Massive Ascites (massive + ascites)

Distribution by Scientific Domains


Selected Abstracts


Massive ascites after living donor liver transplantation with a right lobe graft larger than 0.8% of the recipient's body weight

CLINICAL TRANSPLANTATION, Issue 4 2010
Yasumasa Shirouzu
Shirouzu Y, Ohya Y, Suda H, Asonuma K, Inomata Y. Massive ascites after living donor liver transplantation with a right lobe graft larger than 0.8% of the recipient's body weight. Clin Transplant 2010: 24: 520,527. © 2009 John Wiley & Sons A/S. Abstract:, Background:, There are only limited data on post-transplant ascites unrelated to small-sized grafts in living donor liver transplantation (LDLT). Methods:, The subjects were 59 adult patients who had received right lobe LDLT with a graft weight-to-recipient weight ratio (GRWR) > 0.8%. Patients were divided into either Group 1 (n = 14, massive ascites, defined as the production of ascitic fluid > 1000 mL/d that lasted longer than 14 d after LDLT) or Group 2 (n = 45, no development of massive ascites). Patients were followed for a median period of 3.0 yr (range, 0.5,7.5 yr). Results:, Group 1 had both higher Model for End-Stage Liver Disease score and Child-Pugh score than Group 2. Portal venous flow volume just after reperfusion was significantly greater in Group 1 than Group 2 (307.8 ± 268.8 vs. 176.2 ± 75.0 mL/min/100 g graft weight, respectively; p < 0.05). Post-transplant infectious complications including ascites infection developed more frequently within the first post-transplant month in Group 1. Massive ascites was significantly associated with early graft loss (p < 0.05). Conclusion:, Post-transplant massive ascites associated with portal over-perfusion into the graft liver can develop in patients with a GRWR over 0.8%. Recipients with post-transplant massive ascites require careful management to prevent infection. [source]


Association of non-alcoholic steatohepatitis (NASH) with chronic neutrophilic leukemia

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2004
Chikashi Yoshida
Abstract: A 54-yr-old female having chronic neutrophilic leukemia (CNL) associated with severe liver injury is presented. Physical examination on admission showed severe jaundice, hepatosplenomegaly, massive ascites, and pretibial edema. Complete blood count showed a hemoglobin level of 9.1 g/dL, platelet count of 25.8 × 104/,L, and white blood cell count of 36.6 × 103/,L with 89.7% neutrophils. Blood chemistry showed hyperbilirubinemia (21.9 mg/dL) with normal transaminase levels. There was no abnormality in serum cholesterol, triglyceride, or glucose levels. Neutrophil alkaline phosphatase activity was significantly elevated. Bone marrow aspiration showed myeloid hyperplasia with normal karyotype. Rearrangement of the bcr/abl was not detected by either polymerase chain reaction or fluorescence in situ hybridization. Human androgen receptor gene assay (HUMARA) of the bone marrow cells showed clonal proliferation of neutrophils. The patient was diagnosed as having CNL. To evaluate the pathogenesis of the liver injury, a needle biopsy was performed, which showed steatohepatitis with infiltration of neutrophils. As the patient had no history of alcohol abuse, a diagnosis of non-alcoholic steatohepatitis (NASH) was made. Assuming that the infiltration of abnormal neutrophils into the liver contributed to the development of NASH, she was treated with cytoreductive chemotherapy (cytosine arabinoside: 100 mg/d, 1,3 doses/wk). With decreases in white blood cell counts, serum bilirubin levels decreased gradually to 1.5 mg/mL. A postchemotherapy liver biopsy specimen showed marked improvement of the fatty degenerative change. To our knowledge, this is the first report describing the development of NASH in a myeloproliferative disorder. We believe that the infiltration of leukemic cells contributed to the development of NASH in this patient. [source]


Intracavitary administration of OK-432 with subcutaneous priming for malignant ascites in a case of advanced renal cell carcinoma

INTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2002
YUKIO KAGEYAMA
Abstract The intracavitary injection of OK-432 (a streptococcal preparation) with subcutaneous priming has been shown to be an effective immunotherapy for patients with malignant effusion. We applied this treatment in a case of advanced renal cell carcinoma with massive ascites. The patient received 0.2 Klinishe Einheit (KE) OK-432 in the subcutaneous injection twice (day 1 and day 7) followed by 10KE OK-432 intra-abdominal administration (day 9). The treatment was performed safely without major side-effects except for transient pyrexia. A significant reduction of ascites was noted 1 month after the treatment without subsequent re-accumulation. Intracavitary injection of OK-432 with subcutaneous priming seems to be a simple, safe and effective treatment for ascites in advanced renal cell carcinoma. [source]


Power Doppler sonography of the kidney: Effect of Valsalva's maneuver

JOURNAL OF CLINICAL ULTRASOUND, Issue 7 2001
Ryuichi Takano MD
Abstract Purpose It has been reported that an intra-abdominal pressure (IAP) above 15 mm Hg may cause oliguria and that an IAP above 25 mm Hg may cause anuria. Because Valsalva's maneuver yields an IAP exceeding 180 mm Hg, it is presumed to affect renal perfusion. We evaluated the ability of power Doppler sonography to depict the changes in renal blood flow during Valsalva's maneuver. Methods Seven healthy men aged 21,24 years and 1 50-year-old man with massive ascites participated in the study. With each healthy subject lying in a supine position, longitudinal power Doppler sonograms of the kidney were obtained and analyzed semiquantitatively during Valsalva's maneuver. Also, in the patient with massive ascites, power Doppler sonography was performed before and after paracentesis. Results Along with an increase in IAP, monitored as expiratory pressure during Valsalva's maneuver, power Doppler signals decreased as indicated by both visual impression and computer scores. In the patient with massive ascites, signal intensity increased after paracentesis. Conclusions Our results demonstrated that an increase in IAP within the physiologic range affects renal perfusion and that power Doppler sonography depicts semiquantitatively the change in renal blood flow. © 2001 John Wiley & Sons, Inc. J Clin Ultra- 29:384,388, 2001. [source]


Another patient with an umbilical hernia and massive ascites: What to do?

