Prevention of genital prolapse following Burch colposuspension: comparison between two surgical procedures

 Our objective was to evaluate the efficacy of cul-de-sac obliteration in preventing pelvic floor anatomical defects formation following Burch colposuspension. We evaluated 441 patients who had undergone Burch colposuspension. The patients were divided into two groups: group A (132 patients) who underwent Burch colposuspension only, and group B (309 patients) who had had a concomitant cul-de-sac obliteration. Cul-de-sac obliteration was performed using two different techniques, the Moschocowitz procedure in 131 patients, and approximation of the sacrouterine ligaments in 178 patients. The follow-up period was 8.6 years (range 3–16). In total we found 43/441 (9.7%) postoperative anatomical defects. Obliteration of the cul de sac significantly (P<0.0001) reduced the formation of anatomical defects compared to Burch colposuspension. In a comparison of the two surgical procedures for cul-de-sac obliteration, the approximation of the sacrouterine ligaments was significantly more effective than either the Moschcowitz procedure (P<0.001) or the Burch colposuspension alone (P<0.001). The Moschcowitz procedure reduced the formation of anatomical defects to 15/131 (11.4%) compared to Burch colposuspension only (25/132; 18.9%), but statistically the difference was insignificant. The time of anatomical defect detection was significantly reduced after cul-de-sac obliteration: 2 years 6/25 (24%) in group A compared to 1/8 (5.5%) in group B (P<0.01). After 5 years the detection rate was 64% (16/25) and 22.2% (4/18) respectively (P<0.01). It was concluded that cul-de-sac obliteration using approximation of the sacrouterine ligaments significantly reduced the incidence of anatomical defect formation following Burch colposuspension. A long follow-up period is needed to evaluate the truce incidence. Received: 2 October 2002 / Accepted: 2 July 2002     

A not-so-basic case of metabolic alkalosis: an analysis featuring Leendert Paul and emphasizing Occam’s razor

A patient had the onset of a severe degree of metabolic alkalosis associated with a very large daily loss of diarrheal fluid. Because the expected acid-base disorder in this setting is metabolic acidosis, factors that could result in the markedly increased concentration of bicarbonate (HCO₃⁻) in plasma (P ₃) were sought. In our approach, there is an emphasis on electroneutrality, mass balance, a quantitative analysis, and the application of basic concepts in physiology at the bedside. We suggest that there were 3 major factors that could explain why the P ₃ was so high. First, a severe degree of extracellular fluid volume contraction was probably the most important factor that raised her P ₃. Second, there may have been an unusual way to have an electroneutral addition of HCO₃⁻ and removal of chloride ions from her extracellular fluid compartment. Third, the diarrheal fluid could have contained little HCO₃⁻ because of a down-regulated intestinal secretion of HCO₃⁻. This analysis challenges the traditional pathophysiology of metabolic alkalosis.     

Antibody response to bacteriophage hyaluronidase in acute glomerulonephritis after group A streptococcal infection

In a test of the hypothesis that lysogeny of group A streptococci by a temperate bacteriophage might confer nephritogenicity, 283 sera from 69 patients were examined for IgG and IgM antibodies to M 49 streptococcal bacteriophage hyaluronidase. The IgG and IgM response to bacteriophage hyaluronidase was greatest in M 49 streptococci-infected individuals with nephritis, but M 49 streptococci-infected subjects without nephritis also had a greater immune response than did subjects infected with serotypes other than M 49. Although antibody to bacterial hyaluronidase was detected in all Streptococcus-infected groups, antibody to M 49 streptococcal bacteriophage hyaluronidase usually was found in only M 49 streptococci-infected patients. Although the greatest IgG and IgM antibody response to bacteriophage hyaluronidase can be demonstrated in individuals with glomerulonephritis, the antibody response does not indicate a direct relation of lysogeny and nephritis because subjects with and without nephritis after M 49 streptococcal infection all had a significant rise in antibody titer.     

High frequency of precancerous lesions of gastric cancer associated with Helicobacter pylori and response to treatment,in Chiapas,Mexico

Stomach cancer is the second cause of death in Mexico in patients with malignant tumors. This disease represents a public health problem. A strong association has been described between chronic infection with Helicobacter pylori and gastric cancer. This malignancy is preceded by a series of preneoplastic conditions, including chronic atrophic gastritis (CAG), intestinal metaplasia (IM), and dysplasia. The objective of this study was to establish the prevalence of preneoplastic conditions associated with infection of Helicobacter pylori in the state of Chiapas and its eradication with antibiotics. Persons infected with Helicobacter pylori and with CAG were identified by serology against CagA protein and serologic levels of gastrin. An endoscopy with biopsy was performed at the beginning of the study, and at 6 weeks and 1 year thereafter. A total of 281 people were enrolled and randomly assigned to treatment or placebo group. CAG was found in 59%, IM in 51%, and dysplasia in 13%. In intent-to-treat and per-protocol analysis, Helicobacter pylori was eliminated in 70 and 76%, respectively. These results indicate high frequency of preneoplastic conditions associated with Helicobacter pylori and an excellent eradication rate. They also offer a possible alternative for preventing gastric cancer.     

Intrathoracic pressure fluctuations move blood during CPR: Comparison of hemodynamic data with predictions from a mathematical model

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21–32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was <0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378–426 N), flow was significantly increased when the duration of compression was increased from short (13%–19% of the cycle) to long (40%–47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures. Thus vital organ perfusion pressures and flow for manual external chest compression are dependent on the duration of compression, but not on rates of compression of 60 and 150/min. These data are of course similar to those produced by vest CPR, where intrathoracic pressure is manipulated without sternal displacement, and to those predicted for movement of blood by intrathoracic pressure changes. These data are, however, opposite to those produced by cardiac deformation and to those predicted for movement blood by direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR.