Ajsm284184.qxd

Acute Compartment Syndrome Due to Ruptured Baker Cyst After Nonsurgical Management of an
Anterior Cruciate Ligament Tear : A Case Report
Aimee Lynn Schimizzi, Amir A. Jamali, Kenneth D. Herbst and Robert A. Pedowitz The online version of this article can be found at: can be found at:
The American Journal of Sports Medicine
Additional services and information for
Acute Compartment Syndrome Due to
Ruptured Baker Cyst After Nonsurgical
Management of an Anterior Cruciate
Ligament Tear
A Case Report
Aimee Lynn Schimizzi, MD, Amir A. Jamali, MD, Kenneth D. Herbst, MD,and Robert A. Pedowitz,* MD, PhDFrom the Department of Orthopaedic Surgery, University of California, San Diego, San Diego,California Keywords: compartment syndrome; Baker cyst; anterior cruciate ligament; fasciotomy, coagulopathy
Acute compartment syndrome is a clinical entity seen most thrombophlebitis. That day, the patient underwent an MRI often after extremity trauma. However, acute compartment study, which confirmed the ACL tear in addition to a tear of syndrome can also follow atraumatic bleeding into a closed the posterior horn of the medial meniscus as well as a rup- compartment.2,19,28,41 This case report describes an occur- tured Baker cyst. He was treated with rest, elevation, warm rence of acute compartment syndrome in the setting of bleed- compresses, and scheduled doses of ibuprofen. The patient ing from a ruptured Baker cyst. Five previous cases of acute did well for the next 5 days. At that time, he had an acute compartment syndrome in the setting of a ruptured12,23,31,38 increase in pain with increased swelling. A repeat ultrasound or dissecting16 Baker cyst have been reported. This article was negative for DVT. Compartment pressures were meas- highlights a sixth case and emphasizes the importance of ured and ranged between 15 and 20 mm Hg. A diagnosis of potential contributing factors such as antithrombotic med- possibly evolving acute compartment syndrome was made, ications and mechanical factors such as leg curls and venous and a venous compression device was placed on the foot (Plexipulse, NuTech, San Antonio, Tex) to assist with venousreturn and decrease swelling. The patient was dischargedhome with this device. He came to the emergency depart- ment 6 hours later with markedly increased swelling andtense compartments.
A 49-year-old man was initially evaluated with a 1-month his- The patient’s medical history was significant for Gilbert tory of a ruptured left ACL. He was treated with activity mod- syndrome, benign prostatic hypertrophy, and depression.
ification and gradual range of motion restoration. He began He had no history of coagulation or bleeding problems.
working aggressively on hamstring strengthening exercises Routine medications included fluoxetine (Prozac) 10 mg using prone leg curls with a roller that contacted on the prox- imal posterior calf. Three weeks later, he came to the clinic Physical examination revealed a healthy-appearing man with increased left leg pain and swelling. Examination at that in moderate pain. On musculoskeletal examination of the time revealed pain with passive toe dorsiflexion (Homans left knee, there were posterior fullness, tense swelling of all sign). A duplex ultrasound revealed no evidence of deep lower leg compartments, and increased pain with passive venous thrombosis (DVT). He was diagnosed with superficial flexion and extension of the left ankle. Dorsalis pedis andposterior tibial artery pulses were palpable. On neurologicexamination of the affected extremity, there was slightly *Address correspondence to Robert A. Pedowitz, MD, PhD, decreased sensation to light touch in the deep peroneal Professor, Department of Orthopedics (8894), University of California,San Diego, 350 Dickinson Street, San Diego, CA 92103-8894 (e-mail: nerve distribution. Compartment pressures were as follows: superficial posterior, 78 mm Hg; deep posterior, 69 mm Hg; No potential conflict of interest declared.
lateral, 79 mm Hg; and anterior, 78 mm Hg—confirming adiagnosis of acute compartment syndrome.
