- Email: [email protected]
The pseudothrombophlebitis syndrome: A reappraisal
The Pseudothrombophlebitis By Scott Blumberg
T
HE pseudothrombophlebitis (PTP) syndrome, secondary to changes in the structural integrity of popliteal (synovial) cysts, has been reported primarily in patients with rheumatoid arthritis who have overt knee arthropathies. Our experience has been quite different, and in this regard we report eleven consecutive patients without chronic or readily discernible arthropathies who were admitted to the general medical service of an acute care hospital with the PTP syndrome. An intact, nondissecting popliteal cyst or the lack of an arthrographically demonstrable cyst was found in half of the patients, and is entirely consistent with the PTP syndrome. The pseudothrombophlebitis syndrome encompasses a group of disorders characterized by acute inflammation of the calf, giving rise to signs and symptoms of deep vein thrombophlebitis (DVT). However, intrinsic abnormalities of the vasculature are distinctly uncommon. Changes in the structural integrity of popliteal (synovial) cysts, including rupture with extravasation of synovial fluid and dissection into the calf, are a frequent cause of PTP. The therapeutic implications of this diagnosis are of utmost importance; anticoagulation is used for DVT while antiinflammatory agents and local measures for PTP. The majority of patients previously reported with this syndrome have an inflammatory arthropathy, most commonly rheumatoid arthritis, but noninflammatory disorders such as osteoarthritis, trauma, and meniscal tears have also been described.lm5 Previous series by Katz et From the Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School and Beth Israel Hospital, Boston, Massachusetts Scott Blumberg, M.D.: Clinical and Research Fellow in Medicine, Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School, and Beth Israel Hospital; Fred G. Kantrowitz, M.D.: Chiej. Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School and, Beth Israel Hospifal. Address reprint requests to Fred G. Kantrowifz. M.D., Department of Medicine Beth Israel Hospital, Boston, Massachusetts, 02215 o 1981 by Grune & Stratton, Inc. 0049-0172/81/1004-0005$01.00/0
278
Syndrome:
A Reappraisal
and Fred G. Kantrowitz
al.’ and Perri et a1.6 were based upon patients admitted to rheumatic disease units or preselected due to their underlying rheumatic disease. Our experience has been different, and we therefore report eleven patients without chronic or readily discernible arthropathies who were admitted to the general medical service of an acute care hospital with the PTP syndrome. MATERIALS
AND
METHODS
Patient Selection During the years 197551978, I I patients admitted to the general medical service of the Beth Israel Hospital and initially thought to have DVT were seen in consultation by our rheumatology unit. Venography showed no evidence of DVT, and the arthrographic findings and/or clinical course were considered diagnostic of the PTP syndrome. These patients form the basis of this report, and since there is no inpatient rheumatic disease ward in our hospital, they also represent all patients admitted with PTP.
Arthrography Arthrograms were performed to confirm the presence of an intact, dissected, or ruptured popliteal cyst, and to evaluate the possibility for internal knee derangement. Technically, a double contrast technique was employed using ten ml of water soluble contrast material (Renograffin@ ~ 60) and up to 50 ml of air. These were introduced into the knee joint after a routine arthrocentesis was performed. The patient was then ambulated for 5 minutes and films obtained of both knee and calf in Rexion and extension (anterior-posterior, lateral views). Specific views to evaluate the menisci were also obtained. If a popliteal cyst was not visualized during the procedure, delayed films were obtained several hours later when possible. An intact popliteal cyst is defined arthrographically as a cyst demonstrating a smooth contour without evidence of dissection or rupture. A dissected popliteal cyst maintains its smooth contour and extends along the fascial planes into the calf, below the confines of the popliteal fossa. A ruptured cyst loses its smooth contour with extravasation of contrast material into the soft tissues of the calf.
