BackgroundAnaphylaxis is an acute, potentially fatal medical emergency. Myocardial injury or infarction in the setting of an anaphylaxis can be due the anaphylaxis itself, when it is known as Kounis syndrome or it can also be due to the effect of epinephrine treatment. Epinephrine is considered as the cornerstone in management of anaphylaxis. Myocardial infarction secondary to therapeutic doses of adrenaline is a rare occurrence and only a few cases have been reported in literature. The mechanism of myocardial injury was considered to be due to coronary vasospasm secondary to epinephrine as the coronary angiograms were normal on these occasions.Case presentationA 21-year- old previously healthy male got admitted to the local hospital with an urticarial rash and difficulty in breathing, one hour after ingestion of prawns for which he was known to be allergic. He was treated with 0.5 ml of intramuscular adrenaline (1:1000) which was administered to the lateral side of the thigh, following which he developed palpitations and tightening type central chest pain. Electrocardiogram showed ST segment depressions in leads III, aVF and V1 to V5 and he was transferred to a tertiary care hospital. The second electrocardiogram, done 2 h later, showed resolution of ST segment depressions but new T inversions in leads I and aVL. Troponin I was elevated with a titer of 2.15 ng/ml. He was treated with sublingual GTN in the emergency treatment unit and the symptoms resolved. Transthoracic 2D echocardiogram and stress testing with treadmill was normal and CT coronary angiogram revealed normal coronary arteries.ConclusionHere we present a case of a young healthy adult with no significant risk factors for coronary artery disease who developed myocardial infarction following intramuscular administration of therapeutic dose of adrenalin for an anaphylactic reaction. The postulated mechanism is most likely an alpha receptor mediated coronary vascular spasm. However the use of adrenaline in the setting of life threatening anaphylaxis is life saving and the benefits far outweigh the risks of adverse effects. Therefore the purpose of reporting this case is not to discourage the use of adrenaline in anaphylaxis but to make aware of this potential adverse effect which can occur in the acute setting.

BackgroundDengue is a common arthropod-borne viral infection in Sri Lanka which is spread by the mosquitos of the genus Aedes. The clinical features of dengue include high-grade fever associated with arthralgia and myalgia. However, dengue virus is not considered an arthritogenic virus. We report a case of a previously healthy young female who presented with imaging-confirmed right-sided sacroiliitis 10 days after developing dengue fever. This is the first reported case that shows a possible link between dengue infection and development of arthritis.Case presentationA 14-year-old Sri Lankan female presented to our medical unit with right buttock and hip pain of 3 weeks’ duration. She had serologically confirmed dengue infection 10 days prior to the onset of buttock pain. A clinical examination revealed features of right sacroiliitis. An X-ray of her sacroiliac joint showed joint space widening and reactive bone changes. Magnetic resonance imaging of her pelvis and sacroiliac joint confirmed the diagnosis of acute sacroiliitis. She had an erythrocyte sedimentation rate of 110 mm first hour with a normal C-reactive protein. Her human leukocyte antigen-B27, rheumatoid factor, antinuclear antibody, chikungunya antibody, hepatitis serology, Brucella serology, and tuberculin skin test were negative. She was treated with nonsteroidal anti-inflammatory drugs and showed gradual improvement.ConclusionsAfter excluding possible causes for sacroiliitis, we postulated that sacroiliitis in the index case could have been caused or triggered by dengue virus infection. However there is a possibility that the sacroiliitis merely coincided with the dengue virus infection. This case illustrates the possibility that dengue virus could have a link with the development of arthritis in the same manner as other arthritogenic viruses; possible mechanisms for this include direct invasion of the synovium and the joint tissue by the virus, immune complex formation and deposition in the joint tissue, and immune dysregulation. Further studies are needed in this field to gain more knowledge, as dengue infection is highly prevalent in Sri Lanka.

BackgroundSpinal cord infarction is an uncommon condition. Anterior cord syndrome present with paraparesis or quadriparesis with sparing of vibration and proprioceptive senses. The common causes of anterior cord syndrome are aortic dissection and aortic surgical interventions. Spontaneous unruptured nondissected aortic aneurysms with intramural thrombus can rarely cause anterior cord infarctions.Case presentationWe report a case of anterior spinal cord syndrome due to aneurysm of the thoracic aorta with a mural thrombus. A 64 year old male presented with sudden onset paraparesis with a sensory level at T1 with preserved sense of proprioception and vibration. The MRI panspine revealed increased T2 intensity in the anterior portion of the spinal cord from C5 to T10 level with characteristic ‘owl eye’ appearance on axial imaging. The CT aortogram detected aneurysmal dilatation of the ascending aortic, arch and descending thoracic aorta with significant intimal irregularities, calcified atherosclerotic plaques and a small mural thrombus.ConclusionThe possible mechanisms postulated are occlusion of ostia of radicular arteries by the atherosclerotic plaques and mural thrombus or thromboembolism to the anterior spinal artery. Nondissected atherosclerotic aortic aneurysms should be considered in patients presenting with spinal cord infarctions especially in the presence of vascular risk factors and smoking.

The pathophysiology of severe dengue is related to increased capillary permeability and plasma leakage into extracellular space. A simple, low cost risk prediction tool for plasma leakage will be useful for clinicians practicing in rural areas without imaging facilities. Study design: A prospective observational study was carried out over 12 months at the National Hospital, Sri Lanka enrolling patients with confirmed diagnosis (via NS1 antigen testing) of early dengue infection. Clinical features on admission and investigation results on D3, D5 and D7 of the illness were recorded. Evidence of plasma leakage was confirmed by ultrasonography. Results: A total of 179 patients met the inclusion criteria (males; 91, 50.8%, mean age: 31.6 years, SD ± 14.7). Sixty seven patients (67/173, 38.7%) had ultrasonographic evidence of plasma leakage. Several clinical features (severe vomiting, severe diarrhoea, abdominal pain and liver tenderness) as well as mean differences of some investigations were significantly associated with progression to plasma leakage. However, only liver tenderness on day 3 emerged as independent significant predictors of critical phase in the adjusted analysis (specificity: 93%, sensitivity: 44%). Conclusions: Having liver tenderness by day 3 of the illness is helpful to identify a subgroup of patients at risk of plasma leakage.