Kinematics of Trauma - Report Example

TRAUMA Table of Contents Newton’s First Law of Motion to a Trauma Patient 3 2. Conservation of Energy Law to a Trauma Patient 4 3. Physiological Changes in the Cushings Reflex 5 4. Syndromes Associated with Spinal Cord Injury 7 4.1. Anterior Cord Syndrome 7 4.2. Central Cervical Cord Syndrome 7 4.3. Brown-Sequard Syndrome 8 4.4. Horner’s Syndrome 8 5. Haemothorax and Pneumothorax 9 6. References 11 1. Newton’s first law of motion to a trauma patient when a vehicle strikes a pole As described by Newton’s first law of motion, “An object will remain at rest or in motion with constant velocity unless acted on by a net external force” (Ostdiek and Bord, 2008). In when a car crashes into a wall, an unbalanced force acts upon the car to almost immediately decelerate it to rest. Thus, having same effect to passengers if they are strapped to the car by seat belts since any object that is tightly strapped or connected to the moving body will share its motion whether decelerating or accelerating. Also, as the car maintains a constant speed, the passengers maintain a constant speed as well (Physics Classroom, 1996). Considering a scenario wherein a passenger is not wearing a seatbelt. Results will be catastrophic because passengers will not share same motion with the car. Thus, when the car hits the wall and stops abruptly, the passenger would maintain its velocity forward and throw him towards the dashboard and windshield that can cause serious head and spinal cord injuries. Furthermore, passengers not wearing seatbelts would hit the objects in front of them with the same speed as the car crashes to the wall (Brooks, 2004). Newton’s Law of Motion can also explain the importance of having headrests on car seats that functions as an important safety feature protecting passengers on the event of a rear-end collision. In the absence of it, when a force hits the rear end of the car an abrupt forward acceleration will occur. The car seat will push the passenger’s torso forward along its movement but his head will remain at rest causing the head to appear like it snapped back. This scenario would result to a neck injury called whiplash. Thus, having a headrest is vital to a ensure passenger safety (NEL, 2004). 2. Conservation of energy law to a trauma patient when a vehicle hits a wall.  Traumatic injury occurs when the body’s tissues are exposed to energy levels beyond their tolerance. (Be-Safe Paramedics, 2009). The law of conservation of energy states that “Energy cannot be created or destroyed, only converted from one form to another” (Ostdiek and Bord, 2008). Energy generated from a sudden stop or start of a vehicle must be transformed to the following forms, thermal, electrical, chemical, radiant, or mechanical (American Academy of Orthopaedic Surgeons (AAOS), 2010). Since the passengers are travelling at the same speed as the car before the collision, their kinetic energy is transformed to an energy that causes the trauma injuries, also called energy dissipation (Be-safe Para medics, 2009). In a car crash, the kinetic energy is dissipated into mechanical energy as the car body crumples in a collision, and further dissipated in the form of injury as the passengers sustain fractures or other body trauma (AAOS, 2010). Cars are designed with consideration of the laws of energy. Passenger restraint devices, such as seatbelts, are designed to hold the occupant in place and prevent secondary injuries from throwing around the passenger in the compartment or being ejected from the vehicle. Supplemental Restraint Systems, such as airbags, are very useful at absorbing energy, and vehicle crumple zones and bumpers absorb energy form crashes (Good Samaritan EMS System, 2008). The most common and complex injury in a car accident is the blunt trauma. “. . . an injury pattern produced by the wounding forces of compression and changes in speed . . . may disrupt tissue structures and cause direct or indirect injury” (Be-Safe Paramedical, 2009­­). Direct pressure or compression to a specific organ or tissue structure is the most common force applied in blunt trauma.3. Briefly explain why the physiological changes in the Cushings Reflex occur in severe head injured patients Cushing’s reflex is defined as a hypothalamic response to brain ischemia wherein the sympathetic nervous system is activated which causes increased peripheral vascular resistance with a subsequent increase in blood pressure (BP) that activates the parasympathetic nervous system through the carotid artery, baroreceptors, which results in vagal-induced bradycardia. Brain ischemia leads to cushing’s reflex due to the poor perfusion that results from increased ICP caused by head bleeds or mass lesions (Liferidge, 2007). Cushing’s triad, the clinical manifestation of Cushing’s reflex, is a form of hypertension, bradycardia, and irregular respirations or Cheyne-Stokes breathing. Cushings triad poses an impending threat of having brain herniation, and thus, the need for decompression methods. Temporary methods include the use of “mannitol, hyperventilation, and elevation of the head of bed” (Liferidge, 2007). Treatment of any patient with head or spinal injury involves making an accurate assessment “to identify the extent of injury, prevention of further damage to the brain and spinal cord, and maintenance of cerebral perfusion pressure and end-organ function” (Mazzafero, n.d.). In the diagnosis process, the examiner should observe the presence of bradycardia while taking the pulse. A rapidly expanding intracranial lesion will cause the pulse to drop, respiration will slow, and blood pressure often rises, causing a cushing reflex due to tonsiller herniation (Weisberg, Garcia, and Strub, n.d). The brain is protected by the bones that make up the cranial vault. This protection, however, is a two-edged sword. “Although the cranium helps protect the brain from injury, it also can injure the brain by limiting tissue expansion following injury” (Bledsoe, 2009). Brain tissues are similar with all other body tissues on its response to injury with swelling and bleeding. The difference is that the brain is confined to the space of the cranial vault which easily gets filled when the starts to swell. When the spaces are filled, the pressure will increase or the ICP. Normal ICP ranges from 5-15mmHg (Bledsoe, 2009). An increase in the intracranial pressure (ICP) will affect the brain by also increasing cerebral blood flow or by causing brain herniation (Hong, n.d). Brain tissues would tend to herniate across an opening in the presence of a high pressure gradient. Among the four situations wherein herniation can occur, the tonsillar herniation has a closest association with cushing’s reflex. According to Hong (n.d.), “Tonsillar herniation occurs when the posterior fossa pressure is high enough to cause the cerebellar tonsils can herniated through the foramen magnum, compressing the medulla.” It is also characterised by the loss of consciousness and cardiovascular and respiratory problems that leads to fluctuating blood pressure and irregular breathing. The increase in ICP in the brain results to an oedema. It is characterized by, first, the compression of the blood vessels in the brain resulting to reduced blood flow and brain ischemia that will cause the arteries leading to the brain to dilate increasing further the capillary pressure and ICP that would worsen the oedema. Since blood flow is reduced, oxygen delivery to the brain tissues decreases. This reduces the function of the capillaries and causes capillary leakage and permeability. Furthermore, brain cells lose their energy supply that leads to intracellular pump failure and then cell death (Bledsoe, 2007). 4. Briefly define the following syndromes associated with spinal cord injury:  4.1 Anterior Cord Syndrome  According Schneider (as cited by Tator, n.d.), “the anterior cord syndrome is associated with the complete paralysis with hyperesthesia at the level of the lesion and an associated sparing of touch and some vibration sense.” The condition can be illustrated as a large disk herniation compressing the anterior aspect of the cord that results to damage, by rough splitting, to the anterior and lateral white matter tract and to the grey matter (Tator, n.d.). The tracts involved in this type of lesion are the bilateral horn cells corticospinal tracts, spinothalmic and autonomic. It is typically diagnosed as anterior spinal artery occlusion which is an associated with the MRI spinal cord as an elongated ‘‘pencil-like’’ lesion in the anterior cord. Also, it occurs on settings such as aortic surgery, spinal angiography, vasculitis, embolic source, aortic/vertebral dissection, hypotension, and prothrombotic states (Jacob and Weinshenker, 2008). 