Transfusion related acute lung injury (TRALI) has been an upcoming cause of transfusion related mortality. It is characterized by the sudden development of non cardiac related pulmonary edema after transfusion of blood products. According to the Food and Drug Administration (FDA), in the past two reporting years, it has been the leading cause of transfusion related deaths. It is of severe importance for physicians, nurses and also laboratory scientists to become familiar with the presentations of TRALI since many cases will remain unnoticed or will be misdiagnosed as fluid overload, or acute lung injury of other etiology. In order to properly diagnose a patient with TRALI, there are several criteria that needs to be followed. There needs …show more content…
Intravenous immunoglobulin (IVIG) has the capacity to cause TRALI if it contains a significant amount of anti-leukocyte antibodies directed against antigens on the recipient’s leukocytes. Reactions triggered by IVIG are much more rare than the ones triggered by plasma containing blood products. As with any transfusion reaction, it is imperative to comprehend the pathophysiology of this condition. There are two main mechanisms as to why TRALI can occur. There is an immune and a non immune mechanism of action. The immune mechanism is antibody mediated. It is believed that ninety percent of the time the antibodies originate in the donor blood product, and ten percent of the time the antibodies originate in the recipient. The antibodies are against HLA I, HLA II or HNA. Leukocyte antibodies can activate neutrophils directly, through anti HLA class I or anti HNA, or neutrophils can be activated indirectly by anti HLA class II . After being activated, either directly or indirectly, neutrophils release a neutrophil activating substance. Once other neutrophils are activated the produce reactive oxygen substances and release enzymes, such as elastase. Elastase causes the endothelium to become more permeable for plasma constituents, ultimately leading to pulmonary edema. The non immune mechanism relies on the patient’s pre existing condition as an underlying factor in the onset of TRALI. There
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The clinical picture of acute pulmonary embolism (PE) is not similar from various aspect of its pathophysiological course presenting from minimal symptoms to variety of severity of disease like severe hypoxia, hypotension, right heart failure and death1. Massive pulmonary embolism is defined as obstruction of blood flow to a lobe or multiple segments of the lung, or for unstable hemodynamics, i.e. failure to maintain blood pressure without supportive measures.” This case highlights about aggressiveness of treatment and role of thrombolytic therapy for a severely hemodynamic unstable patient2.
There are challenges that Dr. Correia goes through on occasion. One problem he has is working with the patient’s provider and figuring out what exactly the provider wants him to do. Sometimes it’s difficult to figure out what specific tests the provider wants to have Dr. Correia do. Another problem Dr. Correia comes across is when all the tests show nothing wrong so he has to figure out the puzzle of what’s going on with the patient. After figuring out what is wrong with the patient, it also might to difficult to tell the patient if the test results came out bad.
Ed's blood count is low due to the increased destruction of RBC's. Erythropoesis cannot keep up with the destruction of RBCs, thus a blood transfusion is probably needed. This is done to allevia anemia, increase blood volume and to improve immunity against the parasites that have infected Ed's body.
A.W., a 52-year-old woman disabled from severe emphysema, was walking at a mall when she suddenly grabbed her right side and gasped, “Oh, something just popped.” A.W. whispered to her walking companion, “I can’t get any air.” Her companion yelled for someone to call 911 and helped her to the nearest bench. By the time the rescue unit arrived, A.W. was stuporous and in severe respiratory distress. She was intubated, an IV of lactated Ringer’s (LR) to KVO (keep vein open) was started, and she was transported to the nearest emergency department (ED).
As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the patient begins to show organ dysfunction. The cardiovascular system also begins to fail, the blood pressure does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., renal failure, pulmonary failure, hepatic failure). As sepsis progresses to septic shock, the blood pressure drops, and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs. Adventitious lung sounds occur throughout the lung fields, not just in the upper fields of the lungs.
Venkataraman, Ramesh, and Michael R. Pinsky. "Toxic Shock Syndrome." Medscape. 16 July 2010. Web. 17 Oct. 2011. <http://emedicine.medscape.com/article/169177- overview>.
