Tumor Lysis Syndrome Clinical Pathway — Inpatient, ICU
Cohort
This pathway is to be used for children with a new diagnosis or new relapse of a hematological malignancy or bulky solid tumor with presence of high-risk criteria.
The pathway is intended to identify those at risk for TLS, guide prophylactic management, and treatment of electrolyte derangements for TLS.
Children with bulky metastatic solid tumors are also at risk of TLS and have increased mortality with TLS. Providers should utilize a high degree of suspicion if child has advanced bulky metastatic disease.
Some examples of solid tumors with increased risk of TLS include:
- Metastatic medulloblastoma
- Metastatic neuroblastoma
- Metastatic colorectal cancer
- Hepatocellular carcinoma
- Melanoma
- Advanced germ cell tumors
Exclusion Criteria
Infants < 28 days old. Patients receiving CART therapy or maintenance chemotherapy.
Novel Agents Associated with TLS
Children with bulky metastatic solid tumors are also at risk of TLS and have increased mortality with TLS. Providers should utilize a high degree of suspicion if child has advanced bulky metastatic disease.
- Alvocidib
- Bortezomib
- Carfilzomib
- Dinaciclib
- Docetaxel
- Flavopiridol
- Ibrutinib
- Lenalidomide
- Pazopanib
- Venetoclax
TLS Definition
Tumor lysis syndrome (TLS) is a life-threatening oncologic emergency and needs a high index of suspicion in a patient with a newly diagnosed malignancy. Early intervention and a prophylactic strategy as defined in the pathway can prevent serious morbidity and mortality. TLS usually occurs in tumors with a very high proliferation index, such as in hematological malignancies (acute lymphoblastic leukemia, Burkitt leukemia/lymphoma, and diffuse large B-cell lymphoma), but can occur with any malignancy such as those with coexisting conditions such as renal failure or dehydration, or with delivery of novel targeted therapies.
TLS is a consequence of destruction of cancer cells, either spontaneously or after initiation of cytotoxic chemotherapy. This leads to a release of intracellular contents into the bloodstream. Massive release of uric acid, potassium, and phosphorous occurs, which can overwhelm normal physiological excretion. TLS thus consists of a constellation of metabolic derangements, including hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia and the resultant clinical sequelae, including cardiac arrhythmias, acute kidney injury (AKI), precipitation of uric acid or formation of calcium phosphate stones in the kidney, seizures and even death.
Several historic Classifications have been devised for TLS, including those by Hande and Garrow in 1993, modified by Cairo and Bishop in 2004, and remodified by Howard et al. in 2011, which include definitions for both laboratory and clinical TLS. The pathway was formed based on these sources and updated to reflect that even a significant single metabolic derangement can portend serious TLS.