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Ascites - from Basics to Bedside CHAPTER Ascites - From Basics to Bedside 71 Harbir Kaur Rao, Rajinder Singh Gupta INTRODUCTION little or no fluid in the peritoneal cavity but women The term ascites denotes the pathological accumulation normally may have up to 20ml depending on the phase of fluid in the peritoneal cavity. Healthy men have of menstrual cycle. Causes of ascites may be classified into two pathophysiologic categories: That associated Table 1: Causes of Ascites with the normal peritoneum and that which occur due to Normal Peritoneum Diseased peritoneum a diseased peritoneum. Cirrhosis accounts for 84 percent (SAAG < 1.1g/dL) of all cases of ascites, whereas Cardiac ascites, peritoneal Portal hypertension carcinomatosis and mixed ascites resulting from cirrhosis (SAAG > 1.1g/ dL) Infections and a second disease account for 10-15% of cases. Less 1. Hepatic congestion Bacterial peritonitis common causes of ascites include massive hepatic Congestive heart failure Tuberculous peritonitis metastasis, peritoneal tuberculosis, and pancreatitis and Nephrotic syndrome. Various causes of ascites are Constrictive pericarditis Fungal peritonitis enumerated in Table 1. Tricuspid insufficiency HIV-associated peritonitis PATHOGENESIS Budd-Chiari syndrome Malignant conditions Pathogenesis of ascites is different in cases with cirrhosis Veno-Occlusive disease Peritoneal carcinomatosis and without the cirrhosis. 2. Liver Disease Primary mesothelioma Pathogenesis in Cirrhosis Cases Cirrhosis Pseudomyxoma peritonei The presence of portal hypertension contributes to the Alcoholic Hepatitis Massive hepatic development of ascites in patients who have cirrhosis. metastases There is an increase in Intrahepatic resistance, causing Fulminant hepatic increased portal pressure, but there is also vasodilatation failure Hepatocellular carcinoma of the splanchnic arterial system, which in turn Massive hepatic Other Conditions results in an increase in portal venous inflow. Both of metastases Familial mediterranean these abnormalities result in increased production of Hepatic Fibrosis fever splanchnic lymph. Vasodilating factors such as vascular endothelial growth factor and nitric oxide are responsible Acute Fatty liver of Vasculitis for the vasodilatory effect. These hemodynamic changes pregnancy Granulomatous peritonitis cause activation of the RAAS with the development of 3. Portal vein occlusion Eosinophilic peritonitis hyperaldosteronism and hence sodium retention. These Hypoalbuminemia renal effects of increased aldosterone also contribute (SAAG < 1.1g/dL) to the development of ascites. Sodium retention causes Nephrotic syndrome Cirrhosis Protein- losing enteropathy Portal Hypertensi on Severe malnutrition with Anasarca Splanchnic vasodiltation Miscellaneous conditions (SAAG < 1.1g/dL) ↑ Splanchnic pressure Arterial underfilling Chylous ascites Pancreatic ascites Lymph formation Activation of Bile ascites vasoconstrictors and Formation of ascites antinatriuretic factors Nephrogenic ascites Myxedema (SAAG > 1.1g/ dL) Plasma Volume Expansion Sodium Retention Ovarian disease Fig. 1: Development of Ascites in Cirrhosis 330 fluid accumulation and expansion of extra cellular fluid may be present. Anasarca results from cardiac failure volume which results in the formation of peripheral or nephrotic syndrome with hypoalbuminemia. Finally, oedema and ascites. Sodium retention is the consequence firm lymph nodes in the left superclavicular region or of a homeostatic response caused by the under filling of umbilicus may suggest intra-abdominal malignancy. arterial circulation secondary to arterial vasodilatation in The physical examination is relatively insensitive for the splanchnic vascular bed. Because the retained fluid is detecting ascitic fluid. In general, patients must have constantly leaking out of the intravascular compartment in at least 1500mL of fluid to be detected reliably by this to peritoneal cavity, the sensation of vascular filling is not method. Even the experienced clinician may find it achieved and the process continuous. Hypoalbuminemia difficult to distinguish between obesity and small-volume and reduced oncotic pressure also contribute to the loss of ascites. Abdominal ultrasound establishes the presence of fluid from the vascular compartment into the peritoneal fluid. cavity. Hypoalbuminemia is due to decreased synthetic function in the liver. Figure 1 is brief illustration of Physical Examination Pathogenesis of ascites in cirrhosis. Physical examination should include an assessment for signs of systemic disease. The presence of Pathogenesis in the Absence Of Cirrhosis lymphadenopathy, especially supraclavicular HEPATOLOGY Ascites in the absence of cirrhosis generally results lymphadenopathy (Vorchow’s node), suggests metastatic