Safety Devices in Motor Vehicles Have Been Proven to Save Lives - Assignment Example

Trauma Studies Student’s Name Course Instructor Date Trauma Studies Part 1 Kinematics Q1. Safety devices in motor vehicles have been proven to save lives. Explain how they prevent /limit injuries, and provide evidence of the effect?  According to the Australian Bureau of Statistics, in 2010, there were 1,248 fatal road accidents in Australia, claiming the lives of 1,367 people [ABS24]. This means that there are 1,367 lives that could have been saved if appropriate measures had been put in place to prevent the loss of life during motor vehicle accidents. What are the safety devices used to save lives in traffic accidents and how do they save lives? The first and perhaps most important safety device in a vehicle is the safety belt. Safety belts are basically straps that hold a passenger or driver in the car seat. Safety belts are designed differently for people of different weights and sizes. For instance, safety belts for kids are different from similar belts used by adults. It is henceforth important that people ensure that the right safety belts are installed in their cars. How do safety belts save lives? In an article aptly titled Seat Belts: How They Save Lives, Orenstein (2009) explains that safety belts provide a 5-way protection to users. The first of the five protective ways of safety belts is that they keep the occupants inside the vehicle. People who get thrown out of a vehicle during an accident are four times likely to die opposed to those inside. Secondly, safety belts restrain the stronger parts of the body, preventing hurting. Third, safety belts protect users by spreading any force from the collision and hence minimize injury. Safety belts also protect individuals by slowing down the body, and enabling the body to absorb the change in speed without moving violently. Finally, safety belts protect individuals by holding the body in a position in which the brain and spinal cord is protected [Bet09]. The second important safety device used in vehicles is the airbag. Innovation has greatly influenced the use of airbags and they can now be placed in strategic parts of a vehicle in order to prevent injuries to people during an accident. For instance, Ford has inflatable safety belts, which can function as airbags [Uni132]. An airbag system is composed of crash sensors, air bag modules with ready inflators, and a diagnostic module that has a readiness indicator [Wal13]. Air bags depend on the crash detection system to be launched. When an accident occurs and the crash is detected, the air bags inflate immediately. Airbags are deployed in less than a second when an accident occurs, and save the life of vehicle occupants by preventing them from hitting the steering wheel, the dashboard, the windshield and other parts of the car that a person may be thrown to hit. Airbags are not a substitute for safety belts and should be used with them [CDC13]. Other means that can be used to save lives in accidents are not safety devices per se, but are measures that can reduce the risk of accidents e.g. rearview cameras, impact warning signs etc. References ABS. (2012, May 24). Year Book Australia: Transport: Accidents,. Retrieved December 12, 2013, from Australian Bureau of Statistics website: http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/by%20Subject/1301.0~2012~Main%20Features~Accidents,%20injuries%20and%20fatalities~189 CDC. (2013). Save Lives, Save Dollars: Prevent Motor Vehicle–Related Injuries. Retrieved december 12, 2013, from CDC: http://www.cdc.gov/injury/pdfs/cost-MV-a.pdf Orenstein, B. W. (2009, May 20). Seat Belts: How They Save Lives. Retrieved December 12, 2013, from Every Day Health: www.everydayhealth.com/healthy-living/wearing-your-seat-belt.aspx United States Automobile Association. (2013). 