Tumour Lysis syndrome

Can be spontaneous or treatment related
Massive released of intracellular nucleic acids, phophshate, k+
Often has a drop in calcium as phos-binds to it
Malignant cells have 4x the phosphate of non-malignant counterparts
Hyperphos is less common in the spontaneous tumour lysis setting as the growing cells can take up released phosphate so end up establishing an equilibrium
Can have high K – consider pseudokyperk in leukaemia/highly cellular disease
Can manifest with AKI, cardiac arrhythmia, or seizure.

Classic tumours: Fast growing, highly cellular

AKI

Uric Acid is high -> Intracellular purine nucleic acids are catabolized to xanthine and hypoxanthine, which get converted to uric acid by the enzyme xanthine oxidase.
Uric acid is poorly soluble in water, precipitates in an acidic environment (like distal tubules and collecting ducts).
Calcium-phosphate crystals can also precipitate out into tubules.
Epitaxy: Uric acid crystals and calcium phosphate crystals form a seed layer for each other. Calcium phosphate coats the otherwise soluble uric acid. Thus, the pathological crystals are mixed.
AKI - > higher concentrations -> more crystallisation ->vicious cycle

Prophylactic hydration and rasburicase is best option

Very careful and frequent labs. HDU/ITU possibly.
Treat K+ medically if possible, RRT on the table
volume resuscitate with N.Saline
- 2 ml/kg/hour or atleast 3 litres per day
- Avoid calcium containing fluids
Non calcium binder may have a role, like sevelamer
Caution replacing calcium as may worsening Ca-Phos precipitation, let it ride low as feasible but treat if symptomatic

recombinant urate oxidase
breaks down uric acid into allantoin, which is water-soluble and non-nephrotoxic
contraindicated in G6PD def
in patients with G6PD deficiency, uric acid metabolism leads to hydrogen peroxide generation leading to methemoglobinemia and, in severe cases, Hemolysis
Haemolysis usually occurs 2 to 3 days after starting rasburicase
Monitor closely if no pre chemo genetic testing was done – especially Mediterranean/African ancestry
Note that the post-rasburicase uric acid level for monitoring needs to be processed urgently (ideally in a lithium heparin tube, and on ice) to stop the rasburicase from continuing to reduce uric acid in vitro

QHMAC

3mg (i.e. 2 x 1.5mg vials) as a single dose. This dose should bring uric acid into the normal range but can be repeated if necessary. Patients should be monitored and may require a repeat dose every 2-3 days if serum urate returns to greater than norm

Not recommended as xanthine in the urine and serum can be elevated after the administration of allopurinol because of the inhibition of the conversion of xanthine to uric acid.
Xanthine by itself has limited solubility and can crystallize in the renal tubules making the obstructive uropathy associated with tumor lysis syndrome worse
potential drug-to-drug interaction with azathioprine

No to alkanisation of urine

Diuretics for overload if required

severe AKI with life-threatening hyperkalemia, hyperphosphatemia, and hyperuricemia
CVVH etc may be safer