Chylous ascytes secondary to acute pancreatitis: a case report and review of literature
Ascitis quilosa secundaria a pancreatitis: caso clínico y revisión de la bibliografía
J. M. Gómez-Martín1, E. Martínez-Molina2, A. Sanjuanbenito2, E. Martín-Illana3, F. Arrieta1, J. A. Balsa1, I. Zamarrón1, C. Vázquez1,4 and J. I. Botella-Carretero1,4
1Unit of Clinical Nutrition and Dietetics. Department of Endocrinology and Nutrition.
2Department of General Surgery.
3Department of Radiology. ]]>
4CIBER de Fisiopatología de la Obesidad y Nutrición (CIBEROBN). Hospital Universitario Ramón y Cajal. IRYCIS. Madrid. España.
ABSTRACT
Chylous ascites is an uncommon finding which is due to the presence of thoracic or intestinal lymph in the abdominal cavity. It is usually caused by a chronic disruption of the lymphatic system. The present report is one of the rare cases in the literature of chylous ascites secondary to idiopathic acute pancreatitis, which showed a complete resolution with a combination of low fat enteral nutrition with MCT and somatostatin analogs.
Key words: Chylous ascites. Acute idiopathic pancreatitis. Medium chain triglycerides. Somastotin analogs.
RESUMEN
La ascitis quilosa es un hallazgo infrecuente producido por la presencia de linfa de origen torácico o intestinal en la cavidad abdominal. Normalmente es producido por la disfunción crónica del sistema linfático. El caso que presentamos es uno de los pocos casos descritos en la literatura de ascitis quilosa secundaria a una pancreatitis aguda idiopática, que se resolvió completamente con una combinación de dieta enteral baja en grasas con triglicéridos de cadena media y análogos de somatostatina.
Palabras clave: Ascitis quilosa. Pancreatitis aguda idiopática. Triglicéridos de cadena media. Análogos de somatostatina.
Introduction
Chylous ascites is an uncommon finding1 which is due to the presence of thoracic or intestinal lymph in the abdominal cavity.2 It is usually caused by a chronic disruption of the lymphatic system. The proposed pathophysiological mechanism includes the obstruction of the lymph flow through the dilated subserosal lymphatics into the peritoneal cavity which produces collagen deposition, fibrosis, and protein-losing enteropathy. Other mechanisms that have been involved are the exudation of lymph through the walls of congenital or acquired dilated retroperitoneal vessels into the abdominal cavity, and the obstruction from direct trauma of the thoracic duct3. Its diagnosis is based on the biochemical study of the ascitic fluid. The most important and extended diagnostic criterion is the presence of > 2.3 mM (> 200 mg/dl) of triglycerides in ascitic fluid.1,2,4,5.
Acute and chronic pancreatitis are known causes of chylous ascites. By causing inflammation of the abdominal structures, with compression of the lymphatic vessels, lymph effuses into the abdominal cavity. Besides it can also produce pleural lymphatic effusion and consequent chylothorax.6
Eight cases of chylous ascites associated with acute pancreatitis have been reported so far. Three of them occurred in alcohol drinkers, two associated with enolic acute pancreatitis7,8 and the other one in acute on chronic pancreatitis.9 Three other cases took place in hyperlipidemia-associated acute pancreatitis, two during pregnancy,10,11 and the other one in a familiar hyperlipidemia context.12 The remaining two cases occurred in patients with gallbladder stone disease.13,14 Here we report an uncommon case of insidious chylous ascites following a severe acute idiopathic pancreatitis, in a 68y old woman, which was resolved with somatostatin analogs and artificial nutritional support.
Case report
A 68y old woman came to the emergency room suffering from upper abdominal pain, nausea, and occasional vomiting which started several hours before. The patient had not any relevant medical history, she was not an alcohol drinker, nor had she suffered from pancreatitis before. At admission she had an arterial pressure of 112/62 mmHg, a heart rate of 80 beats per minute, and a temperature of 36o C. Physical examination revealed only an epigastric pain irradiated to both left and right hypochondria without peritoneal irritation.
The first blood test showed a serum amylase of 5,257 U/L, lypase of 8,392 U/L, leucocytes of 17,700 per μL, with transaminases, and other analytical parameters within normal ranges. Radiological images of thorax and abdomen did not show any pathological findings, and abdominal ultrasound showed a normal biliary duct diameter without gallstones, and a hypogenic, globulous, and increased in size pancreas. The pancreatic tail was not well defined in ultrasound, which suggested an incipient pancreatic collection.