Results The predominantly male patients range in age from 17-83 yr.‘-” The majority of patients’-” had symptoms referable to the popliteal fossa or calf and not the knee, both initially and at time of presentation. Although no patient experienced overt knee trauma immediately before the onset of their initial symptoms, 4 patients had engaged in “nonroutine” activities (ie, jogging, dancing, Seminars in Arthritis and Rheumafism, Vol. 10, No. 4 (May),
198 1
279
kneeling). There was a distant history of knee trauma in three patients, two of whom had intermittent knee locking since their injuries. Two patients had prior episodes of acute calf inflammation diagnosed as DVT and muscle strain. An additional patient had rheumatoid arthritis of 20 yr duration, which had been in remission for the past 10 yr. No other patient had evidence of a systemic rheumatic disease or a seronegative spondyloarthropathy. Pertinent findings on physical examination included knee effusions in 6-l 1 patients with effusions detected the following morning in three additional patients. The volume of fluid aspirated varied from 6 ml to 45 ml. Excluding effusions, 7-1 I patients had normal knee examinations while four had mild knee tenderness. A popliteal mass was noted in 5 patients. All patients had calf tenderness and swelling; 6 had a positive Homan sign and 4 had pedal edema. Synovial fluid analysis was performed in 7 patients; 6 of the fluids were noninflammatory. Hemorrhagic or serosanguinous fluids were found in two patients with prior knee injuries who recently jogged, in one patient with severe osteoarthritis, and in one patient initially anticoagulated with sodium heparin for presumed DVT. This latter patient, in addition to the hemarthrosis, developed hematuria and hematochezia. No patient had evidence of a septic or crystal induced synovitis. All patients had roentgenograms of the knee, which were not helpful diagnostically in the majority of cases. Two patients had osteoarthritis, one mild and the other severe; two had small patellar spurs and one had patellar hyperostosis with superior whiskering. The remainder”‘] had entirely normal films. Venography was performed as the initial diagnostic procedure in nine patients, and was negative for DVT in all. However, three venograms demonstrated extrinsic compression of popliteal and proximal calf veins. Two patients did not undergo venography, one of whom had a previous hypersensitivity reaction to dye. Arthrography was performed in all except three patients, two of whom had relative contraindications (previous hypersensitivity reaction to dye, anticoagulation). Four patients had dissection and/or rupture of a popliteal cyst, while three had an intact cyst alone. One arthro-
gram did not demonstrate a popliteal cyst, but clearly showed a medial meniscal tear. Another patient with a ruptured popliteal cyst had also had a lateral meniscal tear. Therapeutically, each patient received bed rest, elevation of the involved extremity, and hot, moist compresses. These measures alone frequently resulted in demonstrable improvement. Only one patient was initially anticoagulated; this was discontinued after venography was negative for DVT. The remainder of the patients were given nonsteroidal antiinflammatory agents or an intraarticular (knee) corticosteroid instillation. All patients were markedly improved at time of discharge with decreased pain, tenderness and swelling of the calf and knee. DISCUSSION
The differentiation between the pseudothrombophlebitis syndrome and true deep venous thrombosis is of utmost importance with respect to therapeutic implications. Previous studies, some based upon referrals to specialized rheumatic disease units, have emphasized the high frequency of underlying inflammatory knee arthropathy, especially rheumatoid arthritis.‘v3 We report a series of patients admitted to an acute care private hospital who were seen in consultation by our rheumatology unit and ultimately diagnosed as having the PTP syndrome. Surprisingly, only one female patient in our predominantely male series had an underlying, chronic, systemic rheumatic disease, and her rheumatoid arthritis, which had been in remission for 10 yr, was not the cause of her present knee arthropathy. The remainder of the patients had internal knee derangement (meniscal tears), structural joint disease (osteoarthritis), or no discernible rheumatic disease. Subtle trauma (dancing, jogging) and distant injuries to the knee can be key historical features in patients with the PTP syndrome. The presence of an overt knee arthropathy in these patients with PTP was uncommon. Although 9-l 1 patients had knee effusions, only 4 patients were found to have another sign of joint inflammation (ie, tenderness) on examination of the knee. Arthrography demonstrated dissection or rupture of a popliteal cyst in half of our patients. However, intact, nondissecting cysts or the