10 Car Safety Features That Could Save Your Life. Retrieved December 12, 2013, from United States Automobile Association: https://www.usaa.com/inet/pages/advice-auto-safetyfeatures?akredirect=true Walters Forensic Engineering. (2013). Air Bags Save Lives. Retrieved December 12, 2013, from Walters Forensic Engineering: http://www.waltersforensic.com/articles/accident_reconstruction/vol2-no2.htm. Head Trauma Q2. Explain how measures taken in the pre-hospital environment can prevent or limit raised intracranial pressure in traumatic brain injuries. Support with evidence. Q2. Explain how measures taken in the pre-hospital environment can prevent or limit raised intracranial pressure in traumatic brain injuries. Support with evidence. Traumatic brain injury is the sudden damage suffered by the brain when the head is subjected to a sudden hard blow or a jolt [Nob13]. Traumatic brain injury occurs in vehicle and motorcycle crashes, in sports injuries, in assaults, falls or any types of blows to the head. In an accident that causes TBI, the head is impacted by a blunt object on one side, making the brain to crash against inside of the skull. The brain is a soft tissue, and when it crashes against the skull, it bruises and bleeds. Intracranial hemorrhage or inflammation caused by TBI increase intracranial pressure. Other causes of increased intracranial pressure after TBI include intracranial hematomas, cerebral ischemia, and cerebral edema [Kee05]. TBI is the leading cause of death in individuals between 1 and 44 years of age. The pre-hospital care of a patient with TBI is very important, if not the most important phase of treatment. Emergency response to a TBI patient is aimed mainly preventing greater harm or injury, making the patient safe, and preventing elevation of intracranial pressure. In the pre-hospital care of a patient with Traumatic brain injury, it is important that the head and neck movement be minimized or avoided in totality. This is vital because any movement of the neck or head may increase intracranial hemorrhage and henceforth increase intracranial pressure. Movement of the head and neck after traumatic brain injury can also worsen the injury to the head and brain [Mar04]. Pre-hospital care of patients with traumatic head injuries in efforts to limit elevation of intracranial pressure should involve hyperventilation of the patient by placing him or her in recovery position and checking for airway obstruction [The13]. One of the causes of raised intracranial pressure is ischemia and hypoxia due to poor ventilation, especially in comatose and unconscious patients. Poor ventilation raises intracranial pressure because carbon dioxide, which is concentrated in tissues with poor ventilation, is a vasodilator. Hyperventilation, or supply of oxygen significantly reduces the diameters of cerebral arterioles, hence decreases intracranial pressure. Lastly, intracranial pressure can be lowered or prevented from rising in TBI patients through the administration of mannitol or hypertonic saline. Mannitol can be administered through infusion or through a bolus. Mannitol increases the osmotic gradient between the blood and the brain, and hence water is drawn from the edematous brain to the vascular system, reducing intracranial pressure significantly. Hypertonic saline, at a concentration of about 7.5% to 23% is effective in lowering intracranial pressure. This is because hypertonic saline has anti-inflammatory changes and increases the osmotic and hemodynamic pressure, resulting to leaking of water into the vascular system [Shi08]. In conclusion, the measures that can be used to limit intracranial pressure due to traumatic head injury include, first, the stabilization of the patient without movement of the head or neck. This is important because it prevents further injury to the head and prevents further increase in intracranial pressure due to traumatic brain injury. Hyperventilation, mannitol administration, and administration of hypertonic saline are also effective in reducing intracranial pressure. References Andaluz, N. (2013, February). Traumatic Brain Injury (TBI). Retrieved December 12, 2013, from The May Field Clinic: http://www.mayfieldclinic.com/PE-TBI.htm Henry, M. C., & Stapleton, E. R. (2004). EMT Prehospital Care, 3rd Ed. New York, NY: Mosby/Jems. Keefe, K., & LeFlore, J. (2005). Management of Increased Intracranial Pressure in the Criticall Ill Child With an Acute Neurological Injury. AACN Advanced Critical Care, Vol. 16, No. 2, 212-231. The State Government of Victoria. (2013, September 24). Head Injuries- First Aid. Retrieved December 12, 2013, from The State Government of Victoria: http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Head_injuries_first_aid