Pijnmanagement na VKB reconstructie

1. Pijnmanagement na VKB-reconstructie Timothy Vranken AIOS orthopedie
2. Inhoud 1. VKB problematiek 2. Pijn problematiek 3. Wat is pijn 4. Hoe werkt pijn 5. Pijnbehandeling bij VKB reconstructie 6. Virtual reality 7. Virtual reality (VR) bij VKB reconstructie
3. 1. VKB problematiek • Interesse in klinische tool om return to sport te bepalen • Return to sport test batterij (zoals bijvoorbeeld single hop test) • Probleem: huidige sport test batterij is te gefocust op de biologie van herstel
4. 1. VKB problematiek • 88% van atleten met VKB ruptuur verwachten dat ze terug naar huidige niveau van sport kunnen terugkeren • Echter, maar 55% van de atleten keert terug op het oude niveau na VKB reconstructie • De competitieve jonge atleet (<20 jaar) die terugkeert naar een pivoterende sport heeft een hoog risico (30-40%) op ipsi- of contralateraal VKB letsel Bron: A. Gokeler, et al. 2022. Return to sports after ACL injury 5 years from now: 10 things we must do. Journal of experimental orthopaedics.
5. 1. VKB problematiek • Operatietechniek • RCT 2021 bij (semi)professionele voetballers : geen verschil in graft falen na 2 jaar follow-up tussen hamstring en BPTB • Systematic review 2021 van 17 RCT’s: geen verschil in graft falen > 10 jaar follow-up tussen hamstring en BPTB • Laterale extra-articulaire tenodese RCT 2020: 25% re-reruptuur in ACLR versus 4% re-ruptuur in ACLR + LET Bron:Guglielmetti et al. 2021. Prospective and randomized clinical evaluation of hamstring versus petallar tendon autograft for anterior cruciate ligament reconstruction in soccer players. Orthopaedic journal of sports medicine. Matar et al. 2021. A systematic review of randomized controlled trials in anterior cruciate ligament reconstruction: standard techniques are comparable (299 trials with 25 816 patienten). Arthroscopy, sports medicine, and rehabilitation. ng autograft versus patellar tendon autograft for ACL reconstruction: is there a difference in graft failure rate? A meta-analysis of 47 613 patienten Getgood et al. 2020. Lateral extra-articular tenodesis reduces failureof hamstring tendon autograft anterior cruciate ligament reconstruction: 2-year outcomes from the stability study randomized controlled trial. American Journal of Sports mediccine.
6. 1. VKB problematiek • Revalidatie • Huidige focus op herstel spierkracht (BFR), uithouding en neuromusculaire controle • Ontoereikend • Neurofysiologische en neurocognitieve adaptatie van centraal zenuwstelsel na ligamentair letsel • Huidige return to sport functionele testen zijn relatatief makkelijke motorische testen in een voorspelbare omgeving en derhalve ontoereikend
7. 1. VKB problematiek • Pijn • Verschil in pijnbeleving tussen sporters en niet-sporters • Verschil in endogene pijn inhibitie • Correlatie tussen algemene fitheid en activatiekracht van het brein en functionele connectiviteit • Postoperatieve pijn is geassocieerd met psychologische en fysieke paraatheid voor return to sport Bron: Pettersen et al. 2020. Pain processing in elite and high level athletes compared to non-athletes. Frontiers in Psychology. Geisler et al. 2021. Neural mechanisms of pain processing differ between endurance athletes and non-athletes: a functional connectivity magnetic resonance imaging study. Human brain mapping. Betsch et al. 2021. Postoperative pain is associated with psychological and physical readiness to return to sports one year after anterior cruciate ligament reconstruction. Arthroscopy, sports mediccine and rehabilitation.
8. 2. Pijn problematiek Voorgeschreven Ziekenhuisopnames door overdosis Overlijden door overdosis Bron: Kalkman et al. 2019. Trends in use and misuse of opioids in the Netherlands: a retrospective, multi-source database study. The Lancet
9. 2. Pijn problematiek • In de Verenigde staten zijn de orthopedisch chirurgen 3de grootste voorschrijvers van opiaten • 1/10 voorschriften voor opiaten komt van een orthopedisch chirurg • Het gebruik van opiaten voor een operatie is de grootste risicofactor voor langdurig gebruik na de operatie Bron: Davey et al. 2021. Pain management strategies after anterior cruciate ligament reconstruction: a systematic review and network meta-analysis. Journal of arthroscopy and related surgery.
