Imaging Use in Focal Rhabdomyolysis of the Left Shoulder

Rhabdomyolysis involves the breakdown of skeletal muscle with the release of intracellular contents into the extracellular space and circulation.1 Diffuse rhabdomyolysis has been found in athletes due to overexertion. However, focal rhabdomyolysis is rare.2,3 The clinical presentation of focal rhabdomyolysis is subtle and nonspecific, with swelling, vague pain, weakness, fatigue, and tea-colored urine.

Early recognition and prompt management are crucial to prevent complications such as compression syndrome, acute renal failure, disseminated intravascular coagulation, cardiac dysrhythmia, or even cardiac arrest. Sonography and magnetic resonance imaging (MRI) can, therefore, be a complementary part of the diagnosis and assessment of the extent of rhabdomyolysis.^4-7

Case History

The patient was a 34-year-old white man with a history of polysubstance abuse who presented to the emergency department (ED) with numbness and weakness in the left arm and hand, pain in the left side of his neck, and 3 days of intermittent amnesia with confusion. He had used IV heroin about 2 weeks prior to admission and used tobacco and alcohol daily. He reported no current medications or known allergies. The patient was in a monogamous relationship with a same-sex partner.

On physical examination, vital signs were within normal limits. He was in distress, confused, and disoriented as to time and place. An extremity examination revealed 1/5 strength in the extensors of the left elbow, left wrist, and left fingers with normal strength noted in the right upper extremity as well as the lower extremities. No sensory deficits were noted. The patient’s skin was warm and dry. Remarkable laboratory findings included creatine kinase (CK) 1,744 U/L, creatinine (Cr) 1.9 mg/dL, ALT 1,065 U/L, AST 319 U/L, ALP 159 U/L. A urine toxicology screen was positive for cocaine and opiates, and the urine analysis dip was negative for red blood cells, white blood cells, and protein. A differential diagnosis favored a left arm inflammatory reaction to IV drugs, although rhabdomyolysis was questioned.

A neurology consult was obtained, and a bedside electroencephalography test was performed in the ED by the neurologist, showing mild left occipital slow wave abnormality with no epileptiform discharges. A chest X-ray and computed tomography (CT) scan of the head and cervical spine were unremarkable, other than incidental mild prominence of the ventricles.

Over the next 24 hours, the patient was hydrated with IV normal saline without bicarbonate. His altered mental status, urine output, and biochemical abnormalities returned to normal, except for the serum CK, which decreased to 917 U/L. He had minimal improvement in his left upper extremity nerve palsy symptoms; however, he was deemed to be stable for discharge with follow-up in the clinic.

Instead of a clinic follow-up, the patient returned to the ED 7 days later, with progressive weakness of the left arm, forearm, and wrist. The patient noted that his weakness was so significant that he had to move his left arm with his right arm. He also reported extremity swelling and increasing paresthesias involving the lateral aspect of his left arm and hand, dizziness, and left neck pain. A physical examination revealed 3/5 strength at the left deltoid and left triceps, and 0/5 strength in the left fingers and grip. Remeasurement of CK was 54 U/L and Cr was 0.9 mg/dL. Compartment pressures were not measured.

Magnetic resonance imaging using multiplanar spin echo T1 and fast spin T2 weighted and post-IV 16cc Omniscan contrast sequences of the left shoulder were performed, showing multiple patchy T2 hyperintense focal areas with peripheral enhancement in the muscles of the posterior shoulder and in the tissues adjacent to the brachial plexus in the neck and shoulder (Figures 1A, 1B, and 1C). Sonography with matrix array linear 6-15 MH3 transducer was performed, which demonstrated patchy focal hypoechoic areas of muscle with enlarged, thickened, and disrupted muscle, representing devitalized muscle without any drainable fluid collection or abscess (Figures 2A, 2B, 2C, and 2D).

Magnetic resonance imaging and magnetic resonance angiogram scans of the brain and cervical spine with and without contrast were unremarkable. At that time, a definitive diagnosis was made of focal rhabdomyolysis and compressive neuropathy of the brachial plexus posterior cord, leading to brachial plexopathy of the left shoulder.

The patient was treated with hydration, a left arm sling, elevated left arm, and ibuprofen 600 mg qid to reduce inflammation. His swelling decreased markedly, and there was a slight improvement in pain and mobility at a 2-week neurology clinic follow-up. The patient lost contact after that.

Discussion

Rhabdomyolysis is caused by diverse etiologies. Most commonly, it is generalized and occurs due to overexertion, crush injury, steroid use, metabolic abnormalities, and certain medications and illicit drugs.^1,2 The most likely etiology of rhabdomyolysis in patients presenting to the ED without significant trauma is of substance abuse, especially with ethanol, heroin, amphetamines, cocaine, and other sedatives or stimulants.^1-3 The patient presented in this case study had a history of drug abuse, with a positive urine toxicology screen for cocaine and opiates. He had been intermittently confused and amnesic for 3 days prior to presentation, during which he may have been lying on his shoulder for a prolonged period.