Stivert, S., & Manley, G. (2008). Prejhospital Management of Traumaric Brain Injury. Neurosurgical Focus, Vol. 25, No. 4, E5. Spinal Trauma Q3. Explain how you would treat a patient with neurogenic shock relating your treatment to the pathological process of this type of shock. Neurogenic shock is a kind of distributive shock that occurs after injury to the spinal cord, especially an injury caused by blunt trauma. Neurogenic shock mainly results to an unopposed vagal tone i.e. there is loss of the sympathetic tone which initiates shock response and a decrease in tissue perfusion [Eli13]. The most affected region in neurogenic shock is the cervical region of the vertebra, then the thoracolumbar junction comes second, the thoracic region third, and finally the lumbar region. It is important to differentiate neurogenic shock from spinal shock, which involves a temporary loss of the spinal reflex activity [Eme09]. Neurogenic shock is mainly manifested by the triad of bradycardia, hypothermia and hypotension. The pathophysiology of the shock is that loss of sympathetic tone at the t1-t12 results to massive vasodilatation, impaired thermo-regulation ad inhibition of baro-receptor response [Eli13]. The treatment of neurogenic shock is difficult because the injury to the spinal cord is often irreversible [Med13]. Treatment of neurogenic shock is aimed at alleviating hypotension, bradycardia and hypothermia. Decreased vascular resistance due to vasodilation which increases venous capacity leads to hypovolemia and hypotension in neurogenic shock. To restore normal blood pressure in neurogenic shock patients, fluid resuscitation is necessary. Neurogenic shock patients are henceforth infused with isotonic solutions such as crystalloid, which contains ringer’s lactate and 0.9% sodium chloride, or colloid, which contains blood products and albumin [Eli13]. Hemodynamic response should be monitored continuously to avoid causing hypertension. In cases where fluid administration does not improve perfusion, inotropic agents, for example dobutamine at 2.0-20.0 µg/kg or dopamine at 2.5-20.0 µg/kg, can be added to improve cardiac contractions and henceforth improve perfusion pressure and cardiac output [Eme09]. Vasopressin is also used in treatment of hypotension in neurogenic shock [HGu08]. In neurogenic shock, vasopressin has several therapeutic effects. It is a peripheral vasoconstrictor that results to vasoconstriction throughout the body while it potentiates other vasoconstrictors [Tat11]. Vasopressin also increases serum cortisol and at low concentrations, it acts as a diuretic [Tat11]. Hypotension can also be treated with norepinephrine and/or phenylephrine. Treatment for hypotension in neurogenic shock restores normal blood pressure, improves tissue perfusion hence avoiding ischemia, and improves thermoregulation. In cases of severe bradycardia, patients can be treated with atropine at 0.5-1.0 mg IV up to a total dose of 3.0 mg [Eme09]. Bradycardia can also occur as a reflex from treatment with phenylephrine. It can also be treated using glycopyrrolate and inotropic vasoconstrictors such as norepinephrine and dopamine[Eli13]. In summary, the treatment of neurogenic shock involves treatment for hypotension using fluid resuscitation, vasoconstrictors, and inotropic agents. These treatments restore normal blood pressure in neurogenic shock patients and improve tissue perfusion. Increased blood supply to tissues avoids ischemia and improves thermoregulation. Bradycardia is treated using atropine or inotropic agents that increase cardiac output. References Emergency Medicine. (2009, March 11). Neurogenic Shock. Retrieved December 12, 2013, from Emergency Medicine website: http://emergencymed.wordpress.com/2009/03/11/neurogenic-shock/ Guly, H., Bouamra, O., & Lecky, F. (2008). The Incidece of Neurogenic Shock in Patients with Isolated Spinal Cord Injury in the Emergency Department. Resuscitation, Vol. 76, 57-62. Kuznetso, T. (2011, June 20). Hypotension and Shock Treatment. Retrieved December 12, 2013, from Armenian Medical Network: http://www.health.am/vein/more/hypotension_shock_treatment/ Mack, E. H. (2013). Neurogenic Shock. The Open Pediatric MEdicine Journal, Vol. 7, Suppl 1: M4, 16-18. Medicine Net. (2013, August 10). Medical Shock. Retrieved December 12, 2013, from