Lateral lumbar interbody fusion (XLIF) is a minimally invasive option to lumbar surgery. This procedure is done from the side rather than the front or back resulting in reduced time for operation, fewer recovery days, minimal scarring, reduced blood loss, less post-operative pain, and quicker return to daily activities. It is an outpatient procedure which is not appropriate in every situation.
This procedure is performed with one or more tiny incisions and a medical device called a retractor that’s used to spread apart overlying tissue to give the doctor a clear view of the spine. The retractor and dilator system used in the lateral lumbar interbody fusion is called MaXcess™ which allows the surgeon to reach the spine via a lateral view from the side with minimal muscle and ligament tampering and no disruption to abdominal muscles.
The recovery process is quicker than with traditional surgery. The patient can get up and walk immediately following the procedure, minor pain afterwards, and the results are immediately apparent rather than having to wait for a gradual return to normalcy as in the traditional fusion surgery.
Over 400 published clinical studies support the procedure, documenting positive clinical outcomes as comparted to traditional posterior fusion procedures.
Rehabilitation is an important part of the recovery process for a TBI patient. The program should be customized to the person based on their strengths and capacities and modified over time to adapt to changing needs. This usually involves a team of rehabilitation specialists in multi-specialties. Individually tailored programs generally include physical therapy, occupational therapy, speech/language therapy, physiatry, psychology/psychiatry, and social support. There are several options for rehabilitation: home-based, hospital outpatient, hospital inpatient, comprehensive day programs, supportive living programs, independent living centers, club-house programs, school based programs for kids and others.
The overall goal is to improve the patient’s ability to function at home, work and in society. This is done through helping the patient adapt to disabilities or to modify their environment to make every day activities easier. Medications must be carefully prescribed because TBI patients are more susceptible to side effects and may react adversely to some pharmacological agents. It is also important for family members to provide support for the TBI patient through involvement in their rehabilitation program.
Here is an article that speaks to a personal experience one may have with TBI injured loved one: https://www.brainline.org/article/introduction-rehabilitation-healing-brain.
Throughout the recovery process TBI victims will undergo tests and procedures which will assist with diagnosis, prognosis, and treatment decisions.
Neurological monitoring/neuromonitoring: Intracranial pressure monitors track the amount of pressure in the brain to help manage brain swelling.
Neuroimaging studies: Computed tomography (CT scans) or MRI is used to identify bleeding and injured parts of the brain, and to determine if surgery is necessary.
Electroencephalogram (EEG): Measure electrical activity in the brain, show location/extent of injury and can be used to diagnose seizures.
Informal bedside neurological exam and formal behavior assessment scale: Used to determine a person’s level of impaired consciousness. Typically testing for basic reflexes, following a moving object with the eyes, performing basic commands and communication.
Guest Blogger: Dennis Brown, MD
On July 2, 2017, the prestigious “Journal of American Medical Association” (JAMA) published an authoritative medical study regarding radiofrequency denervation (ablation) procedures for chronic low back pain titled "Effect of Radiofrequency Denervation on Pain Intensity Among Patients With Chronic Low Back Pain," which concluded "The findings do not support the use of radiofrequency denervation to treat chronic low back pain from these sources" (facet joints, sacroiliac joints or a combination of facet joints, sacroiliac joints, or intervertebral disks).
It is medically probable radiofrequency denervation is not medically reasonable or necessary for the treatment of chronic low back pain.
Reference: Johan N. S. Juch, MD; Esther T. Maas, PhD; Raymond W. J. G. Ostelo, PT, PhD, et l Effect of Radiofrequency Denervation on Pain Intensity Among Patients With Chronic Low Back Pain The Mint Randomized Clinical Trials, JAMA. 2017;318(1): 68-91.doi:10.1001/jama.2017.7918
Low back problems are a necessary evil of being human due to our anatomy and physiology. This is of great importance in many medicolegal claims in which an injury or repetitive stress exposure is alleged to have caused low back problems, thereby attempting to shift responsibility for the costs imposed by low back problems from the individual and his or her health insurance (if applicable) to the liability policyholder/employer and the liability/workers compensation insurance carrier. The high prevalence of low back problems in the general population makes differentiating between idiopathic problems and those caused by an accident or repetitive stress exposure extremely difficult. It is also complicated by the fact that the idea of a manifestation of a preexisting condition is at odds with our folk understanding of temporal proximity and causality, i.e. if two things happen near in time, we tend to assume they are causally related, with the first thing causing the second thing.
Human beings perform many cognitive tasks exceptionally well. Accurately assigning causation is not one of them. In particular, we are prone to making a priori assumptions about how things work and then confirming our assumptions (confirmation bias) post hoc (post hoc ergo propter hoc fallacy). Low back pain is a notable example: we often associate low back pain with lumbar disc pathology discovered on post-injury MRI despite the fact that we know from the medical literature large percentages of the general population have similar MRI findings but no low back pain. We make the assumption based on our assessment of human anatomy and physiology that lumbar discs work in a certain way and when they are compromised it must cause discernible effects such as low back pain. We then see evidence of compromised lumbar discs in persons who complain of low back pain following an injury or exposure and we leap to the bias-confirming post hoc conclusion that the pathology or compromised condition is causing the pain. So strong is this impulse that we ascribe causation even though we are well-aware of the medical literature demonstrating that disc pathology is an exceedingly poor proxy for low back pain. The coup de grace of this faulty reasoning is the post hoc association between disc pathology and pain: physicians will regularly conclude that a specific event or long term exposure caused a herniated disc despite the person being in a population cohort in which it is at least as likely than not that herniated disc was present before the injury or exposure. The only reasonable way one could reach this conclusion is with a pre-injury MRI showing there was not a herniated disc.
The problem with this sort of faulty reasoning is that it can lead to treatment that is extraordinarily expensive but ineffective. In a low back pain claim with post-injury evidence of a herniated disc, the treatment is often a discectomy/laminectomy with or without fusion. If the herniated disc was not causing the pain, the surgery will have been unnecessary. While the placebo effect will almost certainly result in some short term improvement, the long term outcomes are likely to be, at best, no different than they would have been with conservative therapy because the treatment will have been aimed at discal pathology that was benign. The triers of fact in the medicolegal systems will, however, require the workers compensation or liability carriers to absorb the costs of surgery, including non-medical costs that are recoverable under the different systems (such as indemnity payments in worker’s compensation or wage loss and pain and suffering in personal injury), because they are likely to believe the opinion that the herniated disc is the problem. This belief is based on the folk (mis)understanding of cause and effect.
There is an expression in statistics that has been borrowed by cognitive psychologists: regression to the mean. It simply holds that unusual states, events, or findings tend to be temporary and regress over time to the average or status quo. This is true with many non-malignant medical conditions as well. This is both profound and somewhat dispiriting because it means that most of these conditions will get better over time regardless of treatment. It is hence a fallacy to ascribe efficacy to treatment or causation based on recovery following treatment when a condition simply regresses to the mean because it would have regressed to the mean regardless of treatment.
Much attention has been paid to this phenomenon in the context of overusing antibiotics. Most people who go the doctor for upper respiratory infections wait to seek treatment until the condition has been present for some time. They then go to the doctor, ask for antibiotics, take antibiotics, and recover from the condition. These persons then assume that the antibiotics caused the improvement. The problem with the assumption is that most of these persons almost certainly had viral infections that simply got better according to the natural course of the condition. ANTIOBIOTICS DO NOT AFFECT VIRUSES AT ALL. The fact that the condition improved after starting antibiotics was due to the simple fact that the person started the antibiotics at about the time the condition would improve on its own. The antibiotics had nothing to do with the condition improving because ANTIBIOTICS ARE 100% INEFFECTIVE AGAINST VIRUSES.
The same holds true for many persons with low back pain who undergo surgery to remove a herniated disc. Low back pain usually stabilizes over time after an acute exacerbation regardless of treatment. Given enough time, it is highly likely that the person would have gotten better or at least recovered to the same extent regardless of the treatment received (including no treatment). The fact that the person improved after surgery does not indicate that the surgery caused the improvement. Instead, the relation of surgery and improved low back pain is almost certainly coincidental. We regress to the mean. That the surgery occurred and improvement subsequently happened is not evidence that the surgery was effective or that the herniated disc was causing the low back pain.
How do we know this? The medical literature is replete with evidence to that end. Take for example the study, “Influence of Low Back Pain and Prognostic Value of MRI in Sciatica Patients in Relation to Back Pain.” The study was undertaken to evaluate the correlation between MRI findings and outcomes in patients with sciatica alone versus patients with sciatica and back pain. As the authors note, “it remains unclear to what extent morphological changes seen on MRI in sciatica patients are associated with back pain, rather than being a representation of irrelevant differences between individuals.” The study found “that herniated discs and nerve root compression on MRI were more prevalent among patients with predominantly sciatica compared to those who suffered from additional back pain.” Interestingly, patients with sciatica and low back pain but without a herniated disc or nerve root compression fared worse after one year than those patients with a herniated disc or nerve root compression. And “remarkably large disc herniations and extruded disc herniations were … equally distributed between the two groups,” causing the authors to conclude that “the worldwide accepted mechanical compression theory therefore seems not to offer a sufficient explanation for the cause of the disabling back and leg symptoms in sciatica.”
