Incidence of Low Back Pain After Lumbar Discectomy for Herniated Disc and Its Effect on Patient-reported Outcomes

Background

Long-term postdiscectomy degenerative disc disease and low back pain is a well-recognized disorder; however, its patient-centered characterization and quantification are lacking.

Questions/purposes

We performed a systematic literature review and prospective longitudinal study to determine the frequency of recurrent back pain after discectomy and quantify its effect on patient-reported outcomes (PROs).

Methods

A MEDLINE search was performed to identify studies reporting on the frequency of recurrent back pain, same-level recurrent disc herniation, and reoperation after primary lumbar discectomy. After excluding studies that did not report the percentage of patients with persistent back or leg pain more than 6 months after discectomy or did not report the rate of same level recurrent herniation, 90 studies, which in aggregate had evaluated 21,180 patients, were included in the systematic review portion of this study. For the longitudinal study, all patients undergoing primary lumbar discectomy between October 2010 and March 2013 were enrolled into our prospective spine registry. One hundred fifteen patients were more than 12 months out from surgery, 103 (90%) of whom were available for 1-year outcomes assessment. PROs were prospectively assessed at baseline, 3 months, 1 year, and 2 years. The threshold of deterioration used to classify recurrent back pain was the minimum clinically important difference in back pain (Numeric Rating Scale Back Pain [NRS-BP]) or Disability (Oswestry Disability Index [ODI]), which were 2.5 of 10 points and 20 of 100 points, respectively.

Results Systematic Review

The proportion of patients reporting short-term (6–24 months) and long-term (> 24 months) recurrent back pain ranged from 3% to 34% and 5% to 36%, respectively. The 2-year incidence of recurrent disc herniation ranged from 0% to 23% and the frequency of reoperation ranged from 0% to 13%.

Prospective Study

At 1-year and 2-year followup, 22% and 26% patients reported worsening of low back pain (NRS: 5.3 ± 2.5 versus 2.7 ± 2.8, p < 0.001) or disability (ODI%: 32 ± 18 versus 21 ± 18, p < 0.001) compared with 3 months.

Conclusions

In a systematic literature review and prospective outcomes study, the frequency of same-level disc herniation requiring reoperation was 6%. Two-year recurrent low back pain may occur in 15% to 25% of patients depending on the level of recurrent pain considered clinically important, and this leads to worse PROs at 1 and 2 years postoperatively.     

Orthopaedic Surgeons Receive the Most Industry Payments to Physicians but Large Disparities are Seen in Sunshine Act Data

Background

Industry payments made to physicians by drug and device manufacturers or group purchasing organizations are now reported to the Centers for Medicare and Medicaid Services (CMS) as a part of the Physician Payments Sunshine Act. Initial reports from the program show that orthopaedic surgeons lead all physician specialties in total and average industry payments. However, before further discussion of these payments and their implications can take place, it remains to be seen whether these figures are a true reflection of the field of orthopaedic surgery in general, rather than the result of a few outlier physicians in the field. In addition, the nature and sources of these funds should be determined to better inform the national dialogue surrounding these payments.

Questions/Purposes

We asked: (1) How do industry payments to orthopaedic surgeons compare with payments to physicians and surgeons in other fields, in terms of median payments and the Gini index of disparity? (2) How much do payments to the highest-receiving orthopaedic surgeons contribute to total payments? (3) What kind of industry payments are orthopaedic surgeons receiving? (4) How much do the highest-paying manufacturers contribute to total payments to orthopaedic surgeons?

Materials and Methods

We reviewed the most recent version of the CMS Sunshine Act Open Payments database released on December 19, 2014, containing data on payments made between August 1, 2013 and December 31, 2013. Data on total payments to individual physicians, physician specialty, the types of payments made, and the manufacturers making payments were reviewed. The Gini index of statistical dispersion was calculated for payments made to orthopaedic surgeons and compared with payments made to physicians and surgeons in all other medical specialties. A Gini index of 0 indicates complete equality of payments to everyone in the population, whereas an index of 1 indicates complete inequality, or all income going to one individual.

