Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
A case of inflammatory ascites E. Guidetti, M. Galassi, L. Croci, B. Stagni, C. Crespi, F. Tovoli & L. Bolondi To cite this article: E. Guidetti, M. Galassi, L. Croci, B. Stagni, C. Crespi, F. Tovoli & L. Bolondi (2014) A case of inflammatory ascites, Acta Clinica Belgica, 69:3, 204-207, DOI: 10.1179/2295333713Y.0000000001 To link to this article: http://dx.doi.org/10.1179/2295333713Y.0000000001
Published online: 13 Mar 2014.
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Gazi University]
Date: 25 March 2016, At: 22:41
Case Report
A case of inflammatory ascites E. Guidetti1, M. Galassi1, L. Croci1, B. Stagni2, C. Crespi2, F. Tovoli1, L. Bolondi1 1
Department of Medical and Surgical Sciences, University of Bologna, Italy, 2Department of Digestive Diseases and Internal Medicine, Bologna University Hospital Authority St. Orsola-Malpighi Polyclinic, Italy
Downloaded by [Gazi University] at 22:41 25 March 2016
Case background: Ascites appears mainly as a consequence of portal hypertension in patients with liver cirrhosis, or can be caused by several other causes, such us congestive heart failure, peritoneal malignancy, or tuberculosis. In some cases, ascites can pose a diagnostic challenge for clinicians and in some patients, despite thorough and extensive work-up, the origin of this ascites remains unknown. Case report: In the unusual case hereby reported, a 52-year-old man developed severe ascites in a few weeks, in the absence of known liver disease or congestive hearth failure. We performed laboratory analysis, endoscopic, and imaging investigations, including abdominal contrast-enhanced computed tomography and 18-fluorodeoxyglucose-positron emission tomography. Peritoneal fluid analysis showed exudative fluid without neoplastic cells. A diagnostic laparoscopy with multiple diagnostic biopsies was carried out, but no macroscopic cause of the ascites was found; histopathological examination showed minimal aspects of diffuse and non-specific chronic inflammation. Conclusions: We decided to empirically treat the patient with steroid therapy (methylprednisolone: 0.5 mg/ kg/day). Over a period of 6 weeks, his ascites resolved and at 2 months, he was in remission on low-dose methylprednisolone. Our final hypothesis was reactive inflammatory ascites. The literature on ascites and its management has also been reviewed. Keywords: Ascites, Polyserositis, Paracentesis
Introduction Ascites is a frequent symptom in clinical practice and one of the major causes of hospitalization in internal medicine. Nonetheless, differential diagnosis process may sometimes require an extensive work-up for the clinician. Herein, we report a case of male patient who came to our attention for a rapid onset of ascites without a history of liver disease, malignancies, autoimmune disease, or malignancies. Diagnostic work-up, including laparoscopy, did not show any major causes of ascites. A diagnosis of ‘inflammatory ascites’ was made and the patient was successfully treated with empirical steroid therapy.
Case Report A 52-year-old man patient was admitted to our clinic in October 2012, complaining abdominal distension and abdominal pain lasting for 2 months, associated with mild dyspnoea. He reached an isolated febrile peak a few days before the onset of the symptoms. His past medical history was not significant. He denied recent travels abroad, as well as alcohol, tobacco, or drugs intake at admission.
