Ascites CHAPTER 61 391 Test Comment peritoneal metastases, but these are found in only about two-thirds of patients with ascites related to malignancy Other tests Total protein, glucose, LDH Gram stain Ziehl–Neelsen stain and testing for Mycobacterium tuberculosis DNA if suspected tuberculosis Amylase if suspected pancreatitis EDTA, ethylene diaminetetra-acetic acid; LDH, lactate dehydrogenase. TABLE 61.3 Causes of ascites according to the serum–ascites albumin gradient (SAAG) High SAAG (11 g/L or greater) (associated with portal hypertension) • Cirrhosis • Alcoholic hepatitis • Hepatic outfl ow obstruction: – Budd–Chiari syndrome (thrombosis of one or more of the large hepatic veins, the inferior vena cava, or both) – Hepatic veno-occlusive disease • Cardiac ascites: – Tricuspid regurgitation – Constrictive pericarditis – Right-sided heart failure Low SAAG (<11 g/L) (associated with peritoneal neoplasms, infection and infl ammation) • Peritoneal carcinomatosis • Peritoneal tuberculosis • Pancreatitis • Serositis • Nephrotic syndrome • Myxedema • Meig syndrome Ascites TABLE 61.4 Spontaneous bacterial peritonitis • Defi ned as spontaneous infection of ascitic fl uid in the absence of an intra-abdominal source of infection • It is a common complication of ascites due to cirrhosis • Prevalence among patients with ascites is between 10% and 30% • Causes fever (70%), abdominal pain (60%), abdominal tenderness (50%) and change in mental state (50%) • Diagnosis based on fi nding of >250 neutrophils/mm 3 of ascitic fl uid • Aerobic Gram-negative bacteria, especially Escherichia coli, are the commonest organisms • May be complicated by hepatorenal syndrome (in up to 30% of patients, see Table 62.5): IV albumin solution 1.5 g/kg at diagnosis and 1 g/kg 48 h later may reduce the likelihood of hepatorenal syndrome developing, and improve prognosis • Treat with third-generation cephalosporin, e.g. cefotaxime 2 g 8-hourly IV daily for 5 days, followed by quinolone PO for 5 days • Recurrence is common (estimated 70% probablility of recurrence at 1 year). Consider prophylaxis with quinolone or co-trimoxazole. TABLE 61.5 Management of ascites due to cirrhosis • Restrict dietary sodium intake to ∼50 mmol/day • Start diuretic therapy with spironolactone 100 mg daily + furosemide 40 mg daily PO, as single morning doses • Monitor daily weight. Target weight loss is 0.5 kg daily in patients without peripheral edema and 1 kg daily in those with peripheral edema • Increase the doses of spironolactone (by 100 mg steps) and furosemide (by 40 mg steps) every 3–5 days if target weight loss is not achieved, to maximum doses of spironolactone 400 mg daily and furosemide 160 mg daily (as single or divided doses) • Reduce the spironolactone dose if there is hyperkalemia • Amiloride (10–40 mg daily) can be substituted for spironolactone if there is symptomatic gynecomastia • If there is tense ascites, consider a single paracentesis (to remove 5 L), followed by dietary sodium restriction and diuretic therapy. Albumin solution (8 g albumin per liter of ascites removed) should be given IV during paracentesis. Seek advice from a hepatologist/ gastroenterologist Ascites CHAPTER 61 393 ALERT Patients who develop ascites as a complication of cirrhosis have a poor prognosis (2-year survival ∼50%), and should be referred to a hepatologist for consideration of liver transplantation. Further reading Gines P, et al. Management of cirrhosis and ascites. N Engl J Med 2004; 350: 1646–54. Menon KVN, et al. The Budd–Chiari syndrome. N Engl J Med 2004; 350: 578–85. Soares-Weiser K, et al. Antibiotic treatment for spontaneous bacterial peritonitis. BMJ 2002; 324: 100–2. Thomsen TW. Paracentesis. N Engl J Med 2006; 355: e21. Acute liver failure 62 Acute liver failure 394 Suspected acute liver failure (Tables 62.1, 62.2) Jaundice with abnormal behavior or reduced conscious level and prolonged prothrombin time not corrected by vitamin K 10 mg IV Key observations (Table 1.2) Stabilize airway, breathing and circulation Treat/prevent hypoglycemia: start glucose 10% IV infusion, initially 1 L 12-hourly Focused assessment (Table 60.1) Urgent investigation (Table 62.3) Grade 3 or 4 hepatic encephalopathy? (Table 