Lecture 4. Response to Injury & Pain Management (Part 2) PDF

RESPONSE TO INJURY & PAIN MANAGEMENT By: Dr. Walid Abouelnaga Associate Professor of Physical Therapy PhD, MSc, PT Your Date Here Your Footer Here 1 TYPES OF THE BODY TISSUES 1- Epithelial tissue: Stratified squamous epitheli...

RESPONSE TO INJURY & PAIN MANAGEMENT By: Dr. Walid Abouelnaga Associate Professor of Physical Therapy PhD, MSc, PT Your Date Here Your Footer Here 1 TYPES OF THE BODY TISSUES 1- Epithelial tissue: Stratified squamous epithelium of the epidermis of the skin. 2- Connective tissues: which are 3 types: a. Connective tissue proper with soft matrix. b. Cartilage with rubbery matrix. c. Bone with solid matrix. 3- Muscular tissues. 4- Nervous tissues. CONNECTIVE TISSUE PROPER C.T is formed of 3 parts: (A)- Connective tissue cells: e.g. Fibroblasts and Mast cells. (B)- Connective tissue fibers: e.g. Collagenous fibers, Elastic fibers and Reticular fibers. (C)- Matrix: ground interstitial substance. The C.T cells and fibers are embedded in a soft jelly-like substance called the matrix. CONNECTIVE TISSUE CELLS 1- Fibroblast: Is the most important and commonest C.T cell which is responsible for the formation of the C.T fibers and repair of injury. 2- Mast Cell: Mast cells secrete heparin, which is anticoagulant as well as chemotactic factor as histamine. CONNECTIVE TISSUE FIBERS 1- White Collagenous Fibers: Are formed of protein called collagen, which is glue-like substance arranged in bundles. 2- Yellow Elastic Fibers: Are elastic in nature (stretchable) and formed of protein called elastin. 3- Reticular Fibers: Are formed of protein called reticulin and arranged in the form of fine network. PHASES OF WOUND HEALING There are four phases of wound healing: 1- Hemostasis phase: which stops the bleeding 2- Inflammatory phase: which prepares the area for healing. 3- Fibroblastic phase: which rebuilds the structure. 4- Remodeling phase: which is the final form. HAEMOSTASIS Hemostasis (stop the active bleeding) occurs within minutes of the initial injury unless there are underlying clotting disorders. In wound healing the platelet acts to seal off the damaged blood vessels as follow: ✓ The blood vessels themselves constrict in response to injury but this spasm ultimately relaxes. ✓Then the platelets aggregate and adhere to the exposed collagen. Your Date Here Your Footer Here 7 ✓ They also secrete factors which interact with and stimulate the intrinsic clotting cascade through the production of thrombin, which in turn initiates the formation of fibrin from fibrinogen. ✓ The fibrin mesh strengthens the platelet aggregate into a stable hemostatic plug. ✓Finally, platelets also secrete cytokines which is recognized as one of the first factors secreted in initiating subsequent steps. Your Date Here Your Footer Here 8 Your Date Here Your Footer Here 9 INFLAMMATORY PHASE ▪ Clinically inflammation is the second stage of wound healing. This stage usually lasts up to 4 days post injury. ▪ It presents as erythema, swelling and warmth often associated with pain. 12/05/1446 10 PHAGOCYTOSIS In the wound healing, the first job to be done is to clean up the debris, this is done by the neutrophils or PMN’s (polymorphonucleocytes) as follow: ✓ The inflammatory response causes the blood vessels to become leaky releasing plasma and PMN’s into the surrounding tissue. ✓ The neutrophils phagocytize debris and microorganisms and provide the first line of defense against infection. They are aided by local mast cells (mast cells & injured vessels will release histamine which cause more vasodilatation & increase permeability). 12/05/1446 11 ✓ As fibrin is broken down as part of this clean-up the degradation products attract the next cell involved - the macrophage. ✓ Macrophages are able to phagocytize bacteria and provide a second line of defense. ✓ They also secrete a variety of chemotactic and growth factors such as fibroblast growth factor (FGF), epidermal growth factor (EGF), transforming growth factor beta (TGF-B) and interleukin-1 (IL-1) which appears to direct the next stage. 12/05/1446 12  This inflammation is needed for healing, but balance of this inflammation is also needed because: If there is no inflammation → no healing. Too little inflammation → slow healing. Balanced inflammation → proper & good healing. Too much inflammation →excessive scar formation. 