Correspondence to: E. Guidetti, Department of Medical and Surgical Sciences, University of Bologna, Via Massarenti 9, 40100 Bologna, Italy. Email: [email protected]
204
ß Acta Clinica Belgica 2014 DOI 10.1179/2295333713Y.0000000001
He has no fever, his blood pressure was 120/ 80 mmHg, and his pulse rate was 96 beats/min. Heart and lung physical examination was normal. Ascites was detected at abdominal examination without hepatosplenomegaly or palpable abdominal masses or superficial lymphoadenopaties. There was no oedema in his extremities and hepatojugular reflex was absent. No signs of hepatic disease, such as icterus or spider naevi, were found. Abdominal ultrasound examination revealed massive ascites without signs of chronic liver disease or portal venous hypertension (Fig. 1). Patient was treated with high dose of furosemide without reduction of ascites. Laboratory tests showed elevated C-reactive protein (63.6 upper normal limit) with normal erythrocyte sedimentation rate and fibrinogen serum levels, and slightly increased beta2-microglobulin (6.3 mg/ dl, normal values ,2 mg/dl). Complete blood cells count, liver, kidney, thyroid function tests, serum electrolytes, prothrombin time, total proteins, albumin, and immunoglobulins C3 and C4 were within normal range. No proteinuria was detected at urinalysis. Neoplastic markers (including CA 19-9, carcinoembryonic antigen, alpha-fetoprotein, and prostate-specific antigen) were normal.
Acta Clinica Belgica
2014
VOL.
69
NO.
3
Guidetti et al.
Downloaded by [Gazi University] at 22:41 25 March 2016
Figure 1 Abdominal ultrasound shows severe ascites without signs of liver cirrhosis.
Antinuclear antibodies, extractable nuclear antigen antibodies, and antineutrophilic cytoplasmic antibodies were absent. HIV and hepatitis B and C virus serum markers resulted negative. A diagnostic paracentesis was performed with evacuation of 5 l of yellow clear ascitic fluid. Chemical–physical examination of the fluid showed total proteins 5120 mg/dl, albumin 3.1 g/dl, glucose 109 mg/dl, lactate dehydrogenase 1294 U/l, total bilirubin 0.54 mg/dl, and total amylase of 43 U/l. Serum–ascites albumin gradient (SAAG) was suggestive of exudative ascites (0.39 g/dl). Cell count performed on the ascitic fluid revealed 390 cells/mmc (35% lymphocites, 35% mono-macrophages, 20% neutrophils, 7% eosinophils, 3% basophils). Lymphocyte typing described a cellularity represented by phenotypically normal T and B lymphocytes. Peritoneal fluid levels of CA 19-9 and carcinoembryonic antigen were within normal range and no malignant cells were found at the cytological examination. Cultures for bacteria and mycobacteria, as well as PCR for Mycobacterium tuberculosis, were negative. QuantiFERON test was negative. An abdominal contrast-enhanced computed tomography scan was obtained to further investigate the hypothesis of some neoplastic process and confirmed the presence of severe ascites with a small amount of pleural and pericardial effusions. An inhomogeneous region in the pancreatic head and some centimetric mesenteric lymph nodes were described, but no clear evidence of focal mass lesion was found. The endoscopic ultrasound examination revealed an increased in size of pancreatic gland with an inhomogeneous echotexture, but without focal lesions (consistently with chronic pancreatitis). In addition, an 18-fluorodeoxyglucose-positron emission tomography demonstrated minimum hyperfixation
Inflammatory ascites
at the level of aorto-caval and mesenteric lymph nodes with very low levels of standardized uptake values. Colonoscopy and esophagogastroduodenoscopy including mucosal biopsies were unremarkable. The electrocardiogram was normal and the echocardiography confirmed a minimal pericardial effusion. Since the cause of ascites remained obscure, our patient underwent a diagnostic laparoscopy with evacuation of 13 l of ascites. Multiple random biopsies of the parietal and visceral peritoneum and hepatic parenchyma were performed. No macroscopic lesions of major abdominal organs and peritoneum were found. Histopathological examination of biopsy specimen revealed focal hepatic steatosis and minimal aspects of diffuse chronic inflammation of the peritoneum. No findings consistent with neoplastic processes or chronic liver diseases were found. We decided to empirically treat our patient with steroid drugs (methylprednisolone 0.5 mg/kg/day). Over a period of 6 weeks, his ascites resolved and 2 months later, he was in remission on low-dose methylprednisolone. One month after the treatment, an ultrasonographic examination and contrastenhanced computed tomography revealed complete resolution of ascites and lymphoadenopaties. The repetition of biochemistry examination showed the normalization of C-reactive protein and beta2microglobulin’s value.
