Rhabdomyolysis: Advances In Diagnosis And Treatment

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Abstract

Rhabdomyolysis is a potentially life-threatening condition caused by a breakdown of skeletal muscle and the release of the intracellular contents into the circulatory system. There are many possible causes, including crush injury, excessive muscular activity, medications, infections, and varied metabolic, connective tissue, rheumatologic, and endocrine disorders. It is vital that emergency clinicians consider the diagnosis when patients present with circumstances known to be high-risk for rhabdomyolysis, including intoxication, prolonged immobilization, and/or altered mentation. Optimal crystalloid selection is still debated, but immediate, aggressive intravenous volume expansion is indicated to prevent myoglobinuric renal failure. Serum potassium levels must be obtained and electrocardiograms must be evaluated to identify lifeand limb-threatening complications of hyperkalemia. This review examines the current evidence on symptoms and diagnostic methods as well as standard first-line treatments of rhabdomyolysis. In addition, evidence from animal models on urine alkalinization with sodium bicarbonate infusion is discussed.

Case Presentations

You receive an EMS notification for a patient with a potential “tib-fib” fracture. EMS reports a prolonged extrication of a night crew construction worker whose lower leg was trapped underneath a steel beam after a scaffolding collapse. EMS notes an obvious deformity to the mid-lower leg, with tense edema and bluish discoloration of the toes and delayed capillary refill. A large-bore IV was placed prior to extrication, and a rapid crystalloid infusion was initiated. Upon arrival, you note the absence of a dorsalis pedis pulse in addition to the tense edema of the lower leg and cyanotic digits. Your concern for compartment syndrome is confirmed with a Stryker needle registering a compartment pressure of 55 mm Hg. You notify the trauma surgeon of the need for fasciotomy and advise the OR. While this is happening, you get a call from the lab with a “panic value” of a CK level of 37,000 U/L, and the nurse reports gross blood output from the Foley catheter. His BUN is 28 and his creatinine is 4.

Case Presentations

Shortly thereafter, a nurse informs you of a new patient who “just doesn't look well.” You assess the patient, a 69-year-old woman who is coughing up green sputum, saturating 89% on room air, and is febrile, tachypneic, and tachycardic with a blood pressure of 86/40 mm Hg. The patient's daughter informs you that her mother was just released from the hospital 6 days earlier after being treated for pneumonia. You suspect septic shock and instruct the nurse to place a nonrebreather mask on the patient. You administer broad-spectrum antibiotics, draw cultures and labs (including a venous lactate and a cardiac panel), and initiate a 30-cc/kg crystalloid infusion. The blood pressure normalizes, so you breathe a sigh of relief, but soon after, the lactate returns elevated at 8 mmol/L, which confirms your suspicion for severe sepsis. The nurse places a Foley catheter and reports that there is scant and “dark” urine in the bag. The WBC count returns at 18.4, and her BUN and Cr are 32 and 5.5, respectively. You note that the BUN:Cr ratio is odd, considering her previously normal renal function; you expected an increased ratio due to prerenal azotemia from severe sepsis. You then notice that the CK level is 67,000 U/L with normal MB fraction. To confirm your hunch, you check the UA, which returns positive for “blood” but does not show any red blood cells in the sediment.

Case Presentations

These 2 cases remind you that rhabdomyolysis has many causes, but the treatment in all cases is based on an aggressive hydration strategy. You recall that sodium bicarbonate infusion may be indicated and wonder: when, how, and to whom should it be initiated? You also wonder, “Is there anything else I can do for these patients that would mitigate against complications from renal failure?”

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