Pathophysiology of Adult Respiratory Distress Syndrome - Case Study Example

Topic:  PATHOPHYSIOLOGY OF ADULT RESPIRATORY DISTRESS SYNDROME Introduction A clinical syndrome, known as acute respiratory distress syndrome or ARDS, is characterised by an acute and diffuse life – threatening injury of the alveolar - capillary of the lungs, and its diverse aetiology leads to low levels of oxygen in the blood and eventually to respiratory failure refractory to oxygen therapy (Isselbacher et al., 1995; Jaeger, 1995; Robbins et al., 1995; Swierzewshi, 2000; Hansen-Flaschen, 2001; MacIntyre, 2005; Harms, 2007; NIH, 2008; American Lung Association Lung Disease Data, 2008). ARDS, formerly known as RDS, stiff lung, wet lung, and shock lung, is characterised by rapid and difficulty of breathing, which can occur to anybody especially among the critically ill patients (American Lung Association Lung Disease Data, 2008). MacIntyre (2005) noted a variety of aetiologies that lead to lung injury in ARDS. These are: sepsis, contusion of the lung, aspiration, pancreatitis, and other processes associated with a systemic inflammatory response. ARDS is also known as a diffuse injury of the pulmonary parenchyma associated with noncardiogenic oedema of the lung that results to severe respiratory distress and hypoxemic failure of the lung. Diffuse alveolar damage (DAD) is the pathologic hallmark for ARDS (Conrad, 2005). Pathophysiology and Pathologic Changes in ARDS: According to Swierzewshi (2000), a variety of conditions from blood – borne infection (sepsis), major trauma, and pneumonia can also cause ARDS. In addition, multiple transfusions, salt water inhalation, smoke inhalation of chemicals that are toxic, vomit aspiration, narcotics, sedatives, tricyclic antidepressant overdosage, and shock from any cause are also liked with ARDS (American Lung Association Lung Disease Data, 2008). In ARDS, the alveoli are inflamed that causes them to be filled with liquid and subsequently collapse. The exchange of gas ceases once the alveoli collapses resulting to starvation of body from oxygen (Swierzewshi, 2000). This syndrome develops within 24 - 48 hours from the injury; however, Swierzewshi (2000) noted that this condition considerably varies from patient to patient and its mortality rate ranges from 35 – 50 percent. MacIntyre (2005) and Robbins et al., (1995) stated that the sequestration of the pulmonary neutrophil and aggregation of intravascular fibrin aggregates are known to be the early pathologic changes in ARDS. MacIntyre added that inflammatory changes and loss of function of the surfactant results to alveolar instability and collapse. On the other hand, MacIntyre (2005) added that right to left shunting of the blood as well as mismatching of ventilation – perfusion of the blood that causes severe hypoxemia resulted from the formation of the oedema and alveolar instability collapse. In ARDS, MacIntyre noted that pulmonary hypertension results from the following: vasoconstriction, thrombosis, perivascular edema and inflammation, and eventually, interstitial fibrosis. In some cases, overt right ventricular failure develops with severe pulmonary hypertension (MacIntyre, 2005). A. Alveolar Injury Swierzewshi (2000) noted that actual exchange of gasses takes place in a very thin cell that makes up the alveoli known as the type I epithelial cells. In ARDS, the barrier of the alveolar epithelial cell breaks allowing the alveolar epithelial space to flood giving difficulty for the oxygen to break into the capillaries (Swierzewshi, 2000). Moreover, Swierzewshi stated that type II alveolar cells can also be affected by ARDS. B. Alveolar Capillaries Injury Swierzewshi (2000) stated that in ARDS, cellular debris and fibrin blocks the capillaries that results to the cessation of the production of the surfactant that leads to eventual collapse of the alveoli. The following are the phases of ARDS pathogenesis (Conrad, 2005): (1) Exudative phase: This is also known as the initial phase where the endothelium injury occurs as well as inflammation and exudation of fluids is noted. (2) Proliferative Phase: This phase is characterised by fibroblast and other cellular elements influx and proliferation. During this phase, the injury starts to resolve or to some extent, become persistent. (3) Fibrosis phase of healing: This phase is marked by the resolution of inflammation and development of various degrees of fibrosis of the lungs. Incidence and Mortality Rate American Lung Association Lung Disease Data (2008) noted that black men have higher rates of morality due to ARDS compared to women and other races. Lack of oxygen rather than lung failure per se usually results to death. American Lung Association Lung Disease Data added that the chances of survival for ARDS patients can be predicted