The American Journal of Sports Medicine, Vol. 34, No. 4 Radiographs of the left lower extremity were notable for DOI: 10.1177/0363546505284184 2006 American Orthopaedic Society for Sports Medicine soft tissue swelling. Complete blood count showed a mildly The American Journal of Sports Medicine elevated white blood cell count, with a normal differential, cyst, increasing the diagnostic difficulty.26 Five previous normal hematocrit, and normal platelets. The patient’s cases of a ruptured Baker cyst leading to compartment syn- bleeding time was elevated to 17.5 minutes, the prothrom- drome have been reported in the literature.12,16,23,31,38 bin time was 10.8 minutes, and the partial thromboplastin Acute compartment syndrome is most commonly associ- time was 26.3 minutes. The patient was taken emergently ated with extremity trauma. However, acute compartment to the operating room and underwent 4-compartment fas- syndromes induced by medication or concurrent disease- ciotomy. At the time of surgery, the muscle appeared viable induced bleeding have been reported in the litera- and had no evidence of necrosis. After the fascial releases, ture.4,12,19,23,28,31,38,41 The medications most commonly intramuscular pressures were below 20 mm Hg in all com- implicated are aspirin, warfarin, and heparin.2,4,19,41 Anouchi partments. The wound was carefully inspected, and no et al2 reported misdiagnosis of rupture of the medial head of active bleeding was noted from either the skin edges or the the gastrocnemius, “tennis leg,” treated with heparin for deeper tissues. The skin edges were reapproximated using suspected DVT with progression to compartment syndrome.
vessel loops and staples. The patient was admitted and Our patient had been treated with the nonsteroidal anti- started on intravenous antibiotics. His pain was markedly inflammatory drug (NSAID) ibuprofen. The NSAIDs are fre- improved postoperatively. His numbness also gradually quently used medications with approximately 60 million improved during the next several days.
prescriptions written per year in the United States.33 The For the first 12 hours postoperatively, the wound mechanism of action is inhibition of prostaglandin formation remained relatively bloodless. During the next 12 hours, he from arachidonic acid by inhibition of the enzyme cyclooxy- had a significant increase in bleeding from the wound. A genase (COX).33 Two isoenzymes of COX have been identified, hematology consultation was obtained. During the first 4 COX-1 and COX-2. COX-1 appears to be a “housekeeping” days of the admission, the patient had elevation of his enzyme in multiple tissues such as the kidney, stomach, and bleeding time to greater than 20 minutes and a drop in his blood.33 Cox-2 appears to be the isoenzyme primarily respon- hematocrit from 45% to 18.4%. With the recommendation of sible for the inflammatory response.33 The NSAIDs inhibit the hematology service, the patient was treated with trans- platelet aggregation by inhibiting platelet production of fusions of packed red blood cells and platelets. In addition, thromboxane A2, which is required for platelet thrombus his fluoxetine was discontinued. He was started on tran- formation.6,22 The NSAIDs such as nabumetone (Relafen) examic acid, a potent thrombolysis inhibitor.17 The patient’s and etodolac (Lodine) have predominant activity at COX-2.
hematologic status improved with these interventions.
These medications appear to have improved clinical safety On postoperative day 5, the patient underwent an MR profiles with decreased gastric and hematologic complica- angiogram to rule out an underlying arteriovenous malfor- tions.10,22,25,36 In addition, in vitro studies have demonstrated mation or aneurysm as a possible cause for the initial com- that nabumetone has significantly less inhibition of platelet partment syndrome. The MR angiogram showed a ruptured thromboxane A2 synthesis than do naproxen and Baker cyst and an adjacent hematoma. No arteriovenous indomethacin.10,22 Newer COX-2 specific inhibitors, such as malformation or aneurysms were noted.
celecoxib (Celebrex) and rofecoxib (Vioxx), have higher affini- He was taken back to the operating room on postopera- ties for COX-2 activity to provide a greater safety profile rel- tive day 5 and underwent irrigation and debridement of his ative to older NSAIDs.8,14,18,27 The patient in this case report wounds. A large hematoma was revealed in the lateral com- was taking ibuprofen, an older NSAID with both anti-inflam- partment wound. This hematoma was debrided and sent for bacteriology culture, which had negative results. A minimal In addition to ibuprofen, the patient was taking fluoxe- amount of superficial muscle appeared nonviable and was tine. Fluoxetine (Prozac) is an antidepressant medication debrided. The underlying muscle appeared normal and was that inhibits central nervous system neuronal uptake of contractile. All wounds were closed.
