A 78-year-old white man presented to our department with a sudden onset of a medial lower leg pain on the right side. The patient had a history of osteoarthritis and a total knee replacement 1 year ago on the right side. Moreover, his past medical history included long-term treatment (more than 2 years) with Diclofenac (twice daily 50 mg), but he had no history of gastrointestinal bleeding or any other nonsteroidal anti-inflammatory drug (NSAID)-related side effects.The day before presentation, he had been cleaning his garden but no traumatic event occurred during this work. Approximately 16 hours later pain got worse and he sought medical attention in our outpatient clinic. Upon initial examination, the patient was unable to walk without crutches. A slight swelling was visible at the medial side of the proximal lower leg. Ankle dorsiflexion and plantarflexion were decreased because of pain. The tibial and dorsalis pedis pulses were easily palpable and there was normal capillary refill time in all toes; moreover, there was no neurologic deficit. At the urgent care facility, radiographs were taken and interpreted as negative for fracture or any bony expansive mass. To assess intracompartmental tumor magnetic resonance imaging (MRI) scan and ultrasound examination was performed and revealed a hematoma in the deep and superficial posterior compartment of the lower leg.Routine laboratory screening revealed normal red and white blood and platelet count. International normalized ratio, prothrombin, and partial thromboplastin times were normal, but skin-bleeding time was slightly elevated. There was no affection of the individual clotting factors and no evidence for a von Willebrand Disease. To assess altered thrombocyte function resulting from NSAID intake, different platelet aggregation tests were performed. This examination demonstrated an impaired thrombocyte function with a clear reduction of adrenaline (to 29%) and arachidon acid (to 4%) mediated platelet aggregation. In contrast, adenosine diphosphate (ADP)-, collagen-, and ristocetin-induced platelet aggregation was not affected.Next, compartment pressures were measured using a portable hand-held device. The deep posterior compartment pressure was elevated and a few hours later a sensory deficit on the medial side of the foot was detectable. The patient was taken immediately to the operating room where fasciotomies of the deep and superficial posterior compartments were performed and the hematoma was removed through a single skin incision.Postoperative examination revealed normal sensation, active ankle dorsiflexion and plantarflexion, and no evidence of compartment syndrome recurrence. The patient did not receive any platelet transfusions or platelet therapy. A persistent slight bleeding from the inferior pole of the scar was observable for 10 days but required no surgical intervention. Control laboratory screenings revealed normal platelet aggregation to adrenaline and arachidon acid 10 days after omitting the daily intake of Diclofenac, thus suggesting a dire...

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