Case Study of Ms Foley-Free-Samples for Students-

This assignment is about a patient named Ms. Martha Foley, a 35 year old lady who is suffering from acute pulmonary oedema and was admitted in the hospital prior to 5 days because of post multi-trauma caused by a car accident. She is also suffering from multiple fractures in both legs and smoke inhalation as being trapped in car for 15 minutes. This paper has been divided into two parts. Part 1 contains the description of Ms. Foley and her history along with the treatment in the hospital and the analysis of the Observation Chart and Fluid Balance Chart. It also contains a brief description of acute pulmonary oedema, its pathophysiology and the implications of nursing assessment of this situation. Part 2 contains the inter-professional model of care required for Ms Foley while in hospital. Ms. Foley is a full time worker at a supermarket and is a victim of domestic violence from her former partner. She had a good relationship and support from her friends and co-workers. The day of the accident she and her friend Ms. Annie Jones were travelling in the same car. Ms. Jones was also admitted in the same hospital. Ms. Foley was a smoker of 10 cigarettes per day and also intake drugs such as methamphetamines IV and cocaine. But don’t drink alcohol and is a vegetarian. She had suffered from left sided heart failure in the past and is treated by cardiomyopathy. Fluid balance chart describes that Ms. Foley is given compound Sodium acetate was given intravenously from 01:00 am to 08:00 am at 200mls per hour and only 100mls is drained out through urine. It has been shown in appendix 1. Observation chart describes about the general physical conditions of Ms. Foley during the time of her admission in the hospital. The following things were measured: Acute pulmonary oedema is a type of disease in which the alveoli gets filled up with fluid and the person is unable to breathe. As the fluid gets accumulated creates misbalance in exchange of gases and leads to dyspnoea and hypoxia. Acute pulmonary oedema (APO) is caused by two main mechanisms. The first mechanism is elevations in pulmonary pressures due to severe increase in intra-cardiac pressure of chambers and second is severe lung injury causing increase in pulmonary vascular permeability (Liesching et al. 2014). Pulmonary oedema caused due to lung injury is termed as acute respiratory distress syndrome (ARDS) while pulmonary oedema which is due to acute elevations in pulmonary micro vascular pressures is termed acute cardiogenic pulmonary oedema (Lavin et al. 2015). The pathophysiology of these two types of oedema is almost different due to which their treatments are also different. This document relates specifically to acute cardiogenic pulmonary oedema (Zeiss 2016). Acute cardiogenic pulmonary oedema is caused by an intense ischemic occasion bringing about cardiovascular brokenness. Intense diastolic disappointment may likewise be caused from hypertension and atherosclerosis. Less generally the intense sight might be optional to other essential occasions, for example, intense valvular issue or arrhythmia (Elias et al. 2015). The acute cardiac dysfunction that happens from a background marked by myocardial ischemia brings about expanded cardiovascular end diastolic weights which thus result in hoisted pneumonic micro vascular weights and the improvement of intense cardiogenic aspiratory oedema (Vlaar and Juffermans 2013). There is a decrease in cardiovascular yield with ensuing solid enactment of the thoughtful sensory system and the renin-angiotensin framework. This outcomes in lifted blood weights and expanded delayed consequences on the heart starting a gooey cycle of expanded myocardial oxygen request and further lessening in cardiovascular yield (Luks et al. 2014). In the problems of heart failure there are homeostatic systems that prompt liquid maintenance and pneumonic blockage. In APO there might be starting of liquid fill up, however the essential pathophysiology won't be reliant on the benchmark liquid status. It is significant that s number of these patients is hemoconcentrated on introduction because of the gathering of up to 2 litres of liquid in their lungs (Spoletini et al. 2015). They may then show up hemodiluted 24 hours after the fact when they are in the recuperation stage. As it were they give off an impression of being enduring a more prominent plasma volume as of now, which is suggestive that the issue is not fundamentally a liquid over-burden