VCOM Carolinas Research Day 2023

Clinical Case-Based Reports

Warfarin-Induced Compartment Syndrome following Low-velocity Minor Crush Injury. Teresa Perez, OMS III. Dr. Lewis Dickinson, MD Edward Via College of Osteopathic Medicine-Carolinas

Abstract # CBR-21


Case report


References It is essential to emphasize the posed risk of long-term anticoagulant therapy leading to acute compartment syndrome even in low-velocity minor crush injuries. When compartment syndrome is identified in patients on long term anticoagulant therapy the management is made more challenging with wound management and the need for transfusion. Even in the setting of minor trauma physicians should closely evaluate and monitor patients on anticoagulants for acute compartment syndrome. When physicians start long-term anticoagulant therapy, it is also imperative that they thoroughly explain the risks and benefits to the patient. Emphasizing the bleeding risk associated can help in initiating earlier evaluations and addressing concerns. Allowing for prompter attention to care will ultimately lead to better outcomes and fewer complications in these cases of acute compartment syndrome. Considering anticoagulants' role in wound healing, physicians must monitor recovery closely. Compartment syndrome is a diagnosis traditionally associated with significant trauma. The traditional diagnosis is with a combination of physical exam findings and, if necessary, compartment pressures or direct nerve stimulation. However, it is important to emphasize that the associated long-term warfarin therapy poses an increased risk for compartment syndrome and the increased difficulty in management. This risk is explicitly associated with warfarin as it has a high bioavailability (12). In an article published in the American Journal of Emergency Medicine, they describe 5 cases of acute compartment syndrome following minor trauma (13). It is important to note that two of those 5 cases were associated with the isolated risk factors of long-term anticoagulant therapy. Other cases of compartment syndrome complicated by anticoagulant therapy can also be noted by Osteo, Titolo, and Devatoglu (14) (15) (16). In this case, we illustrate the importance of addressing compartment syndrome in a timely manner. It is possible that a delay in treatment could have been avoided if the patient had fully understood the risks of warfarin treatment. It is important to recognize that delays lead to complications, such as permanent nerve damage, muscle contracture, and kidney injury (18). Our patient experienced elevated creatine kinase, which led to decreased kidney function which was managed with intravenous fluids, his kidneys showed good improvement with a positive downward trending creatinine throughout his hospital course. Prompt management is vital because Schmidt discusses that muscle necrosis can begin as soon as 2 hours following injury and lead to elevated creatine kinase levels compromising an individual’s kidney function (19). It is important to note that there was the appropriate decision for delayed primary closure in this case. Jones described that the average stay following fasciotomy is typically 4.5 days (20). In our case, we decided to use negative pressure wound therapy for prolonged time. This form of therapy allows for bleeding to be controlled to promote better wound healing and maintain low pressures within the compartment (19). Because the patient needed to be restarted on anticoagulant therapy, management with negative pressure therapy was still difficult to control. The eschars that resulted were directly linked with the continued bleeding in the compartment from muscle damage and a combination of anticoagulation therapy. Prolonged bleeding led to poor wound healing and the necessary debridement several weeks following his initial presentation. The management of this patient has likely been more difficult owing to the balance of wound healing versus obligated anticoagulant therapy due to a mechanical heart valve.

Compartment syndrome is estimated to occur in 7.3 per 100,000 males. The development of this condition can be exacerbated by certain risk factors (1). A common underrepresented risk factor is the associated use of long-term anticoagulant therapy for lower-velocity injuries. This case discusses a lower velocity and minor crush injury that resulted in emergent lower extremity compartment syndrome in the setting of long-term warfarin therapy. A 51-year-old male presented to the emergency department with left lower extremity pain. He had a history of mechanical aortic valve and was placed on warfarin therapy with an INR goal of 2.5. The night before arriving at the emergency department, he reported driving 2-3 mph in his golf cart and turning it over on its side. He felt minimal injuries and decided to prolong immediate medical attention. The following morning, however, he began to experience severe pain, numbness, and discoloration of the left lower extremity. He reported to the emergency room, and upon initial examination, the patient showed moderate ecchymosis of the left lower extremity with tenderness to palpation with tightness. There was concern for compartment syndrome and the patient underwent a CT angiogram which showed no acute vascular injury or acute traumatic fractures. However, a 41 cm hematoma from the level of the distal thigh into the lesion to the level of the mid to distal tibia was discovered. He underwent a four-compartment fasciotomy and was placed on negative pressure wound therapy. There are a limited number of cases of compartment syndrome following a low velocity and minor crush injury complicated by long-term anticoagulant therapy. It is essential to acknowledge chronic anticoagulant treatment's role in this patient’s case. It showcases the importance of educating patients on warfarin treatment to seek medical attention following even minor injuries due to the increased risk of potential compartment syndrome.

