Much of what a chiropractor does falls within the scope of physical medicine.
Physical medicine and rehabilitation involves the management of disorders that alter the function and performance of the patient. Emphasis is placed on the optimization of function through the combined use of medications, physical modalities, physical training with therapeutic exercise, movement & activities modification, adaptive equipment and assistive device, orthotics (braces), prosthesis, and experiential training approaches.
Common conditions that we treat are back pain, neck pain as well as extremity problems that fall within the chiropractic scope of practice.
Although each patient presents with unique needs for care, the overall scheme of treatment typically involves three stages of management which commonly follow the physiological healing process. In brief, care involves pain & inflammation control, remedial therapeutic care, followed by rehabilitation to the extent that is clinically indicated by findings and the needs of the patient.
Below, if you are so inclined, please find more information on soft tissue injury and repair physiology. This hopefully will give you some additional insight to the healing process and why physical medicine procedures can be of benefit.
The Healing Process after Injury
Following tissue injury, the process and that leads to recovery is divided into three overlapping phases --inflammation, Repair and Remodeling. (Evans 1980; Hardy 1989; Enwemeka 1989; Barlow and Willoughby 1992). R. McKenzie, 2003, page 56. Each part of this process is essential to the structure and function of the final result.
For optimal tissue repair, all phases of this process need to be completed in the appropriate time frame.
Important to Note Connective tissue and muscle do not regenerate if damaged, but are replaced by inferior fibrous scar tissue (Evans 1980; Hardy 1989), thus, proper management is necessary to manage through the healing phases.
The First Stage of Injury Repair
Inflammation Exudate Build Up: Exudates are materials such as fluid, cells and cellular debris from blood vessels after injury. After tissue damage/injury, inflammatory cells with specialized functions are released and attracted to the damaged area. There is an increase in local blood supply. There is leaking of plasma proteins and leukocytes from the blood vessels. White blood cells accumulate at the site of the injury. (Enwemeka 1989; Evans 1980). The cells will be involved in the clearance of dead and dying cells and any foreign matter prior to the re-growth of new vascular channels and nerves into the damaged area. Pain results from the presence of noxious inflammatory chemicals and heightened mechanical sensitivity.
Just as tissue damage always causes inflammation, so inflammation always causes the tissues to become hypersensitive (Levine and Taiwo 1994). The inflammatory irritants sensitize the local pain receptor system and lower the thresholds at which the system is triggered, creating a state of "peripheral sensitization" (Cousins 1994; Woolf 1991). Allodynia; in this situation, the application of relatively minor mechanical stresses causes pain that under normal circumstances would not occur.
Primary hyperalgesia; noxious stimuli create exaggerated responses, and there may be a spread of hyper-responsiveness to non-injured tissues, called secondary hyperalgesia (Cousins 1994; Levine and Taiwo 1994).
At this stage, there will be aching at rest, tenderness, and exaggerated pain on touch and movement (Levine and Taiwo 1994).
Protect, Rest, Ice, Compress, Elevate (P.R.I.C.E.) Rest, at this point, has an obvious important effect of reducing exudates (production response) and protecting the injured tissue from further damage.
Don’t Rest Too Long Rest beyond this stage of healing serves no useful purpose and is in fact detrimental. Early mobilization optimizes tissue healing. Commonly, individuals avoid activity because of association with pain. If this tendency is prolonged, some individuals develop habitual activity avoidance behaviors, thus retarding the repair process.
Most Painful For 3 to 10 Days Aching will progressively lessen while healing and repair begins during the first 3 to 10 days after inflammatory cells, which were the source of chemically mediated pain, decrease in numbers until by the third week after injury none are present (Enwemeka 1989).
Re-triggering; It’s not uncommon at this point, to experience increased pain from normal mechanical loads causing irritation due to re-triggering a chemical inflammatory response, reproducing a constant aching pain. This represents an interface between mechanics and resolving inflammatory state.
Early Movement Guards Against Early Mobility Loss In the acute stage a fibrin mesh forms in the inflammatory exudates and seals the injury. During this time the application of ice, compression, elevation and gentle movements are indicated to reduce the inflammatory exudates (Evans 1980). A greater amount of exudates means more fibrin will form and the more inextensible will be the tissue repair. (mobility loss)
Ordinarily, after the fifth day the inflammatory cells begin to be replaced by fibroblasts, which begin to lay down fibrils of collagen; thus, continued measures to reduce inflammation are of less value. From a clinical standpoint, many times patients continue to re-aggravate the injury and thus reapplication of acute stage management modalities may be necessary.
