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1
1942-, Zapol Warren M., and Falke Konrad J, eds. Acute respiratory failure. New York: Dekker, 1985.
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2
C, Bone Roger, George Ronald B, and Hudson Leonard D. 1938-, eds. Acute respiratory failure. New York: Churchill Livingstone, 1987.
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3
Vincent, Jean Louis, and Peter M. Suter, eds. Cardiopulmonary Interactions in Acute Respiratory Failure. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83010-5.
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4
Jean-Philippe, Derenne, Similowski Thomas 1961-, and Whitelaw William A. 1941-, eds. Acute respiratory failure in chronic obstructive pulmonary disease. New York: M. Dekker, 1996.
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5
Enright, Stephanie. Cardiorespiratory alterations following positional adjustment in critically ill mechanically ventilated patients with acute respiratory failure. Manchester: University of Manchester, 1997.
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6
Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
8
Cardiopulmonary interactions in acute respiratory failure. Berlin: Springer-Verlag, 1987.
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9
Cardiopulmonary Interactions in Acute Respiratory Failure. Springer, 2011.
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10
Wise, Matt, and Simon Barry. Respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0135.
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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnia). Hypoxaemia is defined as an arterial blood partial pressure of oxygen (PaO2) of <8 kPa, and hypercapnia as an arterial blood partial pressure of carbon dioxide (PaCO2) of >6 kPa. Respiratory failure is divided into two different types, conventionally referred to as type 1 and type 2. The distinction between these two is important because it emphasizes not only different their pathophysiological mechanisms and etiologies, but also different treatments. The preferred terminology and definitions are as follows: oxygenation failure (type I respiratory failure), PaO2 of <8 kPa; ventilation failure (type 2 respiratory failure), PaCO2 >6 kPa. Respiratory failure may be acute (onset over hours to days), or chronic (developing over months to years); alternatively, there may be an acute deterioration of a chronic state.
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Millar, Professor Ann B., Dr Richard Leach, Dr Rebecca Preston, Dr Richard Leach, Dr Richard Leach, Dr Wei Shen Lim, Dr Richard Leach, et al. Respiratory diseases and respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.0005.
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Chapter 5 covers respiratory diseases and respiratory failure, including clinical presentations of respiratory disease, assessment of diffuse lung disease, hypoxaemia, respiratory failure, and oxygen therapy, pneumonia, mycobacterial infection, asthma, chronic obstructive pulmonary disease (COPD), lung cancer, mediastinal lesions, pneumothorax, pleural disease, asbestos-related lung disease, diffuse parenchymal (interstitial) lung disease, sarcoidosis, pulmonary hypertension, acute respiratory distress syndrome, bronchiectasis and cystic fibrosis, bronchiolitis, eosinophilic lung disease, airways obstruction, aspiration syndromes, and near-drowning, pulmonary vasculitis, the immunocompromised host, sleep apnoea, and rare pulmonary diseases.
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Wise, Matt, and Paul Frost. ICU treatment of respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0149.
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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnoea). Respiratory failure can develop over years when it is due to conditions such as kyphoscoliosis or motor neuron disease, or minutes in the case of an acute asthma attack or pneumothorax. In this context, respiratory failure is often called acute (e.g. asthma), chronic (e.g. kyphoscoliosis), or acute on chronic (kyphoscoliosis complicated by pneumonia). Chronic respiratory failure is characterized by compensatory mechanisms which aim to adjust the pH of the blood back to the normal physiological range and involve the retention of bicarbonate by the kidney. This topic covers the etiology of respiratory failure as well as signs, symptoms, diagnosis, investigations, prognosis, and treatment.
13
Visouli, Aikaterini N., and Antonis A. Pitsis. Acute heart failure: heart failure surgery and transplantation. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0054.
