Rhabdomyolysis

Rhabdomyolysis is a condition in which muscle cells are damaged and myocyte content are released into the plasma. Rhabdomyolysis can be completely asymptomatic with elevation of muscle enzymes in the blood. However, extensive muscle damage can result in a severe increase in myoglobin and potassium ions - arrhythmias and acute renal failure.

If rhabdomyolysis is suspected, renal function, coagulation status, ionogram, circulatory parameters and lung function should be monitored.

=Definition of Disease=

Rhabdomyolysis is the rapid breakdown of muscle that causes the release of intracellular contents, including protein pigment myoglobin, into the extracellular space and bloodstream (McCance and Huether, 2014).

=Pathophysiology and Disease Described=

Rhabdomyolysis is sometimes interchangeably called myoglobinuria, crush syndrome, or compartment syndrome. Myoglobinuria – was first described in victims of crush injuries during WWII. It refers to the presence of muscle protein in the urine. More recent causes include individuals who become unresponsive and immobile for long periods as a result of drug and alcohol overdoses (McCance and Huether).

Crush Syndrome – describes injuries that result from the crushing of a body part and primarily involves the pathophysiology involving the kidneys and coagulation syndrome (McCance, and Huether).

Compartment Syndrome – the consequences of increased intracompartmental pressure of a muscle. Compartment syndromes occurs when increased venous pressure compromises blood flow to the affected area. This leads to decreased arterial inflow, ischemia, and edema (McCance and Huether).

Physiological interruptions in the sarcolemmal membrane allow the muscle constituents to be released. Complications include: •	hyperkalemia because of the release of intracellular potassium into the circulation •	metabolic acidosis from freeing of intracellular phosphorus and sulfate, which are both negative ions •	acute renal failure as myoglobin precipitates in the tubules, thereby obstructing flow through the nephron and causing injury •	disseminated intravascular coagulation (DIC) caused by activation of the clotting cascade by sarcolemma damage and release of intracellular components as a result of the damaged muscle tissue

=Genetics=

Possibly caused from a hereditary enzyme disorders

=Epidemiology=

Direct muscle injury is the most common cause, however, other causes include drugs, toxins, endocrinopathies, malignant hyperthermia, neuroleptic malignant syndrome, heatstroke, hypothermia, electrolyte alterations, diabetic ketoacidosis and non-ketotic hyperosmolar coma, severe hypo- or hyperthyroidism and bacterial or viral infections (Cervellin, Comelli, Lippi, 2010).

=Signs and Symptoms=

(McCance and Huether, 2014)

1.	Pain out of proportion to the injury

2.	Paresthesias to affected area

3.	Pallor to affected area

4.	Pulselessness

5. 	Paralysis

6.	Systemic symptoms of fever, malaise, fever and tachycardia, nausea and vomiting

The classic triad of muscle pain, weakness and dark urine is classic for rhabdomyolysis, but some patients may not experience pain  or muscle weakness. Dark colored urine as a result of myoglobinuria may be the first and only symptom.

=Diagnosis=

Elevated creatinine kinase level – a level 5 times the upper limit of normal is used to identify rhabdomyolsis (about 1000 units/L). Once CK levels exceed 5000 units/L, acute renal failure is likely (McCance and Huether).

•	Women – normal value – 5-25 units/L

•	Men – normal value – 5-35 units/L

Test for myoglobinuria – obtain a clean catch urine sample

•	Normal result is negative, normal value ranges vary among laboratories

•	Visual inspection of tea colored urine

Serum Ca+ level

•	Hypocalcemia is seen early in the course of myoglobinuria and is followed by late hypercalcemia

Ultrasound

•	A recent study evaluated the appearance of rhabdomyolysis in damaged muscle tissues and found abnormalities in muscle texture and subcutaneous tissue, and areas of liquid (McCance and Huether).

Measurement of rising compartment pressure •	Can be directly measured by inserting a wick or slit catheter into the muscle

=Treatment=

The goals of treatment include maintaining adequate urinary flow and the prevention of kidney failure.

Forced hydration with 1.5-2 L of sterile saline solution should be started immediately, followed by 1.5-2 L/h. Following hospital admission, continuous hydration should be ensured, alternating the saline solution with a 5% glucose solution. In the presence of myoglobinuria, urine should be alkalinized by use of sodium bicarbonate solution (Cervellin, Comelli and Lippi, 2010).

Mannitol can be used to cause an osmotic diuresis or bicarbonate to alkalinize the urine. However, these treatments have not been       shown to consistently improve outcomes (McCance and Huether, 2014).

Fasciotomy and debridement of affected tissues are recommended for reducing elevated intracompartmental pressures

=Links=

PubMed.gov – retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20298139

=Related Current Articles=

Dejardins, M. and Strange, B. (2013). Pre-hospital treatment of traumatic rhabdomyolysis. Emergency Nurse, 21(8), 28-33.

Zimmerman, J. and Shen, M. (2013). Rhabdomyolysis. Chest 144(3), 1058-1065.

=References=

Cervellin, G., Comelli, I., and Lippi, G. (2010). Rhabdomyolysis: historical Background, clinical, diagnostic and therapeutic features. ''Clinical Chem Lab Med, 48(6):749-756. doi: 10.1515/CCLM.2010.151''

Mccance, K. and Huether, S. (2014). Pathophysiology: the biologic basis for Disease in adults and children. St. Louis, MI: Mosby, and imprint of Elsevier Inc.