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VENOUS DIGEST ARTICLE LIST 1996

As the editors of the Venous Digest scan the world literature for articles which will be abstracted each month, the yearly contents become a complete summary of scientific information relating to venous disorders.

This is a listing of articles published last year.

COAGULATION
1. Coexistence of hereditary homodystinuria and Factor V Leiden: Effect on thrombosis. Mandel H, Brenner B, Berant M, et al. N Engl J Med 1996; 334:763-68. (11/96)
2. Hyperhomodysteinemia as a risk factor for deep vein throm-bosis. Heijer MD, Kostter T, Blom HJ, et al. N Engl J Med 1996; 334:759-62. (11/96)

DEEP VENOUS THROMBOSIS
1. The superficial femoral vein: A potentially lethal mis-nomer. Bundens WP, Bergan JJ, Halasz NA, et al. JAMA 1995; 274:1296-98. (1/96)
2. Prevalence of deep venous thrombosis among patients in medical intensive care. Hirsch DR, Ingenito EP, Goldhaber SZ. JAMA 1995; 27:335-37. (1/96)
3. Heparin thromboprophylaxis via indwelling subcutaneous teflon cannula. Pouw L, Kilsby D, Francis P, Tulloh B. Aust NZ J Surg 1995; 65:793-95. (11/96)
4. Prospective 12-year followup study of clinical and hemo-dynamic sequelae after deep vein thrombosis in low-risk patients (Z¸rich study). Franzeck UJ, Schalch I, J”ger KA, et al. Circulation 1996; 93:74-79. (6/96)
5. Thrombolytic therapy. Verstraete M. Br J Med 1995; 311:581-82. (5/96)
6. The syndrome of the coup de fouet: Is it always a benign disease? Antignani PK, Todini AR, DiFortunato T, et al. Dermatol Surg 1995; 21:872-75. (4/96)
7. Successful restoration of renal allograft function with urokinase thrombolysis in the setting of phlegmasia cerulea dolens. Marks MJ, Pais SO, Bartlett ST. J Vasc Interven Radiol 1995; 6:279-82. (3/96)
8. La fragmentation manuelle des thromboses veineuses profundes. Richaud C, Bouchet JY, Bosson JL, et al. J des Maladies Vasculaires 1995; 20:166-71. (1/96)
9. Surgical treatment of septic deep venous thrombosis. Kniemeyer HW, Grabitz K, Buhl R, et al. Surgery 1995; 118:49-53. (1/96)

DIAGNOSIS: REFLUX
1. Venous reflux in symptom-free vascular surgeons. Labropoulos N, Delis KT, Nicolaides AN. J Vasc Surg 1995; 22:150-54. (1/96)
2. Proximity penetrating extremity trauma: The role of duplex ultrasound in the detection of occult venous injuries. Gagne PJ, Cone JB, McFarland D, et al. J Trauma 1995; 39:1157-63. (11/96)
3. Duplex ultrasound assessment of the venous status of the swollen leg. Tong Y, Royle J. Aust NZ J Surg 1995; 65:784-86. (6/96)