60.1) Transfer to intensive therapy unit (ITU) Consider elective ventilation Transfer to high- dependency unit (HDU) Known chronic liver disease? Exclude/treat precipitants (Table 62.2) Supportive care (Tables 62.4, 62.5) Suspect fulminant hepatic failure (Table 62.1) Supportive care (Tables 62.6, 62.7) Urgent hepatology opinion Transfer to liver unit Continue care locally No Yes No Yes CHAPTER 62 395 Acute liver failure TABLE 62.1 Causes of fulminant hepatic failure (FHF) Cause Comment Drug-related Paracetamol poisoning (p. 75): the commonest cause of FHF in the UK; AST/ALT typically >3500 units/L Idiosyncratic reaction (usually occurs within 6 months of starting drug; many drugs implicated, e.g. co-amoxiclav) Viral hepatitis Hepatitis A, B, C, D or E virus Herpes simplex virus (a rare cause; usually seen in patients taking immunosuppressive therapy or in third trimester of pregnancy) Ischemic ‘Shock liver’ hepatitis May occur after cardiac arrest or prolonged hypotension, or in severe congestive heart failure, and therefore often associated with acute renal failure Markedly raised AST/ALT Budd–Chiari Due to acute hepatic vein thrombosis syndrome Typically occurs in women age 20–40 years Presents with right upper quadrant pain, hepatomegaly and ascites Underlying hematological disorder (e.g. polycythemia rubra vera, paroxysmal nocturnal hemoglobinuria) or other cause of thrombophilia (p. 227) Diagnose by duplex ultrasound of hepatic veins and IVC Acute fatty Occurs in last trimester of pregnancy liver of Often associated with pre-eclampsia (p. 552) pregnancy Continued 396 SPECIFIC PROBLEMS: GASTROINTESTINAL/LIVER/RENAL Acute liver failure Cause Comment Autoimmune Consider if there are other autoimmune disorders hepatitis (e.g. hemolytic anemia, idiopathic thrombocytopenic purpura, type 1 diabetes, thyroiditis, celiac disease) Autoantibodies (antinuclear antibodies, antismooth muscle antibodies) and hypergammaglobulinemia usually present Amanita Suspect if the patient has eaten wild mushrooms phalloides Usually associated with severe gastrointestinal poisoning symptoms (nausea, vomiting, diarrhea, abdominal pain), which develop within hours to one day of ingestion Wilson disease Suspect in a patient age <30 with liver failure and hemolytic anemia (giving markedly elevated bilirubin) Kayser–Fleischer rings are present in ∼50% Serum ceruloplasmin is typically low (but may be normal in ∼15% and is often reduced in other forms of ALF) and serum/urinary copper levels high Alkaline phosphatase and urate are low Malignant May occur in breast cancer, small cell lung cancer, infi ltration lymphoma and melanoma Associated with hepatomegaly Diagnosis made by imaging and biopsy Cause unclear Retake the drug history Consider transjugular liver biopsy ALF, acute liver failure; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IVC, inferior vena cava. CHAPTER 62 397 Acute liver failure ALERT Contact your regional liver unit urgently if you suspect fulminant hepatic failure, to discuss management and transfer. TABLE 62.2 Causes of decompensation of chronic liver disease • Infection, especially spontaneous bacterial peritonitis (p. 392) • Alcoholic hepatitis (p. 404) • Acute gastrointestinal hemorrhage (p. 365) • Acute viral hepatitis • Major surgery and anesthesia • Drugs: diuretics, hypnotics, sedatives and narcotic analgesics • Hypokalemia and hypoglycemia • Constipation 398 SPECIFIC PROBLEMS: GASTROINTESTINAL/LIVER/RENAL Acute liver failure TABLE 62.3 Urgent investigation in acute liver failure Needed urgently • Prothrombin time and coagulation screen • Full blood count and reticulocyte count • Blood glucose • Sodium, potassium, creatinine and urea* • Liver function tests: bilirubin, aspartate transaminase, alanine transaminase, gamma-glutamyl transferase, alkaline phosphatase, albumin • Amylase and lipase • Paracetamol level if unexplained acute liver failure or paracetamol poisoning is suspected • Arterial blood gases, pH and lactate • Blood culture • Urine stick test, microscopy and culture • Microscopy and culture of ascites if present (aspirate 10 ml for cell count (use EDTA tube) and culture (inoculate blood culture bottles) (see p. 389) • Chest