Medicine Net: http://www.medicinenet.com/shock/article.htm Injury Prevention Q4. Your ambulance service is concerned about the amount of trauma occurring in your community, and they are seeking assistance from the paramedics to determine what to do about it. They have invited all interested paramedics to submit a brief summary of some program options they could implement to reduce the amount of trauma. They specifically require the submissions indicate the type of benefits that the program would produce. It is very important to control trauma in a community. The programs that are put in place to reduce the occurrence of trauma in a community are referred to as trauma prevention programs. These programs are basically aimed at educating the public on how to avoid trauma and injury, taking necessary measures to avoid risks in the community, and also ensuring quality care for patients that have suffered trauma. Trauma prevention programs at community level should include: a. Community and Patient Education Patient education is the most effective trauma prevention program in the community. Community education on trauma prevention involves informing people in the society on the causes of trauma and how they can prevent it. Judkins, an Injury Prevention and Outreach Educator at the University Medical Centre in Tucson explains that the best way for the community to deal with trauma and injuries is by avoiding them, and explains that they can be avoided through information [Dan13]. Educating the community on trauma prevention means arming the people with the knowledge and skills required to keep themselves, their friends and relatives safe from trauma. For instance, parents can be educated o how to prevent traumatic injury to their kids. Trauma prevention education also involves outreach to the government and lawmakers to develop public policies that are geared towards reduction of trauma in the community [Dan13]. Education makes the people more cautious, and hence directly reduces incidence of trauma. b. Falls Prevention Programs Robert Carreon, a registered nurse who is the head of trauma prevention in the University of Southern Carolina surgery department explains that injuries due to falls have been rising in recent years [Rob13]. Trauma from falls can be decreased due through education programs as well as measures that make adults more competent in avoiding falls. For instance, adults may be examined for vision to establish their probability to suffer a fall, and hence be advised accordingly. Adult falls may be avoided if people wear appropriate shoes and maintain proper home and recreational safety [Placeholder1]. c. Competent Driving Programs Vehicle accidents are major causes of traumatic injuries in most communities. Most accidents are caused by distracted driving or by teen driving. Programs aimed at creating awareness and advocating for proper driving have been proven to reduce trauma significantly. For instance, in 1998, Florida in USA recorded 50 deaths due to vehicle accidents in prom night, but the number was reduced to zero after implementation of trauma prevention programs in 2006 [Flo13]. d. Kid Safety Programs Kids are usually more prone to trauma than adults. This is because they spend most of their time playing dangerously in the fields. The Danbury Hospital explains that to prevent children trauma, injury prevention programs should focus on making playgrounds safe, improving bicycle safety, making children stay with friends and enhancing home safety by protecting children from hazardous actions, machines etc. [Dan131] References Carreon, R. (2013). Trauma Outreach and Injury Preventio Programs. Retrieved December 12, 2013, from USC: http://www.surgery.usc.edu/acutecare/traumaoutreach-injurypreventionprograms.html CDC. (2013). Adult Falls. Retrieved December 12, 2013, from CDC: http://www.cdc.gov/HomeandRecreationalSafety/Falls/adultfalls.html Danbury Hospital. (2013). Programs and Services: Level II Trauma Center. Retrieved December 12, 2013, from Dabury Hospital website: http://www.danburyhospital.org/en/Our-Services/Care-Centers/Trauma-Center/Programs-and-Services Florida Health. (2013). Trauma Injury Prevention and Outreach Programs. Retrieved December 12, 2013, from Florida Health: http://www.floridahealth.gov/prevention-safety-and-wellness/trauma/ Judkins, D. (2013). Trauma Outreach and Injury Prevention. Retrieved december 12, 2013, from The University of Arizona Department of Surgery: http://surgery.arizona.edu/unit/program/trauma-outreach-injury-prevention Part2 Abdominal trauma and Trauma in Pregnancy Q5.Describe the presentation of abruption placentae caused by blunt trauma. What challenges will you come across when treating a woman with this condition?  