SEVERE CHRONIC VENOUS INSUFFICIENCY
1. Hypodermites phlebopathiques venous sclero-hypodermitis. van der Stricht J, Staelens I. PhlÈbologie 1996; 49:37-40. (12/96)
2. Evaluation of vascular and metabolic deficiency in patients with large leg ulcers. Balaji P, Mosley JG. Ann R Coll Surg Engl 1995; 77:270-72. (12/96)
3. The management of leg ulcers. Nelson BA, Ruckley CV, Dale J, Morison M. J Wound Care 1996; 5:73-76. (10/96)
4. Stockings and the prevention of recurrent venous ulcers. Samson RH, Showalter DP. Phlebology 1996; 22:373-76. (10/96)
5. Comparison of leg compression stocking and oral horse-chestnut seed extract therapy in patients with chronic venous insufficiency. Diehm C, Trampisch HJ, Lange S, et al. The Lancet 1996; 347:292-94. (10/96)
6. Surgical technique and preliminary results of endoscopic subfascial division of perforating veins. Gloviczki P, Cambria RA, Rhee RY, et al. J Vasc Surg 1996; 23:517-23. (8/96)
7. Preoperative imaging of lower extremity varicose veins: Color-coded duplex sonography or venography? Baldt MM, B–hler T, Zontisch T, et al. Ultrasound in Medicine 1996; 15:143-54. (7/96)
8. Recurrent varicose veins: Investigation of the pattern and extent of reflux with color-flow duplex scanning. Labropoulos N, Touloupakis E, Giannoukas AD, et al. Surgery 1996; 119:406-9. (7/96)
9. Surgical treatment for venous ulcers: Is it worthwhile? Dunn JM, Kernick FVM, Cosford EJ, et al. Ann R Coll Surg Engl 1995; 77:421-24. (6/96)
10. Cutaneous microcirculation in skin lesions associated with chronic venous insufficiency. St¸cker M, Sch–be MC, Hoffmann K, et al. Dermatol Surg 1995; 21:877-82. (6/96)
11. Relation between aetiology and treatment of leg ulcers. Holan V (for debate). Chant ADB (invited comment). Br J Surg 1996; 83:249-50. (5/96)
12. Chronic venous insufficiency of the lower extremities: Experiences with the Linton and Cockett operations modified in 1974 and 1976. Enrici EA, Caldevilla HS. PhlÈbologie 1996; 49:69-80. (4/96)
13. The possible role of ischemia-reperfusion in the pathogenesis of chronic venous ulceration. Greenwood JE, Edwards AT, McCollum CN. Wounds 1995; 7(6):211-19. (4/96)
14. Leg ulcers: Report on a multidisciplinary approach. Akesson H, Bjellerup M. Acta Derm Venereol (Stockh) 1995; 75:133-35. (3/96)

THROMBOEMBOLISM
1. A comparison of low-molecular-weight heparin administered primarily at home with unfractionated heparin administered in the hospital for deep vein thrombosis. Levine M, Gent M, Hirsh J, et al. N Engl J Med 1996; 334:677-81. (11/96)
2. Treatment of venous thromboisis with intravenous un-fractionated heparin administered in the hospital as compared with subcutaneous low-molecular-weight heparin admini-stered at home. Koopman MMW, Prandoni P, Piovella F, et al. N Engl J Med 1996; 334:682-87. (11/96)
3. Venous thromboembolism during pregnancy. Toglia MR, Weg JG. N Engl J Med 1996; 335:108-14. (9/96)
4. Use of antithrombotic agents during pregnancy. Ginsberg JS, Hirsh J. Chest 1995; 108(4):505S-511S. (9/96)
5. Low-molecular-weight heparins and unfractionated heparin in the treatment of patients with acute venous thrombo-embolism; Results of a meta-analysis. Siragusa S, Cosmi B, Piovella F, et al. Am J Med 1996; 100:269-77. (8/96)
6. Phlegmasia complicating prophylactic percutaneous inferior vena caval interruption: A word of caution. Harris EJ Jr, Kinney EV, Harris EJ Sr, et al. J Vasc Surg 1995; 22:606-11. (4/96)
7. Preliminary results of a nonoperative approach to sapheno-femoral junction thrombophlebitis. Ascer E, Lorensen E, Poloina RM, et al. J Vasc Surg 1995; 22:616-21. (2/96)
8. Efficacy of subcutaneous heparin in prevention of venous thromboembolic events in trauma patients. Upchurch Jr GR, Demling RH, Davies J, et al. Am J Surg 1995; 61:749-55. (2/96)
9. Calf vein thrombi are not a benign finding. Lohr JM, James KV, Deshmukh RM, Hasselfeld KA. Am J Surg 1995; 170:86-90. (2/96)

UPPER EXTREMITY VENOUS PROBLEMS
1. Surgical management of brachioaxillary subclavian vein occlusion. Sotturai VS, Lyon R, Ross C, et al. Eur J Vasc Surg 1995; 11:225-29. (6/96)
2. Surgical management of subclavian vein obstruction, including six cases of subclavian vein bypass. Sanders RJ, Cooper MA. Surgery 1995; 118:856-63. (5/96)
3. Phlegmasia cerulea dolens of the upper extremity. Kammen BV, Soulen MC. J Vasc Interven Radiol 1995; 6:283-86. (3/96)

