Trauma and Pain in Wound Healing in a Post Operative Setting - Literature review Example

Trauma and pain in wound healing in a post operative setting. - Pain – the flipside of pleasure – is the inevitable part of life. Pain associated with trauma is a major cause of concern. Pain prevails as long as the recuperation is not mentally identified on the moment. A perfect synch between ‘physical healing point’ and the psychological awareness of it is the real and complete recovery. Healing and recuperation is a natural process that consumes its own time tag. This applies to both physiological and pathological wounds. Wound care in a health care setting comprises efforts that simply support natural healing processes. Nurses in hospitals are more acquainted with wound care procedures, as they devote much of their duty time with patients and their pain. Clear understanding of pain mechanism and healing mechanism at physiological and cognitive levels would facilitate pain treatment in a more comfortable and effective way. Rationale & background: - Although they are well aware of the psychological inhibitions/acceptance of pain in patients, their findings in this direction do not find place in much of the research reports. The scenario may change when nurses in large numbers plunge into the field of research. This paper is paramount to that effort. Aligning psychic frequency of patients in tune with their actual recovery process is the upper most goal of these nurses in treating their wounds. Understanding Neuronal realm of pain mechanism and healing mechanism would facilitate trauma care, since the psychological derivations and research findings come very easily on their way of normal attendance of patients. Pain mechanism: - Successful pain treatment lies in understanding clearly the pain mechanism that generates pain. Advanced researches in this field have opened a floodgate of numerous vistas that are keeping the pain therapy ever reinvigorated. Molecular genetic studies have thrown light on identifying a protein namely, vanilloid receptor. It is found that it is this protein VR1, which is a heat-transducer converting heat energy into electrical signals. These signals are sent to the central nervous system making us experience and feel the heat. Molecular genetic studies have paved way to identify several other transduction molecules leading to measurable growth in pain therapy research. (Cheryl L. Stucky et al, 2001) Neuronal plasticity denotes changes occurring in the established nervous systems. The changes include many aspects such as neuronal structure, connections between neurons and alteration in the quantity and properties of neurotransmitters and receptors. Increased functional activities of neurons are found to decrease pain inhibitory systems in the pain pathway thereby increasing the feel of pain. (Cheryl L. Stucky et al, 2001) . Neuronal plasticity is capable of retaining the pain experience from minutes to hours or even to a greater length of time depending upon the pressures exchanged between the neurons. The study of neuronal plasticity has grown much to the extent that the functions of neuro transmitters are found not simply restricted to signalling (Tomas Hokfelt, 2009, p.2-3) but also involved in tissue growth aspects and functions as modulators. The traditional belief that a neuron would release only one messenger substance too is getting mooted and even the nerve endings and dendrites are found to release a different messenger substance and operate independently. Neuropathic pain or chronic pain: The important area of brain that is related to the perception of pain is the major part of forebrain namely, the ACC – Anterior Cingulate Cortex. The functioning style of ACC assumes response to both noxious and non-noxious stimuli. Non-pyramidal cells of ACC are inhibitory neurons containing GABA (γ-aminobutyric acid) and/or neuropeptides. GABA neurons of hypothalamic origin (Steven R. Vincent, 1982) are generally found to regulate neuro endocrine system. These neurons show typically the reduced spike responses to peripheral noxious stimuli, where as pyramidal cells show excitatory or increased spike responses. The evoked responses recorded from the larger cells of ACC in layer V were found to contain synaptic responses occurring at the outer layers of ACC. Within the local circuits, the inhibitory neurons often