Causes Of Transfusion Related Lung Injury

This can also result in the area of the lungs deprived of blood and oxygen to become necrotic. Numerous diseases and treatments lead to a higher risk of pulmonary embolism. Especially, surgical patients. The anesthetics used in surgeries can affect the lungs by injuring the lung vessels. Also prolonged bed rest can promote venous stasis (Wolters Kluwer, 2017).

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.

There is a considerable controversy regarding the use of OBL in patients with respiratory failure and those on mechanical ventilation because of the potential high morbidity and mortality associated with its use in those patients (20, 21). While the role of OLB has become well established in the diagnosis of interstitial lung disease (18), its utility and safety are more controversial in critically ill patients. Proponents of OLB argue that solid diagnosis of underlying aetiology can be helpful in determination of the best course of treatment (22). Moreover, the risk of biopsy is fairly low if adequate precautions are taken (23). In contrast, opponents of OLB believe that defining the underlying mechanism of injury is largely academic and it will not add new to the treatment of those patients because of the lack of specific therapies for underlying aetiologies of ARDS and respiratory

38. American Journal of Respiratory care and critical care Medicine, Volume 175, issue 7, pages 698 – 704

Hypoxaemia can result when there is inequality in alveolar ventilation and pulmonary perfusion (V/Q mismatch). V/Q mismatch is the most common cause of hypoxia in critically ill patients. It is caused by intrapulmonary shunting of blood resulting from airspace filling or collapse. Findings include dyspnea and tachypnea. Diagnosis is by ABGs and chest x-ray. Treatment usually requires mechanical ventilation.

This is a 50 years old male with no significant past medical history presented initially with shortness of breath and hypoxia and was transferred to the ICU. He was treated for bilateral pneumonia that required prolonged mechanical ventilation via a tracheostomy. He has necrotizing pneumonia and he has been in the hospital for 6 weeks due to the development of multi-organ failure. He was weaned from mechanical ventilation to the point he was tolerating a CPAP/PS mode. Later on, it was noticed that he

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.

During mechanical ventilation, patients are at risk of injuries to their lungs caused by improper settings on ventilators. Mechanical ventilator induced lung injury (VILI) can affect the lung in several ways. Some of the ways the lung become affected is by excessive pressure, excessive volume, and not enough volume. When the lungs are affected by excessive pressure its termed pulmonary barotrauma. On the other hand, if the lungs receive too much volume it’s called volutrauma. However, when the lungs don’t receive enough volume its termed atelectrauma. This paper describes how pulmonary barotrauma, pulmonary volutrauma, and pulmonary atelectrauma affects the lungs during mechanical ventilation and ways to prevent them from happening.

After the onset of hypovolemic shock, the primary goals are to replace blood and fluid volume via IV infusion; maximization of oxygen delivery, and minimization of oxygen demand. Patient is positioned in a manner that supports maximal circulation and airway patency (oxygenation, ventilation, and perfusion). Diligent treatment of fever, fear and pain are necessary to reduce oxygen demand. Humidified supplementary oxygen is given as needed at up to 10 to 15 L/min by non-rebreathing mask or bag-mask ventilation and is monitored continuously through pulse oximetry (McCance, 2010. pp

Mrs. Schafer completed her pulmonary function test prior to the appointment time and she was evaluated by Dr. Theodore J Standiford. Mrs. Schaefer provided an acute report of her injury and symptoms she was experiencing. Dr. Standiford replied that Mrs. Schaefer lung capacity was reduced by a third. (1/3). I inquired if it was the result of the injuries in the MVA. Dr. Standiford replied that they are a contributing factor i.e. flail chest and fluid in her lungs from aggravated congested heart failure. Dr. Standiford noted left crackles breath sounds on his examination and recommended that Mrs. Schaefer return to her cardiologist and that a high resolution CT scan of her lungs be obtained prior to the next appointment to determine if she has

Patient F.F. is a 75-year-old female that arrived to the emergency room and admitted to the floor for left lobe pneumonia from an exacerbation from chronic obstructive pulmonary disease, or COPD. Upon my assessment, the patient was short of breath and required 2 liters of oxygen by nasal cannula to prevent use of accessory muscles and loss of breath. Wheezes were present in the lower lobes of the lungs and breath sounds were diminished. The patient’s oxygen level was 95% on 2 liters of oxygen, but once the oxygen was removed, the oxygen level would drop down to 88%. A productive cough was present with green sputum. The patient reported feeling ‘weak’ and ‘unable to get around like [she] used to.’

Following a painful crisis, acute chest syndrome may start. The sickling in blood vessel deprives a person’s lungs of oxygen damaging lung tissue and the lungs are unable to exchange oxygen properly and at least one segment of the lung is damaged.

ARDS (Acute Lung Distress Syndrome) is a condition where there are buildup of fluid in the tiny air sacs in the lungs that is known as alveoli. This condition will lead to less oxygenation to the body and its main organ such as the lungs,brain and heart, which is hazardous. ARDS occurs when there is important trauma that will affect the lungs by direct or indirectly. When something like this occurs our body response automatically and quickly where it releases many natural molecules into the bloodstream which is called inflammatory reaction. This inflammatory reaction is protective and will help us fight against infection or heal from any injury. However, there will be times where this inflammatory molecules go against which will lead the tiny

Providing anesthesia for lung transplantation (LT) is considered by many to be a major feat in cardiothoracic anesthesia. Some say it involves the most complex manipulation of cardiothoracic physiology, especially when cardiopulmonary bypass (CPB) is not used. There are many indications for end-stage pulmonary disease, from obstructive lung disease to pulmonary vascular disease. Traditionally, ventilation strategies for this population included tidal volumes of 8-12ml/kg to prevent atelectasis and zero PEEP to prevent a shunt of blood flow (Slinger, 2012). This strategy proved to cause harm during the periorperative period. Research now indicates that a reduction in tidal volume with added PEEP not only decreases atelectasis, but it also reduces pulmonary inflammatory response (Coppola, Froio, & Chuimello 2014). These patients already have a decreased respiratory reserve, therefore inducing an inflammatory mediated response with ventilation settings can be detrimental and should be avoided at all costs by the nurse anesthetist. It is imperative for the nurse anesthetist understand the necessity of lung protective ventilation strategies in LT.

According to DiBlasi, even in animal models, the conventional methods cause inflammation of the lungs and sometimes cause injure to the lungs.1 These techniques also cause redundancy in alveolar growth and also affect the efficacy of surfactant produced in the animal lung.1 This is a good signal that these techniques may have serious consequences in the neonate. One of the adverse effects of invasive and mechanical ventilation is ventilator-induced lung injury.1 This complication is defined by the presence of polytrauma (excessive tidal volume) and shear injury to the airways, a condition known as atelectrauma.1 Insertion of the endotracheal tube into the lungs through the airways also causes injury to the lungs and the airways, a condition known as endotrauma.1