Simultaneous Hyperammonemia Syndrome in Multiple Organ Recipients from a Single Donor

Introduction Hyperammonemia is a rare complication post solid organ transplant, with a high mortality. We report a case of hyperammonemic encephalopathy in separate cardiac and lung transplant recipients, likely related to donor derived infection acquired from the same donor. Case Report A 63-year-old male with sarcoid cardiomyopathy on LVAD support and no known hepatic disease received cardiac transplantation. He was extubated on day (D) 4 with normal allograft function and mentation. He received basiliximab induction, steroids, mycophenolate (MMF) and tacrolimus (TAC) on D6. He developed hallucinations on D8 followed by paranoia and reduced GCS on D9, with no focal neurological deficit. Cranial CT/MRI and CSF were unremarkable. Initial blood results showed raised CRP, WCC with mildly elevated urea, creatinine, bilirubin & transaminase. Serum ammonia (NH3) was 549µmol/L. He was intubated and diagnosed with hyperammonemic encephalopathy. Hyperammonemic encephalopathy had also been diagnosed in the lung transplant recipient, a 65-year-old male with COPD, from the same donor. He received basiliximab induction, steroids, MMF and Cyclosporine A (CSA) on D1. He developed right sided hypertonia and reduced consciousness on D6, with elevated NH3 (177µmol/L). Both received Mycoplasma / Ureaplasma combination antibiotics - moxifloxacin and azithromycin (lung), moxifloxacin and minocycline (cardiac); metronidazole, rifaximin, lactulose, ammonia scavengers and dialysis. NH3 normalised by D12 (lung) and D15 (cardiac) with improvement in mental state. At D30, both remain dependent on dialysis with ongoing antibiotics, steroids, and moderate immunosuppression. Both patients required tracheostomy for critical illness myopathy. The aetiology of hyperammonemia is putative, however both recipients had Mycoplasma hominis identified on blood cultures. M. hominis and Ureaplasma spp. were present in bronchial washings in the lung recipient, and sputum, pleural and pericardial fluid from cardiac recipient. The donor had culture negative urethritis at donation with Mycoplasma and Ureaplasma spp. confirmed on retrospective bronchial washing PCR. Summary Hyperammonemia should be suspected in transplant recipients with altered mental state. Transplant units need increased awareness of the potential impact of infection by urease-producing organisms. Hyperammonemia is a rare complication post solid organ transplant, with a high mortality. We report a case of hyperammonemic encephalopathy in separate cardiac and lung transplant recipients, likely related to donor derived infection acquired from the same donor. A 63-year-old male with sarcoid cardiomyopathy on LVAD support and no known hepatic disease received cardiac transplantation. He was extubated on day (D) 4 with normal allograft function and mentation. He received basiliximab induction, steroids, mycophenolate (MMF) and tacrolimus (TAC) on D6. He developed hallucinations on D8 followed by paranoia and reduced GCS on D9, with no focal neurological deficit. Cranial CT/MRI and CSF were unremarkable. Initial blood results showed raised CRP, WCC with mildly elevated urea, creatinine, bilirubin & transaminase. Serum ammonia (NH3) was 549µmol/L. He was intubated and diagnosed with hyperammonemic encephalopathy. Hyperammonemic encephalopathy had also been diagnosed in the lung transplant recipient, a 65-year-old male with COPD, from the same donor. He received basiliximab induction, steroids, MMF and Cyclosporine A (CSA) on D1. He developed right sided hypertonia and reduced consciousness on D6, with elevated NH3 (177µmol/L). Both received Mycoplasma / Ureaplasma combination antibiotics - moxifloxacin and azithromycin (lung), moxifloxacin and minocycline (cardiac); metronidazole, rifaximin, lactulose, ammonia scavengers and dialysis. NH3 normalised by D12 (lung) and D15 (cardiac) with improvement in mental state. At D30, both remain dependent on dialysis with ongoing antibiotics, steroids, and moderate immunosuppression. Both patients required tracheostomy for critical illness myopathy. The aetiology of hyperammonemia is putative, however both recipients had Mycoplasma hominis identified on blood cultures. M. hominis and Ureaplasma spp. were present in bronchial washings in the lung recipient, and sputum, pleural and pericardial fluid from cardiac recipient. The donor had culture negative urethritis at donation with Mycoplasma and Ureaplasma spp. confirmed on retrospective bronchial washing PCR. Hyperammonemia should be suspected in transplant recipients with altered mental state. Transplant units need increased awareness of the potential impact of infection by urease-producing organisms.