1/58. Expeditious diagnosis of primary prosthetic valve failure.Primary prosthetic valve failure is a catastrophic complication of prosthetic valves. Expeditious diagnosis of this complication is crucial because survival time is minutes to hours after valvular dysfunction. The only life-saving therapy for primary prosthetic valve failure is immediate surgical intervention for valve replacement. Because primary prosthetic valve failure rarely occurs, most physicians do not have experience with such patients and appropriate diagnosis and management may be delayed. A case is presented of a patient with primary prosthetic valve failure. This case illustrates how rapidly such a patient can deteriorate. This report discusses how recognition of key findings on history, physical examination, and plain chest radiography can lead to a rapid diagnosis.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
2/58. pH-dependent cocaine-induced cardiotoxicity.Severe cocaine toxicity causes acidemia and cardiac dysfunction. These manifestations are described in 4 patients who presented with seizures, psychomotor agitation, and cardiopulmonary arrest. Their initial laboratory values demonstrated acidemia and electrocardiographic findings that included a prolonged QRS complex and QTc duration and a rightward T40 ms axis deviation. Treatment of the patients with hyperventilation, sedation, active cooling, and sodium bicarbonate infusion led to the normalization of their blood pHs and reversal of their cardiac conduction disorders. Acidemia can contribute to cocaine cardiac disorders by promoting conduction delays, dysrhythmias, and depressed myocardial contractility. Good supportive care corrects the blood pH and cardiac conduction disorders and remains the major focus in the management of patients with cocaine toxicity.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
3/58. Visual hallucinations in recovery from cortical blindness: imaging correlates.OBJECTIVE: To investigate the cerebral metabolic and functional patterns during recovery from cortical blindness. DESIGN: Follow-up study with serial clinical, metabolic, and functional imaging and visual evoked potentials. CASE PRESENTATION: A 24-year-old woman suffered from cortical blindness after cardiac arrest and recovered over a 6-month period. During recovery, she experienced complex visual hallucinations that could be initiated by visual imagery. RESULTS: Initially, the regional cerebral metabolic rate of glucose was severely reduced in the visual and parieto-occipital cortex bilaterally but recovered almost completely. Visual hallucinations led to significant increases of the regional cerebral blood flow in the initially severely hypometabolic parieto-occipital and temporo-lateral cortex. CONCLUSIONS: Recovery of vision was related to normalization of the postlesionally dysfunctional cortex. Visual hallucinations appeared as the clinical correlate of the electrophysiological hyperexcitability of the recovering partially damaged visual cortex.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
4/58. Deaths of children during an outbreak of hand, foot, and mouth disease in sarawak, malaysia: clinical and pathological characteristics of the disease. For the Outbreak Study Group.From April through June 1997, 29 previously healthy children aged <6 years (median, 1.5 years) in Sarawak, malaysia, died of rapidly progressive cardiorespiratory failure during an outbreak of hand, foot, and mouth disease caused primarily by enterovirus 71 (EV71). The case children were hospitalized after a short illness (median duration, 2 days) that usually included fever (in 100% of case children), oral ulcers (66%), and extremity rashes (62%). The illness rapidly progressed to include seizures (28%), flaccid limb weakness (17%), or cardiopulmonary symptoms (of 24 children, 17 had chest radiographs showing pulmonary edema, and 24 had echocardiograms showing left ventricular dysfunction), resulting in cardiopulmonary arrest soon after hospitalization (median time, 9 h). Cardiac tissue from 10 patients showed normal myocardium, but central nervous system tissue from 5 patients showed inflammatory changes. brain-stem specimens from 2 patients were available, and both specimens showed extensive neuronal degeneration, inflammation, and necrosis, suggesting that a central nervous system infection was responsible for the disease, with the cardiopulmonary dysfunction being neurogenic in origin. EV71 and possibly an adenovirus, other enteroviruses, or unknown cofactors are likely responsible for this rapidly fatal disease.- - - - - - - - - - ranking = 36.530662401761keywords = ventricular dysfunction, dysfunction (Clic here for more details about this article) |