The patient was diagnosed of acute pancreatitis, and admitted to the Gastroenterology ward, with intravenous fluid therapy, antibiotics and analgesic drugs. Four days later, an abdominal CT scan was performed. It revealed multiple mesenteric collections, a pancreatic cyst, and fluid in the abdominal cavity, all these findings compatible with an E Balthazar's degree pancreatitis. The following day the patient developed fever of 38o C, and progressive anemia with dyspnea. She moved to the Intensive Care Unit, where she received intravenous antibiotic therapy, blood transfusions, and total parenteral nutrition support. After six days in the Intensive Care Unit she improved, and moved again to the Gastroenterology ward with the following diagnoses: Systemic Inflammatory Response Syndrome (SIRS) possibly triggered by acute pancreatitis, with a severity index of 4.
]]> One week later a study of the ascitic fluid was performed showing a pancreatic amylase > 900 U/L, which confirmed the pancreatic origin of the ascites. That day multiple abdominal drainages were placed in the abdominal collections, somatostatin analogs were started and a nasojejunal tube was placed in order to start enteral nutrition. The patient progressively improved as shown by her clinical and analytical parameters (amylase 44 U/L, lipase 24 U/L, leucocytes 6,000 per μL, Hb 9.1 g/dL). Also the abdominal collections and ascites were reduced and an oral diet was started. Several days later, the patient worsened again with fever of 39o C and abdominal pain. A CT scan was performed showing more abdominal collections and a greater amount of ascitic fluid (fig. 1 and 2).
The patient moved to the General Surgery ward in order to drain abdominal collections. Four days later, a new ascitic fluid analysis showed > 4,000 mg/dL of triglycerides, > 200 mg/dL of cholesterol, no microbiologic findings, and pancreatic amylase in normal range. After the confirmation of chylous ascites, total parenteral nutrition through a Peripheral Inserted Central Catheter (PICC) and somatostatin analogs were started.
Ten days later this catheter was replaced with a jugular central line because of local phlebitis. After twenty one days of total parenteral nutrition, the jugular line had to be removed due to candidemia, and appropriate therapy was started. Culture of the line tip was positive for Candida parapsilosis. At this time enteral nutrition support was progressively introduced. The chosen enteral nutrition formula (MonogenTM, Nutricia Advanced Medical Nutrition-Danone Group) had a 25% of total calories as lipid, and 90% of these lipids were medium chained triglycerides (MCT).
Radiological tests showed a progressive decrease of the intra-abdominal collections and ascitic fluid. The patient was discharged after three months with a low fat diet and oral enteral nutrition (1,500 mL/day of MonogenTM) and subsequently followed-up monthly. Two years later, with radiological evidence of no abdominal collections not any remnant ascitic fluid, she went on a free diet. Her weight increased 8.5 kg (from 45.5 kg to 54 kg) with an increase of body mass index (BMI) of 3.5 kg/m2 (from 18.7 kg/m2 to 22.2 kg/m2) (table I). The patient is now, three years after hospital discharge, on a free diet with a normal body weight and no signs or symptoms of ascites.
Discussion
The incidence of chylous ascites in developed countries is approximately one case per 20,000 admissions, although large epidemiological studies are lacking.1 Among known causes of chylous ascites there are many pathological processes such as cirrhosis, infections, malignancy, congenital defects, traumatism, inflammatory processes, nephropathies and cardiopathies (table II). Two-thirds of all chylous ascites present in developed countries as a consequence of abdominal malignancy1,15 and cirrhosis.16-19 The incidence has increased in the past years due to longer survival of oncologic patients. In contrast infectious etiologies such as tuberculosis20 or filariasis, 21 are responsible for the majority of the cases in developing countries.
After extensive medical database search on Medline and Embase, only eight cases of chylous ascites secondary to acute pancreatitis have been reported in english literature before, with different etiologies (table III). All these cases occurred in the context of alcohol abuse, gallbladder stone disease, or lipids disorders.
Treatment of the underlying cause is a cornerstone in this entity whenever possible.22-24 The resolution of chylous ascites usually takes several weeks,25,26 but in some cases like ours, it may take months, or even some years after resolution of the underlying cause. In our case, we found no specific cause for the acute pancreatitis, so it was regarded as idiopathic. Therefore, the development and resolution of chylous ascites was more insidious than in previous reported cases, and the time between pancreatitis and chylous ascites onset was also longer.7-14 Our case shows for the first time a case of idiopathic acute pancreatitis-associated chylous ascites.