12/05/1446 13 PROLIFERATIVE PHASE ▪ The proliferation stage starts approximately four days after wounding and usually lasts until day (21) in acute wounds depending on the size of the wound. ▪ In the wound healing, once the site has been cleared of debris, the building process (proliferation) begins. ▪ The aim of this phase is to repair and to provide strength to the wound. 12/05/1446 14  (A) Angiogenesis (B) Epithelization (C) Collagen Deposition (D) Wound Contraction 12/05/1446 15  ANGIOGENESIS (VASCULAR SPROUTING): ▪ Healing will not take place unless new blood vessels are present to supply O2 & nutrients to the injured tissues. ▪ Patent vessels at the periphery of the wound develop small buds or sprouts that grow into the wound area to form a capillary loop. ▪ Immobilization is essential during this period. ▪ No heat application. ▪ It lasts for 4 days under normal conditions. 12/05/1446 16 EPITHELIZATION ▪It means epidermal regeneration or surface covering. ▪The undamaged epithelial cells at the wound margin begin to reproduce epidermal mitosis. ▪These undamaged epithelial cells will migrate from the periphery to the center of the wound cavity and as it is still attached to the parent cells → will create a pull around the wound edge. ▪Escher form a temporary barrier for the wound and must not be disturbed until epithelization is complete. ▪With the completion of epithelization, the epithelial margins will release lytic enzyme which cleave the attachment of non-viable tissue and the scab will be detached. 12/05/1446 17 COLLAGEN PRODUCTION ▪ Wound healing occurs with collagen production. ▪ Fibroblast & collagen formation need adequate O2 supply. ▪ Fibroblasts produce Procollagen → divided at specific terminal sites → tropocollagen → collagen filaments → fibril → collagen fiber. ▪ Collagen fibers will accumulate in the wound in an irregular manner. ▪ Wound durability or tensile strength is dependent on microscopic welding between collagen filaments which are called “CROSS LINKS”. ▪ ↑ No. of cross links → ↑ wound tensile strength. 12/05/1446 18 WOUND CONTRACTION ▪ Epithelization close the wound surface only while wound contraction pulls the whole wound together → wound shrinking. ▪ It is done by the action of “myofibroblast”. 12/05/1446 19 12/05/1446 20 REMODELING PHASE ▪ Remodeling the dermal tissues aiming to produce greater tensile strength. ▪ It consists of the deposition of the matrix and its subsequent changes occurs over time. ▪ Type III collagen is replaced by type I. ▪ The principle cell involved in this process is the fibroblast. ▪ Remodeling can take up to 2 years. ▪ Remodeling phase include two phase: o Synthesis-lysis balance. o Collagen fiber orientation. 12/05/1446 21 (A) SYNTHESIS-LYSIS BALANCE: There is balance between formation of new collagen fibers and breakdown of old collagen. Collagen formation oxygen dependent process Collagen breakdown oxygen independent process So, we must apply pressure therapy to control H.S or keloid formation. Pressure therapy must be continued until remodeling is complete; six months to one-year post injury (may be 2 years). 12/05/1446 22 (B) COLLAGEN FIBER ORIENTATION: 1- Induction Theory: ▪ The scar attempts to mimic the characteristic of the original tissue as follow: - Dense tissues induce the formation of a dense, highly cross-linked scar. - Pliable (flexible) tissues induce the formation of a loose, less cross- linked scar. 12/05/1446 23 2- Tension Theory: ▪ There are several internal & external stresses which affect the wound area during the remodeling phase e.g. muscle force, joint movement, splinting, temperature changes. ▪ To produce permanent change in scar configuration, we can use dynamic splints, stretching techniques and functional electrical stimulation. 12/05/1446 24  PAIN MANAGEMENT Definition of Pain : is unpleasant sensation or it is a personal sensation of hurt. Pain Is a Protective Mechanism. Pain occurs whenever any tissues are being damaged, and it causes the individual to react to remove the pain stimulus. 