Download Free Medical Acute Liver Failure PowerPoint Presentation

Acute Liver Failure PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Acute liver failure”.

This medical PowerPoint presentation talks about acute liver failure (ALF), a rapid and severe deterioration of liver function in individuals without pre-existing liver disease. It is a rare but potentially life-threatening condition that can lead to multiple organ failure and death.

The common causes of ALF include viral hepatitis, drug toxicity, and autoimmune diseases. Other less common causes include metabolic diseases, ischemia or hypoperfusion, and acute fatty liver of pregnancy.

Symptoms of ALF can vary but often include nausea, vomiting, abdominal pain, jaundice, and altered mental status. The diagnosis of ALF is made through clinical evaluation, laboratory tests, and imaging studies.

Treatment for ALF involves managing the underlying cause and providing supportive care, including nutritional support, fluid management, and management of complications. In some cases, a liver transplant may be necessary to save the life of the patient.

Prompt diagnosis and treatment are critical in ALF, and individuals who suspect they may have this condition should seek immediate medical attention.

Tags : Acute Liver Failure, hepatic encephalopathy, brain dysfunction, liver failure, coagulopathy, Gastroenterology, Gastroenterology PowerPoint presentation

Published on : May 02, 2023 | Views : 2617 | Downloads : 8

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Acute liver failure Clinical Practice Guidelines
Slide 2-

About these slides These slides give a comprehensive overview of the EASL clinical practice guidelines on the management of acute (fulminant) liver failure The guidelines were published in full in the May 2017 issue of the Journal of Hepatology The full publication can be downloaded from the Clinical Practice Guidelines section of the EASL website Please cite the published article as: European Association for the Study of the Liver. EASL 2017 Clinical Practice Guidelines on the management of acute (fulminant) liver failure. J Hepatol 2017;66:1047–81 Please feel free to use, adapt, and share these slides for your own personal use; however, please acknowledge EASL as the source
Slide 3-

About these slides Definitions of all abbreviations shown in these slides are provided within the slide notes When you see a home symbol like this one: , you can click on this to return to the outline or topics pages, depending on which section you are in Please send any feedback to: slidedeck_feedback@easloffice.eu These slides are intended for use as an educational resource and should not be used in isolation to make patient management decisions. All information included should be verified before treating patients or using any therapies described in these materials
Slide 4-

Chair Julia Wendon Panel members Juan Cordoba, Anil Dhawan, Fin Stolze Larsen, Michael Manns, Frederik Nevens, Didier Samuel, Kenneth J Simpson, Ilan Yaron, Mauro Bernardi (EASL Governing Board Representative) Reviewers Ali Canbay, François Durand, Ludwig Kramer Guideline panel EASL CPG ALF. J Hepatol 2017;66:1047–81
Slide 5-

Outline EASL CPG ALF. J Hepatol 2017;66:1047–81 Disease burden Principal aetiologies
Slide 6-

Methods Grading evidence and recommendations
Slide 7-

Grading evidence and recommendations 1. Guyatt GH, et al. BMJ. 2008:336:924–6;EASL CPG ALF. J Hepatol 2017;66:1047–81 Grading is adapted from the GRADE system1
Slide 8-

Background Definition of ALF Sub-classifications Disease burden Principal aetiologies
Slide 9-

Definition and clinical course of ALF *Patients with an acute presentation of chronic autoimmune hepatitis, Wilson disease and Budd–Chiari syndrome are considered as having ALF if they develop hepatic encephalopathy, despite the presence of a pre-existing liver disease in the context of appropriate abnormalities in liver blood tests and coagulation profile; †Usually INR >1.5 or prolongation of PT EASL CPG ALF. J Hepatol 2017;66:1047–81 In hepatological practice, ALF is a highly specific and rare syndrome, characterized by an acute deterioration of liver function without underlying chronic liver disease
Slide 10-