LIVER TRANSPLANTATION, Issue 1 2008
James D. Perkins M.D. Special Editor
Background Optimal management in patients with umbilical hernias and liver cirrhosis with ascites is still under debate. The objective of this study was to compare the outcome in our series of operative versus conservative treatment of these patients. Methods In the period between 1990 and 2004, 34 patients with an umbilical hernia combined with liver cirrhosis and ascites were identified from our hospital database. In 17 patients, treatment consisted of elective hernia repair, and 13 were managed conservatively. Four patients underwent hernia repair during liver transplantation. Results Elective hernia repair was successful without complications and recurrence in 12 out of 17 patients. Complications occurred in 3 of these 17 patients, consisting of wound-related problems and recurrence in 4 out 17. Success rate of the initial conservative management was only 23%; hospital admittance for incarcerations occurred in 10 of 13 patients, of which 6 required hernia repair in an emergency setting. Two patients of the initially conservative managed group died from complications of the umbilical hernia. In the 4 patients that underwent hernia correction during liver transplantation, no complications occurred and 1 patient had a recurrence. Conclusions Conservative management of umbilical hernias in patients with liver cirrhosis and ascites leads to a high rate of incarcerations with subsequent hernia repair in an emergency setting, whereas elective repair can be performed with less morbidity and is therefore advocated. [source]


Fetal hydrops associated with spontaneous premature closure of ductus arteriosus

PATHOLOGY INTERNATIONAL, Issue 9 2006
Takeshi Kondo
A 36-year-old woman presenting with fetal growth restriction in the 25th week of gestation was referred to Kobe University Hospital where hydrops fetalis was detected. A stillborn fetus, 2012 g in weight and 40 cm in height, was delivered in the 33rd week of gestation. The mother had no past history of non-steroidal anti-inflammatory drug (NSAID) use during the pregnancy. The male fetus showed maceration without macroscopic anomalies, but it was markedly edematous with bilateral pleural effusion and massive ascites. The autopsy revealed an enlarged heart and aortic coarctation in the region of the ductus arteriosus. A mild form of aortic coarctation and premature closure of the ductus arteriosus with fibrous thickening of the wall were observed. The lungs were atelectatic with vascular dilatation and congestion. This is the first documented case of hydrops fetalis caused by spontaneous premature closure of the ductus arteriosus concomitant with aortic coarctation. The findings suggest that some form of idiopathic, or spontaneous, closure of the ductus arteriosus can be one of the causes of chronic fetal heart failure, coarctation of the aorta, and fetal hydrops. [source]


Massive ascites after living donor liver transplantation with a right lobe graft larger than 0.8% of the recipient's body weight

CLINICAL TRANSPLANTATION, Issue 4 2010
Yasumasa Shirouzu
Shirouzu Y, Ohya Y, Suda H, Asonuma K, Inomata Y. Massive ascites after living donor liver transplantation with a right lobe graft larger than 0.8% of the recipient's body weight. Clin Transplant 2010: 24: 520,527. © 2009 John Wiley & Sons A/S. Abstract:, Background:, There are only limited data on post-transplant ascites unrelated to small-sized grafts in living donor liver transplantation (LDLT). Methods:, The subjects were 59 adult patients who had received right lobe LDLT with a graft weight-to-recipient weight ratio (GRWR) > 0.8%. Patients were divided into either Group 1 (n = 14, massive ascites, defined as the production of ascitic fluid > 1000 mL/d that lasted longer than 14 d after LDLT) or Group 2 (n = 45, no development of massive ascites). Patients were followed for a median period of 3.0 yr (range, 0.5,7.5 yr). Results:, Group 1 had both higher Model for End-Stage Liver Disease score and Child-Pugh score than Group 2. Portal venous flow volume just after reperfusion was significantly greater in Group 1 than Group 2 (307.8 ± 268.8 vs. 176.2 ± 75.0 mL/min/100 g graft weight, respectively; p < 0.05). Post-transplant infectious complications including ascites infection developed more frequently within the first post-transplant month in Group 1. Massive ascites was significantly associated with early graft loss (p < 0.05). Conclusion:, Post-transplant massive ascites associated with portal over-perfusion into the graft liver can develop in patients with a GRWR over 0.8%. Recipients with post-transplant massive ascites require careful management to prevent infection. [source]


Generalized lymphedema in a sirolimus-treated renal transplant patient

CLINICAL TRANSPLANTATION, Issue 2 2008
Carmine De Bartolomeis
Abstract:, Generalized lymphedema is an extremely rare effect of sirolimus therapy in renal transplant recipients. We describe the development of this complication in a 56-yr-old woman, who was given an experimental protocol with cyclosporine, sirolimus, steroids, and basiliximab. Following the protocol, after one month, the patient was randomized to the "sirolimus only" group, while cyclosporine was completely suspended and the oral steroids were continued. Three months later, the patient was admitted for severe lymphedema of the lower limbs, with significant weight increase, massive ascites and dyspnea, but excellent renal function. A chest radiography and an ultrasound study of the heart showed a moderate pleural and pericardial effusion. An abdominal ultrasound scan showed two small lymphoceles next to the transplanted kidney, confirmed with a CT scan. After sirolimus discontinuation the generalized lymphedema started to improve and three months later all the symptoms had disappeared. [source]