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Chylous, bloody, and pancreatic ascites

Authors: Andrés Cárdenas, MD, PhD, MMSc, AGAF, FAASLD, Andres Gelrud, MD, MMSc, Sanjiv Chopra, MD, MACP
Section Editor: Bruce A Runyon, MD
Deputy Editor: Kristen M Robson, MD, MBA, FACG

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Dec 2020. | This topic last updated: Jun 10, 2019.

CHYLOUS ASCITES

Chylous ascites is a milky-appearing peritoneal fluid that is rich in triglycerides. It is due to the
presence of thoracic or intestinal lymph in the abdominal cavity [1].

Chylous ascites is an uncommon finding with a reported incidence of approximately 1 per

20,000 admissions at a large university-based hospital over a two-decade period [2].
Malignancy, cirrhosis, and lymphatic disruption after abdominal surgery are leading causes in
adults. In children, congenital lymphatic abnormalities and trauma are the most common
cause. Although there have been no recent large epidemiologic studies, it is generally believed
that the incidence has increased due to the longer survival of patients with cancer and more
aggressive abdominal and cardiothoracic interventions.

Pathophysiology — Chylous ascites develops when there is a disruption of the lymphatic

system, which occurs due to traumatic injury or obstruction (from benign or malignant causes).
Three underlying mechanisms have been proposed [3]:

● Obstruction of the lymph flow due to malignancy, causing leakage from dilated subserosal
lymphatics into the peritoneal cavity. The effects of a continuous elevated pressure of the
intestinal lymphatic system may lead to collagen deposition of the basement membrane of
lymphatics, further impairing the absorptive capacity of the intestinal mucosa. This can
ultimately lead to the development of a protein-losing enteropathy with chronic diarrhea
(steatorrhea), malabsorption, and malnutrition. (See "Protein-losing gastroenteropathy".)

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● Exudation of lymph through the walls of dilated retroperitoneal vessels lacking valves,
which leak fluid through a fistula into the peritoneal cavity (ie, congenital
lymphangiectasia).

● Acquired thoracic duct obstruction from trauma or surgery, causing direct leakage of chyle
through a lymphoperitoneal fistula. (See "Etiology, clinical presentation, and diagnosis of
chylothorax".)

Etiology — There are multiple causes of chylous ascites ( table 1). The most common causes
in Western countries are abdominal malignancy, lymphatic abnormalities, and cirrhosis, which
account for over two-thirds of all cases. By contrast, infectious etiologies (ie, tuberculosis and
filariasis) are responsible for the majority of cases in developing countries. Other causes include
congenital, inflammatory, postoperative, traumatic, and miscellaneous disorders.

In a systematic review of 131 studies (with a total of 190 patients) who had atraumatic chylous
ascites, the most common causes in adults were lymphatic anomalies (32 percent), malignancy
(17 percent), cirrhosis (11 percent), Mycobacterium infection (15 percent), and a variety of
uncommon causes (21 percent) [4]. The high prevalence of lymphatic anomalies and
mycobacterial infection reflects the inclusion of studies from developing and developed
countries. In children, the most common causes were lymphatic anomalies (84 percent)
followed by a variety of uncommon causes (15 percent).

The mechanisms leading to the formation of chylous ascites vary with each condition. As
examples:

● Cardiovascular disease, mainly constrictive pericarditis, right-sided heart failure, and

dilated cardiomyopathy, can lead to the development of chylous ascites by increasing
lymphatic pressure [5,6].

● Increased caval and hepatic venous pressures (vascular obstruction) cause a large increase
in the production of hepatic lymph.

● Cirrhosis causes an increased formation of hepatic lymph. Decompression of the portal

vein in patients with portal hypertension may relieve lymphatic hypertension [7-10].

Malignancy — Malignancy is a common cause of chylous ascites in adults. Lymphoma

accounted for at least one-half to one-third of the cases in one large series of patients identified
over 20 years [2]. Obstruction and invasion into the lymphatic channels leads to the disruption
of normal lymphatic flow [11]. Other neoplastic causes include breast, esophageal, pancreatic,
colon, renal, testicular, endometrial, cervical, ovarian, and prostate cancer; Kaposi sarcoma;
carcinoid tumors; and lymphangiomyomatosis [2,12-14]. Carcinoid tumors should be excluded
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in patients with chylous ascites and secretory diarrhea. (See "Clinical characteristics of well-
differentiated neuroendocrine (carcinoid) tumors arising in the gastrointestinal and
genitourinary tracts".)

