Rhabdomyolysis — SAQ

Stem

A 24-year-old man is brought to the emergency department the morning after a college party at which he had taken MDMA and drunk heavily, then collapsed and lain unconscious on a hard floor for an estimated 8 to 10 hours. He complains of severe aching pain and weakness in both thighs and calves, and on arrival has passed small volumes of dark, tea-coloured urine. On examination he is alert but distressed, dehydrated; pulse 112/min, BP 96/64 mmHg, RR 24/min, SpO2 97% on air, temperature 37.8 C. Both lower limbs are swollen, tense and tender, with marked pain on passive ankle dorsiflexion. The 12-lead ECG shows peaked, narrow T waves and a slightly widened QRS. Initial bloods: CK 38,000 U/L, potassium 7.1 mmol/L, creatinine 220 micromol/L, urea 12 mmol/L, calcium 1.85 mmol/L, phosphate 2.4 mmol/L, venous pH 7.18, bicarbonate 14 mmol/L. Urine dipstick is 4+ blood-positive, but microscopy shows no red cells; the centrifuged supernatant is brown.^[2][5][24]

Questions

a) What is the diagnosis, and which three features in the stem most strongly support it? (2 marks)

Diagnosis: MDMA- and alcohol-associated rhabdomyolysis with prolonged immobilisation, complicated by life-threatening hyperkalaemia, early myoglobinuric AKI and probable compartment syndrome. Supporting features: (i) context — 8–10 hours immobilised after MDMA and alcohol (Melli: illicit drugs, alcohol and prescribed drugs caused 46% of a 475-patient cohort; Richards: rhabdomyolysis in 20% of methamphetamine-positive patients who had CK screened); (ii) biochemistry — CK 38 000 U/L (Stahl mild definition: syndrome plus CK over 1000 IU/L or over 5 times ULN; myoglobinuria and AKI mark severe disease; Veenstra severe spectrum at CK at or above 5000 U/L); potassium 7.1 mmol/L with peaked T waves and QRS widening; calcium 1.85 mmol/L (Veenstra hypocalcaemia at or below 2.00 mmol/L in 41% of severe cases); (iii) urine — dark tea-coloured urine (Cervellin classic triad, although more than 50% never complain of pain or weakness). Melli: urine myoglobin by dipstick/ultrafiltration was positive in only 19%, so a negative qualitative assay would not have excluded the diagnosis — CK carries it.^{[1][2][4][5][24]}

b) Outline your immediate resuscitation, including the specific emergency treatment of his ECG changes. (2 marks)

Continuous cardiac monitoring and two large-bore IV cannulae; catheterise for hourly urine output. Treat hyperkalaemia now because of ECG changes and potassium 7.1 mmol/L: IV calcium salts are primarily indicated for ECG changes or potassium at or above 6.5 mmol/L (Batterink: no included RCT evaluated IV calcium). Then insulin-glucose: 10 units short-acting insulin IV with 50 g glucose (mean potassium fall 0.78 mmol/L at 60 minutes after a 10-unit bolus), or 20 units over 60 minutes with 60 g glucose for potassium over 6.5 mmol/L or marked ECG changes; plus nebulised salbutamol (10 mg peaks at 120 minutes, mean fall 1.29 mmol/L; 20 mg at 90 minutes, mean fall 1.18 mmol/L) — synergistic with insulin. Monitor plasma glucose frequently (hypoglycaemia risk higher in non-diabetic patients with low baseline glucose). Haemodialysis is definitive if refractory. Start vigorous crystalloid in parallel (see c).^[15][16][17]

c) Give the agent, dose, route, rate and target for the cornerstone of definitive treatment. (2 marks)

The cornerstone is early vigorous IV crystalloid, started without waiting for further CK results.^[2][7]

• Agent / route: isotonic crystalloid IV. Prefer lactated Ringer's where the randomised comparison applies: after 12 hours at 400 mL/h, urine pH was higher on lactated Ringer's, with little supplemental bicarbonate and no metabolic acidosis, versus 0.9% saline.^[8]
• Rate: Cervellin pre-hospital 1.5–2 L sterile saline immediately, then 1.5–2 L/h; in extensive rhabdomyolysis Better credits at least 12 L per day of intravenous alkaline solution started at the scene. After admission, alternate saline with 5% glucose.^[2][7]
• Stop / step down when CK is falling (elimination half-life about 25 hours), potassium has normalised and urine output is stable — not on a packed CK-below-1000 stop rule.^[6]

d) He has clinical features of compartment syndrome in both calves. How would you confirm it, and what is the definitive management? (2 marks)

