Summary: A 50-year-old male patient with a history of prostate cancer treated
with iodine-125 seed implants and previously documented degenerative
lumbar spinal stenosis with chronic low back pain presented to the
emergency room with severe low back and right flank pain. The patient
denied any history of trauma or recreational drug use. The patient was
treated with valium and pain medications; however, he experienced no
improvement of symptoms. The patient also noted on the following day
that his urine had darkened. The patient had earlier denied any history
of abdominal pain, jaundice, rectal bleeding, or melena. On laboratory
evaluation at the time of admission, the white cell count was 18000 per
mcl (18000 µL), creatinine was 1.0 mg/dl and BUN 12 mg/dl. Upon
subsequent testing, the patient’s creatine kinase (CK) level was greatly
elevated to 21613 units/L (U/L). The patient’s erythrocyte
sedimentation rate was also elevated and the urine returned positive for
cocaine. The patient’s creatinine level rose over the following days to
4.7 mg/dl. As his back pain worsened, a magnetic resonance image (MRI)
of the lumbar spine was obtained.
Summary: A diagnosis of cocaine-induced
rhabdomyolysis with secondary acute renal failure was made. With
treatment, the patient’s creatine kinase levels decreased and pain
improved over the following week. All fluid cultures were negative for
infection. The patient was discharged after recovery of renal function
and following appropriate counseling regarding recreational drug use.
Cocaine induced rhabdomyolysis with secondary acute renal failure
The MRI scan (Figure 1) revealed diffusely abnormal high signal on
T2-weighted images with corresponding low signal on the T1-weighted
sequences in the perispinal muscles. The muscle architecture was
altered, and there was blurring of the margins between muscle bundles
and an unsharp appearance to the contents of each muscle bundle. Small
areas of confluent necrosis were also appreciated on the right (Figure
1). There was also abnormal enhancement diffusely in these muscles on
postcontrast imaging (Figures 1). The other muscles were within normal
A follow-up MRI obtained one week later showed persistent
signal abnormality (Figures 2); however, new areas of curvilinear T1
high signal appeared in the muscle, representing hemorrhage with loss of
muscle architecture and more prominent areas of confluent necrosis.
Enhancement was again seen and was only slightly decreased in prominence
compared to the preceding study and the areas of confluent necrosis
were clearly delineated (Figure 2). The abnormal signal in the left
muscle complex had slightly improved in the interval.
Rhabdomyolysis is an unusual entity induced by various etiologies.
Recreational use of cocaine is one of the inciting factors for this
condition. The incidence of rhabdomyolysis in patients who use cocaine
varies from 5% to 30% in published reports. It is unclear why cocaine
causes rhabdomyolysis. Hypotheses include cocaine-induced vasospasm with
resultant muscle ischemia, excessive energy demands placed on the
sarcolemma, and direct toxic effects on myocytes. Seizures, agitation,
trauma, and hyperpyrexia may also play a role. In general, the severity
of the rhabdomyolysis parallels the severity of the cocaine
intoxication; patients with very high CK levels tend to have the most
severe complications from this disease. Intravenous cocaine use may be
associated with a higher incidence of rhabdomyolysis-induced acute renal
failure (ARF) compared with smoking cocaine.1
with rhabdomyolysis classically present with complaints of muscle
weakness, swelling, and pain. The myalgias may be focal or diffuse,
depending on the underlying cause of the disease. The patient may also
note dark- or tea-colored urine. However, a high clinical suspicion for
rhabdomyolysis must be maintained in patients at risk because up to 50%
of those with serologically proven rhabdomyolysis do not report myalgias
or muscle weakness.1
Rhabdomyolysis can induce ARF,
particularly in hypovolemic or acidotic individuals. Myoglobinuric ARF
complicates approximately 30% of cases of rhabdomyolysis. Common causes
of the latter include traumatic crush injury, acute muscle ischemia,
seizures, excessive exercise, heat stroke or malignant hyperthermia,
intoxications (eg, alcohol, cocaine), and infectious or metabolic
disorders.2-7 Compartment syndromes may be a cause or a complication of rhabdomyolysis.1,2
recognition of this condition is necessary for initiation of
appropriate therapeutic measures. MRI findings of rhabdomyolysis include
early onset of edema-like changes with increased T2- signal intensity.