VARICOSE VEINS
1. Pelvic congestion syndrome: A new approach to an unusual problem. Mathis BV, Miller JS, Lukens MKI, et al. Am Surg 1995; 61:1016-18. (9/96)
2. Venous reflux at the saphenofemoral junction. Somjen GM, Donlan J, Hurse J, et al. Phlebology 1995; 10:132-35. (9/96)
3. Preliminary experience with an endovascular catheter for electrocoagulation of peripheral veins. Crockett D, Mankin C, Becker MO, et al. J Vasc Technol 1996; 20(1):19-22. (8/96)
4. Treatment of pre-hemorrhagic telangiectasias. Guex JJ. PhlÈbologie 1995; 48(1):41-42. (7/96)
5. Assessment of wall structure and composition of varicose veins with reference to collagen, elastin, and smooth muscle content. Travers JP, Broomkes CE, Evans J, et al. Eur J Vasc Endovasc Surg 1996; 11:230-37. (7/96)

VARICOSE VEINS, SCLEROTHERAPY
1. The intrinsic antimicrobial activity of selected sclerosing agents in sclerotherapy. Sadick NS, Senterfit LB, Klein RF. Dermatol Surg 1996; 22:369-71. (12/96)
2. Review of photothermal sclerosis of leg veins. Goldman MP, Eckhouse S, Photoderm VL Cooperative Study Group. Dermatol Surg 1996; 22:323-30. (12/96)
3. Treatment of acute anaphylaxis. Fisher M. Br Med J 1995; 311:731-33. (8/96)
4. Ambulatory phlebectomy compared to sclerotherapy for vari-cose and telangiectatic veins: Indications and complications. Weiss RA, Weiss MA. Advances in Derm 1996; 11:3-16. (5/96)
5. Sclerotherapy: Continuous-wave, Doppler-guided injections. Cornu-Thenard A, DeCottreau H, Weiss RA. Dermatol Surg 1995; 21:867-70. (2/96)

VARICOSE VEINS, SURGERY
1. Stripping of Giacomini's vein: Is it pathophysiologically necessary? Zierau UTh, Kullmer A, Kunkel HP. VASA 1996; 25:142-47. (9/96)
2. The femoropopliteal vein: Ultrasound anatomy, diagnosis, and office surgery. Georgiev M. Dermatol Surg 1996; 22:57-62. (8/96)
3. Varicose vein surgery and deep venous thrombosis. Campbell WB, Ridler BMF. Br J Surg 1995; 82:1494-97. (7/96)
4. Crossectomy, partial or complete stripping? Review of the literature and discussion. Gorny Ph, Chahine D, Blanchemaison Ph, et al. PhlÈbologie 1996; 49:87-91. (4/96)
5. Day-case varicose vein surgery: Patient suitability and satisfaction. Ramesh S, Umeh HN, Galland RB. Phlebology 1995; 10:103-105. (4/96)
6. Assessment and treatment of varicose veins in the northern region. Lees TA, Holdsworth JD. Phlebology 1995; 10:56-61. (3/96)
7. Ligation, division with or without short or long stripping of the greater saphenous vein: Analysis of the results in 703 patients. Gorny Ph, Chahine D, Payen B, et al. PhlÈbologie 1995; 48(4):487-90. (3/96)
8. Recurrent varicose veins and primary deep venous insufficiency: Relationship and therapeutic implications.
Guarnera G, Furgiuele S, DiPaola M, Camilli S. Phlebology 1995; 10:98-102. (2/96)
9. Reconstruction of venous outflow after inadvertent stripping of the femoral vein. Flis V. Eur J Vasc Endovasc Surg 1995; 10:253-55. (1/96)
10. Flush saphenofemoral ligation and multiple stab phlebectomy preserve a useful greater saphenous vein four years after surgery. Fliegelstone LJ, Salaman RA, Oshodi TO, et al. J Vasc Surg 1995; 22:588-92. (2/96)

VENA CAVA SURGERY
1. Venography with carbon dioxide as a contrast agent. Sullivan KL, Bonn J, Shapiro MJ, Gardiner GA. Cardiovasc Intervent Radiol 1995; 18:141-45. (12/96)
2. Diagnosis, treatment, and prognosis of the leiomyosarcoma of the inferior vena cava: Three cases and summary of published reports. M–nig SP, Gawendo M, Erasmi H, et al. Eur J Surg 1995; 161:231-35. (12/96)
3. Leiomyosarcoma of the inferior vena cava: Report of two cases and a plea for surgical reconstruction. Sinsel NK, Samijn JP, Von Meyenfeldt MF, et al. Eur J Surg 1995; 161:365-68. (12/96)
4. Prophylactic Greenfield filter placement in selected high-risk trauma patients. Khansarinia S, Dennis JW, Veldenz HC, et al. J Vasc Surg 1995; 22:231-36. (11/96)
5. Inferior vena caval filter placement without preoperative venacavography. Mirande RA, Mirande KK, Liu T, Baker WH. Vasc Surg 1996; 29:469-75. (11/96)
6. Operator errors during percutaneous placement of vena cava filters. Kaufman JA, Geller SC, Rivitz SM, Waltman AC. AJR 1995; 165:1281-87. (4/96)
7. Resection of the suprarenal inferior vena cava: The role of prosthetic replacement. Huguet C, Ferri M, Gavelli A. Arch Surg 1995; 130:793-97. (1/96)

