LAUSR

© BMJ Publishing Group Limited 2021. No commercial reuse. See rights and permissions. Published by BMJ. DESCRIPTION A man in his late 60s with a significant history of decompensated alcoholrelated liver disease was admitted to hospital with a 2week history of increasing jaundice and pruritus as well as confusion, drowsiness and a decreased exercise tolerance. Routine bloods revealed an exceptionally elevated corrected calcium level which peaked at 5.17 mmol/L. On admission, Alphafetoprotein (AFP) was also greatly increased (126 278 U/L). These two derangements were later discovered to be due to an underlying diagnosis of hepatocellular carcinoma on CT. Due to his severe hypercalcaemia, the patient was admitted to the coronary care unit for cardiac monitoring and treatment. This patient was treated with immediate fluid resuscitation, intravenous pamidronate and calcitonin in order to reduce his calcium levels. A 12lead ECG was performed (figure 1) which showed Osborn waves (figure 2). This resolved after therapy (figure 3). Although an MRI liver was arranged for a more detailed assessment, unfortunately he deteriorated significantly and became encephalopathic. Despite optimal treatment, the patient died, receiving supportive input from the palliative care team. The Osborn (‘J’) wave is a deflection occurring at the J point (junctional point between the R wave and ST segment) on the ECG. The phenomenon was described first in the early 20th century by Kraus et al in patients with hypercalcaemia but was named decades later after Osborn, who detailed the characteristic deflection induced by experimental hypothermia in animals. Although most commonly associated with hypothermia, rare causes of the presence of Osborn waves on an ECG include hypercalcaemia, as in this case, and subarachnoid haemorrhage. This characteristic deflection is posited to be mediated by the increased prominence of the cardiac transient outward potassium current