Background Tuberculous aortitis is an unusual presentation of a common disease in Sri Lanka. There were no reported cases of tuberculous aortitis from Sri Lanka. Here we report a case of a 40-year-old woman who developed an ascending aortic aneurysm with severe aortic regurgitation caused by Mycobacterium tuberculosis.Case presentationA 40-year-old Sri Lankan female who presented with exertional breathlessness (NYHA II) and weight loss for 4 weeks duration was found to have collapsing pulse and early diastolic murmur at left sternal edge. Transthoracic and transesophageal echocardiogram showed ascending aortic aneurysm with severe aortic regurgitation. Computed tomographic aortography confirmed the diagnosis of aneurysmal dilatation of the ascending aorta. She underwent successful aortic valve replacement and aortic root replacement. The final diagnosis of tuberculous aortitis was made on the basis of macroscopic appearance of inflammation and microscopic confirmation of caseating granuloma. She made a good clinical recovery with category 1 antituberculous chemotherapy.ConclusionsAlthough most cases of aortitis are non-infectious in Sri Lanka, an infectious etiology must be considered in the differential diagnosis because therapeutic approaches differ widely. Tuberculous aortitis may be under diagnosed in Sri Lanka, a country with intermediate tuberculosis burden, as the histological or microbiological diagnosis is not possible in most cases. The clinical and radiological diagnostic criteria for tuberculous aortitis need to be set out in case of aneurysmal aortic disease in the absence of apparent etiology.
IntroductionOrtner’s syndrome is defined as left recurrent laryngeal nerve palsy caused by a cardiovascular pathology. Here we report the case of a 68-year-old man who presented to our hospital with hoarseness, whose initial chest imaging mimicked a thoracic neoplastic process with left pleural effusion. The final diagnosis was Ortner’s syndrome due to the silent rupture of a thoracoabdominal aortic aneurysm. Diagnostic thoracentesis, before computed tomography, in resource-poor settings, may have resulted in an adverse outcome in our case.Case presentationA 68-year-old Sri Lankan man was referred to us by an otolaryngologist for further evaluation of a suspected thoracic malignancy. His presenting symptom was hoarseness of three months duration. He had essential hypertension for the last four years and had a history of 25 pack-years of cigarettes smoking. His chest X-ray showed a left-sided mediastinal mass with mild to moderate pleural effusion. An ultrasound appeared to show an encysted pleural fluid collection. However, we proceeded with computed tomography before diagnostic thoracentesis. The diagnosis of Ortner’s syndrome was made after the computed tomography due to the silent rupture of his thoracoabdominal aortic aneurysm.ConclusionsHoarseness due to left recurrent laryngeal nerve palsy can be the presenting symptom of cardiovascular pathologies, Ortner’s syndrome. Silent rupture of thoracic aortic aneurysms can mimic that of thoracic malignancy, which is reported in literature. We illustrate the importance of a high degree of suspicion of cardiovascular pathology in order to avoid an adverse outcome following diagnostic thoracentesis.
BackgroundBacteremia following Staphylococcus aureus is a serious clinical condition which is often associated with distant metastatic infections. One of the most dreaded complications of Staphylococcus aureus bacteremia is infective endocarditis. Cloxacillin is a common antibiotic prescribed for suspected staphylococcal infections and confirmed methicillin-sensitive Staphylococcus aureus infections. Prolonged use of cloxacillin may lead to neutropenia.Case presentationA 38-year-old Sinhalese man presented to Teaching Hospital Kurunegala, Sri Lanka, complaining of a 3-week history of fever; he was found to have a pansystolic murmur over the apex of his heart. He had leukocytosis with predominant neutrocytosis. His C-reactive protein was 231 mg/l and erythrocyte sedimentation rate was 100 mm/first hour. Transthoracic two-dimensional echocardiography revealed prolapsed mitral valve with 7 × 13 mm vegetation over the posterior mitral valve. On the following day, three blood cultures became positive and were subsequently identified as Staphylococcus aureus. Intravenously administered cloxacillin 3 g 6 hourly was started. Following day 24 of intravenously administered cloxacillin, our patient developed high spike fever. His total white blood cells were: 990/mm3 with 34% neutrophils and 22% eosinophils. His hemoglobin concentration was 9.5 g/dL and platelet count remained normal (202 × 106/mm3). His C-reactive protein was 78 mg/l, erythrocyte sedimentation rate was 95 mm/first hour, and he was otherwise comfortable, showing no signs of sepsis beside the high grade fever. His serum was negative for filarial and Toxoplasma antibodies while stool was negative for oocytes and amoebic cysts. Further, his serum was negative for dengue virus, Epstein–Barr virus, cytomegalovirus, and hepatitis B antibodies. He was clinically well on day 6 after stopping cloxacillin with 44% neutrophils and 18% eosinophils. His C-reactive protein and erythrocyte sedimentation rate became normal, and there was no further plan for cardiothoracic intervention or administration of antimicrobials. He was discharged from hospital and remained well 6 months later.ConclusionThis case report signifies the potential fatal adverse effect of cloxacillin in methicillin-sensitive Staphylococcus aureus infections. Leukopenia is associated with prolonged use of high doses of cloxacillin. In addition to transthoracic two-dimensional echocardiography and inflammatory markers, sequential white blood cells and differential counts would help clinicians to assess the prognosis of patients with infective endocarditis.
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