LET’S BREAK IT DOWN:

RHABDOMYOLYSIS
Vivian Phyo (PGY2 IM Pharmacy Resident)
LEARNING OBJECTIVES

IDENTIFY THE CAUSES AND DESCRIBE THE EVALUATE THE DIAGNOSIS DEVELOP TREATMENT
POTENTIAL RISK FACTORS PATHOPHYSIOLOGY OF AND CRITERIA OF PLANS FOR A PATIENT CASE
OF RHABDOMYOLYSIS COMPLICATIONS RHABDOMYOLYSIS
ASSOCIATED WITH
RHABDOMYOLYSIS
 RHABDOMYOLYSIS
Definition: A state of severe muscle injury or breakdown of muscle tissue
 CAUSES/RISK FACTORS

 Most common: trauma, immobilization, sepsis, and cardiovascular surgeries

 Non-traumatic causes:
• Statin, fibrates, daptomycin, colchicine, zidovudine, anticholinergics, illicit drugs
Medication • Baclofen-withdrawal

• Hyperosmolar hyperglycemic state, diabetic ketoacidosis

Endocrine • Myxedema coma

• Disorders of glycogenolysis, glycolysis, etc. – any disorders in ATP-muscle

Myopathy production

• Polymyositis, dermatomyositis
Autoimmune
• Malignant hyperthermia, neuroleptic malignant syndrome, frostbite
Body temperature
COMPLICATIONS

Disseminated
Electrolyte Acute Kidney
Intravascular
Imbalance Injury
Coagulation (DIC)
1. ELECTROLYTE IMBALANCE

With muscle injury/cell destruction, the content inside muscle cell leaks out into the
blood stream.
What electrolyte changes would you expect?

Hyper or Hypo?
Potassium HYPERkalemia
Phosphate HYPERphosphatemia
BUN/Uric acid HYPERuricemia
Calcium HYPOcalcemia → HYPERcalcemia
2. ACUTE KIDNEY INJURY (AKI)

Multifactorial causes:
1) RAS activation, ↑vasoconstrictor, ↓vasodilator
 Renal vasoconstriction (reduced blood flow to kidneys)
2) Proximal convoluted tubule (PCT): in acidic pH,
recycling of ferrihemate of myoglobin produces
oxygen-free radicals
 PCT cell injury
3) Distal convoluted tubule (DCT): excessive myoglobin
downstream promotes formation of cast
 Obstruction of DCT
3. DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
Thought to be due to thromboplastin released during muscle/vasculature injury
 DIAGNOSIS

 Creatinine Phosphokinase (CPK): 3-5x the ULN (> 1000 IU/L)

 Higher CPK = higher likelihood of AKI

 Urine Analysis (UA): Positive for heme with < 5 RBCs

 Proteinuria may be present
 Myoglobin casts may be present
TREATMENT

Hydration!!! (usually 200-300 ml/hr but up to 10-20 L intake with adequate diuresis)
 Sodium bicarbonate
 MOA: Urine alkalinization to reduce PCT cell injury,
prevent obstruction in DCT, and neutralize hyperuricemia
 Monitor: symptomatic hypocalcemia
 Goal: maintain serum pH < 7.5
 Mannitol (used in crush injury)
 MOA: hyperosmotic agent to reduce intracerebral hemorrhage
and promote urine output
 Avoid in: AKI, oliguria, anuria → volume overload + hyperosmolality
 Potassium-containing fluids (e.g., LR) = AVOID!
Loops - consider if volume overload
Sodium bicarbonate 150 mEq in D5W at 100 ml/hr
PATIENT CASE

EO is a 84 years old male with PMH of HFrEF

(15%, s/p ICD), CAD s/p CABG, CKD II, DM2,
and HTN, who presented with progressive hip
and leg pain for 3 days.
Of note, son reports that patient recently
restarted many medications after PCP visit
last month as patient had been previously
non-compliant. One of the medications
restarted include rosuvastatin 40mg.

Patient was started on:

Sodium bicarbonate 150 mEq in D5W at 100 ml/hr
 SUPPORTIVE CARE
Hyperkalemia
 C – calcium gluconate
 B – beta-agonist or sodium bicarbonate
 I, G – insulin, glucose
 K – kayexalate or lokelma
 D – diuretics
Symptomatic hypocalcemia
(seizures, arrhythmia)
 Calcium gluconate
Hyperuricemia
 Allopurinol (consider if uric acid > 8 mg/dL)
Dialysis – may consider in:
 Anuric AKI
 Refractory hyperkalemia
 Volume overload
 Severe acidosis/uremia
 HD preferred over PD
 CRRT, not HD, may have a role in the
removal myoglobin
QUESTIONS?
Vivian Phyo (PGY2 IM Pharmacy Resident)