When ascites persists after the resolution of the underlying cause, it is recommended a high protein and low lipid diet, the latter in the form of medium chain triglycerides (MCT). This type of triglycerides is directly absorbed from the bowel to the portal circulation, without passing through the lymph vessels, and it reduces the production and flow of lymph. On the other hand, long chain triglycerides in diet must be avoided, as these are converted into free fatty acids and monoglycerides which are transported through the lymphatic system.22,23,25 There are some enteral nutrition products with a high percentage of MCT. We chose one which provides only a 25% of total fat, with 90% as MCT, and also additional supplements of vitamins, minerals and oligoelements. This composition is specially designed for the treatment of chylothorax, chylous ascites, and other processes with impaired lymph circulation.
Somatostatin analogs have been successfully used in different forms of chylous ascites. Somatostatin is known to inhibit a variety of gastrointestinal processes, hormones and secretions. Although they have been used successfully in the treatment of chylous ascites, the mechanism of action in these disorders remains unclear, and need further research.8,25,27-30 Patients who do not improve with enteral nutrition and somatostatin analogs can be managed with home parenteral nutrition with variable results.26,31-33
The present report is one of the rare cases in the literature of chylous ascites seco*ndary to idiopathic acute pancreatitis, which showed a complete resolution with a combination of low fat enteral nutrition with MCT and somatostatin analogs.
References
]]>1. Press OW, Press NO, Kaufman SD. Evaluation and management of chylous ascites. Ann Intern Med 1982; 96: 358-364. [ Links ]
2. Cardenas A, Chopra S. Chylous ascites. Am J Gastroenterol 2002; 97: 1896-1900. [ Links ]
3. Browse NL, Wilson NM, Russo F, Al-Hassan H, Allen DR. Aetiology and treatment of chylous ascites. Br J Surg 1992; 79: 1145-1150. [ Links ]
4. Moss R, Hinds S, Fedullo AJ. Chylothorax: a complication of the nephrotic syndrome. Am Rev Respir Dis 1989; 140: 1436-1437. [ Links ]
5. Kato A, Kohno S, Ohtake T, Takita T, Hirshida A. Chylous ascites in an adult patient with nephrotic syndrome due to membranous nephropathy. Nephron 2001; 89: 361-362. [ Links ]
]]>6. Hurst PA, Edwards JM. Chylous ascites and obstructive lymphoedema of the small bowel following abdominal radiotherapy. Br J Surg 1979; 66: 780-781. [ Links ]
7. Al-Ghamdi MY, Bedi A, Reddy SB, Tanton RT, Peltekian KM. Chylous ascites secondary to pancreatitis: management of an uncommon entity using parenteral nutrition and octreotide. Dig Dis Sci 2007; 52: 2261-2264. [ Links ]
8. Goldfarb JP. Chylous effusions secondary to pancreatitis: case report and review of the literature. Am J Gastroenterol 1984; 79: 133-135. [ Links ]
9. Smith EK, Ek E, Croagh D, Spain LA, Farrell S. Acute chylous ascites mimicking acute appendicitis in a patient with pancreatitis. World J Gastroenterol 2009; 15: 4849-4852. [ Links ]
10. Chuang SC, Lee KT, Wang SN, Kuo KK, Chen JS. Hypertriglyceridemia-associated acute pancreatitis with chylous ascites in pregnancy. J Formos Med Assoc 2006; 105: 583-587. [ Links ]
]]>11. Liu CJ, Yen CL, Chang JJ, Lee TS, Fan KM. Chylous ascites in acute pancreatitis during pregnancy: case report. Chang Gung Med J 2001; 24: 324-328. [ Links ]
12. Khan FY, Matar I. Chylous ascites secondary to hyperlipidemic pancreatitis with normal serum amylase and lipase. World J Gastroenterol 2007; 13: 480-482. [ Links ]
13. Ben-Ami H, Nagachandran P, Assalia A, Edoute Y. Acute transient chylous ascites associated with acute biliary pancreatitis. Am J Med Sci 1999; 318: 122-123. [ Links ]
