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A Guide to Diagnosing and Managing Ascites in Cirrhosis

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Muhammad Salman Faisal, MD; Tavankit Singh, MD; Hina Amin, A guide to diagnosing and MD; Jamak Modaresi Esfeh, MD Department of Internal managing ascites in cirrhosis Medicine (Dr. Faisal) and Department of Gastroenterology, Combined serum and ascites fluid measurements Hepatology and Nutrition (Drs. Singh, Amin, and point to the cause of ascites. For patients with modest Modaresi Esfeh), Cleveland Clinic, Ohio edema, a reduced weight-loss target with diuresis may be acceptable. [email protected] The authors reported no potential conflict of interest relevant to this article. iver cirrhosis is implicated in 75% to 85% of ascites cases doi: 10.12788/jfp.0186 PRACTICE RECOMMENDATIONS in the Western world, with heart failure or malignancy accounting for fewer cases.1 Among patients who have ❯ Calculate the serum ascites L albumin gradient and decompensated cirrhosis with ascites, annual mortality is 2 measure the total ascites 20%. Another study showed a 3-year survival rate after onset 3 protein level to distinguish of ascites of only 56%. It is vital for primary care physicians cirrhotic ascites from that (PCPs) to be alert for ascites not only in patients who have risk caused by heart failure factors for chronic liver disease and cirrhosis—eg, a history of or other disorders. C alcohol use disorder, chronic viral infections (hepatitis B and ❯ Recommend sodium C), or metabolic syndrome—but also in patients with abnor- restriction of 4.9-6.9 g for mal liver function tests and thrombocytopenia. In this review, patients with established we discuss the initial assessment of ascites and its long-term ascites secondary management, concentrating on the role of the PCP. to cirrhosis. C ❯ Avoid giving angiotensin- converting enzyme inhibitors, Pathophysiology: angiotensin receptor Vasodilation leads to a cascade blockers, and nonsteroidal Splanchnic vasodilation is the main underlying event trig- anti-inflammatory gering a pathologic cascade that leads to the development drugs in cirrhosis. C of ascites.4 Initially portal hypertension in the setting of liver Strength of recommendation (SOR) inflammation and fibrosis causes the release of inflammato- A Good-quality patient-oriented ry cytokines such as nitric oxide and carbon monoxide. This, evidence in turn, causes the pathologic dilation of splanchnic circula- B Inconsistent or limited-quality patient-oriented evidence tion that decreases effective circulating volume. Activation C Consensus, usual practice, of the sympathetic nervous system, vasopressin, and renin- opinion, disease-oriented angiotensin-aldosterone system (RAAS) then causes the proxi- evidence, case series mal and distal tubules to increase renal absorption of sodium and water.5 The resulting volume overload further decreases the heart’s ability to maintain circulating volume, leading to increased activation of compensating symptoms. This vicious cycle eventually manifests as ascites.6 A complex interplay of cirrhosis-associated immune dys- function (CAID), gut dysbiosis, and increased translocation of microorganisms into ascitic fluid is also an important aspect 174 THE JOURNAL OF FAMILY PRACTICE | MAY 2021 | VOL 70, NO 4 FIGURE 1 Mechanisms of cirrhosis-associated immune dysfunction (CAID)7,8 Damage to hepatocytes, gut dysbiosis, and increased bacterial translocation expose the compromised host immune system to pathogen-associated molecular patterns and damage-associated molecular patterns. Translocated bacteria activate inflammatory cells in gut-associated lymphoid tissue and mesenteric lymph nodes. This causes parallel processes of widespread systemic inflammation, hemodynamic disturbances, and endothelial activation contributing to many complications of cirrhosis, including ascites. A decrease in the ability to act against pathogens, combined with poor clearance by the reticuloendothelial system, leads to increased susceptibility to infections, including spontaneous bacterial peritonitis. Gut dysbiosis Damage to and Cirrhosis hepatocytes bacterial translocation Cirrhosis-associated DAMPs PAMPs immune dysfunction Immune deficiency Systemic inflammation • Damaged reticuloendothelial system • Increased bacterial translocation activates inflammatory cells in GALT • Poor neutrophil and macrophage and MLNs, leading to: phagocytosis and function - elevated levels of inflammatory • Decreased B- and T-cell proliferation cytokines TNFα, IL6, IFNγ and function - endothelial activation and more • NK cells lose cytotoxic effects inflammatory receptors such as • Decreased production of ICAMs, VCAMs complements by liver • Decreased opsonization • Endothelial dysfunction • Hemodynamic disturbances • Increased susceptibility to bacterial infections Manifestations of