Workplace injuries are often associated with a single, life-altering incident, such as an engine explosion or a fall from a roof. In fact, however, a large proportion of work-related injuries develop over time from the cumulative effect of repetitive movements or postures on the job—from keyboarding to scanning groceries, from hammering nails to holding a jackhammer.
Fortunately, employees may get workers' compensation benefits for repetitive strain injuries (RSIs), as long as they can show that their work duties were to blame.
What Are Repetitive Strain Injuries?
Under state workers' comp systems, RSIs go by different names, such as overuse injuries, repetitive stress injuries, or cumulative trauma (a larger category that includes other injuries that develop over time, like hearing loss from repeated exposure to loud sounds). Whatever the name, RSIs include many different conditions, including carpal tunnel syndrome, bursitis, tendonitis, trigger finger, rotator cuff syndrome, epicondylitis (often called tennis elbow), lower back pain, and more.
Symptoms of Repetitive Strain Injuries
An RSI may involve any or all of several different symptoms in the affected part of your body, including:
- pain, from tenderness and dull aches to throbbing or acute pains
- tingling
- numbness
- loss of strength or coordination, and
- reduced range of motion or flexibility.
In the early stages, you may not notice any symptoms, or you may experience them only when you're doing a particular motion or holding a particular posture. Without treatment, you may eventually experience the pain, weakness, and other symptoms all the time—even after rest—leaving you unable to do your job or even perform simple actions needed for your daily life.
Jobs Most at Risk for Repetitive Strain Injuries
Most people associate RSIs with working at a computer. Given how many jobs regularly require using a keyboard, mouse, and/or touchscreen, it's no surprise that computer-related cumulative injuries to the hands, wrists, and arms are widespread.
But RSIs can develop from a wide range of other job tasks that require repeated micro-movements, frequent lifting and carrying, using vibrating equipment, or holding awkward postures. In addition to the many occupations that involve computer use, other high-risk jobs for RSIs include:
- nurses and health care aides
- janitors and housekeeping cleaners
- grocery and stock clerks
- bus drivers
- delivery workers
- plumbers and pipefitters
- agricultural and meat processing workers
- firefighters
- musicians, and
- professional athletes.
Repetitive Strain Injuries: Prevention and Treatment
It's important to pay attention to the warning signs of an RSI so that it can be caught early on. If you think that your symptoms are related to your job, notify your employer immediately.
You should also see a doctor as soon as possible (though you'll have to follow the rules in your state's workers' comp system for seeking medical treatment for a work-related injury). "Toughing it out" or waiting to get care could not only hinder your recovery, but it might also make it more difficult to get workers' comp benefits.
Be sure to tell the doctor what you were doing when you experienced symptoms, as well as the time of day. The treating physician might say that you need to stop working for a while or work shorter hours to allow your RSI to get better.
The doctor may also prescribe work restrictions, such as frequent breaks, time limits on how long you should do certain tasks, or ergonomic adjustments to your work station or equipment.
Treatment options vary depending on the type of RSI and its severity. For example, carpal tunnel syndrome can be treated with simple rest, wrist supports, medication, or surgery known as a carpal tunnel release.
Filing a Workers' Comp Claim for Carpal Tunnel or Other RSIs
Depending on the laws in your state, you or your employer will need to file a claim in order to start your worker's comp case officially. RSIs are generally covered under workers' compensation, but a few states set special limits on cumulative injuries or require employees to meet higher standards for proving their RSIs were caused by work duties rather than other activities in their life.
In Arkansas, for example, if an injury wasn't related to a specific incident, it's only covered if it's caused by "rapid repetitive motion" or if it involves the back, neck, or hearing loss (Ark. Code Ann. § 11-9-102(4)(A)(ii) (2022)).
Each state has its own deadline for filing workers' comp claims; in the case of cumulative injuries, the time period generally starts when you first experienced some disability (such as missing work or needing medical care) and you knew or should've known that it was caused by your work. (See our state-specific articles on filing workers' comp claims for details on the procedures and deadlines in your state.)
Getting Legal Help
If your employer's insurer balks at paying for your medical care or denies your claim, it would be a good idea to speak with an experienced workers' comp lawyer.
RSIs can be expensive for insurance companies. These injuries resulted in the longest absences from work (among the most common workplace injuries) during several years in early 2000s, according to the U.S. Bureau of Labor Statistics. So insurers often do everything they can to avoid paying benefits.
A skilled and experienced attorney can tilt the scales in your favor by developing the proper medical evidence to support your claim. (Learn more about what a good workers' comp lawyer should do for you.)
Regardless of the research questions to be addressed, clinically and militarily relevant blast-injury models should satisfy the following criteria (Cernak and Noble-Haeusslein, 2010):
the injurious component of the blast is clearly identified and reproduced in a controlled and quantifiable manner.
the inflicted injury is reproducible and quantifiable and mimics components of human blast injuries.
the injury outcome—on the basis of morphologic, physiologic, biochemical, and behavioral measures—is related to the chosen injurious component of the blast.
the mechanical properties—intensity, complexity of blast signature, and duration—of the injurious factor predicts outcome severity.