VENOUS PHYSIOLOGY/PATHOPHYSIOLOGY
1. Ambulatory venous pressure: Correlation with skin condition and role in identifying surgically correctable disease. Payne SPK, London NJM, Newland DJ, et al. Eur J Vasc Endovasc Surg 1996; 11:195-200. (6/96)
2. Venous valvular reflux in veins not involved at the time of acute deep vein thrombosis. Caps MT, Manzo RA, Bergelin RO, et al. J Vasc Surg 1995; 22:524-31. (5/96)
3. The effect of graduated elastic compression stockings on femoral blood flow velocity during late pregnancy. Norgren L, Austrell C, Nilsson L. VASA 1995; 24(3):282-85. (5/96)
4. Idiopathic rupture of the iliac vein. Plate G, Qvarfordt P. Eur J Surg 1995; 161:611-12. (2/96)

VENOUS RECONSTRUCTION
1. Durability of venous valve reconstruction techniques for "primary" and postthrombotic reflux. Raju S, Fredericks RK, Neglen PN, Bass D. J Vasc Surg 1996; 23:357-67. (10/96)
2. Venous injuries: Military versus civilian experience. Ierardi RP, Kerstein MD. Military Med 1995; 160(8):396-98. (2/96)

SAPHENOFEMORAL VALVES: HISTOPATHOLOGICAL OBSERVATIONS AND DIAGNOSTIC APPROACH BEFORE SURGERY
Corcos L, Procacci T, Peruzzi G, et al.
Dermatol Surg 1996; 22:873-80

ABSTRACT AND COMMENTARY BY:
Sidney Rose, MD, FRCS
Manchester, England

The purpose of this paper was to investigate venous valve pathology at the saphenofemoral junction with a special reference to the use of external valve plasty. The methods used were high-resolution echography and duplex examination for preoperative analysis, intraoperative Doppler examination, angioscopy at operation to identify the immediate result of the procedure, and postoperative histopathological examination of the excised vein with its contained valve. The best results with a 10.4% failure rate were obtained in cases of ten years' standing. There was a 50% failure rate in cases of over 20 years' standing. The authors found that in some of the early patients the valves were perhaps already damaged while in the longer-standing cases, 50% had normal and repairable valves which were merely dilated.

The authors removed 66 segments of the proximal saphenous vein containing 42 venous valves. Cross-sections (30) and longitudinal sections (12) were performed using hematoxylin-Essin, Weigert, and Van Gieson stains. The agger of the valve was only studied in the longitudinal sections. In the agger, the pathology looked for was development of intimal plaques, fibrosis, muscle hyperplasia, and sclerosis breakup of the elastic layer. In the cusp, thickening and hyper-trophy and thinning and atrophy were noted. In the annulus, dilation, thickening, and asymmetry were noted. Their results showed that roughly 50% of the veins had abnormal valves. In general, cusp atrophy occurred in combination with parietal ectasis and asymmetry of the annulus.

There were several contradictions and surprises in a number of their cases. They found intraoperative Doppler and angioscopy helpful in establishing the degree of competence obtained by the operative procedure. In the discussion, they felt that external banding reduced vein wall dilation and when the valve was normal, the clinical and hemodynamic result should be satisfactory. If the hemodynamic result was unsatisfactory, then either 1) the valve was not in fact normal or, 2) reduction of the vein wall dilation did not always prevent further evolution of the early atrophy of the cusp. The authors go on to say that the two phenomena are not mutually exclusive.

Finally, the authors feel that the indications for external valve plasty must include a thorough identification of a normal valve by good visualization of cusp thickness and mobility and suggest that repair is limited to early cases which implies that the vein should not be too dilated.

The tables and figures are clearly presented and the intravascular photography is well reproduced. There is an extensive bibliography. This is a very provocative paper and suggests that there is still much to be learned about the pathology and treatment of varicose veins.

