Diffuse Subcutaneous Upper Extremity Edema in the Setting of Rhabdomyolysis: A Case Report : Current Sports Medicine Reports

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General Medical Conditions: Case Reports

Diffuse Subcutaneous Upper Extremity Edema in the Setting of Rhabdomyolysis

A Case Report

Bergman, Cory BS1; Khodaee, Morteza MD, MPH, FACSM2; Hill, John C. DO, FACSM3

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Current Sports Medicine Reports 13(1):p 42-44, January/February 2014. | DOI: 10.1249/JSR.0000000000000028
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While exertional rhabdomyolysis (ER) can occur with any strenuous exercise, it is more common with exercise involving repetitive eccentric contractions than with concentric contractions (5). ER is the result of the breakdown of skeletal muscle fibers due to overexertion with muscle destruction, necrosis, loss of cell membrane integrity, and displacement of intracellular contents into the extracellular space (1). ER is a syndrome entailing muscle soreness, weakness, and possibly brown urine (13). Complications of ER may include acute kidney injury (AKI), compartment syndrome, hyperkalemia, disseminated intravascular coagulation (DIC), and hypocalcemia (1). Diagnosis of rhabdomyolysis is made by clinical evidence of muscle damage and the presence of circulatory muscle cell content including creatine kinase (CK) and myoglobin (16). Elevation in serum myoglobin declines rapidly and may not be present at the time of presentation. Urine myoglobin test may take several days so it cannot be relied upon for treatment decisions. It is generally acknowledged that an increase in CK of five times the upper limit of normal, with symptoms of muscle pain or muscle weakness, and dark urine in the setting of strenuous activity are indicative of ER (3,14).

Case Presentation

A sedentary 32-year-old Caucasian woman presented with bilateral upper extremity swelling 4 d after initiating a new exercise program. The patient’s workout was supervised by a personal trainer and consisted of intense upper body eccentric exercises, which included multiple sets of pull ups. The patient noted dull achy pain localized from her mid-upper arms to lower forearms beginning 2 h postworkout and gradual swelling at the same locations that progressed over the following 4 d. Over the course of the 4 d, her pain abated, but she developed upper extremity stiffness and slight intermittent tingling in her hands. She did not notice color changes over the affected area, cramping, or weakness. She did report a few episodes of mild swelling localized to her shoulders following previous workouts. The patient denied any trauma, immunizations, extraordinary events, or changes to her routine over the week leading up to her symptoms. She was in good health with no recent history of fevers and malaise. She was not taking any supplements or medications. She had normal stools and bowel movements with no recent nausea and vomiting. She reported no decrease in urine output and no urine color changes.

The patient’s physical examination was positive for bilateral upper extremity nonpitting edema from her mid-upper arms to the distal forearms (Fig. 1a and b). The right side was more pronounced than the left. There was no tenderness to palpation over the affected area. She had full painless passive and active range of motion of her wrists, elbows, and shoulders bilaterally. No upper extremity muscle weakness was appreciated. Sensation was intact to light touch and pin prick throughout the upper extremities. Triceps, biceps, and brachioradialis deep tendon reflexes were 2+ and equal bilaterally. Bilateral brachial and radial pulses were regular, strong, and symmetric.

Figure 1:
(A and B) Bilateral upper extremity edema from mid-upper arms to distal forearm bilaterally 4 d postexercise. (C) Resolution ofedema 14 d postexercise.

On the day the patient presented to the clinic, a urine analysis, basic metabolic panel, complete blood count, and CK levels were assessed. The urine dipstick was positive for trace blood. Microscopic urinalysis was negative for red blood cells, which is likely consistent with myoglobinuria. The patient’s CK was 21,300 U·L−1, and liver markers were mildly elevated (Table). The patient’s creatinine and blood urea nitrogen were within normal limits. A diagnostic musculoskeletal ultrasound of the patient’s upper extremities using a linear transducer (Philips L12-3 MHz) revealed subcutaneous edema that was more significant on the right side (Fig. 2). The ultrasound appearance of the upper extremity musculature was normal with organized fascicular architectures (Fig. 2). There were no hypoechoic or hyperechoic foci in any of the muscles examined. Humeral, radial, and ulnar cortexes were normal with no irregularities.

Laboratory values.
Figure 2:
Edema presented in longitudinal view of (A) anterior right arm (epidermis, dermis, and subcutaneous depth of 0.56 cm) and (B) volar aspect of right midforearm (epidermis, dermis, and subcutaneous depth of 0.793 cm).