Other studies demonstrate similar findings that call into question our ability to assign causation of low back pain to herniated discs and nerve root compression. The well-known twin study demonstrates the difficulty in linking specific activities with low back pain. As the authors in that study report, “disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected.” As noted above, other studies have found that large portions of the general population have disc pathology on MRI, but no low back pain. Still other studies find low back pain in the absence of disc pathology on MRI. Despite this evidence, triers of fact routinely base liability decisions on medical opinions that conclude an injury or exposure caused a herniated disc based on a post-injury MRI (which is almost impossible to conclude from a rational, evidentiary perspective in the absence of a pre-injury or exposure MRI) and that the herniated disc is causing low back pain (which runs contrary to the received scientific evidence).
What does this mean for medicolegal claims? It suggests that every claim for injury- or exposure-related back pain based on post-injury MRI scans demonstrating a herniated disc should be carefully scrutinized. In addition, worker’s compensation and liability carriers should take every opportunity to educate triers of fact regarding the lack of a causal nexus between herniated discs and low back pain. Independent medical examiners should point to the relevant literature to begin convincing triers of fact that there is no evidentiary link between low back pain and herniated lumbar discs. In this regard, insurance carriers can look to how the relationship of carpal tunnel syndrome to repetitive keyboard use evolved over time. When these claims first started arising, triers of fact in worker’s compensation accepted the link based on treating physician opinions seemingly without question. This was based on the fact that claimants reported experiencing symptoms while using computer keyboards. The medical literature did not support this association. Independent medical examiners began citing to research finding the opposite: that repetitive keyboarding is not a risk factor for or a cause of carpal tunnel syndrome. In at least some jurisdictions, the triers of fact and treating physicians eventually listened and stopped finding a relationship between repetitive keyboarding and carpal tunnel syndrome.
A similar shift ought to occur in the context of herniated discs and low back pain. While this does not suggest that low back pain itself is unrelated to an injury or exposure, it would radically reduce costs because it would limit surgery for herniated discs to cases where there is discernible nerve impingement causing motor and sensory deficits rather than in cases of low back pain alone. Although human beings are not very good at accurately assessing causation, we can learn to go against our instincts if there is high quality evidence denying causation and experts willing to hammer that point home. It is time to hammer home the point that disc pathology on MRI is poorly correlated to low back pain and limit expensive surgical procedures the efficacy of which is not supported by the medical literature. The simple fact of the matter is that costs for treating a condition that cannot be reliably related to an accident or repetitive stress exposure should not be borne by a liability or worker’s compensation carrier (especially when the condition is poorly correlated with the alleged health effects).
Employment-related meniscus tears are among the more common worker’s compensation claims. The reasons are myriad but are influenced by the fact that most people develop degenerative meniscus tears as they age and the mechanism of injury for an acute tear merely involves twisting the knee, which can occur in even the lightest and most sedentary occupations because all workers who are not wheelchair-bound walk which means all workers are at risk of twisting their knee in a slip, trip, or fall at the workplace. Setting aside the possibility that such an event is idiopathic, if a worker seeks medical treatment for knee pain following an industrial event and a meniscus tear is discovered on an MRI the treating physician usually relates the tear to the event. Standard treatment in most such cases is usually surgical excision of the loose or torn meniscal tissue, more commonly known as a meniscectomy. The assumption driving the surgery is that the meniscus tear is causing the knee pain and resecting the tear will eliminate the pain. The problem with this scenario is that most meniscus tears are degenerative and there is no high quality research demonstrating that meniscectomy is an effective treatment for degenerative meniscus tears. In fact, when researchers recently studied the question they found that exercise was equally effective as meniscectomy to treat knee pain in the presence of a degenerative meniscus tear, according to results published in the British Medical Journal (“BMJ”).
In the worker’s compensation setting, the argument is often made that an industrial event extended a preexisting degenerative meniscus tear in order to justify the surgical intervention (and coverage of the procedure under a worker’s compensation insurance policy). The cost of meniscectomies to the worker’s compensation system is substantial. The medical expenses alone are significantly higher for surgery than for conservative care. In addition, meniscectomies often result in some permanent partial disability. For example, a meniscectomy in Wisconsin carries with it a 5% minimum PPD rating to the lower extremity at the level of the knee and under the AMA Guides a meniscectomy typically results in at least a 1% impairment rating. Surgery also typically necessitates a period of temporary total disability in non-sedentary workers. The findings of the BMJ study should give every employer and worker’s compensation insurer pause and an editorial advocating systemic prohibition of using arthroscopy to treat knee pain that appears in the same issue should spur change.
First, a few things about the study itself. The BMJ study is a level 1, properly designed randomized controlled trial. This is the highest category of medical studies and is considered to produce the best and most reliable evidence available. The BMJ study was conducted in Norway and was a randomized control trial with two parallel intervention groups of 70 patients per group. One group received exercise alone and the other group received partial meniscectomy alone. The participants were 35-60 year old persons of both sexes with a 2+ month history of unilateral knee pain without a major trauma but with a verified medial meniscus tear verified on MRI and no worse than grade 2 arthritic changes on x-ray. The study found that there was no difference in outcomes between the two groups at 3 months and 24 months post-intervention. The meniscectomy group reported better function and greater participation in sports and recreation at 12 months post-intervention, but the effect was gone by 24 months. The authors could “not exclude the possibility that the greater placebo effect from surgery on patient outcomes” may have “mask[ed] the ‘real’ difference in treatment between the groups,” which they postulated could explain the temporary effects observed in the meniscectomy group.
More striking even than the study findings is the accompanying editorial. The authors of the editorial call for a systemic level rule to prevent unnecessary knee arthroscopies from being performed to treat knee pain. As they note, in the last decade:
The editorial authors note there has never been high quality research supporting meniscectomy in an older population with degenerative meniscus tears, but that the procedure was extended to this population based on unverified assumptions:
The conclusion they reach is both astonishing and harsh:
In short, the authors believe the evidence against arthroscopy to treat knee pain is so strong and the evidence for it is so weak that health systems as a whole should stop paying for these procedures. Such a rule would have a significant impact on worker’s compensation claims where meniscectomies are routinely performed to treat degenerative meniscus tears.
We are inundated with messages about the opioid crisis in America. According to the CDC 28,000 people died due to opioid overdose in 2014, at least half of which occurred while using prescription painkillers. There is also evidence that heroin use is increasing as prescription opioids become harder to obtain. In fact, the CDC reports that prescription opioid painkiller use is strongest risk factor for heroin addiction. Those in the worker’s compensation field have seen firsthand the devastation addiction to prescription opioids can cause. In addition to the tragic human costs, cases involving long term prescription opioid painkiller use often have high economic costs that include significant lost time and failure to return to work in addition to the cost of the prescriptions themselves. And this doesn’t begin to touch on the cost that are imposed on the social safety net when long term opioid painkiller use turns into permanent disability. The bottom line is that an effective alternative to prescription opioid painkiller use in chronic pain cases would improve lives, improve society, and most importantly save lives.
The Journal of the American Medical Association (“JAMA”) recently published a report addressing whether mindfulness-based stress reduction might be that effective alternative. The report notes that the CDC recommends physicians “try nonpharmacologic and nonopioid therapies first,” before using opioid painkillers. Hence, it is becoming imperative for physicians to explore alternatives to simply prescribing painkillers. According to the report, “limited research indicates that mindfulness meditation for pain management therapy has promise.” For example, a recent study found that adding mindfulness meditation to a standard pain treatment program increased the percentage of patients who reported meaningful pain reduction from 26.6% to 44.9%. Obviously this is a significant finding. Unfortunately, there are no studies that compare mindfulness-based stress reduction directly with opioid use. The report stresses the importance of performing direct comparison, double-blinded, randomized studies to measure the effectiveness of mindfulness-based stress reduction compared to prescription opioid painkillers.
So why does mindfulness-based stress reduction appear to help at all? There are a number of reasons, but chief among them is the understanding that “pain is a complex phenomenon involving more than a direct nerve impulse from the affected tissue or limb to the somatic sensory cortex” and that “a person’s thoughts and emotions also play a role in pain perception.” This has helped physicians to focus on treatment modalities that “shift chronic pain treatment from a ‘biomedical disease model’ to a ‘patient-centered’ model focused on ‘patient engagement in daily self-management.’” The key is shift between improved quality of life versus elimination of pain, which is often impossible. This turns the patient’s attention away from pain and disability and toward behavioral and psychological interventions and techniques to improve her quality of life. In the words of a mindfulness meditation study participant, “I felt the pain was there, but I was able to let it go. I didn’t dwell on it so much.”
Whether mindfulness-based stress reduction will prove to be a substitute or an effective alternative to prescription opioid painkillers remains to be seen. Nevertheless, the growing awareness that chronic pain is different from and needs to be treated differently than acute pain is positive. The trend is moving toward interventions in chronic pain patients that focus on learning strategies to cope with their pain which in turn increases their ability to function at higher levels. And higher levels of functioning mean less catastrophizing, less disability, and ultimately, less death. A happy coincidence is that it also means a reduction in worker’s compensation costs.