receive innervations from the pyramidal cells and then release GABA on to the perisomatic region of the pyramidal cells. While the above findings of Min Zhuo (2007) reveals the anatomy and role of Anterior Cingulate Cortex of brain structure in the transmission of pain impulses especially in respect of chronic pains, a very recent (2010) finding of the same author (Min Zhuo et al, 2010) indicates that the enzyme ‘protein kinase M zeta’ in the Anterior Cingulate Cortex acts to maintain neuropathic pain. In an animal model, the team was able to find that the pain was either reduced or absent on mice in which the enzyme was blocked at ACC. The team thus concluded that PKMζ could be a new therapeutic target for treating chronic pain. Healing mechanism: - A normal healing cascade begins with an orderly process of haemostasis and fibrin deposition, which leads to an inflammatory cell cascade, characterised by neutrophils, macrophages and lymphocytes within the tissue. This is followed by attraction and proliferation of fibroblasts and collagen deposition and finally the remodelling by collagen cross-linking and scar maturation. In the circumstances of chronic ulcers, pathologic responses leading to fibrosis – an event in which normal structural elements get replaced by distorted, non-functional and excessive accumulation of scar tissue – may occur if any part of the healing sequence is altered. (Robert F. Diegelmann and Melissa C.Evans, 2004) Healing mechanism comprises a wide range of five processes. They are: 1. Soothing. 2. Growth of new blood vessels. 3. Nerve growth. 4. Regeneration of connective tissues and 5. Regeneration of skin. Soothing: This is the initial process that enables healing occurs faster. The neutrophils migrate from blood cells to the site of wound/infection and the macrophages are less mobile than neutrophils and reside in tissues. (Joel D.Ernst, 2000). Complications arising out of the presence of necrotic tissues,(Sharon Baranoski et al, 2008, pp.89) which are dead, devitalised and avascular lead to delayed healing process, since these dead tissues render warm welcome to bacterial proliferation. The macrophages cells that reach the wound are polymorphonuclear leukocytes. These short-lived cells begin the process of phagocytosis by fixing to bacteria, extending their membrane around them, then dissolving and digesting the invading pathogens. Growth of new blood vessels: Undamaged blood vessels around the wound area begin to grow so that blood with sufficient oxygen pass through the wound. This process of budding of new blood vessels from the undamaged remnants is termed angiogenesis. Several researches involving angiogenesis chiefly revolve around angiogenesis in tumor growth with the aim to develop appropriate antiangiogenic strategies like monoclonal antibodies. (David A. Cheresh, 2008, p.2) Angiogenesis as such is a natural process that automatically maintains tissue homeostasis. Tissue homeostasis in turn is dependent on adequate supply of oxygen and nutrients received through blood vessels. Since the cells must be located within the oxygen diffusion limit, that is 100-200 µm, maintenance of vascular network becomes crucial for survival of tissues. Recent studies, however, point their fingers towards low oxygen level as the chief contributor to the onset of angiogenesis.(Reza Forough, 2006. p 1-2) Nerve growth: Nerves regenerate and grow on the wound site. Neuronal damages generally invite laser phototherapy, which accelerates and enhances axonal growth and regeneration after injury or a reconstructive peripheral nerve procedure. Laser activation of nerve cells, their growth and axonal sprouting could be considered as potential treatment for neuronal injury. (Rochind S, 2009) Regeneration of connective tissues: This is the basic and most important part of healing of a wound. Fibroblast cells converge towards the wound area and lay down collagen to support other tissues. Shivananda Nayak et al, (2006 ) found that Flavonoids were known to reduce lipid peroxidation not only by preventing or slowing the onset of cell necrosis but also by improving vascularity. Hence, any drug that inhibits lipid peroxidation is believed to increase the viability of collagen fibrils by increasing the strength of collagen fibres, increasing the circulation, preventing the cell damage and by promoting the DNA synthesis. (Shivananda