issue. By and large of APO the issue is less liquid abundance; rather it is an instance of liquid in the wrong "compartment", (intra-alveolar, as opposed to intra-vascular) (Duffy et al. 2015). The nursing care plan depends upon the appearance of the patient’s respiratory status. To perform the assessment of nursing care for acute pulmonary oedema the nurse must observe the individual’s responses (Akoumianaki et al. 2014). The following are the therapeutic nursing interventions for  acute pulmonary oedema: The initial management of patients with cardiogenic pulmonary edema (CPE) should address the ABCs of resuscitation, that is, airway, breathing, and circulation. Oxygen should be administered to all patients to keep oxygen saturation at greater than 90%. Any associated arrhythmia or MI should be treated appropriately (Lumb 2016). Methods of oxygen delivery incorporate the utilization of a face covering, non-intrusive pressure support ventilation (which incorporates bi-level positive aviation route weight [BiPAP] and consistent positive airway pressure [CPAP]), and intubation and mechanical ventilation (Stocker et al. 2014). The method that will be utilized relies upon the proximity of hypoxemia and acidosis and on the patient's level of cognizance. For instance, intubation and mechanical ventilation may end up noticeably important in instances of tireless hypoxemia, acidosis, or changed mental status. The utilization of non-intrusive weight bolster ventilation in acidotic patients with serious intense cardiogenic aspiratory oedema does not give off an impression of being related with unfavourable results (early mortality and intubation rates) in these patients (Adam, Osborne and Welch 2017). Initial dose: Frusamide is given intravenously and the dosage is 20-40 mg (slowly for 1 to 2 minutes) or may increase the dosage by 20 mg later by 2 hours after the previous dose until the desired diuretic effect has been obtained. Use: Treatment of oedema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, especially when an agent with greater diuretic potential is desired (Soni et al. 2017). Initial dose: 20 to 80 mg orally once; may repeat with the same dose or increase by 20 or 40 mg no sooner than 6 to 8 hours after the previous dose until the desired diuretic effect has been obtained. Maintenance dose: Administer the dose that provided the desired diuretic effect once or twice a day. Maximum dose: 600 mg/day in patients with clinically severe oedematous states. -Oedema may be most efficiently and safely mobilized by giving this drug on 2 to 4 consecutive days each week. -When doses greater than 80 mg/day are given for prolonged periods of time, careful clinical observation and laboratory monitoring are particularly advisable. Use: Treatment of oedema associated with congestive heart failure, cirrhosis of the liver and renal disease, including the nephrotic syndrome, especially when an agent with greater diuretic potential is desired. The Inter-Professional Model of Patient Care (IPMPC ©) was introduced in 2006 when inter-professional collaboration started as a priority of policy agenda in Canada. This model causes the experts to enhance better care the patients and their families which likewise can manage the extra issues of human medicinal services. The models speak to a pedantic program, a group based affair and a between proficient recreation encounter. The instructional program stresses between proficient group building abilities, information of callings, tolerant focused care, benefit taking in, the effect of culture on medicinal services conveyance and a between proficient clinical segment (Maggiore et al. 2014). Nurses were ready for Ms Foley to attend her while she was lying flat on her bed, trying to sit up, and gasping for air. She is worried, stating she is ‘scared’, and that she has a weird feeling that she can only describe as ‘a sense of impending doom’. Vital signs taken and are the following: Pulse 120bpm and regular, BP 100/50, RR 34, SaO2 92% on RA. Her lips have started to turn blue and the nail beds on her fingers are cyanotic. She remains dyspnoeic and desperate for air. She is coughing. The integral part of inter-professional care of nursing is quality improvement. ACHS is a handbook which gives information of management of risks and improvement of quality to assist organisations and to manage the risks at the organisational levels and to ensure that quality of care and services are integrated (Powell et al. 2016). PE teams have