Any person who spends time in claims has run into files in which a patient with back pain has undergone “provocative discography.” The procedure involves injecting intervertebral discs suspected of causing the claimant’s pain with fluid along with “healthy control” discs. Purportedly, if the claimant feels an increase of pain in the suspected disc compared to the “control” discs, then the suspected disc is confirmed as being the cause of the claimant’s back pain. The problem is threefold. First, studies have determined that provocative discography cannot do what it is supposed to do. It cannot identify “discogenic pain.” Second, studies have definitively concluded that not only is provocative discography an ineffective diagnostic tool but also that it causes the degeneration of injected intervertebral discs to accelerate. Third, a recent study published in The Spine Journal (subscription required) found in a 10 year study that provocative discography performed on persons without back complaints actually led to back pain and surgical intervention. Healthnewsreviews.org has an outstanding piece about the study and the lack of coverage in the health news media. This is important because even today, with knowledge that provocative discography is an ineffective diagnostic tool, 70,000 procedures are performed annually in the United States. Anyone involved in medico-legal claims should read the Healthnewsreviews.org piece. Here are some of the highlights:
Such is the import of this study that an orthopedic surgeon interviewed as part of the article flat out stated:
Perhaps the best summary was provided by another doctor consulted for the article. Steven Atlas, MD, MPH, told Healthnewsreviews.org:
The article is worth reading in its entirety. One hopes that discography and its costs, both direct and indirect, will soon disappear from the health care landscape. In the meantime, claims professionals should expect their IME doctors on back pain cases to be familiar with the study and use it in their reports when treating physicians recommend or actually perform provocative discography and use it to diagnose the cause of back pain and the need for surgery.
Last week psychiatrist Jeffrey Zigun, M.D. and psychologist Brad Grunert, Ph.D. spoke at Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on mild traumatic brain injury. Three topics came up repeatedly during the individual experts’ presentations and in the follow-up panel discussion:
The answers to the first two of the three issues are surprisingly simple, while the answer to the third is, or at least can be, much more complicated.
With respect to the question of whether mild traumatic brain injuries can get worse over time, the simple answer according to the experts is “no.” Both Dr. Zigun and Dr. Grunert were clear in their statement that recovery from mild traumatic brain injury follows a predictable recovery. The physical injury to the brain itself reaches maximum medical improvement within a year and all expected improvements in functioning occur within two years of the injury. This is significant because a number of participants in the seminar reported scenarios in which a claimant/plaintiff experienced a precipitous decrease in functioning 12, 18, or even 24+ months after the initial injury. In at least some cases, the decrease in functioning was measured on neuropsychiatric testing and was deemed not to be malingering. Both Dr. Zigun and Dr. Grunert were clear in their presentations and in the panel discussions that such a decrease in functioning would not be due to an underlying mild traumatic brain injury, even if the injury were permanent. Brain injuries get better over time; they don’t yo-yo up and down or suddenly get worse after a period of improvement. Unfortunately, a decrease in functioning after a period of improvement can still be related to the accident. More on this later.
One of the more interesting aspects of the symposium was the discussions about the role of intelligence in recovery from a mild traumatic brain injury. The experts both stressed that intelligence is enormously important in assessing how individuals will recover from permanent mild traumatic brain injury. The reason is that those with more intelligence have more to lose before the loss of function becomes a significant impairment. The example Dr. Grunert used was an academic researcher: she may have some memory impairment following a mild traumatic brain injury, but it may only mean that she has to look up citations she previously had memorized. This will obviously add some time to her research, but it will not impair the quality of the research itself or her ability to write. On the other hand, a factory worker who has to follow a specific procedure when operating a dangerous machine will have no margin for error. If her memory was on the lower end of average to begin with, losing any amount of memory function could cause her to be unable to follow the specific procedure when operating machinery. Since there is no margin of error, the factory worker’s memory impairment would cost her the ability to do her job. Hence, one point both Dr. Zigun and Dr. Grunert made was that impairment following mild traumatic brain injury is often different for persons of high intelligence than it is for persons of lower intelligence.
The trickiest question the experts dealt with is how to determine the fact of a traumatic brain injury. In many cases a person hits their head and the symptoms of concussion are obvious. These might include brief loss of consciousness, dizziness, retrograde and/or anterograde amnesia, headache, wooziness, etc. In other cases the fact of injury might be less obvious. Perhaps the person did not strike their head in a motor vehicle crash, but reported some symptoms consistent with mild traumatic brain injury. Further complicating matters are cases where there is a preexisting history of psychological problems such as depression, anxiety, or other psychological diagnoses. In all cases, Dr. Zigun and Dr. Grunert stressed the importance of early neuropsychological testing. Dr. Grunert noted that neuropsychological testing has a high degree of reliability and specificity. In addition, neuropsychological testing is good at ferreting out malingering from legitimate claims. Early testing also establishes a baseline from which test results should not decline in mild traumatic brain injury.
As the experts and the audience discussed, often the fact of injury is not an issue at the beginning of a claim, though. Instead, the fact of injury becomes an issue after a year or more. Usually, this seems to occur as a result of a decline in functioning, whether supported through neuropsychiatric testing or not. As the experts agreed, simply because a person declines in functioning after a mild traumatic brain injury should have stabilized does not mean that they are not continuing to suffer from a permanent brain injury or that the decline in function is not legitimate or related to the accident. Both Dr. Zigun and Dr. Grunert agreed that a decline in functioning a year or more after a mild traumatic brain injury only means that the brain injury itself is probably not responsible for the decline in functioning. Instead, they pointed to psychological conditions as often being the culprit.
When the audience heard this, many persons wanted to know if the psychological conditions would be related to the accident, especially if there was a preexisting history. As Dr. Zigun noted numerous times, it depends. For example, Dr. Zigun addressed the simple fact that many of the drugs used to treat psychological conditions also have positive effects on the sequelae from traumatic brain injury. Take SSRIs, commonly used to treat depression. Dr. Zigun pointed out that one symptom of depression is memory impairment, which is also a symptom of mild traumatic brain injury. SSRIs help alleviate memory impairment in both depression and mild traumatic brain injury. Dr. Zigun noted that if a person is diagnosed with mild traumatic brain injury, they may very well end up on an SSRI. Once the brain injury stabilizes, the person may be weaned off the SSRI. However, if the person has simultaneously developed depression, weaning her from the SSRI may cause a decrease in functioning related to the depression, including worsening memory impairment. Both experts agreed that the decrease in functioning in such a case could be legitimate but that it would not be related to the mild traumatic brain injury.
How, then, can we determine if a decline in functioning relates to the accident? The answer, unfortunately, is not clear cut. The experts stressed that to evaluate whether a decline in functioning, once determined to be legitimate and not malingering, relates to an accident, the analysis essentially looks to the totality of the circumstances to attempt to parse out the causal factors. The case a number of audience members brought up was the situation in which there is a preexisting history of a psychological condition such as depression which is determined to be the reason for the post-accident decline in functioning. Dr. Zigun and Dr. Grunert agreed that it is exceptionally difficult to determine whether the development of a psychological condition is accident-related. They noted that many factors could cause the onset of depression episode that would be related to the accident. For example, if the mild traumatic brain injury caused a memory impairment that prevents the injured person from returning to work, it would not be unusual for the person to develop depression. The depression would not be caused by the brain injury itself, but rather would be the result of the job loss, which resulted from the brain injury. On the other hand, if the injured person has recovered well and is coping with any residual impairments from the brain injury, the depression is likely to be independent of the brain injury. The bottom line is that declines in psychological functioning in the context of a permanent mild traumatic brain injuries present challenging cases for experts in which causation can only be determined by assessing the totality of the circumstances.
Mild traumatic brain injuries can present vexing cases for claims professionals. As Dr. Zigun and Dr. Grunert discussed, mild traumatic brain injuries can be diagnosed and treated effectively, even in the case of concomitant psychological conditions. We are grateful for their participation in Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium and for the many insights they shared with our audience.
When we think of traumatic brain injury, we typically think of symptoms primarily related to cognition and executive function. Hence, we expect to see memory deficits, difficulty concentrating, and difficulty regulating emotions. We associate the brain with thinking so we often focus on the symptoms related to thinking despite the fact that traumatic brain injury can cause a host of physical symptoms as well.
One of the most troubling physical symptoms is the potential for traumatic brain injury to disrupt the body’s circadian rhythm, or its normal sleeping/waking cycle. According to a 2012 Public Library of Science study, traumatic brain injury, “disrupts the oscillatory expression pattern of several circadian clock and clock-associated genes” in the areas of the brain primarily responsible for regulating the sleep/wake cycle (the suprachiasmic nuclie, or SCN, and hippocampus). In short, traumatic brain injury interferes with our ability to sleep normally. Interestingly, this sleep-impairing aspect of traumatic brain injury has effects on our cognition:
In short, if you don’t sleep normally you don’t think normally. This is problematic for other reasons also since sleep disruption is known to increase the likelihood of developing depression, bipolar disorder, diabetes, hypertension, and metabolic disorders.
