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Cureus 2019-Mar

Delayed Retroperitoneal Hemorrhage as a Complication of Large-volume Paracentesis.

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
Patricia Rojas
Reetika Sachdeva
Wojtek Blonski

Atslēgvārdi

Abstrakts

Large-volume paracentesis (LVP) consists of the removal of more than four liters of ascitic fluid. This procedure can cause complications such as hemorrhage, infection, bowel perforation, circulatory failure, or ascitic fluid leakage. The main presentation of paracentesis-induced hemorrhage is abdominal wall hematoma. An 81-year-old male with a past medical history of obesity and diabetes mellitus presented to our hospital with confusion, new onset black tarry stools, and foul-smelling urine. He was found to be oriented only to person and had abdominal distention with positive fluid wave sign and melanotic stools on rectal exam. Laboratory results elucidated pancytopenia, hypoalbuminemia, elevated aspartate aminotransferase (AST) of 43 U/L, and elevated D-dimer levels. Urinalysis was abnormal, showing >180 white blood cells (WBC) with positive leukocyte esterase and nitrites. Liver ultrasound evidenced cirrhosis. Octreotide drip, ceftriaxone, lactulose, and pantoprazole were initiated for upper gastrointestinal (GI) hemorrhage and cirrhosis. A computed tomography angiogram (CTA) of the chest was positive for bilateral segmental pulmonary embolism, therefore, he also started receiving heparin drip. On the fifth day of admission, an ultrasound-guided paracentesis was done, with six liters of ascitic fluid removed. On the seventh day of admission, the patient presented acute left flank pain with an associated episode of hypotension and drop in hemoglobin. A CTA of the abdomen showed left retroperitoneal hemorrhage but no signs of active bleeding. Heparin drip was discontinued, and the patient was transferred to the intensive care unit (ICU). The patient's hemoglobin was stable throughout the days after ICU admission, and he did not require any more transfusions of packed red blood cells. His respiratory status was steady although heparin was discontinued due to a bleeding episode. He was discharged without anticoagulation therapy due to his high risk for rebleeding. One of the proposed mechanisms leading to variceal bleeding is the rapid decompression of splanchnic circulation due to decreased abdominal pressure. Since the source of bleeding is venous, initially, the patients can be asymptomatic. Treatment can be conservative, surgical or by means of transcatheter interventions. We would like to emphasize the need for the close monitoring of patients undergoing large-volume paracentesis, especially in the setting of anticoagulation therapy, as survival depends upon early diagnosis and treatment. It is important to mention that international normalized ratio (INR) is neither a reliable anticoagulation test nor a predictive factor of bleeding in cirrhotic patients.

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