Pleural effusion as a complication of extrahepatic biliary tract rupture in a dog

1996 ◽  
Vol 32 (5) ◽  
pp. 409-412 ◽  
Author(s):  
MD Barnhart ◽  
LM Rasmussen

Bile pleural effusion associated with traumatic rupture of the extrahepatic biliary tract and bile peritonitis in a dog is described. Pleural and abdominal fluids were identical cytologically and chemically despite a grossly intact diaphragm. Transfer of peritoneal fluid across the diaphragm via lymphatics and subsequent leakage into the pleural space is the likely cause of effusion. Pleural and abdominal fluid accumulation resolved spontaneously with repeated abdominocenteses and supportive care.

2001 ◽  
Vol 49 (2) ◽  
pp. 141-154 ◽  
Author(s):  
K. Vörös ◽  
T. Németh ◽  
T. Vrabély ◽  
F. Manczur ◽  
J. Tóth ◽  
...  

Findings of hepatic and gallbladder ultrasonography were analyzed in 12 dogs with gallbladder and/or extrahepatic biliary tract obstruction and compared with the results of exploratory laparotomy. Hepatic ultrasonography demonstrated normal liver in 2 dogs and hepatic abnormalities in 10 animals. The following ultrasonographic diagnoses were established compared to surgical findings: gallbladder obstruction caused by bile sludge (correct/incorrect: 1/2, surgical diagnosis: choleliths in one case), gallbladder obstruction caused by neoplasm (0/1, surgical diagnosis: mucocele), gallbladder and extrahepatic biliary tract obstruction due to choleliths (3/3), extrahepatic biliary tract obstruction caused by pancreatic mass (1/1) and small intestinal volvulus (1/1). Bile peritonitis caused by gallbladder rupture (4/4) was correctly diagnosed by ultrasound, aided with ultrasonographically-guided abdominocentesis and peritoneal fluid analysis. Rupture of the gallbladder should be suspected in the presence of a small, echogenic gallbladder or in the absence of the organ together with free abdominal fluid during ultrasonography. Laparotomy was correctly indicated by ultrasonography in all cases. However, the direct cause of obstruction could not be determined in 2 of the 12 dogs by ultrasonography alone.


2017 ◽  
Vol 3 (1) ◽  
pp. 205511691771487
Author(s):  
Ronan A Mullins ◽  
Marc A Barandun ◽  
Barbara Gallagher ◽  
Laura C Cuddy

Case summary A 6-month-old spayed female domestic shorthair cat presented for evaluation of suspected bite wounds over the right caudal thorax and left cranial flank. Thoracic radiographs identified a mild right-sided pneumothorax, a small volume of right-sided pleural effusion, with increased soft tissue opacity in the right cranial and middle lung lobes. Abdominal ultrasound identified a very small gall bladder and several small pockets of free peritoneal fluid. Cytological analysis of peritoneal fluid was consistent with a modified transudate. Following initial diagnostic investigations, yellow–orange fluid began to emanate from the right-sided thoracic wound. Biochemical analysis of this fluid was consistent with bile. Exploratory coeliotomy revealed a right-sided radial diaphragmatic tear, with herniation of the quadrate liver lobe and a portion of the gall bladder into the right pleural space. The gall bladder was bi-lobed and avulsion of a single herniated lobe resulted in leakage of bile into the right pleural cavity, without concurrent bile peritonitis (biloabdomen). The cat underwent total cholecystectomy and diaphragmatic defect repair and recovered uneventfully. Relevance and novel information To our knowledge, at the time of writing non-iatrogenic isolated bilothorax without concurrent biloabdomen has not been previously reported in the cat. This case highlights the importance of thorough assessment of cats with seemingly innocuous thoracic bite wounds. Despite the rarity of its occurrence, bilothorax should be considered a differential in cats with pleural effusion, even in the absence of bile peritonitis. We believe that the optimal treatment of cases of bilothorax is multifactorial and should be determined on a case-by-case basis.