This scenario helped me understand the pathophysiologic process of pneumonia and decompensated shock and how they could possibly manifest in children. Since in our first simulation of the semester we learned different methods of assisting a patient in improving his/her breathing status I was better able to intervene and know what to do to improve our patient’s breathing status. However, I have never been exposed to a patient undergoing decompensated shock. Therefore, this time I was able to learn what to do in case a situation as such arises in the future on a real patient. Shock can be due to several reasons such as bleeding or severe dehydration. However, it was apparent in this case that the patient was not externally bleeding, but she was
Mr. Steward’s priority problems include impaired cardiac tissue perfusion, impaired gas exchange, and pain. We are concerned about impaired cardiac tissue perfusion because the pt. is exhibiting signs of myocardial ischemia including chest pain and shortness of breath (Gillespie, 2012). Although we acknowledge that impaired cardiac tissue perfusion can decrease the function of the heart and will have the potential to affect the perfusion and delivery of oxygen to other end organs, our primary focus will be a focused cardiovascular assessment (House-Kokan, 2012). At 1800, Mr. Steward was SOB, had shallow and rapid breathing (RR = 44), and a SaO2 of 72% on RA. Due to the fluid buildup in his lungs, Mr. Steward has impaired gas exchange, and requires supplemental oxygen to maintain his SaO2; this warrants a focused respiratory assessment.
Intravenous (IV) fluids were bolusing; however, when blood pressure was only obtainable manually and revealed that her blood pressure was 74/34, the decision was made to send the patient to the intensive care unit (ICU). There, coagulation studies revealed an elevated PT, PTT, D-dimer, and a decreased fibrinogen count. She received a peripherally inserted central catheter (PICC), a transfusion of two units of packed red blood cells (PRBCs), as well as cryoprecipitate therapy during her treatment in the ICU.
Pulmonary embolism (PE) accounts for up to 30,000 deaths each year. (Beckman, 2014). It has been estimated that nearly one-third of deaths stemming from pulmonary embolism occur within the first hour. (Muckart, 2010). It can prove to be extremely difficult to diagnose pulmonary embolism due to the wide range of symptoms and presentations, or lack there of. (Muckart, 2010; Tarbox & Swaroop, 2013). Some patients with acute pulmonary embolism, possibly as many as 50%, are completely asymptomatic. (Muckart, 2010). Although the clinical presentation can vary dramatically, some of the main symptoms include tachycardia, sub-sternal chest pain, dyspnea, hypoxemia, hypotension and even possibly shock. (Tarbox & Swaroop, 2013). There are several risk factors attributed to PE, including but not limited to, recent immobilization, previous myocardial infarction or cerebral vascular accident, prior surgery or recent trauma. (Tarbox & Swaroop, 2013). Initial symptoms primarily present with severe respiratory distress, but the main adverse effects of PE effect the cardiovascular system due to the fact that the embolus causes an occlusion in the pulmonary vasculature. (Muckart, 2010). The obstruction within the pulmonary artery vastly increases vascular resistance, which results in right ventricular failure; therefore the left ventricular preload is minimized and cardiac output collapses. (Muckart, 2010).
According to the American Lung Association, “Acute respiratory distress syndrome (ARDS) is a rapidly progressive disease occurring in critically ill patients.” ARDS is an extreme manifestation of a lung injury that can be associated with an acute medical problem. This occurs as a result of direct or indirect trauma to the lungs. With nearly 200,000 cases in the United States each year, ARDS is not extremely common (“Acute Respiratory Distress Syndrome”). Most people who acquire this disease are critically ill patients within the hospital. The most common predisposing medical problems of ARDS consist of: shock, trauma, pulmonary infections, sepsis, aspiration, and cardiopulmonary bypass (Ignatavicious, 2013). ARDS is a severe syndrome and even with prompt and aggressive medical treatment, almost fifty percent of those diagnosed do not survive. Those who survive have a longer hospital stay along with recurring hospital admissions throughout their lifetime (“Acute Respiratory Distress Syndrome”). Acute respiratory distress syndrome is a rapidly progressive disease which requires thorough assessment, rapid diagnosis, and emergency treatment measures in order to successfully respond to the disease process.
Early sepsis is defined as “a suspected or proven infection and the systemic response to infection” (Porth & Matfin, 2009). During early sepsis, a hypodynamic state of vasodilation, increased release of pro-inflammatory cytokines, pooling of blood, cellular hypoxia, and vascular damage cause microthrombi. This sequence of events can lead to Systemic Inflammatory Response Syndrome (SIRS) and potential death if undetected and untreated. Detection and
"The common clinical features among the case-patients included a prodromial illness of fever, chills, and myalgia. The prodrome was followed by dyspnea, cough, throbocytopenia, severe hemodynamic instability, neutrophilid with immature forms, atypical lymphocytes, elevated serum levels of lactate dehydrogenase. There was a high mortality rate, approximately eighty percent in the initial group of patients, the chest x-ray examinations revealed a diffuse, interstitial infiltrate that resembled that observed in patients with adult respiratory distress syndrome (ARDS), which is a common pattern in patients