X-ray • Ultrasound of liver, biliary tract and hepatic/portal veins • Pregnancy test in women of child-bearing age For later analysis (if suspected fulminant hepatic failure) • Markers of viral hepatitis (anti-HAV IgM, HBsAg, anti-HBc IgM, anti-HCV, anti-HEV) • HIV test • Autoimmune profi le (antinuclear antibodies, antismooth muscle antibodies, immunoglobulins) • Plasma ceruloplasmin in patients aged <50 (to exclude Wilson disease) • Serum (10 ml) and urine (50 ml) for toxicological analysis if needed • Blood group EDTA, ethylene diaminetetra-acetic acid; HAV, hepatitis A virus; HBc, hepatitis B core; HBsAG, hepatitis B surface antigen; HCV, hepatitis C virus; HEV, hepatitis E virus; IgM, immunoglobulin M. * Urea may be low because of reduced hepatic synthesis; if markedly elevated with a normal creatinine, suspect upper gastrointestinal hemorrhage. CHAPTER 62 399 Acute liver failure TABLE 62.4 Management of decompensated chronic liver disease Look for and treat precipitants (Table 62.2) • If there is ascites, aspirate 10 ml for cell count (use an EDTA tube) and culture (inoculate blood culture bottles) (p. 389) • Assume spontaneous bacterial peritonitis (see Table 61.4) is present if ascitic fl uid shows >250 neutrophils/mm 3 , and treat with cefotaxime 2 g 8-hourly IV • Start empirical antibiotic therapy with cefotaxime 2 g 8-hourly IV if there is fever, even in the absence of focal signs of infection, after taking blood cultures Maintain blood glucose >3.5 mmol/L • Give glucose 10% by IV infusion initially 1 L 12-hourly • Check blood glucose 1–4-hourly and immediately if conscious level deteriorates Maintain fl uid and electrolyte balance • Low sodium diet (∼50 mmol/day) • Potassium supplements to maintain plasma level >3.5 mmol/L • If IV fl uid is needed, use albumin solution or dextrose 5% or 10%. Avoid saline • Treat ascites with spironolactone (plus a loop diuretic if necessary) aiming for weight loss of 0.5 kg/day (see Table 61.5). If ascites is refractory to diuretic therapy, use paracentesis with IV infusion of salt-poor albumin (p. 392) • Check sodium, potassium and creatinine daily. A rising creatinine may refl ect hypovolemia, sepsis, nephrotoxic drugs or hepatorenal syndrome (Table 62.5) Nutrition • Early feeding by mouth or fi ne-bore nasogastric tube, with protein intake 60 g/day Continued 400 SPECIFIC PROBLEMS: GASTROINTESTINAL/LIVER/RENAL Acute liver failure TABLE 62.5 Hepatorenal syndrome Criteria for diagnosis • Chronic or acute liver disease with liver failure and portal hypertension • Plasma creatinine concentration >133 µmol/L, with progressive increase over days to weeks, and oliguria • Exclusion of other causes of renal failure (p. 414) • Urine sodium concentration <10 mmol/L (if not taking diuretic), urine osmolality greater than plasma osmolality, urinary protein excretion <0.5 g/day, urine red cell count <50 mm 3 Management • Treat underlying liver disease • Exclude/treat spontaneous bacterial peritonitis (p. 392) • General management of acute renal failure (p. 410) • Consider treatment with terlipressin (0.5–2.0 mg IV every 4–12 h) for 5–15 days plus albumin solution (1 g/kg IV on day 1, followed by 20– 40 g daily) for 5–15 days: discuss with hepatologist/gastroenterologist Drugs • Start lactulose 30 ml 3-hourly PO until diarrhea begins, then reduce to 30 ml 12-hourly • Give a proton pump inhibitor, ranitidine or sucralfate to reduce the risk of gastric stress ulceration • Give vitamin supplements IV or PO (thiamine and other B group vitamins, vitamin C, vitamin K, folate) • Avoid sedatives and opioids. Other drugs that are contraindicated are listed in the British National Formulary EDTA, ethylene diaminetetra-acetic acid. [...]