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Home , Hepatorenal syndrome

Ascites, Hepatorenal Syndrome, Portal HTN and SBP

Sept 2014

Ascites Excessive free fluid in the peritoneal cavity. >1.5L before clinically apparent.

Starling forces: ↑venous pressure, ↑capillary permeability, hypoproteinaemia, lymphatic obstruction

Causes (75%) Malignancy (15%) - Ca colon, other GI, Ca ovary (Meigs’ syndrome), Hepatic tumour, Lymphoma CCF (3%) TB (2%) (1%) Constrictive pericarditis, Venous obstruction – e.g. Budd-Chiari, Renal failure, Myxoedema

Examination Abdominal distension umbilicus down, Shifting dullness to percussion, Fluid thrill Stigmata of chronic Other masses: Ca colon/ovary, PR exam Lymphadenopathy Kussmaul’s sign for constrictive pericarditis Signs of CCF, hepatojugular reflex, Signs of IBD Kayser-Fleischer Rings (Wilson’s), ,

Investigations Bloods: FBC, LFT, UEC, Coags, TFT, screen Imaging: USS, CT, CXR /Ascitic tap

Paracentesis/Ascitic Tap Types Diagnostic - exudate vs transudate, ?, cancer, etc. Therapeutic or palliative – ↑comfort, ↓, ↑pulmonary fn, ↓effect on venous return

Procedure Pre-procedure: FBC, coags, but studies show no instances sig bleeding even if plts<50 & INR>1.5. Preparation – equipment, explain to patient Aseptic technique Choose site: lower flank (lateral to inf. Epigastric vessels) or midline 2cm below umbilicus (beware bladder) Withdraw 20-60ml for diagnostic tap or connect to a bag and allow as much as possible to drain over 4-6 hrs for therapeutic tap. Give 100ml albumin for every 1L over 3L drained.

Complications All <2%. Serious Cx as haemoperitoneum and bowel perforation <0.1%

Analysis Protein & LDH – for exudate vs transudate The serum ascites-albumin gradient (SA-AG) = (serum albumin conc) - (ascitic albumin conc) <11g/l = Ca, pancreatitis and TB; ≥11g/l = cirrhosis, CCF, nephrotic syn WCC (for SBP: WCC>500 cells, PMN>250 cells, pH<7.35& blood-ascites pH grad>0.1) RBC ( ↑in hepatocellular Ca, some cirrhotics), amylase (↑in pancreatic) Culture (in culture bottles), Cytology www.shakEM.co.nz 1

Management Avoid alcohol A no added salt diet useful in cirrhosis

Spironolactone: ↑sodium excretion and potassium reabsorption in the distal tubule. Monitor K+ levels

Loop , e.g. frusemide added when max doses of the spironolactone reached. If the underlying problem is CCF then treatment aggressively with usual Rx. Therapeutic Paracentesis Transjugular intrahepatic portosystemic shunt (TIPS), portocaval shunt, peritoneovenous shunt.

Complications Hyponatraemia on diuretics Spontaneous Bacterial (SBP) - 10-30% of patients with ascites, mortality rate 20%. - usually E. coli, streptococci and enterococci.

Hepatorenal syndrome Development of ARF in patient with normal kidneys in preexisting acute or chronic

Presentation Signs of sev. liver disease (ascites, jaundice, bleeding disorders, malnutrition, stigmata) Renal failure (oligouria or just increasing serum levels). Salt and water retention with increased ascites and peripheral oedema Hyponatraemia universal (dilutional), hyperkalaemia common

Diagnosis Exclude other causes of ARF in patients with liver failure: Diagnostic criteria are: - Creatinine clearance <40 mL/min or serum creatinine >1.5 mg/dL. - volume <500 mL per day. - Urine sodium <10 mEq/L. - Urine osmolality > plasma osmolality.

Management Type I More serious; progressive ; Cr x2 in 2/52; survival without medical trt <1/12 Rx: fluid restrict, vasconstrictors, iv albumin, renal replacement therapy, consider TIPS, transplant Type II Gradual impairment of renal function Rx: treat as outpatient, sodium restriction, paracentesis for gross ascites

Complications Life threatening bacterial (septicaemia, SPB, pneumonia). Histological changes in the kidneys are minimal and renal function usually recovers well after liver

Prevention Avoid nephrotoxic drugs Early hepatorenal syndrome treated by aggressive expansion intravascular volume with albumin/FFP

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Portal Hypertension Portal pressure gradient of 12mm Hg or more compared with a normal figure of 5- 10mm Hg. It is secondary to many conditions but the commonest is cirrhosis.