The wide-ranging and myriad effects of traumatic brain injury make it essential to obtain an accurate diagnosis early in the process to ensure that the best available treatment is offered. While at least 80% of persons with mild traumatic brain injury will experience a complete recovery, there is small but nontrivial subset of patients whose symptoms will persist as chronic problems. If we are going to administer traumatic brain injury claims effectively, it is imperative that we understand many of the effects from traumatic brain injury are not primarily cognitive in nature but rather are physical.
To learn more about how the physical, cognitive, and psychological aspects of traumatic brain injury relate, check out Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on April 7, 2016.
There are certain medical procedures that are so common in worker’s compensation that we don’t give them a second thought. Partial meniscectomy is among them. Most people assume that an employee with a torn meniscus who is experiencing catching and locking in their knee should have a partial meniscectomy to treat the symptoms, regardless of whether we think the meniscus tear is work-related. Turns out that our assumption might be wrong.
The Annals of Internal Medicine published results from a study (subscription required) which found that arthroscopic partial meniscectomy is ineffective for relieving catching and locking symptoms in the knee. The study was conducted on a group of patients with medial knee pain who had confirmed meniscus tears without evidence of arthritis. The participants in the study were randomly assigned to either the treatment group, which received the partial meniscectomy, or a control group, who received a sham arthroscopy. Participants were not aware of which group they were in to control possible bias.
The results of the study were surprising because in every reported measure, the patients undergoing the sham procedure reported fewer mechanical symptoms post-surgery. The most impressive results were among those patients reporting that they were symptom free following the procedure. Among this group, only 28% of the participants undergoing the actual partial meniscectomy reported being symptom-free while 41% of the participants who underwent the sham procedure reported being symptom-free. The study’s authors were quick to note, however, that trauma-related meniscus tears causing mechanical symptoms in persons under 35 do respond well to partial meniscectomy. On the other hand, they pointed out that “in a degenerative knee, seemingly similar symptoms may not even be caused by the meniscal tear - more likely they are a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further.”
In the worker’s compensation context, the dispute is typically whether a meniscus tear is traumatic or degenerative. Regardless, the ineffectiveness and the possibility that the symptoms might be “a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further” is a good reason to tread cautiously when an employee is diagnosed with a meniscus tear. If the employee’s meniscus tear is degenerative in nature, there is a strong likelihood that a partial meniscectomy will have a temporary benefit at best and in the long run will not ameliorate or slow the progression of degenerative arthritis. Hence, a meniscus tear in an older worker that is deemed to be work-related is highly likely to become an arthritic knee that will need to be replaced. And despite the fact that it is bad medicine and bad science, the arthritis is likely to be blamed on the meniscus tear even though the arthritis was probably the problem in the first place. Hence, it behooves every claims professional to take a serious look at meniscus claims and to defend them vigorously now that we know the proposed surgery may very well not work and may very well lead to additional (more costly) claims.
Pain is a problem that is frequently treated with painkillers. As we are all aware, this has led to a significant problem with addiction to and overdose from opioid painkillers in this country. The reasons for the crisis in prescription opioid addiction and overdose are myriad and have been discussed extensively here and elsewhere. This post is not about the problem, but instead about an opportunity to address it.
The NY Times recently posted an article about the potential to harness the placebo effect to help treat pain which offers an intriguing possibility in the struggle to treat pain without causing addiction and overdose. As Jo Marchant reports, “even when we take a real painkiller, a big chunk of the effect is delivered not by any direct chemical action, but by our expectation that that drug will work. Studies show that widely used painkillers like morphine, buprenorphine and tramadol are markedly less effective if we don’t know we’re taking them.” In fact, placebo effects are so powerful “that drug manufacturers are finding it hard to beat them.” Hence, Marchant suggests that more research should be done to figure out if “prescription” placebos could be used to treat pain.
Marchant recognizes the difficulty with placebos: namely that the effect is generally observed in clinical trials where individuals don’t know if they are getting the active drug or a placebo. In controlled studies, patients expect they will receive a drug that will improve their condition even though they know they might in fact get a placebo. This, as Marchant notes, appears to be a key component of the placebo effect: “[t]he greater our belief that a treatment will work, the better we’ll respond.” There have, however, been studies in which patients knowingly taking placebos still reported statistically significant improvement in their reported level of pain. This leads Marchant to ask the eminently reasonable question, “[w]ith placebo responses in pain so high – and the risks of drugs so severe – why not prescribe a course of ‘honest’ placebos for those who wish to try it, before proceeding, if necessary, to an active drug?”
Pain is ubiquitous in our society and, when chronic, often proves disabling. We know from experience that prescribing opioid painkillers is not the answer to the problem of pain. Perhaps it is time for those of us in the medico-legal world to use whatever muscle we have and advocate for change. A good place to start would be the use of “honest” placebos to treat pain.
At Medical Systems, we don’t often see separated shoulder cases, known to medical professionals as acromioclavicular (“AC”) joint dislocations, because the injuries are acute and painful. Hence, there usually isn’t much dispute about whether the injuries are work/accident-related or not. Still, these injuries happen at workplaces and in personal injury accidents. They are painful and, if severe, usually treated surgically (read, “expensively”).
New research suggests that this is probably the wrong approach. A recent study in the Journal of Orthopaedic Trauma found that surgical repair of moderate and severe AC joint dislocations did not result in improved outcomes versus non-surgical repair, bucking what has been considered common knowledge among doctors. Not only did surgery not improve patient outcomes, but patients that did not have surgery actually recovered faster. In fact, 75% of the non-surgical patients returned to work within 3 months of the injury while only 43% of the surgical patients did. According to the study’s author, "For severe AC joint dislocations, surgery is the common practice but there's not much evidence to suggest this is actually the best treatment." An additional benefit is that those treated non-surgically (use of a sling and rehabilitation) suffered much lower rates of complication. The only noticeable benefit to surgery was that the AC joint appeared more normal after surgery.
One hopes that the medical community will pay attention to the findings and stop recommending surgery for every moderate to severe AC joint dislocation. It would seem that this would be the best result for both claimants with AC joint dislocations and claims professionals managing their claims.
Ankle fractures are not the most common injury in worker’s compensation or personal injury claims, but they do happen. The standard protocol for uncomplicated ankle fractures is immobilization (casting) followed by a supervised exercise program (physical therapy). Results from a recent JAMA study question whether supervised exercise improves outcomes for patients with uncomplicated ankle fractures. In the study, the control followed the standard protocol (supervised exercise after cast removal) while the experimental group received instructions on home exercises but did not participate in a supervised exercise program. The results demonstrated that the control group had no better outcomes in terms of activity limitations or quality of life. The authors conclude that “findings do not support the routine use of supervised exercise programs after removal of immobilization for patients with isolated and uncomplicated ankle fracture.”
Eliminating unnecessary physical therapy from uncomplicated ankle fracture claims presents a good opportunity to reduce claim costs. If treating physicians are unwilling to follow the recommendations of the JAMA study’s authors, setting up an IME or a record review could be a smart move, especially if it can be done before the cast comes off.
Spinal cord injuries are devastating. The U.S. experiences approximately 12,000 spinal cord injuries per year in which the injured person survives the initial accident. For those who survive the initial accident, the road forward is physically arduous, psychologically taxing, and financially burdensome. A spinal cord injury patient can expect to spend well over a month in hospitals and in-patient rehabilitation (and sometimes considerably longer dependent on the severity of the injury and whether there are concomitant cognitive impairments or other comorbidities). In addition, the lifetime costs of spinal cord injuries are extensive, having a present day value ranging from $4,540,000 for a 20-year-old patient with high tetraplegia (spinal cord injury at C1-C4) to $1,460,000 for a 60-year-old patient with paraplegia. The occupational effects are profound, with only 35% of spinal cord injury patients able to achieve a similar pre-injury level of employment 20 years post-injury. Obviously, the costs to employers and worker’s compensation carriers in work-related spinal cord injury claims are enormous and usually lifelong. The costs of spinal cord injuries are massive in the liability context as well. Since the two most common causes of spinal cord injuries are motor vehicle crashes and falls, liability and worker’s compensation claims are relatively common when spinal cord injuries occur.
Certainly no one did more to raise awareness of spinal cord injuries than Christopher Reeve, who suffered a spinal cord injury causing high tetraplegia (C1-C2) after falling from a horse in 1995. Periodically high profile athlete suffer spinal cord injuries that thrust the issue back into the national spotlight. In 2010, Rutgers football player Eric LeGrande sustained a spinal cord injury during a game against army that initially left him paralyzed from the neck down. In October 1995, Travis Roy was just 11 seconds into his first shift in his first game as a hockey player for Boston University when he crashed head-first into the boards and suffered a spinal cord injury that also paralyzed him from the neck down. More recently, Olympic swimmer and multiple gold medal-winning swimmer Amy Van Dyken suffered a spinal cord injury away from athletics in June 2014 when she fell off the all-terrain vehicle she was driving and down a 5-7 foot embankment. The accident injured her spinal cord at T11 and left her paralyzed from the waist down.
