Acute Respiratory Distress Syndrome - Special Academic Support

Do you need this or any other assignment done for you from scratch?

We assure you a quality paper that is 100% free from plagiarism and AI.

You can choose either format of your choice ( Apa, Mla, Havard, Chicago, or any other)

NB: We do not resell your papers. Upon ordering, we do an original paper exclusively for you.

NB: All your data is kept safe from the public.

Click Here To Order Now!

Acute Respiratory Distress Syndrome

Table of Contents

Introduction
Causes
Risk factors
Pathophysiology of ARDS
Diagnostic Tools Used in the Diagnosis and Management of ARDS
Reference List

Introduction

The acute injury of the lung is referred to as acute respiratory distress syndrome (ARDS). In this condition, the amount of oxygen diffusing from the air sacs to the bloodstream is usually very low, thus the disease is highly life-threatening. Direct or indirect insults are the two broad mechanisms through which ARDS may result. According to Udobi and Touijer (2003, p. 315), sepsis, trauma, and severe pulmonary infections are the commonest causes of ARDS. The most common presentation of ARDS includes dyspnea, severe hypoxemia, decreased lung compliance, and diffuse pulmonary infiltrates (Udobi & Touijer 2003, p. 315). In ARDS, hypoxemia is usually not more than 200 mm Hg as the ratio of PaO₂/FIO₂. On a radiograph of the chest, ARDS manifests with pulmonary infiltrates at the bilateral pulmonary. The wedge pressure of the pulmonary artery is identified to be less than 18 mm Hg, though hypertension in the left atrium is not clinically evident.

Causes

The lung can experience injury or inflammation which leads to ARDS if aspiration occurs, when chemicals are inhaled, due to septic shock, pneumonia, or any other form of trauma involving the lung. In ARDS, pressure accumulates in the alveoli thus barring the diffusion of oxygen into the bloodstream. With fluid inside the air sacs, it becomes hard for the lungs to expand since they are not only stiff but also heavy. This leads to low oxygen levels in the blood (hypoxia). It is common to have another organ failure accompanying ARDS (Blaivas 2011).

In the alveoli, injury is seen to take place at the membrane of the capillaries of alveoli. While some alveoli are laden with fluid, others collapse altogether thus interfering with the O₂/CO₂ exchange which occurs in the lungs. Eventually, other vital organs in the body such as the kidneys fail due to insufficient oxygen in the bloodstream (Harman 2011).

Risk factors

There are varied numbers of risk factors associated with the development of ARDS. Pneumonia is a clinical condition that is associated with direct injury of the lung leading to ARDS. If gastric contents are aspirated into the lungs, then direct injury of the lung and subsequent ARDS is almost inevitable (Hopkins et al. 2010). Conditions such as reperfusion pulmonary edema which occur mainly in lung transplantation are also risk factors that lead to ARDS due to direct injury of the lung. Other risk factors which cause direct injury of the lung include pulmonary contusion as well as being in a situation of near-drowning. Bacterial infection of the blood (sepsis) is a risk factor for ARDS but it causes indirect injury to the lung (Matthay 2003). This is also the case with drug overdose, high blood transfusion, and acute pancreatitis among other clinical conditions. Other factors which exacerbate the risk of developing ARDS include being of advanced age as well as smoking cigarettes (Udobi & Touijer 2003).

Pathophysiology of ARDS

Understanding the pathophysiology of ARDS goes a long way in necessitating diagnostic, treatment, and prognostic options. The pathophysiology of the traumatized lung has three phases: exudative, proliferative, and fibrotic phases. It is established that each phase has unique characteristics of the disease. Inflammatory mediators, for instance, lead to exudation of among other components blood cells (red blood cells in specific), proteins, and water from the walls of the alveoli and vasculature. Damage of the alveoli is mainly due to the irreversible damage to the alveolar Type I cells, followed by proteins and fibrin deposition in the spaces that are left. Eventually, the alveoli collapse since Type II cells are eventually damaged hence they cannot produce surfactants (Udobi & Touijer 2003).

The proliferative phase is characterized by the proliferation of Type II cells. Regeneration of epithelial cells may also occur, while a reaction of a fibroblastic nature accompanied by remodeling is also seen in some cases. Progression to the third stage, the fibroblastic phase, occurs in some patients whereby the alveoli are filled with collagen as well as the interstitial beds. This leads to the formation of microcysts (Udobi & Touijer 2003).

