Rhabdomyolysis

Today we discussed rhabdomyolysis. Some important points:

There is a distinction between a CK elevation without other sequellae and rhabdomyolysis, which may involve consequences such as weakness, electrolyte disturbances, renal failure, acidosis, etc. True rhabdomyolysis is unlikely if the CK is below 10000.

Rhabdomyolysis is a syndrome of muscle necrosis and release of intracellular contents into circulation.

Clinical manifestations are myalgias, pigmenturia (positive supernatent for blood after spinning).

Weakness is only present in most severe cases with significant muscle necrosis.

Lab hallmark is increased CK; 10000 range, up to 100000. CK is the MM fraction. Myoglobin from muscle is released together with CK, but myoglobin is cleared before CK, so may see CK up, but not myoglobin

Renal failure- usually oliguric ATN, from tubular deposition of heme pigment casts and iron from myoglobin

Lytes- Disturbances in Na (sometimes high), K (high), PO4 (high), Ca (low), HCO3 (low), uric acid (high). Hypocalcemia may be extreme, from hyperphosphatemia and increased Ca/PO4 product from Ca salt deposition in necrotic muscle.

Can see hypernatremia because free water "3rd spaces" to muscle because of all of the metabolites.

May increase Cr out of proportion to GFR because creatine is broken down to creatinine


DDx of major causes: (for complete list see link below)

1) Trauma/compression
-crush injury
-struggle against restraint
-immobilization from coma, fracture
-compartment syndrome
-surgery; positioning and tourniquets

2) Non-traumatic "exertional"
-extreme exertion (RFs are unfit, hyperthermia, impaired sweating)
-hyperkinetic states: T-C Sz, DT, severe agitation, amphetamine OD

3) Drugs / poisonings
-Malignant hyperthermia: fever, rigidity, muscle contraction
-EtOH, narcotics, anything causing coma leads to compression
-Sympathomimmetics- cocaine, ecstasy, amphetamines
-CO poisoning
-Statins (esp with cyp inhibitors)
-NMS: fever, rigidity, autonomic instability, post-dopamine antagonist (antipsychotic), or withdrawal of anti-parkinsonians

4) Infections (do not usually cause 'rhabdo-level' CK elevations)
-generalized sepsis
-pyomyositis
-viral (HSV, HIV, EBV, Coxsackie, influenza, CMV)

5) Inflammatory (do not usually cause 'rhabdo-level' CK elevations)
-Dermatomyositis, polymyositis, other inflammatory myopathies

6) Metabolic
-hypokalemia, hypophosphatemia: normally, exercise causes shift of K out of cells, which is trigger for pathway leading to muscle hyperemia and increased O2 delivery. If total body K depleted, less shift, less hyperemia, necrosis.
-extreme hypothyroidism
-metabolic myopathies (suspect in recurrent; CPT deficiency most commonly- may present in adulthood)

Management:

1) HYDRATION!- even if euvolemic, lots of NS, or possibly 150mM HCO3 (i.e. "normal bicarb")- goal urine pH >6.5
2) Reverse underlying cause if possible
3) Mannitol for osmotic diuresis (this is controversial). Give 0.5-1g/kg then 0.25-0.5g/kg q4-6h, usu 20-200g/24h as 20% solution in D5. Possible alternative is loop diuretic (also controversial) Replace urine losses with appropriate IV solution- do urine lytes.
4) Correct lyte disturbances, except Ca, which is replaced only if clinically hypocalcemic (i.e. paresthesias, tetany, long QT) or hyperkalemic. NB- in extreme cases, may see profound hypernatremia acutely, from free water loss in muscle.

Link:

Click here for good review from Critical Care

Click here for a paper questioning the use of bicarb and mannitol