Hang in there! An end is in sight!
Second Phase of Your Treatment As the Injury Repairs
It is during this period that appropriate management provides the optimal circumstances for uncomplicated repair.
The Beginning of Therapeutic Movement This stage represents an excellent window of opportunity for the reshaping and molding of scar tissue without great risk of tissue re-injury. This stage commonly lasts three to eight weeks depending on the histologic makeup and relative vascularity of the damaged tissue. Generally speaking, the entire process and scar tissue formation is lengthened if the damaged tissue is less vascular (poor blood supply) in its non-traumatized state. For example, tendons and ligaments require more time for scar tissue formation than muscle or skin.
Two Parts To This Phase (some of the technical stuff) 1. Granulation In the repair phase cellular proliferation begins with rapid increase in collagen (protein) deposition. Damaged nerve endings and capillaries “sprout” and infiltrate the area (Cousins 1994). Capillaries, at the edge of the injured area, send forward buds which then turn and meet each other to form new capillary loops capable of maintaining circulation that insures oxygen and nutritional supply in the relatively hypoxic region where healing tissues meet, and at the same time, enables the removal of metabolic waste products. These new capillaries are fragile and stay within the support of newly synthesized collagen which has already been deposited ahead of the formation of the capillary loops. The highly vascular mass produced gives the surface of the tissue its granular appearance and hence its name -- granulation tissue. (A System of Orthopedic Medicine: Ombregt, Bissschop, J ter Veer 2003, p45) Granulation tissue can act as glue preventing movement between tissue interfaces. Adhesion formation can impair collagen gliding (Hunter 1994; Donatelli & Owen Burkhart 1981). Although the scar tissue can be easily damaged in this phase, controlled movement is helpful. (Maxey & Magnusson. Rehabilitation. 2001, p 6-7)
2. Fibroblastic Component (Maxey & Magnusson. Rehabilitation. 2001,p 6-7) Here, the number of fibroblasts (cells that produce collagen) increases, as does the rate of production of collagen fibers and ground substance. Collagen is laid down at an accelerated rate and finds itself with weak bonds, making tissue elongation much easier. This stage represents an excellent window of opportunity for the reshaping and molding of scar tissue without great risk of tissue re-injury. This stage lasts three to eight weeks depending on the histologic (cellular) makeup and relative vascularity of the damaged tissue. By the fourth or fifth day after injury the amount of collagen is significant and there is a continued but slower increase, up to six weeks, after injury. (A System of Orthopedic Medicine: Ombregt, Bissschop, J ter Veer 2003, p45)
Therapeutic Movement To encourage better organization of repair, gentle tension should be applied to recent injury at about the fifth day (Evans 1989). Gentle tension from controlled movement, applied early in the healing process promotes greater tensile strength in the long run. Progressive increased movement should continue with the goal of full range by the third or fourth week.
Inactivity During Repair (not good) Cellular activity is stimulated by physical stresses to the tissue. With inactivity, collagen turnover still occurs and new collagen is made, but is poorly organized and not oriented along lines of stress. Controlled movement is good!
End of Repair Tissue Still Weak At the end of this phase, fibrous repair is established and a collagen mass is maximal, but the tensile strength of the newly formed tissue is only 15% of normal (Hardy 1989).
Recurrent Pain & Inflammation Over enthusiastic approaches or failure to maintain appropriate activity modification can lead to disruption of healing and recurrent inflammatory responses. After three weeks it is common for the individual to experience recurrent bouts of pain when the repair is stressed.
Treatment Objectives At this stage the tissue is more amenable to therapeutic movement because collagen is being laid down at the injury site at an accelerated rate (tissue repair), forming weak hydrostatic bonds. This intermediate stage of care and healing presents an excellent opportunity for reshaping and molding of the scar that will form, without great risk of re-injury.
