Can pelvic floor injury secondary to delivery be prevented?

The number of women suffering from pelvic floor disorders (PFD) is likely to grow significantly in the coming years with a growing older population. There is an urgent need to investigate factors contributing to the development of PFD and develop preventative strategies. We have reviewed the literature and analyzed results from our own study regarding the association between delivery mode, obstetrical practice and fetal measurements, and damage to the pelvic floor. Based on our findings, we have suggested a flowchart helping the obstetrician to conduct vaginal delivery with minimal pelvic floor insult. Primiparity, instrumental delivery, large fetal head circumference, and prolonged second stage of delivery are risk factors for PFD. Pelvic floor integrity should always be seriously considered in every primiparous woman. All efforts should be aimed at minimizing any insult, which might have a significant impact on the woman’s pelvic integrity and future quality of life.     

Can pelvic floor dysfunction after vaginal birth be prevented?

Introduction and hypothesis

Significant breakthroughs in our understanding of pelvic floor dysfunction have occurred in the past two decades. The next step is to translate this understanding into effective preventative and early intervention strategies to minimize maternal morbidity from vaginal birth. We have learned enough to chart a course toward prevention.

Methods

This article outlines some major advances in understanding the pathophysiology of pelvic floor dysfunction and suggests strategies for future prevention research.

Results

Vaginal birth is the primary risk factor for the development of pelvic floor disorders and this is compounded by forceps use. Age, race, and genetics are also risk factors. Steps to prevent or minimize the development of pelvic floor problems include moderating forceps use and utilizing risk assessment tools to offer cesarean delivery to those at greatest risk.

Conclusion

These actions would represent one giant step forward in advancing the practice of obstetrics into the modern age of personalized medicine.

     

Can sex survive pelvic floor surgery?

Introduction/hypothesis  

Sexual function in women with pelvic organ prolapse (POP) and stress urinary incontinence (SUI) is adversely affected, but data reporting sexual function following surgery are limited. We aimed to determine effect of pelvic reconstructive surgery on sexual function and to evaluate effect of additional continence procedures.     

Can prostate cancer be prevented?

The goal of primary chemoprevention is to decrease the incidence of a given cancer, simultaneously reducing both treatment-related adverse events and mortality. Prostate cancer is an attractive and appropriate target for primary prevention because of its incidence, prevalence, and disease-related mortality; its long latency and molecular pathogenesis; and epidemiologic data indicating that modifiable environmental factors may decrease risk. The Prostate Cancer Prevention Trial (PCPT) demonstrated that finasteride can prevent prostate cancer, albeit with an apparently increased risk of high-grade disease. A substantial amount of epidemiologic, molecular, and clinical evidence suggests that both selenium and vitamin E might also prevent prostate cancer, and this combination is being tested in the Selenium and Vitamin E Cancer Prevention Trial (SELECT). Ultimately, the adoption of a preventive strategy hinges on its potential benefits weighed against the potential risks of the specific agents used.     

Can stronger pelvic muscle floor improve sexual function?

Introduction and hypothesis

This study aims to evaluate the association between pelvic floor muscle (PFM) strength and sexual functioning.

Methods

Retrospective chart review of consecutive all women who were referred with a primary complaint of sexual dysfunction. Women underwent standardized clinical evaluation including pelvic muscle strength which was ranked from 0 (weak) to 2 (strong). The duration of pelvic muscle contraction was also recorded in seconds. Sexual function was evaluated by using a validated questionnaire, the Female Sexual Function Index (FSFI).

Results

One hundred seventy-six women with a mean age of 37?±?11 years were included. Women with strong or moderate PFM scored significantly higher on the FSFI orgasmic and arousal domains than women with weak PFM (5.4?±?0.8 vs. 2.8?±?0.8, and 3.9?±?0.5 vs. 1.7?±?0.24, respectively; P?<?0.001). The duration of PFM contraction was correlated with FSFI orgasmic domain and sexual arousal (r?=?0.26, P?<?0.001; r?=?0.32, P?<?0.0001, respectively).

Conclusions

Our findings suggest that both the orgasm and arousal function are related to better PFM function.     

Can postpyelonephritic renal scarring be prevented?