12/05/1446 25  TYPES OF PAIN: 1- Fast pain: is also described by many alternative names, such as sharp pain, pricking pain, acute pain, and electric pain. This type of pain is felt when a needle is stuck into the skin, when the skin is cut with a knife, or when the skin is acutely burned. It is also felt when the skin is subjected to electric shock. Fast-sharp pain is not felt in most deeper tissues of the body.  2- Slow Pain: Slow pain also goes by many names, such as slow burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain. This type of pain is usually associated with tissue destruction. It can lead to prolonged, unbearable suffering. It can occur both in the skin and in almost any deep tissue or organ. 12/05/1446 27  PAIN RECEPTORS AND THEIR STIMULATION Pain Receptors Are Free Nerve Endings. The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin as well as in certain internal tissues, such as the periosteum, the arterial walls, the joint surfaces.  PAIN PATHWAY ✓The fast sharp pain signals are elicited by either mechanical or thermal pain stimuli; they are transmitted in the peripheral nerves to the spinal cord by small type Ad fibers at velocities between 6 and 30 m/sec. ✓Conversely, the slow-chronic type of pain is elicited mostly by chemical types of pain stimuli but sometimes by persisting mechanical or thermal stimuli. This slow chronic pain is transmitted to the spinal cord by type C fibers at velocities between 0.5 and 2 m/sec.  PAIN PATHWAY Because of this double system of pain innervations, a sudden painful stimulus often gives a “double” pain sensation: a fast-sharp pain that is transmitted to the brain by the Ad fiber pathway, followed a second or so later by a slow pain that is transmitted by the C fiber pathway. Glutamate, the Probable Neurotransmitter of the Type Ad Fast Pain Fibers. Substance P, the Probable Slow-Chronic Neurotransmitter of Type C Nerve Endings.  PAIN PATHWAY First Order Neurone: Begins from the nociceptors (free nerve endings), enters the spinal cord at the posterior column and terminate in lamina V. Fast pain Aδ terminate at lamina I , V. Slow pain C fibers terminate at Lamina II, III. Second Order Neurone: The fibers dicussate to the other side and ascend in the lateral spinothalamic tract and terminate at P.L.V.N of the thalamus (Ventrobasal complex).  PAIN PATHWAY Third order neurone: From ventrobasal complex to somatosensory area (area 3,1,2) which responsible for localization of pain(neospinothalamic pathway). Other fibers (paleosopinothalamic pathway) (chronic pain) terminate in the reticular area of the brain stem which transmits signals into all areas of cerebral cortex and hypothalamus. Thus the chronic pain has a very potent effect for activating the entire nervous system and arouse one from sleep.  PAIN SUPPRESSION (“ANALGESIA”) SYSTEM IN THE BRAIN AND SPINAL CORD The enkephalins: Are found mainly in brain pain control areas e.g. periaquaductal grey matter, raphe magnus nucleus, substantia gelatinosa of the dorsal horn in spinal cord. The endorphins: Are found in large amounts in the hypothalamus and in the pituitary gland. GATE CONTROL THEORY This theory proposes that stimulation of large- diameter afferent fibers (Aβ) activates local inhibitory circuits in the dorsal horn of the spinal cord and prevents nociceptive impulses carried by small-diameter fibers (C and Aδ) from reaching higher brain centers. When Aβ fibers are activated, they send excitatory stimuli through a collateral branch that activates the substantia gelatinosa (SG) interneurons that inhibit the pain fiber terminals and T cell activity. Therefore, SG interneurons close the gate to nociceptive traffic and reduce pain. SUPRA-SPINAL INHIBITION -Stimulation of the periaqueductal grey region of the midbrain and the raphe neucleus in the pons and medulla by ascending neural input from A-delta and C- fibers activates the descending mechanism. -periaqueductal grey stimulates raphe nucleus which in turn sends impulses along the dorso-lateral tract to release enkephalins into the dorsal horn thus inhibiting the transmission of impulses to the second order afferent neurones.  Β- ENDORPHIN AND DYNORPHIN: β- Endorphin (BEP) and Dynorphin are neuroactive peptides with potent analgesic affects. One of the main sources of BEP is the anterior pituitary gland. Prolonged small-diameter afferent fiber stimulation has been thought to trigger the release of BEP from the anterior pituitary gland.