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Cardiac surgery should be considered in all cases of acute heart failure that is attributed to surgically correctable causes. Surgical revascularization, repair of mechanical complications of myocardial infarction, valve repair or replacement, mechanical circulatory support, and heart transplantation represent the main surgical interventions that may be offered in the setting of acute (de novo or decompensated chronic) heart failure. Percutaneous aortic valve replacement should also be considered for patients who are deemed inoperable.
14
Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.
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Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.
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Javed, Jeffrey K., and Jason E. Moore. Respiratory Failure and Hypoxemia (DRAFT). Edited by Raghavan Murugan and Joseph M. Darby. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190612474.003.0006.
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Respiratory failure and hypoxemia are among the most common problems encountered by the rapid response team (RRT) and can lead to rapid patient deterioration and arrest. A brief, systematic approach focusing on treatment priorities such as airway patency, correcting hypoxemia, and supporting work of breathing, allows RRT responders to quickly provide the appropriate level of supportive care and narrow the complex differential diagnosis of acute respiratory failure. This chapter reviews a logical and efficient clinical diagnostic evaluation, therapeutic modalities including rescue treatments and mechanical ventilation, and transport considerations for this patient group. The pragmatic, problem-based clinical approach discussed in this chapter will help RRTs provide effective care for this group of patients.
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Lee, Jan Hau, and Ira M. Cheifetz. Respiratory Failure and Mechanical Ventilation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0006.
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This chapter on respiratory failure and mechanical ventilation provides essential information about how to support children with severe respiratory disorders. The authors discuss multiple modes of respiratory support, including high-flow nasal cannula oxygen, noninvasive ventilation with continuous positive airway pressure and bilevel positive airway pressure, as well as conventional, high-frequency, and alternative modes of invasive ventilation. The section on invasive mechanical ventilation includes key information regarding gas exchange goals, modes of ventilation, patient–ventilator interactions, ventilator parameters (including tidal volume, end-expiratory pressure, and peak plateau pressure), extubation readiness testing, and troubleshooting. The authors also provide the new consensus definition of pediatric acute respiratory distress syndrome. Also included are multiple figures and indispensable information on adjunctive therapies (inhaled nitric oxide, surfactant, prone positioning, and corticosteroids) and respiratory monitoring (including capnography and airway graphics analysis).
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Esquinas, Antonio M. Respiratory Ventilatory Strategies in Acute and Chronic Respiratory Failure in Idiopathic Pulmonary Diseases: A Practical Approach. Nova Science Publishers, Incorporated, 2020.
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18
Esquinas, Antonio M. Respiratory Ventilatory Strategies in Acute and Chronic Respiratory Failure in Idiopathic Pulmonary Diseases: A Practical Approach. Nova Science Publishers, Incorporated, 2020.
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19
Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
20
Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0052.
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Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
21
Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0052_update_001.
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Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
22
Kreit, John W. Respiratory Failure and the Indications for Mechanical Ventilation. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0007.
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Respiratory failure occurs when a disease process significantly interferes with the respiratory system’s vital functions and causes arterial hypoxemia, hypercapnia, or both. Typically, respiratory failure is divided into three categories based on the underlying pathophysiology: ventilation failure, oxygenation failure, and oxygenation-ventilation failure. With severe disturbances in gas exchange, mechanical ventilation is often needed to assist the respiratory system and restore the PaCO2, PaO2, or both, to normal. Respiratory Failure and the Indications for Mechanical Ventilation defines and describes the three types of respiratory failure and reviews the four indications for intubation and mechanical ventilation—acute or acute-on-chronic hypercapnia, refractory hypoxemia, inability to protect the lower airway, and upper airway obstruction.
23
Patel, Sameer, and Julia Wendon. Pathophysiology and causes of acute hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0194.