COMMENTARY

The findings of this study are very much the same as those which have been published before. The conclusions, however, are not quite the same. Edwards in 1940 and more recently Gottlob and May in 1986 came to the conclusion that pathological change in the venous valve was rarely the cause of varicose veins. Venous valves, as those who have tried to examine them in detail will agree, are difficult to identify and to section. It is easy to get an oblique slice since a variation in thickness of the sections will give the impression of thinning or thickening. It is not generally realized that the cusp is considerably longer than the half lumen which it protects in order to be able to come into contact with the opposite member. When the vein is fully dilated, the cross section is very much enlarged. During the fixing process, the cusp retracts and the final picture may be very different from that occurring in vivo.

This is clearly illustrated in the article in Figure 11. This difficulty renders the angioscopic view all the more intriguing but no one supposes that a lot of experience is required before the procedure becomes user friendly. It is certainly not something that could be used in every case.

With regard to the theory of origin all that one can say is that as long as varicose veins occur in the presence of normal valves, it is most likely that the basic lesion is in the wall. If the wall is affected in the region of the valve, then the function of the valve will be interfered with. The function of the valve is, of course, to prevent reflux. We automatically assume that the cause of venous symptoms is due to backward pressure. Perhaps we ought to consider the effects of venous stagnation without reflux as a cause of symptoms such as in venous clusters which do not appear to be connected to the main internal or external saphenous system. With regard to external valve plasty, I believe it could only work temporarily and then only for a brief period of time when there is limited vein wall dilation and in which there are valve cusps which are able to coapt. The sort of case clinically would be difficult to find as symptoms would be minimal and patients would require a good deal of persuasion to subject themselves to surgery.

There may be some indication for the use of external valve plasty in a dilated deep vein where there has been no history of deep venous thrombosis but this is entirely a different story.

Leonardo Corcos and his coauthors are to be commended for undertaking this thought-provoking investigation. Their attention to detail and the manner in which it has been presented is exemplary. They should be encouraged to carry on in the same vein (if you will pardon the expression). 6268b

PREVALENCE AND ETIOLOGY OF LEG ULCERS IN A DEFINED POPULATION OF INDUSTRIAL WORKERS
Nelzen O, Bergqvist D, Fransson I, Lindhagen A
Phlebology 1996; 11:50-54

ABSTRACT AND COMMENTARY BY:
Ralph G. DePalma, M.D.
Y. John Talieh, M.D.
Department of Surgery
University of Nevada School of Medicine
Reno, Nevada

The prevalence of venous ulcer disease in the general population remains unknown, in part due to the varying circumstances in which patients first present to health care professionals. Most patients with venous ulcer disease are seen years after the onset of symptoms. This work, presented both at the Royal Society of Medicine and Societas Phlebologica Scandinavica Venous Forum 1996 by Nelzen, et al., attempted to determine the point prevalence of leg ulcers in a defined population under retirement age.

The authors mailed questionnaires to all 2785 employees at the Volvo motor engine factory in Skovde, Sweden. Employees were asked if they had an open ulcer currently or have ever had an open leg ulcer. An ulcer was defined as any open wound below the knee, including the foot, that took longer than six weeks to heal after onset. There was an 87% response rate. Respondents with a history of leg ulcers then underwent clinical examination, including history, physical examination, and Doppler ultrasonography. Arterial insufficiency was defined as an ankle brachial index less than 0.9, and deep venous insufficiency was defined as reflux in the popliteal vein.

Among the patients examined, 47 (36%) had a true history of leg ulcers. There was no arterial insufficiency detected. Venous insufficiency was found in 33 (59%) of the legs examined. Most venous insufficiency was found in the superficial system (73% vs 27% in the deep system). The point prevalence of open leg ulcers was 0.6% and the overall lifetime prevalence, excluding traumatic causes, was 1.6%. The authors stratified this data according to age and found a point prevalence of 0.4% in respondents ages 30 to 49 and 1% in those ages 50 to 59. These numbers are much higher than previously reported. Further, 75% of those with open ulcers stated that they treated the ulcers independent of health care professionals.

The authors concluded that the point prevalence of open leg ulcers in younger individuals exceeds previously reported figures. They felt that given the large percentage of self-treated individuals with potentially curable venous disease, it would be prudent for health care professionals to inform the public to seek professional care early in order to identify curable causes of venous ulceration.

