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Acute and Chronic Liver Disease

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Acute and Chronic Liver Disease THE LIVER Prof. AMNA JAVED Surgical Unit-2 Acute and Chronic Liver Disease Adequate liver function is essential to survival. Humans will survive for only 24–48 hours in the an-hepatic state despite full supportive therapy. Liver function and tests • Bilirubin is synthesized in the liver and excreted in bile. Increased levels found in, • increased haemoglobin breakdown • hepatocellular dysfunction resulting in impaired bilirubin transport and excretion • biliary obstruction. In patients with known parenchymal liver disease, progressive elevation of bilirubin in the absence of a secondary complication suggests deterioration in liver function. • Serum alkaline phosphatase (ALP) is particularly elevated with cholestatic liver disease or biliary obstruction. It is important to note that routine laboratory analysis of ALP is not isoform-specific and so alkaline phosphatase from a skeletal source may also lead to elevation. • The transaminase levels (aspartate transaminase (AST) and alanine transaminase (ALT)) reflect acute hepatocellular damage, as does the gamma- glutamyl transpeptidase (GGT) level, which may be used to detect the liver injury associated with acute alcohol ingestion. • However, marked liver injury can occur in the presence of normal liver function tests. • The synthetic functions of the liver are reflected in the ability to synthesize proteins (albumin level) and clotting factors (prothrombin time). • The standard method of monitoring liver function in patients with chronic liver disease is therefore serial measurement of bilirubin, albumin and prothrombin time. Main functions of the liver • Maintaining core body temperature • pH balance and correction of lactic acidosis • Synthesis of clotting factors • Glucose metabolism, glycolysis and gluconeogenesis • Urea formation from protein catabolism • Bilirubin formation from haemoglobin degradation • Drug and hormone metabolism and excretion • Removal of gut endotoxins and foreign antigens Impaired liver function • The clinical signs depend on the severity of dysfunction and whether it is acute or chronic failure. Acute liver failure • In the early stages, there may be no objective signs, but with severe dysfunction the onset of clinical jaundice may be associated with neurological signs of liver failure (hepatic encephalopathy), consisting of a liver flap, drowsiness, confusion and, eventually, coma. Causes of acute liver failure • Viral hepatitis (hepatitis A, B, C, D, E) • Drug reactions (halothane, isoniazid–rifampicin, antidepressants, non-steroidal anti-inflammatory drugs, valproic acid) • Paracetamol overdose • Mushroom poisoning • Shock and multiorgan failure • Acute Budd–Chiari syndrome • Wilson’s disease • Fatty liver of pregnancy Treatment of acute liver failure • Supportive therapy is the mainstay of treatment • The overall mortality from acute liver failure is approximately 50%, even with the best supportive therapy. • Short-term results of liver transplantation are poor in comparison with liver transplantation for chronic liver disease Supportive therapy for acute liver failure • Fluid balance and electrolytes • Acid–base balance and blood glucose monitoring • Nutrition • Renal function (haemofiltration) • Respiratory support (ventilation) • Monitoring and treatment of cerebral oedema • Treat bacterial and fungal infection King’s College selection criteria for liver transplantation in acute liver failure • Paracetamol induced • pH <7.30 (irrespective of grade of encephalopathy) or prothrombin time (PT) >100 s + serum creatinine >300 μmol/L + grade 3 or 4 encephalopathy. • Non-paracetamol induced (irrespective of encephalopathy) • PT >100 s or any three of the following: • Age <10 years or >40 years • Aetiology non-A, non-B, halothane or idiosyncratic drug reaction • More than 7 days’ jaundice before encephalopathy • PT >50 s • Bilirubin >300 μmol/L Chronic liver disease • Clinical jaundice indicating impairment of the liver’s ability to metabolise bilirubin. • There is progressive deterioration in liver function associated with a hyperdynamic circulation involving a high cardiac output, large pulse volume, low blood pressure and flushed warm extremities. • Fever , may be due to: • Underlying inflammation and cytokine release from the diseased liver • Secondary bacterial infection • Skin changes: • spider naevi • cutaneous vascular abnormalities that blanch on pressure • palmar erythema • white nails (leuconychia). • Endocrine abnormalities causing hypogonadism and gynaecomastia. • Hepatic encephalopathy i.e. • memory impairment • Confusion • personality changes • altered sleep patterns • slow, slurred speech. • Lethargy • Flapping tremor, demonstrated by asking the patient to extend his or her arms and hyperextend the wrist joint. • Abdominal distension due to ascites is a common late feature. This may be suggested clinically by the demonstration of a fluid thrill or shifting dullness. • Protein catabolism produces loss of muscle bulk and wasting, • Coagulation