Abruptio placentae, also known as placenta abruption, refers to the detachment or the separation of the placenta from the inner uterine wall before delivery. The placenta should remain firmly attached to the uterine wall until delivery. However, in about 1 in every 150 pregnancies, the placenta detaches from the uterine wall resulting in vaginal bleeding [Iri12]. Below is an illustration of the detached placenta during abruption placenta. ion Placental abruption is the most common of vaginal bleeding in the third trimester of pregnancy. It is also a significant cause of maternal mortality. The effects of placental abruption on the mother depend on the severity of the detachment, but the effects of the abruption on the fetus depend largely on the gestational age and the severity. The heart rate of the fetus is most affected by severe abruptions [Rie07]. The presentation/ clinical manifestation of placental abruption can be classified into four classes: Class 0 to class 3. In class 0, the abruption is asymptomatic, and it is diagnosed through finding a blot clot on a delivered placenta. Class 1 includes mild or slight abruption and presents with mild vaginal bleeding, a tender uterus, normal maternal blood pressure, and no fetal distress. Class 2 placental abruption presents with vaginal bleeding, a tender uterus, notable fetal distress, and maternal tachycardia. Class 3 placental abruption presents with heavy vaginal bleeding, uterine tenderness and pain, abdominal pain, low fibrinogen levels in blood, maternal shock, coagulopathy and results to fetal death [Sha13]. Placental abruption is a leading cause of fetal death. As Tikkanen et al. (2009) report, in the UK, 15% of fetuses in cases of placental abruption lose their lives [Tik09]. The mothers are also prone to complications that may result to mortality. It is henceforth of vital importance to manage placental abruption efficiently to avoid maternal and fetal death. Mild cases of placental abruption can be managed through bed rest, while moderate cases may require hospitalization and frequent monitoring. In moderate and severe cases, labor can be induced. Severe placental abruptions are emergencies and caesarean section is performed immediately to avoid fetal death [Iri12]. Treatment of placental abruption involves many challenges. The first challenge is that maternal blood loss can to shock. It is henceforth a challenge to control bleeding as well as try to save the fetus simultaneously. Blood loss can also result to maternal death. Another challenge is that bleeding can also result to hysterectomy (complete removal of the uterus), which may be against the mother’s wishes. The final challenge is ensuring steady supply of oxygen to the fetus. This requires that the fetus be removed as fast as possible and placed in oxygen to prevent fetal brain damage [Sta13]. References Burd, I. (2012, december 9). Placental Abruption. Retrieved december 12, 2013, from University of Maryland Medical center: http://umm.edu/health/medical/pregnancy/labor-and-delivery/placenta-abruptio Deering, S., Meyer, B., Talavera, F., & Smith, C. (2013, June 3). Abruptio Placentae. Retrieved December 12, 2013, from MedScape: http://emedicine.medscape.com/article/252810-overview State Government of Victoria. (2013). Placental Abruption. Retrieved December 12, 2013, from Better Health: http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Placental_abruption Tikkanen, M., Gissler, M., Metsaranta, M., Luukkaala, T., Hiilesmaa, V., Andersson, S., et al. (2009). Maternal Deaths in Finland: Focus on Placental Abruption. Acta Obstetrica et Gynecologia Scandinavica, Vol. 88, No. 10, 1121-1127. Usui, R., Matsubara, S., Ohkuchi, A., Kuwata, T., Watanabe, T., Izumi, A., et al. (2007). Fetal Heart Rate Pattern Reflecting the Severity of Placental Abruption. Archives of Gynecolgy and Obstetrics, Vol. 277, No. 3, 249-253. Burns Q6.You are called to a male who has had his beard catch fire as he was smoking a cigarette whilst on oxygen via nasal prongs. He has soot around his nose, obvious respiratory distress and an audible wheeze. Discuss the pathophysiology of the condition in relation to your management.  