Tumour lysis syndrome

Question 1

definition of tumour lysis syndrome

Answer 1

rapid cell death with initiation of chemo for rapidly proliferating cancers (leukaemia, lymphoma, myeloma) = cell death and

• hyperkalaemia
• hyperphosphtaemia
• secondary hypocalcaemia
• hyperuricaemia
• acute renal failure

risk of arrhythmia

Question 2

TLS prophylaxis

Answer 2

good hydration

Question 3

precautions if at high risk of tumour lysis syndrome

Answer 3

ie when WCC >50x10(9)

Rasburicase (recombinant urate-oxidase, which converts uric acid to an inactive metabolite).

Screen for G6PD deficiency prior to administration of rasburicase.

Allopurinol for intermediate risk (WCC ¼ 10–50 109 /L).

Question 4

epidemiology of tumour lysis syndrome

Answer 4

incidence unknown

most prevalent in haematological malignancies - high proliferating rates, tumour burden, chemosensitivity eg acute lymphocytic leukaemia and Burkitt’s lymphoma

increased age = increased risk - reduced glomerular filtration and comorbidities

Question 5

aetiology of tumour lysis syndrome

Answer 5

most commonly associated with ionitiation of cancer treatment in aggressive haematological malignancies - especially high grade non-Hodgkin’s lymphoma eg Burkitt;s lymphoma, ALL< AML

less in CLL and multiple myeloma

mostly from cytotoxic chemo, but there are reports from other med - steroids, hormones, radio, immunotherapy

risk increases if rapidly dividing, bulk of disease is high and response to treatment good

Question 6

RF for TLS

Answer 6

pre-existing renal impairment

high serum phosphate, K, creatinine, urea and uric acid

dehydration

volume depletion

high serum lactate dehydrogenase, and WCC associated with high tumour volume and increased risk

age not independant RF

Question 7

pathology of TLS

Answer 7

rapid breakdown of large numbers of cancer cells = subsequent release of large amounts of intracellular content (K, phos, nucleic acid) into blood

cancer cells have high turnover rate - so large amounts of nucleic acid products (which transform to uric acid) and phosphate

this overwhelms normal homeostatic mechanisms

large amount of cellular byproducts can = AKI

Question 8

how can TLS cause AKI

Answer 8

hyperuricaemia, acidic urine, and reduced urinary flow - precipitate uric acid crystals, renal tubular obstructuion and a decline in renal function

hyperphosphtaemia = formation of ca phos crystals and precipitation = nephrocalcinosis and urinary obstruction

secondary hypocalcaemia

hyperkalaemia exacerbated by AKI or lactic acidosis

Question 9

signs and sx of TLS

Answer 9

hyperkalaemia, hyperphosphtaemia and hypocalcaemia = cardiac arrhythmias and sudden death

hypocalcaemia = muscle cramps, tetany, seizures

AKI = fluid overload and pul oedema

syncope, chest pain, dyspnoea

N&V

anorexia

diarrhoea

muscle weakness

muscle cramps

lethargy

paraesthesia

lymphadenopathy

splenomegaly

hypertension/hypotension

oliguria/anuria/haematuria

Question 10

Ix for TLS

Answer 10

high serum uric acid

high serum phosphate

high serum K

low serum Ca

FBC - high WCC

high lactate dehydrogenase

high serum creatine

high serum urea - if renal impairment, AKI, dehydration

urine pH - <=5