Cirrhosis — Chylous ascites is present in 0.5 to 1 percent of patients with cirrhosis who have
ascites [7,8,15,16]. The underlying pathophysiology is due to the rupture of serosal lymphatic
channels, which are dilated due to excessive lymph flow (up to 20 liters/day). Why only a subset
of patients with cirrhosis develops it is unclear. It can be a presenting symptom or occur later in
the disease as a consequence of hepatocellular carcinoma, following shunt surgery or a
thoracic duct injury from sclerotherapy [16-18]. An aggressive approach (unless highly
suspected) to exclude malignancy is usually not warranted in a patient with cirrhosis and
chylous ascites. Other causes of portal hypertension, such as portal vein thrombosis, have also
been implicated as a cause of chylous ascites [19,20].

Infectious — Peritoneal tuberculosis and filariasis are the common infectious causes of

chylous ascites.

● Peritoneal tuberculosis occurs worldwide, particularly in areas of low socioeconomic status,

malnutrition, and poor access to medical care [21]. (See "Abdominal tuberculosis".)

● Lymphatic filariasis, a disease caused by the parasite Wuchereria bancrofti, leads to chylous
ascites. This parasite causes a severe inflammatory reaction in the lymphatic vessels,
leading to lymphedema and chylous ascites [22]. (See "Lymphatic filariasis: Epidemiology,
clinical manifestations, and diagnosis".)

● Infection with Mycobacterium avium-intracellulare has been described as a cause of chylous

ascites in patients with AIDS [23-25].

Congenital — Congenital lymphatic abnormalities are more common in the pediatric

population and should be sought in children with chylous ascites.

● Primary lymphatic hypoplasia is a condition characterized by lymphedema, chylothorax,

and/or chylous ascites [26]. Chylous ascites may also be seen with primary lymphatic
hyperplasia [27]. Two forms have been described: "bilateral hyperplasia," in which the
lymphatics are not severely dilated and contain valves; and lymphangiectasia
(megalymphatics), in which the lymphatics are very dilated and lack valves. (See "Clinical
features and diagnosis of peripheral lymphedema".)

● The Klippel-Trenaunay syndrome is an autosomal-dominant disorder in which venous and

lymphatic hypoplastic malformations cause hypertrophy of the tissues of an involved limb,
and it is often associated with chylous ascites [28].
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● The yellow nail syndrome is a disorder of unclear etiology seen in childhood. Patients have
hypoplastic lymphatics leading to chylous effusions. The characteristic triad consists of
lymphedema, pleural effusion and/or chylous ascites, and a yellow discoloration together
with dystrophy of the nails [29]. (See "Protein-losing gastroenteropathy".)

Inflammatory — A variety of inflammatory conditions have been associated with chylous

ascites, including:

● Radiation therapy to the abdomen, causing fibrosis and obstruction of the lymphatic
vessels in the small bowel and mesentery [30].

● Acute or chronic pancreatitis, which can cause the compression of adjacent lymphatic
channels, resulting in chylous ascites and pleural effusions [31].

● Constrictive pericarditis (as described above), which can cause chylous ascites by increasing
hepatic venous pressure, thereby increasing lymph production [6]. This is a reversible and
treatable cause of ascites.

● Other rare inflammatory disorders such as idiopathic retroperitoneal fibrosis or Ormond's

disease, sarcoidosis, retractile mesenteritis, and Whipple's disease [32-36].

Postoperative and traumatic — Chylous ascites can occur early (around one week) after
abdominal surgery due to the disruption of the lymphatic vessels or late (several weeks to
months) due to adhesions or the extrinsic compression of lymphatic vessels [37]. The surgical
procedures that have been associated with chylous ascites include abdominal aortic aneurysm
repair, retroperitoneal lymph node dissection, pancreaticoduodenectomy, inferior vena cava
resection, catheter implantation for peritoneal dialysis, laparoscopic Nissen fundoplication,
distal splenorenal shunts, laparoscopic donor nephrectomy, small bowel and liver
transplantation, and laparoscopic Roux-en-Y gastric bypass [38-51].