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Acute liver failure (ALF) is a rare, life-threatening clinical syndrome, resulting in loss of hepatic metabolic and immunological function, in a person with no prior history of liver disease. Mortality can still exceed 50%. ALF is characterized by hepatic encephalopathy (HE) and coagulopathy, occurring within days or weeks. Establishing aetiology is essential for treatment, prognostication, and liver transplantation consideration. Viral hepatitis and drug-induced liver failure are the two commonest causes worldwide. Aetiology and time of onset of encephalopathy determines prognosis. Disease progression can rapidly result in multi-organ failure. Ammonia has been postulated in the development of HE, cerebral oedema and intracranial hypertension. Coagulopathy can be highly variable, with some patients prothrombotic, or exhibiting balanced coagulation disorders. Systemic inflammatory response syndrome (SIRS) and associated infection are frequently observed. Significant haemodynamic changes are common while renal failure is an independent risk factor for mortality. Respiratory failure is less common. Deranged homeostasis results in severe hypoglycaemia, and metabolic disturbance.
24
Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.
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Dangayach, Neha S., Charles L. Francoeur, Stephan A. Mayer, and Tarek Sharshar. Neuroprotection in Sepsis and Acute Respiratory Distress Syndrome. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0013.
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Diffuse cerebral dysfunction in sepsis and acute respiratory distress syndrome (ARDS) patients is highly prevalent. Delirium and alterations in level of consciousness in septic patients are symptoms that constitute sepsis-associated encephalopathy (SAE), which is distinct from hypoxic encephalopathy. SAE is associated with substantial mortality and long-term cognitive impairment. The underlying pathophysiology of SAE is complex and poorly understood. The pathophysiology of SAE includes neuroinflammation, microglial activation, microcirculatory failure, autoregulation impairment, blood–brain barrier disruption, apoptosis, and development of microinfarcts and microhemorrhages. Apart from standard resuscitation techniques targeted at maintaining adequate cerebral perfusion and oxygenation, specific neuroprotective interventions are not currently available. Given the vast unmet need for improving functional outcome among survivors of SAE, it is a priority for the critical care community to better define, understand, and prevent this common and devastating form of neurological injury.
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(Editor), Zab Mosenifar, and Guy W. Soo Hoo (Editor), eds. Practical Pulmonary and Critical Care Medicine: Respiratory Failure (Lung Biology in Health and Disease). Informa Healthcare, 2006.
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27
Bellani, Giacomo, and Antonio Pesenti. Treating respiratory failure with extracorporeal support in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0105.
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During extracorporeal support or extracorporeal membrane oxygenation (ECMO) blood is diverted from the patient to an artificial lung for gas exchange, then returned into the patient’s circulation once arterialized. While a low-blood-flow bypass can remove comparatively high amounts of CO2, oxygenation is limited by venous haemoglobin saturation and requires high flows. Several technical improvements led to a profound change in the safety and applicability of ECMO in recent years, even permitting the transfer of patients undergoing ECMO. ECMO has been proposed as salvage therapy for the most severe acute respiratory distress syndrome patients—warranting viable levels of oxygenation. In 2009, the ‘CESAR’ trial provided formal evidence in favour of ECMO application in adults with ARDS. An important indication for the early use of ECMO in ARDS came from the outbreaks of H1N1 influenza, when several countries set up networks aimed at coordinating the application of ECMO. Recent reports suggest the use of ECMO in less severe patients with the purpose of removing CO2, decreasing the need for ventilation and ventilator-induced lung injury,
28
Sahetya, Sarina. Acute Uncomplicated Bronchitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0029.
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Acute bronchitis is a respiratory illness characterized predominantly by cough with or without sputum production that lasts for up to 3 weeks in the presence of normal chest radiography. Additional presenting symptoms include rhinorrhea, congestion, sneeze, sore throat, wheezing, low-grade fever, myalgia, and fatigue. Causative organisms include viral and bacterial pathogens. The disease course is characterized by self-limited inflammation of the airways. Chest radiographs should be utilized to distinguish acute bronchitis from pneumonia or interstitial disease. Therapeutic recommendations are typically supportive; however, studies reveal that between 60% and 80% of patients receive unwarranted antibiotic therapy. Only those patients at high risk for serious complications (including patients over 65 with a history of hospitalization, diabetes mellitus, congestive heart failure, or current use of oral glucocorticoids) usually require routine antibiotic therapy directed toward both typical and atypical bacterial pathogens.