14. Pérez Fontán M, Pombo F, Soto A, Pérez Fontán FJ, Rodríguez-Carmona A. Chylous ascites associated with acute pancreatitis in a patient undergoing continuous ambulatory peritoneal dialysis. Nephron 1993; 63: 458-461. [ Links ]
15. Kinney TB, Ferrara SL, Miller FJ, Roberts AC, Hassanein T. Transjugular intrahepatic portosystemic shunt creation as treatment for refractory chylous ascites and chylothorax in a patient with cirrhosis. J Vasc Interv Radiol 2004; 15: 85-89. [ Links ]
]]>16. Cheng WS, Gough IR, Ward M, Croese J, Powell LW. Chylous ascites in cirrhosis: a case report and review of the literature. J Gastroenterol Hepatol 1989; 4: 95-99. [ Links ]
17. Rector WG, Jr. Spontaneous chylous ascites of cirrhosis. J Clin Gastroenterol 1984; 6: 369-372. [ Links ]
18. Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992; 117: 215-220. [ Links ]
19. Sultan S, Pauwels A, Poupon R, Levy VG. Chylous ascites in cirrhosis. Retrospective study of 20 cases. Gastroenterol Clin Biol 1990; 14: 842-847. [ Links ]
20. Jhittay PS, Wolverson RL, Wilson AO. Acute chylous peritonitis with associated intestinal tuberculosis. J Pediatr Surg 1986; 21: 75-76. [ Links ]
]]>21. Patel KC. Filariasis, chyluria and chylous effusion. J Assoc Physicians India 1983; 31: 801-803. [ Links ]
22. Runyon BA, Akriviadis EA, Keyser AJ. The opacity of portal hypertension-related ascites correlates with the fluid's triglyceride concentration. Am J Clin Pathol 1991; 96: 142-143. [ Links ]
23. Runyon BA, Hoefs JC, Morgan TR. Ascitic fluid analysis in malignancy-related ascites. Hepatology 1988; 8: 1104-1109. [ Links ]
24. Isenberg JI, Gilbert SB, Pitcher JL. Ascites with peritoneal involvement in Whipple's disease. Report of a case. Gastroenterology 1971; 60: 305-310. [ Links ]
25. Leibovitch I, Mor Y, Golomb J, Ramon J. The diagnosis and management of postoperative chylous ascites. J Urol 2002; 167: 449-457. [ Links ]
]]>26. Lee YY, Soong WJ, Lee YS, Hwang B. Total parenteral nutrition as a primary therapeutic modality for congenital chylous ascites: report of one case. Acta Paediatr Taiwan 2002; 43: 214-216. [ Links ]
27. Leong RW, House AK, Jeffrey GP. Chylous ascites caused by portal vein thrombosis treated with octreotide. J Gastroenterol Hepatol 2003; 18: 1211-1213. [ Links ]
28. Runyon BA. Care of patients with ascites. N Engl J Med 1994; 330: 337-342. [ Links ]
29. Weinstein LD, Scanlon GT, Hersh T. Chylous ascites. Management with medium-chain triglycerides and exacerbation by lymphangiography. Am J Dig Dis 1969; 14: 500-509. [ Links ]
30. Reubi JC, Horisberger U, Waser B, Gebbers JO, Laissue J. Preferential location of somatostatin receptors in germinal centers of human gut lymphoid tissue. Gastroenterology 1992; 103: 1207-1214. [ Links ]
]]>31. Kroczek RA. Congenital chyloperitoneum: direct comparison of medium-chain triglyceride treatment with total parenteral nutrition. Eur J Pediatr 1985; 144: 77-79. [ Links ]
32. Alliet P, Young C, Lebenthal E. Chylous ascites: total parenteral nutrition as primary therapeutic modality. Eur J Pediatr 1992; 151: 213-214. [ Links ]
33. Huang Q, Jiang ZW, Jiang J, Li N, Li JS. Chylous ascites: treated with total parenteral nutrition and somatostatin. World J Gastroenterol 2004; 10: 2588-2591. [ Links ]
Correspondence:
José I. Botella-Carretero. ]]>
Unit of Clinical Nutrition and Dietetics.
Department of Endocrinology and Nutrition, and CIBER
de Fisiopatología de la Obesidad y Nutrición (CIBEROBN).
Hospital Universitario Ramón y Cajal.
Carretera de Colmenar, km. 9,1.
28034 Madrid. Spain.
E-mail: jbotella.hrc@salud.madrid.org
Recibido: 13-IX-2011.
Aceptado: 17-IX-2011.