Blunt abdominal trauma resulting in intestinal and/or mesenteric injury can also cause chylous
ascites [52]. In children, the Battered Child Syndrome, which accounts for approximately 10
percent of cases of chylous ascites in the pediatric population, should be excluded [53].

Other causes

● Right heart failure and dilated cardiomyopathy can cause impaired drainage of lymph, with
an increase in lymphatic pressure producing stasis, dilation, and chylous ascites [5].
Chylous ascites can also arise as a result of heart failure secondary to thyrotoxic
cardiomyopathy or cardiac amyloidosis [54,55]. Prompt treatment of the heart failure and
hyperthyroid state can resolve the ascites [54].

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● The nephrotic syndrome and focal segmental glomerulosclerosis have been reported to
cause chylous ascites and chylothorax [56-58]. The underlying pathogenesis is not
understood. An illustrative report included 140 patients with nephrotic syndrome, of whom
90 had ascites, and of those, 35 underwent paracentesis [59]. Sixteen patients (52 percent)
had chylous ascites, defined by the presence of milky white ascitic fluid. A limitation of this
study was that triglyceride levels were not measured; thus, some patients may have just
had opalescent effusions.

● Lymphangioleiomyomatosis is a rare disorder of unclear etiology characterized by smooth

muscle proliferation in the lung, lymphatics, and lymph nodes in the mediastinum,
abdomen, and lower cervical region. It affects almost exclusively women of childbearing
age. The disorder can be associated with a variety of clinical manifestations, including
chylous pleural effusions and ascites. (See "Sporadic lymphangioleiomyomatosis:
Epidemiology and pathogenesis".)

● Calcium channel blockers have also been implicated as a cause of chylous ascites in
patients undergoing peritoneal dialysis [60-64].

Clinical manifestations — Chylous ascites frequently presents as progressive and painless

abdominal distention, occurring over the course of weeks to months, depending upon the
underlying cause. The most common presenting symptom was abdominal distension (81
percent) in a systematic review that included 131 studies (with a total of 190 patients) who had
atraumatic chylous ascites [4]. Patients who have undergone abdominal or thoracic surgery
may present with an acute onset.

Patients may complain of weight gain and/or dyspnea resulting from increased abdominal
pressure. Other features include nonspecific abdominal pain, weight loss, diarrhea and
steatorrhea, malnutrition, edema, nausea, enlarged lymph nodes, early satiety, fevers, and
night sweats [2,3,12]. However, in the majority of cases, the diagnosis is not suspected before
performing a diagnostic paracentesis.

Evaluation — A careful history and physical examination should be performed as in any patient
presenting with ascites. The patient should be questioned regarding weight loss or gain,
symptoms of malignancy, family history, recent abdominal surgery, travel, abdominal trauma,
and underlying liver or kidney disease. Constitutional symptoms such as anorexia, weakness,
and malaise are very common, but nonspecific. (See "Evaluation of adults with ascites".)

Findings that may be present on physical examination include a fluid wave, shifting dullness,
pleural effusions, lower extremity edema, lymphadenopathy, cachexia, temporal wasting,
abdominal masses, and hernias. Stigmata of chronic liver disease such as jaundice, palmar
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erythema, spider angiomata of the chest, and encephalopathy may be present in patients with
cirrhosis.

Paracentesis and laboratory data — Abdominal paracentesis is the most important

diagnostic tool in evaluating and managing patients with ascites ( table 2). Chyle typically has
a cloudy and turbid appearance in contrast to the yellow and transparent appearance of ascites
due to cirrhosis and portal hypertension. In some patients with cirrhosis, the appearance of
ascites may be opalescent due to infection or malignancy without actually containing high
levels of triglycerides [65]. (See "Evaluation of adults with ascites".)

The triglyceride levels in ascitic fluid are critical in defining chylous ascites. Triglyceride values
are typically above 200 mg/dL, although some authors use a cutoff value of 110 mg/dL
[1,2,66,67]. The total protein content varies depending upon the underlying cause, ranging
between 2.5 to 7.0 g/dL ( table 2) [66]. The serum to ascites albumin gradient should be
calculated by subtracting the ascitic fluid value of albumin from the serum value to determine if
the ascites is related to portal hypertension or other causes [15,68].