Discussion The main aetiology of ascites is liver cirrhosis followed by cancer, congestive heart failure, tuberculosis, dialysis, pancreatic disease, and other rare causes (Table 1). The most frequent causes of neoplastic ascites are ovarian, endometrial, breast, gastric, colorectal, pancreatic, hepatobiliary, or primary peritoneal carcinomas. Less than 10% of all patient with malignant ascites have tumours of unknown origin.1 The history and physical examination of a patient with new onset ascites often suggests the diagnosis. In particular, the patient’s clinical history should be investigated for liver disease, malignancy, heart failure, pancreatic disease, tuberculosis, underlying bacterial, fungal or parasitic infection, nephrosis, and autoimmune disease. The presence of abdominal distension, peripheral limphedema, and stigmata of cirrhosis such as vascular spiders, palmar erythema, or collateral circulation, should be evaluated on physical examination. Ultrasound can provide information about the presence of abdominal fluid, liver cirrhosis, portal hypertension, venocclusive disease, congestive heart failure, and focal abdominal mass.
Acta Clinica Belgica
2014
VOL .
69
NO .
3
205
Guidetti et al.
Inflammatory ascites
Table 1 Rare aethiology of ascites INFECTIOUS CAUSES Amebiasis Ascariasis Brucellosis Chlamydia peritonitis Salmonellosis Whipple’s disease Complications related to HIV infection Pelvic inflammatory disease IMMUNOLOGICAL DISORDERS Systemic lupus erythematosus Vasculitis HEMATOLOGIC DISORDERS
Downloaded by [Gazi University] at 22:41 25 March 2016
Amyloidosis Histiocytosis X Leukemia Lymphoma Mastocytosis Multiple myeloma OTHER CAUSES Eosinophilic gastroenteritis Nephrotic syndrome Ovarian hyperstimulation syndrome Endometriosis Crohn’s disease Lymphangioleiomyomatosis Myxedema POEMS syndrome Ventriculoperitoneal shunt Familial Mediterranean fever
Paracentesis with ascitic fluid analysis represents the key tool for the diagnosis. Appearance of ascitic fluid can be helpful in differential diagnosis process: clear fluid suggests uncomplicated ascites, milky fluid suggests chylous ascites, torbid fluid can suggest infectious diseases such as spontaneous bacterial peritonitis, and bloody ascites can be due to traumatic paracentesis or neoplastic disease. Ascites can be classified as an exudate or a transudate, based on total protein and the SAAG.2 This gradient correlates with the presence (.1.1 g/dl) or absence (,1.1 g/dl) of portal hypertension, with a specificity of 96.7%.2 If the SAAG is less than 1.1 g/dl or the total protein is more than 2.5 g/dl, in our patients, ascites could be considered as an exudate. In this case, the differential diagnosis should include malignancy, peritoneal carcinomatosis, tuberculosis peritonitis, spontaneous bacterial peritonitis, or secondary peritonitis. On the other hand, an SAAG .1.1 characterizes a transudative ascites; in this case, the differential diagnosis process includes liver cirrhosis, cardiac failure, portal vein thrombosis, Budd–Chiari syndrome, and other minor aetiologies.
206
Acta Clinica Belgica
2014
VOL .
69
NO .
