Tumor Lysis Syndrome (TLS)

Hyperkalemia is what arrests them - Intracellular potassium is 120 to 130 mEq/L and mass lysis dumps it into the circulation at the same moment uric acid obstructive uropathy has closed the exit. Cardiac arrest from arrhythmia is the immediate threat. Get a 12-lead: hyperkalemia produces left or right bundle branch block, bifascicular block, advanced AV block, sinus bradycardia, sinus arrest, asystole, VT, or VF. Peaked T waves may be there, but there is no orderly progression of ECG changes as the potassium rises and a normal ECG does not exclude a lethal arrhythmia. For life-threatening hyperkalemia the recommendation is early hemodialysis, not another round of temporizing.

No succinylcholine - Avoid succinylcholine when the potassium is 5.5 mEq/L or higher. Reach for a non-depolarizer, and remember that in a TLS patient the potassium you drew an hour ago is already stale.

An elective case does not go forward - Elective surgery is postponed when hyperkalemia is suspected. In a high-tumor-burden patient this is not a number to optimize around the OR schedule.

Hypocalcemia is the more dangerous half of the phosphate problem - The hypocalcemia here is secondary to phosphate chelating calcium, and it is more life-threatening than the hyperphosphatemia itself: arrhythmia, tetany, seizure, death. Be deliberate about replacing it — giving calcium chloride or gluconate potentiates calcium phosphate deposition in kidney and soft tissue and worsens the acute kidney injury. Treat symptomatic or arrhythmogenic hypocalcemia, not a lab value. Calcium can stay low even after the phosphate normalizes because of 1,25-vitamin D deficiency.

Bicarbonate is a trade, not a free win - Alkalinizing the urine raises uric acid solubility roughly tenfold, achieved with 40 to 50 mEq/L of sodium bicarbonate in the hydration fluid. It also drops ionized calcium, which can push a marginal hypocalcemia into arrhythmia or tetany, and it favors precipitation of calcium phosphate salts in the tubules, worsening the acute kidney injury. It is only advisable when rasburicase is not readily available, and calcium has to be followed serially if you do it.

Volume is the primary therapy - Rapid crystalloid expansion raises GFR and gets the solutes out. Prophylaxis runs 3 to 3.5 L/m2 per day, or 4 to 5 L per day, started 48 hours before chemotherapy and continued 48 hours after, targeting roughly 3 L of urine output daily. If you are anesthetizing one of these patients, keep the hydration running rather than letting them arrive volume-contracted on top of everything else.

Protect what kidney function is left - Avoid agents that vasoconstrict the renal vasculature: NSAIDs and iodinated contrast are both specifically named. That constrains your postoperative analgesia plan and it matters when the team wants a contrast CT to stage the mass.

Know which prophylaxis they are on - Allopurinol is a xanthine oxidase inhibitor that prevents uric acid formation but does not treat established hyperuricemia; it also raises serum and urinary xanthine, which is itself poorly soluble and can worsen the obstruction. Rasburicase, recombinant urate oxidase given at 50 to 100 U/kg per day IV or IM, converts uric acid to allantoin and actually treats it. Febuxostat is a newer xanthine oxidase inhibitor without allopurinol hypersensitivity syndrome.

Rasburicase and G6PD deficiency - The reaction generates hydrogen peroxide, which causes severe methemoglobinemia or hemolytic anemia in G6PD-deficient patients. If a patient who received rasburicase has a saturation that will not track the PaO2, send a co-oximetry rather than escalating the FiO2.

Continuous, not intermittent, renal replacement - Ions keep pouring out of lysing cells, so intermittent hemodialysis is followed by rebound hyperkalemia and hyperphosphatemia. Continuous renal replacement therapy at a high dialysate or replacement fluid flow rate is the better modality for ongoing solute removal, including for severe hyperphosphatemia. Know what the patient is on and what it is clearing before you take them to the room.

Look at the chest film before you induce - Dyspnea, orthopnea, and tachypnea in these patients can mean airway compression from the primary tumor. Chest x-ray and CT are part of the standard workup for exactly this reason — look at the images yourself and identify a mediastinal mass or pleural effusion before induction rather than discovering it on laryngoscopy.

Follow the labs at the tempo the disease moves - A comprehensive metabolic panel two to three times daily around therapy is the standard: potassium, calcium, phosphate, uric acid, BUN, creatinine, and LDH. A urinalysis with pH, specific gravity, and output is mandatory if they are being alkalinized. A drifting value is the beginning of the syndrome, not noise.

It can start on your table - Rare reports describe tumor lysis syndrome beginning under general anesthesia. In a patient with a high tumor burden — leukemia with a very high white count, high-grade lymphoma, hepatoblastoma, neuroblastoma — an unexplained intraoperative arrhythmia should send you to a potassium and an ionized calcium before you reach for a deeper anesthetic.

Tumor lysis syndrome (TLS) is the most common oncologic emergency: malignant cells break down en masse and dump their contents into the circulation faster than the kidney can clear them. The result is a characteristic quartet — hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. Released nucleic acids are metabolized through xanthine to uric acid, and because humans lack urate oxidase the uric acid crystallizes in the distal tubules, causing obstructive uropathy and a falling glomerular filtration rate; uric acid additionally scavenges nitric oxide, adding vasoconstriction and renal ischemia on top of the mechanical obstruction. Phosphate released from nucleotides chelates calcium, so the hypocalcemia is secondary and deposits calcium phosphate in kidney and soft tissue.

It usually appears about 72 hours after cytotoxic chemotherapy is started, but occurs spontaneously with high-grade hematologic malignancy and has been reported to begin in patients under general anesthesia.