These authors detail how anticoagulation therapy may have complicated the treatment of a patient who sustained acute compartment syndrome after a crush injury.
With a high clinical suspicion, we took him to the operating room and obtained intra-compartmental pressures utilizing a slit catheter (wick catheter). The compartment pressures measured 45, 90 and 70 mmHg through the dorsal medial forefoot, dorsal lateral forefoot and medial calcaneal penetration sites respectively.
We performed a three-incision fasciotomy, stabilized fractures percutaneously with Kirschner wires and performed dermatotraction of the fasciotomy sites with vessel loops. We planned to close the wound two days later in the operating room, but this was abandoned due to the patient’s persistent compartment syndrome-like symptoms while inpatient. He continued to have persistent marked edema to the foot. The patient reported minimal foot pain relief since the time of the index surgery.
In addition to trending creatinine phosphokinase (CPK) levels, there was a spike from post-fasciotomy day one to day two (2,042 to 5,100 U/L with the normal range being between 28 to 174 U/L). We performed a repeat decompression through the initial incisions of each compartment with evacuation of hematoma. Over the subsequent days, the patient’s pain greatly improved with a decrease in opioid analgesic consumption and CPK levels trending downward daily. Four days later, we performed closure. The CPK was 942 U/L and decreased to 271 U/L at discharge the following day. Hemoglobin dropped from 15 g/dL to 12.9 g/dL on post-op day one and remained at approximately that level throughout the inpatient stay.
Having previously performed multiple fasciotomies for compartment syndrome, we reflected on why in this instance compartment release did not appear to completely resolve symptoms at the index surgery. Our initial consideration was an incomplete or inadequate decompression. Another thought pertained to the hospital-mandated anticoagulation therapy. From the day of surgery until discharge, the patient was placed on heparin for DVT prophylaxis, a standard practice at our institution. We were curious if after the decompression fracture stabilization and associated muscular damage from the crush injury, an increased or sustained bleeding into the foot resulted in a compartment syndrome situation. Intra-compartmental bleeding could have resulted in either blocking off a previously decompressed compartment with hematoma and clot, or filling of a missed small foot compartment.
Was there anything in the literature to support our rationale? The answer to this question was yes and no.
The closest example we found was a case report for a patient who sustained an internal pedal degloving injury with fractures.1 The treating physicians suspected compartment syndrome and the patient went for compartment measurement and subsequent fasciotomy with fracture reduction. Despite an open fasciotomy, hematoma and fracture blisters developed with a return of 10 out of 10 pain by post-op day four. The patient had a hematoma evacuation washout. Compartment pressures again were all elevated above the 30 mmHg threshold for fasciotomy. There was no mention of anticoagulation use in the case. (We did attempt to email the article’s noted corresponding author to obtain more specific case information but received no reply after 60 days.)
A second example includes a patient who sustained a calcaneal fracture and acute compartment syndrome based on clinical findings and wick catheter measurements.2 The patient had pedal fasciotomies on admission. On post-op day three, the patient had wound closure with open reduction internal fixation (ORIF) of the calcaneus as well as subtalar joint fusion. Within 48 hours of the surgery, the patient developed fever, leukocytosis, extreme pain to the foot and blister development about the heel. Ruling out deep vein thrombosis (DVT) with a negative ultrasound and infection with negative urinalysis, blood cultures and a chest radiograph, physicians diagnosed the patient with a recurrence of compartment syndrome and performed fasciotomies through the previous incision sites. Again, no mention of anticoagulation use was in the report. (We did attempt to email the article’s noted corresponding author to obtain more specific case information but received no reply after 60 days.)
Further investigation found multiple case reports consisting of situations in which patients on anticoagulation medication (new/acute or chronic) developed compartment syndrome with either idiopathic- or trauma-related events (i.e. fall, fracture, surgery). Examples include:
- Patients taking long-term anticoagulation medicine (ranging from three to eight years) who sustained minor trauma.3 Minor trauma in this study included: pulled thigh or leg muscle, tackle in rugby game, and non-displaced fibular fracture.