These famous athletes and celebrities periodically remind us of both the risk and devastating consequences of spinal cord injury. Fortunately, progress is being made in managing the post-injury effects of spinal cord injury. The most frequently reported-on developments typically involve bionic exoskeletons that help the paralyzed person move their limbs. However, recently medical researchers have been making strides in using electrical stimulation to allow the injured patient voluntarily move paralyzed limbs. In recently reported research, external electrodes were placed over 5 patients’ spinal columns who have suffered from paraplegia for at least two years. The electrodes in combination with the drug buspirone allowed the patients to move their limbs under stimulation, which was not unexpected. What was remarkable is that the patients retained the ability to move their legs even without electrical stimulation after 4 weeks of treatment. As lead researcher Prof. V. Reggie Edgerton noted, "The fact that they regained voluntary control so quickly must mean that they had neural connections that were dormant, which we reawakened." The findings are considered remarkable because the medical and scientific community had accepted that persons with complete paralysis “no longer had any neural connections in the spinal area.;” suggesting that it may be possible to regain motor function without regenerating spinal neurons or using an exoskeleton system.
This research along with the mind-boggling progress that is being made with patient-controlled exoskeleton devices is changing the landscape for spinal cord injury patients. These developments are welcome news for patients, their families, and society alike. As noted above, the occupational and medical costs of spinal cord injuries are enormous. Anything that can return function to patients has the potential to minimize the occupational impact and long-term medical expenses of spinal cord injuries, which is good news for the worker’s compensation and civil liability systems as well. Spinal cord injuries are among the most costly injuries to everyone involved. Improving outcomes in spinal cord injuries will benefit an extraordinary number of individual lives and also the institutions set up to absorb the costs.
Medical News Today has an article on exciting research in the pharmacological management of chronic pain. The research, published in Neuron, found that persons with a particular genetic profile experience considerably less low back pain than the general population. Such persons have a gene variant that causes them to produce less of the protein BH4 than normal. Researchers postulated that BH4 is at least partly responsible for the development of chronic nerve pain. To test the hypothesis, they engineered mice to overproduce BH4 and found these mice were hypersensitive to pain even without injury. They then engineered mice that produced no BH4 and found those mice to have considerably less sensitive to pain than normal.
The real breakthrough, however, was in the researchers’ next step: pharmacological control of BH4. "We wanted to use pharmacologic means to get the same effect as the gene variant," says Alban Latremoliere, PhD, of Boston Children's Kirby Center, who led the current study. As Medical News Today reports, the researchers caused a peripheral nerve injury in laboratory mice and then “blocked BH4 production using a specifically designed drug that targets sepiapterin reductase (SPR), a key enzyme that makes BH4. The drug reduced the pain hypersensitivity induced by the nerve injury (or accompanying inflammation) but did not affect nociceptive pain--the protective pain sensation that helps us avoid injury.” This could be a hugely important development in the pharmacological management of chronic pain in people as the method would offer an option that could effectively manage pain without any of the addictive or other deleterious effects of narcotic pain medication.
Claims with chronic whiplash symptoms that develop after a low-speed motor vehicle accident are often difficult. The defense points to imaging studies that do not demonstrate evidence of pathology. The plaintiff points to a prior history of normal health without any neck problems or pain complaints. Each side points to their evidence and asks the jury (if the case goes to trial) to reach their preferred conclusion:
The defense will point to the low speed of the impact to demonstrate that their position is more credible, i.e. the speed was so low no person could have suffered more than a minor, temporary neck strain. The plaintiff will try to counter this with evidence that the speed of the striking vehicle at impact cannot accurately convey the forces transmitted to the plaintiff’s cervical spinal column and musculature. In truth, there is little direct evidence that supports either side’s position in these claims.
That may be changing, though. Researchers at the Feinberg School of Medicine at Northwestern University have uncovered what may be objective evidence supporting the claims of chronic whiplash injuries that arise in approximately 25% of all rear-end motor vehicle accidents. Specifically, the researchers found evidence of fatty deposits that accumulated in persons who went on to suffer chronic whiplash injuries in fat and water MRI scans taken within one to two weeks after the initial injury. Specifically, the MRI scans demonstrated “large amounts of fat infiltrating the patients’ neck muscles, indicating rapid atrophy.” Lead Investigator James Elliott stated that “we believe this represents an injury that is more severe than what might be expected from a typical low-speed car crash.”
The significance of the findings, if replicated, could be great for personal injury claims involving allegations of chronic whiplash injuries. If the water-fat ratio in neck muscles becomes an accepted objective test of whiplash injury chronicity, it could take the guesswork out of these claims. This of course seems like it would be a boon to plaintiffs’ claims; however, the defense would benefit also because it would limit chronic whiplash injury claims to those with objective evidence of injury. In short, it could potentially provide definitive evidence of which claims are legitimate and which claims are not. A residual beneficial effect for both sides would be more effective treatment. As Elliott notes, chronic whiplash patients “may require a more concerted effort for pain management from their physician and help from a psychologist.” Better treatment started sooner would be good for everyone involved in whiplash claims.
Lately it seems like we are stuck in a feedback loop: yet another study has found a common treatment modality for acute low back pain to be much less effective than assumed. In this case, medical researchers found that low dose oral corticosteroids (i.e. prednisone) did not improve pain and offered only modest functional improvement among patients suffering from acute sciatica due to a herniated lumbar disk. According to lead author Harley Goldberg, DO, a spine care specialist at Kaiser Permanente's San Jose Medical Center, "[t]hese findings suggest that a short course of oral steroids (prednisone) is unlikely to provide much benefit for patients with sciatica due to a herniated disk in the lower back.” Researchers also found that “oral steroids did not reduce the likelihood of undergoing surgery in the year following steroid treatment.” Given the apparently modest benefits of oral steroid treatment for acute sciatica and the known deleterious effects of negative treatment history, it would seem prudent for researchers to verify the results of the study as soon as possible. Otherwise we will all be stuck paying for treatment that doesn’t work and could possibly render later treatment modalities less effective.
Cogito ergo sum. These words of Descartes are more commonly known to English speakers as “I think therefore I am.” But what have they to do with medical treatment or medico-legal claims? Quite a bit actually. Descartes is famous among philosophers (a relative sort of fame) for arguing that the mind and the body are distinct entities. We see evidence of this intellectual approach in our distinction between the biological and the psychological. Take brain injuries as an example. We distinguish between what we consider to be organic, neurological injuries from the psychological effects of injury. Hence the distinction between post-concussion syndrome and post-traumatic stress disorder. The belief in dualism is extended into the legal realm also, where we have higher standards for proving mental only worker’s compensation injuries than mental injuries in worker’s compensation that arise out of a physical trauma. But is our insistence on this dualism, that mind and body are separate entities, valid?
Much research suggests that our conception of mind and body as separate entities is not so clear cut as we would like to believe. A good example of why we should be wary of separating the psychological from the physical involves the placebo effect. Another example involves treatment history. A group of researchers from German universities and Oxford University authored a 2014 study in which they found that treatment history experience has an astonishingly large effect on subsequent treatment, even when the type of treatment changed. In their study they gave patients analgesic medication delivered through a patch and then later switched to a different analgesic medication delivered through a topical cream. They found that those who responded positively to the first treatment also responded positively to the second treatment. More significantly, the authors found that those who responded negatively to the first treatment also responded negatively to the second treatment despite being given a different medication with a different delivery mechanism.
The findings are significant because the study “results may … challenge step care approaches in which treatment failure has to precede the prescription of next-in-line interventions.” The treatment carryover effect could have a big impact on problematic claims where acute injuries become chronic condition and nothing seems to help. As the authors note, “treatment experiences are ubiquitous in clinical care, particularly in patients suffering from chronic diseases. Carry-over effects might therefore be particularly relevant in chronic conditions where treatments often fail repetitively and negative treatment experiences accumulate along the course of the disease.” The authors suggest that targeted therapy, whether explicit psychological counseling or more implicit methods, could be used to address and attempt to overcome negative treatment history.
The study demonstrates that our minds and bodies are not as separate as we sometimes like to think they are. This can be frustrating when administering medico-legal claims because we want concrete answers. We want diagnostic images to have a one-to-one correlation with physical complaints. We want to know that if someone is prescribed a medicine, that it will work. Unfortunately, medical science tells us that the healing and treatment process is more complicated. While the treatment history study demonstrates the unpredictability of the healing process, it does offer learning opportunities. At a minimum, if we see a failed treatment history we then know that the likelihood of the next intervention working is diminished. In addition, knowing the effects of treatment history can provide a reason to have claimants undergo independent medical examinations. Once a pattern of failed treatment history develops, an independent medical examination may be worthwhile to attempt to halt the seemingly endless spiral of failed treatments.
The business of sorting out what is organic or biological from what is psychological is messy and probably futile. Perhaps it is time that we put Descartes to rest and start thinking of the mind and body as inextricably linked, so inextricably linked that they are not in effect different. Ego sum. That’s it. In the claims experience, this should help us deal with and understand the myriad responses to similar injuries that different claimants have.
What is it about shoulders? They seem to cause an inordinate amount of problems, especially when the rotator cuff is involved. And invariably, there is a question as to whether a shoulder claim involves an acute injury, an acute aggravation of a preexisting condition, an occupational injury, or the mere manifestation of a preexisting condition. One of the biggest challenges in claims is determining whether and to what extent a shoulder condition is work-related. Unfortunately, this task is often difficult for physicians too.
