Acute compartment syndrome after restarting warfarin therapy following polyethylene exchange in unicompartmental knee arthroplasty: case report

Abstract

Background

Acute compartment syndrome (ACS) is one of the true emergencies in orthopedics and traumatology. It can lead to permanent damage to skeletal muscles and neurovascular structures if not promptly treated. Although ACS usually occur after major trauma or invasive surgery, it can develop without trauma or after minimally invasive operation in anticoagulated patients.

Case report

A 76-year-old woman underwent a polyethylene exchange in unicompartmental knee arthroplasty (UKA). She had had undergone mitral valve replacement and tricuspid valve annuloplasty, and a pacemaker insertion. She was on warfarin therapy at a dose of 3.5 mg daily. For surgical preparation, she discontinued warfarin for 7 days prior to the surgery, and administered enoxaparin sodium at a dose of 120 mg/day. Warfarin was re-administered at a dose of 3.5 mg/day on POD #7, and no postoperative complications were observed until the sutures were removed on POD #14. However, ACS, caused by arterial branch bleeding, occurred on POD #16, 10 days after restarting warfarin therapy. Emergency fasciotomy was performed to decompress the anterior and posterior compartments of left thigh. Finally, she had minimal neurologic deficits, with a left knee ROM of 0°–100° after 6 months.

Conclusion

Presented case showed that arterial branch bleeding of the surgical site could occur more than 1 week after restarting warfarin therapy, which in turn may leaded to fatal complications such as ACS. Moreover, in anticoagulated patients, postoperative arterial branch bleeding and compartment syndrome can occur following considerably less invasive surgical procedures, such as polyethylene exchange in UKA. Therefore, surgeons should be aware of the possibility of surgical site bleeding and compartment syndrome for more than a week in patients who restarted warfarin therapy postoperatively, regardless of the invasiveness of surgical procedure.

Compartment syndrome; Anticoagulation; Warfarin; Unicompartmental knee arthroplasty.

1. Introduction

Acute compartment syndrome (ACS) is one of the true emergencies in orthopedics and traumatology. It can lead to permanent damage to skeletal muscles and neurovascular structures if not promptly treated [1, 2]. It is a painful condition caused by the increased intracompartmental pressures, which compromise local tissue perfusion [1, 2]. This might be due to a decrease in compartment size (for example, application of a tight dressing) or an increase in the number of intracompartmental structures (for example, in venous obstruction or hematoma formation) [3].

Etiologies that have been associated with compartment syndrome include fractures, crush injury, vascular injury, exercise, intramedullary nailing, prolonged tourniquet application, deep-vein thrombosis, and use of anticoagulants [4, 5]. Although ACS usually occur after major trauma or invasive surgery, it can develop without trauma or after minimally invasive surgery in anticoagulated patients [6, 7, 8]. The use of anticoagulants can cause traumatic or non-traumatic bleeding, which can increase intracompartmental pressure. Finally, increased intracompartmental pressure can lead to ACS.

The present report describes a case of ACS after restarting warfarin therapy following polyethylene exchange in unicompartmental knee arthroplasty (UKA). Although there have been several case reports that presented ACS following minimal invasive surgery in anticoagulated patients [6, 9], few study reported that ACS after restarting warfarin therapy postoperatively.

2. Case report

A 76-year-old woman, who had undergone UKA of both knees 20 years ago, presented with a pain and locking of left knee. Initial knee anteroposterior (Figure 1a) and lateral (Figure 1b) radiographs revealed a broken polyethylene insert and concurrent dislocation of the fragment of left knee. The femoral and tibial components seemed stable. Aspiration of the knee joint revealed serous joint fluid measuring 15 cc, and the analysis confirmed that the fluid was non-inflammatory (white cell count <1000/mm3 and polymorphonuclear leukocytes <25%). The joint fluid culture was negative for organisms. With a suspected diagnosis of wear and breakage of the polyethylene -, but without definite loosening of the femoral and tibial components, a polyethylene exchange surgery was planned.

Figure 1.

The patient's initial radiographs. Anteroposterior (a) and lateral (b) radiographs reveal breakage of the polyethylene insert and dislocation of the fragment (arrows).

The patient's medical history included mitral stenosis, tricuspid valve regurgitation, sick sinus syndrome, cerebral infarction, liver cirrhosis (stage 1, Child-Pugh classification A), and a thyroid nodule. She had an extensive past surgical history. In 1988 and 1998, she had undergone percutaneous mitral balloon valvotomy for mitral valve stenosis. In December 1997, a permanent pacemaker had been inserted to manage her sick sinus syndrome. In 2006, due to progression of severe mitral and tricuspid valve stenosis, she underwent mitral valve replacement and annuloplasty for the tricuspid valve.

