Rhabdomyolysis NGN Case Study

The triad announcing the diagnosis: prolonged immobilization on hard ground, diffusely painful firm muscle, and tea-colored urine that dips positive for blood. A CK of 38,000 confirms massive muscle breakdown.

The urine trick worth knowing: the dipstick reads myoglobin as blood — strongly positive “blood” with few or no red cells on microscopy is the classic rhabdo signature. Calling this a UTI or simple hematuria is the mislabel that wastes hours.

The immediate danger cues: K⁺ 5.9 with peaked T waves (dying muscle dumps potassium), creatinine 2.2 with oliguria (myoglobin is already clogging and poisoning the tubules), volume depletion (overnight on the floor, tachycardic, soft BP), low calcium and high phosphate (the injured muscle is soaking up calcium).

Background cue: the statin — a contributor worth holding, though the floor did most of this.

The cascade: compressed, ischemic muscle lyses and releases its contents — myoglobin (nephrotoxic and tubule-obstructing, especially in acidic, concentrated urine), potassium (dysrhythmia threat), phosphate (binds calcium → hypocalcemia), and acids. Add overnight dehydration and the kidneys take the hit from both directions: low flow and direct toxicity. This is pigment-induced AKI on top of prerenal physiology.

The question every found-down patient deserves: WHY did he fall and stay down? Mechanical slip is the story, but syncope (arrhythmia, MI), stroke, sepsis, and hypoglycemia all drop people on bathroom floors — EKG (running already), troponin, glucose, neuro exam, and infection screen run in parallel. Treating the rhabdo while missing the cause is half a save.

Also on the watch list: the firm, tender right thigh — compressed muscle swells as it reperfuses, and compartment syndrome can develop after rescue, not just before.

1. Hyperkalemia with EKG changes — K⁺ 5.9 and peaked T waves in a patient whose muscle is still leaking is the minutes-scale threat: membrane protection and shifting per protocol come first.

2. The kidneys — the hours-scale threat: myoglobin is actively injuring tubules, and the single best defense is washing it through with aggressive fluids before the AKI becomes established.

3. The limb — the evolving threat: serial compartment checks on that right thigh as fluids and reperfusion swell it.

4. The cause of the fall — solved in parallel, or he’s back on the floor next month.

For the potassium: hyperkalemia protocol with EKG changes — calcium first (membrane), insulin/D50 and albuterol (shift), continuous cardiac monitoring, serial K⁺. (If you’ve worked our hyperkalemia case, this sequence is an old friend — rhabdo is one of its classic causes.)

For the kidneys — the heart of rhabdo care: aggressive isotonic crystalloid, often liters early, titrated to a urine output target of roughly 200–300 mL/hr in significant rhabdo per orders — dilute, fast-flowing urine is the treatment. Hourly I&O via the Foley isn’t monitoring here; it’s the steering wheel.

Holds and cautions: statin and ACE inhibitor held; no NSAIDs for the muscle pain (opioids per orders instead); asymptomatic hypocalcemia is generally not corrected (the calcium comes back out of the muscle later — replacing it now invites rebound hypercalcemia) unless symptomatic or needed for the hyperkalemia.

Trending: serial CK (expect a peak then fall), electrolytes, creatinine, compartment checks, pressure-area skin care — and dialysis stays on the horizon if oliguria and hyperkalemia defeat the fluids.

This is compartment syndrome declaring itself — pain out of proportion, unrelieved by opioids, worse with passive stretch, in a tense compartment. The reperfused, fluid-resuscitated muscle has swollen inside its fascia. And note: a present pulse rules out nothing — pulselessness is the last P, not the first; pain and passive-stretch pain are the early ones.

Act now: notify the provider/surgery immediately — this is a surgical emergency (fasciotomy) measured in hours of muscle and nerve viability. Keep the limb at heart level (elevation drops perfusion pressure into the compartment; dependent positioning worsens swelling), remove anything constrictive, do NOT ice it, and document serial neurovascular checks with times.

The trap inside the moment: chalking the pain up to “he was lying on that side all night.” Escalating analgesia without escalating assessment is how compartments are lost — pain that outruns the story is a finding, not a dosing problem.

Improving: the CK curve over its peak, clearing urine, recovering creatinine, stable potassium — the kidneys took a hit and survived it; the fasciotomy saved the leg the fluids were swelling.

Still in play: fasciotomy wound care and staged closure, PT for the deconditioning and muscle injury, renal function follow-up (some patients keep a CKD souvenir), statin re-evaluation by his provider, and the afib management plan — the fall cause now has a treatment, and likely an anticoagulation conversation.

The system layer: he lay on a floor for ten hours because no one knew. Discharge planning includes a personal emergency response device, a daily check-in arrangement with the neighbor or family, a home fall-hazard review, and bathroom grab bars — the cheapest renal protection he’ll ever get is never spending a night on the tile again.