocardial infarction. However, the improvement in mortality rate achieved with these drugs is tempered by the risk of serious bleeding complications, including intracranial haemorrhage. Tenecteplase is a genetically engineered mutant tissue plasminogen activator. Haemorrhagic complications of tissue plasminogen activator (tPA) are well known. Compared to other tPAs, tenecteplase use leads to lower rates of bleeding complications. Here, we report a case of unusual site of spontaneous bleeding, intralingual haematoma during tenecteplase therapy following acute myocardial infarction, which caused significant upper airway obstruction and required tracheotomy to maintain the patient’s airway. Clinical dilemmas related to securing the airway or reversing the effects of tissue plasminogen activator are discussed. 1. Introduction Tissue plasminogen activators (tPAs) are accepted agents for the therapy of selected cases of acute ischaemic cerebrovascular events, such as myocardial infarction, pulmonary embolism, portal vein thrombosis, and deep venous thrombosis [1, 2]. As a result of its nonselective ability to lyse clots throughout the vascular system, complications caused by bleeding involving various organs and organ systems have been reported. Tenecteplase (TNKase; Genetech Inc.) is an engineered variant of tPA (Activase; Genentech Inc.) designed to have increased fibrin specificity, and its greater efficacy leads to lower rates of bleeding complications [3]. Lingual haematoma is a rare but potentially fatal cause of upper airway obstruction. It is important to recognise this unusual clinical entity early in its course and take the appropriate steps to secure the airway [4]. Here, we report a case of acute airway compromise secondary to a lingual haematoma that developed after administration of recombinant tPA for acute myocardial infarction (AMI). 2. Case Report A 73-year-old male patient presented to the emergency department (ED) with severe retrosternal chest pain, which progressed over time. Electrocardiogram revealed ST-segment elevation in leads D2, D3, aVF, and V4–V6 derivations and ST depression at D1, aVL, and V1–V3 derivations. He had a history of well-controlled hypertension and two prior nonhaemorrhagic strokes without residual deficits. The pulse rate was between 80 and 95？beats/min and blood pressure was 130/90？mmHg. Evaluation of the patient’s coagulation status showed slight increases in prothrombin time and international normalised ratio (13.9？s and 1.4,
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