10. 2. Pijn problematiek • 2020 door sociale isolatie en economische onzekerheid tijdens pandemie stijging >30% van overlijden door overdosis (Verenigde Staten) Data: 2015–2019 — Final data from CDC WONDER; 2020 — National Vital Statistics System, Provisional Drug Overdose Death Counts. Jesse C. Baumgartner and David C. Radley, “The Drug Overdose Mortality Toll in 2020 and Near-Term Actions for Addressing It,” To the Point (blog), Commonwealth Fund, July 15, 2021, updated Aug. 16, 2021.
11. 2. Pijn problematiek Bron: Automation of Reports and Consolidated Orders System (ARCOS) of the Drug Enforcement Administration (DEA), 2010
12. 3. Wat is pijn • Plato (347 B.C.): een emotie • Descartes (1650): het resultaat van fysiek of van psychologisch lijden • Charles Bell (1840): de huid bevat verschillende receptoren die reageren op koude, pijn, warmte en aanraking
13. 3. Wat is pijn • David Wall en Ronald Melzack (1925): gate control theorie • Ronald Melzack (1930): fantoompijn • Roy Grinker (1954): biopsychosociaal model “Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage. Pain is always a personal experience that is influenced to varying degrees by biological, psychological and social factors.”
14. 4. Hoe werkt pijn Woolf et al. 2010. What is this thing called pain. Journal of clinical investigation.
15. 5. Pijnbehandeling bij VKB reconstructie • 2021 systematic review en meta-analyse: 74 RCT’s • Zenuwblokkade: significante daling in pijnscore (VAS), geen verschil tussen de verschillende zenuwblokkades • Voorkeur: adductor kanaal block (geen risico op femoralis neuropraxie) • Intra-articulaire infiltraties: significante daling in pijnscore <12u postoperatief • Voorkeur: bupivacaine en tramadol • Tranexaminezuur: tegenstrijdig bewijs, 1 RCT laat significante daling in VAS scores zien tot 1 maand postoperatief • Voorkeur: IV, niet intra-articulair gezien mogelijk toxisch effect op kraakbeen • Cryotherapie: significante daling in pijnscore direct en tot wel 6 weken postoperatief Bron: Davey et al. 2021. Pain management strategies after anterior cruciate ligament reconstruction: a systematic review and network meta-analysis. Journal of arthroscopy and related surgery.
16. 5. Pijnbehandeling bij VKB reconstructie • Protocol Zuyderland • Bij voorkeur spinale anesthesie zonder sedatie • Minimaliseren van opiaat gebruik: op indicatie wel geven • Dexamethason 8mg IV • LIA (ropivacaine) in hamstring gebied
17. Wat met het opiaten gebruik postoperatief?
18. 6. Virtual reality • Display op het hoofd gemonteerd • Getransporteerd naar een levensechte 3D wereld • Theorie: de stimulatie van de virtuele cortex zorgt voor afleiding, dit leidt op zijn beurt tot de verminderde verwerking van nociceptieve stimuli • Functionele MRI toonde >50% afname in pijn gerelateerde hersenactiviteit Bron: Spiegel et al. 2019. Virtual reality for management of pain in hospitalized patient: a randomized comparative effectiveness trial. Plos one.
19. 6. Virtual reality • Binnen de orthopedie: • Chronische lage rugpijn • TKP • Patellofemoraal pijnsyndroom • Verwijderen fixateur externe • Subacromiale impingement • Fractuur reposities of gipswissels bij kinderen Bron: Koshinski et al. 2022. Virtual reality (VR) in medicine: a systematic review of current applications of VR and potential applications to pediatric orthopaedic surgery. Journal of orthopaedic experience & innovation. Gumaa et al. 2019. Is virtual reality effective in orthopedic rehabilitation? A systematic review and meta-analysis. Journal of physical therapy. Gazendam et al. 2022. Virtual reality rehabilitation following total knee arthroplasty: a systematic review and meta-anaoysis of randomized controlled trials. European society of sports traumatology, knee surgery, arthroscopy. Le May et al. 2020. Immersive virtual reality vs non-immersive distraction for pain mangement of children during bone pins and sutures removal: a randomized clinical trial protocol. Journal of advanced nursing. Ebrahimi et al.2021. The effects of virtual reality training on clinical indices and brain mapping of women with patellofemoral pain: a randomized clinical trial. BMC musculoskeletal disorders.
