Apixaban
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Intra-parenchymal haematoma and intra-renal bleeding: case report A 73-year-old man developed intra‑parenchymal haematoma and intra-renal bleeding during treatment with apixaban. The man was transferred to an emergency department with a 2h history of excruciating mostly nonradiating acute onset right flank pain. He had vomiting thrice in past 2h. He reported that since the kidney biopsy, he had experienced a very low level of right flank discomfort. He received paracetamol [acetaminophen]; however, no effect was noted. His medical history included hypertension, heart failure and atrial fibrillation. For over 2 years, he had been receiving oral apixaban 5mg twice daily for atrial fibrillation. Prior to 26 days of his transfer, he underwent ultrasound‑guided right kidney biopsy. At that time, his vital signs were normal along with soft, non-distended and non-tender abdomen. About a year prior to the biopsy, he had been diagnosed with right‑sided anterior uveitis. Therefore, he was suspected to have features of tubulointerstitial nephritis and uveitis (TINU). Prior to the kidney biopsy, for 2 years, his creatinine remained stable at 1.30 mg/dL. Prior to 3 days of the right kidney biopsy, apixaban therapy was interrupted. On the day of the kidney biopsy, his PTT was 13.2s and protime INR was 1.1. He underwent right kidney biopsy, wherein 18 gauge core biopsy samples were obtained and a sterile dressing was applied. He tolerated the procedure well and had no immediate complications. A renal ultrasound after the biopsy was normal. After 3 days of the biopsy, he restarted apixaban therapy. The kidney biopsy pathology report described 3 tan, cylindrical tissues, each 1.2cm in length and 0.1cm in diameter. The kidney biopsy showed hypertensive nephrosclerosis, moderate interstitial fibrosis and mild interstitial chronic inflammation. At current presentation, a urinalysis showed trace ketones, 2+ blood and 2+ protein. He exhibited increased serum creatinine to 1.86 mg/dL, which was 1.31 mg/dL in a month prior to biopsy (i.e. May 2019). The increase in serum creatinine was consistent with acute kidney injury associated with Page kidney. Blood test showed WBC count 12 K/cmm, platelet count 234 K/ cmm, haemoglobin 11.7 g/dL with normal electrolytes level. His protime INR was 1.3 (normal range: 0.9–1.1) and PTT was 15.5s (normal range: 10.3–13.4) at the time of admission. An abdominal and pelvic contrast‑enhanced CT examination showed an intra‑parenchymal haematoma in the lower pole of the right kidney measuring up to 5.9cm with evidence of active intrarenal bleeding [durations of treatments to reactions onsets not stated]. Therefore, the man immediately underwent a selective renal angiography with coil embolization of a ruptured pseudoaneurysm. He developed reversible contrast induced nephropathy following the double exposure to iodinated contrast from the contrast enhanced CT examination on the day of admission, and second, during the coil embolization procedure. He received IV fluids for leu
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