3
There are a lot of other laboratory examinations to differentiate ascitic fluid. The routine tests include cell count with differential culture in blood culture bottles. Optional tests are represented by glucose concentration, lactate dehydrogenase, Gram stain, and amylase concentration. Finally, unusual tests like tuberculosis smear and colture, cytology, triglyceride, and bilirubin concentration can be performed.1 Further steps in the diagnostic work-up depend on the findings of previous investigations. In our case, we ruled out any major cause of transudative ascites. The presence of pleural and pericardial effusions associated with ascites could induce the suspect of serum membranes inflammation, due to autoimmune disorders, such as lupus erythematosus (SLE), Still’s disease, and others. The occurrence of peritonitis in SLE patients is about 8–11%, but typically, it presents during disease’s flare. Rarely, ascites have been reported as initial presentation of SLE.3 However, in our case, circulating autoantibodies, such as antinuclear antibodies and anti-dsDNA, as well as other classificative criteria for SLE, were absent. Familiar Mediterranean fever is another rare cause of polyserositis with possible massive ascites. It is an autosomal recessive disease characterized by recurrent fever, polyserositis, and abdominal pain.4 In our case, there was no history or family history of recurrent fever. Accordingly, our case could not be framed in any of the major causes of exudative ascites. ‘Ascites of unknown origin’ is defined as a condition in which abdominal effusion aetiology cannot be determined with conventional procedures as laboratory tests, peritoneal fluid analysis ,and imaging investigations. In patients with ascites of unknown origin, laparoscopy in combination with biopsy can disclose the causes of unexplained ascites in the majority of cases. An American laparoscopy study revealed that about 60% of 51 cases with previously unexplained ascites actually suffered from a chronic liver disease or intra-abdominal malignancy.5 Conversely, an African study showed that 40% of 92 cases of ascites of unknown origin had tuberculous peritonitis.6 These data suggest that the origin of ascites changes according to the geographic area and ethnic origin. In 15% of cases, diagnosis remains unexplained even after laparoscopy.7 In our patients, diagnostic laparoscopy with multiple diagnostic specimens was unremarkable. Histology showed diffuse aspects of chronic inflammation, but no definite cause of inflammation was detected. Consequently, our final diagnosis was ‘inflammatory ascites’.
Guidetti et al.
References 1 Runyon BA. Diagnosis and evaluation of patients with ascites. UPTODATE. 2013; http://www.uptodate.com/contents/ evaluation-of-adults-with-ascites. 2 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. 3 Weinstein PJ, Noyer CM. Rapid onset of massive ascites as the initial presentation of systemic lupus erythematosus. Am J Gastroenterol. 2000;95:302–3. 4 Aslan M, Demir G, Esen R, Du¨lger AC, Beg˘enik H, C ¸ elik Y, et al. A rare cause of massive ascites: familial Mediterranean fever. Turk J Gastroenterol. 2012;23:290–3. 5 Gine`s P, Ca´rdenas A, Arroyo V, Rode´s J. Management of cirrhosis and ascites. N Engl J Med. 2004;350:1646–54. 6 Menzies RI, Fitzgerald JM, Mulpeter K. Laparoscopic diagnosis of ascites in Lesotho. Br Med J (Clin Res Ed). 1985;291:473–5. 7 Han CM, Lee CL, Huang KG, Chu CM, Lin SM, Wang CJ, et al. Diagnostic laparoscopy in ascites of unknown origin: Chang Gung Memorial Hospital 20-year experience. Chang Gung Med J. 2008;31:378–83.
Downloaded by [Gazi University] at 22:41 25 March 2016
The febrile peak, which preceded by a week the onset of the polyserositis, suggested a possible reactive ascites. The dramatic and persistent response to the empirical steroid therapy, confirmed at the follow-up, also confirmed our hypothesis of reactive inflammatory ascites. To our knowledge, no data regarding reactive ascites or polyserositis are available in the literature. We therefore suggest that reactive inflammatory ascites should be considered as a rare cause of abdominal effusion, which can require an extensive work-up in order to rule out other more common and life-threatening conditions. Finally, our case also suggests that these patients can greatly benefit from a medium-dose, slowly tapered, steroid therapy.
Inflammatory ascites
Acta Clinica Belgica
2014
VOL .
69
NO .
