Dysphagia, Hyperglycemia, and Presyncope.

There have been over 80 documented cases of swallow syncope-a rare form of reflex or neurally mediated syncope-with most cases associated with an underlying esophageal disorder. Here, we describe the first reported case of swallow syncope or presyncope caused by an infectious esophagitis. Our 65-year-old patient initially developed dysphagia, odynophagia, and presyncope with swallowing. This lead to nutrition and medication avoidance behavior, which was followed by the development of diabetic ketoacidosis. The diagnosis of swallow presyncope was confirmed with a provocative swallow study demonstrating 8 s sinus arrest, and an underlying cause of Candida esophagitis was found by upper endoscopy. Symptoms completely resolved after treatment with micafungin.

From bone to heart: a case of MRSA osteomyelitis with haematogenous spread to the pericardium.

We report a case of a 55-year-old woman with a history of type 2 diabetes mellitus, Charcot arthropathy and end-stage renal disease, who presented with a syncopal episode after undergoing haemodialysis. She had a history of methicillin-resistant Staphylococcus aureus (MRSA) bacteraemia from an unknown source 3 months earlier, which was treated with an 8-week course of intravenous antibiotics. At the time of presentation to the emergency room, she was found to be in refractory shock. Bedside echocardiogram was performed, which showed moderate pericardial effusion. The effusion was later found to be due to MRSA, which was identified in blood and in pericardial fluid cultures. The patient was successfully treated with intravenous daptomycin for 6 weeks. Acute osteomyelitis of her right foot was the source of the MRSA, for which a right below-knee amputation was ultimately performed.

Haemorrhage, hyponatraemia and more than just a hack.

A 43-year-old previously healthy solicitor presented with a 9-day history of cough productive of yellow sputum with a prodrome of sore throat and myalgia. The cough was paroxysmal in nature and severe enough to cause extensive bilateral subconjunctival haemorrhages and cough syncopes multiple times a day, with one bout of associated haematemesis on the day of admission. He was isolated, treated for a presumed atypical chest infection with tazocin and clarithromycin, and monitored carefully until the hyponatraemia on presentation was resolved. Atypical screen and blood cultures were sent off, though unexciting at first, eventually confirmed the unlikely; Bordetella pertussis, much to the surprise of many who had Legionella as the top differential.

[Acute atrioventricular block in chronic Lyme disease]. / Krónikus Lyme-infekcióban észlelt akut atrioventricularis blokk.

The tick bite transmitted Lyme disease is one of the most common antropozoonosis, about 10 000 new infections are reported in Hungary each year. The progress and clinical presentation can vary, and carditis can occur in later stages. A serologically verified Lyme disease caused third degree atrioventricular block in young male presenting with presyncope. Based on the tick-bites mentioned a few weeks prior to hospital admission, Lyme carditis was considered with the administration of antibiotics and monitor observation. Typical skin lesions were not recognized and laboratory findings showed no pathology. An electrophysiological study recorded a predominant supra-His atrioventricular block. Total regression of conduction could be detected later and the serological tests established an underlying Lyme disease. Currently no definite treatment recommendation is available for the potentially reversible Lyme carditis. The tick bite seemed to be the key on our way to diagnosis; however, serological tests proved the disease to be older than one year. A detailed medical history and serological tests are essential in identifying the cause and pacemaker implantation can be avoided.

Recurrent syncope and chronic ear pain.

An elderly gentleman presented to hospital with recurrent blackout episodes consistent with syncope and a 3-month history of right ear pain. Significant postural hypotension was recorded. White cell count and C reactive protein were elevated. MRI of the head and neck revealed a soft tissue abnormality in the right nasopharynx and base of skull. Tissue biopsies were obtained and microbiology specimens revealed a mixed growth of pseudomonas and diphtheroids. There was no histological evidence of malignancy. A diagnosis of skull base infection was made. Infective involvement of the carotid sinus was considered to be the cause of the recurrent syncope and postural hypotension. The patient responded well to a 12-week course of intravenous meropenem. Inflammatory markers returned to normal and a repeat MRI after 3 months of treatment showed significant resolution of infection. The syncopal episodes and orthostatic hypotension resolved in parallel with treatment of infection.

Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis.

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?

[Type-A aortic dissection without chest pain in a patient with Clostridium fallax infection]. / Dissezione aortica tipo A in un paziente con setticemia da Clostridium fallax asintomatico per dolore toracico.

We describe the case of a 64-year-old patient admitted to our hospital because of syncope and suspicion of cardiac tamponade. At admission he had temporary alteration of conscience with clinical evidence of sepsis without chest pain. There was a mild pericardial effusion in absence of clinical and echocardiographic signs of cardiac tamponade. About 36 hours later we found evidence of an aortic dissection and in the blood culture an isolation of Clostridium fallax that we consider the probable cause of this lesion.