Both natural as well as human-generated disasters, which in many cases are linked to destruction including loss of lives and irredeemable belongings, often, devastate one’s normal life and their coping capacity. Although most individuals eventually do well and go back to their previous level of activity after experiencing traumatic events, others tend to initially experience distressing feelings, thoughts, and physical symptoms. These individuals may also engage in risky actions as a way of coping.
Realizing that one has experienced tremendous loss following a natural disaster can be quite traumatizing. This paper will discuss shock as one of the outcomes of trauma, and highlight some of the steps one should take in the case of a natural disaster.
Delegate your assignment to our experts and they will do the rest.
Differences between Cardiogenic, Hypovolemic, Obstructive, Distributive, and Septic shocks and the pathophysiology of each
Shock is generally a state of tissue and cellular hypoxia following reduction of oxygen delivery and/or raised oxygen use or insufficient oxygen utilization (Redl & Gunther, 2012). Though initially reversible, it is important to acknowledge and treat it immediately to avoid development into irreversible organ failure. As already indicated, there are four main kinds of shock that have so far been recognized. Cardiogenic shock signifies a situation in which a person’s heart unexpectedly fails to thrust adequate blood to cater to the body’s needs (Redl & Gunther, 2012). It is quite rare but often fatal if not managed immediately.
The pathophysiology of cardiogenic shock incorporates a cruel twisting circle where ischemia triggers myocardial dysfunction, which in turn heightens myocardial ischemia (Redl & Gunther, 2012). Myocardial stunning and/or sleeping myocardium can improve myocardial dysfunction and exacerbate the cardiogenic shock. Notably, low perfusion pressures with worldwide ischemia results in multi-organ failure. Reperfusion and ischemia can also lead to systematic swelling or in the initial times sepsis following translocation of bacteria or bacterial poisons from the intestines, leading to increased mortality (Redl & Gunther, 2012).
Hypovolemic shock is a deadly condition that is an outcome of losing more than 20% of the body’s fluid or blood reserve (Redl & Gunther, 2012). This serious fluid loss makes it tough for the heart to pump enough quantity of blood to the body. Very young kids and older adults are considered the most prone to this type of shock. With regards to its pathophysiology, the concerned nervous circulatory and neuroendocrine techniques each play a significant role in the homeostatic reaction to intravascular volume reduction (Redl & Gunther, 2012).
The clinical position of hypovolemic shock can either be decompensated, irreversible, or compensated. Superior levels of catecholamines successively lead to amplified heart speed, casoconstriction, and myocardial contractility to uphold cardiac productivity (Redl & Gunther, 2012). Vasoconstriction takes place principally at the splanchnic and peripheral vessels, thus sidetracking blood flow away from the gastroinstestinal region, skeletal muscles, and skin. This is while upholding perfusion to the head and heart (Redl & Gunther, 2012). Renal perfusion can be sufficiently sustained with low to sensible hemorrhages.
Obstructive shock takes place when blood cannot get to where it needs to go. Obstruction of the aortic flow can be distinguished from disorders involving impaired diastolic filling and less cardiac preload, as it results to increased left ventricular afterload (Redl & Gunther, 2012). The pathophysiology of obstructive shock can be grouped as per the location of the obstruction in the vascular structure in relation to the heart. Distributive shock is a position of virtual hypovolemia following pathological redeployment of the total intravascular section and is considered the most common type of shock (Redl & Gunther, 2012). This form of shock usually takes place when there is actually enough blood in the blood vessels but cannot be distributed to the organs. This leads to dilated blood vessels, making the blood not to move as fast as it needs to (Redl & Gunther, 2012). As a result, the heart cannot pump that blood because there is so much space and less pressure to help the blood move through the vessels.
Lastly, Septic shock is a clinical syndrome of dangerous dysfunction caused by a dysregulated reaction to infection (Redl & Gunther, 2012). Here, there is a significant reduction in tissue perfusion and multiple organ or acute failure can take place. Septic shock’s pathogenesis is not totally comprehended. An inflammatory stimulus such as a bacterial contaminant triggers production of proinflammatory mediators, which in turn activate the clotting mechanism and produce microthrombi (Redl & Gunther, 2012). Anti-inflammatory mediators resulting in an unconstructive feedback mechanism oppose these.
Risks of Morbidity and Mortality and the Preparation and Prevention Measures for one Type of Natural Disaster
Environmental disasters usually result in physical destruction of dwellings, human pain and injury, loss of life, and significant losses. Since time immemorial, much of human life, culture, and technology have been defined by regular challenges against the forces of nature (McCance & Huether, 2010). Natural disasters can be earthquakes, hurricanes, tornadoes, fire, floods, drought, and solar flares, among others. Heat wave is a type of natural disaster where heat kills by pushing a person’s body beyond its limits (Veneema, 2013). This natural disaster results in adverse health effects in urban areas more than in rural ones. The number of deaths grouped as heat associated and attributed to other causes increase considerably (McCance & Huether, 2010). Those who are more prone to heat-related mortality are infants, individuals with chronic conditions, the elderly, those confined to beds, and patients under medications that incline them to heatstroke
Basic environmental and behavioral measures are important in the prevention of heat-associated death and illness. Individual prevention strategies should incorporate increased time spent in air-conditioned settings, inclusion of cool baths into a daily routine, and intake of non-alcoholic beverages (Veneema, 2013). Employees and athletes in occupations that require exposure to indoor or outdoor superior temperatures should take extra precautions, including ten to fourteen days to adjust to a setting of predictably superior ambient temperature.