20. 7. VR bij VKB reconstructie • RCT studie in Zuyderland • Gebruik van VR per- en postoperatief • Primaire VKB reconstructies • Primaire uitkomstmaat: pijn • Secundaire uitkomstmaat: angst, pijn catastrofering, opiaten gebruik, opname duur, knie functie • Hypothese: afname van postoperatieve pijn en angst leidend tot afname van kinesiofobie en verbetering van kniefunctie
21. Graag onthouden Behandeling van VKB ruptuur stopt niet bij “het trucje” op OK

Notes de l'éditeur

Bekijk artikelen neurofysiologie en neurocognitie bij ligamentair letsel
Intensity Theory
The theory goes back to the Athenian philosopher Plato (c. 428 to 347 B.C.) who in his work Timaeus, defined pain not as a unique experience, but as an 'emotion' that occurs when the stimulus is intense and lasting. Centuries later, we are aware that especially chronic pain represents a dynamic experience, profoundly changeable in a spatial-temporal manner. A series of experiments, conducted during the nineteenth century, sought to establish the scientific basis of the theory. These investigations, based on the tactile stimulation and impulses of other nature such as electrical stimulations, provided important information concerning the threshold for tactile perceptions and the role of the dorsal horn neurons in the transmission/processing of pain.[8]
Cartesian Dualistic Theory
The oldest explanation for why pain manifested in specific populations was rooted in religious beliefs. Throughout history, religious ideologies have had a substantial influence on people’s thoughts and actions. As a result, the majority of people believed that pain was the consequence of committing immoral acts. There was also a belief that the suffering they endured was the individual’s way to repent for these sins.[9] Although this belief remained popular up until the nineteenth century, this was not due to the lack of other available theories. One of the first alternative scientific pain theories was bravely introduced in 1644 by the French philosopher Renee Descartes (1596-1650). This theory has the name in current literature as the Cartesian dualism theory of pain.[10] The dualism theory of pain hypothesized that pain was a mutually exclusive phenomenon. Pain could be a result of physical injury or psychological injury. However, the two types of injury did not influence each other, and at no point were they to combine and create a synergistic effect on pain, hence making pain a mutually exclusive entity.[11] In an attempt to placate the church, Descartes also included in his theory the idea that pain has a connection to the soul. He claimed that his research uncovered that the soul of pain was in the pineal gland, consequentially designating the brain as the moderator of painful sensations.[1] The dualistic approach to pain theory fails to account for many factors that are known to contribute to pain today. Furthermore, it lacks an explanation as to why no two chronic pain patients have the same experience with pain even if they had similar injuries. Despite these shortcomings, it still provided future researchers with a solid foundation to continue expanding the scientific understanding of the intricate phenomenon of pain.
Specificity Theory
Many scientists continued to do research long after Descartes proposed the dualistic theory of pain. However, it wasn’t until 1811 that another well-known pain theory came onto the scene. This theory, initially presented by Charles Bell (1774–1842), is referred to as the specificity theory.[1][5] This theory is similar to Descartes' dualistic approach to pain in the way that it delineates different types of sensations to different pathways. In addition to the identification of specific pathways for different sensory inputs, Bell also postulated that the brain was not the homogenous object that Descartes believed it was, but instead a complex structure with various components.[1][5] Scientists and philosophers alike spent the next century and a half further developing the specificity theory. One of the many contributors to this theory was Johannes Muller. In the mid-1800s, Muller published in the Manual of Physiology that individual sensations were the result of specific energy experienced at certain receptors. Furthermore, Muller believed that there was an infinite number of receptors in the skin, and this surplus of receptors accounted for the ability of an individual to discriminate between different sensations.[6] In 1894, Maximillian von Frey made another critical addition to the specificity theory that served to advance the concept. This contribution to the theory was the discovery of the four separate somatosensory modalities found throughout the body. These sensations include cold, pain, heat, and touch.[12] This concept correlates well with previous research done regarding this theory of pain, which served to reiterate the presence of distinct pathways for different sensations. Although this theory and the research surrounding it provided significant advancement to the understanding of pain, it still fails to account for factors other than those of physical nature that result in the sensation of pain. Much like the dualistic approach to pain, this theory also lacks an explanation for why sometimes pain persists long after the healing of the initial injury. This incomplete nature of the specificity theory regarding pain etiology necessitated additional theories and continued research.
