Anatomic guide and sonography for surgical repair of leg muscle lacerations

Background

There were over 110,000 leg laceration cases reported in the United States in 2011. Currently, muscle laceration is repaired by suturing epimysium to epimysium. Tendon-to-tendon repair is stronger, restores the muscle's resting length, and leads to a better functional recovery. Tendons retract into the muscle belly following laceration and surgeons have a difficult time finding them. Many surgeons are unfamiliar with leg muscle anatomy and the fact that the leg muscles have long intramuscular tendons that are not visible in situ. A surgical anatomic guide exists to help surgeons locate forearm tendons; no such guide exists for tendons in the leg.

Materials and methods

The leg tendon ends of 11 cadavers were dissected, measured, and recorded as percentages of leg length. High-frequency ultrasound was used to locate tendon ends in three additional cadavers. These locations were compared with the actual tendon ends located via dissection.

Results

There was little variation in tendon end position within the cadaver group, between men and women or right and left legs. The data are presented as an anatomic guide to inform surgeons of the tendon ends' likely locations in the leg.

Conclusion

The location of leg intramuscular tendon ends is predictable and the anatomic guide will help surgeons locate tendon ends and perform tendon-to-tendon repairs. Ultrasound is a potentially effective tool for detection of accurate location of repairable tendon ends in leg muscle lacerations.     

A review of postoperative feeding regimens in infantile hypertrophic pyloric stenosis

Infantile hypertrophic pyloric stenosis is a condition well known to pediatric surgeons. Postoperative length of hospital stay is a financial concern and remains a potential target for reduction in hospital costs. Ultimately, these costs are directly affected by the ability to effectively advance postoperative enteral nutrition. This review will serve to: 1) identify clinically relevant postoperative feeding patterns following pyloromyotomy, 2) review the relevant literature to determine an optimal feeding pattern, and 3) identify possible preoperative predictors that may determine the success of postoperative feeding regiments.     

Pre- and post-intervention study to assess the impact of a sedation protocol in critically ill surgical patients

Introduction

Sedation and pain management for mechanically ventilated critically ill surgical patients pose many challenges for the intensivist. Even though daily interruption of sedatives and opioids is appropriate in medical intensive care unit (ICU) patients, it may not be feasible in the surgical patients with pain from surgical incision or trauma. Therefore we developed an analgesia/sedation based protocol for the surgical ICU population.

Methods

We performed a two-phase prospective observational control study. We evaluated a prescriber driven analgesia/sedation protocol (ASP) in a 12-bed surgical ICU. The pre-ASP group was sedated as usual (n = 100) and the post-ASP group was managed with the new ASP (n = 100). Each phase of the study lasted for 5 mo. Comparisons between the two groups were performed by χ² or Fisher’s exact test for categorical variables and the Mann-Whitney test for nonparametric variables. A P value <0.05 was statistically significant.

Results

We found a significant reduction in the use of fentanyl (P < 0.001) and midazolam (P = 0.001). We achieved sedation goals of 86.8% in the post-ASP group compared to 74.4% in the pre-ASP (P < 0.001). Mean mechanical ventilations days in pre- and post-ASP group were 5.9 versus 3.8 (P = 0.033).

Conclusion

In our cohort of critically ill surgery patients implementation of an ASP resulted in reduced use of continuously infused benzodiazepines and opioids, a decline in cumulative benzodiazepine and analgesic dosages, and a greater percentage of Richmond Agitation Sedation Scale scores at goal. We also showed reduced mechanical ventilation days.     

Complications following hip arthroscopy: a retrospective review of the McMaster experience (2009–2012)

Background

The use of hip arthroscopy has been steadily rising as technology, experience and surgical education continue to advance. Previous reports of the complication rate associated with hip arthroscopy have varied. The purpose of this study was to report our experience with hip arthroscopy complications at a single Canadian institution (McMaster University).