280
absence of a cyst (ie, a normal arthrogram) were also found with equal frequency and are consistent with the diagnosis of PTP. A cogent way of explaining this is by either a transient rupture of the lining of the cyst with extravasation of synovial fluid and subsequent rapid “sealing” of the defect, or rupture of the synovial lining of the true knee joint. Thus, the arthrogram in these instances does not reflect the true pathophysiologic mechanisms operative hours earlier. The marked clinical improvement of all patients with conservative therapy alone, including those patients who lacked arthrographic documentation of a dissected or ruptured popliteal cyst, is further evidence supporting the diagnosis of PTP. Venography demonstrated extrinsic compression of popliteal and proximal calf veins in three patients with PTP. This presumably is secondary to the dissected or ruptured popliteal cyst. Previous reports have noted the concomitant occurrence of DVT with dissected popliteal cysts, and suggested extrinsic compression as a predisposing factor in thrombus formation.7.8 There was no evidence of this in any of our patients. The demonstration of extrinsic compression of popliteal or proximal calf veins is additional evidence suggestive of the PTP syndrome. The differential diagnosis of the PTP syndrome is limited and includes changes in the structural integrity of a popliteal cyst, hematoma, rupture of the plantaris muscle, acute muscle “strain”, and rupture of the head of the gastrocnemius muscle. Popliteal artery aneurysms and pseudoaneurysms, neoplasms, fat pads, lipomata, lymphadenopathy, varicosities, and hemangiomata may cause a popliteal mass, but rarely give rise to the PTP syndrome. The majority of these disorders can be eliminated on the basis of a thorough history and physical examination (ie, activity or sports related acute calf injury, pulsatile popliteal mass with an aneurysm, ecchymosis with a hematoma, inability to stand on the toes with ruptured gastrocnemius muscle). Various procedures have been used to demonstrate dissection, rupture, or the presence of an intact popliteal cyst (ultrasound’,” arthrography,3 radionuclide arthroscintigraphy,“.‘Z CAT scanningt3), but none can exclude DVT. By
BLUMBERG AND KANTROWITZ
utilizing venography as the initial diagnostic procedure, DVT is immediately recognized, and appropriate therapy initiated. The delay that occurs in many hospitals in obtaining emergency diagnostic procedures (arthrogram) and venograms) and the initial, although mistaken, impression of DVT for PTP, frequently leads to inappropriate institution of anticoagulation. The potential morbidity of anticoagulation is well recognized and is exemplified by our patient who developed multiple hemorrhagic complications. We propose that venography be performed initially, and if negative for DVT, a presumptive diagnosis of the PTP syndrome is established. However, arthrography should be considered in an attempt to secure a diagnosis in the positive sense, and to evaluate for internal knee derangement. CONCLUSION
This series of patients with the PTP syndrome secondary to dissection or rupture of a popliteal cyst differs from previous series in the following aspects: (1) the patients were from the general medical service of an acute care hospital, not a specialized rheumatology unit, and were thus not preselected on the basis of underlying rheumatic disease. (2) The presence of an underlying, chronic, inflammatory rheumatic disease or an overt knee arthropathy was uncommon. (3) A history of antecedent subtle trauma or distant significant knee injury may be important historical features. (4) Although not conclusively establishing the diagnosis of PTP secondary to dissection or rupture of a popliteal cyst, a normal arthrogram or one demonstrating an intact, nondissecting popliteal cyst is consistent with that diagnosis. REFERENCES 1. Good AE: Rheumatoid Arthritis, Baker’s cyst, and “thrombophlebitis,” Arthritis Rheum 1964, 7:56-64. 2. Gristina AG, Wilson PD: Popliteal cysts in adults and children. Arch Surg 1964. 88:357-363. 3. Hall AP, Scott JT: Synovial cysts and rupture of the knee joint in rheumatoid arthritis: An arthrographic study. Ann Rheum Dis 1966,25:32-39. 4. Harvey JP, Corcus J: Large cysts in lower leg originating in the knee occurring in patients with rheumatoid arthritis. Arthritis Rheum 1960, 3:218-222. 5. Katz RS, Zizic TM. Arnold WP, Stevens MB: The pseudothrombophlebitis syndrome. Medicine (Baltimore) 1977, 56:151-164. 6. Perri JA, Rodnan GP, Mankin HJ: Giant synovial
