scholarly journals Chylous Ascites Due to Hyperthyroidism and Heart Failure

Author(s):  
Masaki Uchihara ◽  
Jun Ehara ◽  
Keiichi Iwanami ◽  
Koichi Kitamura ◽  
Toshihiko Suzuki ◽  
...  
2021 ◽  
Vol 9 ◽  
pp. 232470962110261
Author(s):  
Tuong Vi Cassandra Do ◽  
Justin Cozza ◽  
Shyam Ganti ◽  
Jayaramakrishna Depa

Chylothorax is a pleural effusion of >110 mg/dL of triglycerides with a milky appearance with transudative being rare. In this article, we present a case of transudative chylothorax with concurrent chylous ascites that is secondary to congestive heart failure (CHF). A 70-year-old male with CHF with ejection fraction of 10%, coronary artery disease status post coronary artery bypass graft, sleep apnea, chronic kidney disease stage 3, and chronic obstructive pulmonary disease presented with worsening abdominal distention, shortness of breath, and increased lower extremities edema. He denied any cough or fever but had orthopnea and paroxysmal nocturnal dyspnea. He requires monthly paracentesis with drainage of 5 to 9 L each time. On physical examination, he had crackles bilaterally with no wheezes or jugular venous distension. His cardiac examination was unremarkable. He did have abdominal distension with dullness to percussion and a positive fluid wave. There was +2 bilateral pitting edema of lower extremities. He had a diagnostic paracentesis where 9.2 L of cloudy milky fluid was drained and therapeutic thoracentesis where 1.1 L of milky fluid was drained. Pleural fluid for triglycerides was 280. His peritoneal fluid had triglycerides of 671 confirming chylous ascites. CHF can lead to chylous ascites due to the increased lymph production in the abdomen, which flows to the thoracic duct. Due to the stiffness at the lymphatic junction, there is high pressure for less flow. The diaphragm plays a role allowing the chylous ascites to be absorb into the thorax.


2019 ◽  
Vol 72 (5) ◽  
pp. 431-433
Author(s):  
Maria Trêpa ◽  
Raquel Baggen Santos ◽  
Marta Fontes Oliveira ◽  
Inês Silveira ◽  
Joana Pires ◽  
...  

2011 ◽  
Vol 147 ◽  
pp. S136
Author(s):  
H.A. Cakmak ◽  
G. Yenidunya ◽  
B. Karadag ◽  
Z. Ongen

2003 ◽  
Vol 22 (7) ◽  
pp. 826-827 ◽  
Author(s):  
Cheng-Hsin Lin ◽  
Ron-Bin Hsu ◽  
Mei-Hwan Wu ◽  
Jou-Kou Wang ◽  
Shoei-Shen Wang ◽  
...  

1995 ◽  
Vol 8 (7) ◽  
pp. 1235-1236 ◽  
Author(s):  
V. Villena ◽  
A. De Pablo ◽  
P. Martín-Escribano

CHEST Journal ◽  
2012 ◽  
Vol 142 (4) ◽  
pp. 130A
Author(s):  
Andres Borja Alvarez ◽  
Samer Ibrahim ◽  
Rajeev Saggar

Author(s):  
George Hug ◽  
William K. Schubert

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.


Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).


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