defect is suggested by the presence of skin bruising. Severity of chronic liver disease • Severity is assessed commonly by two prognostic models • Child–Turcotte–Pugh (CTP) Classification • Model for End-Stage Liver Disease (MELD) score. MELD model • The survival probability of patients with end-stage liver disease is computed based on the • international normalised ratio (INR) • serum bilirubin • serum creatinine LIVER IMAGING • Ultrasound: Standard first-line investigation • Spiral CT: Anatomical planning for liver surgery • MRI: Alternative to spiral CT but superior in characterizing small liver lesions and detecting liver metastases • MRCP: (magnetic resonance cholangiopancreatography) First-line, non-invasive cholangiography • ERCP: (endoscopic retrograde cholangiopancreatography) Imaging the biliary tract when endoscopic intervention is anticipated (e.g. ductal stones) • PTC :(percutaneous transhepatic cholangiography) Biliary tract imaging when ERCP impossible or failed Angiography To detect vascular involvement by tumour • PET: (positron emission tomography) scanning To quantify tumour spread • Laparoscopy/ laparoscopic ultrasound: To detect peritoneal tumour spread and superficial liver metastases LIVER TRAUMA • Liver trauma can be divided into • blunt trauma • penetrating trauma • Blunt injury produces • Contusion • Laceration • avulsion injuries • Often in association with splenic, mesenteric or renal injury. • Penetrating injuries, such as stab and gunshot wounds, • Often associated with chest or pericardial involvement. Blunt injuries are more common and have a higher mortality than penetrating injuries. Diagnosis of liver injury • Liver injury should be suspected in all lower chest and upper abdominal injuries, especially if considerable blood volume replacement has been required. • Focused assessment sonography in trauma (FAST) performed in the emergency room by an experienced operator can reliably diagnose free intraperitoneal fluid. • Patients with free intraperitoneal fluid on FAST and haemodynamic instability, and patients with a penetrating wound, will require a laparotomy and/or thoracotomy once active resuscitation is under way. • If there is massive ongoing blood loss and the rapid development of a coagulopathy, the patient should be directly transferred to the operating theatre while blood products are obtained and volume replacement is taking place. • Patients who are haemodynamically stable should have a contrast- enhanced CT scan of the chest and abdomen as the next step to confirm diagnosis Management of liver trauma • Remember associated injuries • At-risk groups • Stabbing/gunshot in lower chest or upper abdomen • Crush injury with multiple rib fractures • Resuscitate Airway Breathing Circulation • Assessment of injury • CT chest and abdomen with contrast • Laparotomy if haemodynamically unstable • Treatment • Correct coagulopathy • Suture lacerations • Resect if major vascular injury • Packing if diffuse parenchymal injury • The necessity for fresh frozen plasma and cryoprecipitate should be assessed as these patients rapidly develop irreversible coagulopathies due to a lack of fibrinogen and clotting factors. • Standard coagulation profiles are inadequate to evaluate this acute loss of clotting factors, and factors should be given empirically, aided by the results of thromboelastography (TEG), if available. Complications of liver trauma • Intrahepatic haematoma (requires no specific intervention) • Liver abscess ( due to secondary infection of an area of parenchymal ischaemia. treatment is with systemic antibiotics and aspiration) • Bile collection (require aspiration under ultrasound guidance or percutaneous insertion of a pigtail drain) • Biliary fistula (The site of origin is determined by endoscopic or percutaneous cholangiography, and biliary decompression is achieved by nasobiliary or percutaneous transhepatic drainage or stent insertion. If this fails, hepatic lobe resection can be considered) • Hepatic artery aneurysm • Arteriovenous fistula • Arteriobiliary fistula Fistulas are Late vascular complications (precipitating acute heart failure if between the hepatic artery and hepatic vein and acute portal hypertension if arterioportal) or arteriobiliary fistulae (resulting in often painful haemobilia). These are best treated non-surgically by a specialist hepatobiliary interventional radiologist. • Hepatic failure may occur following extensive liver trauma. This will usually reverse with conservative supportive treatment if the blood supply and biliary drainage of the liver are intact. • Development of biliary strictures may occur many years after recovery from liver trauma. • A segmental or lobar stricture, associated with atrophy of the corresponding area of liver parenchyma and compensatory hypertrophy of the other liver lobe, may be treated expectantly. • A dominant extrahepatic bile duct stricture associated with obstructive jaundice may be treated initially with endobiliary balloon dilatation or stenting. But it will usually require surgical correction using a Roux-en-Y hepatodochojejunostomy. Thank You.
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