COMMENTARY

This interesting study defines a point prevalence of venous ulceration among a population of younger active workers. Two important points surface: 1) Most leg ulcers were venous in origin, and 2) in approximately 75% of these individuals, the superficial venous system was at fault.

The importance of these observations cannot be over-emphasized in structuring rational therapy for individuals afflicted with leg ulcers. Superficial venous insufficiency is an important cause of ulceration and is amenable to surgical intervention. For example, among ten patients with "intractable" venous ulcers recently reported,1 seven had superficial disease requiring, in part, saphenous vein stripping from ankle to groin. The results were favorable over extended periods of time. Bi-directional Doppler ultrasonography was useful for the authors in determining sites of venous insufficiency. Duplex scanning would be better. The authors correctly conclude that health care professionals need to be consulted. They will, in turn, need to recognize curable forms of venous ulceration rather than consigning such cases to the waste-basket diagnosis of postphlebitic leg. 6757b

REFERENCES

1. DePalma RG, Kowallek DL. Venous ulceration: A crossover study from operative to nonoperative treatment. J Vasc Surg 1996; 24:788-92.

POSTOPERATIVE THROMBOLYSETHERAPIE (Postoperative Thrombolytic Treatment)
Kolben M, H–þ C, Graeff H.
Internist 1996; 37:619-22

ABSTRACT AND COMMENTARY BY:
Werner Bl”ttler, MD
Zurich, Switzerland

Rapid restoration of blood flow through occluded pulmonary arteries is the goal of treatment in every patient struck with an acute pulmonary embolism. This objective is difficult to achieve. The methods utilized may themselves carry great danger. Pulmonary embolectomy, for example, requires a medical infrastructure which is often not available. As indicated by the authors of this manuscript, such intervention is often associated with a fatal outcome. They cite a study in which pulmonary embolectomy plus caval interruption succeeded in achieving hospital discharge in 10 of 13 patients who were admitted in shock.1

Thrombolysis rather than pulmonary embolectomy is considered an alternative but the pulmonary reperfusion may not occur rapidly enough to reduce dangerously elevated pulmonary artery pressures. One reason for such failure may be the massive thrombus load which is present in the pulmonary vasculature. Another is the fact that the thrombi may be old and poorly susceptible to lysis when they have been dislocated from the extremities to the lungs. Also, thrombolysis itself may stimulate further pulmonary embolization as extremity thrombi are partially dissolved and lose their attachment. Further, it is inevitable that systemic thrombolysis may induce a severe general bleeding tendency, and hemorrhage threatens to ruin even the good results of the reopened pulmonary vasculature. Because of this, contraindications to thrombolysis have been established, and one of the first and highest ranking contraindications is the postoperative state. A 1980 consensus conference suggested a delay of at least ten days from operation before thrombolysis is contemplated.

The most severe thromboembolic events are often seen in patients after major trauma, surgery, and in the puerperium. Such patients typically develop deep venous thrombosis without signs and symptoms, and even herald small emboli which may have occurred silently, even before the patient presents acutely with distressing dyspnea, hypoxemia, shock, or cardiac arrest. Because extremity thrombi take time to enlarge, pulmonary embolism may occur many days after surgery and even after hospital discharge.2 Massive pulmonary embolus occurs earlier at a time within the tenth postoperative day limit which precludes thrombolysis. Thus, the clinical situation presents a dilemma that is most difficult for clinicians to solve. The present authors review the somewhat sparse literature on the subject and come up with the statement that, "one should not renounce thrombolysis in the situation of a postoperative thromboembolic event if there is a vital indication for it." The authors believe that thrombolysis is not only practical but also promising provided that the risks are individually weighed.

Observers of the scene on both sides of the Atlantic are aware of the fact that some physicians on the continent are rather enthusiastic about lysis in thromboembolism despite lacking confirmatory evidence of its benefits. In the United States, data have been provided that most patients will not agree to thrombolysis for femoral thrombosis if they are truly informed about the risks and benefits.3

With this controversial background in mind, I will interpret the data reviewed by Kolben, et al. in the above-captioned article.

COMMENTARY

The authors cite two German studies which present 41 patients who received thrombolysis within 0 to 21 days of operation. Five patients (12%) died because of further embolism, cerebral hemorrhage, or brain damage. Three patients were reoperated, and eight patients (20%) had to be transfused. In other studies which mention thrombolysis, treatment was attempted only after the second postoperative day and the risk of bleeding appears to be less. Nevertheless, dangers associated with thrombolysis are so great that the procedure must be performed cautiously and with strong reasons. In one study, cardiopulmonary resuscitation had to be undertaken in 9 of 15 patients. This suggests that the outcome in these patients would have been poor without thrombolysis.

