Page 109 - Journal of Special Operations Medicine - Summer 2015

intracellular components. This release can be from cel- other causes, such as deep vein thrombosis or compart-
lular membrane injury, cellular hypoxia, adenosine tri- ment syndrome. In general, skeletal muscle swelling is
phosphate exhaustion, electrolyte imbalance resulting rare in rhabdomyolysis; a literature review reveals that
from cell membrane sodium–potassium pump dysregu- only 5% of patients present with muscle edema. Thus,
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lation, and generation of oxidative free radicals due to significant edema may suggest an alternate diagnosis, es-
the disruption of normal cellular processes. In simplis- pecially in the context of decreased peripheral pulses. If
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tic terms, the muscle cells die because they are pushed there is a prolonged period of immobility, pressure sores
beyond their ability to produce energy. The cells sub- may be apparent. Other significant findings on physical
sequently leak intracellular components such as myo- examination may include hyperthermia/hypothermia,
globin, creatinine kinase, and potassium. Myoglobin ecchymosis from crush injury, or deformities, if trauma
diffuses into the plasma. If there is a lot of myoglobin, it is involved. If rhabdomyolysis is suspected based on
overwhelms the protective binding capacity of intravas- the clinical presentation, laboratory evaluation should
cular proteins, allowing it to freely enter the glomerular be performed to diagnose muscle damage and potential
filtrate system of the kidneys. Large quantities of un- end-organ dysfunction. 4
bound myoglobin in the filtrate may form solids, result-
ing in renal tubular obstruction, direct nephrotoxicity, Laboratory Findings
intrarenal vasoconstriction, and acute kidney injury. 4,5
Laboratory tests to help diagnose rhabdomyolysis and
other potential comorbidities include:
Clinical Presentation
The classic triad of rhabdomyolysis comprises: • Complete blood count
• Renal function: blood urea nitrogen (BUN), creatinine,
• Myalgia glucose, calcium, potassium, magnesium, phosphate,
• Generalized weakness and uric acid levels
• Darkened urine • Coagulation profiles: international normalized ratio/
partial thromboplastin time (INR/PTT), and liver
The presentation of rhabdomyolysis, like its many func tion tests
causes, can vary widely. The classic triad is actually seen • Creatine kinase, myoglobin levels
in only about 50% of adult patients, and it may be even • Lactate dehydrogenase (LDH) level
less common in children. Additional symptoms may in-
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clude fever, nausea, and vomiting.
Urinalysis
The patient’s history may allow for specific causes to The diagnosis of rhabdomyolysis is traditionally con-
be associated with the condition. Inquiry about trauma, firmed from the creatine kinase (CK) level. It is an
exertional extremes, exposure to hot or cold environ- easy-to-detect indicator that is sensitive immediately
ments, and medication use provides key factors that after muscle injury. CK levels continues to rise within
may help provide the clinician with a clear picture as 12 hours of muscle injury, peak in 24 to 36 hours, and
to the inciting event. The clinician has to consider the decrease at a rate of 30% to 40% per day. If CK levels
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physiologic effects of the pertinent details in the history. continue to rise past the 36-hour mark, it may indicate
Could the events recalled result in a dehydrated state? ongoing muscle injury and other sources of muscle in-
Did they involve a period of immobility? Could the pa- jury must be investigated. A CK elevation is a sensitive
tient have ingested or been exposed to a toxin? but nonspecific marker for rhabdomyolysis. CK levels
five times the reference range of 40–150 U/L (i.e., higher
In some patients, the history is nonspecific or the key in- than 500U/L) suggest rhabdomyolysis, but typically
formation may not be communicated from the patient. rhabdomyolysis presents at extremes of laboratory val-
Inquiry from other sources such as friends, family, or ues, as high as 100 times the reference range or more.
team members may provide additional information. The total CK level may increase from initial values de-
pending on time from myocyte injury. Total CK levels
should be evaluated every 6 to 12 hours until a peak
Physical Findings
level is established. Peak CK levels higher than 15,000
On physical examination, muscular pain and tenderness U/L, may be predictive of renal failure. 9
over the affected muscle or muscle group is common; this
often corresponds with decreased muscle strength. The Given the pathophysiology of rhabdomyolysis, it may
affected muscle groups most commonly seen in adults make sense to directly measure plasma myoglobin.
include the calves and the lower back. This pain may However, this approach is unreliable because myoglo-
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mimic other conditions, so it is important to consider bin has a half-life of 1 to 3 hours and is cleared from

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