4.2 Central Cervical Cord Syndrome  The central cervical syndrome is characterised by motor impairment which is disproportionately greater than in the upper limbs than in the lower, by bladder dysfunction, most often urinary retention, and by a variable degree of sensory loss below the level of the cord lesion (Merriam, Taylor and McPhail, 1986). This syndrome can be typically observed in older subjects with cervical spondylosis and hypertension injuries (Taylor and Blackwood, 1948, as cited by Merriam, Taylor and McPhail 1986). According to Schneider, “acute compression was an etiological factor in many cases such as cord compression between bony bars or spurs anteriorly and infolded ligament flava posteriorly” (as cited by Tator, n.d). It is clinically difficult to distinguish central cord syndrome with the syndrome of crucial paralysis. However, the use of plain films, computed tomography, and magnetic resonance imaging (MRI) can accurately determine the lesion and thus characterising the specific type of syndrome (Tator, n.d.) 4.3 Brown-Sequard syndrome  Brown-Sequard Syndrome (BSS) is a rare neurological condition, characterized by a lesion in the spinal cord, which is usually caused by an injury to the spine in the region of the neck or back (National Organization of Rare Disorders (NORD), 2005). The syndrome is characterized by “the lost sense of touch, vibrations and/or position in three dimensions below the level of the injury, known as hemiparalysis or asymmetric paresis”. These sensations are accompanied by a loss of the sense of pain and of temperature, called hypalgesia, on the side of the body opposite to the side at which the injury was sustained (NORD, 2005). “Generally treatment for individuals with BSS focuses on the underlying cause of the disorder. Early treatment with high-dose steroids may be beneficial in many cases. Other treatment is symptomatic and supportive” (National Institute of Neurological Disorders and Stroke (NINDS), 2011) 4.4 Horner’s syndrome The Horner’s syndrome is commonly caused by the interruption of a set of nerve fibres from the hypothalamus to the face. It can be a result from injury to one of the main arteries of the brain, injury to nerves in the brachial plexus, cluster head aches, stroke or tumour, and tumour at the top of the lung (Medline Plus, 2012). The syndrome may also be present at birth, characterised by the loss of colour of the iris. Horner’s syndrome may result from any site between the diencephalon and the sympathetic end organs that causes pupillary dilation lag (Pilley and Thompson, 1975). Its symptoms include the decrease in sweating on the affected side of the face, drooping eyelids, sinking of the eyeball into the face, and small pupil (Medline Plus, 2012). 5. Haemothorax is associated with a higher mortality rate than a simple pneumothorax. Why is that the case? Thoracic trauma is one of the major causes of morbidity and mortality in trauma centres, with 25% of the deaths related to injuries within the thoracic cage. Complex problems related to the management of both pneumothorax and haemothorax have been around for 200 years, after the discovery of the conditions (Mowery, et. al., 2011). Around 85% of the reported cases of thoracic injuries do not require surgical intervention, though there are still several questions on the trauma management that cannot be easily answered (Westaby and Brayley, 1990). According to Constantino, Gosselin, and Primack (2006) the separation of the parietal and visceral pleura caused by a haemothorax and pneumothorax, “disrupts the inherent elastic recoil properties of the lung producing passive atelactasis, pulmonary collapse.” Pneumothorax or spontaneous pneumothorax is a condition where air accumulates in the pleural space, between the visceral and parietal pleura, which causes the lung to partially or totally collapse. It happens to 10-30% of patients with blunt chest trauma and most patients with penetrating chest trauma (Voohrees, 2011). Patient may be diagnosed of having chest pain, difficulty breathing, or tachycardia. In addition, the breath sounds may be decreased or absent which is a sign that the lung has already collapsed. Test used to determine pneumothorax includes the use of stethoscope, chest x-ray and arterial blood gases (Medline Plus, 2011). For small pneumothorax, the treatment includes the use of high-flow oxygen through a bag-valve mask and the patient will be allowed to rest. For large pneumothorax, a chest tube will be administered between the ribs into the pleural space around the lungs to facilitate the draining of air from the space and will also allow the lung to re-expand (Medline Plus, 2011). The haemothorax is a condition characterized by the presence of blood in the pleural space that may be caused by blunt or penetrating trauma (Trauma.org, 2004). On some situations, a patient may suffer from a mixed case wherein blood and air accumulates in the pleural space. This is called hemopneumothorax (Voohrees, 2011). As discussed by Voohrees (2011), each side of the chest can hold 30-40% of the patient’s blood volume, around 2000 to 3000 ml. Compared to pneumothorax, haemothorax do carry a higher mortality rate since it creates a problem with both B and C, Breathing and Cardiovascular system respectively, of the ABC’s of cardiopulmonary resuscitation (Westaby and Brayley, 1990). When one side of the chest is full of blood, oxygenation of the lung cannot be done