281
cysts of the calf in patients with rheumatoid arthritis. J Bone Joint Surg 1968,50A:709-719. 7. Gordon GV, Edell S, Brogadir SP, Schumacher HR. Schimmer BM, Dalinka M: Baker’s cyst and true thrombophlebitis. 1979, Arch Intern Med 139:40-42. 8. Prescott SM, Pearl JE, Tikoff G: “Pseudo-pseudothrombophlebitis”: Ruptured popliteal cyst with deep venous thrombosis. (Letter to the Editor) 1978, N Engl J Med 299~1192. 9. Carpenter JR, Hattery RR, Hunder GG, Bryan RS, McLean RA: Ultrasound evaluation of the popliteal space. Mayo Clin Proc 1976, 51:498-503.
10. Moore CP, Sarti DA, Lottie JS: Ultrasonographic demonstration of popliteal cysts in rheumatoid arthritis. Arthritis Rheum 1975, 18:577-580.
11. Schmidt MC, Workman rupture 698.
of a popliteal
JB, Barth WI? Dissection or cyst. Arch Intern Med 1974, 134:694
12. Watkins AE, Poulose KP, Reba RC: Arthroscintigraphy with technetium albumin in diagnosis of pseudophlebitis (Baker’s) Br Med J 1975, 1:86. 13. Cooper RA: Computerized tomography of Baker’s cyst. J Rheumatol 1978, 5:184189.
(Body Scan)
T
HE pseudothrombophlebitis (PTP) syndrome, secondary to changes in the structural integrity of popliteal (synovial) cysts, has been reported primarily in patients with rheumatoid arthritis who have overt knee arthropathies. Our experience has been quite different, and in this regard we report eleven consecutive patients without chronic or readily discernible arthropathies who were admitted to the general medical service of an acute care hospital with the PTP syndrome. An intact, nondissecting popliteal cyst or the lack of an arthrographically demonstrable cyst was found in half of the patients, and is entirely consistent with the PTP syndrome. The pseudothrombophlebitis syndrome encompasses a group of disorders characterized by acute inflammation of the calf, giving rise to signs and symptoms of deep vein thrombophlebitis (DVT). However, intrinsic abnormalities of the vasculature are distinctly uncommon. Changes in the structural integrity of popliteal (synovial) cysts, including rupture with extravasation of synovial fluid and dissection into the calf, are a frequent cause of PTP. The therapeutic implications of this diagnosis are of utmost importance; anticoagulation is used for DVT while antiinflammatory agents and local measures for PTP. The majority of patients previously reported with this syndrome have an inflammatory arthropathy, most commonly rheumatoid arthritis, but noninflammatory disorders such as osteoarthritis, trauma, and meniscal tears have also been described.lm5 Previous series by Katz et From the Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School and Beth Israel Hospital, Boston, Massachusetts Scott Blumberg, M.D.: Clinical and Research Fellow in Medicine, Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School, and Beth Israel Hospital; Fred G. Kantrowitz, M.D.: Chiej. Rheumatology Unit, Department of Medicine and Thorndike Laboratory, Harvard Medical School and, Beth Israel Hospifal. Address reprint requests to Fred G. Kantrowifz. M.D., Department of Medicine Beth Israel Hospital, Boston, Massachusetts, 02215 o 1981 by Grune & Stratton, Inc. 0049-0172/81/1004-0005$01.00/0
278
Syndrome:
A Reappraisal
and Fred G. Kantrowitz
al.’ and Perri et a1.6 were based upon patients admitted to rheumatic disease units or preselected due to their underlying rheumatic disease. Our experience has been different, and we therefore report eleven patients without chronic or readily discernible arthropathies who were admitted to the general medical service of an acute care hospital with the PTP syndrome. MATERIALS
AND
METHODS
Patient Selection During the years 197551978, I I patients admitted to the general medical service of the Beth Israel Hospital and initially thought to have DVT were seen in consultation by our rheumatology unit. Venography showed no evidence of DVT, and the arthrographic findings and/or clinical course were considered diagnostic of the PTP syndrome. These patients form the basis of this report, and since there is no inpatient rheumatic disease ward in our hospital, they also represent all patients admitted with PTP.