In addition to triglyceride levels, ascitic fluid should be sent for cell count, culture, Gram stain,
total protein concentration, albumin, glucose, lactate dehydrogenase, amylase, and cytology
[68,69]. A tuberculosis smear, culture, and adenosine deaminase (ADA) should be performed in
selected cases when tuberculosis is suspected. ADA is an enzyme involved in the conversion of
adenosine to inosine that is released by macrophages and lymphocytes during cellular immune
response. ADA values in peritoneal fluid are used as an indirect guide for the diagnosis of
tuberculous effusions. Studies outside the United States have reported high sensitivity and
specificity in the diagnosis of tuberculous peritonitis in areas of high prevalence for
tuberculosis. By contrast, the utility of ADA measurement in populations with a high prevalence
of cirrhosis, such as in the United States, is limited [70]. The diagnosis of tuberculous peritonitis
usually requires a peritoneal biopsy. (See "Abdominal tuberculosis".)

Standard blood tests including a complete blood count, electrolytes, liver tests, total protein,
albumin, lactate dehydrogenase, triglycerides, cholesterol, amylase, and lipase should be
performed [68,69]. Additional testing should be based upon the clinical setting.

Radiologic studies — Computed tomography (CT) of the abdomen is useful in identifying

pathologic intra-abdominal lymph nodes and masses. In the setting of postoperative or
traumatic causes of chylous ascites, it also helps in determining the extent and localization of
fluid, particularly if there is a suspicion of thoracic duct injury. Other studies such as non-
contrast magnetic resonance (MR) lymphography, lymphangiography and lymphoscintigraphy
can assist in detecting abnormal retroperitoneal nodes, leakage from dilated lymphatics,

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fistulization, and patency of the thoracic duct [19,71]. Lymphangiography (LAG) is the gold
standard in defining cases of obstruction, but it may be associated with several complications
such as tissue necrosis, fat embolism, and hypersensitivity related to the volume and type of
contrast used [71]. In an analysis of 16 patients with 17 chyle leaks who underwent LAG, the
leak was identified in all cases. The initial LAG alone provided the diagnosis and localized the
chyle leak in four patients, whereas a postprocedure CT scan alone provided the diagnosis and
localized the leak in six patients. Both modalities localized the leak in the remaining six patients.
No major side effects were reported [72]. In addition to imaging the lymphatics and identifying
the site of leakage, lymphangiography may also have therapeutic potential. There are reports of
successful embolization of sites of leakage using microcoils or glue in patients with chylothorax
or chylous ascites [73,74].

Management — The underlying cause should be addressed whenever feasible. In most cases,

correction of the underlying pathology will result in the resolution of symptoms and of the
ascites. This is particularly true of patients who have an infectious, inflammatory, or
hemodynamic cause.

Only a few studies have addressed specific treatments aimed at reducing the ascites formation
[37,75,76]. Based upon the limited data, a reasonable initial approach for patients in whom the
cause cannot be found or for those who do not respond to treatment of the underlying
condition is to recommend a high-protein and low-fat diet with medium-chain triglycerides
(MCT). Dietary restriction of long-chain triglycerides (LCT) avoids their conversion into
monoglycerides and free fatty acids (FFA), which are transported as chylomicrons to the
intestinal lymph ducts. By contrast, MCTs are absorbed directly into intestinal cells and
transported as FFA and glycerol directly to the liver via the portal vein. Thus, a low-fat diet with
MCT supplementation reduces the production and flow of chyle [77-79].

MCT is commercially available as MCT oil. The usual initial oral adult dose of MCT oil for use as a
nutritional supplement is 1 tablespoon three to four times per day. Common adverse effects
are nausea, occasional vomiting, abdominal pain, and diarrhea. MCT oils should be mixed with
fruit juices; used on salads and vegetables; incorporated into sauces for use on fish, chicken, or
lean meats; or used in cooking or baking. MCT oil should not be used in patients with advanced
cirrhosis because narcosis and coma may occur. Such patients should be managed with a low-
sodium diet and diuretics such as spironolactone [69]. (See "Ascites in adults with cirrhosis:
Initial therapy".)