3
207
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
A case of inflammatory ascites E. Guidetti, M. Galassi, L. Croci, B. Stagni, C. Crespi, F. Tovoli & L. Bolondi To cite this article: E. Guidetti, M. Galassi, L. Croci, B. Stagni, C. Crespi, F. Tovoli & L. Bolondi (2014) A case of inflammatory ascites, Acta Clinica Belgica, 69:3, 204-207, DOI: 10.1179/2295333713Y.0000000001 To link to this article: http://dx.doi.org/10.1179/2295333713Y.0000000001
Published online: 13 Mar 2014.
Submit your article to this journal
Article views: 28
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Gazi University]
Date: 25 March 2016, At: 22:41
Case Report
A case of inflammatory ascites E. Guidetti1, M. Galassi1, L. Croci1, B. Stagni2, C. Crespi2, F. Tovoli1, L. Bolondi1 1
Department of Medical and Surgical Sciences, University of Bologna, Italy, 2Department of Digestive Diseases and Internal Medicine, Bologna University Hospital Authority St. Orsola-Malpighi Polyclinic, Italy
Downloaded by [Gazi University] at 22:41 25 March 2016
Case background: Ascites appears mainly as a consequence of portal hypertension in patients with liver cirrhosis, or can be caused by several other causes, such us congestive heart failure, peritoneal malignancy, or tuberculosis. In some cases, ascites can pose a diagnostic challenge for clinicians and in some patients, despite thorough and extensive work-up, the origin of this ascites remains unknown. Case report: In the unusual case hereby reported, a 52-year-old man developed severe ascites in a few weeks, in the absence of known liver disease or congestive hearth failure. We performed laboratory analysis, endoscopic, and imaging investigations, including abdominal contrast-enhanced computed tomography and 18-fluorodeoxyglucose-positron emission tomography. Peritoneal fluid analysis showed exudative fluid without neoplastic cells. A diagnostic laparoscopy with multiple diagnostic biopsies was carried out, but no macroscopic cause of the ascites was found; histopathological examination showed minimal aspects of diffuse and non-specific chronic inflammation. Conclusions: We decided to empirically treat the patient with steroid therapy (methylprednisolone: 0.5 mg/ kg/day). Over a period of 6 weeks, his ascites resolved and at 2 months, he was in remission on low-dose methylprednisolone. Our final hypothesis was reactive inflammatory ascites. The literature on ascites and its management has also been reviewed. Keywords: Ascites, Polyserositis, Paracentesis
Introduction Ascites is a frequent symptom in clinical practice and one of the major causes of hospitalization in internal medicine. Nonetheless, differential diagnosis process may sometimes require an extensive work-up for the clinician. Herein, we report a case of male patient who came to our attention for a rapid onset of ascites without a history of liver disease, malignancies, autoimmune disease, or malignancies. Diagnostic work-up, including laparoscopy, did not show any major causes of ascites. A diagnosis of ‘inflammatory ascites’ was made and the patient was successfully treated with empirical steroid therapy.
Case Report A 52-year-old man patient was admitted to our clinic in October 2012, complaining abdominal distension and abdominal pain lasting for 2 months, associated with mild dyspnoea. He reached an isolated febrile peak a few days before the onset of the symptoms. His past medical history was not significant. He denied recent travels abroad, as well as alcohol, tobacco, or drugs intake at admission.