Arthrography Arthrograms were performed to confirm the presence of an intact, dissected, or ruptured popliteal cyst, and to evaluate the possibility for internal knee derangement. Technically, a double contrast technique was employed using ten ml of water soluble contrast material (Renograffin@ ~ 60) and up to 50 ml of air. These were introduced into the knee joint after a routine arthrocentesis was performed. The patient was then ambulated for 5 minutes and films obtained of both knee and calf in Rexion and extension (anterior-posterior, lateral views). Specific views to evaluate the menisci were also obtained. If a popliteal cyst was not visualized during the procedure, delayed films were obtained several hours later when possible. An intact popliteal cyst is defined arthrographically as a cyst demonstrating a smooth contour without evidence of dissection or rupture. A dissected popliteal cyst maintains its smooth contour and extends along the fascial planes into the calf, below the confines of the popliteal fossa. A ruptured cyst loses its smooth contour with extravasation of contrast material into the soft tissues of the calf.
Results The predominantly male patients range in age from 17-83 yr.‘-” The majority of patients’-” had symptoms referable to the popliteal fossa or calf and not the knee, both initially and at time of presentation. Although no patient experienced overt knee trauma immediately before the onset of their initial symptoms, 4 patients had engaged in “nonroutine” activities (ie, jogging, dancing, Seminars in Arthritis and Rheumafism, Vol. 10, No. 4 (May),
198 1
279
kneeling). There was a distant history of knee trauma in three patients, two of whom had intermittent knee locking since their injuries. Two patients had prior episodes of acute calf inflammation diagnosed as DVT and muscle strain. An additional patient had rheumatoid arthritis of 20 yr duration, which had been in remission for the past 10 yr. No other patient had evidence of a systemic rheumatic disease or a seronegative spondyloarthropathy. Pertinent findings on physical examination included knee effusions in 6-l 1 patients with effusions detected the following morning in three additional patients. The volume of fluid aspirated varied from 6 ml to 45 ml. Excluding effusions, 7-1 I patients had normal knee examinations while four had mild knee tenderness. A popliteal mass was noted in 5 patients. All patients had calf tenderness and swelling; 6 had a positive Homan sign and 4 had pedal edema. Synovial fluid analysis was performed in 7 patients; 6 of the fluids were noninflammatory. Hemorrhagic or serosanguinous fluids were found in two patients with prior knee injuries who recently jogged, in one patient with severe osteoarthritis, and in one patient initially anticoagulated with sodium heparin for presumed DVT. This latter patient, in addition to the hemarthrosis, developed hematuria and hematochezia. No patient had evidence of a septic or crystal induced synovitis. All patients had roentgenograms of the knee, which were not helpful diagnostically in the majority of cases. Two patients had osteoarthritis, one mild and the other severe; two had small patellar spurs and one had patellar hyperostosis with superior whiskering. The remainder”‘] had entirely normal films. Venography was performed as the initial diagnostic procedure in nine patients, and was negative for DVT in all. However, three venograms demonstrated extrinsic compression of popliteal and proximal calf veins. Two patients did not undergo venography, one of whom had a previous hypersensitivity reaction to dye. Arthrography was performed in all except three patients, two of whom had relative contraindications (previous hypersensitivity reaction to dye, anticoagulation). Four patients had dissection and/or rupture of a popliteal cyst, while three had an intact cyst alone. One arthro-
