Tumor Lysis Syndrome: Treatment

Tumor Lysis Syndrome is a group of metabolic complications that may arise after treatment of neoplasms, especially in lymphoma and leukemia, and in some cases, even when no previous treatment has been carried out.

The types of lymphoma involved in the disorder are poorly differentiated, such as Burkitt’s lymphoma. On the other hand, acute lymphoblastic and myeloid leukemia could also lead to this disorder. Different types of malignant tumors associated with this disorder, such as melanoma, can rarely be observed.

Typically, the initiation of the syndrome therapy involves chemotherapy and steroids and may arise spontaneously, without carrying out a previous treatment. The factors that trigger this disorder are the complications of cellular debris after the destruction of cancer cells during treatment.

Clinically, tumor lysis syndrome is characterized by:

Hypercalcemia: Symptoms of the disease usually appear only when intracellular potassium levels are very high (more than seven mmol / L) and can lead to heart abnormalities, muscle weakness, or severe paralysis.

Hyperphosphatemia: can lead to acute renal failure due to the accumulation of calcium phosphate crystals in the renal parenchyma.

Hypocalcemia: can lead to tetany, seizures, sudden mental disability, parkinsonian symptoms, papilledema, and myopathy.


Hyperuricemia and hyperuricosuria: acute nephropathy due to uric acid due to hyperuricosuria is the dominant cause of acute renal failure. However, due to an effective treatment for the latter, hyperphosphatemia has become a cause in comparison more infrequent. It should be suspected in cases of tumor lysis syndrome of cancer patients who develop acute renal failure associated with hyperuricosuria. A urinalysis can point to uric acid crystals or amorphous urates. In addition, using urine analysis, it is possible to identify the elevated excretion of uric acid.


The treatment aims to prevent the onset of acute renal failure, which leads to a considerable increase in the clinical manifestations of the syndrome and its clinical consequences. Therefore, it can be done to control hyperuricemia and the prevention of nephrocalcinosis. This is done by renal replacement therapy when it is not possible to control the metabolic alterations in the 6 hours after the prevention is implemented. However, if there is still acute renal injury, extrarenal treatment should be initiated to clear uric acid and phosphate to minimize renal failure. In addition, hydration is essential for this disorder, and drugs that reduce urate levels can also be used.

A literature review/acute complete tumor lysis syndrome: a comprehensive review.

Source: Rev. Bras. Intensive, 20 (3): 278-285, July-September Illus 2008, tab. Language: es; pt.

Abstract: The tumor lysis syndrome is characterized by the massive destruction of malignant cells and the consequent release of their contents in the extracellular space. Although it can occur spontaneously, tumor lysis syndrome usually appears shortly after starting treatment with cytotoxic chemotherapeutic agents. Once released, these metabolites can overwhelm the homeostatic mechanisms that result in hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.

These biological changes can lead to the appearance of various clinical manifestations, including acute renal failure, seizures, and sudden death, which may require intensive care. As the tumor lysis syndrome is associated with a poor prognosis, preventing its occurrence and consequences is also mandatory. This review aims to describe the pathophysiology and clinical and biological manifestations of acute tumor lysis syndrome and provide updated recommendations for prevention.

The articles on tumor lysis published in the last 20 years of the portal www.ncbi.nlm.nih.gov/pubmed/ were selected. The studies mentioned in the selected articles were also used.

Results: Tumor lysis syndrome is a severe and frequent complication in patients with newly diagnosed malignant tumors. Prevention strategies include:

  • Vigorous hydration.
  • Mucolytic agents.
  • Identifying predisposing factors for acute renal injury and in critical patients.
  • The prophylactic methods of renal replacement are necessary to prevent or mitigate their consequences.

However, the optimal timing and prevention modalities remain unknown and can be modified by changes in the spectrum of patients at risk of developing it. The development and validation of strategies based on patient risk are necessary to limit high morbidity and mortality.