Describe the healing of the head lacerations, and the role of sutures in that process. - ANS--Wound Healing Process: 1. Severed blood vessels bleed 2. Inflammatory chemicals are released 3. Local blood vessels become more permeable, allowing WBCs, fluid, clotting proteins, and other plasma proteins to seep into the injured area 4. Clotting occurs; surface dries and forms a scab 5. The clot is replaced by granulation tissue, which restores the vascular supply 6. Fibroblasts produce collagen fibers that bridge the gap 7. Macrophages phagocytize dead and dying cells and other debris 8. Surface epithelial cells multiply and migrate over the granulation tissue 9. The fibrosed area matures and contracts; the epithelium thickens 10. A fully generated epithelium with an underlying area of scar tissue results -Sutures hold the edges the laceration together to: • Reduce size • Speed up healing process • Improve appearance • Improve tissue function Describe the reduction and immobilization of the three leg fractures (specific to the patient's injuries), and how the bone will subsequently heal. - ANS-• open reduction and repair with hardware o due to the amount of fractures and the femur fracture (since it is a major fracture), ♣ even though the fracture is displaced but is not open healing process of fractures • fractures will be immobilized o cast or boot ♣ keep the bones still during the healing process -Fracture Healing Process: 1. Hematoma formation - clot forms, then osteogenic cells form granulation tissue 2. Soft callus formation - fibroblasts produce fibers and fibrocartilage 3. Hard callus formation - osteoblasts produce a bony collar in 6 weeks 4. Bone remodeling - spongy bone replaced by compact bone Give a possible explanation for why the fractures are all right leg. - ANS-all the fractures are on the right leg because you use your right leg to drive Describe the nature (degree and type) of the burns that exist on his hands and face, and how those would be treated. - ANS-• friction burns o most likely first degree • chemical burns o most likely second degree • depends on how close the patient was sitting to the steering wheel -Burn Treatment: • wash and dress burns • wrap in wet, sterile gauze • IV drip for nutrition and fluid replacement pt will already be in IV drip for other medical issues Describe the mechanism of concussion (what happens during concussive injury), relating it to how he sustained the injury (which areas of the brain would be effected note that there was both rapid deceleration followed by rapid acceleration from the rear-end collision. - ANS-• impact from the collision caused indirect force transmitted to the head. o disrupted the RAS o over release of glutamate • rapid acceleration and deceleration o frontal lobe impact ♣ symptoms include: sudden change in behavior, impaired moral judgement, memory loss, declined intelligence, etc. o occipital lobe impact ♣ symptoms include: loss of visual capability, inability to identify colors, and hallucinations Describe the cellular events that occur with spinal cord injury (both immediate and delayed), and relate it to compression of the spinal cord. - ANS--Immediate response to SCI: ¥ Initial mechanical trauma secondary to traction and compression forces. ¥ Direct compression of neural elements by bone fragments, disc material, and ligaments damages CNS and PNS. ¥ Blood vessel damage leads to ischemia. Rupture of axons and neural cell membranes also occurs. ¥ Microhemorrhages occur within minutes in the central gray matter and progress over the next few hours. ¥ Massive cord swelling within minutes, leading to secondary ischemia. ¥ Loss of autoregulation and spinal shock cause systemic hypotension, exacerbate ischemia. ¥ Ischemia, toxic metabolic compounds, and electrolyte changes cause a secondary injury cascade. -Delayed response to SCI: ¥ Hypoperfusion of gray matter extends to the white matter, altering propagation of action potentials along the axons, contributing to spinal shock. ¥ Glutamate is a key element in the. ¥ Massive release of glutamate leads to excitotoxicity -overstimulation of neighbor neurons, production of free radicals, death of healthy neurons. ¥ Excitotoxic mechanisms, via glutamate receptors, kill neurons & oligodendrocytes, leading to demyelination. ¥ Wave of apoptosis affects oligodendrocytes up to 4 segments from the trauma site days and weeks after the initial trauma. Describe the pain pathway. - ANS--Pain Pathway: 1. Nociceptor releases substance P onto spinal interneuron. 2. Second-order neuron transmits signal up spinothalamic tract to thalamus. 3. Third-order neuron relays signal to somesthetic cortex