Vesicocutaneous fistula: An unusual complication of inguinoscrotal hernia

Involvement of the urinary bladder in an inguinal hernia is common, but massive bladder hernia is rare. Most urinary bladder herniations are discovered and repaired during surgery. We report a case of large incarcerated inguino-scrotal hernia, which was reduced only to present as a scrotal abscess and vesicocutaneous fistula; an unusual complication. The patient was managed conservatively due to underlying comorbidities.     

CLINICAL IMPLICATIONS OF ELECTROPHYSIOLOGY STUDY FINDINGS IN PATIENTS WITH CHRONIC BIFASCICULAR BLOCK AND SYNCOPE

Electrophysiology study was performed in 93 patients with bifascicular block and unexplained syncope. Clinical evidence of organic heart disease was present in 33 (35%). Electrophysiological abnormalities were detected in 45 patients (48%). Of these, 36 had distal conduction disease, including 28 with an HV interval > 55 ms (mean 76.4 ms), and eight who developed infraHisian block following either intravenous procainamide (four) or atrial pacing (four). Sick sinus syndrome was evident in six patients and a further two had carotid sinus hypersensitivity. Sustained monomorphic ventricular tachycardia (VT) was induced in only three patients, two of whom also had prolonged HV interval. Among the 93 patients, 45 had therapy which was guided by positive findings at electrophysiology study (Group 1). Of these, 42 received permanent pacemakers, two were treated with combined permanent pacing and antiarrhythmic drug therapy, and one was treated with antiarrhythmic drug alone. In addition, eight patients without electrophysiologic abnormalities were treated empirically by pacing (Group 2). Finally, 40 patients without electrophysiologic abnormalities received no specific therapy (group 3). At a mean follow-up of 39 months (range two-125 months), recurrence of syncope had occurred in 4% of Group 1 patients, and 25% of Group 3 patients (p < 0.05). No patient in Group 2 had had recurrence. Total mortality was 40%, including 47% of patients in Group 1, 25% of Group 2, and 35% of Group 3. Death was sudden in seven patients. We concluded that among patients with bifascicular block and syncope, therapy directed by findings at electrophysiology study was associated with symptomatic improvement, but mortality was not significantly influenced. Patients with no electrophysiological abnormality have a high recurrence of syncope which may relate either to undetected bradyarrhythmia or ventricular tachycardia. These results highlight some limitations in current assessment, including, for programmed ventricular stimulation, significant differences in both stimulation protocols and the definition of ventricular tachycardia.     

Random coil conformation for extended polyglutamine stretches in aqueous soluble monomeric peptides

Several neurodegenerative diseases have been found to be strongly associated with proteins containing a polyglutamine stretch which is greatly expanded from approximately 20 glutamines in normal individuals to more than 40 in affected individuals. A conformational change in the expanded polyglutamine stretch has been suggested to form the molecular basis for disease onset. Model peptides containing polyglutamine tend to aggregate and become insoluble. We have synthesized readily water-soluble monomeric peptides by flanking polyglutamine stretches with sequences rich in alanine and lysine. Circular dichroism measurements show that polyglutamine stretches of length 9 or 17 adopt a random coil configuration in aqueous solution. We think that in the disease-associated peptides for normal individuals the stretches of ～20 glutamines are in a random coil conformation, whereas in affected individuals the polyglutamine stretch may be in some other conformation. Our method to design soluble monomeric peptides containing extended polyglutamine stretches may be generally useful in studying other highly aggregating peptides.     

Functional dyspepsia: New insights into the pathophysiology

Abstract The pathogenesis of functional dyspepsia remains poorly understood. There is increasing evidence pointing to a predominant role of gastroduodenal visceral hypersensitivity in the pathogenesis, where patients have abnormally reduced gastric and small intestinal sensory thresholds. Motor abnormalities observed in subgroups of patients include delayed gastric emptying, antral hypomotility, gastric dysrhythmias, abnormal gastrointestinal reflexes and small intestinal dysmotility, but these may be secondary pheno nena. The central nervous system modifies peripheral visceral afferent pathways and, hente, psychological factors may possibly alter symptom status. Other putative mechanisms include Helicobacter pylori gastritis and gastric acid hypersecretion or sensitivity, but the role of these remain controversial.     

Recognition of Dementia in General Practice: Comparison of General Practitioners' Opinions with Assessments Using the Mini-Mental State Examination and the Blessed Dementia Rating Scale

Mant A, Eyland E A, Pond D C, Saunders N A and Chancellor AH B. Recognition of dementia in general practice: comparisonof general practitioners' opinions with assessments using themini-mental state examination and the Blessed dementia ratingscale. Family Practice 1988; 5: 184–188. In a study of 226 elderly residents in a retirement villagein Sydney, Australia, general practitioners' opinions aboutdementia status had high positive and negative predictive valuesand high specificity, but low sensitivity when evaluated againstthe mini-mental state examination and the Blessed dementia ratingscale. General practitioners were found to disagree with thesetwo measures more often when patients were in advanced old age,and when they considered the patients to be depressed. We concludethat the general practitioner can increase his or her sensitivityto dementia in the elderly by use of either measure.     

