Based on the findings in this and other studies, the decision to use or not use a wound drain following lumbar spine surgery should be left to the surgeon's discretion.
Study Design
Simulate the progression of human disc degeneration.
Objective
The objective of this study was to quantitatively analyze and simulate the changes in cell density, nutrition level, proteoglycan content, water content, and volume change during human disc degeneration using a numerical method.
Summary of Background Data
Understanding the etiology and progression of intervertebral disc (IVD) degeneration is crucial for developing effective treatment strategies for IVD-degeneration related diseases. During tissue degeneration, the disc undergoes losses of cell viability and activities, changes in extracellular matrix composition and structure, and compromise of the tissue-level integrity and function, which is significantly influenced by the inter-coupled biological, chemical, electrical, and mechanical signals in the disc. Characterizing these signals in human discs in vivo is difficult.
Methods
A realistic 3D finite element model of the human IVD was developed based on biomechano-electrochemical continuum mixture theory. The theoretical framework and the constitutive relationships were all biophysics based. All the material properties were obtained from experimental results. The cell-mediated disc degeneration process caused by lowered nutrition levels at disc boundaries was simulated and validated by comparing with experimental results.
Results
Cell density reached equilibrium state in 30 days after reduced nutrition supply at the disc boundary, while the proteoglycan (PG) and water contents reached a new equilibrium state in 55 years. The simulated results for the distributions of PG and water contents within the disc were consistent with the results measured in the literature, except for the distribution of PG content in the sagittal direction.
Conclusions
Poor nutrition supply has a long-term effect on disc degeneration.
Although extremely rare, cauda equina syndrome and severe and/or progressive neurologic deficit caused by lumbar disc displacement can occur during pregnancy. The prevalence of symptomatic lumbar disc herniation during pregnancy may be on the increase because of the increasing age of patients who are becoming pregnant. These cases showed, and the literature confirms, that pregnancy at any stage is no contraindication to magnetic resonance imaging scan, epidural and/or general anesthesia, and surgical disc excision.
The low rate of thromboembolic complications and the cost savings suggest that IPC might be used safely and effectively for thromboprophylaxis in trauma patients.
Background
The intervertebral disc (IVD) receives important nutrients, such as glucose, from surrounding blood vessels. Poor nutritional supply is believed to play a key role in disc degeneration. Several investigators have presented finite element models of the IVD to investigate disc nutrition; however, none has predicted nutrient levels and cell viability in the disc with a realistic 3D geometry and tissue properties coupled to mechanical deformation. Understanding how degeneration and loading affect nutrition and cell viability is necessary for elucidating the mechanisms of disc degeneration and low back pain. The objective of this study was to analyze the effects of disc degeneration and static deformation on glucose distributions and cell viability in the IVD using finite element analysis.
Method of Approach
A realistic 3D finite element model of the IVD was developed based on mechano-electrochemical mixture theory. In the model, the cellular metabolic activities and viability were related to nutrient concentrations, and transport properties of nutrients were dependent on tissue deformation. The effects of disc degeneration and mechanical compression on glucose concentrations and cell density distributions in the IVD were investigated. To examine effects of disc degeneration, tissue properties were altered to reflect those of degenerated tissue, including reduced water content, fixed charge density, height, and endplate permeability. Two mechanical loading conditions were also investigated: a reference (undeformed) case and a 10% static deformation case.
Results
In general, nutrient levels decreased moving away from the nutritional supply at the disc periphery. Minimum glucose levels were at the interface between the nucleus and annulus regions of the disc. Deformation caused a 6.2% decrease in the minimum glucose concentration in the normal IVD, while degeneration resulted in an 80% decrease. Although cell density was not affected in the undeformed normal disc, there was a decrease in cell viability in the degenerated case, in which averaged cell density fell 11% compared with the normal case. This effect was further exacerbated by deformation of the degenerated IVD.
Conclusions
Both deformation and disc degeneration altered the glucose distribution in the IVD. For the degenerated case, glucose levels fell below levels necessary for maintaining cell viability, and cell density decreased. This study provides important insight into nutrition-related mechanisms of disc degeneration. Moreover, our model may serve as a powerful tool in the development of new treatments for low back pain.
Clinicians must not simply decide that a patient with symptoms and a positive diagnostic test has a reason for a specific treatment, and likewise clinicians must not decide that a patient with symptoms and a negative test does not have a clinically important problem. We must also consider the sensitivity, specificity and predictive value of the diagnostic test and the individual characteristics of the patient. Treatment outcome depends on many factors. Point of service decisions vs population based decisions are obviously different. Each patient presents to the treating practitioner on a given day, at a given time, and it is this picture upon which a plan of care is formulated.
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