The hallmark of an acute rotator cuff injury is an asymptomatic shoulder, a discernible traumatic event, and immediate pain and weakness. Unfortunately, this type of presentation accounts for less than 10% of all rotator cuff tears according to some literature. In addition, the medical literature suggests that acute rotator cuff tears are underdiagnosed in emergency departments and often attributed to tendonitis, bursitis, arthritis, or some combination of all three. To further complicate matters, many other conditions of the shoulder, cervical spine, and peripheral nerve system can produce symptoms that are similar to symptoms occurring in rotator cuff tears. And finally, a somewhat sizable percentage of the population has asymptomatic rotator cuff tears which makes the determination of the etiology of the cuff defect difficult to determine.
The best way to assess whether a rotator cuff tear is acute or traumatic is with diagnostic imaging. Numerous studies have found that mid-substance tears are more likely to be acute than insertional tears. The presence of swelling and joint fluid or a hematoma also suggest that a tear is acute. To the contrary, the absence of joint and bursal fluid suggests a chronic tear. The presence of fatty infiltration and the degree of rotator cuff atrophy are also useful findings to assess the chronicity of the tear. Interestingly, at least one study found that the “injury mechanism and the activity at the moment of injury did not correlate with the presence of a rotator cuff lesion,” but also found “a strong age correlation, with a prevalence of RCTs above 50% in patients aged over 50 years…” This study suggests a shockingly high rate of rotator cuff injury resulting from shoulder trauma in persons over 50.
The strong correlation between age and rotator cuff tear caused one study’s authors to postulate that “it is even likely that there [is] no such thing as an acute cuff tear without some previous tendon degeneration.” The authors of another study address the complicated relationship between the chronicity and symptomatic nature of rotator cuff tears and note that the “duration of symptoms does not necessarily reflect the duration a patient has had a rotator cuff tear… It is not understood why full-thickness tears become symptomatic in some individuals and not others.” How then, can any physician determine to a reasonable degree of medical certainty if a particular rotator cuff tear relates to the patient’s employment in the absence of diagnostic imaging that suggests a tear is acute?
In truth, the answer is that any physician who attributes a symptomatic rotator cuff tear to a workplace injury is most likely engaging in speculation if there is no acute traumatic event and no diagnostic imaging evidence demonstrating that the tear is acute. This doesn’t mean that the tear can’t be acute and work-related, simply that there is no reasonable basis for a physician to determine the exact etiology of the tear to a reasonable degree of medical certainty. In handling claims, it is important to recognize these situations and pose the question to the IME doctor directly as to there is any way, given the current state of evidence-based medicine, to determine what caused a rotator cuff tear (or caused it to become symptomatic) to a reasonable degree of medical certainty in the absence of an acute traumatic event, diagnostic imaging evidence that a tear is acute, or occupational risk factors such as repetitive overhead work. If there are no specific risk factors, no precipitating injury, and no diagnostic imaging evidence of an acute tear, the answer should always be “no.”
From a claims perspective, there are several useful things that can be gleaned from the medical literature addressing rotator cuff conditions. First, a definitive assessment of causation in the absence of a discrete, acute precipitating event with imaging evidence demonstrating the presence of an acute tear or an occupational risk factor should be considered impossible. Of course treating surgeons will attempt to relate rotator cuff conditions to workplace injuries that do not meet the above criteria, but it is incumbent from a claims perspective that the IME physician points to the relevant medical literature and explains why it is not possible, to a reasonable degree of medical certainty, to determine the etiology of a rotator cuff tear in the absence of the above criteria.
Second, it should not come as a surprise if an employee over 40 who says they hurt their shoulder and is told that it is just a strain or tendinitis when they go the ER later discovers she has a rotator cuff tear. The medical literature suggests that clinical examination in the emergency setting underestimate the presence of rotator cuff tears. The relevant study found that in the patient population complaining of an acute shoulder injury who have an inability to perform active abduction above 90° and normal radiographs, more than 50% will have rotator cuff tears. In establishing reserves, if the medical records show normal radiographs coupled with an inability to actively abduct the shoulder above 90°, it may be wise to consider the likelihood of a rotator cuff tear requiring surgical intervention to be 50%.
Finally, knowing the different shoulder, neck, and peripheral nerve conditions that have similar symptom constellations to rotator cuff tear will help to assess what the likely diagnosis will be based on the clinical history, examination, and positive findings. Thus, a shoulder complaint that can be localized to the acromioclavicular joint, is more likely to be a shoulder separation or acromioclavicular arthritis than a rotator cuff tear. In another example, a complaint of gradual onset of shoulder pain with weakness that is especially noticeable during sleeping hours is likely to be a chronic rotator cuff tear or advanced impingement syndrome than an acute rotator cuff injury.
The bottom line is that shoulder injuries are often difficult claims, especially when they involve rotator cuffs. Knowing the medical literature about how rotator cuff tears occur and what suggests acute versus chronic tears can help guide the claims analysis. To learn more about the diagnosis, management, and prognosis of rotator cuff tears, join us on February 26, 2015 for the Medical Systems Advanced Medical Topics in Worker’s Compensation in Brookfield, Wisconsin at which Dr. Bartlett will give an in-depth presentation on acute shoulder injuries. Claim handlers and legal professionals alike will gain valuable information on what claims will likely be compensable and what medical information can be used to defend against those which should not be compensable.
The employee is a delivery driver and is in a rollover accident. Miraculously she suffers only minor injuries in the crash. However, she hits the inside part of her right leg near her knee in the rollover and now, 18 months after the rollover, she still can’t go back to regular duty because she has a permanent foot drop. Another employee gets his hand stuck in the machine he works on. The broken bones heal and the tendons are repaired. Unfortunately, it has been difficult returning him to work because he complains of burning pain every time he touches anything with the injured hand and his doctor has permanently restricted him to one-handed work.
What do these claims have in common? Peripheral nerve injuries. Peripheral nerve injuries are complicated, slow-healing, and often result in permanency. Why are they so complicated and what you can do to make peripheral nerve injury claims go as smoothly as possible? In this short primer, we hope to answer some of these questions.
To understand why nerve injuries are so challenging, it helps to know some basic nerve physiology. Nerve cells (neurons) are essentially made up of little factories (axons) that produce chemicals (neurotransmitters) which mediate the electrical signals each nerve cell sends (axon) and receives (dendrite). Nerve cells are not physically connected to each other and must send the electrical signals across a gap (synapse) to the next nerve cell (dendrite). The axon of each nerve cell is encased in fatty cells (myelin) that increase the rate at which electrical signals are transmitted between nerve cells. Branching extensions of the nerve cells (dendrites) receive the electrical signal from the axon of an adjacent nerve cell and transmit the signal to the axon for further transmission. A failure of any part of this process will disrupt the nerve cell’s functioning and cause sensory or motor problems or both.
Unfortunately, nerve injuries take a long time to heal and often heal poorly because of the complex, compound, and disconnected nature of nerve cells. Nerve injuries are categorized according to the degree to which the nerve cells are compromised. There are two classification systems – one use three categories and one using six categories. This post will use the simpler, three part system because it is more concise (the six part system breaks second degree injuries into four subcategories based on the seriousness of the injury). In first degree injuries, or neurapraxia, the nerve remains intact but its signaling ability is damaged. Ordinarily persons suffering first degree injuries recover completely without residual sensory or motor impairment. In second degree injuries, or axonotmesis, the axon is damaged but the surrounding connective tissues remain intact. Recovery takes longer than in first degree injuries, but complete recovery without residual sensory or motor impairment is still the general rule. In third degree injuries, or neurotmesis, both the axon and the surrounding connective tissue are damaged. Recovery is exceptionally long in third degree injuries and typically results in some residual sensory or motor impairment. In addition, surgery is often necessary to restore function in third degree injuries. The alternate classification system essentially divides the axonotmesis category into four parts based on the severity of the insult to the axon.
We will focus on third degree injuries because they are the most difficult to treat and usually result in permanency. In a third degree nerve injury both the axon and supporting connective tissue are injured. This means that the nerve cell must regenerate both the axon and its supporting structure. The regeneration is complicated by a post-injury process called Wallerian degeneration. Approximately 24-36 hours after the initial injury, the axonal injury disintegrates, the myelin sheath degrades, and macrophages and Schwann cells remove the cellular debris from the injury. In third degree injuries, the supporting connective tissue (endoneurium), which is a tubular structure containing individual axonal fibers, is severed. This causes problems because regenerating axonal fibers may meander into surrounding tissue or inappropriate neural tubes, thus failing to reinnervate their proper end organs. The resulting loss of function is analogous to what would happen in a marionette show if the strings to the marionette controllers are cut and then randomly reattached, sometimes to the correct controller, sometimes to the incorrect controller. Nothing really works right.
