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Sections in this case
Question and answer links
- W1: A 52-year-old woman with acute myeloid leukemia and a white count of 140,000/µL is 20 hours into induction chemotherapy. · Answer
- W2: A student summarizes the hyperkalemia treatments for her team. Which summary is correct? · Answer
- Q3: Russ, 58, before his first R-CHOP: bulky DLBCL (14-cm mass), LDH 1,860 U/L (about 6.6 times the upper limit), uric acid · Answer
- Q4: Russ, 04:15: potassium 6.4 mEq/L with peaked T waves in V2–V5 and a QTc of 500 ms; calcium 6.8 mg/dL (corrected 6.9, ion · Answer
- Q5: Russ, 04:40: calcium given, T waves narrower, spasm gone; insulin, dextrose and albuterol given. Still dry, urine 15 mL/ · Answer
- Q6: If you were thinking "tumor lysis syndrome" from Russ's chemistry, and you then learn that his 09:00 urine holds sheaves · Answer
- Q8: Russ has worsening AKI after two acyclovir doses infused over 30 minutes while dehydrated. The fresh urine contains need · Answer
- Q7: Russ, hour 30: potassium back to 6.6 mEq/L with peaked T waves despite a second insulin dose and a binder; phosphorus 10 · Answer
Session S4 · 2026-10-29 · supplementary · 20 min Anchor: Acute kidney injury — tumor lysis syndrome (TLS) and crystal nephropathy · Integrates: the hyperkalemia emergency sequence, hypocalcemia and hyperphosphatemia, AEIOU and when to call, prevention that was missed One-line hook: Tumor lysis has a recognizable high-risk window and can begin even before treatment. When it happens anyway, the PA at the bedside has to give calcium for the right reason, withhold it for the right reason — and know when the answer is dialysis.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q8 · Q7
- Identify the patient at high risk for TLS before chemotherapy and choose the prevention that fits: rasburicase or allopurinol, IV isotonic fluid, frequent chemistry.
- Recognize laboratory and clinical TLS from the big four — potassium, phosphorus, uric acid, calcium — plus the creatinine, and stage the AKI (staging discussed, not tested).
- Sequence hyperkalemia treatment in TLS — stabilize, shift, remove — and decide when and how calcium is safe against a high phosphorus.
- Protect the tubules from crystals in TLS, and recognize a drug-induced crystal nephropathy and its usual culprits.
- Name the findings that mean dialysis now in TLS, and say what dialysis does not fix.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
Two readiness questions. Commit to an answer before you open each callout.
W1The cell-lysis pattern
A 52-year-old woman with acute myeloid leukemia and a white count of 140,000/µL is 20 hours into induction chemotherapy. Which set of results is the tumor lysis pattern?
Potassium high, phosphorus low, uric acid high, calcium high, creatinine rising
Potassium low, phosphorus low, uric acid high, calcium low, creatinine normal
Potassium high, phosphorus high, uric acid high, calcium low, creatinine rising
Potassium high, phosphorus high, uric acid normal, calcium high, creatinine normal
Show answer and explanation · Link to this question
Correct answer: C
Learning point: A dying cancer cell empties itself: potassium and phosphate pour out, and its nucleic acids are broken down to uric acid. Phosphate binds calcium, so calcium falls, and uric acid and calcium phosphate crystallize in the tubules, so the creatinine rises. For bedside recognition, look for at least two absolute abnormalities: uric acid ≥8 mg/dL, potassium ≥6.0 mEq/L, phosphorus ≥4.5 mg/dL or corrected calcium ≤7.0 mg/dL around treatment. The original Cairo–Bishop definition also includes relative changes and defines clinical renal involvement as creatinine ≥1.5 times the upper limit of normal; do not confuse that grading rule with KDIGO AKI staging. Why not the others: A — high calcium with low phosphorus is hypercalcemia of malignancy. B — falling potassium and phosphorus is refeeding. D — lysis raises uric acid and lowers calcium. Course reading: Evidence for this case
W2What each potassium drug actually does
A student summarizes the hyperkalemia treatments for her team. Which summary is correct?