Correspondence to: E. Guidetti, Department of Medical and Surgical Sciences, University of Bologna, Via Massarenti 9, 40100 Bologna, Italy. Email: [email protected]
204
ß Acta Clinica Belgica 2014 DOI 10.1179/2295333713Y.0000000001
He has no fever, his blood pressure was 120/ 80 mmHg, and his pulse rate was 96 beats/min. Heart and lung physical examination was normal. Ascites was detected at abdominal examination without hepatosplenomegaly or palpable abdominal masses or superficial lymphoadenopaties. There was no oedema in his extremities and hepatojugular reflex was absent. No signs of hepatic disease, such as icterus or spider naevi, were found. Abdominal ultrasound examination revealed massive ascites without signs of chronic liver disease or portal venous hypertension (Fig. 1). Patient was treated with high dose of furosemide without reduction of ascites. Laboratory tests showed elevated C-reactive protein (63.6 upper normal limit) with normal erythrocyte sedimentation rate and fibrinogen serum levels, and slightly increased beta2-microglobulin (6.3 mg/ dl, normal values ,2 mg/dl). Complete blood cells count, liver, kidney, thyroid function tests, serum electrolytes, prothrombin time, total proteins, albumin, and immunoglobulins C3 and C4 were within normal range. No proteinuria was detected at urinalysis. Neoplastic markers (including CA 19-9, carcinoembryonic antigen, alpha-fetoprotein, and prostate-specific antigen) were normal.
Acta Clinica Belgica
2014
VOL.
69
NO.
3
Guidetti et al.
Downloaded by [Gazi University] at 22:41 25 March 2016
Figure 1 Abdominal ultrasound shows severe ascites without signs of liver cirrhosis.
Antinuclear antibodies, extractable nuclear antigen antibodies, and antineutrophilic cytoplasmic antibodies were absent. HIV and hepatitis B and C virus serum markers resulted negative. A diagnostic paracentesis was performed with evacuation of 5 l of yellow clear ascitic fluid. Chemical–physical examination of the fluid showed total proteins 5120 mg/dl, albumin 3.1 g/dl, glucose 109 mg/dl, lactate dehydrogenase 1294 U/l, total bilirubin 0.54 mg/dl, and total amylase of 43 U/l. Serum–ascites albumin gradient (SAAG) was suggestive of exudative ascites (0.39 g/dl). Cell count performed on the ascitic fluid revealed 390 cells/mmc (35% lymphocites, 35% mono-macrophages, 20% neutrophils, 7% eosinophils, 3% basophils). Lymphocyte typing described a cellularity represented by phenotypically normal T and B lymphocytes. Peritoneal fluid levels of CA 19-9 and carcinoembryonic antigen were within normal range and no malignant cells were found at the cytological examination. Cultures for bacteria and mycobacteria, as well as PCR for Mycobacterium tuberculosis, were negative. QuantiFERON test was negative. An abdominal contrast-enhanced computed tomography scan was obtained to further investigate the hypothesis of some neoplastic process and confirmed the presence of severe ascites with a small amount of pleural and pericardial effusions. An inhomogeneous region in the pancreatic head and some centimetric mesenteric lymph nodes were described, but no clear evidence of focal mass lesion was found. The endoscopic ultrasound examination revealed an increased in size of pancreatic gland with an inhomogeneous echotexture, but without focal lesions (consistently with chronic pancreatitis). In addition, an 18-fluorodeoxyglucose-positron emission tomography demonstrated minimum hyperfixation
Inflammatory ascites
at the level of aorto-caval and mesenteric lymph nodes with very low levels of standardized uptake values. Colonoscopy and esophagogastroduodenoscopy including mucosal biopsies were unremarkable. The electrocardiogram was normal and the echocardiography confirmed a minimal pericardial effusion. Since the cause of ascites remained obscure, our patient underwent a diagnostic laparoscopy with evacuation of 13 l of ascites. Multiple random biopsies of the parietal and visceral peritoneum and hepatic parenchyma were performed. No macroscopic lesions of major abdominal organs and peritoneum were found. Histopathological examination of biopsy specimen revealed focal hepatic steatosis and minimal aspects of diffuse chronic inflammation of the peritoneum. No findings consistent with neoplastic processes or chronic liver diseases were found. We decided to empirically treat our patient with steroid drugs (methylprednisolone 0.5 mg/kg/day). Over a period of 6 weeks, his ascites resolved and 2 months later, he was in remission on low-dose methylprednisolone. One month after the treatment, an ultrasonographic examination and contrastenhanced computed tomography revealed complete resolution of ascites and lymphoadenopaties. The repetition of biochemistry examination showed the normalization of C-reactive protein and beta2microglobulin’s value.
