Sanjiv Petkar

How to avoid a misdiagnosis in patients presenting with transient loss of consciousness

Daily in the UK, frontline medical and paramedical staff are required to manage patients with “collapse ?cause”. This universal colloquialism refers to patients who have had an abrupt loss of postural tone. Some of these patients would have had a “blackout” or a transient loss of consciousness (T-LOC). The three most important causes of T-LOC are syncope, epilepsy and psychogenic blackouts. Determining the correct cause is an important challenge; if the initial clinical diagnosis is wrong, investigations may be misdirected, and the final diagnosis and treatment incorrect. Syncope is much more common than epilepsy and may present with symptoms akin to the latter. This fact is not well appreciated and often leads to misdiagnosis. This article deals with the clinical features of the three main causes of blackouts, the value of investigations in arriving at a diagnosis and the problem of misdiagnosis. Pathways for managing patients presenting with blackouts are suggested.

Upgrading Patients with Chronic Defibrillator Leads to a Biventricular System and Reducing Patient Risk: Contralateral LV Lead Placement

Increasing numbers of patients with indwelling single‐ or dual‐ chamber internal cardioverter defibrillators (ICDs) will require upgrading of an existing system to a biventricular ICD providing cardiac resynchronization with back‐up defibrillation. Upgrading, usually by the addition of a new left ventricular (LV) lead, can be technically challenging with central venous occlusion or stenosis often being the main obstacle to a successful procedure. We report a new technique of implanting a LV lead from the contralateral side to the existing ICD system to minimize the peri‐ and postoperative risk to the patient.

Tilt-table testing: transient loss of consciousness discriminator or epiphenomenon?

Syncope accounts for 1–1.5% of emergency room visits and up to 6% of general hospital admissions.1–4 Patients with syncope present with a blackout,5 or transient loss of consciousness (T-LOC), and may present in family practice, cardiology, general medicine, accident and emergency, neurology, geriatric medicine, and psychiatry. Generally, a patient with T-LOC can only give limited details of the event, covering premonition and aftereffects. An eye-witness account is essential for filling in details during T-LOC. However, there are important causes of T-LOC other than syncope, e.g. generalized epilepsy and psychogenic blackouts. When patients present having had T-LOC, clinicians seek a test that will discriminate between these important causes. Is tilt-table testing such a test? Tilt testing is a simple, non-invasive test with a low risk of complications.6 The physiological and pathophysiological effects of orthostatic stress by tilt testing have been known for 60 years.7 In 1986, Kenny et al .8 observed a high rate of tilt-induced syncope, with hypotension and bradycardia, in patients with syncope of previously unknown origin when compared with controls. Subsequently, many reports profiled the use of the test, and guidelines and recommendations emerged.6 However, clinical practice featured a very variable yield from a wide range of protocols, varying in duration and angle of tilt, the use of drug provocation to increase yield, and most importantly, the type of patients studied. Such factors presumably underlie the variable yield of tilt-table testing, which is from 26 to 87%.9 The overall reproducibility of a negative response (85–94%)10–14 is higher than that of an initial positive response (31–92%). The impact of these variations in protocol and patient clinical types, and their effect on the interpretation of a test result for T-LOC discrimination, is considered below. Most studies using tilt …

Disappearing hot spot on an indium 111 white cell scan: A case report

Case presentation. In July 2006 an 81-year-old man was admitted to the hospital with perianal discharge and rigors of 3 weeks’ duration. The patient’s medical history revealed an operation for a fistula in ano 6 years ago and significant comorbid cardiac problems, which had started more than 30 years ago. In 1976 he had a myocardial infarction. In 1998, 22 years later, he was admitted to the hospital after a collapse and found to have ventricular tachycardia, and as he was hemodynamically compromised, he underwent external cardioversion. After successful cardioversion, antiarrhythmic drug therapy was started in the form of amiodarone. A few months later, because he continued to have inducible ventricular tachycardia on an electrophysiologic study despite amiodarone, he underwent an implantable cardioverter defibrillator (ICD) implantation in the left infraclavicular area. Seven years later, in September 2005, after a surgical procedure to replace the ICD batteries, he started complaining of pain in and around the ICD site. The device was found to be lying superficially in the chest wall, and therefore he underwent another surgical procedure to rebury it. Unfortunately, despite the reburial procedure, the device eroded through the skin and became infected. A wound swab grew coagulase-negative staphylococci, sensitive to erythromycin, vancomycin, rifampin, and gentamicin and resistant to penicillin and floxacillin. Blood culture showed no growth after 6 days’ incubation. In keeping with current practice, in April 2006, he underwent an extraction of the whole ICD system (box and leads). Guided by the results of the culture and sensitivity of the wound swab, he was treated with antibiotics. During the same hospital stay, after satisfactory control of infection, a totally new ICD system was successfully implanted, this time on the contralateral (right) side, without any complications (Figure 1). On the present admission, the patient was spiking temperatures of up to 38.1°C, associated with rigors. Per rectum (PR) examination revealed a small left-sided perianal fistula with no local inflammation. There were no signs of local inflammation or infection at the sites of the present or previous ICD implantation. The rest of his systemic examination was normal. Investigations revealed a raised white cell count (16.0 10/L; normal, 4.0-11.0 10/L), a raised neutrophil count (14.03 10/L; normal, 2.0-7.5 10/L), and a high C-reactive protein (CRP) level (74 mg/L; normal, 0.3-5.0 mg/L). A chest radiograph showed cardiomegaly with a right-sided ICD implantation. The lung fields were clear (Figure 1). Urine culture and local wound swabs of both the ICD sites were negative. Thyroid function tests and tests for antinuclear antibody, antibody to double-stranded deoxyribonucleic acid, anti-neutrophil cytoplasmic antibody (c-ANCA), and antiglomerular basement membrane antibody were also negative. Blood cultures grew coagulase-negative staphylococci, sensitive to vancomycin and rifampin and resistant to gentamicin and floxacillin. While the patient was being treated with antibiotics, further investigations were undertaken in an attempt to locate the source of infection. Repeat PR examination failed to reveal any evidence of collection in the perianal area. A transthoracic echocardiogram showed poor left ventricular function but no evidence of vegetations, an ultrasound of the upper abdomen was unremarkable except for a Bosniak type 2 cyst in the lower pole of the right kidney, and a computed tomography (CT) scan of the abdomen and pelvis failed to reveal any ischiorectal or intra-abdominal fluid collection. As the patient continued to have pyrexia and a high CRP level despite 10 days of antibiotic treatment and as the source of the staphylococcal infection remained unclear, an indium 111–labeled white cell scan was undertaken. This showed progressive white cell accumulation in the thorax on days 1 and 2 that was localized on the tomographic images, along with low-resolution CT, to be in relation to the ICD lead and possibly the tricuspid valve, but this disappeared on day 3 (Figures 2–5). This raised the possibility of vegetations on the ICD leads or the tricuspid valve (with possible emboliFrom the Manchester Hear Centre and Department of Nuclear Medicine, Manchester Royal Infirmary, Manchester, England. Reprint requests: Parthiban Arumugam, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, England; parthiban. arumugam@cmmc.nhs.uk. J Nucl Cardiol 2008;15:e1-5. 1071-3581/

Atrial fibrillation is under-recognized in chronic heart failure: insights from a heart failure cohort treated with cardiac resynchronization therapy

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