Several other measures have been described in case reports or small observational studies.

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● Orlistat, a reversible inhibitor of gastric and pancreatic lipases, was reported to minimize
ascites and triglyceride levels in ascitic fluid in a patient with chylous ascites due to cirrhosis
[80].

● Somatostatin and octreotide have been used successfully to treat chylous effusions in
patients with the yellow nail syndrome and lymphatic leakage due to abdominal and
thoracic surgery [20,81-85]. Case reports have suggested that both somatostatin and
subcutaneous octreotide are also effective in the management of chylous ascites
[20,83,84,86,87]. The mechanism may involve inhibition of lymph fluid excretion through
specific receptors found in the normal intestinal wall of lymphatic vessels [88,89].

Surgery may benefit patients with postoperative, neoplastic, and congenital causes [12].
However, a systematic review of 36 studies showed that for postoperative chylous ascites,
conservative management was effective in almost all cases [75]. Prior to surgery, a
lymphangiogram or lymphoscintigraphy is helpful in identifying the anatomical location of the
leakage or the presence of a fistula.

In patients with a large amount of ascites, a total paracentesis to relieve abdominal discomfort
and dyspnea should be performed and repeated as needed. The replacement of intravascular
volume with albumin to prevent post-paracentesis circulatory dysfunction is not necessary
unless the patient has cirrhosis. Repeated large-volume paracentesis is a reasonable option for
patients who have end-stage disease not amenable to medical or surgical treatment.

In patients with cirrhosis and chylous ascites refractory to medical therapy and who have
preserved liver function, the insertion of a transjugular intrahepatic portosystemic shunt (TIPS)
can be an effective measure that reduces ascites significantly by decreasing portal pressure
[9,10]. A case series of four patients with cirrhosis revealed that TIPS is safe and effective for the
treatment of cirrhosis-related chylous collections [90]. The placement of TIPS in a patient with
cirrhosis must be carefully evaluated due to the significant problems that may arise after its
placement. (See "Overview of transjugular intrahepatic portosystemic shunts (TIPS)".)

In the past, peritovenous shunting was considered an option for patients who were refractory
to nonoperative treatment. However, shunts were associated with a high rate of complications,
including sepsis, disseminated intravascular coagulation, electrolyte imbalance, small bowel
obstruction, and risk for air embolism, and are thus seldom used. In addition, the high viscosity
of the chyle results in a high rate of shunt occlusion [91,92]. (See "Hepatorenal syndrome",
section on 'Peritoneovenous shunt'.)

BLOODY ASCITES
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Bloody ascites is defined as ascitic fluid in the peritoneal cavity with a red blood cell (RBC) count
greater than 50,000 mm3. The RBC count of ascitic fluid is usually less than 1000 mm3. Ascitic
fluid will be pink colored at a level of approximately 10,000 RBCs.

Etiology — There are several causes of bloody ascites. Bloody ascites occurs in up to 19 percent
of patients with cirrhosis [93]. In such patients, hemoperitoneum may develop spontaneously
or follow a traumatic paracentesis. Most commonly, bloody ascites occurs due to the latter; in
this setting blood usually clots, in contrast to non-traumatic bloody ascites in which the blood is
lysed and will not clot [94]. The presence of non-traumatic bloody ascites in a patient with
cirrhosis is associated with increased morbidity and mortality since such patients frequently
have an underlying malignancy such as hepatocellular carcinoma [93,95,96]. Approximately 20
percent of ascitic fluid samples of patients with malignant ascites are bloody [66]. The majority
of these cases (50 percent) are accounted for by hepatocellular carcinoma [66]. Of samples from
patients with peritoneal carcinomatosis, only approximately 10 percent are bloody. (See
"Malignancy-related ascites".)

Classification — Bloody ascites can be classified according to the underlying cause responsible

for blood leakage. In most cases, the underlying pathophysiology is related to either mass
effect eroding into small vessels or high shear stress over small vessels and lymphatics. These
sites can be divided as follows:

● Hepatic parenchyma – Hepatocellular carcinoma [95], cirrhosis with ruptured varices

[94,96], idiopathic noncirrhotic portal hypertension [94], lymphoma [97], ruptured hepatic
hemangioma [98], and metastatic liver tumors [94].

