Biomedical subjects
Publications and source records attributed to D H Nichols.
Posterior vaginal repair is often poorly understood and ineffectively performed. The goals of reconstructive surgery emphasize relief of symptoms and restoration of normal anatomic relationships and of function. A useful method to preoperatively determine posterior vaginal wall weakness is outlined along with a surgical description of important steps in surgical reconstruction.
There are several treatments from which to choose for the patient with symptomatic uterine prolapse who wishes to retain fertility. Transabdominal construction of a sacrocervical "ligament" with transplanted fascia lata femoris is a useful solution to this problem. The technique is described.
By careful observation of the physical findings in the patient complaining of one of the disorders of genital prolapse, it should be possible to discern the origin of the symptoms and therefore to devise an appropriate treatment that would remedy by reconstruction all of the signs of anatomic weakness. The goals of reconstructive surgery are three: to relieve the symptoms, to restore the anatomy to normal, and to restore the function to normal. When any element of weakness in the pelvic floor is found to be sufficient to produce symptoms that warrant repair, it is the responsibility of the surgeon to identify all the sites of weakness, so that all may be repaired at the same time, sparing the patient the expense, pain, and inconvenience of future readmission for further surgery. These weaknesses all relate to deficiencies of the six major organ systems that are involved in the support of the female pelvis, which may be damaged singly or in any combination. There are various types of cystocele, each of which must be carefully excised if an appropriate surgical treatment is to be given. This may involve correction of cystocele, enterocele, rectocele, prolapse of the uterus, and posthysterectomy prolapse of the vaginal vault. With enterocele, it is possible to correlate the four common types of enterocele with their location, which in turn correlates directly with their treatment. The prevention of complications is emphasized along with the treatment of certain mechanical complications easily recognized at the time of surgery.
In the mouse embryo, neural crest mesenchyme associated with the first and second pharyngeal arches escapes from the epithelium that forms the tips of the midbrain/rostral hindbrain and preotic hindbrain neural folds. To investigate the ultrastructure of crest formation, embryos with four to eight pairs of somites were processed for transmission electron microscopy. In the earliest event related to crest formation, crest precursors in the midbrain/rostral hindbrain elongated and moved all or most of their contents to the basal region of the epithelium. Elongation was probably mediated by apical bands of microfilaments and longitudinally oriented microtubules. Elongated cells then relinquished apical associations while nonelongated cells maintained those associations and withdrew from the basal lamina. This resulted in an epithelium stratified into apical and basal (crest precursor) layers. The coalescence of enlarging extra-cellular spaces opened a delaminate gap between the two layers. Additional crest precursors entered this gap from the apical layer. From the time crest precursors began moving basally, some formed microfilament- and/or microtubule-containing processes, which penetrated the basal lamina. Some of these cells moved their contents into the larger, microtubule-containing processes, perhaps thereby escaping from the epithelium. Soon after elongating cells appeared, the basal lamina beneath the epithelium began to degrade in a pattern unrelated to process formation. This ultimately resulted in disruption of the lamina, dispersal of the basal layer of the epithelium, and release of the crest precursors in the delaminate gap. Once crest formation was complete, the apical layer reformed a basal lamina on a patch-by-patch, cell-by-cell basis. In the preotic hindbrain, elongating crest precursors apparently forced their basal faces through the basal lamina and then relinquished apical association to escape. As a result, the lamina was disrupted before the epithelium could stratify, and enlarged extracellular spaces appeared among mesenchymal cells rather than creating a delaminate gap. The failure of elongation to disrupt the basal lamina in the midbrain/rostral hindbrain and its success in the preotic hindbrain might be due to less-vigorous, less-concerted elongation in the midbrain/rostral hindbrain or to earlier, more rapid degradation of the lamina in the preotic hindbrain.