by determining its causative factor, and the survival rates for patients suffering from ARDS are determined among young patients who have a trauma – related ARDS, patients with milder form of ARDS as well as to patients with fewer chronic problems in health. On the other hand, American Lung Association Lung Disease Data (2008) noted that the function of the lung in most ARDS survivors return to normal in several months. In some patients, lasting lung damage and to areas affected are noted. Classification of ARDS: ARDS is classified as: (1) Primary ARDS This type of ARDS notes lung injury from a direct insult of the lung such as aspiration. (2) Secondary ARDS Secondary ARDS describes injury of the lung as part of systemic process such as injury of the lungs secondary to systemic inflammatory reaction. An example for this is sepsis. Diagnostics Initial test done in patients who are suspected with ARDS are the following (NIH, 2008; Dimov, V. 2008)): (1) Arterial Blood Gas (ABG) Analysis This test is done to establish the level of oxygen in the blood. Consequently, low levels of blood oxygen can be a significant indication of ARDS. Initially, a physician assessing the patient and analysing the ABG of the patient must first to look at the pH value. If the pH is less than 7.35, the patient will be noted to have acidosis and on the other hand, if the pH level is more than 7.45, the patient has alkalosis (Scribd, 2009). Secondly, it is also important to note whether the pH is compensated, within 7.36 – 7.44 or uncompensated, less than 7.35 or more than 7.45 (Woodley and Whelan, 1992; Scribd, 2009). Next, the physician must determine whether the cause of ARDS is respiratory, where the CO2 level is less than 35 or more than 45 (normal CO2 is within 35 – 45 mmHg), or metabolic, the HCO3 level is less than 22 mEq/L or more than 26 mEq/L (normal HCO3 is 22 – 26 mEq/L) (Scribd, 2009). It must also be noted than in interpreting ABG, pH and HCO3 goes the same way and CO2 runs the opposite way. Hence, with increased pH and HCO3, patient is interpreted to have alkalosis and decreased pH and HCO3, acidosis. On the other hand, increased pH and decreased CO2 is noted as acidosis and decreased pH and increased CO2 is alkalosis (Scribd, 2009). To further understand ABG and ARDS, a case of a 40 year – old who was admitted in the Intensive Therapy Unit (ITU) post operatively patient is presented. The patient was noted to have a panicky personality who later died due to ARDS. From the case report, the patient has respiratory alkalosis with hypoxemia. As noted, the patient had a panicky personality and could be hyperventilating leading to acute respiratory alkalosis (Berg and Ongjoco, 2002). Hypoxemia results from the accumulation of fluids in the lung. ABG result can be noted as: pH of more than 45 mmHg, CO2 of less than 35 mmHg, and HCO3 can be normal (Woodley and Whelan, 1992; Berg and Ongjoco, 2002). Woodley and Whelan (1992) noted that increased excretion of renal bicarbonate leading to fall of serum HCO3 is the compensatory response of renal alkalosis. To further understand ARDS, another case of a 19 – year old patient who died due to ARDS after a 15 – day stay at the ITU. In this case, the patient had developed several complications and may have developed pneumonia or pulmonary embolism due to prolonged hospital stay. Hence, based from the diagnosis, the patient may have suffered from acute respiratory acidosis secondary to pneumonia. ABG results for respiratory acidosis are: pH is less than 7. 35 and CO2 is more than 44 mmHg. Woodley and Whelan (1992) added that increased in renal absorption and bicarbonate generation leading to rise in serum HCO3 can be the compensatory response to respiratory acidosis. (2) Chest X – ray This test gives an idea that extra fluids are found in the lungs. (3) Blood Tests These include complete blood count, blood chemistries, and blood culture. Blood tests are done to identify the underlying cause of ARDS. (4) Sputum Culture This test is done to identify the cause of an infection. Other tests done to diagnose patients with ARDS: (1) CT scan This diagnostic study is done to note the presence of fluid in the lungs as well as to look for any impending signs of pneumonia. (2) Cardiopulmonary tests This test is performed to look for signs of heart failure, a condition that causes build up of fluid in the lungs. Treatment: MacIntyre (2005) and NIH (2008) noted that to date, treatment of ARDS offers treating the underlying condition that causes ARDS. MacIntyre added the physiologic markers such as arterial blood gasses and lung mechanics generally guides the conventional support strategies for ARDS. The following blood markers may also help guide therapies: white blood cell count, creatinine and liver function tests. NIH (2008) noted