● Peritoneal involvement – Leiomyoblastoma [99], tuberculosis, and peritoneal dialysis with

sclerosing encapsulating peritonitis [100].

● Adjacent organs – Ovarian cancer [94], endometriosis [101,102], lymphoma [97], prostate
cancer [103], pancreatitis [94], splenic lymphoma [104], bladder rupture [105], and
ruptured ovarian cyst [106].

● Systemic disease – Sarcoidosis [107], systemic lupus erythematosus, immunoglobulin A

vasculitis (Henoch-Schönlein purpura) [108], and parasitic infections (Fasciola hepatica)
[109].

● Cardiovascular disease – Heart failure [110].

● Trauma in patients with cirrhosis – Trauma to spleen or liver following procedures like liver
biopsy, transjugular intrahepatic portosystemic shunt placement, laparoscopy, or
paracentesis.
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Management — In patients with grossly hemorrhagic ascites, paracentesis should be

attempted at a different site to exclude local trauma of a vessel. Abdominal imaging should be
performed with an ultrasound or computed tomography scan if bloody non-traumatic ascites is
confirmed.

Therapy should be directed toward correction of the underlying cause. In cases of traumatic
paracentesis, patients should be observed carefully with strict monitoring of vital signs,
complete blood count, and coagulation studies.

Patients with spontaneously bloody ascites due to cirrhosis in the absence of hepatocellular
carcinoma usually require no special treatment [96]. Patients with bleeding due to the tap itself
usually also have renal failure (based on a study of almost 5000 procedures) and might benefit
from desmopressin [111].

Patients whose bloody ascites is due to hepatocellular carcinoma may benefit from
embolization of the bleeding tumor vessel. An angiogram and surgical consultation should be
sought in patients who continue to show signs of ongoing blood loss (decreasing hemoglobin
level, tachycardia, hypotension).

PANCREATIC ASCITES

Pancreatic ascites is defined as the massive accumulation of pancreatic fluid in the peritoneal
cavity [112]. It mainly occurs due to an ongoing leakage of pancreatic secretions in the
peritoneum due pancreatic duct injury. The level of amylase in the ascitic fluid is typically above
1000 international unit/L, and the ascitic fluid to serum amylase ratio is approximately 6.0 [113].
In one report of eight patients, the ascitic fluid amylase concentration ranged from 280 to 5730
international unit/L, a value more than three times that in the plasma [114].

The most common underlying cause is chronic pancreatitis secondary to alcohol abuse [115]. It
has been described in approximately 4 percent of patients with chronic pancreatitis and in 6 to
14 percent of those with pancreatic pseudocysts [116,117]. It can also occur after an episode of
acute pancreatitis or following a traumatic injury to the pancreas [115]. It has also been
reported to occur after therapeutic endoscopic ultrasonography with fine aspiration of the
pancreas [118,119]. However, as many as two-thirds of patients do not give a history of a recent
attack of pancreatitis [120].

Clinical manifestations — Patients may present with a history of chronic pancreatitis, a recent

episode of acute pancreatitis soon after abdominal trauma, or with new onset ascites. Pain or

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symptoms of pancreatic disease may be absent, especially in alcoholics; as a result, the

diagnosis may be confused with ascites due to cirrhosis and portal hypertension.

A pleural effusion may also be present. In one series, for example, pleural effusion was present
(in addition to pancreatic ascites) in 15 of 28 patients (54 percent) [112,115].

Evaluation — As discussed above, diagnostic paracentesis should be performed in every

patient with ascites. In some cases, the fluid may be serosanguineous or opalescent. If
pancreatic ascites is suspected, routine tests of ascitic fluid such as cell count, culture, Gram
stain, amylase, albumin, and total protein should be obtained. The combination of a serum-
albumin ascites gradient below 1.1 g/dL, a total protein level >3 g/dL, and elevated ascitic
amylase is diagnostic of this condition. In some cases, the white cell count may be elevated due
to concomitant infection of the ascitic fluid. (See "Evaluation of adults with ascites".)

