Within 24 h of admission, he received chemotherapy with single-agent carboplatin as he was felt to be too unwell for standard bleomycin, etoposide and cisplatin chemotherapy. Bleomycin was felt to be inappropriate in view of his breathlessness and etoposide due to his deranged liver function. Later the same day, he became more unwell with grade II encephalopathy and a reduced conscious level. He subsequently became unconscious with a decorticate position, was intubated and transferred to the intensive care unit (ICU). A CT scan and MRI scan of the brain, electroencephalograph and a lumbar puncture were all unremarkable, excluding any obvious neurological cause for the rapid deterioration in his conscious level. In view of his severely deranged liver function, he was managed as a case of hepatic failure with the help of the specialist liver team. There was no serological evidence of hepatitis B/C infection or recent infection with hepatitis A/E viruses, cytomegalovirus or Epstein–Barr virus. Autoantibody and anti-neutrophil cytoplasmic antibody screens were negative. -1-Antitrypsin and ceruloplasmin levels were also normal and there was nothing to suggest a recent paracetamol overdose. A transjugular biopsy of the liver was carried out. Histopathological examination of this confirmed confluent zonal and panacinar necrosis without specific aetiological features; in particular there was no evidence of malignancy in the random biopsy ().
Figure 2 A. Liver biopsy (H&E stain, 20× magnification) showing confluent zonal and panacinar necrosis, with replacement of the parenchyma by areas of haemorrhage. The biopsy has a variegated appearance due to the interposition of haemorrhage (red/pink) (more ...)
His clinical condition and liver enzymes started to improve following his first dose of carboplatin chemotherapy (). After 2 weeks in the ICU, he was transferred to the liver unit and his clinical condition and liver enzymes continued to improve. A reassessment CT scan, approximately 3 weeks after his first cycle of chemotherapy, showed a partial response, with reduction of the retroperitoneal mass from 17 × 13 to 9 × 4 cm. He received a second dose of carboplatin at AUC4 4 weeks after his first dose and tolerated this well.
After further dramatic improvement in his clinical condition he received three further cycles of chemotherapy with etoposide and cisplatin, given at 3-weekly intervals from 7 weeks after his first dose of carboplatin. The cisplatin was given at full dose (100 mg/m2 per cycle), but a reduction in the etoposide dose of two-thirds was used in view of his persisting liver impairment. A post chemotherapy CT scan showed a further reduction in the retroperitoneal mass to 4 × 2.5 cm.
He remained an inpatient throughout his chemotherapy, requiring continuous physiotherapy and occupational therapy input. He was discharged 2 weeks after his final cycle of chemotherapy. At 4 days after discharge, he became unwell and was readmitted with fever. Vegetations were seen on the aortic valve on transthoracic echocardiography and blood cultures grew Enterococci. A diagnosis of bacterial endocarditis was made and approximately 4 weeks after his final cycle of chemotherapy, he underwent an emergency aortic valve replacement with mitral valve debridement and insertion of a metal prosthetic valve. He also required insertion of a pacing device in view of an episode of complete heart block. He recovered well and was discharged a month later.