The trigeminal placode is a thickened region of ectodermal epithelium located along the side of the embryonic head. Mesenchyme escapes from the placode to form neurons of the trigeminal (V) ganglion. To further our knowledge of the morphogenesis of this escape, plastic thick sections were cut from mouse embryos and stained for light microscopy by using a technique which revealed escaping mesenchyme. The escape of trigeminal mesenchyme began at approximately 12 somites of age and was substantially complete by 30 somites. These results provided spatial/temporal orientation for a subsequent electron microscopic study. The first ultrastructural manifestation of escape was the penetration of an otherwise continuous basal lamina by small cell processes. The presence of longitudinally oriented microtubules within these processes suggests that mesenchymal cells escape through the basal lamina by using microtubules to direct/move their contents (e.g., the cell nucleus) into an enlarging process. Nuclei were distorted as they passed into these processes. This distortion suggests that basal lamina, together with a possible contribution from basal microfilaments, forms a rigid obstruction which is disrupted in the region from which a process is formed. In some cases a collar of basal lamina was observed around the necks of processes, but their distal membranes were invariably lamina-free. This lamina-free membrane is possibly that which is newly formed to accommodate the growing process. In later stages of escape, instances were observed in which the lamina was completely absent beneath an escaping cell and partially degraded beneath adjacent cells as well. These instances suggest that enzymatic digestion may play a role in degrading the lamina during mesenchymal escape. Apical desmosomes were often retained beyond the initial stages of escape. Mechanisms involved in their disruption are thus not among those which initiate escape.
Murine neural crest mesenchyme begins its escape from columnar epithelium near the tips of the midbrain-rostral hindbrain neural folds at 4+ to 5 somites of age. At that time the tip of each fold is located dorsolateral to the pharynx. Once crest formation is complete at this earliest site, it leaves behind both crest mesenchyme and overlying squamous epithelium. Crest formation then progresses medially, into the lateral margin of the neural plate. At the same time, this lateral margin elevates as the tip of the neural fold. By the time crest formation ceases at approximately 10 somites, the result of these simultaneous activities is to passively distribute the earliest mesenchyme, formed from the lateralmost epithelium, dorsolateral to the pharynx and the later, more medially derived mesenchyme lateral to the neural tube. Once formed, the crest mesenchyme dorsolateral to the pharynx is displaced ventromedially in a narrow, transient subectodermal space functionally similar to that observed in the chick embryo. Displacement might result from cell motility or the formation of matrix-filled spaces between cells of the mesenchyme. Displaced cells are closely associated with the overlying columnar epithelium. This association precedes their subsequent induction and may reflect preliminary patterning. The crest mesenchyme passively distributed lateral to the neural tube is subsequently displaced medially. Here the formation of enlarged (matrix-filled?) spaces is clearly involved in the initial displacement. Displaced cells proliferate to form the anlage of the trigeminal ganglion. The other major contributor to this ganglion is the trigeminal placode. The placodal epithelium is located dorsolateral to the pharynx of the 12-somite embryo. If the epithelia of the head maintain their relative positions, this placode is derived from the squamous epithelium formed together with the earliest crest mesenchyme. If not, an alternative source is the columnar epithelium located ventromedial to the tip of the 4+- to 5-somite neural fold.
A randomized, double-blind, multicenter trial was initiated to compare the safety and efficacy of piperacillin, cephalothin and cefoxitin in the prophylactic treatment of patients undergoing vaginal hysterectomy. The total dose of each antibiotic was 6 grams given in three equally divided doses. A satisfactory prophylactic response was obtained in 143 of 151 (95 per cent) patients treated with piperacillin, in 82 of 87 (94 per cent) patients treated with cephalothin and in 57 of 60 (95 per cent) patients treated with cefoxitin. The pooled data indicated that the piperacillin treatment group did not differ from the combined cephalosporin treatment groups with respect to prophylactic response, presence of febrile morbidity, fever index, duration of postoperative hospitalization and incidence of reported adverse experiences.