Once the diagnosis has been established, an abdominal computed tomography scan should be
performed to evaluate for a pseudocyst. Many authorities agree that endoscopic retrograde
pancreatography (ERCP) should be performed to localize the site of leakage and to perform
endoscopic therapy (stenting of pancreatic duct) if possible [121-124]. Although there are no
data on the role of magnetic resonance cholangiopancreatography (MRCP) for the diagnosis of
this condition, this test along with secretin stimulation can help demonstrate the normal
pancreatic duct and detect any abnormalities arising from it [125]. Thus, MRCP should be
considered in patients who are poor candidates for ERCP.

Management — Conservative medical treatment should be the first step in managing all

patients. Withholding oral feedings and starting total parenteral nutrition will minimize
pancreatic exocrine secretion [126]. One-third of patients will improve on conservative
management and will not require any further intervention [127]. Treatment with somatostatin
or octreotide together with diuretics and repeated paracentesis may be beneficial for some
patients with mild accumulation of pancreatic ascites [128,129].

Transpapillary pancreatic duct stenting can be attempted in patients with persistent pancreatic
ascites and evidence of ductal disruption by ERCP [114,121-123]. The stent can facilitate healing
of ductal disruptions by partially occluding the leaking duct or bypassing the pancreatic
sphincter, thereby decreasing the intrapancreatic duct pressure. (See "Overview of pancreatic
stenting and its complications".)

Some patients fail medical therapy, ultimately requiring surgery [130]. Indications for surgery
include a persistent or recurrent accumulation of ascites and/or a sudden deterioration of
clinical status. The type of surgical intervention depends upon the ductal anatomy, the site of
the leakage from the pancreatic duct or pseudocyst, and the operative findings. When the
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pancreatic duct is dilated, the ideal procedure is a wide anastomosis between the ruptured duct
and a Roux-en-Y jejunal loop. Patients with a pseudocyst and a mature lining can undergo
internal cyst drainage into a jejunal loop. Distal pancreatic resection followed by duct ligation is
an acceptable alternative if the pancreatic duct is of normal caliber or the abnormality is
localized in the tail of the pancreas [131].

An alternative for patients with pancreatic ascites and evidence of ductal disruption by ERCP is
the placement of a transpapillary pancreatic duct stent [114,121-123]. The stent may facilitate
healing of ductal disruptions by partially occluding the leaking duct or bypassing the pancreatic
sphincter, thereby decreasing the intrapancreatic duct pressure. (See "Overview of pancreatic
stenting and its complications".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Portal hypertension and
ascites".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Fluid in the belly (ascites) (The Basics)")

SUMMARY AND RECOMMENDATIONS

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6/1/2021 Chylous, bloody, and pancreatic ascites - UpToDate

Chylous ascites

● Chylous ascites is a milky-appearing peritoneal fluid that is rich in triglycerides. It develops

when there is a disruption of the lymphatic system, which occurs due to traumatic injury or
obstruction (from benign or malignant causes).

● There are multiple causes of chylous ascites ( table 1). The most common causes in
Western countries are abdominal malignancy and cirrhosis, which account for over two-
thirds of all cases.

● Abdominal paracentesis is the most important diagnostic tool in evaluating and managing
patients with ascites ( table 2). Radiologic evaluation may also be required.

● The underlying cause should be addressed whenever feasible.

● Only a few studies have addressed specific treatments aimed at reducing the ascites
formation. In patients in whom the cause cannot be found or for those who do not respond
to treatment of the underlying condition, we suggest a high-protein and low-fat diet with
medium-chain triglycerides (MCT) (Grade 2C). However, MCT oil should not be used in
patients with advanced cirrhosis because narcosis and coma may occur. Patients who do
not respond to the above measures often need to be treated with ongoing therapeutic
paracentesis. In patients with compensated cirrhosis, a transjugular intrahepatic
portosystemic shunt can be considered.

Bloody ascites

● Bloody ascites is defined as ascitic fluid in the peritoneal cavity with a red blood cell count
greater than 50,000 mm3. There are several causes.

● In patients with grossly hemorrhagic ascites, paracentesis should be attempted at a

different site to exclude local trauma of a vessel. Abdominal imaging should be performed
with an ultrasound or computed tomography scan if bloody non-traumatic ascites is
confirmed. Therapy should be directed toward the correction of the underlying cause.

