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Books on the topic 'ALF(Acute Liver Failure)'

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Published: 21 February 2023

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1

Piracha, Kashif. Acute Liver Failure. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-26911-0.

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2

International, Congress of Liver Diseases (10th 1995 Basel Switzerland). Acute and chronic liver diseases: Molecular biology and clinics : proceedings of the 87th Falk Symposium (X International Congress of Liver Diseases, Part II of the Basel Liver Week 1995), held in Basel, Switzerland, October 19-21, 1995. Dordrecht: Kluwer Academic Publishers, 1996.

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3

Demetriou, A. A., and Frederick D. Watanabe. Support of the acutely failing liver. 2nd ed. Georgetown, Tx: Landes Bioscience, 2000.

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4

BSG-SK&F International Workshop. (11th 1990 Ferndown, England). Acute liver failure: Improved understanding and better therapy ; proceedings of the eleventh BSG/SK & F International Workshop 1990, organized by the Education and Science Committee of the British Society of Gastroenterology, Dormy Hotel, Ferndown, Dorset, UK, 24-25 September 1990. Welwyn Garden City, Hertfordshire: SmithKline Beecham, 1991.

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5

BSG/SK, &. F. International Workshop (11th 1990 Ferndown England). Acute liver failure: Improvedunderstanding and better therapy : proceedings of the eleventh BSG/SK&F International Workshop 1990 : organised by the Education and Science Committee of the British Society of Gastroenterology, Dormy Hotel, Ferndown, Dorset, UK, 24-25 September, 1990. Welwyn Garden City: Smith Kline Beecham, 1991.

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6

Keshav, Satish, and Palak Trivedi. Acute liver failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0209.

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Acute liver failure (ALF) is the term given to a potentially reversible condition characterized by rapid deterioration in hepatocyte function, coagulopathy, and encephalopathy in the absence of preexisting liver disease.
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7

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Acute liver failure. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0063.

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Definition 476Aetiology 476Therapy 480Complications 480Transplantation 484Liver support system 484Prognosis 485Acute liver failure (ALF) in children is defined as ‘a rare multisystem disorder in which severe impairment of liver function, with or without encephalopathy, occurs in association with hepatocellular necrosis in a patient with no recognized underlying chronic liver disease’. Liver function is considered severely impaired if prothrombin time (PT) is >15 s or international normalized ratio (INR) is >1.5 and not corrected by vitamin K, in the presence of hepatic encephalopathy (HE) or a PT >20 s or INR >2.0 in the absence of HE....
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8

Wang, Cynthia, and Michelle Y. Braunfeld. Acute Liver Failure. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0035.

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Acute liver failure produces widespread physiologic derangements including encephalopathy, coagulopathy, peripheral vasodilation, a systemic inflammatory response, and multiorgan failure. Morbidity is significant, and mortality is 50%. The classification of liver failure and the various etiologies, including viral hepatitis, drug-induced, toxins, and autoimmunity are reviewed here. The multisystem effects of acute liver failure influence all aspects of perioperative care and adequate supportive care during this time is crucial to providing the best possible outcome for the patient. Specific treatment objectives and recommendations are discussed, and the anesthetic management with regard to drug choices, hemodynamic goals, and intraoperative monitoring is reviewed.
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9

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.
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10

Joshi, Deepak, and Georg Auzinger. Management of acute hepatic failure in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0196.

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Acute liver failure occurs in patients with acute hepatic necrosis resulting in hepatic encephalopathy, jaundice and coagulopathy. Acute liver failure is a multisystem disorder. The management is initially supportive. Intravenous N-acetylcysteine is recommended for all patients. Brain dysfunction is common. Elective intubation is recommended for all patients who develop Grade III hepatic encephalopathy. Liver transplantation is an appropriate and viable treatment for acute liver failure. Early and safe transfer to a transplant centre for transplant assessment is advised.
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11

Patel, Sameer, and Julia Wendon. Diagnosis and assessment of acute hepatic failure in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0195.

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Establishing the aetiology of acute hepatic failure is essential for correct and timely management. An exhaustive history and examination is crucial in targeting investigations and initiating management. Clinical assessment allows risk stratification, identifying those patients who can be managed locally from those best served in a specialist centre with liver transplantation capability. History should focus on the presenting problem, time of onset and speed of deterioration, and establish features consistent with hyperacute, acute or subacute ALF to guide prognostication. Examination should initially focus on rapid assessment and resuscitation before searching for signs leading to more specific differential diagnoses. Investigations should encompass the variety of potential causes, ranging from basic to more specialist studies. Prognostication is critical for stratification of those patients who may benefit from a potentially life-saving transplantation. Several risk stratification and predictive tools exist to differentiate those patients likely to recover, those unlikely to survive despite maximal intervention, and those who would potentially benefit from transplantation.
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12

O’Brien, Alastair. Pathophysiology, diagnosis, and assessment of acute or chronic hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0199.

