A 45-year-old male with known alcoholic liver cirrhosis presents with worsening ascites.
Which ONE of the following is the next MOST appropriate management step?
Answer: D: In a cirrhotic patient, ascites is caused by a combination of portal hypertension, hypoalbuminaemia, and poor renal management of sodium and water. These patients are usually responsive to salt restriction and diuretics and therefore the mainstay of treatment of patients with cirrhosis and ascites includes education regarding dietary sodium restriction and oral diuretics. Fluid restriction is not necessary in treating most patients with cirrhosis and ascites. Similarly, it is sodium restriction, not fluid restriction, that results in weight loss as fluid follows sodium passively. However, severe hyponatraemia does warrant fluid restriction and a reasonable threshold for fluid restriction is a serum sodium <120–125 mmol/L.
The usual diuretic regimen consists of a combination of a single morning dose of oral spironolactone and frusemide, beginning with 100 mg of the former and 40 mg of the latter. The doses of both oral diuretics can be increased simultaneously every 3–5 days (maintaining the 100 mg: 40 mg ratio) if weight loss and natriuresis are inadequate. Usual maximum doses are 400 mg/day of spironolactone and 160 mg/day of furosemide. Spironolactone can be used as a single agent; however, hyperkalaemia and its long half-life limit its use. As a result, it is mainly reserved for patients with minimal fluid overload. Single-agent furosemide has been shown to be less efficacious than spironolactone. Starting with both drugs appears to be the preferred approach in achieving rapid natriuresis and maintainig normokalemia. In the largest, multicentre, randomised controlled trial performed in patients with ascites, dietary sodium restriction and a dual diuretic regimen has been shown to be effective in more than 90% of patients in achieving reduction in the volume of ascites to acceptable levels. Serial paracentesis remains an alternative for patients refractory to medical therapy.
Outpatient treatment can be attempted initially if no precipitants are identified. However, some patients with cirrhosis and ascites also have gastrointestinal haemorrhage, hepatic encephalopathy, bacterial infection, and/or hepatocellular carcinoma, and may require hospitalisation for definitive diagnosis and management of their liver disease as well as management of their fluid overload.
Reference:
Regarding serial therapeutic paracentesis performed in patients with liver cirrhosis and recurrent ascites, which ONE of the following is TRUE?
Answer: A: Various sites are suitable for abdominal paracentesis. One site is approximately 2 cm below the umbilicus in the midline where the fasciae of the rectus abdominis join to form the fibrous, thin, avascular linea alba. Large collateral veins may occasionally be present and should be avoided. Another site is the left lower quadrant (LLQ). The abdominal wall in the LLQ, 3 cm cephalad and medial to the anterior superior iliac spine, has been shown to be thinner and with a larger pool of fluid than the midline and is usually a good choice for needle insertion for performance of therapeutic paracentesis. This is also the preferred site by many clinicians as abdominal obesity increases the midline thickness. The right lower quadrant (RLQ) may be a suboptimal choice in the setting of a dilated cecum (due to lactulose) or an appendectomy scar. It is important to remain lateral to the rectus sheath at all times to avoid the inferior epigastric arteries; these vessels are located midway between the pubis and anterior superior iliac spines and then run cephalad in the rectus sheath.
The removal of up to 5–6 L of ascitic fluid is regarded as routine and is well tolerated, and for therapeutic purposes, at least this volume should be removed. Up to 10 L may be safely removed in most patients with chronic ascites. One controversial issue regarding therapeutic paracentesis is the role of colloid replacement. So far, studies have failed to show more clinical morbidity and mortality in patients not receiving colloids. However, there has been no study large enough to demonstrate decrease survival in patients who are given no plasma expander compared with patients given albumin. Current recommendations do not recommend colloid replacement for a single paracentesis of <5 L, but it remains optional, due to lack of evidence, if larger volumes are removed. The recommended infusion is 6–8 g of intravenous albumin per litre of ascitic fluid removed.
As many as two-thirds to three-quarters of patients undergoing paracentesis will have a coagulopathy. However, the only prospective study to evaluate the complications of paracentesis determined that transfusion-requiring abdominal haematomas occurred in <1% of cases despite the fact that 71% of patients had an abnormal prothrombin time (PT). Because transfusion-requiring haematoma is so unlikely, even in this population, prophylactic administration of fresh frozen plasma or platelets is not standard and is associated with considerable cost, in addition to the risk of transfusion-related complications, with little net gain. Furthermore, routine tests of coagulation do not reflect the bleeding risk in patients with cirrhosis. Therefore, for patients undergoing repeated therapeutic paracentesis, in the absence of prior problems or obvious clotting issues, obtaining preprocedure platelet count and INR is not routine.
Serial paracentesis should preferably be reserved for the 10% of patients who truly fail medical therapy. It is therefore important that the patient’s compliance with dietary sodium restriction be reviewed and appropriate adjustment of oral diuretics should occur before discharge.
References:
A 51-year-old male presents with decompensated chronic liver disease. He has tense ascites and slight confusion and you want to perform a diagnostic as well as therapeutic paracentesis to exclude peritonitis.
Which ONE of the following statements is TRUE?
Answer: B: A standard 3.8-cm (1.5-inch) metal needle can be used in most cases and can safely be left in the abdomen during a therapeutic tap for intervals of an hour or more without injury. An 18-gauge needle is preferred for large-volume therapeutic paracenteses because this permits expeditious outflow, whereas a smaller-gauge (20- to 22-gauge) needle may be sufficient for diagnostic taps and lessen the likelihood of post-procedural ascitic fluid leak through the wound site. Plastic sheath cannulas tend to kink and run the risk of being sheared off into the peritoneal cavity. The needle should be inserted slowly in 5-mm increments to detect undesired entry of a vessel and to help prevent unnecessary puncture of the small bowel. Continuous manual aspiration should be avoided because it may attract bowel or omentum to the end of the paracentesis needle with resultant occlusion.