Pyelonephritis in childhood may, in the worst cases, lead to long-term cardiovascular morbidity due to tubulointerstitial renal scarring. Renal damage is the end result of an interplay between (1) urinary tract anatomy and function, (2) bacterial virulence factors, and (3) the host innate immune system, which on the one hand manages bacterial clearance, but on the other causes tubulointerstitial inflammation, which underlies the renal scarring. It is unclear how common postpyelonephritic scarring is, and how many of the "scars" in fact represent congenital renal hypoplasia. We do, however, know that some situations have an increased risk for scars, i.e., large renal-uptake defects on initial renal scintigraphy or pyelonephritis in young girls with dilating vesicoureteral reflux. It seems logical that antiinflammatory or antioxidant therapy given concomitantly with antibiotics should lower the risk of postpyelonephritic scarring. Animal studies give some support to this idea, but research on humans has been surprisingly scant. In this issue of Pediatric Nephrology, we publish a study that indicates that antioxidant therapy with vitamin A or E given to children with pyelonephritis may indeed lower the risk for renal scarring. This is a track that needs to be pursued further.     

Can acute renal failure be prevented?

Correction of salt and volume depletion is paramount in the prevention of renal damage. Measures which stimulate intense filtration of glomeruli in acute renal failure, such as the use of atrial natriuretic peptide analogues, theophylline, dopamine, or growth factors should be regarded with caution, since they all increase metabolic workload in the outer medulla and hence aggravate medullary hypoxia. Neither frusemide, dopamine nor dopexamine have been shown to be better than aggressive saline loading in preventing acute renal failure in at risk patients. Until new clinical studies emerge, avoidance of nephrotoxic insults where possible, monitoring of circulating concentrations of potentially nephrotoxic drug levels and volume loading coupled with supportive measures is recommended. When volume depletion persists, usual blood pressure cannot be restored and patients remain oliguric, early referral to the intensive care unit is paramount. The mortality rate in patients with acute renal failure is high; therefore, measures which reduce the incidence and progression of renal dysfunction will be of benefit.     

Can bone loss in rheumatoid arthritis be prevented?

Rheumatoid arthritis (RA) is a systemic inflammatory disease that can lead to local joint deformations (bone erosions and joint space narrowing) and to extra-articular phenomena, including generalized osteoporosis. In addition, in patients with RA, the risk of vertebral and nonvertebral fractures is doubled. High disease activity (inflammation), immobility, and glucocorticoid use are common factors that substantially increase fracture risk in these patients, on top of the background fracture risk based on classical risk factors such as high age, low body mass, and female gender. New insights on the links between the immune system and the bone system, the field of osteoimmunology, have shown that local and generalized bone loss share common pathways. The receptor activator of nuclear factor κB ligand/osteoprotegerin pathway (RANKl/OPG) is one of the most important pathways, as it is (strongly) upregulated by inflammation. In modern treatment of RA with biologics, for example, TNFα-blocking agents and combination therapy of conventional disease-modifying antirheumatic drugs (DMARDs), clinical remission is a realistic treatment goal. As a consequence, in recent studies, it has been documented that both local and generalized bone loss is absent or minimal in those patients who are in clinical remission.     

Can secondary extremity compartment syndrome be diagnosed earlier?

BACKGROUND: In 2002, our institution published a 5-year retrospective review of 10 patients who developed secondary extremity compartment syndrome (SECS) with a mortality rate of 70%. Since then, we have aggressively screened for the development of SECS in high-risk patients. We postulate that awareness of SECS and vigilant monitoring for its development would result in earlier diagnosis and treatment and improved outcome. METHODS: Retrospective review of all patients at a level I trauma center developing SECS from 2002 to 2006. Data collected included demographics, mechanism of injury, injury complex, blood transfused prior to development of SECS, affected extremities, creatinine, creatine phosphokinase, management, and outcome. RESULTS: Seventeen of 11,468 trauma patients (.148%) developed SECS. Mean admission hematocrit was 31.7 +/- 8.9, mean admission base deficit was -13.3, mean worst base deficit was -17.8, and average Injury Severity Score was 36.3 +/- 16.6. Patients received 20.9 +/- 11.0 units of blood and 24.6 +/- 14 L of crystalloid prior to the development of SECS. Average time from admission to diagnosis of the SECS was 32.6 hours. Acute renal failure developed in 6 (35%) patients; 4 required dialysis, and 3 died. The number of affected extremities ranged from 1 to 4. Of the 46 affected extremities, 39 were salvaged and 7 required amputation. Mortality was 35.3%. CONCLUSIONS: SECS is an uncommon, but devastating complication in severely injured patients with hypotension undergoing massive transfusion, and developing systemic inflammatory response syndrome. Vigilance increases detection. While the overall mortality was reduced by half, patients requiring dialysis have a 75% mortality.     