- Patients who sustained minor trauma (i.e. leg/calf strain, gastrocnemius tear), were misdiagnosed as having venous thrombosis and received anticoagulation medication.3,4
- Patients who had joint total hip or total knee arthroplasty, received routine post-op anticoagulation medication and developed subsequent compartment syndrome.5,6 A literature review by Shaath and colleagues of total knee arthroplasty and compartment syndrome found that there was a delay range of 14 to 192 hours between replacement surgery and fasciotomy for suspected compartment syndrome.6 Complications from this delay in diagnosis include sensory deficits, weakness, muscle loss, foot drop and amputation.5,6
- Patients who had trauma fixation, received post-op anticoagulation medication and developed subsequent compartment syndrome.7 An interesting example includes a patient who sustained left femur and left tibia fractures in a motor vehicle accident, and had emergent retrograde nailing of the femur and external fixation application for the tibia. He started on heparin at post-op day one and at post-op day 12, developed a right leg compartment syndrome requiring a four incision leg fasciotomy.7
- One patient presented to the ED with chest pain, received a diagnosis of acute myocardial infarction, and started on anticoagulation medication.8 Without any history of traumatic events, an idiopathic onset of compartment syndrome developed 12 hours later. He required an arm fasciotomy.
Aside from the aforementioned degloving and calcaneal fracture cases, the search did not yield any examples of post-fasciotomy patients having a “new” acute incident of compartment syndrome, such as the recent situation we described above. While recurrent compartment syndrome cases exist in the literature, authors have described them as long-term secondary events or occurring after a new trauma event.2
Some interesting case examples of latent recurrent compartment syndrome include: development of reflex sympathetic dystrophy secondary to a crush injury resulting in hyperemia and a subsequent compartment syndrome five weeks later (Chokshi and colleagues); compartment syndrome secondary to an ischemia-reperfusion situation after a percutaneous thrombolysis vascular procedure (Kerkar and coworkers, 2016); compartment syndrome secondary to viral myositis (Kerkar and coworkers, 2016); and compartment syndrome secondary to a suspected connective tissue disorder with a female patient undergoing 60 to 70 fasciotomies between ages 27 and 43 (Barajas and colleagues, 2013).9–11 A few key points derived from this review of recurrent compartment syndrome cases include omission of closing the deep fascia, the use of split-thickness skin graft closure methods and consideration of genetic workup.11,12
Muscular and osseous trauma can naturally result in hemorrhage into the surrounding tissue and compartments. Adding anticoagulation medication increases patients’ susceptibility to exacerbated bleeding, ultimately leading to hemorrhage, increasing intra-compartmental pressures, and resulting in an acute compartment syndrome scenario. Whether it is a relatively minor trauma, high energy crush injury with or without fracture, or surgical trauma, each instance has the potential to cause disproportionally greater intra-compartmental bleeding while a patient is on anticoagulation medication.3,5 Despite this plausible hypothesis, a review of compartment syndrome after total knee arthroplasty by Shaath and colleagues found only half the cases in the literature examined reported anticoagulant use during the course of clinical events.6 The two aforementioned cases with acute compartment syndrome development (internal degloving, calcaneal fracture) also do not mention anticoagulation use during the timeline of events.1,2
A constant theme throughout multiple articles was the need to have a definitive diagnosis of DVT prior to implementing anticoagulation therapy as treatment without confirmatory diagnosis can be hazardous.3,4 A key consideration is the assessment of pain and its location. With compartment syndrome, things to consider include continued severe pain not relieved by opioid analgesics, continued or increased swelling, firm compartments and neurological symptoms or deficit (e.g., loss of two-point discrimination).5 This can sometimes be difficult in a post-operation setting when opiates are often required or in extremity surgery when patients receive a local block (e.g., popliteal and saphenous nerve, ankle ring block with Marcaine or Exparel® (Pacira Pharmaceuticals)) for pain relief, but may mask some of these important clinical cues. One benefit to foot decompression is its distance from the popliteal vessels in potentially differentiating DVT from compartment syndrome. However, one should always rule out DVT prior to considering compartment syndrome.5
Labs may be of benefit including trends in CPK, chloride (Cl), blood urea nitrogen (BUN) and hemoglobin levels.5,13 The protein CPK is found in muscle. Researchers have cited cellular ischemia or muscular damage as generating the release of CPK from injured cells.13 Although no true threshold comparing CPK values against compartment syndrome presentation exists in the literature, one study determined that using cutoff values of CPK greater than 4,000 U/L, chloride greater than 104 mg/dL and blood urea nitrogen less than 10 mg/dL could be of benefit to diagnosis. Specifically, the presence of two out of the three elevated lab values resulted in a sensitivity and specificity of 0.87 and 0.76 for compartment syndrome, respectively, with a total accuracy of 0.86.13 A drop in hemoglobin may also be suggestive of continued hemorrhage into a fascial compartment.5 If all else fails, direct wick catheter compartment measurement may be required with normal ranges between 0 to 8 mmHg and levels greater than 30 mmHg indicate need for fasciotomy.6
We remain unsure as to how the patient’s compartment syndrome recurred. Did we miss a compartment in the index release? Did hemorrhage and hematoma clot off a decompressed compartment? Did his DVT prophylaxis play a role? In hindsight, we wish we had remeasured compartment pressure during the revision surgery to test these hypotheses. His hemoglobin remained relatively stable throughout the hospital stay after the initial fasciotomy, suggesting bleeding may not have been a factor. However, foot compartments are small and minimal blood loss could easily fill a compartment.