29
Macagno, Francesco, and Massimo Antonelli. Therapeutic strategy in acute or chronic airflow limitation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0112.
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The fragility of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) accounts for their frequent hospitalization and their high intensive care unit risk. Therapy for AECOPD is varied and the need for hospitalization must be always carefully evaluated, considering the risk factors related to the presence of multi-resistant pathogens or the need of invasive procedures. The prolonged use of oxygen therapy requires an accurate monitoring of blood gases and continuous oximetry. Inhalation therapy can be performed using nebulizers, predosed aerosols or powders for inhalation. Corticosteroids for oral and systemic use now play an established role in AECOPD, because bacterial infections account for 50% of exacerbations. Non-invasive ventilation (NIV) must be considered the first option in AECOPD patients and acute respiratory failure if there are no contraindications. The careful monitoring of the patient and the response to NIV are indispensable elements for therapeutic success.
30
Innes, J. Alastair. Respiratory complications and management of severe CF lung disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0006.
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This chapter covers the most common medical complications of severe CF lung disease, excluding the treatment of infection exacerbation. The section on haemoptysis covers severity assessment, medical and interventional radiological approaches to managing this problem. The particular risks of pneumothorax in CF are then discussed, including the factors guiding referral to surgery. The management of acute and chronic respiratory failure in CF is covered. This includes the indications for home oxygen and for non-invasive ventilation, and guidance on how these should be used in CF. Finally, there is a section on terminal care in cystic fibrosis, covering the management of the transition to palliative management at the end of life, and appropriate strategies to support patient and family in advanced disease.
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Sever, Mehmet Şükrü, and Raymond Vanholder. Acute kidney injury in polytrauma and rhabdomyolysis. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0252_update_001.
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The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.
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Gardiner, Matthew D., and Neil R. Borley. Core surgical skills and knowledge. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199204755.003.0015.
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This chapter begins by discussing the basic principles of fluid and electrolyte homeostasis, fluid therapy, healthcare-associated infection, microorganisms and antimicrobials, preoperative assessment, and acute pain, before focusing on the key areas of knowledge, namely deep venous thrombosis, pulmonary embolism, respiratory tract infection, asthma, chronic obstructive pulmonary disease, acute respiratory failure, ischaemic heart disease, heart failure, cardiac arrhythmias, hypertension, diabetes mellitus, acute renal failure, stroke, acute confusional state, and haematological conditions. The chapter concludes with relevant case-based discussions.
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Spoletini, Giulia, and Nicholas S. Hill. Non-invasive positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0090.
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Non-invasive ventilation (NIV) has been increasingly used over the past decades to avoid endotracheal intubation (ETI) in critical care settings. In selected patients with acute respiratory failure, NIV improves the overall clinical status more rapidly than standard oxygen therapy, avoids ETI and its complications, reduces length of hospital stay, and improves survival. NIV is primarily indicated in respiratory failure due to acute exacerbations of chronic obstructive pulmonary disease, cardiogenic pulmonary oedema and associated with immunocompromised states. Weaker evidence supports its use in other forms of acute hypercapnic and hypoxaemic respiratory failure. Candidates for NIV should be carefully selected taking into consideration the risk factors for NIV failure. Patients on NIV who are unstable or have risk factors for NIV failure should be monitored in an intensive or intermediate care units by experienced personnel to avoid delay when intubation is needed. Stable NIV patients can be monitored on regular wards.
34
Carton, James. Lung pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0005.
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This chapter discusses lung pathology and covers respiratory malformations, respiratory failure, acute respiratory distress syndrome (ARDS), bronchiectasis, cystic fibrosis, pulmonary thromboembolism, pulmonary hypertension, asthma, chronic obstructive pulmonary disease (COPD), bacterial pneumonia, idiopathic pulmonary fibrosis (IPF), hypersensitivity pneumonitis, lung carcinoma, pleural effusion, pneumothorax, and malignant mesothelioma.