Pattern Theory
Following the specificity theory, there were a handful of other philosophies introduced regarding the sensation of pain. Of these philosophies, the pattern theory of pain has the greatest coverage in the scientific literature. The American psychologist John Paul Nafe (1888-1970) presented this theory in 1929. The ideas contained in the pattern theory were directly opposite to the ideas suggested in the Specificity theory in regards to sensation. Nafe indicated that there are no separate receptors for each of the four sensory modalities. Instead, he suggested that each sensation relays a specific pattern or sequence of signals to the brain. The brain then takes this pattern and deciphers it. Depending on which pattern the brain reads, correlates with the sensation felt.[5][13] At the time of its introduction, the pattern theory gained significant popularity among many researchers. However, through further research and the discovery of unique receptors for each type of sensation, it can be stated with certainty, that this theory is an inaccurate explanation for how we feel pain.
Gate Control Theory
In 1965, Patrick David Wall (1925–2001) and Ronald Melzack announced the first theory that viewed pain through a mind-body perspective. This theory became known as the gate control theory.[14] Melzack and Wall’s new theory partially supported both of the two previous theories of pain but also presented more knowledge to advance the understanding of pain further. The gate control theory of pain states that when a stimulus gets sent to the brain, it must first travel to three locations within the spinal cord. These include the cells within the substantia gelatinosa in the dorsal horn, the fibers in the dorsal column, and the transmission cells which are located in the dorsal horn as well.[6][15]The substantia gelatinosa of the spinal cord's dorsal horn serves to modulate the signals that get through, acting similar to a “gate” for information traveling to the brain.[13] The sensation of pain that an individual feels is the result of the complex interaction among these three components of the spinal cord. Simply stated, when the “gate” closes, the brain does not receive the information that is coming from the periphery to the spinal cord. However, when the signal traveling to the spinal cord reaches a certain level of intensity, the “gate” opens. Once the gate is open, the signal can travel to the brain where it is processed, and the individual proceeds to feel pain. The information mentioned above accounts for the physical component of pain, but as stated earlier, the Gate Control Theory was one of the first to acknowledge that psychological factors contributed to pain as well. In their original study, Melzack and Wall suggested that in addition to the control provided by the substantia gelatinosa, there was an additional control mechanism located in cortical regions of the brain.[15] In more recent times, researchers have postulated that these cortical control centers are responsible for the effects of cognitive and emotional factors on the pain experienced. Current research has also suggested that a negative state of mind serves to amplify the intensity of the signals sent to the brain as well.[16] For example, somebody who is depressed has a “gate” that is open more often, allowing more signals to get through, increasing the probability that an individual will experience pain from an otherwise normal stimulus. Also, there are reports that certain unhealthy lifestyle choices will also result in an “open gate,” which in turn leads to pain that is disproportionate to the stimulus.[17][18] The gate control theory has proven to be one of the most significant contributions to the study of pain throughout history. The concepts that Melzack and Wall introduced to the study of pain are still utilized by researchers today. Even though this theory initiated the idea that pain wasn’t solely a result of physical injury but rather a complex experience, influenced by cognitive and emotional factors, there was still additional research necessary to comprehend the mechanisms and etiology of pain completely. This need precipitated the introduction of the following two philosophies regarding pain.