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Cirrhosis is an increasing problem and prognosis following intensive care unit admission is poor. Acute on chronic liver failure (ACLF) is a separate entity to cirrhosis with organ failure at the core of this syndrome. Infection and the associated systemic inflammatory responses are the most important precipitants of ACLF. Clinical assessment should follow the standard airway breathing circulation disability exposure approach to the critically-ill patient.
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13

O’Brien, Alastair. Management of acute or chronic hepatic failure in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0200.

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Acute on chronic liver failure is characterized by an acute deterioration of liver function in a patient with previously compensated cirrhosis secondary to a precipitating event. It is most commonly associated with a very poor prognosis and early identification of the precipitating cause is essential to successfully attempt to reverse decompensation. The most common precipitant is infection and a high index of suspicion is required. Other management is largely supportive with close attention to renal dysfunction being particularly important. All patients admitted to the intensive care unit with complications of cirrhosis warrant consultation with a transplant centre to determine whether they fulfil the criteria for transplantation and for expert advice.
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14

undifferentiated, Roger Williams, Jean-Pierre Benhamou, William M. Lee, and Jacques Bernuau. Acute Liver Failure. Cambridge University Press, 2010.

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15

Shanmugam, Naresh P., and Sanjay Bansal. Acute liver failure. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0069.

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The chapter on acute liver failure includes the definition, aetiology, and management of this condition. It discusses the frequently associated complications (neurological, haemodynamic, coagulopathy, infectious, and metabolic) and its prognosis, as well as the role of liver transplantation and liver support systems in its management.
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16

M, Lee William, and Williams Roger 1931-, eds. Acute liver failure. Cambridge: Cambridge University Press, 1997.

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17

Benhamou, Jean-Pierre, and Jacques Bernuau. Acute Liver Failure. Edited by William M. Lee and Roger Williams. Cambridge University Press, 1996. http://dx.doi.org/10.1017/cbo9780511575044.

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18

undifferentiated, Roger Williams, Jean-Pierre Benhamou, William M. Lee, and Jacques Bernuau. Acute Liver Failure. Cambridge University Press, 2011.

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19

undifferentiated, Roger Williams, Jean-Pierre Benhamou, William M. Lee, and Jacques Bernuau. Acute Liver Failure. Cambridge University Press, 2011.

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20

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
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21

Liver Failure: Acute and Acute on Chronic. Springer, 2020.

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22

Pyrsopoulos, Nikolaos. Liver Failure: Acute and Acute on Chronic. Springer International Publishing AG, 2021.

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23

Pyrsopoulos, Nikolaos T. Acute Liver Failure, an Issue of Clinics in Liver Disease. Elsevier - Health Sciences Division, 2018.

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24

(Editor), R. Schmid, L. Bianchi (Editor), H. E. Blum (Editor), W. Gerok (Editor), K. P. Maier (Editor), and G. A. Stalder (Editor), eds. Acute and Chronic Liver Diseases: Molecular Biology and Clinics (Falk Symposium). Springer, 1996.

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25

Shi, Yu, Yu-Chen Fan, Tao Chen, and Cornelius Engelmann, eds. Acute-On-Chronic Liver Failure: Natural History, Mechanism, And Treatment. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-830-3.

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26

A, Demetriou A., ed. Support of the acutely failing liver. Austin, Texas: R.G. Landes, 1994.

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27

Demetriou, Achilles A. Support of the Acutely Failing Liver (Tissue Engineering Intelligence Unit). Landes Bioscience, 2000.

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28

Burdmann, Emmanuel A. Leptospirosis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0191.

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Leptospirosis is one of the most prevalent zoonotic diseases worldwide. Pathogenic spirochaetes are shed in the urine of infected mammals to the environment. Humans are infected through contact with contaminated material. Leptospirosis is more prevalent in tropical and subtropical areas, but exists in all continents except Antarctica. The disease is difficult to diagnose and hence frequently neglected. Its clinical picture ranges from a mild flu-like disease to a life-threatening form with pulmonary haemorrhage, liver failure and acute kidney injury (AKI), called Weil disease, which may affect 10% of those with clinical disease. Typically, fever, myalgia and headache progress to nausea and vomiting, jaundice, red eyes, and other manifestation affecting skin, brain, and other organs.Kidney involvement, characterized by acute tubulointerstitial nephritis, is nearly universal. It may be clinically manifested as a tubulopathy with urinary electrolytes wasting, hypokalaemia and hypomagnesaemia and/or as AKI, which is more frequently non-oliguric. Antibiotic therapy may reduce hospitalization time and AKI frequency. Otherwise management is supportive, including timely and adequate dialysis support.
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29

Bosch, Annet M., and Elaine Murphy. Galactosemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0002.