Sub-classifications of ALF 1. O'Grady JG, et al. Lancet 1993;342:2735; 2. Bernal W, et al. Lancet 2010;376:190201; EASL CPG ALF. J Hepatol 2017;66:1047–81 Weeks from development of jaundice to development of HE1 +++ High severity; ++ Medium severity; + Low severity; +/- Present or absent
Slide 11-

Burden of ALF in Europe EASL CPG ALF. J Hepatol 2017;66:1047–81 Rare syndrome whose true prevalence across Europe is unknown Incidence of virally induced ALF has declined substantially in Europe Remains the most common cause worldwide Most frequent aetiology of ALF in Europe is now drug-induced liver injury (DILI)
Slide 12-

Principal aetiologies of ALF EASL CPG ALF. J Hepatol 2017;66:1047–81 Viral Hepatitis B, A, E (less frequent CMV, HSV, VZV, Dengue) Drugs Paracetamol, anti-tuberculous, chemotherapy, statins, NSAIDs, phenytoin, carbamazepine, ecstasy, flucloxacillin Vascular Budd–Chiari syndrome, hypoxic hepatitis Pregnancy Pre-eclamptic liver rupture, HELLP, fatty liver of pregnancy Other Wilson disease, autoimmune, lymphoma, malignancy, HLH Toxins Amanita phalloides, phosphorus ALF
Slide 13-

Aetiology of ALF varies with geography *’Other causes’ refers to identified causes that are not: HAV, HBV, HEV, paracetamol or other drugs Bernal W, Wendon J. New Eng J Med 2013;369:252534 Bangladesh HEV 75% HBV 13%Unknown 6% Germany Other causes* 28% Unknown 21% HBV 18% India HEV 44% Unknown 31% HBV 15% Japan HBV 42% Unknown 34% Other drugs 9% Sudan Unknown 38% Other causes* 27% HBV 22% UK Paracetamol 57% Unknown 17% Other drugs 11% USA Paracetamol 39% Other causes* 19% Unknown 18% Top three causes of ALF in selected countries
Slide 14-

Guidelines Key recommendations
Slide 15-

Topics EASL CPG ALF. J Hepatol 2017;66:1047–81 Assessment and management at presentation Organ-specific management Cardiovascular Respiratory Gastrointestinal Metabolic Acute kidney injury and renal replacement therapy Coagulation Sepsis, inflammation and anti-inflammatory The brain in ALF Artificial and bioartificial liver devices Liver transplantation Paediatric ALF Click on a topic to skip to that section
Slide 16-

Assessment and management at presentation EASL CPG ALF. J Hepatol 2017;66:1047–81 Immediate measures Exclude cirrhosis, alcohol-induced liver injury or malignant infiltration Initiate early discussions with tertiary liver/transplant centre Even if not immediately relevant Screen intensively for hepatic encephalopathy Determine aetiology To guide treatment and determine prognosis Assess suitability for liver transplant Contraindications should not preclude transfer to tertiary liver/transplant centre Transfer to a specialized unit early If the patient has an INR >1.5 and onset of hepatic encephalopathy or other poor prognostic features
Slide 17-

Assessment and management at presentation *Should be performed preferably by a transjugular route, in an experienced centre, with access to a histopathologist with liver experience EASL CPG ALF. J Hepatol 2017;66:1047–81 Immediate measures Exclude cirrhosis, alcohol-induced liver injury or malignant infiltration Initiate early discussions with tertiary liver/transplant centre Even if not immediately relevant
Slide 18-

Assessment and management at presentation EASL CPG ALF. J Hepatol 2017;66:1047–81 Immediate measures Determine aetiology to guide treatment, especially LTx Primary or secondary causes of ALF and need for transplantation No indication for emergency LTx Possible indication for emergency LTx
Slide 19-

Differential diagnosis based on clinical features EASL CPG ALF. J Hepatol 2017;66:1047–81 No indication for emergency LTx Possible indication for emergency LTx
Slide 20-

Aetiologies with no indication for LTx EASL CPG ALF. J Hepatol 2017;66:1047–81 Malignant infiltration of the liver and acute ischaemic injury are not indications for LTx
Slide 21-