Smoking while on oxygen therapy or even near oxygen administration equipment is strongly prohibited [SHR12]. This is because though oxygen does not burn per se, it facilitates burning, and nourishes fire to a great extent. In the case of this patient, his beard caught fire because there was a high concentration of oxygen around him because he was on oxygen therapy. Because of high oxygen concentration in his airways, the patient should have inhaled hot gases and smoke as his beard burnt. This is evidenced by the presence of soot around his nose. In essence, the patient suffered smoke inhalation. Smoke inhalation is a dangerous cause of death due to fires. Smoke inhalation causes injury through several different mechanisms [Kei13]. The first mechanism is thermal injury to the upper airway, which is caused by inhalation of hot smoke or gas, leading to burning of the region above the oropharynx. The second mechanism through which smoke inhalation causes injury is through chemical injury and irritation caused to the airways by soot. Smoke inhalation also causes asphyxiation, which involves insufficient or poor exchange of oxygen and carbon dioxide in the lungs. Finally, smoke inhalation causes injury to the respiratory system through carbon monoxide poisoning. Carbon monoxide gas is produced during combustion, and then it is oxidized by oxygen to carbon dioxide. The pathophysiology of smoke inhalation injury involves inflammatory response to injury and irritation, and carbon monoxide poisoning. Above the oropharynx, smoke inhalation causes thermal injury to the respiratory mucosa, and triggers an inflammatory response that can result to occlusion of the airways. However, heat is effectively dissipated by the moist airways and hence never causes significant damage below the oropharynx [MMa09]. The inhalation of irritants in smoke, which include soot and tobacco in this case, triggers a cascade of inflammatory events that result to pulmonary edema and airway obstruction. Toom, Maybauer, Greenwood and Fraser (2010) explain that the most important event in the pathophysiology of smoke inhalation injury is the activation of the classic complement pathway by irritant substances resulting to production of cytokines and chemokines [MTo10]. For instance, there is production of nitric oxide synthase which results to production of nitric oxide which is a powerful vasodilator. Carbon monoxide occurs in smoke inhalation because hemoglobin binds to carbon monoxide with about 250 times the affinity of hemoglobin to oxygen. Binding of carbon monoxide to hemoglobin results to carboxy-hemoglobin, which is unable to transport oxygen [MTo10]. The management of the above patient would require restoring oxygen therapy using hyperbaric oxygen. Hyperbaric oxygen, at around there bars, would reduce the half-life of carbon dioxide bound to hemoglobin 320 minutes in normal air to 23 minutes [Kei13]. It is important to put patients with smoke inhalation injury on oxygen therapy fast in order to avoid neurological damage due to poor perfusion [Lau11]. Because the above patient presents with wheezing, an indicator of obstruction, intubation would be important to avoid more airway obstruction. In summary, the patient has suffered from smoke inhalation injury, and should be managed through hyperbaric oxygen therapy. Anti-inflammatory medication should also be given to prevent more airway obstruction. References Knott, L. (2011, April 20). Inhalation Injury. Retrieved December 12, 2013, from Patient.co.uk: http://www.patient.co.uk/doctor/Inhalation-Injury.htm Lafferty, K. A., Alcock, J., Bonhomme, K., Martinez, C., & Wiener, S. (2013, August 26). Smoke Inhalation Injury. Retrieved December 12, 2013, from MedScape: http://emedicine.medscape.com/article/771194-overview Maybauer, M., & Reyberg, S. (2009). Pathophysiology of Acute Lung Injury in Severe Burn and Smoke Inhalation Injury. Anaesthetist, Vol. 58, 805-812. SHR Nursing Policy Committee. (2012, April 4). Practices and Policies: Oxygen Adminstration. Retrieved December 12, 2013, from Saskatoon Health Region : http://www.saskatoonhealthregion.ca/about_us/documents/Nursing%20Affairs/Oxygen_Administration-1115.pdf Toon, M., Maybauer, M., Greenwood, J., & Fraser, J. (2010). Managemet of Acutre Smoke Inhalation Injury. Critical Care and Resuscitation, Vol. 12, No. 1, 53-61. Thoracic Trauma Q7. You are called to a patient with a penetrating chest wound. Support with evidence your management of this patient in relation to fluid administration.  