properly and thus compromise breathing and the patient loses blood into his chest cavity that compromises circulation of blood (Voohrees, 2011). The diagnosis of small-moderate haemothorax cannot be detected by physical examination, chest x-ray, FAST, or CT scan is necessary. For larger cases, it is detected clinically (Poudre Valley Health Systems, n.d.). The complexity of treating haemothorax associates it with having higher mortality that pneumothorax. However, advances in technology would provide a more faster and efficient way of addressing cases of haemothorax and pneumothorax. Previously, trauma teams were limited to the ability of detecting less than 500 ml of blood on radiography. Currently, smaller volumes can be detected via chest computed tomography. Finally, minimally invasive surgery such as Video-assisted thoracoscopic surgery (VATS) has growing role in the diagnosis and therapeutic interventions and management of trauma patients (Mowery et. al., 2011). References American Academy of Orthopaedic Surgeons (AAOS). (2010). Advanced Assessment and Treatment of Trauma. USA: Jones & Bartlett Learning. Be-Safe Paramedical. (2009). Kinematics of Trauma. Retrieved from http://www.be-safe.co.za/index.php/news/37-kinematics-of-trauma Bledsoe, B. E. (2009). Understanding Cushing Reflex. Retrieved from http://mediczone.org/index.php?option=com_content&view=article&id=10:understandingcushings-reflex&catid=5:street-science&Itemid=37 Brooks, R. (2004). The Physics of Driving. Codman Academy Charter Public School. Retrieved from fc.codmanacademy.org/branches/physicsofdriving1/index.php?module=pagemaster&PAGE_user_op=view_page&PAGE_id=2&MMN_position=2:2 Constantino, M., Gosselin, M. V., Primack S. L. (2006). The ABC’s of Thoracic Trauma Imaging. Seminars in ROENTGENOLOGY, 209-225. doi:10.1053/j.ro.2006.05.005 Griff, J. (2000). Understanding Car Crashes: It’s basic Physics. Florida: Insurance Institute for Highway Safety Good Samaritan EMS System. (2008). Trauma: Let’s be blunt about it. Retrieved from http://www.loyolaems.com/ce/ce_jul08.pdf Hong, A. (n.d). The Acute Management of Head Injuries. Retrieved from http://www.worldscibooks.com/medsci/5413.html Jacob, A., & Weinshenker, B. G. (2008). An Approach to the Diagnosis of Acute Transverse Myelitis. Semin Liver Dis, 28(1), 105-120. Liferidge, A. (2007). Cushings Reflex and Triad. Retrieved from https://umem.org/pearl_view.php?p=133 Mazaferro, E.M. (2009). Treatment of Head and Spinal Trauma. Wheat Ridge. Medline Plus. (2011). Collapsed Lung. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/article/000087.htm Medline Plus (2012). Horner syndrome. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/article/000093.htm Merriam, W.F., Taylor, T. K. F., Ruff, S.J., & McPhail, M.J., (1986). A Reappraisal of Acute Traumatic Central Cord Syndrome. The Journal of Bone and Joint Surgery 68(5), 708-713. Mowery, N. T., Gunter, O. L., Collier, B. R., Diaz, J. J., Huat, E., Hildreth A., Holevar, M., Mayberry, J., & Streib, E. (2011). Practice Management Guidelines for Management of Hemothorax and Occult Pneumothorax. The journal of TRAUMA Injury, Infection and Critical care. 70(2). 510-518. National Institute of Neurological Disorders and Stroke. (2011). NINDS Brown-Sequard Syndrome Information Page. Retrieved from: http://www.ninds.nih.gov/disorders/brown_sequard/brown-sequard.htm National Organization of Rare Disorders (NORD). (2005). Brown Sequard Syndrome. Retrieved from http://www.rarediseases.org/rare-disease-information/rare-diseases/byID/950/viewAbstract NEL. (n.d). Newton’s First Law of Motion. Retrieved from http://www.lakeheadschools.ca/scvi_staff/childs/Gr11_physics_web/downloadable_content/unit3/textpdf3/phys11_3_2.pdf Ostdiek, V. J., & Bord, D. J. (2008). Inquiry into Physics. Australia: Thomson Brooks/Cole. Pilley, S. F. J., & Thompson H.S. (1975). Pupillary ‘dilation lag’ in Horner’s syndrome. British Journal of Opthalmology, 59, 731-735. Physics Classroom. (1996). The Car and Wall. Retrieved from http://www.physicsclassroom.com/mmedia/newtlaws/cci.cfm Poudre Valley Health System. (n.d.). Pneumothorax/ Hemothorax. Retrieved from http://pvhs.org/documents/Trauma/PneumothoraxHemothorax.pdf Tator, C. H., (n.d.). Clinical Manifestation of Acute Spinal Cord Injury. Trauma Organization. (2004). Chest Trauma Haemothorax. Retrieved from http://www.trauma.org/archive/thoracic/CHESThaemo.html Voohrees, J. V. (2011). Thoracic & Abdominal Trauma. Journal CME article. 5-11. Weisberg, L.A., Garcia, C., & Strub, R. (n.d.). Essentials of Clinical Neurology: Head Trauma. Retrieved from http://www.psychneuro.tulane.edu/neurolect/ Westaby, S., Brayley, N. (1990). Thoracic Trauma - I. BMJ, 300, 1639-1643. doi: 10.1136/bmj.300.6741.1710 Read More