... Miura F Flow charts for the diagnosis and treatment of acute cholangitis and cholecystitis: Tokyo guidelines J Hepatobiliary Pancreatic Surg 20 07; 14: 27 34 UK Working Party on Acute Pancreatitis UK guidelines for the management of acute pancreatitis Gut 2005; 54 (suppl III): iii1–iii9 Wada K, et al Diagnostic criteria and severity assessment of acute cholangitis: Tokyo guidelines J Hepatobiliary Pancreatic... endocarditis (p 203) and myeloma as causes of renal failure • Has renal failure followed cardiac catheterization via the femoral artery (raising the possibility of renal atheroembolism)? • Has the patient been exposed to any nephrotoxic drugs (including contrast media) or poisons? Consider occupational exposure to toxins Examination • Key observations (see Table 1.2) and systematic examination (see Table... transplantation Crit Care Med 2003; 31: 299–305 Polson J, Lee WM American Association for the Study of Liver Diseases position paper: the management of acute liver failure Hepatology 2005; 41: 1 179 – 97 Acute liver failure Complication 403 Alcoholic hepatitis 63 Alcoholic hepatitis T A B L E 63 1 Alcoholic hepatitis: diagnosis and management Clinical features and blood results • Malaise • Jaundice • Nausea... Surgical opinion Urgent ultrasound of biliary tract Biliary drainage by ERCP ALT, alanine aminotransferase; ERCP, endoscopic retrograde cholangiopancreatography Biliary tract disorders and acute pancreatitis Disorder 408 S P E C IFIC PROBLEMS: GASTROI NTESTI NAL/LI VE R/RE NAL T A B L E 64 2 Acute pancreatitis: clinical features and management Comment Common causes Biliary tract disorders and acute pancreatitis... catheter to monitor urine output and, in patients over 60 or with cardiac disease, a central venous catheter so that central venous pressure can be monitored to guide fluid replacement Manage acute renal failure along standard lines (Table 65.5) Acute renal failure Element AL ERT Contact your renal unit early about patients with acute renal failure, before the plasma creatinine is >400 µmol/L T A B... basis of raised bilirubin and clinical cholangitis Nutritional support (enteral feeding by nasoenteric tube beyond the ligament of Treitz, in the absence of substantial ileus) ALT, alanine aminotransferase; APACHE II, severity of illness scoring system based on acute physiology and chronic health evaluation; ERCP, endoscopic retrograde cholangiopancreatography Further reading Indar AA, Beckingham IJ Acute... ventilated Management of complications • See Table 62 .7 Acute liver failure Ask for help • Ask for help from your local gastroenterologist/hepatologist or discuss management with the regional liver unit 402 S P E C IFIC PROBLEMS: GASTROI NTESTI NAL/LI VE R/RE NAL Acute liver failure T A B L E 62 7 Management of complications of acute liver failure Complication Management Cerebral edema Cerebral edema occurs... for alcoholic hepatitis: what’s next? J Hepatol 2005; 43: 526–33 Stewart SF, Day CP The management of alcoholic liver disease J Hepatol 2003; 38 (suppl I): S2–S13 Alcoholic hepatitis Management of alcoholic hepatitis • Seek advice from a gastroenterologist/hepatologist • Avoid diuretics and ensure adequate volume replacement (use 4.5% human albumin solution and/or salt-poor albumin; avoid normal saline)... Hypoglycemia, hypocalcemia, hypomagnesemia and disseminated intravascular coagulation may occur Identification of severe acute pancreatitis APACHE II score of 8 or more Organ failure (shock, respiratory failure, renal failure) Continued CH AP TE R 64 Element 409 Comment Pleural effusion on admission chest X-ray C-reactive protein >150 mg/L Substantial pancreatic necrosis (at least 30% glandular necrosis... into muscle Acute renal failure from hypovolemia and renal tubular obstruction, tubular damage and renal vascoconstriction Metabolic effects of muscle injury: hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia Management of severe rhabdomyolysis Diagnose and treat underlying cause Vigorous fluid resuscitation with normal saline Transfer the patient to high-dependency unit Put in a bladder catheter . potassium, creatinine and urea* • Liver function tests: bilirubin, aspartate transaminase, alanine transaminase, gamma-glutamyl transferase, alkaline phosphatase, albumin • Amylase and lipase •. Diagnosis made by imaging and biopsy Cause unclear Retake the drug history Consider transjugular liver biopsy ALF, acute liver failure; ALT, alanine aminotransferase; AST, aspartate aminotransferase;. Substantial pancreatic necrosis (at least 30% glandular necrosis on contrast-enhanced CT) Management of Fluid resuscitation acute Cardiovascular/respiratory support pancreatitis Analgesia with