As earlier mentioned, ARDS is considered to have set in if PaO₂/FiO₂ ratio goes below 200 mm Hg, thus differentiating the condition from acute lung injury (ALI) which is usually a precursor (Udobi & Touijer 2003). ARDS early phase is considered as the initial 72hrs after lung injury. In this stage, inflammatory reactions are the capital characteristics whereby the alveolar-capillary barrier is damaged during the inflammatory reactions. Pulmonary edema resulting from the inflammation interferes with the exchange of gases, thus resulting in respiratory failure. It is for this reason that mechanical ventilation is called for during the early phase of ARDS (Putensen et al., 2009).

Mechanical ventilation, however, comes with its risks since if not well administered it may result in further injury to the air sacs. This is because tidal breaths from the ventilation mechanisms lead to collapse and shear opening of any unstable air sac. Overdistension of the intact alveoli may also result as the tidal volume increases leading to trauma. The barrier between the endothelium and epithelium may also be damaged due to the increased volume and pressure during mechanical ventilation, and this followed by proinflammation mediators released at the injured parts exacerbates the injury (Bream-Rouwenhorst et al. 2008).

Continued inflammation recruits neutrophils to the lungs and activation of neutrophils cause further damage to the lungs due to the release of proteases and arachidonic acid. A vicious cycle of lung damage may ensue in this process. If recovery does not take place at this stage, ARDS progresses into the next phase which is referred to as the mid- or exudative phase. It is pertinent to note that the clinical course of ARDS may differ among patients due to various factors such as the presence of other illnesses like diabetes mellitus among other factors. Intervention at the exudative phase, therefore, is highly determined by the prevailing factor(s). The exudative phase comes between day 3 and day 7 after lung injury. In this phase, it is common to find protein-rich hyaline membranes inside of the alveolar. Cellular debris also tends to accumulate. Alveolar damage is usually of diffuse nature and gas exchange is poorly handled, thus hypoxemia is a common phenomenon.

As a result of inflammatory damage in the alveoli and mechanical violations from mechanical ventilation, pathogenic events are experienced. For instance, metabolism, as well as the work of the surfactant, is disrupted and more inflammatory mediators are released. The complement pathway is also activated. Since multiple organ failure is the principal cause of death in ARDS, most patients progress to the third phase and only a few succumb in the second phase. However, the disease state at the second phase usually culminates into multiple organ failure (Ware & Matthay 2000).

The fibroproliferative phase is the last stage which mostly occurs between day 8 and day 28. Fibrosis is usually evident due to the organization of hyaline membranes. On the lining of the walls of the air, sacs can be seen as Type II cells of the alveolar and differentiation of the fibroblasts into myofibroblasts. At the interstitium, there is the deposition of a matrix that is rich in collagen leading to the destruction of alveoli, constriction of vascular area, and eventual chronic inflammation (Timby & Smith 2005). Mechanical ventilation at this stage usually fails to correct the situation and most patients succumb. It is for this reason that pharmacological interventions targeting phase three should aim at preventing fibrosing alveolitis. Fibrosis is usually the main barrier to any intervention at this stage. It is therefore advisable to intervene during the initial stage of ARDS if severe damage is to be circumvented.

Diagnostic Tools Used in the Diagnosis and Management of ARDS

In ARDS treatment, it has been established that computed tomography scanning can be used to come up with a positive end-expiratory pressure (PEEP) (Brower et al. 2004). Caironi, Langer & Gattinoni (2008) indicate that since PEEP can lead to both the benefit of reducing derecruitment of the alveoli and the disadvantage of hyperventilation which comes with PEEP, computed tomography, therefore, provides an avenue for monitoring pathophysiology in order to realize a balance between the benefits and the likely injury emanating from PEEP. CT scanning is particularly important in showing lung hyperventilation, including in patients who receive low tidal volume during PEEP (Desai et al. 1999). While there are gaps for further research as regards coming up with the right PEEP, it is evident that CT scanning is a beneficial intervention in ARDS patients. Caironi, Langer & Gattinoni (2008) however caution that using low tidal volume is not universally beneficial, hence other techniques of achieving respiratory support should be explored. Some of the suggested techniques include performing lung ultrasound as well as the use of electrical impedance tomography (Goodman & Gattinoni 2006).

