Laura K. Frye, MD, Member-At-Large

 

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
 

 

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
 

 

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

Given the severe risks associated with HALT, vigilance is vital, particularly in intubated and sedated patients where monitoring of neurologic status is more challenging. Protocols may involve routine serum ammonia monitoring, polymerase chain reaction testing for mycoplasma and ureaplasma at the time of transplant or with postoperative bronchoscopy, and empiric antimicrobial treatment. No definitive ammonia threshold exists, but altered sensorium with elevated levels warrants immediate and more aggressive treatment with levels >75 μmol/L. Early testing and symptom recognition can significantly improve survival rates in this potentially devastating condition.

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868