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This patient's preceding flu-like illness would be in keeping with development of a viral pericarditis. Pericarditis presents with pleuritic chest pain in association with systemic features related to the underlying pathogen. The ECG changes were likely to be rate related. ACS is a possibility, but the nature of the chest pain was atypical and the patient's only risk factor was smoking making it an unlikely diagnosis especially at such a young age. This patient was partially treated for acute coronary syndrome (ACS) with aspirin based on dynamic ECG changes. 2 This patient also had a family history of aortic aneurysm which may represent a risk factor for dissection especially if in association with connective tissue disease, although there was no suggestion of this. 1 The pain was not the typical central chest pain radiating to the back which is often described in association with aortic dissection and the chest radiograph did not show any mediastinal widening which is sometimes a radiological feature, although the diagnostic accuracy is higher for PA radiographs (sensitivity 90%) than AP radiographs (sensitivity 72%). The D-dimer is usually raised in acute aortic dissection and values of less than 500 mg/mL have been shown to be a useful screening tool to identify patients who do not have an acute aortic dissection. Additionally, the blood pressure difference between the two arms would have supported this diagnosis (although this actually turned out to be a red herring). The nature of the chest pain would also have been consistent with an aortic dissection, especially its severity and sudden onset. The patient did not, however, have any risk factors for PE and maintained oxygen saturations of over 96% on air. PE was a reasonable suggestion based on a history of pleuritic chest pain in a young patient alongside sinus tachycardia on the ECG and a high A-a gradient on the arterial blood gas (suggesting a ventilation/perfusion mismatch) and the raised D-dimer. There is a wide differential diagnosis for this patient's symptoms. Monospot test was positive confirming EBV infection and accounting for the liver function and haematological abnormalities.Īnteroposterior (AP) chest radiograph showed clear lung fields with no mediastinal widening.ĬT pulmonary angiogram was negative for PE.ĬT angiogram of the aorta (thorax and abdomen) excluded an aortic dissection but revealed a large grade III subcapsular haematoma of the spleen of 3.8 cm depth affecting more than 50% of its surface with underlying splenomegaly of 16 cm ( figure 1). Biochemical investigation revealed deranged liver function tests with bilirubin 33 mmol/L, alkaline phosphatase 283 IU/L and alanine aminotransferase 583 IU/L. Haematological investigation revealed a high white cell count of 27×10 9/L with lymphocytosis (16.3×10 9/L) and mild neutrophilia (8.9×10 9/L) and a D-dimer of 1135 ng/mL (250 ng/mL is the cut-off for PE). Alvelolar-arterial gradient was 28 (expected 11) suggesting a V/Q mismatch. Initial ECG demonstrated sinus tachycardia with no ischaemic features but subsequent ECG showed new T-wave inversion in leads III, aVF and V 6.Īrterial blood gas showed normal pH, base excess and bicarbonate with partial pressure of oxygen 10 kPa but a high lactate of 3.4 mmol/L. He was found to have a 24 mm Hg blood pressure difference between the left and right arms. His abdomen was soft with minimal epigastric discomfort and no palpable organomegaly. Clinically there was no deep vein thrombosis and Well's score for pulmonary embolism (PE) was 4.5 indicating intermediate risk.
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His chest pain was localised to the upper left chest, made worse by movement and inspiration but not chest wall palpation. Cardiovascular and respiratory examinations were unremarkable. His oxygen saturations were 96% on room air. He was tachycardic with a heart rate of 111 bpm and his blood pressure was 135/73 mm Hg. On examination he was sweaty and pale and in severe pain. He had a 6 pack-year smoking history but no illicit drug use. His father had an abdominal aortic aneurysm but there was no other notable family history. He had a medical history of pericarditis 5 years previously but no risk factors for ischaemic heart disease. He denied a productive cough and did not have any calf swelling or haemoptysis. He described a flu-like illness in the preceding week when he suffered from fever and a sore throat which were resolving. It was worsened by inspiration and movement and associated with sweating, shortness of breath and an episode of vomiting. A 29-year-old man presented with a 5 h history of sudden onset of severe sharp pain in his left upper chest.