Therapeutic movement is achieved with various forms of passive (manual) and active movement therapy. This stage physiologically lasts for three to eight weeks. If this phase of healing is left unattended, a greater amount of unorganized scar tissue may form leaving the soft tissues less elastic, less flexible and the joint less mobile. Therapeutic movement helps promote more organized and more functional scar tissue, and more functional, stable joints.
From this stage we will transition you to more independent, active forms of therapy called rehabilitation. Rehabilitation exercises balance out old and recently developed muscle imbalances. It also ensures that the tissues mature and strengthen properly. This will better enable you to carry out normal and more demanding activities with less chance of recurrent problems.
If repair phase is retarded, remodeling may remain incomplete. Thus, optimal function may not be restored and persistent problems are considered more likely.
Phase Three (Remodeling) In the remodeling phase, collagen begins to solidify and shrink. Nonetheless, collagen synthesis is still occurring and additional therapeutic benefit can be attained with appropriate intervention as the tissues continue to mature (7). Progressive resistance exercises are implemented into the treatment plan, directed at hypertrophy and hyperplasia of the maturing injured tissue (18). If therapeutically unattended, the collagen fibers may still develop significantly more unorganized scar tissue, shrinkage, cross-linking and remain immature (weaker & less functional). Once the tissues mature, management becomes a more difficult proposition as the tissue reverts to a more inactive and non-pliable status. Most of your benefit at this stage will come from therapeutic exercise, typically performed at home. However, continued passive manual may still be beneficial during remodel because of the contractive nature of the healing dense connective tissue (ligaments). At this stage the treatment plan is to wean you off passive care as much as possible but at the same time carefully monitor and manage against intersegemental stiffening of the injured area. This theoretically is more applicable with spinal joints because of the multiple segments involved. Active movement exercises may fail to isolate some segments. This is determined by how you feel and by clinical findings by palpation on each subsequent visit as we extend the period of time between visits.
Remodeling can last for 12 months, sometimes more after injury. Because of the protracted nature of remodeling, it's important in many cases, to continue active therapeutic movement for some time after you feel better! This is clearly established in the medical literature. The maturation (remodeling) time is different in every individual based on a multitude of independent variables unique to each individual. Again, any ongoing care is based on clinical findings as visit frequency is reduced. Additional rehabilitation addressing muscle strength, balance, coordination is based on clinical indication and individual physical demands.
Failure to Remodel/Repair Tissue
Self-perpetuating Inflammation (A System of Orthopedic Medicine: Ombregt, Bissschop, J ter Veer 2003, p45) Orthopedic medicine also deals with chronic repetitive strains and tissue disruptions, overuse phenomenon and excessive tension on the devitalized tissues. Here the reaction of the tissues involved is often not linear; inflammation may be prolonged and the formation of scar tissue excessive and inappropriate. Without proper movement there is no balance between formation and lysis of the regenerating elements of the involved tissue. Proper alignment of collagen does not result and the scar tissue tends to remain poorly organized. With that, any small stress applied to an inappropriate tissue is sufficient to disrupt newly formed fibers in the healing breach. This in turn starts another inflammatory response and a vicious cycle of chronic repetitive disruptions of inferior quality connective tissue will result. In such circumstances, with chronic recurrent inflammation, the function of the affected areas continues to deteriorate and leads to further tissue damage.
Refractory (stubborn) Pain If a chronic self-perpetuating inflammation has become established, the local infiltration of corticosteroid may interrupt the process. The scar then becomes painless and the tissue, no longer deprived of its functional motion and appropriate stress, again remodels. Another less invasive approach is deep tissue manipulation. (A System of Orthopedic Medicine: Ombregt, Bissschop, J ter Veer 2003, p45)
Scar Contraction Recently formed scar tissue will always shorten unless it is repeatedly stretched. This contracture occurs from the third week to the sixth month after the beginning of the inflammation stage. (McKenzie) Contracture of old scar tissue may occur for years after the problem originated (Evans 1980; Hunter 1994). Nonfunctional cross-linking between newly synthesized collagen fibers, at the time of repair, can act to prevent full movement.
Muscles: A similar functional impairment may affect contractile tissues, and although this may restrict end-range flexibility, it is most commonly exposed with restricted movements that stress the muscle tendon.
Hyper-sensitization of Scar Nerve endings infiltrate this area during the repair process and thus can make the scar tissue a sensitized nodule of abnormal tissue (Cousins 1994).
