Tumor Lysis Syndrome

When intracellular components are released at a faster rate in to blood stream it may accumulate as constellation of electrolyte abnormalities is referred as Tumor Lysis Syndrome (TLS). It may cause acute renal failure and metabolic acidosis. TLS is characterized by the following

• Hyperkalemia
• Hyperphosphatemia
• Hypocalcaemia
• Hyperuricemia

Release of intracellular potassium, inorganic and organic phosphate may end up in apoptosis thereby inducing hyperkalemia and hyperphosphatemia. If hyperphosphatemia is severe and prolongs then it may result in calcium concentration to come down thereby hypocalcaemia will develop very rarely. Hyperuricemia result in ultimate breakdown of nucleic acids. Individual with hematological neoplasms may develop Tumor Lysis Syndrome just before administration of chemotherapy with high dose concentration. Patients with Burkitt lymphoma and lymphoblast may show development of TLS. Individual with solid tumors of large size may undergo rapid proliferation of cells resulting in TLS. High LDH levels lead continuous of lysis of cells. Patients with TLS may have very less glomerular filtration rate and high susceptible to electrolyte distribution as and when compared to individuals with normal functioning renal cells.

Hyperkalemia

Hyperkalemia is an electrolyte abnormality which can develop tumor lysis syndrome. Plasma concentration is more in case of hyperkalemia as cell lysis results in release of more intracellular stores. When individuals are with hemolysis, thrombocytosis, marked leukocytosis may develop pseudohyperkalemia. It also source partial depolarization, prolonged depolarization, flaccid paralysis and muscular weakness. Worst threatening part of hyperkalemia is ventricular arrhythmia. Symptoms of hyperkalemia are weakness, cardiac arrest, EKG changes, paralysis, muscle cramps, nausea, bard arrhythmias, tachyarrhythmia, etc. Calcium gluconate reduce the symptoms to extent in specific cellular membrane excitability. Other methods are hemodialysis and continuous venous hemofiltration helps to reduce the serum potassium level.

Hyperphosphatemia

Similar to hyperkalemia, serum potassium level increases when cell lysis occurs. Individuals with thrombocytosis may cause spurious hyperphosphatemia. Extra osseous calcification may develop hyperphosphatemia. When this condition prolongs for a longer time then it may result in deceased calcium level in serum. It leads to renal expansion except for the individuals with renal failure. Agent like aluminium based antacids help gut from being absorbed. Phosphate binder and Sevalamer can also be used for this purpose. Hemodialysis is best option to treat the individuals with renal failure.

Hypocalcaemia

Direct manifestation of hyperphosphatemia is hypocalcaemia.  When serum calcium level decreases it may result in hypoalbuminemia. To overcome this over alkalinization helps in binding of calcium to proteins and hence the calcium level is maintained. Hormone such as parathyroid hormone may result in proper maintenance of calcium level. Symptoms of hypocalcaemia are tetany, heart block, ventricular arrhythmias, hypotension, laryngospasm, paresthesias and muscle switching. Biphosphonates helps in treatment of cancer related hypocalcaemia.

Hyperuricemia

Patients with hyperuricemia should access risk development. Symptoms of Hyperuricemia are vomiting, joint pain, crystalluria, flank pain, anuria, azotemia, diarrhea, nausea and oligouria. Allopurinol, a type of health check treatment prevents hyperuricemia. Rasburicase is used to treat prophylaxis and hyperuricemia of individuals who may develop malignant cells when cell lysis occurs.

Questions:

• What are the risk factors of tumor lysis syndrome?
• Give signs and symptoms of tumor lysis syndrome.
• What are pretreatment for tumor lysis syndrome?
• Describe each types of tumor lysis syndrome.
• What are common causes of tumor lysis syndrome?