Aetiologies with possible indication for LTx EASL CPG ALF. J Hepatol 2017;66:1047–81 Drug-induced liver injury is the most frequent cause of severe ALI and ALF Especially paracetamol overdose
Slide 22-

Aetiologies with possible indication for LTx EASL CPG ALF. J Hepatol 2017;66:1047–81 Viral and autoimmune ALF HBV (most common), HAV, HEV, and VZV, HSV-1 and -2 (rare) can cause ALF Existence of other autoimmune conditions should raise suspicion of autoimmune hepatitis
Slide 23-

Aetiologies with possible indication for LTx EASL CPG ALF. J Hepatol 2017;66:1047–81 Uncommon aetiologies In most cases a potential positive effect of specific intervention will be too late to be beneficial Consideration for emergency LTx should not be delayed
Slide 24-

General support outside ICU: anamnesis *Based on the individual case; †Specialist input required EASL CPG ALF. J Hepatol 2017;66:1047–81 Questions for patients and relatives at admission
Slide 25-

General support outside ICU *Including LDH, conjugated and unconjugated bilirubin and creatinine kinase; †Low urea is a marker of severe liver dysfunction; ‡ANAs, ASMA, anti-soluble liver antigen, globulin profile, ANCAs, HLA typing EASL CPG ALF. J Hepatol 2017;66:1047–81
Slide 26-

General support outside ICU *Glycaemic target ± 140 mg/dl, Na 135–145 mmol/l; EASL CPG ALF. J Hepatol 2017;66:1047–81 In case of HE Transfer to an appropriate level of care (ideally critical care) at the first symptoms of mental alterations Quiet surrounding, head of bed >30°C, head in neutral position and intubate, ventilate, and sedate if progression to >3 coma Low threshold for empirical start of antibiotics if haemodynamic deterioration and/or increasing encephalopathy with inflammatory phenotype In case of evolving HE, intubation and sedation prior to the transfer Ensure volume replete and normalize biochemical variables (Na, Mg, PO4, K)
Slide 27-

Assessment and management at presentation EASL CPG ALF. J Hepatol 2017;66:1047–81 Immediate measures Assess suitability for liver transplant and initiate early discussions with transplant unit Even if not immediately relevant Suggested criteria for referral of cases of ALF to specialist units
Slide 28-

Assessment and management at presentation EASL CPG ALF. J Hepatol 2017;66:1047–81 Immediate measures Transfer to a specialized unit early Evolution of ALF is highly unpredictable Experience of specialized units is required to improve patient outcomes
Slide 29-

Organ-specific management EASL CPG ALF. J Hepatol 2017;66:1047–81 Main organ-specific complications in ALF Coagulation/haemostasis Unbalanced haemostasis Thrombocytopenia Infection Bacterial, fungal Pneumopathy Septicaemia Urinary infection Haemodynamic Hyperkinetic syndrome Arrhythmia Neurological = cerebral oedema Acute liver failure Pulmonary Pneumopathy Acute respiratory distress syndrome Pulmonary overload Cranial hypertension Brain death Metabolic Hypoglycaemia Hyponatraemia Hypophosphataemia Hypokalaemia Renal Toxic Functional
Slide 30-

Organ-specific management: cardiovascular EASL CPG ALF. J Hepatol 2017;66:1047–81 Most patients presenting with ALF or severe ALI develop systemic vasodilation with reduced effective central blood volume
Slide 31-

Organ-specific management: respiratory EASL CPG ALF. J Hepatol 2017;66:1047–81 Invasive airway management is required in the face of progression to high-grade HE to ensure airway protection
Slide 32-

Organ-specific management: gastrointestinal EASL CPG ALF. J Hepatol 2017;66:1047–81 Guidance regarding nutritional needs in patients with ALF is largely empirical Oral nutrition should be encouraged in patients with ALI Progressive HE or anorexia is likely to result in decreased calorie intake
Slide 33-