Calcium steadies the heart but lowers no potassium; insulin and albuterol shift it into cells; urine, binders and dialysis remove it
Calcium lowers the potassium within minutes; insulin removes it in the urine; a binder protects the heart until dialysis can start
Insulin protects the heart muscle; calcium drives potassium into bone; albuterol removes it through the kidney within the hour
Bicarbonate is the most reliable potassium drug; calcium is reserved for levels above 8.0; binders are the first emergency step
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Three jobs, three kinds of drug. Stabilize: IV calcium steadies the heart-muscle membrane for 30–60 minutes without lowering potassium at all. Shift: insulin with dextrose — with glucose checks, because hypoglycemia comes late when the kidney is injured — and high-dose nebulized albuterol move potassium into cells for a few hours. Remove: only urine, a gut binder or dialysis takes potassium out of the body; everything else wears off. Why not the others: B — calcium lowers nothing and insulin removes nothing. C — the roles are scrambled. D — bicarbonate is unreliable alone, calcium follows the ECG rather than a number, and binders are slower than the shift drugs. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3
Russ, 58, a rural mail carrier, had six weeks of drenching night sweats and a 9-kg weight loss before a CT found a 14-cm abdominal nodal mass: diffuse large B-cell lymphoma (DLBCL), an aggressive lymphoma. He has hypertension and nothing else. On day 0 he was admitted for his first cycle of R-CHOP (rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone), started at 10:00, under the ward's standard lymphoma order set: allopurinol (begun two days earlier), "encourage oral fluids," and chemistry the next morning. No IV fluid was ordered. Nauseated, he vomited twice and drank about 600 mL.
At 19:00 the nurse found a band of grouped blisters wrapping from his left lower chest to his back — herpes zoster (shingles) — with three blisters outside the band. With chemotherapy just begun, oncology ordered IV acyclovir 10 mg/kg (880 mg) every 8 hours; the 20:00 dose ran in over 30 minutes, and the 04:00 dose was running when things changed.
At 04:10 on day 1 — 18 hours after the chemotherapy began — Russ called the nurse: his lips and fingertips were tingling, and his hands had cramped into claws when the blood-pressure cuff inflated. He had passed 120 mL of urine since 20:00.
Vitals: T 37.4 °C · heart rate 112 · BP 104/60 · respiratory rate 18 · SpO₂ 97 % on room air · weight 87.0 kg (88.0 on admission). Exam: dry mouth; flat neck veins; lungs clear; no edema; a firm mass filling the left abdomen; zoster as above; Chvostek sign (tapping the facial nerve in front of the ear twitches the corner of the mouth) and Trousseau sign (carpal spasm under the inflated cuff) both positive. Bladder scan 40 mL.