5/58. Alarming atrioventricular block and mitral valve prolapse in the kearns-sayre syndrome.kearns-sayre syndrome (KSS) is a multisystem mitochondrial disorder characterized by the invariant triad: onset before 20, progressive external ophthalmoplegia and pigmentary retinal degeneration, plus at least one of the following: complete (or not) heart block, cereberal dysfunction and CSF protein above 100 mg/dl. Autopsies from patients with KSS revealed widespread tissue distribution mtDNA deletions. These deletions result in significantly lower activities of the enzymes of the respiratory chain. The same deletion of mitochondrial dna present in skeletal muscle is found in myocardial tissue. An 18-year-old girl diagnosed with the KSS was admitted to our hospital because of an upper respiratory tract infection and dysphagia. ECG showed cardiac conduction defects. The patient had no history of syncope. At her surface ECG there was a complete RBBB (QRS duration approximately 130 ms), a clockwise rotation with an axis of approximately 90 degrees and a slight QT prolongation (420 ms). echocardiography showed prolapse with thickening and degeneration of both mitral valve leaflets but without mitral regurgitation. The patient was started on a diet rich in potassium and pharmaceutical therapy with magnesium oxide (240 mg of elemental Mg p.o. per day), 1 g of calcium carbonate t.i.d., vitamin d (calcitriol 0.25 microg p.o. per day) and coenzyme Q(10) 100 mg daily and discharged 6 days later with slightly improved biochemical profile but apparent clinical improvement. Urgent pacemaker implantation was decided but unfortunately the patient died due to acute cardiac arrest 10 days later.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
6/58. Idiopathic cardiac asystole presenting as epileptic seizures.Cardiac asystole has been associated with partial or generalized seizures (anoxic seizure) but, despite the previous descriptions, is still an underdiagnosed entity. The authors report 2 cases of cardiac asystole mimicking seizure disorder. The apparent cause of seizures in both cases was primary cardiac asystole caused by sinus node dysfunction. Both patients underwent emergent cardiac pacemaker implantation with complete resolution of their seizure/syncopal episodes. The importance of cardiac monitoring in patients who present with seizure-like events is emphasized.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
7/58. Progressive delayed-onset dystonia after cerebral anoxic insult in adults.The basal ganglia, especially the globi pallidi (GP), are highly vulnerable to generalized cerebral anoxia/hypoxia. We report on 2 new cases with delayed-onset generalized dystonia due to cerebral anoxia. The onset of dystonia in both of our patients was delayed by about 2 months. In both cases, the unusual feature was the progressive worsening and the spread of dystonia over many years after delayed onset. dystonia progressed for 16 years in Case 1 and for 4 years in Case 2. Furthermore, initial magnetic resonance imaging (MRI) scan of Case 1 showed mild changes of the internal capsule sparing the basal ganglia. Years later, in line with clinical progression, the follow-up MRI scan showed isolated bilateral lesions involving the entire GP. MRI scans in Case 2 showed bilateral lesions of caudate and lentiform nuclei. There may be several mechanisms underlying delayed and progressive symptoms after time-limited brain anoxia. We hypothesize that anoxia-induced excitotoxicity resulting in mitochondrial dysfunction and subsequent apoptosis may explain, at least partly, the delayed-onset and progressive extrapyramidal syndromes seen in these patients.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
8/58. Clusters of ventricular fibrillation in a patient with an implantable cardioverter difibrillator treated with amiodarone.A 44 year-old man with severe left ventricular dysfunction resulting from an old myocardial infarction developed clusters of ventricular fibrillation (VF). Although coronary bypass surgery was performed and heart failure was well controlled, the VF recurred during amiodarone therapy. Despite multiple deliveries of shocks by an implantable cardioverter defibrillator, the electrical storm could not be terminated. Some substrate for rapid ventricular tachyarrhythmias, refractory to class III drugs, can lead to death from arrhythmia.- - - - - - - - - - ranking = 35.530662401761keywords = ventricular dysfunction, dysfunction (Clic here for more details about this article) |
9/58. Transient obstructive sleep apnea and asystole in association with presumed viral encephalopathy.Evidence suggests that untreated obstructive sleep apnea (OSA) can lead to hypertension, cardiovascular disease, and stroke. Conversely, the systemic effects of a wide variety of critical illnesses can lead to CNS dysfunction, which can precipitate respiratory failure. Reported is a patient in whom an acute encephalopathy may have been responsible for transient OSA.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
10/58. Neuropsychological deficits of a U.S. Army pilot following an anoxic event as a function of cardiac arrest.Anoxic encephalopathy occurs as a result of cardiac arrest, respiratory distress, or carbon monoxide poisoning. This is a case report on the neuropsychological deficits of anoxia in an otherwise previously healthy 36-year-old male pilot. The patient was taking an over-the-counter supplement that included an herb called Ma Huang on the day of his cardiac arrest. Ma Huang is reported to potentially present an increased risk of cardiac infarctions and central nervous system dysfunctions. Several instances of death have been linked to Ma Huang. The patient produced a neuropsychological profile that evidenced impairments in executive functioning, memory, language, attention, intellectual and academic functioning, as well as motor speed and coordination, all of which are consistent with diffuse brain damage. This case adds to the body of literature documenting the physical and neuropsychological effects of anoxia, as well as the effects of ephedrine-based supplements, such as Ma Huang.- - - - - - - - - - ranking = 1keywords = dysfunction (Clic here for more details about this article) |
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