Stem Cell Migration and Proliferation During Severe Anemia

The pluripotential stem cell (CFU) compartment of marrow and spleen wasevaluated in mice subjected to an intense erythroid stimulus associated withphenylhydrazine-induced anemia. Erythroid hyperplasia occurred in both marrow and spleen. CFU in the marrowgradually declined to approximately 50per cent of control levels (day 5) whiletheir numbers in the spleen increased(fourfold) by day 3 and were maintainedat this level for several days. Thesechanges in numbers of marrow andsplenic CFU were not associated withCFU proliferation. Thereafter, CFU inthe marrow, but not in the spleen, entered active cell cycle. The data suggestthat CFU migrate from marrow to spleenduring the demands of severe anemia.The induction of marrow CFU into cyclefurther suggests a negative feedback,which, perhaps through cell-cell interaction, maintains stem cells at a criticalcompartment size. The failure of splenicCFU to cycle may reflect the converseeffect, i.e. an inhibition on stem cell proliferation in the wake of an expandedstem cell pool.

Submitted on March 17, 1970 Revised on May 14, 1970 Accepted on June 9, 1970     

LATE ONSET HUNTINGTON'S DISEASE AS A CAUSE OF DEMENTIA: WHERE SHOULD THE CLINICIAN'S INDEX OF SUSPICION LIE?

Our experience with two genetically confirmed cases of late onset Huntington's disease (HD) in a longitudinal dementia research study suggested that clinical misdiagnosis can easily occur. We therefore undertook genetic testing for HD in a further 84 elderly subjects, 81 of whom had come to postmortem; 75 subjects had dementia and nine were normal controls. A quarter of the demented group had demonstrated extrapyramidal symptoms in life but in none had HD formed part of the differential diagnosis. Although no genetically confirmed cases were found in this second group, the original cases serve as a reminder that late onset HD is a cause of dementia. Genetic confirmation should be sought when the condition forms part of the final differential diagnosis. Further studies conducted in the routine clinical setting are now required since it is in this environment that late onset HD is likely to be misdiagnosed in favour of other forms of dementia.     

Integration of Merged Delayed‐Enhanced Magnetic Resonance Imaging and Multidetector Computed Tomography for the Guidance of Ventricular Tachycardia Ablation: A Pilot Study

MDCT/MRI Fusion for the Guidance of VT Ablation . Background: Delayed enhancement (DE) MRI can assess the fibrotic substrate of scar‐related VT. MDCT has the advantage of inframillimetric spatial resolution and better 3D reconstructions. We sought to evaluate the feasibility and usefulness of integrating merged MDCT/MRI data in 3D‐mapping systems for structure–function assessment and multimodal guidance of VT mapping and ablation. Methods: Nine patients, including 3 ischemic cardiomyopathy (ICM), 3 nonischemic cardiomyopathy (NICM), 2 myocarditis, and 1 redo procedure for idiopathic VT, underwent MRI and MDCT before VT ablation. Merged MRI/MDCT data were integrated in 3D‐mapping systems and registered to high‐density endocardial and epicardial maps. Low‐voltage areas (<1.5 mV) and local abnormal ventricular activities (LAVA) during sinus rhythm were correlated to DE at MRI, and wall‐thinning (WT) at MDCT. Results: Endocardium and epicardium were mapped with 391 ± 388 and 1098 ± 734 points per map, respectively. Registration of MDCT allowed visualization of coronary arteries during epicardial mapping/ablation. In the idiopathic patient, integration of MRI data identified previously ablated regions. In ICM patients, both DE at MRI and WT at MDCT matched areas of low voltage (overlap 94 ± 6% and 79 ± 5%, respectively). In NICM patients, wall‐thinning areas matched areas of low voltage (overlap 63 ± 21%). In patients with myocarditis, subepicardial DE matched areas of epicardial low voltage (overlap 92 ± 12%). A total number of 266 LAVA sites were found in 7/9 patients. All LAVA sites were associated to structural substrate at imaging (90% inside, 100% within 18 mm). Conclusion: The integration of merged MDCT and DEMRI data is feasible and allows combining substrate assessment with high‐spatial resolution to better define structure–function relationship in scar‐related VT. (J Cardiovasc Electrophysiol, Vol. 24, pp. 419‐426, April 2013)     

Malfunction of Subpectorally Implanted Cardiac Resynchronization Therapy Defibrillators Due to Weakened Header Bond

Malfunction of Subpectorally Implanted Cardiac Resynchronization Therapy . Background: Implantable cardioverter defibrillator (ICD) implantation has increased significantly over the last 10 years. Concerns about the safety and reliability of ICD systems have been raised, with premature lead failure and battery malfunctions accounting for the majority of reported adverse events. We describe the unique mode of presentation, diagnosis, and management of cardiac resynchronization therapy defibrillators (CRT‐D) malfunctions that were caused by weakened bonding between the generator and header. Methods and Results: Between June 2008 and December 2009, 22 Teligen? ICDs and 24 Cognis? CRT‐Ds were implanted subpectorally at our institution, until a product advisory was issued. Of 24 Cognis? CRT‐D implants, 3 patients presented with CRT‐D malfunctions. All our cases presented with initially intermittent and then persisting increases in shock lead impedance, associated with nonphysiological noise in the shock electrogram channels. These issues were rectified by generator change. Postexplant laboratory analysis confirmed inadequate bonding between device header and titanium casing in all cases, resulting in loosening and rocking of the header followed by fatigue‐induced fracture of the shock circuitry. Conclusion: Weakened bonding between the header and generator casing of subpectorally implanted CRT‐Ds can result in fractures and malfunction of the HV circuit. Physicians monitoring patients with devices affected by the product advisory should remain vigilant in order to diagnose and manage similar device malfunction expediently. (J Cardiovasc Electrophysiol, Vol. 24, pp. 351‐355, March 2013)