When nerve cells start regenerating after Wallerian degeneration, the process is slow. Within four days of the injury, the injured axons start sending sprouts toward the neurolemma (tube comprised of Schwann cells surrounding the axon). Schwann cells produce growth factors that attract the sprouts. If a sprout reaches a neurolemma, it grows into the tube and advances approximately 1 mm per day until it reaches and reinnervates the target tissue. Surgery may be necessary to guide the sprouts into the neurolemma when the gap is too wide or scar tissue has formed. This regeneration and repair phase can last many months. Human peripheral neurons are capable of initiating a regenerative response for at least 12 months after an injury. Hence, it can be well after a year from the date of injury before a treating physician or an IME doctor will be able to place a patient who sustained a peripheral nerve injury at maximum medical improvement.
Further complicating matters, third degree injuries do not usually heal completely. Several factors can contribute to an incomplete recovery. First, intramuscular fibrosis (scarring) may hinder the muscle contraction a nerve impulse produces. Erroneous cross-reinnervation may result in impaired functioning (the marionettes with crossed strings). The imperfect regeneration also results in sensory deficits, especially in proprioception (how the body perceives itself in space), that rarely go away completely. Even in first and second degree nerve injuries, sensory recovery often takes 6-12 months, so determining whether and to what degree permanent sensory impairment has resulted can take a year or more post-injury.
The site of the injury itself and the regeneration process can result in the development of neuromas or gliomas, which can increase pain and disability. If surgical realignment or stump approximation does not occur, the migration of axoplasm may form a neuroma, which is an errant scaffolding (structure) for axonal migration. Essentially, the strands of axonal fibers get tangled as they seek the distal nerve stump, forming a ball of connective tissue and axonal fibers. While some neuromas cause no problems, many are painful and impair functioning.
Treatment and rehabilitation following peripheral nerve injury present their own challenges. For example, in nerve injuries with extensive damage a graft may be needed to connect the two ends of viable nerve. Using a graft will leave the patient with a large area of numbness that the donor nerve previously innervated. The size of this area of numbness will shrink over time, but will not go completely away resulting in residual permanency for loss of sensation at a site remote from the injury. In addition, nerve regeneration itself can be uncomfortable and accompanied by paresthesia (pins and needles) as the target tissue is reinnervated.
Some of the direct consequences of peripheral nerve injury included:
Unfortunately neuropathic pain is not well-understood and is difficult to treat. Anticonvulsants and tricyclic antidepressants are the most popular drugs for neuropathic pain. “Complete relief is very difficult and only 40-60% of patients achieve partial relief.” The persistence and refractory nature of neuropathic pain causes psychological distress and is difficult to understand for persons who are accustomed to the way more typical musculoskeletal pain responds to conventional analgesic medications. From a claims standpoint, neuropathic pain presents great impediments to returning claimants to work because claimants are conditioned to equate pain with physical disability and loss of function, but neuropathic pain frequently does not impair function and is only disabling from a psychological perspective (not to diminish the psychological distress that neuropathic pain causes). It is critical for return to work efforts that the treating physicians and occupational/physical therapists convey the distinction between neuropathic and musculoskeletal pain to the claimant to avoid protracted disability beyond the period of actual physical impairment caused by the injury.
Weakness and loss of function are common complications of third degree nerve injuries because even in the best case scenario nerve regeneration is imperfect. As noted above, weakness and loss of function result from many complicating factors including slow regrowth causing irreparable muscle atrophy, imperfect regrowth resulting in loss of function, and the presence of scar tissue in the muscle preventing normal contracture. This presents challenges to the claim handler who must attempt to gauge return to work, appropriate rehabilitation, and permanent partial disability. EMG can determine the rate at which nerves are growing and muscles are reinnervating, but functional use/restoration will lag behind reinnervation. The reinnervated muscles have been without innervation for a time, so the body must relearn how to use the muscles again which takes time. In addition, the muscles are usually reinnervated imperfectly, so the body is not only relearning how to use the newly innervated muscles, but it is also learning a new neural pattern of action. The body cannot rely on muscle memory to speed the relearning process because the newly configured reinnervation is different than it was before, meaning muscle memory itself is altered or lost.
Some studies have found that conservative therapies can be used alone or in conjunction with surgery to help restore function in peripheral nerve injuries. Laser phototherapy “maintains functional activity of the injured nerve for a long period, decreases scar tissue formation at the injury site, decreases degeneration in corresponding motor neurons of the spinal cord and significantly increases axonal growth and myelinization.” In addition, acupuncture has been found to be an effective treatment modality in improving the rate of recovery. In managing nerve injury claims, it is important to know what therapies work and what do not. Effective claim handlers should be conversant in treatment modalities that can hasten recovery and improve ultimate function so they can ensure patients with peripheral nerve injuries receive the treatment that will get them to an end of healing the fastest and will minimize the inevitable permanent partial disability rating.
Even with effective conservative treatment modalities such as laser phototherapy or acupuncture, recovering function and building strength in peripheral nerve injuries are long and arduous processes that require skilled therapy and a motivated patient. If either variable is lacking, recovery is likely to be compromised. A supreme difficulty for claim handlers is managing the nerve injury case where either the employee lacks motivation or their choice of treating therapist appears to be wanting in some fashion. Early engagement in the claim can help foster a “can do” attitude in the injured worker and a positive relationship with the therapist so that he or she pushes the worker and provides the highest and best evidence-supported rehabilitative care.
The Medical Systems, Inc. “Advanced Topics in Worker’s Compensation Symposium” will address these and other issues related to severe, acute industrial injuries to the hand and wrist with Dr. Jan Bax. Join us to learn why severe hand and wrist injuries present such difficult challenges, what the best medical and surgical treatments of these injuries are, and what strategies you can utilize to help claimants get the best physical recovery and (in the process) lower your costs.
A recent development finds an alternative to postoperative pain management in knee replacement surgery that appears to offer more effective pain relief and potentially speedier recovery. Researchers found that when they injected “a newer long-acting numbing medicine called liposomal bupivacaine into the tissue surrounding the knee during surgery…[p]atients had pain relief for up to two days after surgery and better knee function compared with the traditional method." One of the study’s authors noted that “many patients were able to walk comfortably within hours after surgery.”
It is estimated that more than half of American adults diagnosed with knee arthritis will have a knee replacement at some point. Given the prevalence of knee replacement surgery both in the general patient and worker’s compensation patient populations, any development that can improve pain relief and increase early knee function could have a profound impact. Prescription pain reliever abuse continues to vex society and intraoperative techniques that can reduce the need for postoperative narcotic pain relief can only help the problem. In addition, faster restoration of knee function has the potential to speed rehabilitation and end of healing. If this new technique fulfills its early promise, it could have a significant and positive effect on reducing costs and recovery time of knee replacements. In the worker’s compensation setting, this would be a welcome development.
Andreas Goebel, a lecturer in molecular and clinical pharmacology at the University of Liverpool, has an article at The Conversation about an exciting development in the understanding of how chronic pain works, which offers possible insight into treating Complex Regional Pain Syndrome (“CRPS”), among other chronic pain conditions. Historically, CRPS has been considered primarily a brain problem. The article points out that recent research suggests autoantibodies are implicated in CRPS by “binding to peripheral tissues, prompting sensory nerves to misfire.” The working theory is that trauma, even minor trauma, induces inflammation which causes the binding/misfiring sequence and this in turn causes the central nervous system to become “wound up.” Once the central nervous system is wound up, it malfunctions, causing the unusual and often intractable symptoms of CRPS. As Goebel reports, the discovery of autoantibodies’ role in pain development is important because “there are treatment methods … designed to reduce or remove antibodies,” which may well prove effective in treating CRPS, especially if treatment is initiated early in the progression of the disease. These findings could prove important as claims involving CRPS typically have high disability and medical expenses and are difficult to process and close in a timely manner. Any effective treatment options would have the potential to change CRPS claims processing radically for the better.
Medical News Today reports on an interesting development in treatment of noise-induced hearing loss. Researchers from the University of Michigan and Harvard Medical School used gene therapy to reverse partial hearing loss in mice. The mice’s genes were manipulated to increase production of a protein (NT3) necessary to keep the connection between the ear’s hair cells and the nerve cells that communicate with the brain “super-fast,” also called a “ribbon synapse.” Exposure to noise and normal aging can damage the ribbon synapse, leading to hearing loss. By increasing production of the protein NT3, researchers were able to repair damage to ribbon synapses and restore hearing.
This is exciting news for anyone handling worker’s compensation claims because hearing loss claims plague myriad employers. Researchers noted that rather than pursuing gene therapy in human subjects, the most likely way to increase production of NT3 in humans would be through the use of drugs, a number of which researchers have already identified as candidates. From a worker’s compensation perspective, the possibility of reversing hearing loss would represent a substantial development in what has previously been a permanent condition manageable only through the use of hearing aids. However, the use of pharmaceuticals to treat hearing loss would have costs. How substantial those would be is impossible to guess. Regardless, it is worth monitoring the research to see if the same finding can be reproduced in human subjects.