A 51-year-old male presented to the emergency department following a golf cart accident the previous night. He reported that the golf cart was going at a speed of approximately 2-3 MPH when the golf cart fell over on top of him. That night he felt no acute pain and decided to defer medical attention. The following morning, he started to experience severe pain, numbness, and discoloration of his left lower extremity. His past medical history included a bicuspid aortic valve which required a replacement and chronic warfarin therapy Upon preliminary physical exam his left lower extremity showed decreased range of motion at the ankle, with moderate ecchymosis extending from the distal mid-thigh to the lower ankle, tenderness to palpation along areas of ecchymosis with the area feeling very firm and tight, and decreased capillary refill noted in the left foot. The patient’s initial laboratory values revealed a hemoglobin of 13.5 gm/dL, INR of 2.4 which is his targeted goal. CT angiogram of the aorta and bilateral lower extremity runoff showed no significant arterial injury. No tibia and fibula fracture but a minor acute fracture of the posterior medial aspect of the left talus. There was a large conglomerate of multiple hematomas extending from the level of the distal thigh into the to the level of the mid-to-distal tibia. The hematoma measured 41 cm in craniocaudal dimension. Prior to taking the patient to the operating room, he was given 1,500 units of prothrombin complex concentrate and started on prophylactic antibiotics. The patient was taken emergently to the operating theater and was placed under general anesthesia. He then underwent four-compartment fasciotomy through lateral and medial incisions of the left calf. A 300cc hematoma was evacuated as the four compartments were released. The muscles of all four compartments appeared to be viable, responding to electrocautery as hemostasis was obtained. Negative pressure wound therapy was placed on his incision sites with plan for a delayed primary closure. The patient’s anticoagulant therapy was held on the initial day of his surgery while monitoring for postoperative bleeding. On post-operative day one he was restarted on anticoagulation therapy. His laboratory values on that day revealed creatinine kinase showed a reassuring downward trend however hemoglobin decreased to 10.9 gm/dL, creatinine increased to 1.6, and GFR declined to 50. His decline in kidney function was addressed with judicious isotonic intravenous fluid replacement. On day 2 of his hospital course, he developed significant eschar on his anterior shin, which can be seen in figure 1.1 and 1.2. On hospital day three, his hemoglobin dropped to 6.7 gm/dL, and was transfused 1 unit of packed red blood cells. Anticoagulation was held and wound vac was changed at bedside with relief of a recurrent hematoma in the anterior lower leg. Anticoagulation was restarted the following day and required no further blood transfusions. Five days following the fasciotomy, the patient was taken to the operating theater with successful closure of the medial aspect of his left lower extremity. The lateral incision unable to be approximated without tension, therefore negative pressure wound therapy was reapplied to the lateral incision with plans of potential closure or skin graft placement. Seven days following the second surgical procedure, the patient underwent skin graft placement for his lateral incision with the graft donor site coming from his left anterior thigh. On post operative day 21, negative pressure wound therapy was removed and the patient was discharged with plans for outpatient follow up. The eschars demarcated and it was decided to bring him back for debridement of the anterior surface of the leg with potential wound vac and skin graft place, see figure 2.1 the procedure was done 39 days following the patient’s initial procedure. Figure 2.2 shows the patient following excisional debridement. Following debridement, the patient was discharged with an at home wound vac with plans of skin graft of the anterior lower leg. The patient gave verbal and written consent for all documentation and imaging provided.

Figure 1.1

Figure 1.2

Figure 2.1

Clinical Presentation of Compartment Syndrome The 5 P’s Pain


Figure 2.2

Pulse Pallor Paresthesia Paralysis

Figure 1.1 Postoperative day two, patient developed significant eschar on his anterior shin. Figure 1.2 Postoperative day two, eschar noted on anterior shin

Figure 2.1 Patient’s wound healing before debridement Figure 2.2 Patient’s wound healing post debridement


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