Discussion The main aetiology of ascites is liver cirrhosis followed by cancer, congestive heart failure, tuberculosis, dialysis, pancreatic disease, and other rare causes (Table 1). The most frequent causes of neoplastic ascites are ovarian, endometrial, breast, gastric, colorectal, pancreatic, hepatobiliary, or primary peritoneal carcinomas. Less than 10% of all patient with malignant ascites have tumours of unknown origin.1 The history and physical examination of a patient with new onset ascites often suggests the diagnosis. In particular, the patient’s clinical history should be investigated for liver disease, malignancy, heart failure, pancreatic disease, tuberculosis, underlying bacterial, fungal or parasitic infection, nephrosis, and autoimmune disease. The presence of abdominal distension, peripheral limphedema, and stigmata of cirrhosis such as vascular spiders, palmar erythema, or collateral circulation, should be evaluated on physical examination. Ultrasound can provide information about the presence of abdominal fluid, liver cirrhosis, portal hypertension, venocclusive disease, congestive heart failure, and focal abdominal mass.
Acta Clinica Belgica
2014
VOL .
69
NO .
3
205
Guidetti et al.
Inflammatory ascites
Table 1 Rare aethiology of ascites INFECTIOUS CAUSES Amebiasis Ascariasis Brucellosis Chlamydia peritonitis Salmonellosis Whipple’s disease Complications related to HIV infection Pelvic inflammatory disease IMMUNOLOGICAL DISORDERS Systemic lupus erythematosus Vasculitis HEMATOLOGIC DISORDERS
Downloaded by [Gazi University] at 22:41 25 March 2016
Amyloidosis Histiocytosis X Leukemia Lymphoma Mastocytosis Multiple myeloma OTHER CAUSES Eosinophilic gastroenteritis Nephrotic syndrome Ovarian hyperstimulation syndrome Endometriosis Crohn’s disease Lymphangioleiomyomatosis Myxedema POEMS syndrome Ventriculoperitoneal shunt Familial Mediterranean fever
Paracentesis with ascitic fluid analysis represents the key tool for the diagnosis. Appearance of ascitic fluid can be helpful in differential diagnosis process: clear fluid suggests uncomplicated ascites, milky fluid suggests chylous ascites, torbid fluid can suggest infectious diseases such as spontaneous bacterial peritonitis, and bloody ascites can be due to traumatic paracentesis or neoplastic disease. Ascites can be classified as an exudate or a transudate, based on total protein and the SAAG.2 This gradient correlates with the presence (.1.1 g/dl) or absence (,1.1 g/dl) of portal hypertension, with a specificity of 96.7%.2 If the SAAG is less than 1.1 g/dl or the total protein is more than 2.5 g/dl, in our patients, ascites could be considered as an exudate. In this case, the differential diagnosis should include malignancy, peritoneal carcinomatosis, tuberculosis peritonitis, spontaneous bacterial peritonitis, or secondary peritonitis. On the other hand, an SAAG .1.1 characterizes a transudative ascites; in this case, the differential diagnosis process includes liver cirrhosis, cardiac failure, portal vein thrombosis, Budd–Chiari syndrome, and other minor aetiologies.
206
Acta Clinica Belgica
2014
VOL .
69
NO .