ECG, 04:15: sinus tachycardia 112, PR 160 ms, QRS 96 ms, peaked T waves in V2–V5, QTc 500 ms.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| R-CHOP, cycle 1 | standard doses | IV (prednisone PO) | day 0 (prednisone days 0–4) | DLBCL |
| Allopurinol | 300 mg | PO | once daily since day −2 | TLS prevention |
| Acyclovir | 880 mg (10 mg/kg) | IV over 30 min | every 8 hours since 20:00, day 0 | Herpes zoster |
| Ondansetron | 8 mg | IV | every 8 hours as needed | Nausea |
| Amlodipine | 5 mg | PO | once daily | Hypertension |
| Test | Day −5 (diagnosis) | Day 0, 08:00 (before chemo) | Day 1, 04:10 (hour 18) | Reference range |
|---|---|---|---|---|
| Sodium (mEq/L) | 139 | 138 | 137 | 136–145 |
| Potassium (mEq/L) | 4.4 | 4.9 | 6.4 | 3.5–5.0 |
| Chloride / bicarbonate (mEq/L) | 103 / 25 | 103 / 23 | 104 / 20 | 98–107 / 22–28 |
| Anion gap (mEq/L) | 11 | 12 | 13 | 8–12 |
| BUN (mg/dL) | 16 | 22 | 46 | 8–20 |
| Creatinine (mg/dL) | 1.0 | 1.6 | 2.9 | 0.7–1.3 |
| Uric acid (mg/dL) | 7.8 | 9.1 | 14.0 | 3.5–7.2 |
| Phosphorus (mg/dL) | 3.9 | 4.7 | 8.9 | 2.5–4.5 |
| Calcium, total (mg/dL) / albumin (g/dL) | 9.2 / 3.9 | 8.9 / 3.9 | 6.8 / 3.9 | 8.5–10.5 / 3.5–5.0 |
| Corrected calcium (mg/dL) | 9.3 | 9.0 | 6.9 | 8.5–10.5 |
| Ionized calcium (mmol/L) | — | — | 0.88 | 1.12–1.32 |
| Magnesium (mg/dL) | 2.0 | 2.1 | 2.2 | 1.7–2.4 |
| LDH (U/L) | 1,420 | 1,860 | 2,450 | 140–280 |
Corrected calcium = measured + 0.8 × (4.0 − albumin) = 6.8 + 0.8 × 0.1 = 6.9. Magnesium is normal, so it is not the cause. Creatinine 2.9 ÷ baseline 1.0 = 2.9 times: KDIGO stage 2 (eGFR not valid — creatinine is moving); urine 120 mL over 8 hours is 0.17 mL/kg/h. All four Cairo-Bishop laboratory criteria are met, plus an AKI and ECG changes: clinical TLS.
Q3The prevention that was missed
Russ, 58, before his first R-CHOP: bulky DLBCL (14-cm mass), LDH 1,860 U/L (about 6.6 times the upper limit), uric acid 9.1 mg/dL, phosphorus 4.7 mg/dL, creatinine 1.6 mg/dL (1.0 five days earlier), nauseated and drinking little. Which pre-emptive plan matched his risk and already abnormal chemistry?
Allopurinol 300 mg daily from two days before, oral fluids encouraged, and chemistry the next morning
Rasburicase after a G6PD check, IV isotonic fluid before the first dose, and chemistry every 4–6 hours
Allopurinol with a sodium bicarbonate drip to keep the urine pH above 7, and chemistry every 12 hours
Oral fluids only, because TLS prophylaxis is reserved for Burkitt lymphoma and the acute leukemias
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Russ was high risk on the counts the TLS lecture and handout list — high-grade lymphoma over 10 cm, LDH more than twice normal, uric acid above 7.5, a rising creatinine, a dry patient — and his morning panel already met two Cairo-Bishop criteria. High risk means rasburicase, an enzyme that converts existing uric acid to soluble allantoin (check G6PD first: it causes hemolysis in G6PD deficiency), IV isotonic fluid before chemotherapy, titrated to urine output, and chemistry every 4–6 hours. Allopurinol only blocks new uric acid and takes a day or two to act. Why not the others: A — inadequate for this patient, who already has laboratory TLS; merely encouraging oral fluid is not an adequate intermediate-risk hydration plan either. C — urinary alkalinization is no longer recommended in TLS; it precipitates calcium phosphate. D — bulky high-grade lymphoma is on the high-risk list too. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q4 · Q5 · Q6 · Q8
Every abnormality on that 04:10 panel needs an order in the next hour — and two of them, the potassium and the phosphorus, pull the calcium decision in opposite directions.
