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capstone > Tumor Lysis Syndrome > Flashcards

Tumor Lysis Syndrome Flashcards

Vincent

1
Q

what is TLS

A

rapid lysis of cells leading to the release of massive quantities of intracellular components into the bloodstream

caused by cytotoxic tx or spontaneous lysis

subsequent catabolism can lead to emergent life threatening conditions

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2
Q

what are some dx lab values for TLS

A

Uric acid > 8 mg/dL
Phosphate > 4.5 mg/dL
Potassium > 6 mEq/L
Corrected calcium < 7 mg/dL

At least 2 criteria observed within a 24 hour period

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3
Q

what are some clinical dx factors of TLS

A

Meets criteria for AKI
Sx: cardiac dysrhythmia, seizure, neuromuscular irritability, HoTN, HF, sudden death, etc.

Lab dx + at least one of the clinical criteria listed above

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4
Q

what are some risk factors for TLS

A

New dx of advanced stage diffuse large B-cell lymphoma (DLBCL) w large retroperitoneal mass → aggressive hematologic malignancy w large tumor burden “bulky disease”

Older age/pre-existing renal dysfunction

Pre-existing LDH elevation

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5
Q

What is considered high risk for TLS

A

Hematologic malignancies (leukemias and lymphomas)
– Advanced stage (3-4)
–Bulky disease
– Acute leukemia w WBC > 100
– LDH > 2*ULN

Pre-existing renal dysfunction or oncologic renal involvement

Uric acid or electrolytes > ULN

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6
Q

what is considered intermediate risk for TLS

A

Solid tumors that are highly sensitive, advanced stage, or large tumor burden:
– Neuroblastoma, SC lung cancer**

Hematologic malignancies w lower WBC and LDH cut offs
– Not advanced stage or bulky

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7
Q

what is considered low risk for TLS

A

Most solid tumors except those that are highly chemo sensitive advanced stage or large tumor burden

CML

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8
Q

what is hyperuricemia

A

Purine nucleic acids are catabolized into hypoxanthine → kidneys unable to clear uric acid fast enough → uric acid crystallization and deposition in renal tubules → AKI or renal failure

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9
Q

Tx recommendations for hyperuricemia

A

Hydration (goal urine output: ~ 100 mL/hour)

Allopurinol or rasburicase
– Per FDA: Febuxostat limited to patients who cannot tolerate other agents due to an increased risk of AE (SJS, cardiac, all cause mortality)

Goal: normalize uric acid level

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10
Q

allopurinol is preferred for …

A

ppx agent for patients at risk of developing TLS

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11
Q

what is the MOA of allopurinol

A

blocks conversion of nucleic acids released from cancer cells: hypoxanthine to xanthine to uric acid

Does not remove existing uric acid

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12
Q

Allopurinol AE

A

pruritic rash, diarrhea, hypersensitivity skin reactions

HLA-B*5801 allele = increased risk of severe cutaneous AE

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13
Q

allopurinol dose

A

600 mg x1, then 300 mg daily
Start tx 1-2 days prior to chemotherapy and continue for at least 7-10 days or until signs of TLS are absent

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14
Q

Allopurinol special population

A

renal dose adjust in CKD

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15
Q

Allopurinol DDI

A

6-MP, azathioprine

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16
Q

what to monitor w allopurinol

A

repeat uric acid levels according to TLS protocol and renal function

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17
Q

rasburicase is preferred for …

A

Preferred agent for lab or clinical TLS tx. May also be used as ppx in high risk pts

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18
Q

Rasburicase MOA

A

decreases uric acid by converting it into inactive metabolite (allantoin), easily excreted in urine.

Does not inhibit formation of uric acid

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19
Q

Rasburicase dose

A

0.1-0.2 mg/kg/day for up to 7 days

*Single fixed dose
Uric acid < 12 mg/dL: 3 mg x 1
Uric acid > 12 mg/dL: 6 mg x 1

Monitor every 4-6 hours and readmin as necessary

20
Q

Rasburicase AE

A

hypersensitivity (anaphylaxis), oxidative hemolytic anemia, methemoglobinemia

21
Q

rasburicase special population

A

no renal adjustments
CI in G6PD deficiency

22
Q

Rasburicase clinical pearls

A

Special lab: creates false uric acid serum results → blood sample must be collected and put on ice w assay performed within 4 hours