3
There are a lot of other laboratory examinations to differentiate ascitic fluid. The routine tests include cell count with differential culture in blood culture bottles. Optional tests are represented by glucose concentration, lactate dehydrogenase, Gram stain, and amylase concentration. Finally, unusual tests like tuberculosis smear and colture, cytology, triglyceride, and bilirubin concentration can be performed.1 Further steps in the diagnostic work-up depend on the findings of previous investigations. In our case, we ruled out any major cause of transudative ascites. The presence of pleural and pericardial effusions associated with ascites could induce the suspect of serum membranes inflammation, due to autoimmune disorders, such as lupus erythematosus (SLE), Still’s disease, and others. The occurrence of peritonitis in SLE patients is about 8–11%, but typically, it presents during disease’s flare. Rarely, ascites have been reported as initial presentation of SLE.3 However, in our case, circulating autoantibodies, such as antinuclear antibodies and anti-dsDNA, as well as other classificative criteria for SLE, were absent. Familiar Mediterranean fever is another rare cause of polyserositis with possible massive ascites. It is an autosomal recessive disease characterized by recurrent fever, polyserositis, and abdominal pain.4 In our case, there was no history or family history of recurrent fever. Accordingly, our case could not be framed in any of the major causes of exudative ascites. ‘Ascites of unknown origin’ is defined as a condition in which abdominal effusion aetiology cannot be determined with conventional procedures as laboratory tests, peritoneal fluid analysis ,and imaging investigations. In patients with ascites of unknown origin, laparoscopy in combination with biopsy can disclose the causes of unexplained ascites in the majority of cases. An American laparoscopy study revealed that about 60% of 51 cases with previously unexplained ascites actually suffered from a chronic liver disease or intra-abdominal malignancy.5 Conversely, an African study showed that 40% of 92 cases of ascites of unknown origin had tuberculous peritonitis.6 These data suggest that the origin of ascites changes according to the geographic area and ethnic origin. In 15% of cases, diagnosis remains unexplained even after laparoscopy.7 In our patients, diagnostic laparoscopy with multiple diagnostic specimens was unremarkable. Histology showed diffuse aspects of chronic inflammation, but no definite cause of inflammation was detected. Consequently, our final diagnosis was ‘inflammatory ascites’.
Guidetti et al.
References 1 Runyon BA. Diagnosis and evaluation of patients with ascites. UPTODATE. 2013; http://www.uptodate.com/contents/ evaluation-of-adults-with-ascites. 2 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. 3 Weinstein PJ, Noyer CM. Rapid onset of massive ascites as the initial presentation of systemic lupus erythematosus. Am J Gastroenterol. 2000;95:302–3. 4 Aslan M, Demir G, Esen R, Du¨lger AC, Beg˘enik H, C ¸ elik Y, et al. A rare cause of massive ascites: familial Mediterranean fever. Turk J Gastroenterol. 2012;23:290–3. 5 Gine`s P, Ca´rdenas A, Arroyo V, Rode´s J. Management of cirrhosis and ascites. N Engl J Med. 2004;350:1646–54. 6 Menzies RI, Fitzgerald JM, Mulpeter K. Laparoscopic diagnosis of ascites in Lesotho. Br Med J (Clin Res Ed). 1985;291:473–5. 7 Han CM, Lee CL, Huang KG, Chu CM, Lin SM, Wang CJ, et al. Diagnostic laparoscopy in ascites of unknown origin: Chang Gung Memorial Hospital 20-year experience. Chang Gung Med J. 2008;31:378–83.
Downloaded by [Gazi University] at 22:41 25 March 2016
The febrile peak, which preceded by a week the onset of the polyserositis, suggested a possible reactive ascites. The dramatic and persistent response to the empirical steroid therapy, confirmed at the follow-up, also confirmed our hypothesis of reactive inflammatory ascites. To our knowledge, no data regarding reactive ascites or polyserositis are available in the literature. We therefore suggest that reactive inflammatory ascites should be considered as a rare cause of abdominal effusion, which can require an extensive work-up in order to rule out other more common and life-threatening conditions. Finally, our case also suggests that these patients can greatly benefit from a medium-dose, slowly tapered, steroid therapy.
Inflammatory ascites
Acta Clinica Belgica
2014
VOL .
69
NO .
3
207
