A 66-year-old, former smoker and drinker of approximately 70 g of alcohol a day.
Early menopause under estrogen treatment for more than 20 years
She was admitted to another hospital one month before due to right hydrothorax.
He was diagnosed with hepatic hydrothorax with liver biopsy diagnostic of poorly evolved macro-micronodular cirrhosis, with moderate activity and focal steatosis.
The viral, metabolic and autoimmune study of liver disease was negative.
Cardiopulmonary pathology was ruled out as the cause of pleural effusion, as well as infectious or tuberculous pleuropulmonary pathology.
Lack of response to hydrosaline restriction and diuretic treatment, the patient underwent evacuation accentesis and chest tube for symptomatic relief.
She was admitted to our hospital one month later for recurrent right hydrothorax.
Physical examination revealed hypoventilation of the lower 2/3 of the right lung field.
Blood count showed leukocytosis of 20,500/μL with 77% of PMN, without anemia or thrombopenia.
Biochemistry showed a creatinine of 1.9 mg/dl, with sodium 129 mEq/litre; potassium 5.4 mEq/litre; total protein: 5.68 g/dl; fibrinogen: 680 IU/dl; coagulation protein: 50 mg/dl; total protein:
Tuberculosis was ruled out by determining acid-resistant bacilli and gamma-interferon in pleural fluid and by the negativity of the Mantoux reaction.
Malignancy was ruled out by pleural fluid cytology and pleural biopsies.
Abdominal Doppler ultrasound showed signs of chronic liver disease without morphological or hemodynamic signs of portal hypertension, with minimal ascites and right pleural effusion.
After verifying that there was no response to treatment with hydrosaline restriction and diuretics, a thoracic tube was placed as symptomatic treatment of hydrothorax draining 2000-2500 cc of liquid per day.
Complications of pleural effusion included prerenal renal failure due to high output and hypoproteinemia with hypoalbuminemia.
In an attempt to control pleural fluid production, a minithoracotomy with talc pleurodesis was performed, which was not effective.
Because of the failure of the pleurodesis, it was decided to place a PPPD, after finding in the pressure measurements data of mild portal hypertension (free-claving pressure gradient: 13 mmHg) suggestive of hepatic hydrothorax.
This led to a transient decrease in thoracic output (2-3 days).
Dysfunction of the IPPP was ruled out by Doppler ultrasonography.
Liver transplant is discouraged due to recent alcohol consumption.
5 days later we decided to start treatment with octreotide at a dose of 25 μg/h i.v. on the first day, 50 on the second 100 other days.
The patient had a very good response to this treatment, with a progressive decrease in the output through the chest tube, which allowed its removal without subsequent recurrence of the pleural effusion.
A 10 mg dose of subcutaneous octreotide was administered before discharge.
In the following six months, she had no pleural effusion or ascites under treatment with 25 mg of aldactone per day.