Organ-specific management: metabolic EASL CPG ALF. J Hepatol 2017;66:1047–81 ALF is frequently associated with electrolyte and metabolic imbalance Hypoglycaemia and hyponatraemia Acidosis Alterations in serum phosphate, magnesium, ionised calcium and potassium
Slide 34-

AKI and renal replacement therapy EASL CPG ALF. J Hepatol 2017;66:1047–81 4080% of ALF patients referred to liver units have AKI Associated with increased mortality and longer hospital stays Increased age, paracetamol-induced ALI, SIRS, hypotension, and infection increase risk
Slide 35-

Rapid changes in PT or INR are characteristic of ALF Significant prognostic value Common in ALF Thrombocytopenia Reduced circulating pro- and anti-coagulant proteins Increased PAI-1 Abnormal coagulation does not translate to increased risk of bleeding Most patients’ coagulation is normal despite abnormal INR and PT Coagulation: monitoring and management 1. Agarwal B, et al. J Hepatol 2012;57:780–6;EASL CPG ALF. J Hepatol 2017;66:1047–81
Slide 36-

Coagulation: monitoring and management EASL CPG ALF. J Hepatol 2017;66:1047–81 Prophylactic correction of coagulation or platelet levels is not necessary May instead adversely affect prognosis May increase the risk of thrombosis or transfusion-related acute lung injury
Slide 37-

Sepsis, inflammation and anti-inflammatory management *Guided by the use of biomarkers EASL CPG ALF. J Hepatol 2017;66:1047–81 Patients with ALF are at increased risk of developing infections, sepsis and septic shock Severe, untreated infection may preclude LTx and complicate the post-operative course ALF is associated with dynamic immune dysfunction Imbalance can contribute to organ failure and death
Slide 38-

The brain in ALF: hepatic encephalopathy EASL CPG ALF. J Hepatol 2017;66:1047–81 HE tends to fluctuate May progress from a trivial lack of awareness to deep coma Multiple additional manifestations Headache, vomiting, asterixis, agitation, hyperreflexia and clonus Clinical diagnosis is one of exclusion Course dictated by outcome and phenotype of liver failure Usually parallels evolution of liver function parameters Neurological outcomes may be worse in some circumstances Coexistence of infection Presence of inflammation without sepsis Other organ failure
Slide 39-

The brain in ALF: management of HE *Grade 3 coma in this context is not defined by asterixis (hepatic flap) but by the development of marked agitation and frequent aggression with a decrease in GCS (usually E1–2, V 3–4 and M4); †Grade 4 coma is associated with marked reduction in GCS (E1, V 1–2 and M1–3); ‡This may protect from ICH and reduce the risk of seizures; §e.g. levetiracetam or lacosamide (prophylactic use of antiepileptic drugs is not warranted) EASL CPG ALF. J Hepatol 2017;66:1047–81 Regular clinical and neurological examination to monitor progression in a quiet environment On progression to Grade 3 HE:* Intubate and provide mechanical ventilation to protect the airway, prevent aspiration and provide safer respiratory care On progression to Grade 4 HE:† Minimize risk of pulmonary barotraumas Target PaCO2 between 4.5–5.5 kPa (34–42 mmHg) and use propofol as a sedative agent‡ Add a short-acting opiate for adequate analgesia In case of concern of seizure activity: Monitor EEG Administer antiepileptic drugs with low risk of hepatotoxicity§
Slide 40-

Brain oedema-induced ICH is a classic complication of HE in ALF Incidence of ICH has decreased recently1 Improvements in preventative medical care Use of emergency LTx in high-risk patients2 Still may affect one-third of cases who progress to Grade 3 or 4 HE Risk of ICH is highest in patients with: Hyperacute or acute phenotype Younger age Renal impairment Need for inotropic support Persistent elevation of arterial ammonia The brain in ALF: intracranial hypertension *Proportion of 1,549 patients with ALF developing clinical signs of ICH. Error bars are 95% CI; p<0.000011. Bernal W, et al. J Hepatol 2013;59:74–80; 2. Bernal W, et al. J Hepatol 2015;62(1 Suppl):S112–20; EASL CPG ALF. J Hepatol 2017;66:1047–81 0 20 40 Patients developing ICH (%) Decrease in the incidence of ICH in patients with ALF*1 Years 1973–78 1979–83 1984–88 1989–93 1994–98 1999–2003 2004–08 60 80 100
Slide 41-