Methods

We performed a retrospective chart review of 2 hip arthroscopists at the same institution to identify patients who had undergone the index surgery and had been followed for a minimum of 6 months postoperatively. We used a standard data entry form to collect information on patient demographic and clinical characteristics, including age, sex, surgical indication and type of complication if any.

Results

A total of 211 patients underwent 236 hip arthroscopies. The mean age at time of surgery was 37 ± 13 years and mean follow-up was 394 ± 216.5 days. The overall complication rate associated with hip arthroscopy was 4.2% (95% confidence interval 2.3%–7.6%). We identified 4 major and 6 minor complications.

Conclusion

Overall, hip arthroscopy appears to be safe, with minor complications occurring more frequently than major ones. However, surgeons should recognize the possibility of serious complications associated with this procedure. Future research should focus on prospective designs looking for potential prognostic factors associated with hip arthroscopy complications.     

Cyclodextrin Protects Podocytes in Diabetic Kidney Disease

Diabetic kidney disease (DKD) remains the most common cause of end-stage kidney disease despite multifactorial intervention. We demonstrated that increased cholesterol in association with downregulation of ATP-binding cassette transporter ABCA1 occurs in normal human podocytes exposed to the sera of patients with type 1 diabetes and albuminuria (DKD⁺) when compared with diabetic patients with normoalbuminuria (DKD⁻) and similar duration of diabetes and lipid profile. Glomerular downregulation of ABCA1 was confirmed in biopsies from patients with early DKD (n = 70) when compared with normal living donors (n = 32). Induction of cholesterol efflux with cyclodextrin (CD) but not inhibition of cholesterol synthesis with simvastatin prevented podocyte injury observed in vitro after exposure to patient sera. Subcutaneous administration of CD to diabetic BTBR (black and tan, brachiuric) ob/ob mice was safe and reduced albuminuria, mesangial expansion, kidney weight, and cortical cholesterol content. This was followed by an improvement of fasting insulin, blood glucose, body weight, and glucose tolerance in vivo and improved glucose-stimulated insulin release in human islets in vitro. Our data suggest that impaired reverse cholesterol transport characterizes clinical and experimental DKD and negatively influences podocyte function. Treatment with CD is safe and effective in preserving podocyte function in vitro and in vivo and may improve the metabolic control of diabetes.Diabetic kidney disease (DKD) is responsible for nearly half of the incidents of end-stage kidney disease in the U.S. (1), yet our current understanding of the pathophysiological processes responsible for DKD has led to limited improvements in patient outcomes. Multifactorial intervention reduces the rate of progression of DKD but does not prevent end-stage kidney disease in type 1 (T1D) or type 2 diabetes (T2D) (2,3). A key factor for this translation gap is the current lack of adequate mechanistic insight into DKD in humans.The kidney glomerulus is a highly specialized structure that ensures the selective ultrafiltration of plasma so that essential proteins are retained in the blood (4). Podocytes are glomerular epithelial cells that contribute to the glomerular filtration barrier through a tight regulation of actin cytoskeleton remodeling (4). Currently, the diagnosis of DKD relies on the detection of microalbuminuria (5). However, a growing body of evidence suggests that key histological lesions precede the development of albuminuria (6,7); among them, decreased podocyte number (podocytopenia) has been described as an independent predictor of DKD progression (8–12). Although we have previously shown that podocyte insulin resistance and susceptibility to apoptosis is already present at the time of onset of microalbuminuria in experimental models of DKD, the cause of podocyte injury in early DKD remains unknown (13).We used a previously established cell-based assay in which differentiated human podocytes are exposed to 4% patient sera for 24 h (14) to identify new pathways and targets in DKD. Podocytes exposed to the sera of patients with DKD showed increased cholesterol accumulation in association with downregulation of ATP-binding cassette transporter 1 (ABCA1) expression that was independent of circulating cholesterol.ABCA1 is a major regulator of cellular cholesterol homeostasis by mediating efflux to lipid-poor apolipoprotein acceptors in the bloodstream (15). ABCA1 genetic variants are strongly associated with the risk of coronary artery disease (16). Furthermore, the capacity of patient sera to induce ABCA1-mediated cholesterol efflux in macrophages is impaired in patients with T2D and incipient or overt nephropathy (17). Excessive cholesterol accumulation has been described in glomeruli of rodent models of T1D and T2D (18–20) and may contribute to DKD development and progression. Finally, inactivating mutations of ABCA1 result in Tangier disease, which causes premature atherosclerosis and proteinuria (21).Although interventions that increase ABCA1 expression (such as liver X receptor agonists) may be beneficial in DKD, they have a relatively high incidence of adverse events (22) as well as intrinsic lipogenic effects (23). We used β-cyclodextrins, cyclic oligosaccharides consisting of seven β(1-4)-glucopyranose rings, to remove cholesterol from differentiated human podocytes in vitro and from diabetic animals in vivo. The exact mechanism by which cyclodextrins (CDs) remove cholesterol from cells is not completely understood, but the formation of cholesterol/CD inclusion complexes at the membrane surface plays an important role in this process (24).We hypothesized that 2-hydroxypropyl-β-cyclodextrin, which was recently approved by the U.S. Food and Drug Administration (FDA) for the cure of Niemann-Pick disorder (25,26), would be an effective way to sequester cholesterol and to protect podocytes from cholesterol-dependent damage in DKD in vivo and in vitro.     