Neuromatrix Model
Almost thirty years after introducing the gate control theory of pain, Ronald Melzack introduced another model that contributed to the explanation of how and why people feel pain. Until the mid-1900s, most theories of pain implied that this experience was exclusively due to an injury that had occurred somewhere in the body. The thinking was that if an individual suffered an injury, whether it be through trauma, infection, or disease, a signal would transmit to the brain which would, in turn, result in the sensation of pain. Although Melzack had contributed to these previous theories, it was his exposure to amputees that were experiencing phantom limb pain in well-healed areas that prompted his inquiry into this more accurate philosophy of pain. The theory he proposed is known as the neuromatrix model of pain. This philosophy suggests that it is the central nervous system that is responsible for eliciting painful sensations rather than the periphery.[19][23] The neuromatrix model denotes that there are four components within the central nervous system responsible for creating pain. The four components are the “body-self neuromatrix, the cyclic processing, and synthesis of signals, the sentinel neural hub, and the activation of the neuromatrix.”[13]According to Melzack, the neuromatrix consists of multiple areas within the central nervous system that contribute to the signal, which allows for the feeling of pain. These areas include the spinal cord, brain stem and thalamus, limbic system, insular cortex, somatosensory cortex, motor cortex, and prefrontal cortex.[19] The signal that these areas of the central nervous system work together to create is responsible for allowing an individual to feel pain, and he referred to as the “neurosignature.” Furthermore, this theory states that input coming in from the periphery can initiate or influence the neurosignature, but these peripheral signals cannot create a neurosignature of their own.[13] This idea that peripheral signals can alter the neurosignature is an important concept when considering the effect that nonphysical factors have on an individual’s experience with pain. Melzack’s theory claimed that not only are there specific neurosignatures that elicit certain sensations, but when there is an alteration in a certain signal, this allows for memory formation of these particular experiences.[19] If the same circumstances occur again in the future, it is this memory that allows for the same sensation to be felt. In addition to the hypothesis that pain was a product of different patterns of signals from the central nervous system, the neuromatrix model continued to elaborate on the idea that was initially brought forward in the gate control theory, that pain can be affected not only by physical factors but by cognitive and emotional factors. Melzack suggested that hyperactivity of the stress response has a direct effect on pain. Hyperactivity of the stress response is when an individual exposed to increased levels of stress experiences a higher level of pain.[19] Taking all of these claims into consideration, it is evident that pain is a complex issue that cannot be accounted for by physical factors alone. Even though the neuromatrix model further established the idea that pain gets influenced by cognitive and emotional factors as well as physical factors, it still fails to account for social constructs of pain. Therefore, a new theory of pain must be utilized to appropriately explain the mechanism behind pain and why each individual’s experience with pain is unique.
Biopsychosocial Model
The biopsychosocial model provides the most comprehensive explanation behind the etiology of pain. This specific theory of pain hypothesizes that pain is the result of complex interactions between biological, psychological, and sociological factors, and any theory which fails to include all of these three constructs of pain, fails to provide an accurate explanation for why an individual is experiencing pain.[20][21] Although the term biopsychosocial was not introduced until 1954 by Roy Grinker (1900-1993), a neurologist and psychologist, there have been many physicians who had considered the utility of using such a model to approach the management of a patient’s pain long before this.[22][23] One of the most prominent physicians who utilized this more comprehensive approach to pain was John Joseph Bonica (1917-1994), a Sicilian American anesthesiologist at Madigan Army Hospital, known as the founding father of the discipline of pain medicine. In the 1940s, Bonica was caring for many patients who had returned home from World War II and were now experiencing debilitating pain due to injuries they had suffered in the war. He had recognized that the pain these wounded soldiers were experiencing was rather complex and not easily managed. This situation led him to propose that to adequately manage these patients, physicians needed to create interprofessional pain clinics comprising multiple disciplines.[24] At this moment in history, there was little support for the idea that pain was more than just the result of an injury, and Bonica was relatively unsuccessful in establishing these clinics. It wasn’t until 1977 that the biopsychosocial model was scientifically suggested as an explanation for the etiology of some medical conditions. George Engle claimed that to treat disease adequately, one must consider multidimensional concepts and manage the whole patient instead of focusing on a single issue.