found their place in health care. Teams do not replace the physician-patient relationship, but rather enhance it—creating a more comprehensive, efficient, and tailored health care experience (Short et al. 2014). The care convention was created by the IP group amid a CPE workshop and encouraged group gatherings. It was utilized as the guide by medical caretakers or doctors associates who gave mind at the visits. Components of the IP mind convention included visual signs, for example, publications on the exam room dividers that represent the body frameworks affected by diabetes, and an envelope with data, worksheets and apparatuses created by the IP group on parts of connecting with relatives for help, eating regimen, exercise and medical administration. Thus through the above discussion it can be concluded that Ms. Martha Foley had an accident and detected by acute pulmonary oedema which is a type of disease in which the lungs is filled up with fluid. At first in this task there had been included clinical assessment tools; pathophysiology and its applications; nursing care plan; nursing interventions; pharmacological uses of frusamide; inter-professional model of care, its risk management and its implications Adam, S., Osborne, S. and Welch, J. eds., 2017. Critical care nursing: science and practice. Oxford University Press. Akoumianaki, E., Maggiore, S.M., Valenza, F., Bellani, G., Jubran, A., Loring, S.H., Pelosi, P., Talmor, D., Grasso, S., Chiumello, D. and Guà ©rin, C., 2014. The application of esophageal pressure measurement in patients with respiratory failure. American journal of respiratory and critical care medicine, 189(5), pp.520-531. Duffy, M., Jain, S., Harrell, N., Kothari, N. and Reddi, A.S., 2015. Albumin and furosemide combination for management of edema in nephrotic syndrome: a review of clinical studies. Cells, 4(4), pp.622-630. Elias, B., Barginere, M., Berry, P.A. and Selleck, C.S., 2015. Implementation of an electronic health records system within an interprofessional model of care. Journal of interprofessional care, 29(6), pp.551-554. Lavin, M., Harper, E. and Barr, N., 2015. Health information technology, patient safety, and professional nursing care documentation in acute care settings. OJIN: The Online Journal of Issues in Nursing, 20(2). Liesching, T., Nelson, D.L., Cormier, K.L., Sucov, A., Short, K., Warburton, R. and Hill, N.S., 2014. Randomized trial of bilevel versus continuous positive airway pressure for acute pulmonary edema. The Journal of emergency medicine, 46(1), pp.130-140. Luks, A.M., McIntosh, S.E., Grissom, C.K., Auerbach, P.S., Rodway, G.W., Schoene, R.B., Zafren, K. and Hackett, P.H., 2014. Wilderness Medical Society practice guidelines for the prevention and treatment of acute altitude illness: 2014 update. Wilderness & environmental medicine, 25(4), pp.S4-S14. Lumb, A.B., 2016. Nunn's Applied Respiratory Physiology eBook. Elsevier Health Sciences. Maggiore, S.M., Idone, F.A., Vaschetto, R., Festa, R., Cataldo, A., Antonicelli, F., Montini, L., De Gaetano, A., Navalesi, P. and Antonelli, M., 2014. Nasal high-flow versus Venturi mask oxygen therapy after extubation. Effects on oxygenation, comfort, and clinical outcome. American journal of respiratory and critical care medicine, 190(3), pp.282-288. Powell, J., Graham, D., O’Reilly, S. and Punton, G., 2016. Acute pulmonary oedema. Nursing Standard, 30(23), pp.51-60. Short, K.R., Kroeze, E.J.V., Fouchier, R.A. and Kuiken, T., 2014. Pathogenesis of influenza-induced acute respiratory distress syndrome. The Lancet infectious diseases, 14(1), pp.57-69. Soni, L., Ansari, M., Thakre, N., Singh, A., Bhowmick, M. and Rathi, J., 2017. Development and in-vitro evaluation of Furosemide Solid Dispersion using different Water Soluble Carriers. International Journal, 6(2), pp.2571-2575. Spoletini, G., Alotaibi, M., Blasi, F. and Hill, N.S., 2015. Heated humidified high-flow nasal oxygen in adults: mechanisms of action and clinical implications. CHEST Journal, 148(1), pp.253-261. Stocker, R., Lenzlinger, P.M. and Stover, J.F., 2014. Contemporary intensive care treatment for patients with severe multiple trauma. In General Trauma Care and Related Aspects (pp. 95-109). Springer Berlin Heidelberg. Vlaar, A.P. and Juffermans, N.P., 2013. Transfusion-related acute lung injury: a clinical review. The Lancet, 382(9896), pp.984-994. Zeiss, A.M., 2016. Cognitive Behavioral Therapy as an Integral Component of Interprofessional Care. Cognitive and Behavioral Practice, 23(4), pp.441-445