Immediate onset of action

$$

No concern utilizing allopurinol and rasburicase together

23
Q

what is the most life threatening abnormality of TLS

A

hyperkalemia

24
Q

hyperkalemia possible sx

A

cardiac conduction abnormalities, arrhythmia, widening of QRS, muscle weakness, sudden cardiac death, etc

25
Q

what to monitor in hyperkalemia

A

EKG- continuous cardiac rhythm monitoring

26
Q

classes of hyperkalemia

A

mild/mod: ≥ 5-6.5 mEq/L and asymptomatic

Severe: sx OR ≥ 6.5 mEq/L

27
Q

tx for mild/moderate hyperkalemia

A

Acute shift:
IV insulin regular 0.1 U/kg x 1 or 10 U x 1:
Followed by 25-50 gram of dextrose 50%
Less common shifting agents: albuterol nebulizer, sodium bicarb IV

Elimination:
IV loop diuretics – quick onset
K binders – slow onset
Ex: lokelma, kayexalate, etc

28
Q

tx for severe hyperkalemia

A

Same tx options as mild/moderate AND

IV calcium gluconate 1-2g over 2-5 minutes to stabilize the heart

Renal replacement therapy (RRT) if life threatening or refractory

29
Q

what happens when there is high levels of phosphate

A

increased risk of calcium/phosphate precipitation
Precipitate builds up and injures renal tubules → worsening AKI or failure
Secondarily causes hypocalcemia

30
Q

is tx of hyperphosphatemia necessary if mild and asymptomatic in TLS

A

no

Pharmacologic tx not indicated unless severe/sx

31
Q

hyperphosphatemia tx

A

Preventative measures
Initiate low phosphate diet
Avoid phosphorus in fluids

Pharmacologic tx:
Non-calcium phosphate binders (sevelamer hydroxide, lanthanum carbonate, etc)
Renal replacement therapy (RRT)– indicated in sx or refractory cases

32
Q

hypocalcemia sx

A

muscle cramps, tetany, seizures, arrhythmias

33
Q

is tx of hypocalcemia necessary for those who are asymptomatic in TLS

A

Tx not recommended due to increased risk of precipitate formation w phosphorous

34
Q

is tx of hypocalcemia necessary for those who are symptomatic or have severe hypocalcemia in TLS

A

yes

Tx at lowest effective dose
Calcium gluconate 50-100 mg/kg over 2-5 minutes

35
Q

monitoring for hypocalcemia

A

EKG (continuous cardiac monitoring), corrected Ca or ionized Ca every 4-6 hours

36
Q

AKI Tx

A

Hydration – IV NS
Goal urine output: ~100 mL/hr OR 3 L/day
Consider mild diuresis to achieve goal
Avoid LR due to phos/calcium + K

Tx the underlying problem: hyperuricemia, hyperphosphatemia, etc

Eliminate other possible nephrotoxic agents

May have to consider RRT in severe cases w volume overload or oliguria

37
Q

when to consider Renal replacement therapy

A

severe/refractory hyperkalemia

severe/refractory hyperphosphatemia

Acidosis

Fluid overload unresponsive to diuretics

Uremia causing encephalopathy

38
Q

when does TLS occur

A

within first 48-72 hours after cytotoxic therapy initiation

39
Q

when can first lab signs of TLS be observed

A

within 6-24 hours after initiation

40
Q

when can ppx tx be dc for TLS

A

7-10 days

41
Q

what are exacerbating meds of TLS

A

Thiazides: increase uric acid
Lithium: increase uric acid
ACE/ARB: increase K and may worsen AKI
IV fluids w electrolyte additives: increase electrolyte supplements
Multivitamin: increase electrolyte supplement
Cholecalciferol: increase calcium and risk for calcium/phos precipitate
Nephrotoxic meds: NSAIDs, aminoglycosides, etc

42
Q

what are the guideline directed preventative measures for hydration

A

PO/IV fluids starting at least 24 hours prior to start of start of tx

goal UO: 100 ml/hr or 3 L per day

not urinary alkalization anymore

43
Q

what are the guideline directed preventative measures for urate lowering therapy

A

allopurinol or rasburicase

allopurinol is preferred ppx agent

44
Q

what are the guideline directed preventative measures for vigilant lab and clinical monitoring**

A

Low risk: once daily

Intermediate: every 8-12 hours

High: every 4-6 hours

45
Q

what are the guideline directed preventative measures for cytoreduction considerations

A

Case-to-case basis

Consider starting steroids or hydroxyurea to decrease tumor burden prior to tx initiation

capstone (14 decks)

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