Despite concerns regarding haemorrhagic complications (abdominal wall haematomas and haemoperitoneum) in patients with ascites, it is sufficiently rare, regardless of the PT. In a study of 1100 large-volume paracentesis, there were no haemorrhagic complications despite platelet counts as low as 19,000 cells/mm3 and INRs as high as 8.7 (75% >1.5 and 26.5% > 2). The risks and cost of prophylactic blood products may exceed the benefit. Traditional recommendations suggest the administration of platelets to patients with levels <50,000/mm3 and to give fresh frozen plasma to those with a PT exceeding 20 seconds (1.5 times the therapeutic level). However, this practice is not evidence supported and current recommendations are to reserve the use of FFP and platelets for clinically evident hyperfibrinolysis (threedimensional ecchymosis/haematoma) and disseminated intravascular coagulation.
Clinical assessment for detection of spontaneous bacterial peritonitis by emergency clinicians is only 75% sensitive. Furthermore, 5% of patients are asymptomatic. Although it is common in cirrhotic patients, SBP is difficult to diagnose because signs of abdominal pain and fever are not always present, and physical examination does not always demonstrate abdominal tenderness. Patients who are diagnosed with ascites for the first time, or who have ascites and develop fever, abdominal pain, GI bleeding or encephalopathy, should undergo paracentesis to check for SBP. Ascitic fluid infection is sufficiently common (12% in a recent series) at the time of admission that it is recommended that all patients with ascites admitted to hospital should undergo abdominal paracentesis.
A 42-year-old female with known liver cirrhosis and ascites presents with an unexplained fever. You perform an ascitic tap.
Which ONE of the following is TRUE?
Answer: A: The diagnosis of SBP is made when there is a positive ascitic fluid bacterial culture and an elevated ascitic fluid absolute PMN count ≥ 250 cells/mm3 (0.25 x 109 /L) without an evident intraabdominal, surgically treatable source of infection.
However, treatment should commence immediately and one should not wait until the ascitic fluid culture grows bacteria as it may result in the death of the patient from overwhelming infection. Microscopy is usually available before culture results. While patients with ascitic polymorphonuclear (PMN) counts ≥ 250 cells/mm3 is presumed to have bacterial peritonitis and should receive empirical antibiotic, infection can also be present in some patients before there is a neutrophil response (i.e. <250 cells/mm3 ). Therefore, in a clinical setting compatible with ascitic fluid infection (fever, abdominal pain or unexplained encephalopathy), all patients should receive empiric antibiotic therapy awaiting culture results. Clinical examination is not helpful in separating patients who need surgical intervention (secondary peritonitis) from those who have SBP and need only antibiotic treatment. In contrast, the initial ascitic fluid analysis can assist in distinguishing between spontaneous and secondary peritonitis and it is useful to order an ascitic fluid gram stain, culture, total protein, LDH and glucose in patients with ascitic fluid PMN count ≥ 250 cells/mm3. The characteristic analysis in the setting of free perforation is PMN ≥ 250 cells/mm3 (usually thousands), multiple organisms on gram stain and culture, as well as at least two of the following criteria:
However, these criteria are only 50% sensitive in detecting non-perforation secondary peritonitis. When ascitic fluid is collected in a syringe or tube, positive cultures are obtained in about 50% of cases compared with 80% if inoculated into a blood culture bottle prior to administration of antibiotics. Gramnegative enteric organisms, primarily E. coli, are the most frequently identified organisms in SBP.
Polymicrobial and anaerobic infections have been reported but are not common. A third-generation cephalosporin, such as cefotaxime, is usually sufficient in treating SBP. Anaerobic coverage should be added if secondary peritonitis is suspected.
A 44-year-old female with known liver cirrhosis and portal hypertension presents with acute hepatic encephalopathy. She is apyrexial with no clinical evidence of infection. Regarding her management, which ONE of the following is TRUE?
Answer: C: Lactulose, a nonabsorbable disaccharide, is the first-line treatment in patients with hepatic encehalopathy. It is effective via various mechanisms:
Lactulose should be given at 30 mL orally, 1–2-hourly initially to induce a rapid laxative effect. Once a laxative effect has been achieved, the dosage should be reduced to lactulose 30 mL orally, 3–4 times daily. In unconscious patients or patients who cannot swallow, lactulose may be given by nasogastric tube or mixed with water and given rectally as a retention enema.
Antibiotics such as neomycin reduce intestinal ammonia production by acting against urease-producing bacteria. However, its efficacy has never been demonstrated, and there is significant risk of ototoxicity and nephrotoxicity with long-term use. Neomycin is currently not recommended. However, a nonabsorbable oral antibiotic, rifaximin, has been shown to reduce repeated episodes of hepatic encephalopathy, even in patients taking lactulose regularly. Rifaximin is not registered for use in Australia but is available via the Special Access Scheme. If no precipitant of acute encephalopathy is readily identifiable, the patient should be started on empirical treatment for infection while waiting for the results of a septic work-up. One gram of intravenous ceftriaxone daily or 1g of cefotaxime 8-hourly are suggested regimens. When culture results become available, modify the antibiotic therapy appropriately. Continue therapy until the clinical signs of infection have resolved (usually for 5–10 days). Antibiotics can be stopped earlier if an alternative precipitant is identified.
Contrary to previous practice, protein restriction is not recommended in patients with acute encephalopathy. However, oral and nasogastric feeding should be suspended in patients with severe encephalopathy who do not have airway protection.
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