Acute appendicitis in the developing world is a morbid disease

IntroductionAcute appendicitis in the developing world has a markedly different disease profile to that in the developed world.MethodsA retrospective study was undertaken over a four-year period at a university hospital in South Africa to review the disease spectrum and the clinical outcome of acute appendicitis.ResultsA total of 1,004 patients (54% male, median age: 18 years) with intraoperatively confirmed appendicitis were reviewed. Over half (56%) were from the urban district within the city of Pietermaritzburg and the remaining 44% were from the rural health district. The median duration of illness from onset to definitive care was 4 days. Sixty per cent of appendices were perforated and associated with intra-abdominal contamination. Forty per cent of patients required reoperation to control intra-abdominal sepsis. Ten per cent required admission to the intensive care unit. The median overall length of hospital stay was 5 days. The mortality rate was 1%.Rural patients had a longer median duration of illness (3 vs 5 days, p<0.001) as well as a more advanced disease profile associated with perforation and severe intra-abdominal sepsis (19% vs 71%, p<0.001). Female patients had a longer median duration of illness (3 vs 4 days, p<0.001), were more likely to present with severe intra-abdominal sepsis (31% vs 54%, p<0.001) and were more likely to require a laparotomy (50% vs 73%, p<0.001). The total cost of managing the entire cohort of 1,004 patients over the 4-year period was £2,060,972.ConclusionsAcute appendicitis in South Africa is a serious disease associated with significant morbidity. Late presentation is common. Female and rural patients have the worst clinical outcomes, with significant cost to the health system.     

Factors Predisposing to the Development of Atrial Fibrillation

Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so-called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff-Parkinson-White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.     

Plasminogen activator inhibitor type‐1 is an independent marker of metabolic disorders in young adults born small for gestational age

Summary. Background: Metabolic syndrome (MS) has been associated with being born small for gestational age (SGA). In epidemiological studies plasminogen activator inhibitor type‐1 (PAI‐1) levels have been associated with MS. Few studies have examined this association in subjects born SGA. Patients and methods: Five hundred and fifty‐seven SGA adults (birth weight < 10th percentile) were compared with 671 subjects with a birth weight between the 25th and 75th percentiles (control group). MS was defined using the World Health Organization (WHO) definition. Active PAI‐1 was measured on citrated plasma with bio‐immunoassay. Results: MS was more prevalent in the SGA group (8.7%) than in the control group (5.5%; P = 0.03). In both groups, PAI‐1 concentrations were significantly correlated with waist circumference, plasma triglycerides, homeostatic model assessment‐insulin resistance (HOMA‐IR) and associated with male sex and MS. PAI‐1 concentrations were significantly increased in the SGA group (12.2 ± 21.2 vs. 10.0 ± 13.5 IU mL^?1, P = 0.03) and this remained after adjustment of metabolic variables (P = 0.009). PAI‐1 concentrations above 4.9 IU mL^?1 (= median of PAI‐1 concentration in the control group) were present in 94% of the subjects with MS. Moreover, the adjusted odds ratio (OR) for having elevated PAI‐1 was 1.48 (1.08; 1.95) in the SGA group in comparison with the control group (P = 0.005). Conclusions: PAI‐1 plasma concentrations were significantly increased in SGA subjects independently of MS. These data suggest that elevation of PAI‐1 concentrations might be an indication of an abnormal secretion at the level of the adipose tissue, endothelial cells or liver and implicated in metabolic disorders reported in SGA subjects.     

Alternate Ventriculo-Atrial Wenckebach Conduction during Ventricular Tachycardia

Although pacing-induced ventriculo-atrial (VA) Wenckebach conduction has been previously described, the occurrence of this phenomenon during ventricular tachycardia has received little attention. The latter is defined as 2:1 VA block in which the conducted beats show progressive lengthening of VA conduction until the sequence is terminated by two or three blocked ventricular beats. This phenomenon was observed in a 16-year-old boy who underwent electrophysiologic study for ventricular tachycardia as a late complication of surgical correction of tetralogy of Fallot. During pacing-induced ventricular tachycardia with a morphology similar to that of the spontaneous tachycardia, 8:4 alternating VA block was observed. This sequence suggested that the AV node was the site of block, the 2:1 block being located at the upper level, and the VA Wenckebach block at the lower level. Alternate VA Wenckebach conduction appears as a possible cause of variation in atrial depolarization intervals during ventricular tachycardias with short cycle lengths.