Results

A total of 15,376 orthopaedic surgeons receiving payments during the 5-month period were identified, accounting for USD 109,846,482. The median payment to orthopaedic surgeons receiving payments was USD 121 (interquartile range, USD 34–619). The top 10% of orthopaedic surgeons receiving payments (1538 surgeons) received at least USD 4160 and accounted for 95% of total payments. Royalties and patent licenses accounted for 69% of all industry payments to orthopaedic surgeons.

Conclusions

Even as a relatively small specialty, orthopaedic surgeons received substantial payments from industry (more than USD 110 million) during the 5-month study period. Whether there is a true return of value from these payments remains to be seen; however, future ethical and policy discussions regarding industry payments to orthopaedic surgeons should take into account the large disparities in payments that are present and also the nature of the payments being made. It is possible that patients and policymakers may view industry payments to orthopaedic surgeons more positively in light of these new findings.

Level of Evidence

Level III, Economic and Decision Analysis.     

Can Near-infrared Spectroscopy Detect and Differentiate Implant-associated Biofilms?

Background

Established bacterial diagnostic techniques for orthopaedic-related infections rely on a combination of imperfect tests that often can lead to negative culture results. Spectroscopy is a tool that potentially could aid in rapid detection and differentiation of bacteria in implant-associated infections.

Questions/purposes

We asked: (1) Can principal component analysis explain variation in spectral curves for biofilm obtained from Staphylococcus aureus, Staphylococcus epidermidis, and Pseudomonas aeruginosa? (2) What is the accuracy of Fourier transformed-near infrared (FT-NIR)/multivariate data analysis in identifying the specific species associated with biofilm?

Methods

Three clinical isolates, S aureus, S epidermidis, and P aeruginosa were cultured to create biofilm on surgical grade stainless steel. At least 52 samples were analyzed per group using a FT-NIR spectrometer. Multivariate and principal component analyses were performed on the spectral data to allow for modeling and identification of the bacterial species.

Results

Spectral analysis was able to correctly identify 86% (37/43) of S aureus, 89% (16/18) of S epidermidis, and 70% (28/40) of P aeruginosa samples with minimal error. Overall, models developed using spectral data preprocessed using a combination of standard normal variant and first-derivative transformations performed much better than models developed with the raw spectral data in discriminating between the three classes of bacteria because of its low Type 1 error and large intermodel distinction.

Conclusions

The use of spectroscopic methods to identify and classify bacterial biofilms on orthopaedic implant material is possible and improves with advanced modeling that can be obtained rapidly with little error. The sensitivity for identification was 97% for S aureus (95% CI, 88-99%), 100% for S epidermidis (95% CI, 95–100%), and 77% for P aeruginosa (95% CI, 65–86%). The specificity of the S aureus was 86% (95% CI, 3–93%), S epidermidis was 89% (95% CI, 67–97%), and P aeruginosa was 70% (95% CI, 55–82%).

Clinical Relevance

This technique of spectral data acquisition and advanced modeling should continue to be explored as a method for bacterial biofilm identification. A spectral databank of bacterial and potentially contaminating tissues should be acquired initially through an in vivo animal model and quickly transition to explanted devices and the clinical arena.     

Connective Tissue Growth Factor Modulates Adult β-Cell Maturity and Proliferation to Promote β-Cell Regeneration in Mice