Can pelvic tilting be ignored in total hip arthroplasty?

INTRODUCTION

The orientation of acetabular component is influenced by pelvic tilt, body position and individual variation in pelvic parameters. Most post-operative adverse events may be attributed to malposition of the component in the functional position. There is evidence that orientation of the pelvis changes from the supine to standing position. Authors report a case of recurrent dislocation after total hip arthroplasty due to excessive pelvic tilting.PRESENTATION OF CASE A 69-year old female with coxarthrosis had undergone total hip replacement with recurrent dislocation of the hip on bearing weight in spite of using constrained acetabular component.

DISCUSSION

Our case report substantiates the influence of pelvic tilt, incurred by a sagittal deformity of spine, on dynamic orientation of the acetabular cup which was positioned in accordance with the anatomic landmarks alone. If the reference is only bony architecture and dynamic positions of the pelvis are not taken into account, improper functional orientation of the acetabular cup can result in sitting and standing positions. These can induce instability even in anatomically appropriately oriented acetabular component.

CONCLUSION

The sagittal position of pelvis is a key factor in impingement and dislocation after total hip arthroplasty. Pelvic tilting affects the position of acetabular component in the sagittal plane of the body as compared with its anatomic position in the pelvis. We suggest a preoperative lateral view of spine-pelvis, in upright and supine position for evaluation of a corrective adaptation of the acetabular cup accordingly with pelvic balance.     

Association between pelvic floor muscle trauma and pelvic organ prolapse 20 years after delivery

Introduction and hypothesis

It is known that pelvic floor muscle trauma (PFMT) after vaginal delivery is associated with pelvic organ prolapse (POP) symptoms (sPOP) and signs (POP-Q ≥2) in patient populations. Our aims were to establish the prevalence and investigate a possible association between PFMT and sPOP and POP-Q ≥2 in healthy women 20 years after their first delivery.

Methods

During 2013 and 2014 we conducted a cross-sectional study among 847 women who delivered their first child between 1990 and 1997. Women responded to a postal questionnaire and were offered a clinical examination including prolapse grading and pelvic floor ultrasonography. The main outcome measures were sPOP, POP-Q ≥2 and PFMT, defined by levator avulsion or a levator hiatal area on Valsalva manoeuvre of >40 cm² on ultrasonography.

Results

Of the 847 eligible women, 608 (72 %) were examined. Data on POP symptoms, POP-Q stage, levator avulsion and levator hiatal area were available in 598, 608, 606 and 554 women, respectively, and of these 75 (13 %) had sPOP, 275 (45 %) had POP-Q ≥2, 113 (19 %) had levator avulsion and 164 (30 %) had a levator hiatal area >40 cm². Levator avulsion was associated with POP-Q ≥2 with an odds ratio (OR) of 9.91 and a 95 % confidence interval (CI) of 5.73 – 17.13, and with sPOP (OR 2.28, 95 % CI 1.34 – 3.91). Levator hiatal area >40 cm² was associated with POP-Q ≥2 (OR 6.98, 95 % CI 4.54, – 10.74) and sPOP (OR 3.28, 95 % CI 1.96 – 5.50).

Conclusion

Many healthy women selected from the general population have symptoms and signs of POP 20 years after their first delivery, and PFMT is associated with POP-Q ≥2 and sPOP.

     

Modulation of cartilage's response to injury: Can chondrocyte apoptosis be reversed?

Osteoarthritis is characterized by a chronic, progressive and irreversible degradation of the articular cartilage associated with joint inflammation and a reparative bone response. More than 100 million people are affected by this condition worldwide with significant health and welfare costs. Our available treatment options in osteoarthritis are extremely limited. Chondral or osteochondral grafts have shown some promising results but joint replacement surgery is by far the most common therapeutic approach. The difficulty lies on the limited regeneration capacity of the articular cartilage, poor blood supply and the paucity of resident progenitor stem cells. In addition, our poor understanding of the molecular signalling pathways involved in the senescence and apoptosis of chondrocytes is a major factor restricting further progress in the area. This review focuses on molecules and approaches that can be implemented to delay or even rescue chondrocyte apoptosis. Ways of modulating the physiologic response to trauma preventing chondrocyte death are proposed. The use of several cytokines, growth factors and advances made in altering several of the degenerative genetic pathways involved in chondrocyte apoptosis and degradation are also presented. The suggested approaches can help clinicians to improve cartilage tissue regeneration.