Old Problems Can Remodel With older injuries, the remodeling of collagen by applying a long-term structured exercise program may be necessary. By applying regular stress sufficient to provide tension without damage, collagen undergoes chemical and structural changes that allow elongation and strengthening of the affected tissue. (McKenzie 2004) Because tissue turnover is slow, one must recognize it may be a slow process. If the contracture has been present for some time, the remodeling (exercise) program will have to be followed for several months; Evans (1980) reports that some patients may have to exercise for the remaining years of their life.
Arem and Madden (1976) showed that old scar tissue might be unresponsive to a remodeling program, especially where the original healing process has been interrupted by repeated re-injury, causing the production of more inflammatory exudates.
Applying tension to injuries should be routinely practiced, especially prior to routine increased use and sporting activities (Hunter 1994).
Potential Causes of Chronic or Recurrent Pain Problems
Central Sensitization The plasticity of the central nervous system following a barrage of peripheral input can cause pathological changes that maintain the pain states in the absence of peripheral pathology (Johnson 1997; Siddall & Cousins 1997).
Persistent peripheral nociceptive input can induce changes in the central nervous system (Woolf 1991; Melzack 1988). This can lead to the sensitization of neurons in the dorsal horn, a state characterized by reduced thresholds and increased responses to a afferent input, such that normal mechanical stimuli is interpreted as pain.
There may be heightened responses to repeated stimuli, expansion of receptor fields and spontaneous generation of neuronal activity (Johnson 1997; Siddall & Cousins1997; Dubner 1991; cousins 1994). In other words, the pain seems to spread.
Nociceptive (pain) signals can also be initiated due to altered parts of the peripheral or central nervous system, which can produce the effect of localized “Phantom” pain in a part of the periphery where tissue damage no longer exists (Bogduk 1993).
Allodynia, Secondary Hyperalgesia, & Ectopic Pain Pain can radiate and be felt in uninjured areas adjacent to the original problem (secondary hyperalgesia), normal movement can be painful (allodynia), repeated movements can exaggerate pain responses, and pain signals can fire off without any appropriate stimulus (ectopic pain signals).
Other Chronic Pain Factors With the passage of time, neuropsychological, psychological and social factors may come to dominate the maintenance of pain and the link to the original tissue damage may become minimal (Waddell 1998; Adams 1997).
Psychological and behavioral attitudes and responses, as well as the process of nociception, shape individual’s experience of pain (Waddell 1998).
Psychosocial factors, and (Bokduk 1993; Johnson 1997).
Factors affecting pain responses are cultural, learned behavior, meaning of pain, fear and anxiety, neuroticism, lack of control of events, passive coping style and focus on the pain (Cousins 1994).
Depression, anxiety, passive coping and attitudes about pain are related to pain and disability.
Yellow Flag Catastrophising, hyper-vigilance about symptoms and fear avoidance behavior or attitudes and beliefs have been highlighted as being particularly significant, thus psychosocial factors, which can have a prognostic significance and termed “yellow flags“.
Chronic pain sufferers often feel little or no control over the pain, and helplessness that tends towards anxiety and depression, which in turn can make people more concerned about symptoms (Adams 1997).
Activity Avoidance The fear -- avoidance model (activity avoidance) proposes that some individuals react to a pain experience by continued avoidance of any activity that they think might hurt, long after rest is of any therapeutic value, leading ultimately to disability and exaggerated pain behavior (Lethem et al. 1983).
Although these factors can undermine treatment attempts, mechanical therapy is still found helpful for many patients with persistent symptoms. A mechanical assessment should never be denied to patients according to the duration of their symptoms. (McKenzie 2003, page 64)
Discordant Pain Often, healthcare professionals seem unable to deal with chronic pain behaviors, some of whom imply it is primarily “in their heads“, as the pain is “apparently discordant with discernible abnormalities” (Awerbuch 1995).
Inappropriate Behaviors Usually Consequential Not Cause of Chronic Pain
Important to note: Maladaptive or inappropriate behavior in the face of ongoing pain states does not represent malingering; it should be remembered that on the whole, the emotional disturbances are more likely to be a consequence of chronic pain rather than its cause (Gamsa 1990).
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