A 47-year-old man was referred from an outside facility with complaints of recurrent falls. He had been referred to a neurologist for evaluation of recurrent unexplained syncope. Each event was non-convulsive, random, and preceded by a sudden loss of balance that would progress to falling due to altered mental status. There was no apparent triggering factor, post-event confusion, or loss of either bowel or urinary continence. He had been evaluated twice at a local healthcare facility for these falls, but no cause was identified.He was referred to us on the third presentation after suffering multiple facial and thoracic injuries. He had no evident cardiopulmonary symptoms. Because he was adopted, he had no knowledge of any family history history of cardiac events. His past medical history included bipolar disorder, tobacco abuse, alcohol dependence, and atypical facial pain. His home medications were carbamazepine, lamotrigine, olanzepine, diazepam, and venlafaxine. The only recent change in his medications was a carbamazepine dose reduction because a provider at an outside facility had thought that this might be contributing to his symptoms. On review of his past medical records (more than 10 years prior), left ventricular hypertrophy had been mentioned, but it had not been followed-up in subsequent evaluations. Previous computerized tomography (CT) of the head and neck had been unremarkable.Clinically, the patient was alert, awake, and oriented. Blood pressure was 123/63 mmHg, pulse 83 beats/minute, temperature 99.6ºF, respirations 20 breaths/ minute, and oxygen saturation 95% on room air. He had no orthostatic hypotension. The physical examination was normal except for the multiple facial swellings and left-sided chest wall tenderness he had sustained from the falls. Apical hypertrophic cardiomyopathy (AHC) is a rare variant of hypertrophic cardiomyopathy. Since its description by Sakamoto in 1976 in Japanese patients, our understanding of this entity has evolved. Although cardiac magnetic resonance imaging has emerged as the gold standard for diagnosing AHC, clinical attention must be drawn to the unique electrocardiographic features that provide the initial clues to making the diagnosis. In this case, we present a 47-year-old man with AHC who presented with recurrent syncope, but anomalies on his electrocardiogram went unnoticed on two clinical encounters. He was subsequently admitted to our service and rapidly diagnosed after we observed the very classical findings in the plain twelve lead electrocardiogram done at the time of admission. In a clinical encounter involving a patient presenting with recurrent syncope, special attention must be focused on the electrocardiogram to decipher the unique diagnostic features it might show.

Case PresentationA previously healthy woman, age 26 years, presented with abdominal pain, progressive fatigue, and purpuric skin rash over the extremities that began 7 days after beginning a treatment with trimethoprim-sulfamethoxazole (TMP-SMX) for a Klebsiella pneumoniae urinary tract infection. She also complained of exertional shortness of breath with no cough, hemoptysis, or other cardiopulmonary symptoms. No history of bleeding gums or hematochezia was present. A detailed interrogation did not demonstrate any other recent clinical complaints or the administration of any other type of medication beyond TMP-SMX. Physical examination revealed a young woman in no obvious distress, with a body mass index of 27 and stable vital signs. She had pallor and icterus of the mucus membranes but had no bleeding gums or rectal bleeding. She had a non-itchy, purpuric skin rash over her extremities, as well as petechiae. The rest of her physical examination was unremarkable. Thrombotic thrombocytopenic purpura (TTP) is a hematological disease characterized by microangiopathic hemolytic anemia and thrombocytopenia. Although the link between ADAMTS13 deficiency and idiopathic TTP has been well-established, the role of trimethoprimsulfamethoxazole (TMP-SMX) in the pathogenesis of TTP is not yet well elucidated. To the best of our knowledge, there have been only two previous reports linking this medication with the development of TTP. We present the case of a healthy woman, age 26 years, who developed TTP during TMP-SMX therapy for urinary tract infection. She was found to have ADAMTS13 deficiency with anti-ADAMTS13 antibodies. Her condition responded to discontinuation of the TMP-SMX, plasmapheresis, and rituximab therapy. We speculate that the acquired ADAMTS13 deficiency might have been triggered by the TMP-SMX therapy.

A man, aged 61 years, on etanercept treatment for ankylosing spondylitis, presented to the emergency room with altered mental status. He had been discovered at his vacation cabin by emergency services after his family was unable to contact him. His past medical history was significant for systemic hypertension and tobacco abuse. He had no known allergies, nor any recent head trauma, splenectomy, immunodeficiency disorders, or history of alcoholism. He had been receiving etanercept 50 µg subcutaneously every week on a continuous basis for the past 4 years. Other medications included acetaminophen, metoprolol, and omeprazol. His vaccinations were up to date, including a 23-valent pneumococcal polysaccharide vaccine that had been given before starting etanercept.The initial physical examination on arrival to the emergency room revealed an unresponsive male with a Glasgow coma scale of 6/15 (eye opening, 2; verbal response, 1; motor response, 3). His vitals signs included blood pressure 140/80 mmHg, pulse 150 beats/minute, temperature 103ºF, respirations 50 breaths/ minute with stridor, and oxygen saturation of 82% on room air. The patient was also noted to have nuchal rigidity, left-sided hemiparesis, and facial drooping, as well as a positive Kerning's and Brudzinski's sign (more evident on the right side). The remainder of the physical examination, including ear canal and tympanum were unremarkable. The patient had a generalized seizure for which he received intravenous (IV) lorazepam and phenytoin. He was intubated for airway protection and admitted to the intensive care unit. An electrocardiogram Brain abscess formation as a sequelae of community-acquired pneumococcal meningitis is extremely rare, accounting for less than 1% of all meningitis complications. Although metastatic seeding from a distal peripheral septic focus has been observed, this phenomenon most commonly occurs in the context of ear, nose and throat infections, post-cranial neurosurgical procedures, traumatic open cranial injury, or immunosuppression. We present the case of a man, 61 years old, on etanercept therapy for ankylosing spondylitis who developed multiple brain abscesses as a complication of pneumococcal meningitis. We believe that the predisposition to this extremely rare complication of a particularly aggressive pneumococcal meningitis was most likely due to the underlying immunosuppression resulting from etanercept therapy. As far as we know, this case is the first report linking multiple brain abscess formation in a patient with community-acquired pneumococcal meningitis with etanercept therapy.