Clinical applications of magnets on cardiac rhythm management devices.

The growing indications for permanent pacemaker and implantable cardioverter defibrillator (ICD) implantation have increased the number of patients with these cardiac rhythm management devices (CRMDs). Cardiac rhythm management devices occasionally perform inappropriately in response to electromagnetic interference (e.g. surgical electrocautery) or lead noise over-sensing (e.g. lead fracture). Temporary reprogramming of the CRMDs using device programmers can prevent these untoward device responses. However, these programmers are device manufacturer specific and require technically qualified personnel to operate. This could cause delayed patient care and increased use of resources in certain clinical situations. Alternatively, clinical magnets, when appropriately positioned over the device site, can change the pacing to an asynchronous mode in pacemakers and suspend tachycardia therapies in ICDs. Although readily available, clinical magnets have not been widely used for this purpose, perhaps due to the unfamiliarity with the variable responses of CRMDs to magnet application. This article provides a comprehensive overview of the current literature on the mechanism of action and the specific responses of various CRMDs to clinical magnets.

Life-threatening hyperkalemia from nutritional supplements: uncommon or undiagnosed?

Potassium chloride and other potassium compounds are used by the general public as salt substitutes, muscle-building supplements, and panacea. Severe hyperkalemia from oral potassium is extremely rare if kidney function is normal because of potassium adaptation. The oral potassium dose has to be large enough to overcome the normal renal excretory mechanisms to cause severe hyperkalemia. This occurs most commonly in patients with renal impairment or those who take potassium-sparing diuretics, angiotensin receptor blockers, or angiotensin-converting enzyme inhibitors. We present two unique cases of near-fatal hyperkalemia from nutritional supplements containing potassium. The first case was due to salt-substitute intake, whereas the second case was from a muscle-building supplement. Both patients suffered cardiac arrest, but were successfully resuscitated and survived. The acuity of intake and excessive quantity overwhelmed the kidneys' ability for adaptation. Potassium toxicity affects multiple organ systems and manifests in characteristic, acute cardiovascular changes with electrocardiographic abnormalities. Neuromuscular manifestations include general muscular weakness and ascending paralysis may occur, whereas gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis that may lead to perforation. Once an urgent situation has been handled with intravenous push of a 10% calcium salt, short-term measures should be started with agents that cause a transcellular shift of potassium, namely, insulin with glucose, ß2-agonist, and NaHCO(3). Patients are unaware of these potentially serious adverse effects, and there are inadequate consumer warnings. Clinicians should be vigilant in monitoring potassium intake from over-the-counter supplements.

Pericardial effusion impending tamponade: a look beyond Beck's triad.

Clinical diagnosis of chronic or slowly progressing pericardial effusion with impending tamponade remains a challenge, particularly when classical physical signs are subtle or absent. A high index of suspicion should be entertained in such cases in the appropriate setting even when the clinical signs and symptoms are missing. We present two cases where the pericardial effusion was missed in the emergency department due to subtle clinical features or mistaken for a more familiar "look-a-like" presentation. A review of the literature and an analysis of various clinical parameters of published cases were performed. It is pivotal that physicians should not only be aware of the limitations of the traditional clinical signs, but also be familiar with the use of other subtle findings and the importance of other modalities that may potentially enhance the sensitivity in diagnosing chronic pericardial effusion impending tamponade.

Bronchocutaneous fistula after chest-tube placement: A rare complication of tube thoracostomy.

Bronchocutaneous fistula is a pathologic communication between the bronchus, pleural space, and subcutaneous tissue. It can occur as a complication of positive pressure ventilation and pneumonectomy. Diagnosis is made by imaging studies. Treatment options are endoscopic repair, parietal pleurectomy, and pleurodesis. Our patient is a 53-year-old woman who had a difficult chest-tube placement for complicated parapneumonic effusion. Computed tomography scan revealed a fistulous tract from the bronchus to the skin at the site of the original chest tube, and chest x-ray film revealed a subcutaneous fistulous air tract in the lateral chest. It is usually an acquired condition; congenital bronchocutaneous fistula is rare. We report a case of bronchocutaneous fistula after chest-tube placement.

Retinal histopathology of an XLRP carrier with a mutation in the RPGR exon ORF15.

X-linked retinitis pigmentosa comprises the severe forms of RP, with early onset of night blindness, rapid constriction of visual fields and eventual loss of central acuity. Of the five distinct XLRP loci identified on the X chromosome, mutations have been found only in the RP2 and RPGR genes. Of these, mutations in RPGR are more common, particularly in a mutational hot spot that was identified in the newly discovered exon ORF15. We report on an extended family with a microdeletion in RPGR exon ORF15 and the retinal histopathology of a female carrier of this mutation. We found a 1bp deletion at position 632 in exon ORF15 in affected members of family XLRP-319. This mutation alters the reading frame of the predicted RPGR protein, resulting in a premature stop codon. The mutation segregated with disease in three generations of the family and was associated with severe early onset retinal disease in affected men. The retina from a 75 year old carrier female donor had slight photoreceptor loss in the less diseased areas. More severe atrophy with retinal pigment epithelium (RPE) migration was present in areas of the mid- and far periphery. By immunocytochemistry, loss of rhodopsin labelling in rods was found in the areas of focal atrophy and loss of uniform cone spacing was apparent even in well preserved regions. Small multifocal areas of outer retinal degeneration were present in the better preserved regions of the eye. In these foci, rod and cone loss did not coincide. The dissociation of rod and cone degeneration in areas of focal disease is consistent with random X-inactivation early in embryonic development and the occurrence of distinct patterns of radial (rod) and tangential (cone) dispersion during clonal expansion early in photoreceptor differentiation.