In the later phases, imaging demonstrates evidence of muscle fiber
destruction manifested as loss of normal architecture, areas of necrosis
and cavitation, abnormally elevated T1 signal representing hemorrhage,
and abnormal enhancement. Some of these findings are difficult to
differentiate from other causes of myonecrosis, which include sickle
cell crisis, crush injuries, diabetic myonecrosis, compartment syndrome,
and severe ischemia. Infection with abscess formation also presents
with similar features. Some of these conditions have features that can
help in differentiating them from rhabdomyolysis, such as involvement of
the subcutaneous soft tissue and fat in crush injury, while others may
present similar to rhabdomyolysis.8-11 Eliciting a good
history usually provides a clue to the underlying etiology. However, as
described above, some of these conditions may occur in tandem; for
example, sickle cell crises may lead to myonecrosis with subsequent
compartment syndrome and rhabdomyolysis. In general, severity of the
signal intensity alterations correlates with severity of injury.3
Rhabdomyolysis should be entertained in the sudden onset of muscle pain
and/or acute renal failure, especially in the setting of cocaine use,
severe exertion, and trauma. MRI findings are helpful in determining the
presence of this entity, which can be confirmed by testing the serum
for elevated CK levels. It is important to remember that up to 50% of
cases may be silent, without accompanying pain or muscle weakness, and
the MRI findings may be the only suggestion of rhabdomyolysis.1
Early diagnosis allows the institution to provide appropriate
management, given the frequency of acute renal failure in such patients.
- Botempo LJ. Rhabdomyolysis. In: Marx J, Walls R, Hockberger R, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 6th ed. Philadelphia, Pa: Mosby Elsevier; 2006:chap 125.
- Brady HR, Brenner BM. Acute renal failure. In: Kasper DL, Braunwald E, Hauser S, eds. Harrison’s Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill Medical Publishing Division; 2006:chap 260.
- Abraham B. Malignant hyperthermia susceptibility: Anaesthetic implications and risk stratification. QJM. 1997;90:13-18.
- Singhal PC, Rubin RB, Peters A, et al. Rhabdomyolysis and acute renal failure associated with cocaine abuse. J Toxicol Clin Toxicol. 1990;28:321-330.
- Welch RD, Todd K, Krause GS. Incidence of cocaine-associated rhabdomyolysis. Ann Emerg Med. 1991;20:154-157.
- Roth D, Alarcon, FJ, Fernandez JA, et al. Acute rhabdomyolysis associated with cocaine intoxication. N Engl J Med. 1988;319:673-677.
- Counselman FL, McLaughlin, EW, Kardon, EM, Bhambhani-Bhavnani, AS.
Creatine phosphokinase elevation in patients presenting to the emergency
department with cocaine-related complaints. Am J Emerg Med. 1997;15:221.
- May DA, Disler DG, Jones, EA, et al. Abnormal signal intensity in
skeletal muscle at MR imaging: Patterns, pearls, and pitfalls. Radiographics. 2000;20:S295–S315.
- Kakuda W, Naritomi, H, Miyashita, K, Kinugawa, H. Rhabdomyolysis lesions showing magnetic resonance contrast enhancement. J Neuroimaging. 1999;9:182-184.
- Stock KW, Helwig A. MRI of acute exertional rhabdomyolysis--in the paraspinal compartment. J Comput Assist Tomogr. 1996;20:834-836.
- Lamminen AE, Hekali, PE, Tiula, E, et al. Acute rhabdomyolysis:
evaluation with magnetic resonance imaging compared with computed
tomography and ultrasonography. Br J Radiol. 1989;62:326-330.