2020 ◽  
Vol 22 (3) ◽  
pp. 141-145
Author(s):  
Krishna Chandra Devkota ◽  
S Hamal ◽  
PP Panta

Pleural effusion is present when there is >15ml of fluid is accumulated in the pleural space. It can be divided into two types; exudative and transudative pleural effusion. Tuberculosis and parapneumonic effusion are the common cause of exudative pleural effusion whereas heart failure accounts for most of the cases of transudative pleural effusion. This study was a hospital based cross sectional study performed at Nepal Medical College during the period of January 2016-December 2016. A total of 50 patients who fulfilled the inclusion criteria were enrolled. Pleural effusion was confirmed by clinical examination and radiology. After confirmation of pleural effusion, pleural fluid was aspirated and was analysed for protein, LDH, cholesterol. The Heffner criteria was compared with Light criteria to classify exudative or transudative pleural effusion. Among 50 patients, 30 were male and 20 were female. The mean age of patient was 45.4±21.85 years. The sensitivity and specificity of using Light criteria to detect the two type of pleural effusion was 100% and 90.9%, whereas using Heffner criteria was 94.87%, 100% respectively(P<0.01). There are variety of causes for development of pleural effusion and no one criteria is definite to differentiate between exudative or transudative effusion. In this study Light criteria was more sensitive whereas Heffner criteria was more specific to classify exudative pleural effusion. Hence a combination of criteria might be useful in case where there is difficulty to identify the cause of pleural effusion.


Author(s):  
Martino Handoyo ◽  
Titong Sugihartono

Hepatic hydrothorax is a transudative pleural effusion which presents in 5-10% patients with liver cirrhosis. Although fairly uncommon, it is associated with higher morbidity and lower survival rate. The mechanism is yet to be understood fully, but the most widely accepted pathogenesis involves the presence of portal hypertension, diaphragmatic defects, and negative intrathoracal pressure, all of which lead to the formation of unidirectional passage of ascitic fluid from peritoneal cavity into pleural space. Due to its origin, the pleural effusion has similar characteristics to ascitic fluid. We herein report the case of a 60-year-old woman with advanced liver cirrhosis and right-sided moderate hepatic hydrothorax. Treatment given to the patient includes diuretics, sodium restriction, and repeated thoracentesis. Subsequent evaluation of the patient revealed improvement both clinically and radiologically.


Chest Imaging ◽  
2019 ◽  
pp. 165-170
Author(s):  
Christopher M. Walker

Pleural effusion discusses the radiographic and computed tomography (CT) manifestations of this entity. Pleural effusion is classified based on pleural fluid analysis using Light’s criteria: transudative and exudative. Free pleural fluid collects in the most dependent aspect of the pleural space due to gravitational effects. It exhibits a meniscus configuration on upright chest radiography. Pleural effusion in a supine or semiupright patient is more difficult to identify but may be suspected in cases with a homogeneous or gradient-like opacity over the lower hemithorax, elevation of the hemidiaphragm contour, or an apical cap. Subpulmonic pleural effusion manifests with lateral displacement of the apex of the ipsilateral hemidiaphragm contour and increased distance between the gastric air bubble and pseudodiaphragmatic contour. Exudative pleural effusion should be suspected in cases with CT findings of pleural thickening, enhancement, septations, and/or loculations.


Chest Imaging ◽  
2019 ◽  
pp. 155-158
Author(s):  
Christopher M. Walker

The chapter titled introduction to pleural disease discusses the imaging and clinical features of diseases of the pleura. The pleural space is a potential space located between the visceral and parietal pleural surfaces. Pleural effusion and pneumothorax are the most common manifestations of pleural disease and are caused by a wide variety of disease processes. Pleural thickening may be related to benign or malignant processes. Bilateral discontinuous nodular pleural thickening is characteristic of pleural plaques. Pleural thickening with calcification may also be seen in fibrothorax. Malignant pleural disease may manifest with pleural effusion, pleural nodules or masses, or a combination of the two. There are several CT features suggestive of malignant pleural thickening including circumferential pleural thickening, pleural nodules or masses, involvement of the mediastinal pleural surface, and pleural thickening measuring greater than 1 cm in thickness. Metastatic disease is the most common pleural neoplasm. Mesothelioma is uncommon but remains the most common primary pleural malignancy and is almost always seen in patients with previous asbestos exposure. Pleural abnormalities must be differentiated from pulmonary processes. Pleural masses may exhibit obtuse angles with the adjacent pleural surfaces, displace rather than engulf adjacent pulmonary vasculature, and may exhibit the incomplete border sign.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Eunjue Yi ◽  
Tae Hyung Kim ◽  
Jun Hee Lee ◽  
Jae Ho Chung ◽  
Sungho Lee

