Tumor Lysis Syndrome
Tumor lysis
syndrome refers to the constellation of metabolic disturbances that occurs when
large numbers of neoplastic cells are killed rapidly, leading to the release of
intracellular ions and metabolic byproducts into the systemic circulation.
Clinically, the syndrome is characterized by rapid development of
hyperuricemia,hyperkalemia, hyperphosphatemia, hypocalcemia, and acute kidney injury. [1, 2] (See Pathophysiology, Etiology, Prognosis, Presentation, and Workup.)
Epidemiology
International occurrence
The incidence of tumor lysis syndrome is unknown. The prevalence
varies among different malignancies; bulky, aggressive, treatment-sensitive
tumors are associated with higher frequencies of tumor lysis syndrome. In
studies of frequency in patients with intermediate-grade or high-grade
non-Hodgkin lymphomas, laboratory evidence of tumor lysis syndrome (42%)
occurred much more frequently than the symptomatic clinical syndrome (6%). In
children with acute leukemia receiving induction chemotherapy, silent
laboratory evidence of tumor lysis syndrome occurred in 70% of cases, but
clinically significant tumor lysis syndrome occurred in only 3% of cases.
As advances are made in cancer treatment and as high-dose
regimens become more commonplace, tumor lysis syndrome incidence may increase
and the syndrome may emerge in a broader spectrum of malignancies.
Age-related demographics
Although tumor lysis syndrome occurs in all age groups, advanced
age leading to impaired renal function may predispose patients to clinically
significant tumor lysis syndrome owing to a decreased ability to dispose of
tumor lysis byproducts.
Prognosis
Early recognition of signs and symptoms of patients at risk for
tumor lysis syndrome, including identification of abnormal clinical and
laboratory values, can lead to successful prevention of the otherwise
life-threatening complications of the condition.
Potential complications of tumor lysis syndrome include uremia
and oliguric renal failure due to tubule precipitation of uric acid, calcium
phosphate, or hypoxanthine.
Severe electrolyte disturbances, such as hyperkalemia and
hypocalcemia, predispose patients to cardiac arrhythmia and seizures.
Iatrogenic complications, such as pulmonary edema from overly
vigorous hydration or metabolic alkalosis from excess exogenous administration
of bicarbonate, can also occur and are life threatening if not immediately
addressed.
Acute kidney injury
Renal tubule precipitation of uric acid, calcium phosphate, or hypoxanthine
causes acute kidney injury. This is often oliguric (<400 mL daily) in
nature, leading to volume overload and complications of hypertension and
pulmonary edema.
High blood urea nitrogen (BUN) levels due to increased protein
catabolism and renal impairment can be severe enough to result in pericarditis,
platelet dysfunction, and defective cellular immunity. Renal dysfunction can be
severe enough to require dialysis, but with prompt supportive measures, it is
usually reversible.
Cardiac arrhythmia
Hyperkalemia can lead to electrocardiographic changes and
life-threatening cardiac arrhythmia, including asystole. Severe potassium
elevation can cause electrocardiographic alterations such as peaked T waves,
flattened P waves, prolonged PR interval, widened QRS complexes, deep S wave,
and sine waves. Hypocalcemia can lead to QT interval lengthening, which
predisposes patients to ventricular arrhythmia.
Metabolic acidosis
Acute kidney injury and the liberation of large amounts of
endogenous intracellular acids from cellular catabolism result in acidemia.
This acidemia causes a decrease in serum bicarbonate concentration and a high
anion gap acidosis (see the Anion Gap calculator).
Acidemic states can worsen the many electrolyte imbalances
already present in tumor lysis syndrome; intracellular uptake of potassium is
hindered, uric acid solubility is decreased, and extracellular shift of
phosphate is promoted. Calcium phosphate solubility, however, improves in
acidic conditions.
The myriad of metabolic disorders must be assessed and treated
rapidly. Proper fluid management, alkalinization of the urine, correction of
acidosis, and attention to infections are the mainstays of therapy.
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