that treatment of patients with ARDS include oxygen, fluids, and medicines. (1) Oxygen The main goals for ARDS treatment are to bring oxygen to the lungs and to the vital organs in the body such as the kidneys and the brain, and to treat conditions that causes ARDS (NIH, 2008). Initially, oxygen is given through nasal prongs or oxygen mask. If the desired level of oxygen doesn’t increase, oxygen is provided by means of intubation, which can be attached to a mechanical ventilator so that the desired amount of oxygen is received and conversely, remove the carbon dioxide from the body. The aforementioned process, otherwise known as the positive pressure ventilation, is maintained until the patient can spontaneously breathe on his own at a normal rhythm (Swierzewshi, 2000; NIH, 2008). (2) Fluids Fluids are given through IV line to improve blood flow and to supply nutrition to the body. NIH (2008) stated that fluids must be given in the right amount because too much fluid in the lung leads to difficulty in acquiring the amount of oxygen needed by the body. On the other hand, less amount of fluid limits flow of blood and oxygen to the organs in the body (NIH, 2008). (3) Medicines Medicines such as diuretics, salbutamol, corticosteroids and surfactant therapy are given by the physicians to prevent and treat infections as well as to relieve discomfort (Brower, 2001; Barclay, 2002; Martin, 2003; Martin, 2005; Brett, 2007; NIH, 2008; Baltic, 2008; Douglas, 2008). Complications ARDS can develop into several complications while patient is treated in the hospital. These include: (1) Infection In the hospital setting, pneumonia can be the most common infection for patients. Patients who are on a ventilator are also at risk for infections; however, the two aforementioned conditions can be treated with antibiotics (NIH, 2008). (2) Pneumothorax Pneumothorax that results from air pressure brought about by mechanical ventilation leads to lung (NIH, 2008; Meng et al., 2008). Nevertheless, this can be treated by removing the air in the lung through tube placement into the chest (NIH, 2008). Aside from pneumothorax, volutrauma is also considered to be the most common complication of mechanical ventilation (Swierzewshi, 2000). (3) Scarring of the Lung Scarring of the lungs can also be caused by ventilator; however, this condition oftentimes heals prior to patient’s discharge (NIH, 2008). (4) Clotting of Blood Clotting of blood can lead to a serious condition known as pulmonary embolism. NIH (2008) noted that this condition may have caused by prolonged patient inactivity. Prognosis Fein et al. (1983) stated that the prognosis for ARDS is poorly defined. ARDS is usually preceded by shock and thrombocytopenia that worsens the prognosis of ARDS significantly (Fein et al., 1983). Isselbacher et al. (1995) noted that the overall rate of mortality of ARDS is 50%. The prognosis of ARDS varies with intrinsic mortality of the underlying pathology. References: American Lung Association Lung Disease Data (2008) Acute Respiratory Distress Syndrome. 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Available at: http://emedicine.medscape.com/article/808260-overview (Accessed 21 January 2009). Dimov, V. (2008) Pneumonia and Metabolic Acidosis in a 35-kilogram Man. Available at: http://clinicalcases.org/2004/02/pneumonia-and-metabolic-acidosis-in-35.html (Accessed 21 January 2009). Douglas, D (2008) Salbutamol Shows Promise against ARDS. Thorax, 63 (2008), 215 -220. Fein, A., Lippmann, M., Holtman, H., Eliraz, A. and Goldberg, S. (1983) ‘The Risk Factors, Incidence, and Prognosis of ARDS following Septicemia’, Chest Journal, 83(1983), 40 – 42. Fujii, T. and Phillips, B. (2003) ‘Quick Review: ARDS’, The Internet Journal of Pulmonary Medicine’, 3 (1), pp. 1531 – 2984. Gnanasekaran, I. and Grosu, H. (2007) ‘Top 10 Clinical Pearls in Acid-base Disorders’, The American Journal of Managed Care, 53(1). Hansen-Flaschen, J. (2001) Understanding ARDS. Available at: http://www.ards.org/learnaboutards/whatisards/brochure/ (Accessed 24 January 2009). Harms, R. (2007) ARDS. 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Available at: http://www.nhlbi.nih.gov/health/dci/Diseases/Ards/Ards_WhatIs.html (Accessed 21 January 2009). Robbins, S., Cotran, R., and Kumar, V. (1995) Pathologic Basis of Disease. 2nd Edition. Philadelphia: W.B. Saunders Company. Scribd (2009). Simple Method of Acid – Base Balance Interpretation. Available at http://www.scribd.com/doc/2161655/ABG-Made-Easy (Accessed 25 January 2009) Swierzewski, S. III (2000) Acute Respiratory Distress Syndrome. Available at: http://www.pulmonologychannel.com/ards/index.shtml (Accessed 22 January 2009). Woodley, M. and Whelan, A. (ed) (1992) Manual of Medical Therapeutics. 27th Edition. Missouri: Little, Brown, and Company. Read More