Chronic Treatment With a Melanocortin-4 Receptor Agonist Causes Weight Loss,Reduces Insulin Resistance,and Improves Cardiovascular Function in Diet-Induced Obese Rhesus Macaques

The melanocortin-4 receptor (MC4R) is well recognized as an important mediator of body weight homeostasis. Activation of MC4R causes dramatic weight loss in rodent models, and mutations in human are associated with obesity. This makes MC4R a logical target for pharmacological therapy for the treatment of obesity. However, previous studies in rodents and humans have observed a broad array of side effects caused by acute treatment with MC4R agonists, including increased heart rate and blood pressure. We demonstrate that treatment with a highly-selective novel MC4R agonist (BIM-22493 or RM-493) resulted in transient decreases in food intake (35%), with persistent weight loss over 8 weeks of treatment (13.5%) in a diet-induced obese nonhuman primate model. Consistent with weight loss, these animals significantly decreased adiposity and improved glucose tolerance. Importantly, we observed no increases in blood pressure or heart rate with BIM-22493 treatment. In contrast, treatment with LY2112688, an MC4R agonist previously shown to increase blood pressure and heart rate in humans, caused increases in blood pressure and heart rate, while modestly decreasing food intake. These studies demonstrate that distinct melanocortin peptide drugs can have widely different efficacies and side effects.Maintenance of body weight and energy homeostasis requires balance between energy intake and expenditure and is achieved via the interaction between central and peripheral signals. The central melanocortin system is one of the key neural circuits involved in mediating the integration of information from both sites. Proopiomelanocortin is a prohormone that is processed into multiple bioactive peptides, including α-melanocyte–stimulating hormone (MSH), β-MSH, γ-MSH, and the endogenous opioid β-endorphin (1). α-MSH, or its analogs, are potent inhibitors of food intake and increase energy expenditure to promote weight loss in rodent and rhesus macaque models (2–5). Central melanocortins are involved in many physiological functions, including stress responses; however, their actions on the regulation of food intake and energy expenditure have been a focus.Melanocortin-4 receptor (MC4R) is the main melanocortin receptor involved in the regulation of food intake and energy expenditure, primarily through modulation of sympathetic outflow (6–8). MC4R has a broad distribution, including expression in several peripheral tissues, such as muscle, kidney, and lung (9). The importance of MC4R in the maintenance of body weight homeostasis is highlighted by genetic studies in humans and mice. MC4R^−/− mice are hyperphagic, have increased adipose and lean mass, and develop insulin resistance (10). In humans, mutations in the proopiomelanocortin gene (11) and the MC4R gene have a similar phenotype (12–14).Although the effects of MC4R agonists on energy/glucose homeostasis (15,16) make it an attractive target for a therapeutic agent, the potential side effects of increasing heart rate and blood pressure have been a major limitation (17). Indeed, recent studies reported by Greenfield et al. (18) showed that acute peripheral administration with a centrally acting MC4R selective agonist increased blood pressure and heart rate in moderately obese humans. There is an obvious concern in treating obese individuals with a high risk of hypertension and cardiovascular disease with a weight loss therapy that is exacerbating these same risks. In the current study, we use a diet-induced obesity (DIO) nonhuman primate model (NHP) to determine if long-term treatment with the MC4R-specific agonist BIM-22493 can reduce food intake and adiposity without adversely affecting cardiovascular function.     