Confirm with compartment pressure monitoring. McQueen: 53 of 116 tibial fractures exceeded an absolute 30 mmHg in the first 12 hours, and a 30 mmHg absolute threshold would have sent 50 patients (43%) to fasciotomy — the absolute number over-triages. Decompress when diastolic minus compartment pressure falls under 30 mmHg; three patients met that rule, all had fasciotomy, and none of 116 had sequelae. Schmidt: decompressive surgical fasciotomy is the only effective treatment. Restore circulating volume before release: reperfusion can surge potassium and myoglobin (Better: early mortality from hypovolaemic shock, hyperkalaemia, acidosis and myoglobinuric AKI).^[7][18][19]

e) Two days later he is oliguric with a creatinine of 540 micromol/L, refractory hyperkalaemia at 7.0 mmol/L despite medical therapy, and pulmonary oedema. State the indications for renal replacement therapy, and explain why his early hypocalcaemia should not be treated with IV calcium on the number alone. (2 marks)^[9][17]

Petejova: do not start RRT on the myoglobin or CK concentration. Use the delayed-strategy triggers tested in AKIKI: severe hyperkalaemia, metabolic acidosis, pulmonary oedema, blood urea nitrogen over 112 mg per decilitre, or oliguria beyond 72 hours. He already has refractory hyperkalaemia, acidosis and pulmonary oedema. STARRT-AKI: accelerated RRT did not reduce 90-day mortality (43.9% vs 43.7%) and caused more adverse events (23.0% vs 16.5%). AKIKI: 49% of delayed-strategy patients never received RRT.^[9][20][21]

Early hypocalcaemia is expected (Veenstra 41% at or below 2.00 mmol/L). Das: calcium homeostasis is biphasic — rebound hypercalcaemia in recovery can be severe and refractory to loop diuretics, low-calcium haemodialysis and calcitonin. Reserve IV calcium salts for ECG changes or potassium at or above 6.5 mmol/L, and monitor through both phases.^[4][17][23]

References18ShowHide

1. [1]Stahl K, Rastelli E, Schoser B A systematic review on the definition of rhabdomyolysis J Neurol, 2020.PMID 30617905
2. [2]Cervellin G, Comelli I, Lippi G Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features Clin Chem Lab Med, 2010.PMID 20298139
3. [3]Zutt R, van der Kooi AJ, Linthorst GE, et al. Rhabdomyolysis: review of the literature Neuromuscul Disord, 2014.PMID 24946698
4. [4]Veenstra J, Smit WM, Krediet RT, et al. Relationship between elevated creatine phosphokinase and the clinical spectrum of rhabdomyolysis Nephrol Dial Transplant, 1994.PMID 7970089
5. [5]Melli G, Chaudhry V, Cornblath DR Rhabdomyolysis: an evaluation of 475 hospitalized patients Medicine (Baltimore), 2005.PMID 16267412
6. [6]Mikkelsen TS, Toft P Prognostic value, kinetics and effect of CVVHDF on serum of the myoglobin and creatine kinase in critically ill patients with rhabdomyolysis Acta Anaesthesiol Scand, 2005.PMID 15954972
7. [15]Batterink J, Cessford TA, Taylor RA Pharmacological interventions for the acute management of hyperkalaemia in adults Cochrane Database Syst Rev, 2015.PMID 35658162
8. [7]Better OS, Abassi ZA Early fluid resuscitation in patients with rhabdomyolysis Nat Rev Nephrol, 2011.PMID 21587227
9. [8]Cho YS, Lim H, Kim SH Comparison of lactated Ringer's solution and 0.9% saline in the treatment of rhabdomyolysis induced by doxylamine intoxication Emerg Med J, 2007.PMID 17384382
10. [9]Petejova N, Martinek A Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review Crit Care, 2014.PMID 25043142
11. [16]Harel Z, Kamel KS Optimal dose and method of administration of intravenous insulin in the management of emergency hyperkalemia: a systematic review PLoS One, 2016.PMID 27148740
12. [17]Geldermann N, Dzimiera J, Fischer H, et al. Acute hyperkalaemia in emergency care: evidence-based approaches Emerg Med J, 2026.PMID 41506858
13. [18]McQueen MM, Court-Brown CM Compartment monitoring in tibial fractures. The pressure threshold for decompression J Bone Joint Surg Br, 1996.PMID 8898137
14. [19]Schmidt AH Acute compartment syndrome Orthop Clin North Am, 2016.PMID 27241376
15. [20]Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of initiation of renal-replacement therapy in acute kidney injury N Engl J Med, 2020.PMID 32668114
16. [21]Gaudry S, Hajage D, Schortgen F, et al. Initiation strategies for renal-replacement therapy in the intensive care unit N Engl J Med, 2016.PMID 27181456
17. [23]Das A, Silva J, Miyata K, et al. Rhabdomyolysis-induced resistant hypercalcemia during the recovery phase of acute kidney injury Cureus, 2026.PMID 42306390
18. [24]Richards JR, Wang CG, Fontenette RW, et al. Rhabdomyolysis, methamphetamine, amphetamine and MDMA use: associated factors and risks J Dual Diagn, 2020.PMID 32644906