[32] This methodology takes into account that the human body cannot be divided into separate categories when considering treatment options. Instead, it is beneficial to acknowledge the fact that illness and disease are the results of complex interactions between biological, psychological, and sociological factors, and they all affect an individual’s physical and mental well-being.[33]Although Bonica had technically been the first physician to comprehend the importance of using a biopsychosocial approach to pain, John D. Loeser, another anesthesiologist, has been credited as the first person to use this model in association with pain.[25] Loeser suggested that four elements need to be taken into consideration when evaluating a patient with pain. These elements include nociception, pain, suffering, and pain behaviors. Nociception is the signal that is sent to the brain from the periphery to alert the body that there is some degree of injury or tissue damage. Pain, on the other hand, is the subjective experience that occurs after the brain has processed the nociceptive input. The last two components of pain that merit consideration is suffering and pain behaviors. The thinking is that suffering is an individual’s emotional response to the nociceptive signals and that pain behaviors are the actions that people carry out in response to the experience of pain. Both of these can be either conscious or subconscious.[25] Loeser’s four elements of pain account for the biological, psychological, and sociological factors that can create or influence an individual’s experience with pain. Failing to consider any one of these four elements when determining the cause or establishing a management plan could be a consideration as inadequate assessment or care. With a better understanding of what is causing a patient to experience pain, the doctor is provided with a more accurate foundation to begin formulating a treatment plan. Loeser’s findings prove that the Biopsychosocial Model of pain offers the most comprehensive philosophy and provides the framework that is needed to start appropriate therapy to manage patients with chronic pain adequately
What exactly, from a neurobiological perspective, is pain? Pain is actually three quite different things, although we and many of our physicians commonly fail to make the distinction. First, there is the pain that is an early-warning physiological protective system, essential to detect and minimize contact with damaging or noxious stimuli. This is the pain we feel when touching something too hot, cold, or sharp. Because this pain is concerned with the sensing of noxious stimuli, it is called nociceptive pain (Figure (Figure1A),1A), a high-threshold pain only activated in the presence of intense stimuli (1). The neurobiological apparatus that generates nociceptive pain evolved from the capacity of even the most primitive of nervous systems to signal impending or actual tissue damage from environmental stimuli. Its protective role demands immediate attention and action, which occur by virtue of the withdrawal reflex it activates, the intrinsic unpleasantness of the sensation elicited, and the emotional anguish it engages. Nociceptive pain presents itself as something to avoid now, and when engaged, the system overrules most other neural functions.

The second kind of pain is also adaptive and protective. By heightening sensory sensitivity after unavoidable tissue damage, this pain assists in the healing of the injured body part by creating a situation that discourages physical contact and movement. Pain hypersensitivity, or tenderness, reduces further risk of damage and promotes recovery, as after a surgical wound or in an inflamed joint, where normally innocuous stimuli now elicit pain. This pain is caused by activation of the immune system by tissue injury or infection, and is therefore called inflammatory pain (Figure (Figure1B);1B); indeed, pain is one of the cardinal features of inflammation. While this pain is adaptive, it still needs to be reduced in patients with ongoing inflammation, as with rheumatoid arthritis or in cases of severe or extensive injury.
Finally, there is the pain that is not protective, but maladaptive, resulting from abnormal functioning of the nervous system. This pathological pain (Figure (Figure1C),1C), which is not a symptom of some disorder but rather a disease state of the nervous system, can occur after damage to the nervous system (neuropathic pain), but also in conditions in which there is no such damage or inflammation (dysfunctional pain). Conditions that evoke dysfunctional pain include fibromyalgia, irritable bowel syndrome, tension type headache, temporomandibular joint disease, interstitial cystitis, and other syndromes in which there exists substantial pain but no noxious stimulus and no, or minimal, peripheral inflammatory pathology. The clinical pain syndrome with the greatest unmet need, pathological pain is largely the consequence of amplified sensory signals in the central nervous system and is a low-threshold pain. By analogy, if pain were a fire alarm, the nociceptive type would be activated appropriately only by the presence of intense heat, inflammatory pain would be activated by warm temperatures, and pathological pain would be a false alarm caused by malfunction of the system itself. The net effect in all three cases is the sensation we call pain. However, because the processes that drive each are quite different, treatments must be targeted at the distinct mechanisms responsible.

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