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Rickman, Otis B. Critical Care Medicine. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0148.
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Critical care medicine is a multidisciplinary branch of medicine encompassing the provision of organ support to patients who are severely ill. All areas of medicine may have relevance for critically ill patients; however, this review focuses only on aspects of cardiopulmonary monitoring, life support, technologic interventions, and disease states typically managed in the intensive care unit (ICU). Airway management, venous access, respiratory failure, mechanical ventilation, acute respiratory distress syndrome, shock, and sepsis are reviewed.
36
Kreit, John W., and John A. Kellum. Mechanical Ventilation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.001.0001.
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Mechanical Ventilation—Physiology and Practice provides a comprehensive review of the physiological principles underlying mechanical ventilation, as well as practical approaches to the management of patients with respiratory failure. The book explains instrumentation and terminology, ventilator modes and breath types, ventilator alarms, how to write ventilator orders, and how to diagnose and correct patient–ventilator asynchrony. It also discusses the physiological assessment of the mechanically ventilated patient and the diagnosis and management of dynamic hyperinflation, and describes how to manage patients with the acute respiratory distress syndrome (ARDS), severe obstructive lung disease, and right ventricular failure; how to “wean” patients from the ventilator; and how and when to use noninvasive ventilation.
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Garner, Justin, and David Treacher. Intensive care unit and ventilation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0009.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by rapidly developing hypoxaemic respiratory failure and bilateral pulmonary infiltrates on chest X-ray. ALI/ARDS are a relatively frequent diagnosis in protracted-stay patients in the intensive care unit. The pathology is a non-specific response to a wide variety of insults. Impaired gas exchange, ventilation-perfusion mismatch, and reduced compliance ensue. Mechanical ventilation is the mainstay of management, along with treatment of the underlying cause. Mortality remains very high at around 40%. The condition is challenging to treat. Injury to the lungs, indistinguishable from that of ARDS, has been attributed to the use of excessive tidal volumes, pressures, and repeated opening and collapsing of alveoli. Lung-protective strategies aim to minimize the effects of ventilator-induced lung injury. Use of low tidal volume ventilation has been shown to improve mortality. Emerging ventilatory therapies include high-frequency oscillatory ventilation and extracorporeal membrane oxygenation.
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Masip, Josep, Kenneth Planas, and Arantxa Mas. Non-invasive ventilation. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0025.
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During the last 25 years, the use of non-invasive ventilation has grown substantially. Non-invasive ventilation refers to the delivery of positive pressure to the lungs without endotracheal intubation and plays a significant role in the treatment of patients with acute respiratory failure and in the domiciliary management of some chronic respiratory and sleep disorders. In the intensive and acute care setting, the primary aim of non-invasive ventilation is to avoid intubation, and it is mainly used in patients with chronic obstructive pulmonary disease exacerbations, acute cardiogenic pulmonary oedema, or in the context of weaning, situations in which a reduction in mortality has been demonstrated. The principal techniques are continuous positive airway pressure and bilevel pressure support ventilation. Whereas non-invasive pressure support ventilation requires a ventilator, continuous positive airway pressure is a simpler technique that can be easily used in non-equipped areas such as the pre-hospital setting. The success of non-invasive ventilation is related to the adequate timing and selection of patients, as well as the appropriate use of interfaces, the synchrony of patient-ventilator, and the fine-tuning of the ventilator.
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Masip, Josep, Kenneth Planas, and Arantxa Mas. Non-invasive ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0025_update_001.