Stimulation of endogenous β-cell expansion could facilitate regeneration in patients with diabetes. In mice, connective tissue growth factor (CTGF) is expressed in embryonic β-cells and in adult β-cells during periods of expansion. We discovered that in embryos CTGF is necessary for β-cell proliferation, and increased CTGF in β-cells promotes proliferation of immature (MafA⁻) insulin-positive cells. CTGF overexpression, under nonstimulatory conditions, does not increase adult β-cell proliferation. In this study, we tested the ability of CTGF to promote β-cell proliferation and regeneration after partial β-cell destruction. β-Cell mass reaches 50% recovery after 4 weeks of CTGF treatment, primarily via increased β-cell proliferation, which is enhanced as early as 2 days of treatment. CTGF treatment increases the number of immature β-cells but promotes proliferation of both mature and immature β-cells. A shortened β-cell replication refractory period is also observed. CTGF treatment upregulates positive cell-cycle regulators and factors involved in β-cell proliferation, including hepatocyte growth factor, serotonin synthesis, and integrin β1. Ex vivo treatment of whole islets with recombinant human CTGF induces β-cell replication and gene expression changes consistent with those observed in vivo, demonstrating that CTGF acts directly on islets to promote β-cell replication. Thus, CTGF can induce replication of adult mouse β-cells given a permissive microenvironment.     

Defects in Mitochondrial Efficiency and H2O2 Emissions in Obese Women Are Restored to a Lean Phenotype With Aerobic Exercise Training

The notion that mitochondria contribute to obesity-induced insulin resistance is highly debated. Therefore, we determined whether obese (BMI 33 kg/m²), insulin-resistant women with polycystic ovary syndrome had aberrant skeletal muscle mitochondrial physiology compared with lean, insulin-sensitive women (BMI 23 kg/m²). Maximal whole-body and mitochondrial oxygen consumption were not different between obese and lean women. However, obese women exhibited lower mitochondrial coupling and phosphorylation efficiency and elevated mitochondrial H₂O₂ (mtH₂O₂) emissions compared with lean women. We further evaluated the impact of 12 weeks of aerobic exercise on obesity-related impairments in insulin sensitivity and mitochondrial energetics in the fasted state and after a high-fat mixed meal. Exercise training reversed obesity-related mitochondrial derangements as evidenced by enhanced mitochondrial bioenergetics efficiency and decreased mtH₂O₂ production. A concomitant increase in catalase antioxidant activity and decreased DNA oxidative damage indicate improved cellular redox status and a potential mechanism contributing to improved insulin sensitivity. mtH₂O₂ emissions were refractory to a high-fat meal at baseline, but after exercise, mtH₂O₂ emissions increased after the meal, which resembles previous findings in lean individuals. We demonstrate that obese women exhibit impaired mitochondrial bioenergetics in the form of decreased efficiency and impaired mtH₂O₂ emissions, while exercise effectively restores mitochondrial physiology toward that of lean, insulin-sensitive individuals.     

Longitudinal Assessment of Neuroanatomical and Cognitive Differences in Young Children With Type 1 Diabetes: Association With Hyperglycemia

Significant regional differences in gray and white matter volume and subtle cognitive differences between young diabetic and nondiabetic children have been observed. Here, we assessed whether these differences change over time and the relation with dysglycemia. Children ages 4 to <10 years with (n = 144) and without (n = 72) type 1 diabetes (T1D) had high-resolution structural MRI and comprehensive neurocognitive tests at baseline and 18 months and continuous glucose monitoring and HbA_1c performed quarterly for 18 months. There were no differences in cognitive and executive function scores between groups at 18 months. However, children with diabetes had slower total gray and white matter growth than control subjects. Gray matter regions (left precuneus, right temporal, frontal, and parietal lobes and right medial-frontal cortex) showed lesser growth in diabetes, as did white matter areas (splenium of the corpus callosum, bilateral superior-parietal lobe, bilateral anterior forceps, and inferior-frontal fasciculus). These changes were associated with higher cumulative hyperglycemia and glucose variability but not with hypoglycemia. Young children with T1D have significant differences in total and regional gray and white matter growth in brain regions involved in complex sensorimotor processing and cognition compared with age-matched control subjects over 18 months, suggesting that chronic hyperglycemia may be detrimental to the developing brain.     