How to Set Up for Disaster Closet in the Emergency Department, What Items It Should Contain, Who Should Have Access, If It Should Be Blocked and Type of Drills that Should Be Conducted
Emergency closets should be situated at the hospital ambulance bay entrance in instances of disaster. An emergency closet should contain Mass Casualty Incidents packets in which are specific roles and accountabilities to be achieved soon after the activation of the Emergency Management Plan (Veneema, 2013). The fitting Personal Protective Equipment should be used depending on the kind of the vital sanitization (McCance & Huether, 2010). In instances when the Emergency Department is at capacity with patients, areas in the hospital should be used as expanded observation and expanded care space.
Any disaster patient that has been exposed to radioactive and/or other contaminated poisons or materials should be transported to the decontamination region before transportation to the main treatment region. The only individuals having access to the calamity closet in the Emergency Department ought to be the nursing supervisors, hospital operators, senior emergency residents, pediatric residents, patient representatives, and hospital police patrol supervisors. Some of the drills that should be conducted include the functional drill, which incites an emergency in the most representative way possible, short of shifting genuine individuals and equipment to a real site; tabletop drill which is a facilitated evaluation of an emergency situation in a non-official, stress-free setting; and full-scale drill which is the closest to the real thing (Veneema, 2013). This is usually a lengthy occurrence, taking place on location using personnel and equipment that would be called upon in a genuine occurrence.
The Pathophysiology of Burns and the Differences between First, Second, and Third Degree Burns; Potential Complications of Each
Though burns are cutaneous wounds, the effects tend to influence almost all systems of a person’s body. Kids and the elderly have thinner skin and are thus more probable to sustain a deeper burn injury. The total morbidity linked to a burn wound is determined by fraction Total Body Surface Area involved, manifestation of breath injury, burn depth, and patient age (Daigler, Kapalschinski & Lenhardt, 2015). Extensive burn wounds produce a systematic reaction that tugs fluid from the vascular system into the interstitial area (Garcia-Espinoza, et al., 2017). This is worsened in burns higher than 20% TBSA by a significant vessel seepage into the microvasculature and comprehensive edema.
Burns tend to differ in terms of seriousness and type. First-degree burns are usually minor likened to other burns and result in reddening and pain of the epidermis (Daigler, Kapalschinski & Lenhardt, 2015). Second-degree burns affect both the skin and dermis, causing inflammation, swelling, pain, and blistering, while third-degree burns go through the dermis, affecting deeper tissues. They lead to white or darkened, seared skin that may become deadened (Garcia-Espinoza, et al., 2017). In some instances, the level of burn a person has will transform. This happens if their damaged skin keeps spreading and the injury grows deeper (Daigler, Kapalschinski & Lenhardt, 2015). Burns can result in numerous complications, with the inclusion of bone and joint issues and infection.
The Pathogenesis and Progression of Ebola and What Safety Concerns were addressed during the 2014 Outbreak
The Ebola virus is a destructive pathogen that instigates a superiorly dangerous hemorrhagic infection syndrome in people and nonhuman primates. It was initially discovered near the Ebola River valley in the course of an outbreak in 1976, in Zaire. The inherent host of the virus is still unknown, thus making it difficult to apply programs to manage or get rid of viral reservoirs of transmission to human populace (Baize, et al., 2014). The Ebola virus tends to replicate very effectively in different cells, yielding large quantities of sickness in macrophages, dentritic cells, monocytes, and other cells (Veneema, 2013). This replication in monocytes prompts the discharge of superior levels of inflammatory chemical signals.
The cells lining the interior of blood vessels, monocytes, liver cells, and macrophages are the chief targets of infection. Macrophages are the initial cells infected with the virus, which then results in cellular death (McCance & Huether, 2010). Endothelial cells can be infected in a span of three days following exposure to the Ebola virus (Feldmann, 2014). The widespread hemorrhage that takes place in affected individuals causes hypovolemic shock and edema.
During the 2014 epidemic, a number of security concerns were tackled. For instance, the risk of infection for the healthcare workers when caring for Ebola virus patients when not wearing Personal Protection Equipment was among the concerns (McCance & Huether, 2010). Another major concern was for those involved in epidemic reaction and health care to the virus, with the inclusion of violence, extra working hours, dehydration from using heavy PPE, psychological distress, and ergonomic issues associated with handling loads and bodies.
Conclusion
During and after a traumatic event or disaster, it is normal to experience unusual and strong emotions. Generally, traumatic experiences are quite common. About two-thirds of individuals in the overall populace tend to experience a significant traumatic to occurrence at some point in their lives. Coping with these emotions and accessing help when you most need it to help recover from a traumatic event goes along way when healing. Therefore, it is important for governments and the communities as a whole to explore ways, and be well equipped and ready to handle the traumas and losses that follow after a natural disaster.
References
Baize, S., et al. (2014). ‘Emergence of Zaire Ebola virus disease in Guinea.’ N Engl J Med , 371. Pp. 1418.
Daigeler, A., Kapalschinski, N., & Lehnhardt, M. (2015). ‘Therapy of burns.’ Chirurg , 86. Pp. 389-401.
Feldmann, H. (2014). ‘Ebola – A growing threat?’ N Engl J Med , 371. Pp. 1375.
Garcia-Espinoza, J.A., et al. (2017). ‘Burns: Definition, classification, pathophysiology and initial approach.’ Gen Med , 5. Pp. 298.
McCance, K.A., & Huether, S.E. (2010). Pathophysiology: The biologic basis for disease in adults and children . 7 th Edition. St. Loius: Mosby.
Redl, H., & Gunther, S. (2012). Pathophysiology of shock, sepsis, and organ failure . New York: Springer Science & Business Media.
Veneema, T.G. (2013). Disaster nursing and emergency preparedness: For chemical, biological, and radiological terrorism and other hazards . New York, NY: Springer Publishing.
