In sportsmens, Anabolic-Androgenic Steroids administration is a problem that needs attention. Use of anabolic-androgenic steroids could cause both short and long term side effect. One of these side effects is rhabdomyolysis which is cause to compartment syndrome. While the frequency of compartment syndrome increases in athletes due to overuse and exercise, Anabolic-Androgenic steroid use also increases the frequency. With formation of compartment syndrome, muscle and nerve damages may be observed. A 34 years old healthy male bodybuilder using anabolic and androgenic steroids who presented in emergency department with hypopotassemia and drop foot without any trauma. While potassium replacement , patient’s left leg swollen and pain with passive dorsiflexion and plantar flexion movement , inability to dorsiflex of left foot , decreased great toe extension. After electrodiagnostic studies and magnetic resonance imaging support , the patient was taken to emergency operation. After a period of delay , the patient was admitted to our rehabilitation program. Absence of any trauma, compartment syndrome could be seen due to exercise and rhabdomyolysis. It is easier to diagnose compartment syndrome in the presence of trauma for physicians. It should be considered that compartment syndrome may develop without any trauma.
In sportsmens, Anabolic-Androgenic Steroids administration is a problem that needs attention. Use of anabolic-androgenic steroids could cause both short and long term side effect . One of these side effects is rhabdomyolysis which is cause to compartment syndrome. Anabolic-Androgenic Steroids cause compartment syndrome , both through rhabdomyolysis and with direct effect of hypopotasemmia and also rhabdomyolitic effect of hypopotassemia [2-4]. While the frequency of compartment syndrome increases in athletes due to overuse and exercise, Anabolic-Androgenic steroid use also increases the frequency [4-6]. With formation of compartment syndrome, muscle and nerve damages may be observed [7-9].
This case report discusses a male bodybuilder using anabolic and androgenic steroids who presented in emergency department with hypopotassemia and drop foot without any trauma. Informed consent was obtained from patient.
A 34 years old healthy male patient presented to emergency deparment with weakness and fatique. He had mild left leg pain; but there is no sign of swelling. The day prior to his presentation, patient has fatique after exhausting exercise and he tought it was typical post exercise muscle soreness. He has no trauma in history. His past medical history contains using anabolic and androgenic steroid for the last 2 years and he attend bodybuilding activities at least 4 times each week for 4 years. On physical examination, the left leg was slightly erythematosus , tender and warm ; her had no systemic fever and vital signs are stabilized. Laboratory findings demonstrated serum potassium level 2,60 mmol/l (referance range 3,5-5,1mmol/l) , creatinine kinase 1061,7 U/l (referance range 0-171 U/l) , AST 72 U/l (referance range <50 U/l) and ALT 133,4 U/l (referance range 0-50 U/l). Intravenous potassium started to given and maintain close follow up and continuous electrocardiography monitoring. While potassium replacement , patient’s left leg swollen and pain with passive dorsiflexion and plantar flexion movement , inability to dorsiflex of left foot , decreased great toe extension. But he had plantar flexion with maximal resistance over full of range of motion. The posterior tibial and dorsalis pedis artery pulses were both palpable.
Radiographies of leg and ultrasound imaging were negative for any abnormalities. Left crural magnetic resonance imaging did demonstrate “The left tibialis showed an intra-muscular edema and mild mass effect on the tibialis anterior muscle. Isolated diffuse inflammation in the tibialis anterior muscle is consistent with myositis. Fluid collection was observed in the anterior section. In the muscle T1A and T2A series, iso-hyperintense signal changes were observed. Compatible with inflammation-intramuscular hematoma”(Figure 1-2). Control laboratory findings demonstrated potassium level normalized but creatinine kinase 11700 U/l , AST 328,1 U/l , ALT 210,7 U/l. Electrodiagnostic studies demonstrated “Left Tibialis Anterior Muscle is fibrotic and left deep branches of Peroneal nerve has full axonal damages.” The patient was diagnosed with acute compartment syndrome of anterior compartment of left leg with rhabdomyolysis. In treatment, left peroneal nerve exploration was done and suggest rest and hydration. The orthopedist thought no need for fasciotomy. But there is no information of intracompartmental pressure measurement. After surgery, patient’s manuel muscle test score in left M. tibialis anterior is 0/5 , in left M. extensor hallucis longus is 0/5. The patient was discharged home and physical therapy began six months after discharge because of patient had a traffic accident. He had operated due to multiple fractures in right tibia, fibula and calcaneus.
Figure 1: Magnetic resonance imaging of cruris, T1 weighted coronal section.