gram did not demonstrate a popliteal cyst, but clearly showed a medial meniscal tear. Another patient with a ruptured popliteal cyst had also had a lateral meniscal tear. Therapeutically, each patient received bed rest, elevation of the involved extremity, and hot, moist compresses. These measures alone frequently resulted in demonstrable improvement. Only one patient was initially anticoagulated; this was discontinued after venography was negative for DVT. The remainder of the patients were given nonsteroidal antiinflammatory agents or an intraarticular (knee) corticosteroid instillation. All patients were markedly improved at time of discharge with decreased pain, tenderness and swelling of the calf and knee. DISCUSSION
The differentiation between the pseudothrombophlebitis syndrome and true deep venous thrombosis is of utmost importance with respect to therapeutic implications. Previous studies, some based upon referrals to specialized rheumatic disease units, have emphasized the high frequency of underlying inflammatory knee arthropathy, especially rheumatoid arthritis.‘v3 We report a series of patients admitted to an acute care private hospital who were seen in consultation by our rheumatology unit and ultimately diagnosed as having the PTP syndrome. Surprisingly, only one female patient in our predominantely male series had an underlying, chronic, systemic rheumatic disease, and her rheumatoid arthritis, which had been in remission for 10 yr, was not the cause of her present knee arthropathy. The remainder of the patients had internal knee derangement (meniscal tears), structural joint disease (osteoarthritis), or no discernible rheumatic disease. Subtle trauma (dancing, jogging) and distant injuries to the knee can be key historical features in patients with the PTP syndrome. The presence of an overt knee arthropathy in these patients with PTP was uncommon. Although 9-l 1 patients had knee effusions, only 4 patients were found to have another sign of joint inflammation (ie, tenderness) on examination of the knee. Arthrography demonstrated dissection or rupture of a popliteal cyst in half of our patients. However, intact, nondissecting cysts or the
280
absence of a cyst (ie, a normal arthrogram) were also found with equal frequency and are consistent with the diagnosis of PTP. A cogent way of explaining this is by either a transient rupture of the lining of the cyst with extravasation of synovial fluid and subsequent rapid “sealing” of the defect, or rupture of the synovial lining of the true knee joint. Thus, the arthrogram in these instances does not reflect the true pathophysiologic mechanisms operative hours earlier. The marked clinical improvement of all patients with conservative therapy alone, including those patients who lacked arthrographic documentation of a dissected or ruptured popliteal cyst, is further evidence supporting the diagnosis of PTP. Venography demonstrated extrinsic compression of popliteal and proximal calf veins in three patients with PTP. This presumably is secondary to the dissected or ruptured popliteal cyst. Previous reports have noted the concomitant occurrence of DVT with dissected popliteal cysts, and suggested extrinsic compression as a predisposing factor in thrombus formation.7.8 There was no evidence of this in any of our patients. The demonstration of extrinsic compression of popliteal or proximal calf veins is additional evidence suggestive of the PTP syndrome. The differential diagnosis of the PTP syndrome is limited and includes changes in the structural integrity of a popliteal cyst, hematoma, rupture of the plantaris muscle, acute muscle “strain”, and rupture of the head of the gastrocnemius muscle. Popliteal artery aneurysms and pseudoaneurysms, neoplasms, fat pads, lipomata, lymphadenopathy, varicosities, and hemangiomata may cause a popliteal mass, but rarely give rise to the PTP syndrome. The majority of these disorders can be eliminated on the basis of a thorough history and physical examination (ie, activity or sports related acute calf injury, pulsatile popliteal mass with an aneurysm, ecchymosis with a hematoma, inability to stand on the toes with ruptured gastrocnemius muscle). Various procedures have been used to demonstrate dissection, rupture, or the presence of an intact popliteal cyst (ultrasound’,” arthrography,3 radionuclide arthroscintigraphy,“.‘Z CAT scanningt3), but none can exclude DVT. By