It is realized that acute lung injury may result from exposure to damaging agents such as toxic compounds from industrial processes and other potential bioterrorism agents. It is for this reason that Lindsay (2010) has suggested the use of new therapeutic approaches for ARDS. Lindsay (2010) suggests that the development of novel treatment strategies for ARDS can be helpful in averting casualties as well as the characteristic pulmonary edema which accompanies ARDS (Manthous 2010). As such, it is identified that there is a need to move from the conventional ventilation and fluid management strategies and employ pharmacological options, which aim at enhancing recovery of the compromised blood/air barrier of the alveoli. This therapeutic approach is particularly applicable with ARDS resulting from chemical injury (Lindsay 2010).

While the pharmacological approaches are still under development stages, there is the promise that some growth factors such as keratinocyte, epithelial and basic fibroblast growth factors (KGF, EGF, and bFGF respectively) are the most likely candidates so far. It is important to employ a growth factor that shows specificity for the epithelium of the lung alveoli. As such, the hepatocyte growth factor is ruled out as a potential pharmacological intervention. It is suggested that trefoil factor family (TFF) peptides show a lot of promise in the short term since they help the epithelial activities spread fast, thus allowing quick repair of mucosal surfaces injured in ARDS (Lindsay 2010).

To achieve better intervention outcomes with mechanical ventilation in ARDS therapy, it is advisable that mechanical ventilation is initiated early. Hu et al (2010) advise that providing effective mechanical ventilation for the first three days results in improved outcomes. Hue et al (2010) identified that when mechanical ventilation is not given sufficiently in the early stages of ARDS functional performance of the lung deteriorates due to increased injury. However, it is evident that controlled Vt ventilation may change the course of the pathophysiology, resulting in better outcomes and increased survival. In fact, low vte has been established as an effective intervention in lowering ARDS mortality among adult patients (Russel & Walley 1999).

Each of the three phases of ARDS can be addressed by specific pharmacological interventions targeting the pathophysiologic characteristics in these phases. It is pertinent to note that as per current research, pharmacotherapy interventions that can effectively treat ARDS have not been established. Nevertheless, there is still promise in the suggested pharmacotherapy interventions. Where ARDS results from direct injury among pediatric interventions, replacement of exogenous surfactant is indicated as an effective intervention as it reduces mortality rate (Bosma, Taneja & Lewis 2010).

Linden et al (2009) studied the use of extracorporeal membrane oxygenation (ECMO) in ARDS. In a follow-up study to identify how this intervention would affect long-term pulmonary health, the authors identified that there was commendable restitution in pulmonary function. There was a reduced spread of morphological changes and lung injury associated with the use of ventilators. It is however important to note that while ECMO in ARDS treatment is a promising intervention, fibrosis is not thwarted completely. Improved pulmonary health due to this intervention should however be harnessed.

Litmathe and Dapunt (2010) emphasize the effectiveness of double ECMO when treating ARDS at its severe stage. In a patient who developed ARDS from pneumonia resulting from herpes simplex, Litmathe and Dapunt (2010) reported full recovery in the patient. Important to note is that the patient was administered virostatic therapy systemically in addition to double ECMO. It is also worth noting that in addition to double ECMO, the researchers used other systems for assisting in lung function as intravascular dissemination was spreading wide. It is therefore evident that ARDS requires multiple interventions if positive treatment outcomes are to be realized.

Combining pharmacotherapy interventions with conventional mechanical ventilation has been found to reduce the time required to administer low tidal volume ventilation. It also helps in instances where fluid management is the conventional method of ARDS management (Bream-Rouwenhorst et al. 2008). The pharmacological options which are effective in these cases include the use of corticosteroids in moderate doses (Hooper & Kearl 1996). Most other pharmacological interventions such as the use of prostaglandins or nitric oxide have however not demonstrated any efficacy in ARDS treatment (Adhikari et al. 2007). This, therefore, proves that effective management of ARDS is way beyond reach; thus calling for further research. It is however important to utilize the promising benefits of the conventional treatments such as mechanical ventilation, prone positioning (Morell 2010; Balas 2000), and fluid management, with complementation of pharmacological interventions where they have been shown to be effective. Most important in ARDS management is to intervene during the first phase of the condition as the pathological situation has not deteriorated. Severe pathological outcomes of the progressed ARDS in the second and third phases reduce the likelihood of successful recovery, regardless of the intervention measure adopted.