Q4The first drug, and the trap
Russ, 04:15: potassium 6.4 mEq/L with peaked T waves in V2–V5 and a QTc of 500 ms; calcium 6.8 mg/dL (corrected 6.9, ionized 0.88 mmol/L) with perioral tingling, a Chvostek sign and carpal spasm; phosphorus 8.9 mg/dL; bicarbonate 20 mEq/L; dry, with 15 mL/h of urine. What do you give first?
No calcium: with a phosphorus of 8.9, any calcium will precipitate in his kidneys; give insulin with dextrose and a binder
A calcium gluconate infusion titrated to a total calcium above 8.5, since the Chvostek sign shows dangerous hypocalcemia
IV sodium bicarbonate to shift the potassium and alkalinize the urine for the uric acid; calcium only if he seizes
Monitored IV calcium per emergency protocol for ECG changes and tetany, then potassium-shifting treatment; do not chase a normal calcium value
Show answer and explanation · Link to this question
Correct answer: D
Learning point: Hyperkalemia kills first in TLS, and peaked T waves mean the heart is already affected, so IV calcium goes in now — carpal spasm with a long QT is a second, independent reason. Give monitored calcium and reassess the ECG and symptoms; then shift potassium with insulin/dextrose and nebulized albuterol, following serial glucose monitoring. Persistent severe symptoms may require additional specialist-directed calcium. What you do not do is infuse calcium to normalize the number: every milligram meets a phosphorus of 8.9 and can precipitate as calcium phosphate in the kidney. Lower the phosphate, and the calcium follows. Why not the others: A — withholding calcium from a hyperkalemic ECG trades the heart for the kidney. B — normalizing calcium unnecessarily increases calcium-phosphate precipitation risk; use the minimum required for dangerous symptoms or ECG findings. C — bicarbonate lowers ionized calcium further and precipitates calcium phosphate in alkaline urine. Course reading: Evidence for this case
Q5Fluid, urate and phosphate
Russ, 04:40: calcium given, T waves narrower, spasm gone; insulin, dextrose and albuterol given. Still dry, urine 15 mL/h, BP 106/62, lungs clear; uric acid 14.0 mg/dL, phosphorus 8.9 mg/dL, creatinine 2.9 mg/dL; G6PD screen sent. What is the plan for the next 24 hours?
Isotonic saline as a bolus, then a rate titrated to urine output and lungs; rasburicase once G6PD is normal; a binder
Furosemide 80 mg IV to restart the urine first, then saline at 75 mL/h so that a failing kidney is not flooded with fluid
A sodium bicarbonate drip to a urine pH above 7, plus a second allopurinol dose to dissolve the uric acid crystals faster
No fluid while he is oliguric, and dialysis this morning for a uric acid of 14 before the crystals in his tubules can set
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Crystals form where urine is scant and concentrated, so the first treatment is flow: potassium-free isotonic saline, a bolus and then a rate individualized to perfusion, hourly urine output and frequent lung/weight reassessment — a kidney full of crystals may not answer. Rasburicase clears the uric acid already there (send later levels on ice, or the enzyme keeps working in the tube); a phosphate binder is an adjunct. No bicarbonate: alkaline urine precipitates calcium phosphate, and urinary alkalinization is no longer recommended in TLS. Why not the others: B — a loop diuretic in a dry patient worsens perfusion. C — alkalinization is out, and allopurinol cannot dissolve urate. D — he is dry, not overloaded, and a urate number alone is not a dialysis indication. Course reading: Evidence for this case
09:00. The G6PD screen was normal at 06:10, and rasburicase ran at 06:30. On saline at 250 mL/h after a 1-L bolus, Russ is making 40 mL of urine an hour; potassium 5.4; the spasm has not returned. The nephrology fellow sends fresh urine for microscopy before the next antiviral dose.
Concordance-style practice — no expert panel stands behind the key. "Unchanged" means the finding does not move the hypothesis.