Figure 2: Magnetic resonance imaging of cruris, T2 weighted axial section. After six months from traffic accident, patient is internated to ?i?li Hamidiye Etfal Training and Research Hospital Physical Medicine and Rehabilitation clinic. In our physical examination, manuel muscle testing revealed in left M. Tibialis Anterior is 1/5, Left m. Extensor Hallucis Longus is 1/5 and left M. Peroneus longus is 2/5. In left deep peroneal nerve sensorial line , with painful stimulation and light touching sensation was decreased. On the other hand , inversion and eversion of right leg were slightly restricted. Initial therapy focused on passive range of motion strectching exercises of ankle especially to dorsiflexion and the lower extremity muscle strengthening. The patient rehabilitation process included 5 session per week and also functional electrical stimulation to m. Tibialis anterior and m. Extensor hallucis longus is performed. Electrodiagnostic studies which is repeated in hospitalization revealed in the left tibialis anterior muscle, indefinite, long-term, short amplitude, infrequent MUPs were observed, in the Extensor Hallucis Longus and Extensor Digitorum Brevis muscles, MUP was not obtained, infrequent polyphasic MUPs in the left peroneus longus muscle were observed, in the deep branch of the peroneal nerve is consistent with severe axonal involvement.
After 1 month treatment, patient externated and continued with outpatient therapy. In discharge, Muscle strength of M. Tibialis anterior, m. Extensor hallucis longus and peroneus longus increased as 1 grade. And patient had near normal sensation in deep peroneal nerve distribution. Ankle foot orthosis is not considered because the patient has no trouble in walking.
Rhabdomyolysis may occur in normal subjects after strenuous exercise and patients who have potassium deficient in exercise as a consequence of drug administration, hot climate or some disease [10,11]. Although mechanism of potassium deficiency leads to rhabdomyolysis has not been clear, some litherature has proved potassium release from contracting skeletal muscle into interstitial tissue of muscle dilates arteriolles and potassium ion may be a major factor mediating muscle blood flow balance. In potassium deficiency, skeletal muscle blood flow decrease and during strenuous exercise myonecrosis and rhabdomyolysis could occur as a consequence of relative ischemia [2,3]. In rhabdomyolysis, blood creatine kinase level increases due to muscle destruction [12, 13].
Some bodybuilders use anabolic androgenic steroids cause of they believe that steroids allow increased period of intensive training to enhance muscle strenght . The most prevalent reason of use anabolic steroid is to promote muscle strenght and mass. Some medications cause hypokalemia through a variety of mechanisms, including intracellular potassium shifting, increased renal loss, and/or stool loss. Mineralocorticoids and glucocorticoids cause especially increase renal loss of potassium and increase blood level of sodium .In potassium deficiency, rhabdomyolysis could occur in any muscle of body. Steroids may also cause localized rhabdomyolysis in injection region .
Compartment syndrome of leg is most frequently presents in anterior compartment . In anterior compartment, there are 3 components: first one is muscles which are tibialis anterior muscle, extensor hallucis longus muscle, extensor digitorum longus muscle and peroneus tertius muscle ; second is blood supply which are branches of tibialis anterior artery and last one innervation is deep peroneal nerve . Therefore pressure of compartment increase may cause deep peroneal nerve damage. At the end of deep peroneal nerve injury, drop foot can be observed.
The compartment syndrome is not rare complication of nontraumatic rhabdomyolysis. Vice versa, rhabdo-myolysis often occurs after compartment syndrome. Acute exertional compartment syndrome of lower extremity is a rare cause of leg pain and often characterized by increasing pressure within a closed fascial space in the absence of trauma [7,12]. Each muscular compartment is tightly closed anatomic space that has little capacity to expand. Cause of any reason, pressure of compartment rises to a level higher than blood pressure, leading to a reduction in myocyte oxygenation and resulting in muscle necrosis and nerve damages [7-9]. Chronic exertional compartment syndrome is self limiting and benign condition compare to acute exertional compartment syndrome . The most majority of compartment syndrome occurs with trauma, fractures and crush injuries and less common reasons are excessive use and exercise . The diagnosis is often delayed due to rarity of atraumatic compartment syndrome [7,13].There are five P’s of compartment syndrome ; pain, paresthesia, pallor, pulseless and paralysis. Generally presenting symptoms are pain and parestesia ; late symptoms are others [7,17,18]. In late stages of acute compartment syndrome pain can be absent. Paresthesia indicates early nerve ischemia but paralysis may indicates both nerve and muscle damage .In diagnosis, Measurement of intracompartmental pressure is important. Compartment pressures higher than 30 mmHg of diastolic blood pressure is diagnostic supporter of compartment syndrome .Our case’s one of deficit is there is no information about intracompartmental pressure measurement because of inadequate patient’s paper filling. The treatment of compartment syndrome is decrease pressure in each involved compartment. Modality of treatment is emergent fasciotomy [5,21]. But in our patient , fasciotomy hadn’t performed and beside of that just nerve exploratation had performed.
Absence of any trauma , compartment syndrome could be seen due to exercise and rhabdomyolysis. It is easier to diagnose compartment syndrome in the presence of trauma for physicians. It should be considered that compartment syndrome may develop without trauma. The metabolic disorders of the patient and the drugs used are effective in the development of the compartment syndrome.