Abstract Background The aim of this study was to investigate the clinical manifestation and predictive risk factors of pleural empyema developing during treatment of the pyogenic liver abscess. Methods Medical records of patients with the liver abscess in our institution were reviewed retrospectively. Enrolled patients were classified into four groups; Group 1: patients without pleural effusion, Group 2: patients with pleural effusion and who were treated noninvasively, Group 3: patient with pleural effusion and who were treated with thoracentesis, and Group 4: patients with pleural effusion that developed into empyema. Patient characteristics, clinical manifestation, and possible risk factors in development of empyema were analyzed. Results A total of 234 patients was enrolled in this study. The incidence rate of empyema was 4.27% (10 patients). The mean interval for developing pleural effusion was 5.6 ± 6.35 days. In multivariate analysis, risk factors for developing pleural effusion included the location of the liver abscess near the right diaphragm (segment 7 and 8, OR = 2.30, p = 0.048), and larger diameter of the liver abscess (OR = 1.02, p = 0.042). Among patients who developed pleural effusions, presences of mixed microorganisms from culture of liver aspirates (OR = 10.62, p = 0.044), bilateral pleural effusion (OR = 46.72, p = 0.012) and combined biliary tract inflammation (OR = 21.05, p = 0.040) were significantly associated with the need for invasive intervention including surgery on effusion. Conclusion The location of the liver abscess as well as pleural effusion, elevated inflammatory markers, and combined biliary tract inflammation may be important markers of developing pleural complication in patients with pyogenic liver abscess.


2000 ◽  
Vol 279 (6) ◽  
pp. C1744-C1750 ◽  
Author(s):  
Yuanlin Song ◽  
Baoxue Yang ◽  
Michael A. Matthay ◽  
Tonghui Ma ◽  
A. S. Verkman

Continuous movement of fluid into and out of the pleural compartment occurs in normal chest physiology and in pathophysiological conditions associated with pleural effusions. RT-PCR screening and immunostaining revealed expression of water channel aquaporin-1 (AQP1) in microvascular endothelia near the visceral and parietal pleura and in mesothelial cells in visceral pleura. Comparative physiological measurements were done on wild-type vs. AQP1 null mice. Osmotically driven water transport was measured in anesthetized, mechanically ventilated mice from the kinetics of pleural fluid osmolality after instillation of 0.25 ml of hypertonic or hypotonic fluid into the pleural space. Osmotic equilibration of pleural fluid was rapid in wild-type mice (50% equilibration in <2 min) and remarkably slowed by greater than fourfold in AQP1 null mice. Small amounts of AQP3 transcript were also detected in pleura by RT-PCR, but osmotic water transport was not decreased in AQP3 null mice. In spontaneously breathing mice, the clearance of isosmolar saline instilled in the pleural space (∼4 ml · kg−1· h−1) was not affected by AQP1 deletion. In a fluid overload model produced by intraperitoneal saline administration and renal artery ligation, the accumulation of pleural fluid (∼0.035 ml/h) and was not affected by AQP1 deletion. Finally, in a thiourea toxicity model of acute endothelial injury causing pleural effusions and lung interstitial edema, pleural fluid accumulation in the first 3 h (∼4 ml · kg−1· h−1) was not affected by AQP1 deletion. These results indicate rapid osmotic equilibration across the pleural surface that is facilitated by AQP1 water channels. However, AQP1 does not appear to play a role in clinically relevant mechanisms of pleural fluid accumulation or clearance.


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