Clinical and hemodynamic findings in patients in other studies are not thoroughly reported. Without these data, it is difficult to assess the relationships of risk and benefit. The present authors deal with the aspects of risk implying that benefits would be assumed to be very great in every case. Based on the quoted and other evidence,4-6 the following statements can be made:

1. Postoperative thrombolysis should not be attempted unless a patient with a suggestive history is hemodynamically unstable or in shock (systolic blood pressure under 100 mmHg, heart rate over 120/min, PaO2 under 60 mmHg, PA pressure over 25 mmHg, right ventricular systolic pressure over 40 mmHg).

2. Thrombolysis should be performed in a patient who was in good health prior to the thromboembolic episode.

3. Diagnosis by pulmonary angiography should be prompt, and hemodynamic information should guide the management.

4. A bolus of 10 or 20 mg of small rTPA followed by an infusion of 50 to 100 mg or bolus of 2,200 IU/kg bodyweight of UPA followed by an infusion of the same amount per hour have been used.

5. Thrombolysis should be stopped when the pulmonary artery pressure falls. This may occur within two hours and lysis can be terminated at that time, or at least after 12 hours of therapy.

Recurrence rate of pulmonary embolism is high. Therefore, a temporary removable caval umbrella may provide protection with a minimum of long-term complications. Bleeding complications have to be anticipated and transfusions should be readied. Surgical intervention may be necessary in some patients to control hemorrhage.

In conclusion, previously healthy patients with massive life-threatening pulmonary emboli (but only those) deserve an immediate attempt to lyse pulmonary emboli even in the postoperative situation. The hazards of this form of treatment are acknowledged but may be bearable with the use of a regimen of short lysis time and support of modern intensive care. 5793b

REFERENCES
(Not quoted by authors)

1. Gulba DC, Schmid C, Borst RG, et al. Medical compared to surgical treatment for massive pulmonary embolism. Lancet 1994; 343:576-77.

2. Huber O, Bounameaux H, Borst F, Rohner A. Postoperative pulmonary embolism after hospital discharge: An underestimated risk. Arch Surg 1992; 127:310-13.

3. O'Meara JJ, McNutt RA, Evans AT, et al. A decision analysis of streptokinase plus heparin as compared with heparin alone for deep vein thrombosis. N Engl J Med 1994; 330:1864-69.

4. Alpert JS, Smith R, Carlson J, et al. Mortality of patients treated for pulmonary embolism. JAMA 1976; 236:1477-80.

5. Lilienfeld DE, Chan E, Ehland J, et al. Mortality from pulmonary embolism in the United States, 1962-1984. Chest 1990; 98:1067-72.

6. Goldhaber SZ, Haire WD, Feldstein ML, et al. Alteplase versus heparin in acute pulmonary embolism: Randomized trial assessing right ventricular function and pulmonary perfusion. Lancet 1993; 341:507-11.

MINI ABSTRACTS
John J. Bergan, M.D.
Items of Interest Which Have Crossed the Editor's Desk
(Provided for reference purposes and general interest)

Vascular Biology of the Human Saphenous Veins
Allen SP, Chester AH, Dzimiri NF, et al.
Ann Saudi Med 1995; 4:378-84

This review article discusses the biological properties of the saphenous vein endothelium and its vascular smooth muscle. Further, it discusses the interactions between endothelial cells, platelets, leukocytes, and the muscle cells following endothelial injury. The role of these properties and interactions as the saphenous vein serves as a conduit are elucidated.

Reconstruction Veineuse Chirurgicale Devant un Envahissement Tumoral du Systeme Cave SupÈrieur: Štude RÈtrospective de 7 Cas
Jeanfaivre T, PÈgis JD, Enon B, Tuchais E.
J Chir (Paris) 1996; 133:61-64

In this report, seven patients are reported, five of whom had compression of the superior vena cava. This compression was relieved within 24 hours and did not recur. As expected, reconstruction had no effect on the tumor itself and only one patient is still alive after five years. If a tumor is localized, resection is indicated as it contributes to improvement of patient comfort and, as indicated by the single case, may have a potential for cure.