The brain in ALF EASL CPG ALF. J Hepatol 2017;66:1047–81 Regular clinical and neurological examination is mandatory Detection of early signs of HE and progression to high-grade HE is critical
Slide 42-

The brain in ALF EASL CPG ALF. J Hepatol 2017;66:1047–81 Additional monitoring is required in some patients
Slide 43-

Artificial and bioartificial liver devices *HVP defined as exchange of 8–12 or 15% of ideal body weight with fresh frozen plasma, for 3 days was superior to SMT regarding transplant-free and overall hospital survival Larsen FS, et al. J Hepatol. 2016;64:69–78; EASL CPG ALF. J Hepatol 2017;66:1047–81 Liver-assist devices are intended to provide a ‘bridge’ to LTx or recovery of liver function, reducing the need for transplant Experience with ‘liver support devices’ to date has been disappointing High-volume plasma exchange improved outcome in an RCT in ALF* Grade of evidence Grade of recommendation 0 0 20 14 40 60 80 100 28 42 56 70 84 Time (days) Cumulative proportion surviving (%) 7 21 35 49 63 77 91 HVP (n=92) SMT (n=90)
Slide 44-

LTx has been the most significant development in the treatment of ALF in 40 years and has transformed survival 1-year survival following emergency LTx for ALF is now around 80% Selection for LTx depends on: Accurate prediction of survival without transplant Consideration of the survival potential after LTx Consideration of whether a patient is too sick to transplant Impact of liver transplantation in ALF 1.Germani G, et al. J Hepatol 2012;57:288–96; EASL CPG ALF. J Hepatol 2017;66:1047–81 Patient survival after liver transplantation for ALF, Europe 1988–20091 p<0.001 for survival 2004–2009 vs. previous time periods
Slide 45-

ALF poor prognosis criteria in use for selection of candidates for liver transplantation *Bilirubin not included in paracetamol criteriaEASL CPG ALF. J Hepatol 2017;66:1047–81 A variety of prognostic evaluation systems are used to select candidates for transplantation Common prognostic criteria: Patient age Presence of HE Liver injury severity (magnitude of coagulopathy or jaundice) In general, falling aminotransferases, increasing bilirubin and INR, and shrinking liver are poor prognostic signs Should result in considering transfer of patient to a transplant centre
Slide 46-

Criteria for emergency liver transplantation EASL CPG ALF. J Hepatol 2017;66:1047–81
Slide 47-

Comparison of traditional criteria for emergency liver transplantation compared with new alternatives *Gc-globulin is a multifunctional protein involved in the scavenging of actin released from necrotic cells1 1. Schiodt FV et al. Liver Transpl 2005;11:1223–7; EASL CPG ALF. J Hepatol 2017;66:1047–81 Many new marker studies report better diagnostic performance than existing criteria Often small in size, have limited methodological quality and are seldom internally or externally validated Few (if any) have been adopted internationally and cannot be recommended for routine use
Slide 48-

Liver transplantation EASL CPG ALF. J Hepatol 2017;66:1047–81 Evaluation of patient prognosis is key at the earliest opportunity
Slide 49-

Liver transplantation EASL CPG ALF. J Hepatol 2017;66:1047–81 Evaluation of patient prognosis is key at the earliest opportunity
Slide 50-

Paediatric ALF EASL CPG ALF. J Hepatol 2017;66:1047–81
Slide 51-

Most common aetiologies of ALF in children ALF Viral Most common aetiology in Asia and South America Drugs Paracetamol Indeterminate Around 50% of cases in Europe and North America tend to have severe disease and a high fatality rate without LTx. ~10% of these patients develop bone marrow failure Neonatal Gestational alloimmune liver disease (neonatal haemochromatosis) Other Haemophagocytic lymphohistiocytosis Autoimmune Mitochondrial hepatopathy Metabolic disease e.g. Wilson disease
Slide 52-

