Miller·Anesthesia management of liver transplantation (3) Pathophysiology of end-stage liver disease

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Anesthesia for kidney transplantation in China 2019 Liver transplantation anesthesia for liver transplantation (1) In 1963, shortly after the effectiveness of azathioprine and prednisone in kidney transplantation was determined, Dr.
Strazl performed the first case of human liver transplantation.
transplant
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· Cyclosporine was introduced in 1979 · The National Health Consensus Conference in 1983 announced the end of liver transplantation🧪, which made liver transplantation enter a new era : Decompensated cirrhosis, malignancy, acute liver failure, metabolic diseases.
Early TIPS in patients with advanced cirrhosis and variceal bleeding can increase the 1-year survival rate to 86%.
In the United States, chronic liver disease and cirrhosis 5th leading cause of death Liver failure with life-threatening complications: hepatic encephalopathy, ascites, gastrointestinal bleeding or sepsis Trends: Malignancy and non-alcoholic fatty liver NASH still increasing The problem is the shortage of organ donors, which has resulted in almost 12% of patients dying each year while waiting for the past 10 years
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·Recurrent infection and newly transplanted liver failure can have dire consequences ·Indications for liver transplantation in children: cholestatic disease, malignancy, metabolic disease and acute severe hepatitis Liver transplantation anesthesia Cell inflammation and necrosis--fibrosis--blood flow obstruction--portal hypertension and portosystemic shunt Severe portal hypertension: the pressure difference between portal vein and hepatic vein exceeds 10-12mmHg--ascites, esophageal variceal bleeding may occur , hepatic encephalopathy, hepatorenal syndrome and other complications
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Cardiovascular complications: Hyperdynamic circulation with high cardiac output and low resistance is a hallmark of end-stage liver disease.
Increased blood volume in patients with dilated splanchnic vascular bed results in a significant reduction in effective circulatory volume.
R: Portal hypertension—production of vasodilatory factors A large increase--the circulatory system weakens the response to sympathetic stimulation--the dosage of vasoconstrictor drugs is often required to be increased clinically.
It may be complicated by cirrhotic cardiomyopathy--heart failure is likely to occur.
The myocardium has insufficient chronotropic function and insufficient hemodynamic response to severe fluctuations in hemodynamics
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There are also some QT interval prolongation, and caution should be used when administering QT prolonging drugs
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(Note: Amiodarone, Oxytocin, Droperidol, Ondan) · The risk factors for coronary artery disease in liver transplantation are similar to other patients, and NASH has become the main indication.
The best way to check for severe coronary artery disease
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· Therefore, coronary angiography should be considered when the possibility of coronary heart disease is high
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Pulmonary complications · 50-70% of patients with chronic liver disease have shortness of breath · Pay attention to HPS--hepatopulmonary syndrome--progressive hypoxemia 1⃣️Portal hypertension 2⃣️Partial pressure of oxygen lower than 80 when inhaling air 3⃣️Evidence of internal vasodilation · Oxygen partial pressure <50 predicts increased mortality PPHTN--portal pulmonary hypertension--dyspnea, fatigue, limited activity tolerance 1⃣️portal hypertension 2⃣️mean pulmonary artery pressure>25 3⃣️pulmonary wedge pressure <15 4⃣️PVR>240 dyn.
s.
cm-5 or 3 wood.
Optimal screening method--TTE tricuspid regurgitation velocity to assess right ventricular systolic pressure--estimation of pulmonary artery systolic pressure.
Moderate to severe pPHTN is associated with mortality.
Pulmonary vasodilators: prostaglandins (epoprostenol), phosphodiesterase inhibitors (sildenafil), endothelin inhibitors (bosentan), calcium channel blockers -- contraindicated (mesenteric vasodilation -- further worsening of portal hypertension) Liver transplantation anesthesia (3) Renal insufficiency caused by renal hypoperfusion and sodium retention · HRS hepatorenal syndrome -- advanced liver cirrhosis -- circulatory changes -- prerenal abnormalities -- dysfunction · Renal function is the only way to calculate MELD score One of the three variables is an important risk factor for mortality
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Risk factors: parenchymal lesions, sepsis, nephrotoxic damage, and hypovolemia
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·HRS--local production of vasodilatory factors after portal hypertension, especially NO caused--decreased circulating blood volume--decreased arterial blood pressure--RAAS system activation--severely reduced renal perfusion and significantly reduced glomerular filtration rate ·Treatment - vasopressin, somatostatin, alpha receptor agonist demethylation, deoxygenation and volume expansion ·Dialysis treatment at least twice a week for more than 6 consecutive weeks should consider combined liver and kidney transplantation
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Hepatic encephalopathy HE - hyperammonemia - but the severity is not related to its level.
Patients with cirrhosis are very sensitive to sedative drugs and have impaired liver metabolism, and possible drug-related encephalopathy should be carefully investigated
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Treatments to reduce blood ammonia levels include the use of the nonabsorbable disaccharide lactulose and the nonabsorbable antibiotics neomycin and metronidazole
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Ascites Most common complication Serum-ascites albumin difference >1.
1 mg/dl indicates portal hypertension with 97% accuracy Rapid correction of hyponatremia is detrimental and can cause central pontine myelination in patients with cirrhosis Lysis
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• Once refractory ascites occurs, treatment options are usually limited
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Varicose veins, portal hypertension-increased splanchnic blood flow resistance-formation of portal systemic collateral circulation-NO production exacerbates splanchnic vasodilation.
Esophagogastroduodenoscopy is the gold standard for diagnosing varicose veins
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Intravascular volume resuscitation, correction of severe coagulopathy, pharmacological control of portal pressure, and endoscopic variceal ligation should be used in combination for acute variceal hemorrhage
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·Early endoscopic variceal ligation combined with drug therapy is the preferred treatment for acute variceal bleeding
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Coagulation function, dynamic process, PT, APTT results are abnormal, and patients with liver cirrhosis are usually considered to have bleeding tendency, however, these experiments can only reflect the activities of some procoagulant factors, and do not consider and evaluate the concomitant reduction of anticoagulant factors
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Hypercoagulation occurs when anticoagulant factors are disproportionately reduced and procoagulant factors are increased and coagulation predominates
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· The fibrinolytic system in patients with cirrhosis has many abnormalities that may accelerate fibrinolysis
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Thrombosis in the early stage of DIC - followed by extensive fibrinolysis - coagulation factor consumption - bleeding A good lesson on anesthesia management for liver transplantation - TEE, another perspective of anesthesia for liver transplantation (Ji Xiaolin) Here is a summary of what you want! ! ~~The 2021 updated version of the good books are all in the WeChat store~END Grateful heart Thank you for having you