Pain is a difficult and an amorphous concept. The most common understanding of pain is what we feel when our nociceptors are stimulated. A nociceptor is a receptor on a sensory nerve that responds to damaging or potentially damaging stimuli and sends a signal to the brain that is interpreted as pain. When a child falls down and is asked, “does it hurt?” they are referring to nociception. One of the problems we encounter in relation to pain is that not everything that we might classify or categorize as “pain” is wholly or even partially related to nociception. Grief, for example, can be painful but obviously does not implicate nociception, despite the fact that psychic pain can be described in somatic terms or be physically felt or manifested.
The problem with pain is that we have a medical model for addressing concerns related to the body that tends to subsume everything suboptimal as pathological. One of the tenets of the medical model is that a certain level of physical function is optimal and that everything that is not optimal is somehow pathological and amenable to cure. This idea ignores the reality of physical diversity and can turn normal human experience into a medical condition to be treated rather than a normal aspect of life to be lived through or with. The physical changes that occur with aging are a good example of how we medicalize normal human development and attempt to “cure” that which is not pathological. As a culture, we seem to have fallen into the trap of thinking that every medicalized problem has a cure, including the physical changes that occur with age. Hence, we pathologize normal aspects of growing old as “chronic” pain and treat them as if a cure were possible.
Human bodies have tissues that degrade over time; human bodies are also less resilient over time. This is not to say that age-related physical changes do not vary widely in their effects based on individual experience or that lifestyle has no effect on the changes, but rather is an observation that human bodies do not function as well in the 6th decade of life as they do in the 3rd decade of life, all things being equal. In short, we get old.
Getting old is a fact over which we have some influence. We can maintain a healthy weight, eat a diet rich in fiber and fruits and vegetables, maintain an active lifestyle, get adequate sleep, etc. These things will help us to avoid accelerating the aging process within our tissues. In addition, our genetic makeup plays a significant role in how our bodies’ age. Unfortunately, the influence we have does not stop aging or the physical effects of aging. No matter how healthy our weight or our diet or our lifestyle, collagen becomes less elastic, spinal discs desiccate, articular cartilage wears. In the claims world we often feel the effects of medicalizing age because claimants will try to link the normal effects of aging with a worker’s compensation claim or a personal injury claim. Unfortunately, the effects are often exceedingly expensive as such claimants seek seemingly unending treatment to cure the incurable: age. Both claimants and claims administrators would be better served if treating physicians identified age-related degenerative changes and gave patients options to help them cope with the changes better rather than promising panaceas (usually in the form of surgery) that do not help.
Medical News Today reports on a study published in the Journal of Bone and Joint Surgery (subscription required) which found that patients whose opioid use was increasing prior to spine surgery had worse outcomes than those whose opioid use was not. As Medical News Today notes, studies have shown that opioid use prior to spine surgery frequently leads to worse outcomes, but "the studies did not account for differences in opioid consumption among patients." In this new study, the authors concluded that, "increased preoperative opioid use was a significant predictor of worse health outcomes at 3 and 12 months following surgical treatment..." While this news is not particularly surprising to those in the medico-legal world, it does offer an opportunity to ask IME physicians a targeted question about the appropriateness of spine surgery in claimants with a demonstrated history of opioid dose escalation which should ensure that the physician's opinion explicitly relies on evidence-based medicine and hence is more credible.
Evidence continues to mount that arthroscopy to treat osteoarthritis of the knee is no better than sham surgery or conservative care. The German Institute for Quality and Efficiency in Health Care (IQWiG) published a final report (executive summary available here) on May 12, 2014 that consisted of a meta-analysis of various studies comparing arthroscopy to various modalities, including sham surgery and strengthening exercises. The report’s authors concluded that:
While this information is not new, it bolsters the conclusion that arthroscopy to treat osteoarthritis of the knee is no more effective than other modalities, including conservative care and doing nothing. The standard of care does appear to be shifting toward the abandonment of arthroscopy to treat osteoarthritis of the knee; however, the procedure is still performed occasionally. In managing claims, it is important to ensure that approval for any arthroscopic knee procedure be based on evidence-based medicine. Insurance carriers should not be expected to bear the cost of procedures the benefit of which “is not proven.” In addition, injured plaintiffs and employees should not be expected to bear the risks of surgical complications and extended recovery periods for procedures the benefit of which “is not proven.”
Medical News Today reports on a recent finding from Johns Hopkins that most spine surgeons do not follow recommendations for presurgical screening for depression and anxiety. This is significant because depression and anxiety are known to increase recovery times and reduce the likelihood of a successful outcome. According to one researcher quoted in the Medical News Today article,
Interestingly, the study found that surgeons in private practice and at community hospitals were more likely to provide presurgical screening than were surgeons affiliated with university hospitals. In addition, surgeons with more than 15 years of practice and those performing 200+ spinal surgeries per year were more likely to provide screening.
Considering the enormous expense of spine surgery, it would seem wise for claims handlers to exert whatever influence or control available to ensure that claimants receive proper presurgical psychological screening before undergoing recommended spine surgery. This also seems to be an area in which the insurance industry (including group health carriers) could and should exert its influence to make presurgical psychological screening mandatory in spine surgery cases.
Medical News Today has an article about exciting research from the United Kingdom regarding management of back pain. The article notes that:
To accomplish the targeted care, general practitioners participating in the study gave patients a 9 part questionnaire to evaluate the severity of their back problems. Patients were then placed low risk, medium risk, and high risk categories, with treatment individualized based on the level of risk. Importantly, the low risk patients were not given intensive treatment but were simply reassured about their back pain and given strategies for managing it. Medium and high risk patients received "more intensive treatments led by [physical therapists]."
Prior research found that targeted treatment of back pain was effective, but this is the first evidence that targeted care is effective at the family practice level of care. Medical News Today quotes Professor Alan Silman, medical director of Arthritis Research UK:
Critically, the research found that the targeted approach to back pain does not increase costs. Whether the results can be duplicated remains to be seen, but the study offers a promising method for early, cost-effective intervention in persons suffering from back pain. The fact that the protocol resulted in a 50% reduction in workplace absence is remarkable and reason enough to attempt to replicate the findings so they can be implemented as standard care in general medical practices. Professor Silman put it to Medical News Today best:
Researchers at the University Of Texas Health Sciences Center at Houston, Rice University, and Shriners Hospital for Children-Houston recently published findings in the Journal of Bone and Joint Surgery (subscription required) regarding use of antibiotic-containing microspheres that could lead to their use in joint replacement surgeries. Researchers found that antibiotic-containing microspheres could significantly reduce the rate of infection in joint replacement surgery:
Porous metal implants that were coated with the microspheres prevented infection in 100 percent of the 11 specimens. In the tissue and bone surrounding implants that were not coated with the antibiotic delivery system, infection occurred at a rate of 64 percent. (Emphasis added).
According to a press release announcing the findings, the infection rate in joint replacement surgery is between 1% and 3%. While this is a low figure, one million persons per year undergo hip and knee replacements alone. This means that between 10,000 and 30,000 patients develop an infection after joint replacement surgery. As anyone who has been involved with a claim in which a joint replacement became infected knows, the costs of infection can be staggering. Often the original prosthesis will have to be removed to treat the infection. Sometimes patients end up effectively undergoing three joint replacements because an antibiotic-impregnated temporary prosthesis is used to treat the infection, which will then be taken out when the infection is cleared and replaced with a second permanent prosthesis. The lead researcher, Catherine Ambrose, Ph.D., noted:
[m]ade of biodegradable polymers, the antibiotics are gradually released over a period of weeks and eventually the microspheres dissolve, allowing sufficient time to prevent or treat an infection while reducing the likelihood of additional surgeries.
Better preventing and controlling infections in joint replacement surgeries would greatly decrease both costs and human suffering.The use of microspheres is exciting for reasons other than simply reducing the rate of infection. When persons develop an infection after a joint replacement, they are typically given systemic antibiotics. Microspheres offer a significant advantage when it comes to side effects because they are administered directly at the surgical site. According Ambrose, "[t]he microspheres could be administered directly at the surgical site, eliminating the need for systemic antibiotics that impact the entire body." Systemic antibiotics are hard on the body. They often cause gastrointestinal problems (and in extreme cases can lead to the development of infection with clostridium difficile, or c diff). Systemic antibiotics can also cause fever, rash, and potentially more extreme, though rare, side effects.It will be interesting to follow the use of antibiotic-containing microspheres in joint replacement surgery. If they prove as effective in practice as they have in the preliminary, preclinical trial, they will eliminate much suffering while reducing costs and improving outcomes in joint replacement surgeries.
Researchers recently discovered that persons suffering from lumbago (low back pain) alter their movements because they fear possible back pain. Researchers believe that this behavior can contribute to acute low back pain becoming chronic. Essentially, "[t]hey are trapped within a vicious circle: fearing the suffering linked to movement, they lose their mobility, and the pain persists." Most interesting was the fact that patients in the study felt less pain when researchers told them they were going to feel less pain even when the pain stimulus being applied was higher. As the author of the article points out, "it seems that the first pain-reliever to be administered to a patient suffering from acute lumbago should be a generous dose of reassuring words, in order to prevent the illness from becoming chronic."This is potentially an important development for the medico-legal world because the costs of surgical intervention on worker's compensation and personal injury claims are staggering and any method for helping patients manage acute low back pain to prevent it from becoming chronic would represent a huge cost savings.