Full textAbstract:
During the last 25 years, the use of non-invasive ventilation has grown substantially. Non-invasive ventilation refers to the delivery of positive pressure to the lungs without endotracheal intubation and plays a significant role in the treatment of patients with acute respiratory failure and in the domiciliary management of some chronic respiratory and sleep disorders. In the intensive and acute care setting, the primary aim of non-invasive ventilation is to avoid intubation, and it is mainly used in patients with chronic obstructive pulmonary disease exacerbations, acute cardiogenic pulmonary oedema, or in the context of weaning, situations in which a reduction in mortality has been demonstrated. The principal techniques are continuous positive airway pressure and bilevel pressure support ventilation. Whereas non-invasive pressure support ventilation requires a ventilator, continuous positive airway pressure is a simpler technique that can be easily used in non-equipped areas such as the pre-hospital setting. The success of non-invasive ventilation is related to the adequate timing and selection of patients, as well as the appropriate use of interfaces, the synchrony of patient-ventilator, and the fine-tuning of the ventilator.
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Masip, Josep, Kenneth Planas, and Arantxa Mas. Non-invasive ventilation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0025_update_002.
Full textAbstract:
During the last 25 years, the use of non-invasive ventilation has grown substantially. Non-invasive ventilation refers to the delivery of positive pressure to the lungs without endotracheal intubation and plays a significant role in the treatment of patients with acute respiratory failure and in the domiciliary management of some chronic respiratory and sleep disorders. In the intensive and acute care setting, the primary aim of non-invasive ventilation is to avoid intubation, and it is mainly used in patients with chronic obstructive pulmonary disease exacerbations, acute cardiogenic pulmonary oedema, or in the context of weaning, situations in which a reduction in mortality has been demonstrated. The principal techniques are continuous positive airway pressure and bilevel pressure support ventilation. Whereas non-invasive pressure support ventilation requires a ventilator, continuous positive airway pressure is a simpler technique that can be easily used in non-equipped areas such as the pre-hospital setting. The success of non-invasive ventilation is related to the adequate timing and selection of patients, as well as the appropriate use of interfaces, the synchrony of patient-ventilator, and the fine-tuning of the ventilator.
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Masip, Josep, Kenneth Planas, and Arantxa Mas. Non-invasive ventilation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0025_update_003.
Full textAbstract:
During the last 25 years, the use of non-invasive ventilation has grown substantially. Non-invasive ventilation refers to the delivery of positive pressure to the lungs without endotracheal intubation and plays a significant role in the treatment of patients with acute respiratory failure and in the domiciliary management of some chronic respiratory and sleep disorders. In the intensive and acute care setting, the primary aim of non-invasive ventilation is to avoid intubation, and it is mainly used in patients with chronic obstructive pulmonary disease exacerbations, acute cardiogenic pulmonary oedema, immunocompromised or in the context of weaning, situations in which a reduction in mortality has been demonstrated. The principal techniques are continuous positive airway pressure, bilevel pressure support ventilation and more recently, high flow nasal cannula. Whereas non-invasive pressure support ventilation requires a ventilator, the other two techniques are simpler and can be easily used in non-equipped areas by less experienced teams, including the pre-hospital setting. The success of non-invasive ventilation is related to an adequate timing, proper selection of patients and interfaces, close monitoring as well as the achievement of a good adaptation to patients’ demand.
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Fischer, Kevin M., and Shannon S. Carson. Chronic Multiple Organ Dysfunction. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0013.
Full textAbstract:
This chapter reviews the clinical syndrome of chronic multiple organ dysfunction (MOD) following acute critical illness. Chronic MOD, also referred to as chronic critical illness, occurs in patients who have survived the acute phase of their illness or injury but remain dependent on life support for weeks or months. This condition presents unique physiologic and metabolic abnormalities distinct from those encountered in the acute illness. These include neuroendocrine and immune dysregulation, ICU-acquired weakness, persistent respiratory failure, and brain dysfunction. The symptom burden for these patients is high, and long-term survival is limited for elderly patients and those for whom MOD persists for weeks. Comprehensive and systematic programmes will need to be designed and implemented involving bundled best-practice interventions in order to reduce the incidence and treat the consequences of chronic MOD.
