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Wednesday, 6 February 2019

Tumor Lysis Syndrome



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. [12(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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