Compared with the injuries caused by an impact or acceleration– deceleration force, the mechanistic factors underlying blast injuries are extremely complex. Hence, an appropriate and clinically relevant blast-injury model should be based on sufficient knowledge of shock-wave physics and on the characteristics of the injurious environment generated by an explosion and clinical manifestations of resulting injuries. Substantial interspecies differences in responses to blast exposure across different mammalian species make it imperative that research studies of blast effects and the mechanism by which they are produced consider the possible advantages of using species similar in size to humans, and caution should be exercised in extrapolating to humans observations made in rodents and isolated cells and tissues.
The design and choice of a specific model depend on the goal of research and the component of clinical CNS injury that one wishes to simulate (Cernak, 2005; Risling and Davidsson, 2012). Given the complex nature of blast injuries, it is obvious that the conditions used in a model to reproduce some aspects of blast injuries should be defined with rigor; otherwise, the results obtained will lack military and clinical relevance and can be dangerously misleading. Indeed, despite the growing literature on experimental blast injuries, the results of studies are difficult to compare because of vast differences in methods and experimental conditions (Panzer et al., 2012). Figure 3-5 is a schematic depiction of the decision-making steps in the process of choosing a model for blast research. First, the researcher should clarify the blast effects to be reproduced. If the choice is primary blast, the researcher should ensure that the animals are fixed so that there will be no blast-induced acceleration of the body and head during the exposure.
In a situation in which the body or head is allowed to move, the injury mechanisms involve both primary and tertiary blast effects, which could introduce difficulties in the proper interpretation of results. Next, a decision should be made about the biologic complexity of the research study because this will dictate the choice of research environment, the means of generating a shock wave, the choices of models and their positioning, and the length of the experiment. Thus, on the basis of the research question and the complexity, a choice is made between nonbiologic models and biologic models. The nonbiologic models provide an experimental platform for analyzing interactions between blast loading and different types of materials; the information gained is extrapolated to biologic materials at different levels of scaling. The nonbiologic models can be computer simulations and surrogate physical models. Biofidelic models (mechanical models with computerized sensors that mimic particular human characteristics) are helpful for characterizing the physics of the blast-induced mechanical changes in the brain or head. They are made from synthetic materials, such as glass and epoxy or polyurethane. Multiple displacement and pressure sensors molded into the organs' material are used to record biomechanical measures, such as linear and angular acceleration, velocity, displacement, force, torque, and pressure (Desmoulin and Dionne, 2009; Ganpule et al., 2012; Roberts et al., 2012).
Nonbiologic models can be useful in recording biomechanical alterations induced by blast load and suggesting potential consequences, but they are incapable of providing insight into the mechanisms of later physiologic alterations; hence the need for biologic models. The latter models use biologic systems of differing complexity and include in vitro, ex vivo, and in vivo models. In vitro models based on cell cultures can be useful for characterizing cell responses to blast loading in a highly controlled experimental environment (Effgen et al., 2012; Panzer et al., 2012). Ex vivo models use an organ or a segment of a specific tissue, such as brain or spinal cord, taken from the organism and placed in an artificial environment that is more controlled than is possible with in vivo experiments. As with all blast-injury models, applying operationally relevant loading histories is critical for the in vitro and ex vivo models. Only if blast-loading conditions that are realistic and that mimic what would happen at the cellular or tissue level in a person exposed to a militarily relevant blast environment are used can the mechanisms of the energy transfer to the tissue and the resulting biologic response be reliably analyzed (Effgen et al., 2012).
The success of a research study that uses biologic models, especially at the whole-animal level, depends on rigorous selection of the species to be used as experimental models. The choice of animal species depends on the focus of the study (Cernak, 2005). Many investigators have accepted rodent models as the most suitable choice for trauma research. The relatively small size and low cost of rodents permit repetitive measurements of morphologic, biochemical, cellular, and behavioral characteristics that require relatively large numbers of animals; for ethical, technical, and financial reasons, such measurements are less achievable in phylogenetically higher species (Cernak, 2005). However, because of substantially anatomic and physiologic differences, especially in the circulatory and nervous systems, it has been suggested that rodents should not be the sole choice in blast-injury research.