Adnexal torsion is an interesting, uncommon, and potentially lethal condition that may arise most unexpectedly in women of any age, but particularly during the reproductive years. It is generally unilateral and may involve either normal or pathologically enlarged ovary or tube, or both organs. The condition may be partial or complete, the latter often resulting in gangrene and marked exacerbation of symptoms. If untreated, it may progress to necrosis and gangrene, followed by peritonitis, which may be lethal. Prompt diagnosis, in which timely diagnostic laparoscopy and ultrasound evaluation of the pelvis may be helpful, provides the opportunity for prompt laparotomy with untwisting of the torsion and stabilization of the adnexa by suture and cystectomy, if possible, extirpation if not. Organ conservation requires a clear need to preserve reproductive or ovarian function, so cystectomy is generally preferable to oophorectomy.
Five sonographic cases are presented with images that demonstrate normal arcuate arteries and peripheral uterine blood vessels. These vascular structures are shown in both the longitudinal and transverse sections, and should not be confused with pathology such as Nabothian cysts, hydrosalpinx, pelvic inflammatory disease, hydatid cysts of Morgagni, endometriosis, or abnormal pelvic varices.
When pelvic reconstructive surgery is being considered, it is important that the presence of cystocele be carefully and accurately assessed preoperatively and intraoperatively so that appropriate correction can be achieved. Continence is under the influence of urethral tone and the response of the proximal urethra to changes in intra-abdominal pressure. Cranial elevation of a rotated vesicourethral junction to a normal retropubic position should be provided. Any surgical technique that alters the normal axis of the vagina should be accompanied by simultaneous obliteration of the cul-de-sac of Douglas to lessen the chance of postoperative enterocele and subsequent eversion of the vault of the vagina. When massive vaginal eversion causes displacement of the vesicourethral junction, a restoration of vaginal depth and axis by posthysterectomy transvaginal sacrospinous colpopexy with appropriate colporrhaphy will relocate a defective urethrovesical site to a higher and retropubic level within the pelvis, where the proximal urethra may once again be responsive to changes in intra-abdominal pressure.
When pelvic reconstructive surgery is being considered, it is important that the presence of cystocele be carefully and accurately assessed preoperatively and intraoperatively so that appropriate correction can be achieved. Continence is under the influence of urethral tone and the response of the proximal urethra to changes in intra-abdominal pressure. Cranial elevation of a rotated vesicourethral junction to a normal retropubic position should be provided. Any surgical technique that alters the normal axis of the vagina should be accompanied by simultaneous obliteration of the cul-de-sac of Douglas to lessen the chance of postoperative enterocele and subsequent eversion of the vault of the vagina. When massive vaginal eversion causes displacement of the vesicourethral junction, a restoration of vaginal depth and axis by post-hysterectomy transvaginal sacrospinous colpopexy with appropriate colporrhaphy will relocate a defective urethrovesical site to a higher and retropubic level within the pelvis, where the proximal urethra may once again be responsive to changes in intra-abdominal pressure.
It is evident that the maintenance and reestablishment of urinary continence is in large part dependent, during times of intraabdominal stress, upon maintenance of an intraurethral pressure higher than that within the bladder. It is important that the presence of cystocele be carefully and accurately assessed preoperatively and intraoperatively so that correction appropriate to its etiologic circumstance can be achieved. Continence is under the influence of urethral tone, as well as the response of the distal urethra to changes in intraabdominal pressure. Cranial elevation of the vesicourethral junction, as may be required, may be provided by any one of several different or combined surgical techniques. When vaginal inversion causes displacement of the vesicourethral junction, a restoration of vaginal depth and axis by transvaginal sacrospinous fixation with appropriate colporrhaphy will relocate a defective urethrovesical site to a higher level within the pelvis where it may once again be responsive to changes in intraabdominal pressure.
If retention or removal of the postmenopausal ovary is to receive similar attention at vaginal hysterectomy as at abdominal hysterectomy, more consideration must be given to the development of safe and secure techniques for vaginal oophorectomy. Technical problems relating to exposure and accessibility are obviously more pronounced with a transvaginal surgical approach. When salpingo-oophorectomy is surgically inaccessible, oophorectomy may often be performed. A stitch embodying a single penetration of the mesovarium is described for suture ligation.
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