Muscle Fibers are Injured at the Time of Acute and Chronic Rotator Cuff Repair

BackgroundRotator cuff tears are a common source of shoulder pain and disability. Even after surgical repair, some patients continue to have reduced function and progression of fatty degeneration. Because patients with chronic cuff tears often experience muscle shortening, it is possible that repairing the tendon to its anatomic footprint induces a stretch-induced muscle injury that could contribute to failures of the repair and perhaps ongoing pain.Questions/purposesWe hypothesized that, compared with acutely torn and repaired muscles, the stretch that is required to repair a chronically torn cuff would result in more muscle fiber damage. Specifically, we asked: (1) Is there muscle fiber damage that occurs from repair of an acutely torn rotator cuff and does it vary by location in the muscle; and (2) is the damage greater in the case of repair of a chronic injury?MethodsWe used an open surgical approach to create a full-thickness rotator cuff tear in rats, and measured changes in muscle mass, length, and the number of fibers containing the membrane impermeable Evans Blue Dye after acute (1 day) or chronic (28 days) cuff tear or repair in rats. Differences between groups were tested using a one-way ANOVA followed by Tukey’s post hoc sorting.ResultsChronic tears resulted in 24% to 35% decreases in mass and a 20% decrease in length. The repair of acutely and chronically torn muscles resulted in damage to 90% of fibers in the distal portion of the muscle. In the proximal portion, no differences between the acutely torn and repaired groups and controls were observed, whereas repairing the chronically torn group resulted in injury to almost 70% of fibers.ConclusionsIn a rat model, marked injury to muscle fibers is induced when the tendons of torn rotator cuffs are repaired to their anatomic footprint.

Clinical Relevance

In this animal model, we found that repair of chronically torn cuff muscles results in extensive injury throughout the muscle. Based on these findings, we posit that inducing a widespread injury at the time of surgical repair of chronically torn rotator cuff muscles may contribute to the problems of failed repairs or continued progression of fatty degeneration that is observed in some patients that undergo rotator cuff repair. Therapeutic interventions to protect muscle fiber membranes potentially could enhance outcomes for patients undergoing rotator cuff repair. To evaluate this, future studies that evaluate the use of membrane sealing compounds or drugs that upregulate endogenous membrane-sealing proteins are warranted.     

Involuntary Wheel Running Improves but Does Not Fully Reverse the Deterioration of Bone Structure of Obese Rats Despite Decreasing Adiposity

This study investigated whether exercise or antioxidant supplementation with vitamin C and E during exercise affects bone structure and markers of bone metabolism in obese rat. Sprague–Dawley rats, 6-week old, were fed a normal-fat diet (NF, 10 % kcal as fat) and a high-fat diet (HF, 45 % with extra fat from lard) ad libitum for 14 weeks. Then, rats on the high-fat diet were assigned randomly to three treatment groups for additional 12 weeks with forced exercise: HF; HF + exercise (HF + Ex); and HF with vitamin C (0.5 g ascorbate/kg diet) and vitamin E (0.4 g α-tocopherol acetate/kg diet) supplementation + exercise (HF + Ex + VCE). At the end of the study, body weight and fat (%) were similar among NF, HF + Ex, and HF + Ex + VCE, whereas HF had greater body weight and fat (%) than other groups. Compared to NF, HF had elevated serum leptin, tartrate-resistant acid phosphatase (TRAP), and IGF-1; increased trabecular separation and structural model index; and lowered bone mineral density, trabecular connectivity density, and trabecular number in distal femur, while HF + Ex and HF + Ex + VCE had elevated serum TRAP and decreased bone volume/total volume and trabecular number of distal femurs. Compared to HF, HF + Ex and HF + Ex + VCE had decreased serum TRAP and osteocalcin and improved bone structural properties of the distal femur. These findings suggest that exercise, while decreasing body fat, does not fully protect against the negative skeletal effects of existing obesity induced by a high-fat diet. Furthermore, vitamin C and E supplementation has no additional benefits on bone structural properties during exercise.