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Kenneth D. Brandt, MD
Clinical Professor of Medicine
University of Kansas Medical Center
Kansas City, Kansas
The patient, a 68 year old housewife and avid gardener who has been married for 38 years to a malpractice attorney, presented with an acute increase in her usual left knee discomfort for the previous 36 hours, which she now described as “7 or 8 out of 10” and “burning,” and so severe that she could bear no weight on the extremity.
She had been in good health except for chronic low-grade pain in her left knee during the past 8 years, which had been gradually worsening with activity, such as kneeling in her garden to pull weeds and plant flowers and shrubs, and getting down on the carpet to play with her 1-year-old granddaughter. Prior to this recent flare-up, her knee pain had led her to curtail such activities and to use over-the-counter analgesics and nonsteroidal anti-inflammatory drugs, which she took as needed. It had not disturbed her sleep previously, but was aggravated by walking on hills and climbing stairs. She reported that the left leg occasionally buckled when she walked, but she had never fallen. She had become aware of a crackling sensation in the left knee in recent months, especially with climbing stairs; morning stiffness in the left knee lasted 10 to 15 minutes and was of mild-moderate severity. She also reported gelling in her left knee with inactivity, such as sitting for hours watching TV or in a concert hall.
Her past history was entirely unblemished, except for some exercise-induced precordial pain 1 year earlier led to a work-up that excluded myocardial infarction and was otherwise negative. Aspirin 81 mg daily, was prescribed, which she been taking since that time. In addition, she has been taking naproxen 500 mg in the morning and 250 mg after supper, and acetaminophen, 1000 mg up to 4 g/day as needed, for her knee pain.
On physical examination the patient was 64” tall, weighed 174 pounds, and had a body mass index of 29.9. Her blood pressure was 138/88, pulse 92 and regular. Oral temp was 98.8° F. The left knee was held in 45° of flexion. Except for the findings in the left lower extremity, the physical exam was unremarkable. Non-tender, 1+ pitting edema was present around the left ankle. The left calf was very tender on compression, slightly swollen, and warm to the touch. No cords were palpable, but Homan’s sign was strongly positive on the left.
In a standing anteroposterior radiograph, the left knee showed moderate medial tibiofemoral compartment joint space narrowing, with osteophytosis and subchondral bony sclerosis under the medial tibial plateau. (Slide 1) A lateral view showed radio-opacity in the left suprapatellar pouch. (Slide 2)
A venogram was negative, but because of the swollen and tender calf and strongly positive Homan’s sign, the patient was hospitalized and anticoagulation with heparin was started. Naproxen and low-dose aspirin were continued. Warm compresses to the left lower extremity, 20 minutes 4 times a day, were ordered. A hydrocodone/acetaminophen combination was prescribed for the severe left lower extremity pain.
Diagnosis and Treatment
Pseudothrombophlebitis, due to leakage of a popliteal (Baker’s) cyst, is not an uncommon cause of diagnostic confusion in patients with knee osteoarthritis (OA). (Slide 3) The correct diagnosis may be established either by ultrasonography (Slide 4) or by arthrography after an injection of contrast material into the involved knee. (Slide 5) The sensitivity of each procedure is approximately 95%, with each picking up an occasional case that is missed by the other. An arthrogram offers the advantage of providing an opportunity to obtain a sample for synovial fluid analysis at the time of arthrocentesis, prior to injection of the contrast material. The presence of a popliteal cyst may be revealed merely by obtaining a lateral radiograph of the knee immediately after injection of 30 cc to 50 cc of air into the joint at the time of arthrocentesis.
In patients with knee arthritis and a popliteal cyst, a narrow connection between the cyst and the joint can be demonstrated.1 A Bunsen-valve mechanism permits passage of synovial fluid from the knee into the cyst, but flow does not occur in the opposite direction.2 Pressure in the cyst may exceed that in the knee and be great enough to lead to a rupture of the cyst wall.2,3 In most cases, popliteal cysts are painless but when they leak or rupture acutely, spilling synovial fluid into the soft tissues of the calf, they produce a clinical syndrome which may be indistinguishable from that produced by deep vein thrombosis, with swelling and tenderness of the calf, a positive Homan’s sign, and, occasionally, ecchymosis around the ankle.4-6 Rupture or leakage of a pop-liteal cyst often responds to bed rest, avoidance of weight bearing, and local application of heat. If a large effusion is present in the knee, an intrarticular injection of steroid may be helpful.
The patient may not readily distinguish the pain due to pseudothrombophlebitis from that due to the knee OA. Pseudothrombophlebitis should be suspected in any patient presenting with signs and symptoms of thrombophlebitis in the lower extremity, especially if a history of knee arthritis or clinical evidence of knee effusion is present. In some cases, a rupture of a synovial cyst may be the initial indication of the underlying knee arthritis.7
It is essential to differentiate pseudothrombophlebitis from bona fide thrombophlebitis. Anticoagulation, which is indicated in the latter case, is contraindicated in pseudothrombophlebitis because it may lead to bleeding into the leg.7,8 As in the present case, an emergency fasciotomy may be required for treatment of an iatrogenic compartment syndrome, with compression of nerves, blood vessels, and muscle by blood within a closed space, whose ability to expand is limited by the fascia. If decompression is not achieved it may result in tissue death due to a lack of oxygenation, as the blood vessels are compressed by the raised pressure within the compartment. In the above patient, anticoagulation with heparin, given because of the presumption of a deep vein thrombosis - and superimposed on the patient’s daily low-dose aspirin therapy for cardiovascular prophylaxis - increased her risk of bleeding.
- Taylor AR, Rana NA. A valve. An explanation of the formation of popliteal cysts. Ann Rheum Dis. 1973;32:419-421.
- Jayson MI, Dixon AS. Valvular mechanisms in juxta-articular cysts. Ann Rheum Dis. 1970;29:415-420.
- Solomon L, Berman L. Synovial rupture of knee joint. J Bone Joint Surg Br. 1972;54:460-467.
- Katz RS, Zizic TM, Arnold WP, Stevens MB. The pseudothrombophlebitis syndrome. Medicine. 1977;56:151-164.
- Soriano ER, Catoggio LJ. Baker’s cysts, pseudothrombophlebitis, pseudo-pseudothrombophlebitis: where do we stand? Clin Exp Rheumatol. 1990;8:107-112.
- Wigley RD. Popliteal cysts: variations on a theme of Baker. Semin Arthritis Rheum. 1982;12:1-10.
- Eyanson S, MacFarlane JD, Brandt KD. Popliteal cyst mimicking thrombophlebitis as the first indication of knee disease. Clin Orthop. 1979;144:215-219.
- Tait GB, Bach F, Dixon J. Acute synovial rupture: further observations. Ann Rheum Dis. 1965; 24: 273- 277
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