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Leaver, Susannah, and Timothy Evans. Hypoxaemia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0085.
Full textAbstract:
Hypoxaemia is a reduction in the partial pressure of oxygen in the blood below 8 kPa/60 mmHg. Hypoxaemia results from one, or several, or a combination of causes. Calculating the alveolar–arterial gradient can help to delineate the cause. Acute respiratory failure manifests in a number of ways, the most sensitive indicator being an increased respiratory rate. Diagnosis is dependent on a comprehensive history, examination in combination with appropriate blood tests, and imaging. Hypoxaemia is the final common pathway of a number of conditions and the exact cause may not be immediately apparent. Despite this, the same management principles apply. A trial of non-invasive ventilation can be used to support patients during respiratory failure who do not require immediate endotracheal intubation. However, it is recommended that this is instituted for a preset trial period (e.g. 1–2 hours) in an HDU/ICU setting where facilities for definitive airway management are available. Invasive ventilation aims to facilitate treatment of the underlying condition whilst minimizing side effects through lung protective ventilatory strategies.
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Dondorp, Arjen M. Other tropical diseases in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0294.
Full textAbstract:
A wide range of tropical infectious diseases can cause critical illness. Knowledge of the local epidemiology where the disease is acquired is essential. In addition, local resistance patterns of common bacterial pathogens can be very different in tropical countries, so that antibiotic regimens might need adaptation. The ‘surviving sepsis’ guidelines are not always appropriate for the treatment of tropical sepsis. Both diseases require a more restricted fluid management. Leptospirosis is another important tropical disease that can cause sepsis with liver and renal failure or ARDS with pulmonary haemorrhages. Neglected tropical diseases causing neurological syndromes include trypanosomiasis (Sub-Saharan Africa) and rabies. Several viruses in the tropics can cause encephalitis. Recent epidemics of respiratory viruses causing life-threatening pneumonia have had their origins in tropical countries, including severe acute respiratory syndrome, influenza A subtype H5N1 (‘avian influenza’), and recently Middle East respiratory syndrome coronavirus.
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Ramsay, Michelle, and Mike Polkey. Non-invasive ventilation and chronic obstructive pulmonary disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0012.
Full textAbstract:
Non-invasive ventilation is one of the major advances in respiratory medicine over the last century. It can be lifesaving for patients in acute hypercapnic respiratory failure, improving gas exchange and pulmonary mechanics and reducing the need for endotracheal intubation. Adherence to therapy is key to its success, and many patients find this a significant challenge. This case report will examine the pitfalls of initiating non-invasive ventilation, provide a brief overview of the current British Thoracic Society non-invasive ventilation guidelines, and describe common causes of a chronic obstructive pulmonary disease patient ‘failing’ non-invasive ventilation and an approach to the long-term management of the frequently exacerbating chronic obstructive pulmonary disease patient.
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Hulse, Elspeth J., and Michael Eddleston. Management of pesticide and agricultural chemical poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0330.
Full textAbstract:
Poisoning with agricultural chemicals is common in rural Asia-Pacific with up to 300,000 annual deaths from pesticide self-poisoning. The pharmacokinetics and pharmacodynamics of pesticides can vary markedly depending on the chemicals ingested, the pesticide’s lipid solubility, enzyme reactivation, co-ingested toxicants, and extent of decontamination and organ dysfunction. Diagnosis and management is based on clinical signs and standard investigations. Staff should wear standard universal precaution attire for examining and treating patients; nosocomial poisoning is rare. Management of poisonings should include careful airway intervention and administration of oxygen, except in suspected paraquat poisoning. Organophosphorus insecticide poisoning causes a cholinergic crisis with excess airway secretions and acute respiratory failure. Patients should be treated with intravenous atropine and observed for the neuromuscular disorder ‘intermediate syndrome’, which can cause further paralysis and respiratory failure after 24 hours. Few antidotes exist for other agricultural chemical poisonings with the mainstay of treatment being supportive standard ICU care.