Extensive studies conducted in Albuquerque, New Mexico, and confirmed by British, German, and Swedish findings demonstrated substantial differences in blast tolerance among 15 mammals (Bowen et al., 1968a; Richmond et al., 1967, 1968). Body size–dependent differences in blast tolerance have been explained on the basis of lung density: the lung density in larger species—including humans, monkeys, cats, and dogs—is only about one-half that in smaller species, such as rodents (see Figure 3-6). In contrast, the lung volumes relative to body mass are three times greater in large species than in smaller animals (White et al., 1965). The body size of the animal model is an important consideration for extrapolating to humans; however, size is only one factor to be considered when validating a model. In addition, substantial interspecies differences in body geometry influence blast–body and blast–head interactions (Bass et al., 2012). The body position of the animal also has an important effect on blast-injury severity. Animals facing an incoming shock-wave front with their chest and abdomen (that is, in the supine position with the shock wave coming from above) provide the most efficient conditions for the shock wave's energy transfer and thus sustain the highest mortality and the most severe injuries (Cernak et al., 2011). In blast-injury modeling, especially when acceleration is included as one of the mechanistic factors, the basic principles of scaling laws should be carefully considered (Bass et al., 2008, 2012). For example, a given blast–head scenario, calculation of the net loading scales for a cross-sectional area of the skull, even if other measures are identical, shows that a specimen 20 times as large would experience one-twentieth the acceleration. However, there are other important anatomic differences between human and animal heads, such as bone volume fraction, trabecular separation, trabecular number, and connectivity density (Bauman et al., 2009; Holzer et al., 2012). Interspecies differences in the structure and arrangement of blood vessels (Vriese, 1904) should also be taken into account in choosing models to reproduce blast injury. For example, the internal carotid artery in lower vertebrates directs the blood to the brain parenchyma through the posterior branch without a contribution from the basilar artery, whereas the two posterior branches in higher vertebrates stem from a single, central branch at the basilar artery (Casals et al., 2011). This anatomical difference could significantly influence the shock-wave propagation through the cerebral vasculature.
It has been shown that phylogenetic maturity has a decisive role in the brain's response to a high-pressure environment (Brauer et al., 1979), and this should be taken into account in planning blast-induced neurotrauma (BINT) experiments. Characterization of basic molecular and gene injury mechanisms that have persisted through evolution might use phylogenetically lower species such as rodents, whereas establishing the pathogenesis of impaired higher brain functions would require larger animals that have a gyrencephalic brain (one that has convolutions).
A short overview of experimental results of biologic models, mainly at the whole-animal level, provides information on mechanisms that potentially underlie long-term functional deficits or organ failure.
Experimental studies of primary blast-induced biologic responses are performed either in an open environment or in laboratory conditions. In open-field exposure studies, animals are exposed to a blast wave that is generated by detonation of an explosive (Axelsson et al., 2000; Bauman et al., 2009; Lu et al., 2012; Richmond, 1991; Saljo and Hamberger, 2004; Savic et al., 1991). Such an experimental setting is comparable with in-theater conditions, but the physical characteristics (such as homogeneity of the blast wave) are less controllable, so a broader array of biologic response should be expected.
Experiments performed in laboratory conditions use shock tubes (in which compressed air or gas generates a shock wave) or blast tubes (in which explosive charges generate a shock wave) (Nishida, 2001; Robey, 2001). The tubes focus the blast-wave energy from the source to the subject; this maximizes the blast energy (Reneer et al., 2011) without the exponential decay of the shock wave's velocity and pressure that is seen in free-field explosions (Celander et al., 1955).
The induction system routinely used in blast-exposure models consists of a cylindric metal tube divided by a plastic or metal diaphragm into two main sections: driver and driven. The anesthetized animals are fixed individually in holders that prevent movement of their bodies in response to the blast. The high pressure in the driver section is generated by an explosive charge or compressed gas and ruptures the diaphragm when it reaches the material's tolerance to pressure. After the diaphragm ruptures, the shock wave travels along the driven section with supersonic velocity and interacts with the animal. The blast overpressure duration can be varied by changing the size of the high-pressure chamber (Celander et al., 1955). The compressed atmospheric air in the tube fails to expand as quickly as would an ideal gas when the membrane is ruptured and also fails to generate a broad range of overpressure peaks. Use of a light gas, such as helium, improves the performance of the shock tubes because of the increased speed of sound in such types of gas (Celander et al., 1955; Lu and Wilson, 2003).
Although shock and blast tubes are convenient means of generating shock waves, they lack the ability to generate other factors of the blast environment, such as acoustic, thermal, optical, and electromagnetic components (Ling et al., 2009). A wide range of blast overpressure sustained for various durations has been used in single-exposure experimental studies. In most studies, the animals are subjected to a shock or blast wave that has a mean peak overpressure of 52–340 kPa (7.54–49.31 psi) on the nearest surface of an animal's body (Cernak et al., 2001b; Chavko et al., 2007; Clemedson et al., 1969; Saljo et al., 2000).
Most experiments used rodents (mice and rats) (Cernak et al., 2001a; Long et al., 2009), but some have used rabbits (Cernak et al., 1997), sheep (Savic et al., 1991), pigs (Bauman et al., 2009), or nonhuman primates (Bogo et al., 1971; Damon et al., 1968; Lu et al., 2012; Richmond et al., 1967).