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There are three known inherited disorders of galactose metabolism: classic galactosemia (galactose-1-phosphate uridyltransferase deficiency), galactokinase deficiency, and uridine diphosphate galactose 4-epimerase deficiency. Classic galactosemia presents in the newborn period with liver and renal impairment and failure to thrive. Acute symptoms resolve when lactose is excluded from the diet, but long-term complications are frequent and include neurocognitive and social difficulties, speech and language problems, motor problems, and premature ovarian insufficiency. Patients with galactokinase deficiency develop cataracts, while the clinical spectrum of uridine diphosphate galactose 4-epimerase deficiency is broad, from a benign condition to a severe disorder similar to classic galactosemia. All are autosomal recessive conditions. Diagnosis is by measurement of enzyme activity in erythrocytes, confirmed by mutation analysis of the specific genes, GALT, GALK, or GALE.
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30

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Paediatric liver transplantation. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0065.

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• Indications and contraindications 496• Timing of transplantation 497• Pre-transplant assessment 498• Types of liver transplantation 500• Immediately after transplantation 501• Complications 502Liver transplantation is now a standard treatment for: • Acute liver failure• Chronic liver failure•...
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31

Fourneau, Inge. Potentially Reversible Model of Acute Liver Failure in the Pig: A Model to Test the Efficiency of a Bioartificial Liver (Acta Biomedica Lovaniensia, 240). Leuven Univ Pr, 2001.

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32

Kortgen, Andreas, and Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.

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Impaired hepatic function is a common event in intensive care unit patients and as the liver plays a central role in drug metabolism and excretion this may lead to profound changes in pharmacokinetics. Underlying mechanisms are altered enzyme function of phase I and phase II metabolism, altered transporter protein function together with cholestasis and hepatic perfusion disorders. Moreover, multidrug therapy may lead to induction and inhibition of these enzymes and transporter proteins. In addition, changes in plasma protein binding and volumes of distribution of drugs are common. Altogether, these changes may not only lead to sometimes unpredictable plasma levels of xenobiotics, but also to drug-induced liver injury when hepatocellular accumulation of noxious substances occurs. Concomitant renal dysfunction may further complicate this situation. Pharmacodynamic alterations might also occur. In conclusion, the clinician must carefully evaluate medication given to patients with hepatic failure. Therapeutic drug monitoring should be performed wherever available to guide therapy.
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33

Hegarty, Rob, and Tassos Grammatikopoulos. Metabolic liver disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0060.

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The chapter on metabolic liver disease covers the metabolic disorders that affect the liver. It covers the important features in the history that may raise the suspicion of such a condition, as well as the clinical features that may be found. A detailed differential is discussed depending on the clinical presentation, for example, acute liver failure, infantile cholestasis, neonatal ascites, or acidosis and ketosis. Suggested investigations and the general management of these conditions are also included.
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34

Arroyo, Vicente, Mónica Guevara, and Javier Fernández. Renal failure in cirrhosis. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0247.

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A major event in liver cirrhosis is the development of a progressive deterioration of circulatory function due to splanchnic arterial vasodilation and impairment in cardiac function. This feature determines a homeostatic activation of the renin–angiotensin–aldosterone system, sympathetic nervous system, and antidiuretic hormone. The splanchnic microcirculation is resistant to the vasoconstrictor effect of these systems. Therefore, the homeostasis of arterial pressure in cirrhosis occurs in the extrasplanchnic, mainly renal circulation. The activation of these systems produces renal fluid retention, which accumulates as ascites, and water retention and dilutional hyponatraemia. In the latest phase of cirrhosis, when circulatory dysfunction is severe, renal vasoconstriction is intense and patients develop type 2 hepatorenal syndrome (HRS) and refractory ascites.Type 1 HRS is an acute and rapidly progressive renal failure that occurs in the setting of a precipitating event, commonly an infection. Patients with type 1 HRS also present with rapid deterioration of liver function (encephalopathy, jaundice) and relative adrenal insufficiency. The mechanism of this multiorgan failure is an acute deterioration in circulatory function due to both an accentuation of arterial vasodilation and of cardiac dysfunction.There is no specific test for the diagnosis of HRS. The most accepted diagnostic criteria are those proposed by the International Ascites Club which are based on the exclusion of other types of renal failure. The course of renal failure following treatment of the precipitating event of HRS is another important diagnostic feature.The treatment of choice of tense ascites in cirrhosis is paracentesis associated with intravenous albumin infusion. Moderate sodium restriction and diuretics (spironolactone alone or associated with furosemide) are subsequently given to prevent re-accumulation of ascites. Diuretics are the treatment of choice in patients with moderate ascites. Patients with type 2 HRS and refractory ascites (not responding to diuretics) could be treated by frequent paracentesis or by the insertion of a transjugular intrahepatic portosystemic shunt (TIPS).Terlipressin plus albumin is the treatment of choice in type 1 HRS
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35

Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.

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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
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36

Jalan, Rajiv, and Banwari Agarwal. Extracorporeal liver support devices in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0198.

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Liver failure is common and carries high morbidity and mortality. Liver transplantation (LT) is the only definitive treatment available performed as an emergency in acute liver failure and electively for chronic liver disease. In the last 50 years, a number of extracorporeal liver support devices and modifications have emerged , some of them purely mechanical in nature aimed at detoxification, while others are cell based systems possessing bio-transformational capability. Mechanical devices are mainly based on albumin dialysis, albumin being a key transporter protein that is severely deficient and irreversibly destroyed in liver diseases. Despite a sound scientific rationale and good safety profile, none of the currently available devices have shown enough promise to be incorporated in routine clinical practice, their use being limited to specific clinical situations. This chapter describes currently available devices, their operational characteristics, current evidence of their utility and limitation, and the future developments in the field of extracorporeal liver support.
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37

Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
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38

Moore, Professor Kevin, Dr Marcus Harbord, and Dr Daniel Marks. Gastroenterology and hepatology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.0008.

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Chapter 8 discusses gastroenterology and hepatology as it relates to acute medicine, including presentation, examination, and investigations, acute upper GI bleeding, acute gastroenteritis, jaundice, complications of cirrhosis, acute liver failure, infections and the liver, complications in liver transplant recipients, pregnancy and the liver, inflammatory bowel disease, acute pancreatitis, and malnutrition and chronic gastrointestinal disease.
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39

Stacey, Victoria. Gastroenterology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199592777.003.0013.

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Acute gastrointestinal bleeding - Acute upper gastrointestinal bleeding - Acute lower gastrointestinal bleeding - Vomiting - Diarrhoea - Inflammatory bowel disease (IBD) - Liver failure - Alcoholic liver disease/withdrawal syndromes - SAQs
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40

Williams, Ashleigh, and John Christie. Hepatic disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0007.

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This chapter describes the anaesthetic management of the patient with liver disease and its sequelae. Acute liver failure and chronic liver failure are discussed, together with their anaesthetic implications on coagulation and drug metabolism. Major sequelae of liver disease are discussed, including portal hypertension, varices, and hepatorenal syndrome. The preoperative investigation and optimization, treatment, and anaesthetic management of the patient with liver failure are described. The investigation and management of post-operative liver dysfunction are described. The anaesthetic management of acute oesophageal variceal haemorrhage and transjugular intrahepatic portosystemic shunt (TIPSS) are described.
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41

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Gastroenterology and hepatology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0009.

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Chapter 9 covers the basic science and clinical topics relating to gastroenterology and hepatology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers basic science, gastrointestinal investigation, malabsorption and malnutrition, inflammatory bowel disease, acute upper gastrointestinal haemorrhage, lower gastrointestinal bleeding and related disorders, gastrointestinal infections, gastrointestinal cancer, miscellaneous gastrointestinal problems, normal liver and biliary function, variceal disease, hepatic tumours, acute (fulminant) liver failure, haemochromatosis, Wilson disease (hepatolenticular degeneration), Alpha-1 antitrypsin deficiency, alcohol-induced liver disease, hepatitis, biliary diseases, and non-alcoholic fatty liver disease.
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42

Adam, Sheila, Sue Osborne, and John Welch. Gastrointestinal problems and nutrition. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0009.

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The chapter includes the background gastrointestinal (GI) physiology and pathophysiology commonly seen in critical care, including the immune functions of the gut. Acute gastrointestinal bleeding, the acute abdomen, liver failure and dysfunction, liver support systems and transplantation, and the management of acute pancreatitis are covered. Physical examination techniques, diagnostic information, and history are reviewed. The rationale for the importance of nutritional support in critical care, the techniques and complications of enteral feeding tube placement , the types of parenteral intravenous (IV) access, including peripherally inserted central catheter (PICC) lines, and the monitoring of delivery of enteral and parenteral nutrition are detailed. The complications associated with enteral tube placement and management and parenteral intravenous access and management are also included.
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43

Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.