Pancreatic ascites

● Pancreatic ascites is defined as a massive accumulation of pancreatic fluid in the peritoneal

cavity. The most common underlying cause is chronic pancreatitis secondary to alcohol
abuse.

● We suggest conservative medical treatment as the first step in managing all patients
(Grade 2C). Patients should be kept fasted and started on parenteral nutrition. As many as

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one-third of patients will resolve with this measure alone.

● In patients who do not respond to conservative management, we suggest treatment with

octreotide (50 micrograms given subcutaneously three times daily for two consecutive
weeks) and endoscopic retrograde pancreatography for pancreatic duct stenting (Grade
2C). In patients who fail the above, we suggest evaluation for surgery.

Use of UpToDate is subject to the Subscription and License Agreement.

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in acute and chronic pancreatitis. Digestion 1999; 60 Suppl 2:23.

130. Gómez-Cerezo J, Barbado Cano A, Suárez I, et al. Pancreatic ascites: study of therapeutic
options by analysis of case reports and case series between the years 1975 and 2000. Am J
Gastroenterol 2003; 98:568.

131. da Cunha JE, Machado M, Bacchella T, et al. Surgical treatment of pancreatic ascites and
pancreatic pleural effusions. Hepatogastroenterology 1995; 42:748.

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GRAPHICS

Causes of chylous ascites

Neoplastic (common in adults) Infectious

Lymphoma Tuberculosis

Other cancers (see text) Filariasis (Wuchereria bancrofti)

Lymphangiomyomatosis Mycobacterium avium intracellulare

Carcinoid tumors Inflammatory

Kaposi's sarcoma Radiation

Cirrhosis (common in adults) Pancreatitis

Congenital (common in children) Constrictive pericarditits

Primary lymphatic hypoplasia Retroperitoneal fibrosis

Yellow nail syndrome Sarcoidosis

Klippel-Trenaunay syndrome Celiac sprue

Primary lymphatic hyperplasia Whipple's disease

Bilateral hyperplasia Retractile mesenteritis

Intestinal lymphangiectasia
Trauma
Postoperative Blunt abdominal trauma
Abdominal aneurysm repair Battered child syndrome
Retroperitoneal node dissection

Catheter placement for peritoneal dialysis

Inferior vena cava resection

Laparoscopic nissen fundoplication

Laparoscopic nephrectomy

Other causes
Right heart failure

Dilated cardiomyopathy

Nephrotic syndrome

Calcium channel blockers

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Characteristics of ascitic fluid in chylous ascites

Color Milky and cloudy

Triglyceride level Above 200 mg/dL

Cell count Above 500 (predominance of lymphocytes)

Total protein Between 2.5 - 7.0 g/dL

SAAG Below 1.1 g/dL*

Cholesterol Low (ascites/serum ratio <1)

Lactate dehydrogenase Between 110 - 200 IU/liter

Culture Positive in selected cases of tuberculosis

Adenosine deaminase Elevated in cases of tuberculosis

Cytology Positive in malignancy

Glucose Under 100 mg/dL

Amylase Elevated (>40 IU/liter) in cases of acute or chronic pancreatitis

SAAG: serum-ascites albumin gradient; IU: international units.

* Level above 1.1 g/dL in chylous ascites secondary to cirrhosis.

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Contributor Disclosures
Andrés Cárdenas, MD, PhD, MMSc, AGAF, FAASLD Grant/Research/Clinical Trial Support: Boston
Scientific Corporation [Endoscopy in biliary complications after liver transplantation]. Consultant/Advisory
Boards: Boston Scientific Corporation [Endoscopy in biliary complications after liver
transplantation]. Andres Gelrud, MD, MMSc Consultant/Advisory Boards: AbbVie [Pancreatic exocrine
insufficiency]; Boston Scientific [Biliary, pancreatic, and enteral stents]; Akcea [Pancreatitis]; Ariel [Genetic
testing]. Speaker's Bureau: AbbVie [Pancreatic insufficiency]. Sanjiv Chopra, MD, MACP Nothing to
disclose Bruce A Runyon, MD Consultant/Advisory Boards: Mallinckrodt. Kristen M Robson, MD, MBA,
FACG Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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