Aetiology Prehepatic Thromboses: portal vein, splenic vein Congenital portal vein atresia or stenosis Extrinsic compression e.g. tumour Splanchnic arteriovenous fistula Intrahepatic Cirrhosis, Acute , Acute and fulminant hepatitis, Primary biliary cirrhosis Idiopathic Myeloproliferative or metastatic disease infiltration Polycystic liver disease Granulomatous disease (Sarcoid, TB), Venoocclusive disease, Schistosomiasis Vitamin A toxicity Posthepatic IVC obstruction, Budd-Chiari syndrome, RHF, Constrictive pericarditis, Tricuspid regurgitation Arterial-portal venous fistula, ↑Portal or splenic blood flow

History Jaundice, blood transfusion, especially abroad. Sexual or drug taking lifestyle. Family history of liver disease such as Wilson's disease or hereditary haemochromatosis Alcohol consumption

Complications Haematemesis or melaena are features of upper GI and suggest bleeding varices Mental changes e.g. lethargy, irritability & changes in sleep suggest encephalopathy Increased abdominal girth and rapid weight gain suggests ascites Abdominal pain and fever suggest spontaneous peritonitis

Examination May indicate liver disease, porto-systemic anastomosis and hyperdynamic circulation. Jaundice, spider naevi, palmar erythema, Dupuytren's contracture, asterixis Abdo exam: ascites, splenomegaly, dilated epigastric veins, caput medusa, haemorrhoids Testicular atrophy and gynaecomastia, Muscle wasting Examination of the pulse shows a bounding, hyperdynamic circulation with warm periphery

Investigations LFTs, FBC, platelets, PTT, Albumin Screen for Anti-nuclear antibody, anti-mitochondrial antibody, anti-smooth muscle antibody Ferritin, Alpha-1-antitrypsin, Ceruloplasmin Doppler USS - ascites, portal blood flow, thrombosis of portal/splenic veins. Liver & spleen anomalies CT or MRI may show portal vasculature and be useful if USS inconclusive. Endoscopy to exclude or treat any oesophageal varices.

Management Aims is to reduce bleeding by reducing portal pressure Bed rest, restrict intake of salt to <90mmol/day, water restriction www.shakEM.co.nz 3

Drugs Reduce portal pressure with: beta blockers (propranolol), vasodilators (ISMN), splanchnic vasoconstrictor (, analogue), and lanreotide Reduce ascites with diuretics (spironolactone at high dose ± frusemide), paracentesis

Surgical

Portocaval shunts are no longer used but instead procedures such as transjugular intrahepatic portosystemic shunts (TIPS). Liver transplantation is the ultimate treatment. Ligation seems better than sclerotherapy to treat active bleeding

Complications: Variceal haemorrhage (esp. oesophageal)

Spontaneous Bacterial Peritonitis Epidemiology High mortality (for 1 st episode – 68% survival at 1/12, 30% survivial at 3/12) 30% of ascitic patients will develop SBP in 1yr

Risk factors Hepatic cirrhosis, nephrotic syndrome, peritoneal

Pathophysiology Infection of ascitic fluid without intra-abdominal focus; ascitic fluid has low levels of complement and opsonic activity; incr risk if low protein ascites E coli 30%; Grp D entero 15%; other staph 15%; staph aureus 10%; klebsiella 10%; pseudomonas 5%; anaerobes 5%

Assessment 5% asymptomatic; fever 40% sens; afebrile patients has worst prognosis; AP 95%; encephalopathy 50%

Investigation Paracentesis: macroscopically abnormal in >95%; WCC >1000 (sens 80%); neut >250 (sens >95%, spec 20%); decr glu, incr protein; gram stain positive in 10-50% (95% spec), bacteria rarely grown Bloods: cultures positive in 50%; LFTs; FBC

Management Abx: ceftriaxone 2g IV OD or cefotaxime 2g IV TDS; in dialysis pt, Abx can be intraperitoneal (ceftazidime and cephazolin initially); vancomycin into CAPD bag used if proven gram +ive infection Other: mng ; IV albumin 1.5g/kg may help decr renal failure www.shakEM.co.nz 4