Q6Evidence update
If you were thinking "tumor lysis syndrome" from Russ's chemistry, and you then learn that his 09:00 urine holds sheaves of needle-shaped crystals, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The chemistry already strongly establishes TLS. Needle-like crystals raise concern for an additional crystal nephropathy in a dehydrated patient receiving IV acyclovir, but morphology alone does not identify the material: uric acid can also form needles. Retain TLS and investigate a possible concurrent drug-related injury. Review acyclovir indication, renal dosing, infusion rate and hydration with pharmacy; do not turn a suggestive sediment finding into a proven second diagnosis. Why not the others: A and B discount strong biochemical evidence without a contradictory finding. D can be defended if the student explains that urate crystals would support TLS, while acknowledging that the material is unconfirmed; E overstates the diagnostic weight of nonspecific morphology. C is the preferred formative response, not an expert-panel score. Course reading: Evidence for this case
Q8The next acyclovir dose
Russ has worsening AKI after two acyclovir doses infused over 30 minutes while dehydrated. The fresh urine contains needle-shaped crystals. What is the safest next prescribing action?
Give the next full dose over 15 minutes so treatment finishes before dialysis
Continue the same regimen because TLS explains all kidney findings
Pause the next dose for immediate oncology/ID/pharmacy review of need, renal dosing, hydration and an infusion of at least one hour if continued
Add bicarbonate solely to alkalinize the urine while continuing the rapid infusion
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Rapid IV acyclovir in a dehydrated patient with impaired clearance increases crystal-injury risk. The label requires infusion over at least one hour, adequate hydration and renal adjustment. The crystals suggest a possible additional process, not chemical proof; urgently balance antiviral need against toxicity and adjust the next order. Why not the others: A increases the infusion hazard; B overlooks a modifiable exposure; D leaves the unsafe regimen in place and adds inappropriate TLS alkalinization. Course reading: Evidence for this case
The next acyclovir dose was paused for review. Oncology, ID and pharmacy retained treatment for immunocompromised zoster, with renal-adjusted timing and infusion over at least one hour; ongoing hydration followed the changing volume examination.
Part 3 — Course and Decisions
Answers for this section: Q7
16:00, day 1 — hour 30. As the potassium crept back up, a dose of sodium zirconium cyclosilicate (a potassium binder) and a second dose of insulin with dextrose went in at 12:30. Since noon Russ has made 10 mL of urine an hour, but the saline has kept running at 250 mL/h with no one rechecking him; he is 3.8 L in since 04:00. Weight 90.0 kg; fine crackles at both lung bases; SpO₂ 93 % on 2 L; neck veins visible at 10 cm. The cramps are back, with Chvostek and Trousseau signs.
| Test | 04:10 | 09:00 | 16:00 | Reference range |
|---|---|---|---|---|
| Potassium (mEq/L) | 6.4 | 5.4 | 6.6 (peaked T waves again) | 3.5–5.0 |
| Phosphorus (mg/dL) | 8.9 | 8.6 | 10.2 | 2.5–4.5 |
| Calcium, total (mg/dL) | 6.8 | 7.0 | 6.5 | 8.5–10.5 |
| Uric acid (mg/dL; on ice after rasburicase) | 14.0 | 2.1 | 1.9 | 3.5–7.2 |
| Bicarbonate (mEq/L) | 20 | 19 | 17 | 22–28 |
| Creatinine (mg/dL) | 2.9 | 3.2 | 3.6 | 0.7–1.3 |
| Urine output (mL/h) | 15 | 40 | 10 | at least 44 (0.5 mL/kg/h) |
Creatinine 3.6 ÷ 1.0 = 3.6 times baseline: stage 3.
Q7Is it time?
Russ, hour 30: potassium back to 6.6 mEq/L with peaked T waves despite a second insulin dose and a binder; phosphorus 10.2 mg/dL with recurrent carpal spasm; urine 10 mL/h for four hours despite 3.8 L of saline; crackles and SpO₂ 93 % on 2 L; uric acid 1.9 mg/dL; creatinine 3.6 mg/dL. What now?