Before the planned surgical procedure, one of the most important perioperative and postoperative concerns for this patient was the dose adjustment of her anticoagulants. As prescribed by her cardiologist, she was on warfarin at a dose of 3.5 mg daily. The target international normalized ratio (INR) was 2.5–3.5 according to the American College of Chest Physicians (ACCP) and the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines [8]. For surgical preparation, warfarin was discontinued for 7 days prior to the surgery. Considering the high risk of thromboembolism or stroke after the discontinuation of warfarin, she was administered enoxaparin sodium at a dose of 120 mg/day via subcutaneous injection for 5 days as a bridging therapy, with the last dose administered 2 days before the surgery. Her INR was 1.15 on the day of surgery.

The patient was positioned supine under general anesthesia. General anesthesia was induced with propofol (60 mg) and remifentanil (5 ml/h) infusion. Rocuronium (40 mg) was also administered to achieve appropriate neuromuscular blockade. Anesthesia was maintained with a continuous infusion of remifentanil (5 ml/h) and desfluane (6 vol%) with 6 L/min of oxygen. A tourniquet was tied on her left thigh with a pressure of 250 mmHg, and an incision was made along the scar of the previous incision. Breakage and dislocation of the UKA polyethylene bearing were observed during the procedure (Figure 2a). In addition, synovial hypertrophy and inflammation were observed in the suprapatellar pouch area, and synovectomy was performed. The femoral and tibial components were stable. The previously inserted bearing was removed and replaced with another of the same size (Figure 2b). Precise bleeding control was performed throughout the surgical field, including the synovectomy site. Her blood pressure was maintained at 120/50 mmHg during the surgery by the anesthesiology team. At the end of the procedure, a drainage tube was inserted. Pneumatic tourniquet was released after wound closure. Anesthesia and surgery lasted 90 min and 65 min, respectively.

Figure 2.

Intraoperative findings and postoperative radiographs. a) During the surgery, breakage and dislocation of the unicompartmental knee arthroplasty polyethylene bearing were observed. The previously inserted bearing was removed and replaced with another of the same size. b) Postoperative radiographs.

On postoperative day (POD) #1, 15 cc of blood drained through the tube, which was subsequently removed. Knee joint ROM exercises were started using a continuous passive motion (CPM) machine. Intramuscular injections of enoxaparin at 120 mg/day were restarted on POD #2. After observing that the surgical incision site and the patient's condition were stable, warfarin was re-administered at a dose of 3.5 mg/day on POD #7. The sutures were removed on POD #14. By then, joint effusion had been minimal and any wound problems were not identified.

On POD #16, severe swelling with acute pain developed on the operated knee joint, and 130 cc of blood was aspirated. Despite the discontinuation of warfarin, swelling of the knee joint and thigh worsened, and the patient's serum hemoglobin level dropped from 9.2 g/dL (POD #16) to 6.5 g/dL (normal 12.0–16.0 g/dL) on POD #19. Her blood pressure (BP) decreased to 70/40 mmHg, with a pulse rate of 150 beats per minute (bpm), and she developed severe swelling of the thigh with intractable pain. Vascular evaluation of the left lower extremity was performed to locate the site of bleeding. Under ultrasonographic guidance, the left femoral artery was used for angiography via the vascular sheath. Contrast extravasation was noted from a branch of the superior geniculate artery (Figure 3). Embolization was performed with N-butyl 2-cyanoacrylate (NBCA, enbucrilate; 1:1 mix) on the bleeding foci. Her BP increased to 100/60 mmHg after embolization. The following day, her BP decreased again to 70/40 mmHg, and she continued to suffer from severe thigh swelling and unbearable pain. The pressure in the lateral thigh compartment was found to be 25 mmHg. Under the clinical impression of a compartment syndrome, emergency fasciotomy using a lateral thigh incision was performed (Figure 4). The anterior and posterior compartments were decompressed. For further management of the open wound, a vacuum-assisted closure (VAC) device was applied. She was then transferred to the intensive care unit (ICU).

Figure 3.

To locate the focus of bleeding, left lower extremity angiography was performed using the left femoral artery under ultrasonographic guidance. Contrast extravasation is noted from a branch of the superior geniculate artery (arrow). Embolization was performed.

Figure 4.

The patient suffered continuous, severe swelling of the thigh and unmanageable pain even after embolization. With the clinical impression of compartment syndrome, emergency fasciotomy using a lateral thigh incision was performed. The anterior and posterior compartments were decompressed.

A VAC pressure of 75 mmHg was intermittently applied to the wound. Five pints of packed red blood cells (pRBCs) had already been transfused during the surgery, but three more pints were transfused postoperatively. Her systolic BP was maintained between 80 and 90 mmHg in the ICU. Three days after fasciotomy, her BP normalized to 110/70 mmHg, and the INR was noted to be 1.92. One week after fasciotomy, her general condition was stable, the VAC system was removed and secondary closure of the lateral incision wound was performed. One week after secondary closure, warfarin at a dose of 3.5 mg/day and enoxaparin at a dose of 120 mg/day were restarted under consultation with the cardiology department. After 3 days, the INR was noted to be 1.5, and enoxaparin was discontinued.