Will this change how we practice? We are not sure at this point. Some things we may consider include initial use of mechanical modalities such as sequential compressive devices, elastic stockings, early physical therapy encouraging out of bed habits, and extremity range of motion exercises instead of chemical anticoagulation. We liken incentive spirometer use to be very similar to encouraging patients to make a calf squeezing contraction in multiple sets per day to promote circulation while admitted to the hospital. Once one has performed a successful fasciotomy and closure, adding any desired anticoagulation medication may be (more) appropriate.
From this review, we feel as though we have raised more questions than when we started. However, we now have better insight into some of the intricacies and considerations when attempting to diagnose compartment syndrome in patients who may be susceptible to this condition.
Questions for discussion: Does anyone strictly utilize non-pharmacological methods of DVT prophylaxis in patients with compartment syndrome? What are your criteria for closure of a fasciotomy (standard number of days, lab values, pain)? Does anyone use long-term local anesthetic blocks like Marcaine, Exparel® or patient-controlled analgesia (PCA) after a compartment syndrome decompression for patient pain control?
Dr. Hood is a fellowship-trained foot and ankle surgeon, and associate at Premier Orthopaedics and Sports Medicine in Malvern, PA. Follow him on Twitter at @crhoodjrdpm.
Dr. Hollinger is a fellowship-trained foot and ankle surgeon and associate at Martin Foot and Ankle in York, PA.
Dr. Miller is the Fellowship Director of the Pennsylvania Intensive Lower Extremity Fellowship and Residency Director of the Phoenixville Hospital PMSR/RRA in Phoenixville, PA. He currently practices at Premier Orthopaedics and Sports Medicine in Malvern, PA.
1. Bingham AL, Fallat LM. Empty toe phenomenon: a rare presentation of closed degloving injury of the foot. J Foot Ankle Surg. 2015;55(4):842-.
2. Ramanujam CL, Wade J, Selbst B, Belczyk R, Zgonis T. Recurrent acute compartment syndrome of the foot following a calcaneal fracture repair. Clin Podiatr Med Surg. 2010;27(3):469-474.
3. Hay SM, Allen MJ, Barnes MR. Acute compartment syndromes resulting from anticoagulant treatment. BMJ. 1992;305(6867):1474-1475.
4. Collins IE, Waite J, Gundle R. Acute compartment syndrome following therapeutic anticoagulation for suspected dvt. Inj Extra. 2005;36(7):253-254.
5. Nadeem RD, Clift B, Martindale JP, Hadden W, Ritchie IK. Acute compartment syndrome of the thigh after joint replacement with anticoagulation. J Bone Joint Surg. 1998;80(5):866-868.
6. Shaath M, Sukeik M, Mortada S, Masterson S. Compartment syndrome following total knee replacement: a case report and literature review. World J Orthop. 2016;7(9):618-622.
7. McLaughlin JA, Paulson MM. Delayed onset of anterior tibial compartment syndrome in a patient receiving low-molecular-weight heparin. J Bone Joint Surg. 1998;12(80-A):1789-1790.
8. Hettiaratchy S, Kang N, Hemsley C, Powell B. Spontaneous compartment syndrome after thrombolytic therapy. J R Soc Med. 1999;92(9):471-472.
9. Chokshi BV, Lee S, Wolfe SW. Recurrent compartment syndrome of the hand: a case report. J Hand Surg Am. 1998;23(1):66-69.
10. Kerkar AP, Farber A, Kalish JA, Siracuse JJ. Recurrent lower-extremity compartment syndrome after four-compartment fasciotomy secondary to acute limb ischemia. Ann Vasc Surg. 2016;30:306.e5-306e.7.
11. Barajas BD, Sun A, Rimoin DL, Reinstein E. Recurrent compartment syndrome in a patient with clinical features of a connective tissue disorder. Am J Med Genet Part A. 2013;161(6):1442-1446.
12. Kotak BP, Bendall SP. Recurrent acute compartment syndrome. Injury. 2000;31(1):66-67.
13. Valdez C, Schroeder E, Amdur R, Pascual J, Sarani B. Serum creatine kinase levels are associated with extremity compartment syndrome. J Trauma Acute Care Surg. 2013;74(2):441-447.