decompensated cirrhosis, including ascites DAMPs, damage-associated molecular patterns; GALT, gut-associated lymphoid tissue; ICAMs, intercellular adhesion molecules; MLNs, mesenteric lymph nodes; NK, natural killer; PAMPs, pathogen-associated molecular patterns; VCAMs, vascular cell adhesion molecules. of the pathogenesis.7 CAID (FIGURE 1)7,8 is an to the effects of damage-associated molecu- immunodeficient state due to cirrhosis with lar patterns (DAMPs) from hepatocytes and reduced phagocytic activity by neutrophils pathogen-associated molecular patterns and macrophages, T- and B-cell hypopro- (PAMPs) from the gut microbiota on the im- liferation, and reduced cytotoxicity of natu- mune system, which leads to many of the ral killer cells. In parallel, there is increased manifestations of decompensated cirrhosis production of inflammatory cytokines due including ascites.8 CONTINUED MDEDGE.COM/FAMILYMEDICINE VOL 70, NO 4 | MAY 2021 | THE JOURNAL OF FAMILY PRACTICE 175 TABLE Initial work-up for possible cirrhosis-associated ascites History • Ask about abdominal fullness, recent weight gain, ankle edema. • Ask about risk factors for liver disease and ascites: alcohol abuse; features of metabolic syndrome; drug use; unsafe sexual practices; history of travel; history of cardiac, renal, or thyroid disease; or malignancy. Physical exam • Check for distended abdomen, flank dullness, positive shifting dullness, and fluid thrill. • Look for signs of chronic liver disease: spider angiomas, jaundice, caput medusae, tremor/asterixis, palmar erythema, gynecomastia. Labs, imaging • Order blood tests: complete blood count, comprehensive metabolic panel, prothrombin time/ international normalized ratio. • Consider ordering ultrasound to detect abdominal fluid, even if it’s not clinically apparent; it can also detect abnormal liver morphology and signs of portal hypertension (eg, splenomegaly), or locate a site for paracentesis. A Doppler exam can detect patency of hepatic vasculature. Paracentesis • Check cell count and differential, albumin, and total protein on all samples. • Calculate SAAG in ascitic fluid (see FIGURE 2). • Consider obtaining cytology, adenosine deaminase, triglyceride, gram stain, and culture. SAAG, serum ascites albumin gradient. Key in on these elements ascites, may include spider angiomas on the of the history and exam upper trunk (33% of cirrhosis patients),13 Each step of the basic work-up for ascites pro- gynecomastia (44% of cirrhosis patients),14 vides opportunities to refine or redirect the palmar erythema, jaundice, asterixis, and diagnostic inquiry (TABLE). abdominal wall collaterals including caput medusa.15 History We suggest a systematic and targeted Generally, patients with ascites present with approach to using various physical exam weight gain and symptoms of abdominal maneuvers described in the literature. If the distension, such as early satiety, nausea, and patient has a full/distended abdomen, per- vomiting. Besides cirrhosis, rule out other cuss the flanks. If increased dullness at the causes of ascites, as treatment differs based flanks is detected, check for shifting dullness, on the cause.9 Also ask about histories of can- which indicates at least 1500 mL of fluid in the cer and cardiac, renal, or thyroid disease.10 abdomen.16 Keep in mind that a 10% chance Patients with ascites in the setting of of ascites exists even if shifting dullness is liver disease usually are asymptomatic in its absent.17 Maneuvers such as the puddle sign early stages. Common complaints are vague and fluid thrill are less accurate than shift- abdominal pain, generalized weakness, mal- ing dullness, which has 83% sensitivity and aise, and fatigue.11 Ask patients about risk fac- 56% specificity in detecting ascites.17 Patients tors for liver disease such as obesity, diabetes, with cirrhosis also have a high likelihood of hypertension, alcohol use, unsafe sexual complications from ascites such as inguinal, practices, recent travel, and needle sharing umbilical, and other hernias. or drug use. Due to a strong association be- tween obstructive sleep apnea and fatty liver disease, consider screening at-risk patients Diagnostic work-up for sleep apnea.12 includes blood tests and ultrasound ❚ Blood tests. The initial work-up for asci- Physical exam tes should include complete blood count, When there are risk factors for liver disease, complete metabolic panel, and prothrombin examine the patient for stigmata of cirrhosis time/international normalized ratio.18 and ascites. Signs of liver disease, aside from ❚ Abdominal ultrasound is recommend- 176 THE JOURNAL OF FAMILY PRACTICE | MAY 2021 | VOL 70, NO 4 ASCITES IN CIRRHOSIS ed as the first-line imaging test.19 Aside from lated by subtracting the level of ascitic fluid detecting ascites, it can give an estimate of albumin
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