Reference List

Adhikari, N. K., Burns, K. E., Friedrich, J. O., Granton, J. T., Cook, D. J., & Meade, M. O., 2007. Effect of nitric oxide on oxygenation and mortality in acute lung injury: systematic review and meta-analysis. British Medical Journal, 334, 7597, 779.

Balas, M. C., 2000. Prone positioning of patients with acute respiratory distress syndrome: applying research to practice. Critical Care Nurse, 20(1), 24-36.

Blaivas, A. J., 2011. Acute respiratory distress syndrome. MedlinePlus. Web.

Bosma, K. J., Taneja, R. & Lewis, J. F., 2010. Pharmacotherapy for prevention and treatment of acute respiratory distress syndrome current and experimental approaches. Drugs, 70(10), 1255-1282.

Bream-Rouwenhorst, H. R., et al., 2008. Recent developments in the management of acute respiratory distress syndrome in adults. American Journal of Health-Systemic Pharmacology, 65:29-36

Brower, R. G., Lanken, P. N., MacIntyre, N., et al., 2004. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. New England Journal of Medicine, 351, 32736

Caironi, P., Langer, T., & Gattinoni, L., 2008. Acute lung injury/acute respiratory distress syndrome pathophysiology: what we have learned from computed tomography scanning. Current Opinion in Critical Care, 14, 64-69.

Desai, S., Wells, A., Rubens, M., Evans, T., & Hansell, D., 1999. Acute respiratory distress syndrome: CT abnormalities at longterm follow-up. Radiology, 210, 2935.

Goodman, L. R., & Gattinoni, L., 2006. Multidetector CT evaluation of acute respiratory syndrome. In Schoepf, U. J., Multidetector-row CT of the thorax. New York, NY: Springer.

Harman, E. M., 2011. Acute Respiratory Distress Syndrome (ARDS). eMedicineHealth. Web.

Hooper, R. G., Kearl, R. A., 1996. Established adult respiratory distress syndrome successfully treated with corticosteroids. South Med J., 89,359-64

Hopkins, R. O., et al., 2010. Blood glucose dysregulation and cognitive outcome in ARDS survivors. Brain Injury, 24(12): 14781484.

Hu, X. et al., 2010. Incidence, management and mortality of acute hypoxemic respiratory failure and acute respiratory distress syndrome from a prospective of Chinese paediatric intensive care network. Acta Pædiatrica/Acta Pædiatrica 99, 715721.

Linden, V. B. et al., 2009. ECMO in ARDS: a long-term follow-up study regarding pulmonary morphology and function and health-related quality of life. Acta Anaesthesiologica Scandinavica, 53, 489-495.

Lindsay, C. D., 2010. Novel therapeutic strategies for acute lung injury induced by lung damaging agents: The potential role of growth factors as treatment options. Human and Experimental Toxicology, 701-724.

Litmathe, J. & Danput, O., 2010. Double ECMO in severe ARDS: report of an outstanding case and literature review. Perfusion, 25(6), 363-367.

Manthous, C. A., 2010. A practical approach to adult acute respiratory distress syndrome. Indian Journal of Critical Care Medicine, 14(4), 196-201.

Matthay, M. A., (Ed), 2003. Acute respiratory distress syndrome. New York, NY: CRC Press.

Morrell, N., 2010. Prone positioning in patients with acute respiratory distress syndrome. Nursing Standard, 24(21), 42-45.

Putensen, C., et al., 2009. Meta-analysis: Ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury. Annals of Internal Medicine, 151:566-576.

Russel, J. A., & Walley, K. R., (Eds), 1999. Acute respiratory distress syndrome. Cambridge, UK: Cambridge University Press.

Timby, B. K., Smith, N. E., 2005. Essentials of nursing: care of adults and children. Philadelphia, PA: Lippincotts Williams & Wilkins.

Tripathi, M., et al., 2009. Evaluation of lung infiltration score to predict postural hypoxemia in ventilated acute respiratory distress syndrome patients and the lateralization of skin pressure sore. Indian Journal of Critical Care Medicine, 63(9), 392-401.

Udobi, K. F., & Touijer, K., 2003. Acute respiratory distress syndrome. American Family Physician, 67(2), 315-322.

Ware, L. B., & Matthay, M. A., 2000. The acute respiratory distress syndrome. New England Journal of Medicine, 342(18), 1334-1349.

Click Here To Order Now!