Run the saline faster and give furosemide 200 mg IV to force a diuresis, then recheck all the chemistry in six hours
Repeat the calcium, stop the saline, and call nephrology for urgent dialysis: potassium, phosphate and volume are failing
Start a calcium infusion to hold the calcium above 8 and add a second binder; dialyze only if the potassium passes 7.0
Hold off on dialysis: the uric acid is down to 1.9 and the creatinine has not reached 4.0, so the kidney is turning the corner
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Dialysis treats complications, not numbers, and Russ now has three: hyperkalemia back with ECG changes despite treatment, phosphate climbing with symptomatic hypocalcemia, and oliguria with fluid in his lungs — the E and O of AEIOU plus TLS's own phosphate trigger. Calcium again for the ECG and the spasm, no more saline, and call now, because dialysis takes time to arrange. Know its limits: it removes potassium, phosphate, uric acid and fluid, but the lymphoma keeps dying, so levels rebound after each session — recheck every few hours and expect more than one session. Why not the others: A — fluid into an oliguric, crackling patient goes to his lungs. C — the calcium drip is the precipitation trap, and waiting for 7.0 is waiting for an arrhythmia. D — the uric acid is fixed, but potassium, phosphate and volume are not; no creatinine threshold is required. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q8 · Q7
Dialysis began at 19:00 through a temporary catheter. After the first session potassium was 4.6 and phosphorus 6.1; by morning they had rebounded to 5.7 and 8.0, and Russ needed sessions on days 2 and 3 while the lymphoma finished breaking down. The cramps stopped after day 2; the acyclovir continued at a kidney-adjusted dose, each dose over an hour. Urine output returned on day 4, dialysis stopped, and the creatinine — peak 4.4 on day 3 — was 2.0 at discharge on day 9 and 1.3 on day 21, when cycle 2 ran with rasburicase, IV fluid from the evening before and chemistry every 4–6 hours: no clinical TLS. At three months: creatinine 1.1 mg/dL (eGFR 78 at steady state) — resolved. The oncology order set now asks two questions before the first dose: is this patient high risk, and is IV fluid running?
Clinical Pearl — Hyperkalemia kills first In TLS potassium is the lethal number. Pair it with the ECG, give calcium for ECG changes, shift with insulin and albuterol, and remember the tumor keeps releasing it — recheck every few hours.
Clinical Pearl — Calcium for the heart and the spasm, not the number Give a monitored bolus for hyperkalemic ECG changes whatever the phosphate, and for tetany, seizure or a long QT. Do not give calcium merely to normalize the laboratory value during hyperphosphatemia. Use the minimum needed for dangerous symptoms or ECG changes with monitoring, while controlling phosphate; persistent symptoms require urgent specialist reassessment.
Clinical Pearl — Allopurinol stops new urate; rasburicase removes old High-risk patients get rasburicase (after a G6PD check) and IV isotonic fluid before the first dose. Send post-rasburicase urate on ice. No urinary alkalinization in TLS.
Clinical Pearl — The crystal family Uric acid (TLS), acyclovir (high-dose IV, fast, dry), high-dose methotrexate, sulfonamides (TMP-SMX, sulfadiazine). Prevention depends on the drug: renal dosing, appropriate hydration and the correct route/rate. Acyclovir infusion must last at least an hour; high-dose methotrexate has a separate alkalinization protocol. Do not generalize that protocol to TLS or every crystal-forming drug.
Pitfall — The wrong order set Russ was high risk on the morning of chemotherapy — bulky disease, an LDH more than six times normal, uric acid 9.1, creatinine already 1.6 — and got an intermediate-risk plan with no IV fluid. Recognize risk before treatment while remembering that spontaneous TLS also occurs.
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q8 · Q7
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-16, aki-21, aki-22, aki-23, aki-24, aki-25, lytes-13, lytes-17, lytes-19.