So Bored I Worked Out: Rhabdomyolysis

New year, new beginnings, and new resolve. A 31 year-old slightly overweight male visits the emergency department a week after New Years with a chief complaint of muscle soreness. He had recently attended a soulcycle session with his girlfriend as part of his new year’s resolution to lose some of his winter weight. The next day he was extremely sore (more than expected) and started to have dark urine (not expected). Our enthusiastic exerciser has rhabdomyolysis.

What is rhabdomyolysis? What are the common causes?

Rhabdomyolysis is a syndrome precipitated by injury to skeletal muscle cells resulting in release of intracellular contents such as creatine kinase, myoglobin, potassium, phosphate, and lactate dehydrogenase. Common causes include trauma, immobilization secondary to intoxication or altered level of consciousness, and exercise related injury. Other possible etiologies include autoimmune and genetic disorders, infectious and as well as certain medications.

What are the signs and symptoms of rhabdomyolysis?

Common symptoms include weakness, fatigue, fever, muscle soreness, and pain. It is important to note that muscle symptoms are present in only half the cases. Therefore, rhabdomyolysis can occur without any signs or symptoms. Clinical suspicion must be high when suggested by history.

What are the complications?

Complications from rhabdomyolysis are largely due in part to consequences of muscle necrosis. Widespread release of potassium and phosphorus leads to hyperkalemia and hypocalcemia (secondary to deposition of calcium phosphate). This is further complicated by tubular obstruction from uric acid and free myoglobin that can lead to acute renal failure.

It is important to note that neither the degree of creatine kinase elevation nor myoglobinuria is predictive of acute renal failure.

How is rhabdomyolysis diagnosed?

Elevated serum creatine kinase (CK) is the best indicator of muscle injury. While the degree of elevation correlates with the severity of muscle damage, it does not predict renal failure or other morbidities. Five times the normal limit has been accepted as the requirement for diagnosis of rhabdomyolysis. CK levels peak 24-72 hours after muscle injury.

Myoglobin is also released and can be detected in the urine faster than elevated CK. It is cleared in 1-6 hours, so it is not very sensitive. The myoglobin level takes several days for results to return so the UA is often used as a screening alternative. The UA will show presence of heme without RBCs in the urine.

What is the treatment for rhabdomyolysis?

Aggressive hydration with IV fluids is essential in preventing and treating acute renal failure. Consider a foley catheter in patients with high suspicion for ARF in order to monitor urine output (UOP). The recommendation is 24-72 hours of crystalloid with a goal UOP of 2ml/kg/hour or 200-300ml/hour.

The use of sodium bicarbonate and mannitol had been recommended in the past, but there is no prospective study indicating their benefit. The rationale was that alkalinization of urine would decrease toxicity of myoglobin in the renal tubules. Mannitol was thought to increase osmotic diuresis resulting in increased flushing of the renal tubules. They are not without risk as sodium bicarbonate may cause hypokalemia, hypocalcemia, and metabolic alkalosis, and mannitol may cause osmotic diuresis in a hypovolemic patient.

One should treat electrolytes disturbances such as hyperkalemia and hypocalcemia accordingly. Replete calcium only if patient is symptomatically hypocalcemic. If the rhabdomyolysis is severe enough to cause acute oliguric tubular necrosis, hemodialysis may be necessary. Most patients recover their renal function with prompt treatment.

References:
Counselman, F. and B. Lo. “Chapter 89. Rhabdomyolysis.”Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Eds. Judith E. Tintinalli, et al. New York, NY: McGraw-Hill, 2015. n. pag. AccessMedicine.Web. 8 Jan. 2017.

Sauret J. and G. Marinides. “Rhabdomyolysis.”Am Fam Physician. 2002 Mar 1;65(5):907-913.

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3 Comments

ablumenberg · January 12, 2017 at 1:36 am

Awesome post Andy!!

Rhabdomyolysis can also have some pretty interesting laboratory abnormalities.

Creatinine may be artifactually elevated because creatine (a phosphate – ATP buffer found in myocytes) registers as creatinine on many standard assays. If the event which caused the rhabdomyolysis was within a short time window and there is a significant creatinine elevation this is unlikely to represent a true creatinine elevation. If a patient were to acutely lose 90% of their renal function (i.e., almost equivalent to bilateral nephrectomies), their creatinine would be expected to rise by only 1.8 – 2.0 mg/dL in 24 hours. (1)
Consider rhabdomyolysis if you ever see a patient’s creatinine rise at a faster rate than on this graph: http://jasn.asnjournals.org/content/20/3/672/F3.expansion.html
For example, if a patient had a creatinine of 1.2 mg/dL yesterday and 5.0 mg/dL today then consider rhabdomyolysis.

Transaminases (AST/ALT) are elevated because these enzymes are found in skeletal muscle. The transaminases are involved in gluconeogenesis which occurs in myocytes during starvation. AST/ALT are erroneously called “liver function tests.” True liver function tests include ammonia level, prothrombin time, albumin, and other assays of hepatically-produced proteins. Transaminase elevation in rhabdomyolysis does NOT indicate liver injury (2).

Lactate dehydrogenase is elevated any time there is cell lysis. LDH is required for glycolysis and is found in nearly all living cells (animals, plants, bacteria, etc.). A little *recent* history of medicine: LDH and AST were used as a cardiac biomarker to detect acute myocardial infarction before troponin and CK-MB assays were developed. (3)

1. http://jasn.asnjournals.org/content/20/3/672.full
2. https://www.ncbi.nlm.nih.gov/pubmed/20407858
3. https://www.ncbi.nlm.nih.gov/pubmed/1086587

Andy · January 16, 2017 at 7:35 pm

thanks for the info adam!

Jordan Dow · July 7, 2017 at 12:45 pm

Ca will precipitate after combining with the released Phosphate. Repleting Ca only in the symptomatically hypocalcemic patients prevents them from becoming hypERcalcemic once the Ca precipitates back out. Beware the stones, bones and proverbial psychiatric overtones…