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Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
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44

Harding, Sian E. The Exquisite Machine. The MIT Press, 2022. http://dx.doi.org/10.7551/mitpress/12836.001.0001.

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How science is opening up the mysteries of the heart, revealing the poetry in motion within the machine. Your heart is a miracle in motion, a marvel of construction unsurpassed by any human-made creation. It beats 100,000 times every day—if you were to live to 100, that would be more than 3 billion beats across your lifespan. Despite decades of effort in labs all over the world, we have not yet been able to replicate the heart's perfect engineering. But, as Sian Harding shows us in The Exquisite Machine, new scientific developments are opening up the mysteries of the heart. And this explosion of new science—ultrafast imaging, gene editing, stem cells, artificial intelligence, and advanced sub-light microscopy—has crucial, real-world consequences for health and well-being. Harding—a world leader in cardiac research—explores the relation between the emotions and heart function, reporting that the heart not only responds to our emotions, but it also creates them. The condition known as Broken Heart Syndrome, for example, is a real disorder that can follow bereavement or stress. The Exquisite Machine describes the evolutionary forces that have shaped the heart's response to damage, the astonishing rejuvenating power of stem cells, how we can avoid heart disease, and why it can be so hard to repair a damaged heart. It tells the stories of patients who have had the devastating experiences of a heart attack, chaotic heart rhythms, or stress-induced acute heart failure. And it describes how cutting-edge technologies are enabling experiments and clinical trials that will lead us to new solutions to the worldwide scourge of heart disease.
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45

Alvis, Bret, and Amy Robertson. Hepatic Encephalopathy. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0075.

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Hepatic encephalopathy is a complication of both acute and chronic liver failure. The disease can range from mild cognitive deficits to deep coma. Ammonia accumulation and inflammation are the two most accepted causes of hepatic encephalopathy. It is important to confirm an elevated serum ammonia level and rule out alternative causes of neurological derangements. Nonabsorbable disaccharides are the mainstay of treatment; however, the only definitive treatment is liver transplantation. Pertinent anesthetic considerations include avoiding benzodiazepines, understanding the implications of diminished hepatic function, and recognizing factors that may contribute to increased intracranial cerebral pressure. Proper assessment and management of the patient presenting with hepatic encephalopathy will be discussed.
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46

Dionisi-Vici, Carlo, Diego Martinelli, Enrico Bertini, and Claude Bachmann. HHH Syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0020.

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Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is an autosomal recessive disorder of the urea cycle characterized by impaired transport of ornithine across the inner mitochondrial membrane. As seen in other urea cycle defects, in the acute phase the disease is characterized by intermittent episodes of hyperammonemia accompanied by vomiting, lethargy, and coma, with or without signs of acute liver failure. The disease course is characterized by a pyramidal tract dysfunction associated with myoclonic seizures and cerebellar symptoms. Most patients reaching adulthood manifest variable degrees of cognitive impairment and abnormal behavior. Long-term treatment consists of a low-protein diet supplemented with citrulline, arginine, or ornithine. Protein restriction may be combined with sodium benzoate. If plasma creatine levels are low, creatine supplementation should be instituted. Acute treatment is similar to other urea cycle defects.
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47

Orellana, Renán A., and Jorge A. Coss-Bu. Nutrition and Gastrointestinal Emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0014.

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Appropriate nutrition must be tailored to the specific needs of individual patients. Needs depend on the child’s baseline nutritional status, the severity of disease, and specific organ dysfunction. Enteral nutrition is preferable whenever possible. Parenteral nutrition may be necessary when efforts to supply adequate nutrition enterally are contraindicated or unsuccessful. Patients with symptoms of acute abdomen require prompt recognition of surgical and nonsurgical disorders. Upper gastrointestinal hemorrhage may require transfusion of blood products, vasoactive drug infusion to minimize ongoing losses, and endoscopy following stabilization. Pancreatitis typically requires an orogastric/nasogastric tube for decompression, aggressive pain management, and radiological evaluations. Abdominal compartment syndrome needs to be recognized promptly to avoid further injury. Acute liver failure commonly leads to multiorgan system dysfunction and death. Specific therapy is available only in a minority of cases, and outcome depends on excellent supportive care, prompt evaluation by a pediatric gastroenterologist, and referral to a transplant center.
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48

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0029.

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Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.
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49

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0029_update_001.

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Abstract:
Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.
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50

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0029_update_002.

Full text
Abstract:
Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.
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