Osteochondritis Dissecans Knee Histology Studies Have Variable Findings and Theories of Etiology

Background

Although many etiological theories have been proposed for osteochondritis dissecans (OCD), its etiology remains unclear. Histological analysis of the articular cartilage and subchondral bone tissues of OCD lesions can provide useful information about the cellular changes and progression of OCD. Previous research is predominantly comprised of retrospective clinical studies from which limited conclusions can be drawn.

Questions/purposes

The purposes of this study were threefold: (1) Is osteonecrosis a consistent finding in OCD biopsy specimens? (2) Is normal articular cartilage a consistent finding in OCD biopsy specimens? (3) Do histological studies propose an etiology for OCD based on the tissue findings?

Methods

We searched the PubMed, Embase, and CINAHL databases for studies that conducted histological analyses of OCD lesions of the knee and identified 1560 articles. Of these, 11 met our inclusion criteria: a study of OCD lesions about the knee, published in the English language, and performed a histological analysis of subchondral bone and articular cartilage. These 11 studies were assessed for an etiology proposed in the study based on the study findings.

Results

Seven of 11 studies reported subchondral bone necrosis. Four studies reported normal articular cartilage, two studies reported degenerated or irregular articular cartilage, and five studies found a combination of normal and degenerated or irregular articular cartilage. Five studies proposed trauma or repetitive stress and two studies proposed poor blood supply as possible etiologies.

Conclusions

We found limited research on histological analysis of OCD lesions of the knee. Future studies with consistent methodology are necessary to draw major conclusions about the histology and progression of OCD lesions. Inconsistent histologic findings have resulted in a lack of consensus regarding the presence of osteonecrosis, whether the necrosis is primary or secondary, the association of cartilage degeneration, and the etiology of OCD. Such studies could use a standardized grading system to allow better comparison of findings.     

Health Policy Implications of Outcomes Measurement in Orthopaedics

Background

An emphasis on “value” over volume in health care is driving new healthcare measurement, delivery, and payment models. Orthopaedic surgery is a major contributor to healthcare spending and, as such, is the focus of many of these new models.

Where Are We Now?

An evaluation of “value” in orthopaedics requires information that has not traditionally been collected as part of routine clinical practice. If value is defined as patient outcomes in relation to healthcare costs, we need to collect information about both [32]. In orthopaedics, patient-reported functional status is not routinely measured, and a poor understanding of the costs associated with the provision of musculoskeletal care limits our ability to quantify and report on financial measures [10].

Where Do We Need to Go?

To improve the value of musculoskeletal care, we need to focus on both improving outcomes and controlling costs. To improve outcomes, orthopaedists must agree on a set of outcome measures for appropriate care and advocate for their collection through the use of registries. Orthopaedic registries in several countries provide best practices for this information collection and sharing [20]. In the United States, we should make comparable investments in registries to measure patient-reported outcomes. To address escalating costs, we need to improve the accuracy of cost data by applying modern cost accounting processes.

How Do We Get There?

Orthopaedists should take a leadership position in the promotion and implementation of value-based health care by advocating for the use of registries to measure risk-adjusted patient specific outcomes, negotiating with payors for value-based payment incentives and applying modern cost accounting processes to control costs rather than waiting for public and private payors to define components of the value equation that will affect how orthopaedic surgeons are evaluated and compensated in the future.