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Nava, Stefano, and Luca Fasano. Ventilator Liberation Strategies. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0039.
Full textAbstract:
The weaning process should ideally begin as soon as the patient is intubated and continue through the treatment of the cause inducing acute respiratory failure. Weaning includes the assessment of readiness to extubate, extubation, and post-extubation monitoring; it also includes consideration of non-invasive ventilation which has been shown to reduce the duration of invasive mechanical ventilation in selected patients. Weaning accounts for approximately 40% of the total time spent on mechanical ventilation and should be achieved rapidly, since prolonged mechanical ventilation is associated with increased risk of complications and mortality and with increased costs. During mechanical ventilation, medical management should seek to correct the imbalance between respiratory load and ventilatory capacity (reducing the respiratory and cardiac workload, improving gas exchange and the ventilatory pump power). Ventilator settings delivering partial ventilatory pump support may help prevent ventilator-induced respiratory muscles dysfunction. Daily interruption of sedation has been associated with earlier extubation. Critically ill patients should be repeatedly and carefully screened for readiness to wean and readiness to extubate, and objective screening variables should be fully integrated in clinical decision making.
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Aksamit, Timothy R. Diffuse Lung Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0617.
Full textAbstract:
Diffuse lung disease includes a wide range of parenchymal lung diseases that have infectious, inflammatory, malignant, drug, occupational or environmental, and other causes. Although many identifiable causes are recognized, the cause of most cases of diffuse lung disease in many published series is idiopathic. The clinical course may be acute or prolonged and may progress rapidly to life-threatening respiratory failure with death, or it may be indolent over many years. In most instances, a differential diagnosis can readily be formulated by obtaining the medical history, with emphasis on the nature of the symptoms, duration, and pertinent environmental, occupational, drug, and travel exposures.
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Farmer, Brenna M., and Neal Flomenbaum. Management of salicylate poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0317.
Full textAbstract:
Salicylates are weak acids that work as neurotoxins. The goal of management is to keep salicylates out of the brain and enhance elimination. Acute salicylate toxicity manifests as tinnitus, nausea, vomiting, and hyperventilation in a patient who takes a single large ingestion. Chronic salicylate toxicity is associated with long-term use, has a more insidious onset, and symptoms tend to be less severe, resulting in delayed diagnosis. It is more commonly seen in elderly patients. Therapeutic interventions for toxicity include gastrointestinal decontamination, serum and urine alkalinization, and haemodialysis. Mechanical ventilation may lead to clinical deterioration and death in a salicylate-poisoned patient due to worsening acidosis from respiratory failure. This results in severe acidosis, cerebral oedema, pulmonary oedema, and cardiac arrest.
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Latronico, Nicola, Simone Piva, and Victoria McCredie. Long-Term Implications of ICU-Acquired Muscle Weakness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0024.
Full textAbstract:
Intensive care unit-acquired weakness (ICUAW) is a significant and common complication with major implications for survivors of critical illness. ICUAW is a clinical diagnosis made in the presence of generalized muscle weakness that occurs in the setting of critical illness when other causes of muscle weakness have been excluded. Critical illness polyneuropathy and myopathy are the most common causes of ICUAW. Short-term implications of ICUAW include alveolar hypoventilation and an increased risk of pulmonary aspiration, atelectasis, and pneumonia—factors which may contribute to acute respiratory failure and ICU re-admission. In the long term, ICUAW has been associated with physical disturbances, including unsteady gait, sensory loss, foot drop, and, in more severe cases, persistent quadriparesis and ventilator dependency. ICUAW appears to heavily influence the failure of ICU patients to return to baseline health status post-discharge. There is a paucity of evidenced-based therapeutic strategies to reduce the incidence of ICUAW; however, early rehabilitative therapy might represent an effective measure in improving functional status.