Nayak et al, 2006 ) Regeneration of skin: The epithelial cells at the edges of the wound begin to bifurcate, trifurcate and so on. Simultaneously these cells grow towards each other and finally join to form an intact layer of the skin. Skin regeneration involves reconstruction of both epidermal and dermal skin components. This process is accomplished through neo-dermis formation; re-epithelialisation of wound surface and some degree of skin contracture. Normal fibroblasts gradually get to their normal count as the wound heals and myofibroblasts wane. Collagen type I production and the presence of normal fibroblasts are essential for the epithelial cell growth over the neo-dermis.(S.E.James et al, 2009. p161-165) Pain Measurement: - Taking an accurate account of individual pain history with a view to record pathophysiological cause of pain is essential. Intensity of pain in respect of young children and non-responsive patients relies on third-party observation. Quality of pain must be ascertained from the wordings of the patients. This would cover a wide range of presentation like ‘clear, burning, stabbing, shooting, lancinating, dull or gnawing’. On doing the subjective assessment, a keen record of the coping strategies used by individual patients is to be maintained. (Theodoros Theodoridis and Juergen Kraemer, 2009. p35-36). This is because the use of coping strategies does not always depend on the severity of disease and pain. Nina Santavirta (2001) found that in all pain groups distraction was the most commonly used coping strategy. Thus, after taking a comprehensive pain history of individual patient, appropriate basis for efficient pain therapy could be strategised through which, pain could be modulated and repressed by medication. Pain Psychology: - Homeostasis is the metabolic equilibrium actively maintained by complex biological mechanisms, which operate through autonomic nervous system in order to counter the disrupting changes. Recent hypotheses formulate that pain and homeostatic functions of thermoregulation are processed alike in central nervous system, in which non-painful thermal stimuli evoke an affective motivation – sensation of either pleasantness or unpleasantness – that depends on a functional context associated with reflexive autonomic adjustments. Thus, it is self- explanatory that pain experiences include modulation of cardio respiratory activity as well as immediate or delayed behavioural modifications. The defence responses work through the synergic action of the dorsolateral and lateral column of PAG – periaqueductal grey matter – of mesencephelon and the sympathetic nervous system. According to the body’s coping strategies – active and passive – the defence response mechanism is capable of counteracting the homeostatic imbalances elicited by psychological or physical stressors. (Giancarlo Carli, 2009). Exclusive focus on non- clinical approaches reveals that psychological factors have impact in pain management. Platow M.J (2007) et al investigated the social component to pain experiences and pain related behaviours. The team observed that in-group reassurance produced lower levels of physiological arousal than out-group reassurance in a pain setting. One more finding by Gabriel Tan (2006) et al attempting to illustrate the effect of incorporating CAM – Complementary and Alternative Medicine – showed that psychological intervention such as CBT(Cognitive behavioural Therapy) established efficacy in pain treatment. Of the two CAM presented by the team, the self-hypnosis method prompted greater confidence over the clinical application of CES – Cranial Electrotherapy Stimulation, the other CAM. These two findings reveal that non-clinical applications are capable of influencing pain management on selective group of patients. Rigorous and plenteous research in this direction may prove to render viable treatment strategies in which clinical aspects may serve more as data providers. Conclusion: - Pain is an indication of physiological imbalance. The natural defence mechanism employs pain as an indicator in its course of returning to normalcy. Both physiological and psychological stressors contribute to exacerbation of disease and pain. The interconnection between these two is very subtly fixed in brain cells. While recuperation or healing of wounds is purely physiological, the acknowledgement of