BLUMBERG AND KANTROWITZ
utilizing venography as the initial diagnostic procedure, DVT is immediately recognized, and appropriate therapy initiated. The delay that occurs in many hospitals in obtaining emergency diagnostic procedures (arthrogram) and venograms) and the initial, although mistaken, impression of DVT for PTP, frequently leads to inappropriate institution of anticoagulation. The potential morbidity of anticoagulation is well recognized and is exemplified by our patient who developed multiple hemorrhagic complications. We propose that venography be performed initially, and if negative for DVT, a presumptive diagnosis of the PTP syndrome is established. However, arthrography should be considered in an attempt to secure a diagnosis in the positive sense, and to evaluate for internal knee derangement. CONCLUSION
This series of patients with the PTP syndrome secondary to dissection or rupture of a popliteal cyst differs from previous series in the following aspects: (1) the patients were from the general medical service of an acute care hospital, not a specialized rheumatology unit, and were thus not preselected on the basis of underlying rheumatic disease. (2) The presence of an underlying, chronic, inflammatory rheumatic disease or an overt knee arthropathy was uncommon. (3) A history of antecedent subtle trauma or distant significant knee injury may be important historical features. (4) Although not conclusively establishing the diagnosis of PTP secondary to dissection or rupture of a popliteal cyst, a normal arthrogram or one demonstrating an intact, nondissecting popliteal cyst is consistent with that diagnosis. REFERENCES 1. Good AE: Rheumatoid Arthritis, Baker’s cyst, and “thrombophlebitis,” Arthritis Rheum 1964, 7:56-64. 2. Gristina AG, Wilson PD: Popliteal cysts in adults and children. Arch Surg 1964. 88:357-363. 3. Hall AP, Scott JT: Synovial cysts and rupture of the knee joint in rheumatoid arthritis: An arthrographic study. Ann Rheum Dis 1966,25:32-39. 4. Harvey JP, Corcus J: Large cysts in lower leg originating in the knee occurring in patients with rheumatoid arthritis. Arthritis Rheum 1960, 3:218-222. 5. Katz RS, Zizic TM. Arnold WP, Stevens MB: The pseudothrombophlebitis syndrome. Medicine (Baltimore) 1977, 56:151-164. 6. Perri JA, Rodnan GP, Mankin HJ: Giant synovial
281
cysts of the calf in patients with rheumatoid arthritis. J Bone Joint Surg 1968,50A:709-719. 7. Gordon GV, Edell S, Brogadir SP, Schumacher HR. Schimmer BM, Dalinka M: Baker’s cyst and true thrombophlebitis. 1979, Arch Intern Med 139:40-42. 8. Prescott SM, Pearl JE, Tikoff G: “Pseudo-pseudothrombophlebitis”: Ruptured popliteal cyst with deep venous thrombosis. (Letter to the Editor) 1978, N Engl J Med 299~1192. 9. Carpenter JR, Hattery RR, Hunder GG, Bryan RS, McLean RA: Ultrasound evaluation of the popliteal space. Mayo Clin Proc 1976, 51:498-503.
10. Moore CP, Sarti DA, Lottie JS: Ultrasonographic demonstration of popliteal cysts in rheumatoid arthritis. Arthritis Rheum 1975, 18:577-580.
11. Schmidt MC, Workman rupture 698.
of a popliteal
JB, Barth WI? Dissection or cyst. Arch Intern Med 1974, 134:694
12. Watkins AE, Poulose KP, Reba RC: Arthroscintigraphy with technetium albumin in diagnosis of pseudophlebitis (Baker’s) Br Med J 1975, 1:86. 13. Cooper RA: Computerized tomography of Baker’s cyst. J Rheumatol 1978, 5:184189.
(Body Scan)