Thoracic injuries are very common and account for approximately 20-25% deaths due to trauma [Roh12]. Penetrative thoracic injuries are caused by blunt or sharp trauma that pierces the skin around the thoracic cavity, enters through tissues, and creates an open wound. Penetrating trauma implies that the cause of the injury does not go through. Thoracic injuries where an object goes through the thoracic cavity are referred to as perforating injuries [Ste05]. Penetrating thoracic injuries usually cause hypoxic arrests, pneumothorax, massive hemorrhage and cardiac tamponades. Penetrating thoracic injuries also present with the risk that vital organs such as the heart and the lungs might be affected, resulting to massive hemorrhage. In cases where the heart is pierced, exsanguination may result from bleeding from the heart. The massive loos of blood from penetrative thoracic wounds mean that the management of hemorrhage, hypovolemia and hypotension are crucial in management of penetrative thoracic injuries. Shahani et al. (2012) explain that fluid therapy, or volume replenishment, is the cornerstone of penetrative thoracic trauma treatment. Fluid therapy in managing penetrating chest trauma is important in managing hypovolemic/hemorrhagic shock, and treating hypotension. It is important that fluid loss and hemothorax be managed first before fluid therapy is started. This is because infusion of fluids when blood loss is still ongoing is futile because it would result to hemothorax. The control of hemorrhage should henceforth come before fluid infusion. After hemorrhage control is achieved, rapid but controlled fluid infusion aimed at controlling hypovolemia and hypotension should be started. The fluids infused are mainly blood and blood products [Eva05]. The overzealous infusion of fluids, i.e. infusion of very large volumes of fluids, can precipitate renal failure, respiratory insufficiency, abdominal compartment syndrome, and cardiac failure; hence should be avoided [JJe05]. Explaining this better, Shahani et al (2012) assert that continuous infusions of normotonic fluids or blood in patients with penetrative thoracic injuries may result to tissue edema, acute respiratory distress, cardiac compromise and soggy lungs i.e. presence of water in the lungs. This indicates that it is important to control the volume of infusions administered into a patient in management of penetrative thoracic injury[Car07]. Inotropic treatments should be avoided before control of hypotension, hypovolemia, and restoration of proper cardiac function [JJe05]. Inotropic treatments are aimed at increasing the output of the heart by increasing contractions and heart activity. In conclusion, to treat a patient with a penetrating thoracic injury through fluid therapy, which is the focus of this case, involves control of hemorrhage, controlled infusion of blood or blood products, then use of an inotropic infusion to increase cardiac output if necessary. Notably, it is important that blood products and other fluids be warmed before infusion because the patient normally has hypothermia due to massive hemorrhage and poor perfusion. References Evans, B., & Hornick, P. (2005). Penetrating Injuries to the Chest. Surgery, Vol. 25, No. 11, 406-409. Jenkins, J., & Braen, G. (2005). Manual of Emergency Medicine. Hagerstown, MD: Lippincott Williams & Wilkins. Lee, C., Revell, M., & Steyn, R. (2007). The Prehospital Management of Chest Injuries: A Consensus Statement. Emergency Medicine Journal, 220-224. Shahani, R., Galla, J. D., Talavera, F., Schwartz, D. S., Zamboni, P., & Milliken, J. C. (2012, October 3). Penetrating Chest Trauma. Retrieved December 12, 2013, from MedScape: http://emedicine.medscape.com/article/425698-overview#a0112 Stewart, M. (2005). Principles of