the same has to be evoked psychologically. Any disharmony between the two is construed as prolongation of illness. As such, a perfect synch between body condition and mental acceptance lead to speedy recovery. Moleculer studies, cortical imaging studies and studies on synaptic plasticity in alignment with pharmacological, therapeutic and psychological realm throw much light in evolving a better therapeutic strategy for pain treatment and trauma care. A constant updating and research in this arena are sure to place the services of tissue viability nurses at the crown. * * * * * Reference list – Cheryl L. Stucky, Michael S. Gold and Xu Zhang, 2001, “Mechanisms of Pain”, Proceedings of the National Academy of Sciences of USA, Vol.98, No. 21, pp.11845-11846 David A. Cheresh, 2008, pp. 2, “Angiogenesis: in vivo systems Part 2”, Elsevier Inc, Amsterdam, Netherlands. Gabriel Tan, Julie A. Alvarez and Mark P. Jensen, August, 2006, “Complementary and Alernative Medicine approaches to Pain management”, Journal of Clinical Psychology, Vol. 62. No. 11: 1419-1431 Giancarlo Carli, 2009, “An Update on Pain physiology: The Relevance of Craig’s anf Janig’s Hypotheses for Hypnotic Analgesia”, Contemporary Hypnosis, Vol.26. No.1: 4-14, Wiley InterScience Joel D.Ernst, 2000, “Bacterial inhibition of phagocytosis”, Cellular Microbiology, Vol.2. No.5: 379-386 Min Zhuo, June 2007, “Neuronal mechanism for neuropathic pain”, Molecular Pain, Vol.3. No.14: Min Zhuo, Xiang-Yao Li, Hyoung-Gon Ko, Tao Chen, Giannina Descalzi, Kohei Koga, Hansen Wang, Susn S. Kim, Yuze Shang, Chuljung Kwak, Soo-Won Park, Jaehoon Shim, Kyungmin Lee, Graham L. Collingridge and Bong-Kiun Kaang, December 2010, “ Alleviating Neuropathic Pain Hypersensitivity by Inhibiting PKMζ in the Anterior Cingulate Cortex”, Science Magazine, Vol. 330. No. 6009: 1400-1404 Nina Santavirta, Hjordis Bjorvell, Svetlana Solovieva, Hannu Alaranta, Kari Hurskainen and Yrjo T. Konttinen, 2001, “Coping Strategies, Pain, and Disability in Patients with Hemophilia and related Disorders”, Arthritis Care and Research, Vol. 45: 48-55 Platow M.J, Nicholas J. Voudouris, Melissa Coulson, Nicola Gilford, Rachel Jamieson, Liz Najdovski, Nicole Papaleo, Chelsea Pollard and Leanne Terry, August, 2007, “In-group reassurance in a pain setting produces lower levels of physiological arousal: direct support for a self-categorization analysis of social influence”, European Journal of Social Psychology, Vol. 37, No.4: 649-660 Reza Forough, 2006, pp.1-2, “New Frontiers in Angiogenesis”, Springer, Netherlands Robert F. Diegelmann and Melissa C.Evans, January 2004, “Wound Healing: an Overview of Acute, Fibrotic and delayed healing”, Frontiers in Bioscience, Vol. 9: 283-289 Rochind S, 2009, “Phototherapy in peripheral nerve regeneration:From basic science to clinical study”, Neurosurgery Focus, Vol.26. No.2:E8 retrived from www.healinglightseminars.com/listing/Nerve%20Regeneration.pdf on 10.dec.2010 S.E.James, S.Booth, P.Gilbert, I.Jones and R.Shevchenco, 2009, pp.161-165, “Clinical Approaches to Skin Regeneration” in (Eds) Matteo Santin, “Strategies in regenerative medicine: integrating biology with materials design”, Springer Science+Business Media, New York Sharon Baranoski and Elizabeth A.Ayello, 2008, pp. 89,“Wound Care Essentials: Practice Principles”, Lippincott Williams and Wilkins, USA Shivananda Nayak, Steve Sandiford, Andrew Adogwa, Poorna Nalabothu and Vidyasagar Bogadi, April, 2006, “Evaluation of wound healing activity of Allamandha Cathartica L. and Laurus Nobilis L extracts on rats”, BMC Complementary and Alternative medicine, Vol. 6. No.12: doi:10.1186/1472-6882-6-12 Steven R.Vincent, Tomas Hokfelt and Jang-Yen Wu, 1982, “GABA Neuron Systems in Hypothalamus and the Pituitary Gland: Immunohistochemical demonstrationUsing Antibodies against GlutamateDecarboxylase”, Neuroendocrinology, Vol. 34. No.2: 117-125 Tomas Hokfelt, pp. 2, “Coexistence of Neuro Messenger Molecules – A perspective”, in (Eds) Rafael Gutierrez, 2009, “Co-Existence and Co-Release of Classical Neurotransmitters: Ex Uno Plures”, Springer Science+Business Media, New York. Theodoros Theodoridis, Juergen Kraemer, 2009, pp.35-36, “Spinal Injection Techniques”, Georg Thieme Verlag, New York Volker Neugebauer, Weidong Li, Gary C. Bird and Jeong S. Han, June 2004, “The Amygdala and Persistent Pain”, Neuroscientist, Vol. 10 No. 3: 221-234 Read More