from peritoneal carcinomatosis, peritoneal infection or abdominal malignancy. Care should be taken during the pancreatic disease. Peritoneal carcinomatosis can result cardiac examination to evaluate for elevation of jugular from primary malignancies such as mesothelioma or venous pressure (JVP); Kussmaul’s sign (elevation of sarcoma, secondary to abdominal malignancies such as the JVP during inspiration); a pericardial knock, which gastric or colon adenocarcinoma, metastatic disease from may be seen in heart failure of constrictive pericarditis; breast or lung carcinoma or melanoma. Tumour cells or a murmur of tricuspid regurgitation. Spider angiomas, lining the peritoneum produce a protein rich fluid that palmar erythema, dilated superficial veins around the contributes to the development of ascites. Fluid from the umbilicus (caput medusae), and gynecomastia suggest extra cellular space is drawn into the peritoneum, further chronic liver disease. contributing to the development of ascites. Tuberculous peritonitis causes ascites via a similar mechanism; tubercles The abdominal examination should begin with inspection deposited on the peritoneum exude a proteinaceons fluid. for the presence of uneven distention or an obvious Pancreatic ascites results from the leakage of pancreatic mass. Auscultation should follow. The absence of bowel enzymes into the Peritoneum. sounds or the presence of high-pitched localized bowel sounds points toward an ileus or intestinal obstruction. CLINICAL FEATURES An umbilical venous hum may suggest the presence of Symptoms and Signs portal hypertension, and a harsh bruit over the liver is The history usually is one of increasing abdominal girth, heard rarely in patients with hepatocellular carcinoma. with the presence of abdominal pain depending on the Abdominal swelling caused by intestinal gas can be cause. Because most astices is secondary to chronic differentiated from swelling caused by fluid or a solid liver disease with portal hypertension, patients should mass by percussion; an abdomen filled with gas is be asked about risk factors for liver disease, especially tympanic, whereas an abdomen containing a mass or fluid alcohol consumption, transfusions, tattoos, injection drug is dull to percussion. The absence of abdominal dullness, use, a history of viral hepatitis or jaundice, and birth in an however, does not exclude ascites, because a minimum area endemic for hepatitis. A history of cancer or marked of 1500 ml. of ascites fluid is required for detection on weight loss arouses suspicion of malignant ascites. physical examination. Finally, the abdomen should be Fever may suggest infected peritoneal fluid, including palpated to assess for tenderness, a mass, enlargement bacterial peritonitis (spontaneous or secondary). Patients of the spleen or liver, or presence of a nodular liver with chronic liver disease and ascites are at greatest suggesting cirrhoses or tumor. Light palpation of the liver risk for developing spontaneous bacterial peritonitis. In may detect pulsations suggesting retrograde vascular immigrants, immunocompromised hosts, or severely flow from the heart in patients with right-sided heart malnourished alcoholics, tuberculous peritonitis should failure, particularly tricuspid regurgitation. be considerd. EVALUATION Physical examination should emphasize signs of portal Once the presence of ascites has been confirmed, the hypertension and chronic liver disease. Elevated jugular etiology of the ascites is best determined by paracentesis. venous pressure may suggest right-sided congestive heart The left lower quadrant is preferred because of the failure or constrictive pericarditis. A large tender liver is greater depth of ascites and the thinner abdominal wall. characteristic of acute alcoholic hepatitis or Budd-Chiari Paracentesis is a safe procedure even in patients with syndrome. The presence of large abdominal wall veins coagulopathy; complications, including abdominal wall with cephalad flow also suggests portal hypertension; hematomas, hypotension, hepatorenal syndrome, and inferiorly directed flow implies hepatic vein obstruction. infection are infrequent. Signs of chronic liver disease include palmar erythema, Once ascitic fluid has been extracted, its gross appearance cutaneous spider angiomas, gynecomastia, and muscle should be examined. Turbid fluid can result from wasting. Asterixis secondary to hepatic encephalopathy presence of infection or tumor cells. White, milky fluid SAAG volume and ventricular wall stretch. High levels of 331 BNP in serum occur in heart failure and may be useful >1.1 g/dL <1.1g/dL in identifying heart failure as the cause of high-SAAG ascites. Further tests are indicated only in specific clinical Ascites protein Ascites protein <2.5g/dL >2.5g/dL
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