Biomedical subjects
Publications and source records attributed to M R Toglia.
Anorectal disorders are the cause of significant discomfort and embarrassment in women. The onset typically follows childbirth and symptoms increase with age. Anal incontinence, rectovaginal fistula, rectal prolapse, anal fissure, and constipation are considered.
OBJECTIVE: To examine the anatomy of the internal and external anal sphincters in the area of midline obstetric lacerations, to gain insight into sphincter damage and repair. METHODS: The length, craniocaudal extent, and overlap of the internal and external anal sphincters in the perineal body were measured in 17 cadavers. Further anatomic observations were made in four sets of whole pelvis cross-sections taken in the sagittal, coronal, and transverse planes. During the repair of 20 acute fourth-degree lacerations, observations were made to determine the internal sphincter visibility following birth. RESULTS: The external and internal and sphincters overlap by 17.0 mm (standard deviation [SD] 6.9), with the internal sphincter lying between the external sphincter and the anal canal. The internal sphincter extends an additional 12.2 mm (SD 5.9) cranial to the proximal extent of the external sphincter, whereas the caudal margin of the internal sphincter lies 3.7 mm (SD 7.2) cranial to the distal margin of the external sphincter. In pregnant women who sustained a fourth-degree laceration, we found that the internal sphincter can be identified as a rubbery white layer adjacent to the anal submucosa lying between the external sphincter and the anal canal. CONCLUSION: The internal anal sphincter lies between the anal mucosa and the external anal sphincter and extends more than a centimeter above the cranial margin of the external sphincter, a region where it is disrupted when a fourth-degree obstetric laceration has occurred.
Pregnancy is widely recognized to be a physiologic state with a markedly elevated risk for thromboembolic complications. The diagnosis and management of venous thromboembolic events during pregnancy, however, remains controversial because of the lack of prospective, randomized trials that have included pregnant women. Significant progress has been made in the last 10 years in the management of these conditions in the nonpregnant patient and strong clinical guidelines have been established recently. Obstetrician-gynecologists may modify these guidelines and apply them to the pregnant patient based on their knowledge of the physiologic changes in pregnancy. Objective diagnostic techniques should be used liberally when the diagnosis of deep vein thrombosis or pulmonary emboli is considered because early intervention may prevent serious maternal sequelae including death. Heparin remains the anticoagulant of choice during pregnancy because of its proven safety for both the patient and the fetus. It is likely that long-term anticoagulation is necessary when venous thromboembolism occurs antepartum, although the most efficacious regimen has yet to be established. There is some concern about the prolonged use of heparin during pregnancy, particularly regarding the risk of osteopenia.
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OBJECTIVE: To determine the incidence of pelvic fluid collections after hysterectomy, detected by transvaginal sonography and pelvic examination, and to correlate these findings with postoperative febrile morbidity. METHODS: Thirty-eight women, aged 26-65, were studied by pelvic examination and transvaginal sonography 1-5 days after vaginal or abdominal hysterectomy. The sonographer was unaware of the patient's clinical course before the examination and was not involved in clinical decision making. The results of the study were not made available to the treating physician. RESULTS: Transvaginal sonography revealed a sonolucent mass consistent with a fluid collection above the vaginal cuff ranging in size from 3.9-74.7 cm3 in 13 of 38 patients (34.2%). Only one of the 13 fluid collections was evident on pelvic examination performed before ultrasound. Nine of 13 women (69.2%) with fluid collections developed febrile morbidity, compared to three of 25 (12%) who did not have fluid collections (P = .006, Fisher exact test). Cuff cellulitis was clinically diagnosed in seven of the 13 women (53.8%) with fluid collections, compared to none of 25 women without fluid collections (P < .001, Fisher exact test). CONCLUSIONS: Pelvic fluid collections are common after hysterectomy. Women who develop post-hysterectomy fluid collections appear to be at increased risk for the development of febrile morbidity and cuff cellulitis. Transvaginal sonography may facilitate the diagnosis of post-hysterectomy pelvic fluid collections, which are not readily detected by pelvic examination.
OBJECTIVE: To gather, synthesize, and present useful scientific information concerning the anal continence mechanism that will aid obstetrician-gynecologists in managing vaginal birth and evaluating women with anal incontinence not caused by disruption of the external anal sphincter. DATA SOURCES: Sources included a Medline search and reference lists of relevant articles and standard textbooks. METHODS OF STUDY SELECTION: Articles were identified that contained scientific data on the pathophysiology of anal incontinence, the influence of vaginal delivery on the continence mechanism, and therapeutic measures. Only those presenting original research results were included. Studies concerned exclusively with surgical management of the ruptured perineum were excluded. DATA EXTRACTION AND SYNTHESIS: All articles were reviewed and the physiologic data summarized. These findings were grouped by their relevance to each anatomical or physiologic issue involving anal incontinence and by whether they considered the issue of injury at the time of vaginal delivery. The data were then assembled into a functionally oriented overview of the continence mechanism. The subject of injury at the time of vaginal delivery was considered separately against a background of continence pathophysiology. CONCLUSION: Vaginal delivery may initiate damage to the continence mechanism by direct injury to the pelvic floor muscles, damage to their motor innervation, or both. Additional denervation may occur with aging, resulting in a functional disability many years after the initial trauma. These factors should be kept in mind when conducting vaginal birth and planning therapy for anal incontinence.
An automatic pressure infusion system equipped with a fluid warmer has been developed for rapid intravenous infusion of homeothermic fluids. The use of this system for irrigation during operative laparoscopy provides the surgeon with the ability to irrigate at a relatively high flow while avoiding the hypothermic effects of irrigation with cool fluids.
The hepatic removal of plasma chylomicrons was determined for rats fed the following diets: a) containing no triglyceride, b) regular chow diet with 4.5% of its mass as lipid and, c) a corn oil-supplemented chow with triglyceride accounting for 20% of the mass. The fractional hepatic uptake of either radiolabeled chylomicrons or a triglyceride emulsion was reciprocally related to the amount of lipid in the diet. The animals receiving only carbohydrate and protein calories had the most active hepatic uptake of particulate triglyceride and were observed to have a significant decrease in the plasma concentration of the C apolipoproteins. The addition of either C-I, C-II, or C-III apoproteins to the triglyceride emulsion prior to intravenous injection produced a significantly lower hepatic triglyceride recovery of emulsions containing apoC-III. When the plasma of animals fed a fat-free diet was supplemented with human C-III-1 apolipoprotein, the distribution into the liver of either enterally administered fatty acid or parenteral triglyceride was diminished. The triglyceride content in the liver of the rats fed fat-free or corn oil-supplemented diets was significantly greater than that of the control rats and composition was somewhat similar to that of lymph triglyceride. The studies indicate an important influence of dietary lipid on both the partition of plasma triglyceride into the liver and the steady state hepatic triglyceride content.