The patient was treated with observation, oral hydration, and restricted physical activity. She was seen in the clinic 10 d after her initial visit. Laboratories were drawn 4 and 10 d following her initial visit. Within 10 d of her first visit, her symptoms had completely abated. On day 10, she had no swelling on examination and her laboratory values returned to normal limits (Fig. 1c). She was able to resume normal activities by day 10, and at 6 months, she reported no further episodes or exacerbations.


There have been only a few reported cases of isolated upper extremity ER (9,10,14,19). Contrary to our case, all of these cases reported pain as a major symptom. Another important feature of this case was the presence of substantial amount of subcutaneous edema. Clinical presentation of edema has been reported in a few cases of rhabdomyolysis (9,10,12,15,18). However pain seemed to be present in all cases (9,10,12,15,18). Other causes of subcutaneous edema like congestive heart failure, cellulitis, thrombosis, myositis, and drug-induced myopathy should be considered in cases with clinical suspicion for ER.

Ultrasonic appearance of our case was consistent with a significant subcutaneous edema with no noticeable intramuscular edema or abnormality. Ultrasonic features of rhabdomyolysis include homogenous decreased echogenicity, areas of hyperechogenic foci, disorganized muscle fibers, and edema within the muscle (17,18). Lamminen et al. (11) examined the use of imaging modalities in the diagnosis of rhabdomyolysis and found out that the sensitivities of magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound in the detection of rhabdomyolysis were 100%, 62%, and 42%, respectively. Presence of subcutaneous edema on MRI, CT, and ultrasound has been reported in few cases of rhabdomyolysis (9,11,12,15,18). However all of these cases showed substantial evidence of characteristic muscle damage on imaging modalities (9,11,12,15,18).

The complications of rhabdomyolysis can be severe and grave. Severe electrolyte imbalance (e.g., hyperkalemia and hypocalcemia), arrhythmia, and DIC are rare complications of rhabdomyolysis. AKI is a common and important complication of ER. The incidence of AKI in patients with rhabdomyolysis is approximately 5% to 7% (16). AKI occurs in the setting of rhabdomyolysis as a result of serum myoglobin levels exceeding 100 mg·dL−1 (16). At this level, tubule epithelial myoglobin metabolization capacity is overwhelmed and filtered myoglobin accumulates in the tubules leading to tubule damage, AKI, and myoglobinuria (1). Serum CK levels correlate with myoglobin levels, and CK is the preferred marker over myoglobin because of its longer half-life, cost, and laboratory properties (4,5,16). Myoglobinuria occurs when CK levels approach 70,000 U·L−1 (16).

The risk of AKI from any form of rhabdomyolysis is low when serum CK levels are less than 20,000 U·L−1 (4,6,7). Most reported cases of ER that result in AKI have occurred in patients with coexisting medical conditions (4,6,7). Underlying conditions that may increase the risk of AKI include dehydration, nonsteroidal anti-inflammatory drug (4) use, heat, and genetic conditions (1,4–7). Sickle cell trait is a major risk factor for ER (4,13). Repetitive sprints or timed laps may cause exertional sickling and eventually ischemia in athletes with sickle cell traits (7). Levels of serum CK up to 100,000 U·L−1 have been reported in healthy individuals with no renal complications (4). These findings suggest that elevated or extremely elevated CK levels in the setting of ER in healthy individuals may not be predictive of renal failure (1,4–6). There is no consensus on the CK serum level that will precipitate AKI and warrant hospital admission (1,2,4,6).

It remains unclear why the incidence of ER is relatively high among untrained individuals performing repetitive eccentric exercise (4). ER is a potential life-threatening syndrome that may present with nonspecific clinical features like muscle pain, tenderness, and swelling. Screening is performed with urine dipstick and microscopy. Early recognition and prompt management are critical to prevent potential complications. More scientific studies are needed to further understand the clinical course of ER.


Patients with ER can present variably, sometimes including minimal pain and normal renal function. Musculoskeletal ultrasound is an inexpensive rapid office diagnostic tool that can aid in evaluation of a patient suspected of having ER. Severe complications from ER in patients with no coexisting medical conditions are rare (8). Patients presenting with ER with no comorbidity can be managed in the outpatient setting, with close serial monitoring, oral hydration, and restricted physical activity. Complications of rhabdomyolysis can be severe in patients with underlying medical conditions, and clinical judgment must be exercised on a case-by-case basis when determining the management of a patient presenting with ER.

The authors declare no conflicts of interest and do not have any financial disclosures.


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