serotonin.21,29,30 It is metabolized through the liver to inac- After complete healing of the skin incisions, the patient tive metabolites, which undergo renal clearance. According returned to a progressive rehabilitation program. He elected to the Physicians Desk Reference,32 increased bleeding time, not to undergo an ACL reconstruction. He eventually returned anemia, ecchymosis, thrombocytopenia, thrombocythemia, to all of his activities, including expert snow skiing and long- petechiae, purpura, and other blood dyscrasias have been reported as rare side effects of fluoxetine. Increased bleed-ing has been reported in cases of coadministration with warfarin secondary to the inhibition of cytochrome P450.9,11However, in the literature, there are multiple reports of Common diagnostic dilemmas involve the distinction bleeding complications and bruising as a result of the use between a ruptured Baker cyst and thrombophlebitis, as of fluoxetine without concurrent use of antithrom- both syndromes present with extremity swelling, pain, and botics.3,21,30,37,42 In addition, reversible bleeding time pro- pain with passive toe dorsiflexion (Homans sign).7,20 longation has been reported with fluoxetine use.21 Despite Misdiagnosis of a ruptured Baker cyst as thrombophlebitis these reports, no studies have proven fluoxetine causes may lead to nonindicated anticoagulation with progression bleeding dyscrasias. Several small prospective studies have to compartment syndrome.7,12,19,20,31,41 Concurrent popliteal failed to show significant hematologic changes from this vein thrombosis can also occur along with a ruptured Baker drug.1,5,24 These studies had small sample sizes (≤10 subjects) and short follow-up (4 weeks of treatment). Because the 9. Claire RJ, Servis ME, Cram DL Jr. Potential interaction between warfarin functional effect of fluoxetine on inhibition of platelet sodium and fluoxetine. Am J Psychiatry. 1991;148:1604.
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impaired as a result of treatment with ibuprofen in combi- 12. Dunlop D, Parker PJ, Keating JF. Ruptured Baker’s cyst causing pos- terior compartment syndrome. Injury. 1997;28:561-562.
In addition to the pharmacologic and anatomical etiologi- 13. Fordyce MJ, Ling RS. A venous foot pump reduces thrombosis after total hip replacement. J Bone Joint Surg Br. 1992;74:45-49.
cal factors, another possible contributor to the patient’s 14. Geis GS. Update on clinical developments with celecoxib, a new acute compartment syndrome may have been the pneumatic specific COX-2 inhibitor: what can we expect? Scand J Rheumatol.
compression pumps placed on his lower extremities. These compression devices decrease venous stasis and augment 15. Gloviczki P, Fowl RJ, Hollier LH, Dewanjee MK, Plate G, Kaye MP.
fibrinolytic activity.13,40 There is only 1 case report in the lit- Prevention of platelet deposition by ibuprofen and calcium dobesilate erature of acute compartment syndrome resulting from a in expanded polytetrafluoroethylene vascular grafts. Am J Surg.
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malfunctioning pneumatic compression boot.39 The patient 16. Hammoudeh M, Siam AR, Khanjar I. Anterior dissection of popliteal in this case report did not have a malfunctioning pneumatic cyst causing anterior compartment syndrome. J Rheumatol. 1995;22: compression device, but it is theoretically possible that the increased venous return toward the ruptured Baker cyst 17. Harder S, Klinkhardt U, Alvarez JM. Avoidance of bleeding during could have contributed to the increased pressure in the limb surgery in patients receiving anticoagulant and/or antiplatelet ther- and, ultimately, to compartment syndrome.
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18. Hawkey CJ. COX-2 inhibitors. Lancet. 1999;353:307-314.
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19. Hay SM, Allen MJ, Barnes MR. Acute compartment syndromes Specifically, the presence of a ruptured Baker cyst in com- resulting from anticoagulant treatment. BMJ. 1992;305:1474-1475.
bination with pharmacological and mechanical factors con- 20. Hench PK, Reid RT, Reames PM. Dissecting popliteal cyst simulating tributed to the development of compartment syndrome in thrombophlebitis. Ann Intern Med. 1966;64:1259-1264.
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22. Jeremy JY, Mikhailidis DP, Barradas MA, Kirk RM, Dandona P. The extremities with NSAIDs must be tempered by the risk of effect of nabumetone and its principal active metabolite on in vitro bleeding complications, particularly in patients with syn- human gastric mucosal prostanoid synthesis and platelet function.
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25. Lanza FL. Gastrointestinal toxicity of newer NSAIDs. Am J Gastroenterol. 1993;88:1318-1323.
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