Most common aetiologies of ALF in children Dhawan A. Liver Transpl. 2008;14 Suppl 2:S80-4. 331 patients with acute liver failure, data from the USA and Canada (PALFSG data set) Unknown Paracetamol Drug-related Autoimmune hepatitis Hepatitis A Viral (not B) Shock Wilson disease Metabolic Other
Slide 53-

Liver transplantation in children with ALF EASL CPG ALF. J Hepatol 2017;66:1047–81 LTx is the only proven treatment that has improved outcomes in children with ALF who fulfil poor prognostic criteria
Slide 54-

The future for ALF Considerations for future studies
Slide 55-

Burden, definition, assessment, and management EASL CPG ALF. J Hepatol 2017;66:1047–81 Definitions and main clinical features Biomarkers to help predict progression from ALI to ALF Improved tests for subtle HE Review of INR/PT cut-off for definition of ALF in the context of hyperacute, acute and subacute liver failure Burden of ALF within Europe Enrolment of all patients with ALF into a common web-based database with internationally agreed definitions of ALF and sub-classification Internationally accepted assessment of coagulation abnormalities in ALF Development of EU-wide epidemiological studies to define ALF and ALI prevalence and incidence General support management outside ICU Biomarkers to help predict deterioration and likely progression of disease Assessment of volume status and appropriate fluids in a ward setting Point of care assessment for sepsis Assessment and management at presentation Further continuous update of the EALFR Review of criteria defining poor prognosis in the context of modern critical care and support Application of biomarkers to further delineate cofactors in the development of ALF (e.g. paracetamol adducts, viral nucleic acid testing) Considerations for future studies
Slide 56-

Organ-specific management EASL CPG ALF. J Hepatol 2017;66:1047–81 The brain in ALF Accurate non-invasive assessment of ICP should be developed and validated Relationship between inflammation and cerebral irritation Modulators of cerebral inflammation need to be studied Cardiovascular Accurate assessment of volume status with biomarkers for congestion and depletion Studies of microcirculatory status as an endpoint for resuscitation as opposed to pressures Appropriate utilization of VA ECMO in subgroups of patients with ALF and hypoxic hepatitis Respiratory Application of extracorporeal lung support techniques to address risk/ benefit in highly specific subgroups Gastrointestinal Biomarkers for small bowel ileus and failure Renal Monitoring and management of anticoagulation of extracorporeal circuits Appropriate indications for commencing RRT Biomarkers for the prediction of and recovery from AKI Coagulation Role of anticoagulation to improve microcirculation and decrease liver injury Further understanding of coagulation disturbances and critically ill patients with ALF, as well as point of care monitoring Risk of thrombotic complications in the context of ALF and appropriate therapeutic interventions Sepsis, inflammation and anti-inflammatory Integration of inflammatory biomarkers with biochemical and functional markers of liver function Biomarkers to separate infection and inflammation Immunomodulatory therapy to promote liver regeneration and decrease nosocomial sepsis Considerations for future studies
Slide 57-

Artificial and bioartificial liver devices Well-designed RCTs of new liver support systems in well-defined patient cohorts Development of dynamic measures of liver function to assess metabolic and synthetic capacity Antimicrobial clearance and dosing when utilizing various liver support systems such as PE Liver transplantation and artificial liver devices EASL CPG ALF. J Hepatol 2017;66:1047–81 Liver transplantation Prospective studies of high methodological quality and sufficient size, enrolling from multiple centres, to assess the current natural history of ALF Avoid the assumption that transplantation equals non-survival for prognostic modelling purposes Definition and validation of contraindications to transplant in patients with ALF Definition and validation of futility of LTx in patients with ALF Clarification of the role of auxiliary LTx in patients with ALF Definition of long-term outcomes including quality of life in both transplant recipients and spontaneous survivors Biomarkers of regenerative capacity Considerations for future studies