Ballistics and Penetrating Trauma. In M. Stewart, Head, Face, and Neck Trauma: Comprehensive Management (pp. 188-194). ISBN 3-13-140331-4. Pain and Pain Management Q8. Which analgesic is the best for pain of traumatic origin? Support your argument with credible evidence. The best analgesic in the treatment of traumatic pain is morphine. Morphine is an opioid drug that is an effective painkiller used to treat and manage severe pain of traumatic origin [Bri13]. The drug is marketed as tablets, oral liquid, injectable liquid or capsules. The drug is contraindicated in many situations including pregnancy and its use without a prescription is considered a case of drug and substance abuse because it is a narcotic drug. Despite these issues, morphine is the best analgesic for the management and treatment of pain of traumatic origin. My argument that morphine is the best analgesic for treating traumatic pain is supported by research as well as arguments against the other analgesics that are said to be better than morphine. Many studies have been done to establish the effectiveness and efficacy of morphine use as an analgesic against traumatic pain. Most of these studies conclude that morphine is very effective against traumatic pain. One such study was done by Machino, Yukawa, Hida, Oka, Terashima, Kinoshita and Kato on 205 patients who had lower extremity fractures. The researchers did the study from June 2006 to December 2007, and they exposed a group of the patients to morphine and another group to bupivacaine as a control group. The results of the study indicated that morphine provided an additional analgesic effect in the postoperative period of the patient. The researchers also noted that though morphine is associated with more side effects than other analgesics, there is actually no significant difference between the side effects caused by morphine and other strong analgesics, noting that the side effects are themselves very minor complications [Mac10]. This is in keeping with the observation of Meylan, Elia, Lysakowski & Tramer (2009) that the side effects of morphine are rare and very minimal when the drug is used at low doses to treat traumatic pain [NMe09]. Another study on the efficacy of morphine was done by Jennings, Cameron and Bernard (2012) in a randomized trial in which they compared the use of ketamine and morphine to the use of morphine alone. The researchers report that use of ketamine together with morphine is superior than use of morphine alone [PJe12]. In a commentary to this research, McKay (2013) reports that ketamine use gives a greater pain reduction than morphine use, but explains that ketamine causes more adverse effects [Wii13]. The above studies provide scholarly support for the argument that morphine is the best analgesic in treatment of traumatic pain. One argument that is not tackled in the above studies is the argument that morphine is very addictive. The addiction to morphine cannot be refuted, but can be avoided if patients stick to prescriptions. Summarily, morphine is the best analgesic in management of traumatic pain. References British Medical Association and Royal Pharmaceutical Society of Great Britain. (2013). British National Formulary, 66th Edition. London: British Medical Association and Royal Pharmaceutical Society of Great Britain. Jennings, P., Cameron, P., & bernard, S. (2012). Morphine and Ketamine is Superior to Morphine alone for Out-of-Hospital Trauma Analgesia: A Randomized Controlled Trial. Annals of Emergency Medicine, Vol. 59, 497-503. Machino, M., Yukawa, Y., Hida, T., Oka, Y., Terashima, T., Kinoshita, S., et al. (2010). A Prospective Study Randomized Study for Post-Operative Relief of Lower Estremity Fractures: Efficacy of Intrathecal Morphine Administration. Nagoya Journal of Medicine and Science, Vol. 72, 145-150. McKay, W. (2013). Intravenous Analgesia for Out-of-Hospital Traumatic Pain in Adults: Ketamine Gives a Greater Reduction in Pain than Morphine but Causes More Adverse Effects. Evidence Based Nursing, Vol. 16, No. 2, 58-59. Meylan, N., Elia, N., Lysakowski, C., & Tramer, M. (2009). Benefits and Risks of Intrathecal Morphine Without Local Anaesthetic in patients Undergoing Major Surgery: Meta-analysis of Randomized Trials. British Journal of Anaethesia, Vol. 102, 156-167. Read More