The patient was transferred to the general ward with instructions for gentle knee ROM exercises using the CPM machine and walker-assisted ambulation. On POD #40 (from the initial bearing exchange operation), she was able to sit on the side of the bed and perform active and passive knee flexion up to 45° and 90°, respectively. As the thigh pain subsided and the incision wound healed, she was discharged. She continues to visit the outpatient clinic. Six months after the initial surgery, she had minimal sensory and motor deficits of lower extremity, with a left knee ROM of 0°–100°. The patient and her family were informed that data concerning the case would be submitted for publication, and they provided their consent.

3. Discussion

The important highlight of this report is that arterial branch bleeding of the surgical site could occur more than 1 week after restarting warfarin therapy, which in turn may leaded to fatal complications such as ACS. Moreover, postoperative arterial branch bleeding and compartment syndrome can occur following considerably less invasive surgical procedures, such as polyethylene exchange in UKA. In presented case, perioperative risk for bleeding or thromboembolism was adequately managed per the ACCP and ACC/AHA guidelines [10], and no postoperative complications were observed until the sutures were removed on POD #14. However, ACS, caused by arterial branch bleeding, occurred on POD #16, 10 days after restarting warfarin therapy.

Previous literatures reported ACS caused by postoperative bleeding following minimal invasive surgeries or interventions in patients with warfarin therapy. Cagle et al. reported the case of deltoid compartment syndrome following shoulder arthroscopy in patient on warfarin therapy [6]. Moreover, ACSs following simple vein puncture or catheterization in patients with warfarin therapy have been reported [11, 12]. These cases showed ACSs occurred immediately after surgeries or interventions. On the other hands, in our case, there have been no active bleeding until 2 weeks after surgery, and ACS with arterial branch bleeding occurred 10 days after restarting warfarin therapy. To the best our knowledge, there have been few study that reported ACS after restarting warfarin therapy following minimal invasive surgical procedure.

Our patient had a past medical and surgical history of mitral valve replacement and annuloplasty for the tricuspid valve, for which she was on warfarin therapy with a target INR of 2.5–3.5 [10]. The management of perioperative anticoagulation therapy for patients receiving long-term warfarin remains controversial [13]. The risk of bleeding needs to be balanced against the risk of thromboembolism. If anticoagulation needs to be discontinued before surgery, some risk of thromboembolism is unavoidable [14]. We followed the current guidelines, which recommend preoperative discontinuation of warfarin and instead using a bridging regimen with low-molecular-weight heparin during the perioperative phase while the INR normalizes [15]. Warfarin is then resumed after surgery, and the bridging therapy is discontinued once the INR reaches the desired range [15]. In spite of that, in our case, ACS caused by arterial branch bleeding occurred after restarting warfarin therapy. Any protocols cannot provides optimal guidelines for preventing perioperative bleeding or thromboembolism in patients receiving long-term warfarin therapy [16].

As suggested by previous reports in literature [3, 17, 18], prompt diagnosis and management of ACS are critical to prevent major skeletal muscle and neurovascular sequelae. Muscles can tolerate up to 4 h of ischemia; however, after 6 h, the outcome is uncertain, and after 8 h, the damage is irreversible [19]. The diagnosis of ACS is primarily clinical, although it should be noted that pain might be an unreliable symptom as it is subjective and may vary between patients [3]. Measurement of the intracompartmental pressure can be helpful for the diagnosis of ACS, when it is suspected [2]. Early fasciotomy is imperative, and decompression of all affected anatomical compartments is recommended. In the present case, rapid embolization could be performed by angiography, and all affected compartments of thigh were decompressed in time. Finally, she had minimal neurologic deficits, with a left knee ROM of 0°–100° after 6 months.

4. Conclusion

Presented case showed that arterial branch bleeding of the surgical site could occur more than 1 week after restarting warfarin therapy, which in turn may leaded to fatal complications such as ACS. Moreover, in anticoagulated patients, postoperative arterial branch bleeding and compartment syndrome can occur following considerably less invasive surgical procedures, such as polyethylene exchange in UKA. Therefore, surgeons should be aware of the possibility of surgical site bleeding and compartment syndrome for more than a week in patients who restarted warfarin therapy postoperatively, regardless of the invasiveness of surgical procedure.

Declarations

Author contribution statement

All authors listed have significantly contributed to the investigation, development and writing of this article.

Funding statement

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability statement

No data was used for the research described in the article.

Declaration of interests statement

The authors declare no conflict of interest.

Additional information

No additional information is available for this paper.