PULMONARY EMBOLISM FROM LEFT SUBCLAVIAN VEIN THROMBUS FOLLOWING SUPRAPUBIC PROSTATECTOMY DAVID F! GENTILE, M.D. LOUIS R. COS, M.D. KENNETH OURIEL, M.D.

From the Departments of Urology and Vascular Surgery, University of Rochester School of Medicine and Dentistry, Rochester, New York ABSTRACT-Deep venous thrombosis (DVT) of the axillary and subclavian veins accounts for approximately l-2 percent of all recorded deep venous thromboses. Pulmonary embolism from an upper extremity DVT has been reported to vary between 2 percent and 35.7 percent. We report the occurrence of a left subclavian vein DVT with subsequent nonfatal pulmonary embolism in a sixty-two-year-old patient twenty-four hours following suprapubic prostatectomy. A review of the literature is presented, along with pathophysiology, diagnosis, and treatment.

Thromboses of the axillary and subclavian veins account for 1-2 percent of all reported deep venous thromboses (DVT).‘-lo In many instances a cause precipitating the thrombosis can be defined. These may include central venous catheterization, neoplasm, thoracic outlet syndrome, intravenous drug abuse, trauma, congenital venous malformations, implanted pacemakers, the superior vena cava syndrome, heart failure, and hypercoagulability states. l-l5 In addition, there has been reported an upper extremity venous thrombosis associated with oral contraceptive use.12 More frequently, however, the etiology is unclear and the term Paget-Schroetter syndrome is applied, indicating spontaneous, idiopathic, often effort-related, thrombosis of the axillary and subclavian veins.13 As mentioned, if categorized by etiology as trauma or stress-related versus spontaneous, the latter is more common though less frequently reported. The left side is also affected more often than the right in the spontaneous form.3J2 The incidence of pulmonary embolism resulting from a thrombosis of an upper extremity vein varies widely in the literature. Harley et

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a1.,2 in their series of 14 patients with thrombosis of the subclavian or axillary veins documented by phlebography, reported that pulmonary emboli were diagnosed by arteriogram and ventilation-perfusion (V-Q) scan in 5, for an incidence of 35.7 percent. Horattas et al. ,I0 in a retrospective study of all upper extremity DVTs occurring at the Akron General Medical Center over a six-year period, noted an incidence of pulmonary emboli of 12 percent. Most recently, Hauptli et al. I6 found pulmonary emboli in only 2 of 96 patients with proved subclavian vein thrombosis. Of importance, regardless of the actual incidence, Falicov, Resnekov, and Petasnick15 have reported resultant car pulmonale from repeated pulmonary emboli from an axillary vein source. We report the case of a healthy sixty-twoyear-old white man undergoing suprapubic prostatectomy for benign prostatic hyperplasia, in whom acute thrombosis of his left subclavian vein with subsequent pulmonary embolism developed less than twenty-four hours postoperatively. A review of the pathogenesis, diagnosis, and treatment is presented.

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(A) Normal ventilation scan showing no areas of photopenia. (B) Perfusion scan showing segmental filling defect, consistent with high probability of pulmonary embolism.

FIGURES.

Case Report A sixty-two-year-old white man presenting with macroscopic hematuria, nocturia ( x 2), every two- to three-hour daytime frequency, poor stream, dribbling, urge, and urge incontinence underwent a suprapubic prostatectomy for presumed benign prostatic hyperplasia. His past medical history was significant only for hypertension that was treated with chlorthalidone and potassium supplementation. He was a one pack/day cigarette smoker. Physical examination was within normal limits, except for an enlarged prostate (4 +). Chest x-ray film, electrocardiogram, and laboratory values, including prothrombin time, partial thromboplastin time, and bleeding time were also unremarkable. The patient underwent prostatectomy in the usual supine position, using an NzO/Oz/Forane general anesthetic, supplemented with fentanyl and midazolam. A 1Sgauge intracatheter was placed in the left arm and a 20-gauge intracatheter in the right. The blood pressure cuff was placed on the right arm. Vital signs remained stable throughout the procedure, except for an episode of bradycardia to 40, treated with 0.4 mg of atropine. Preoperatively, the patient’s blood pressure was 160/84 mm Hg. It was maintained between 98-122/60-80 mm Hg intraoperatively. The patient was in sinus

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rhythm throughout the operation, with an oxygen saturation (SA02) of 97-100 percent. Operative blood loss was 1,200 cc, replaced with 2,600 cc of crystalloid. No blood transfusions were given, since the patient’s preoperative hematocrit was 48. Operative time was one hour and thirty-five minutes. Pathologic analysis of the removed tissue revealed stromal and glandular hyperplasia with evidence of chronic prostatitis. Several small foci of well to moderately differentiated adenocarcinoma (Gleason grade 5/10) were also found. The following morning, eighteen hours after the completion of the operation, the patient complained of pain in the left side of the chest, worse with inspiration. Findings on physical examination were within normal limits, except for new edema and cyanosis of the left arm. The patient had experienced episodes of left arm swelling in the past, but he had never noted discoloration. Findings on chest x-ray film and electrocardiogram were unchanged. Arterial blood gas measurement revealed a pH of 7.45, a PCOz of 28, and a PO2 of 59. Supplemental oxygen was supplied and a V-Q scan obtained. Mismatched defects were present in the middle and lower lobes of right lung (Fig. l), consistent with a high probability of pulmonary embolism. The patient was immediately given heparin intravenously. Serial creatinine phosphokinase (CPK) determinations showed a

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FIGURE 2. Left arm venogram showing thrombosis in proximal left subclavian vein.

peak value of 430 (3 % MB fraction). Inevitable exacerbation of bleeding from the prostatic bed occurred as a result of heparinization. This was managed with prolonged Murphy drip irrigations and blood transfusions as needed (total of 6 U packed red blood cells were given). A search for the source of the pulmonary embolism consisted of negative color duplex scan of the legs, a color duplex scan of the left arm revealing clot just above the elbow, and a venogram of left arm showing a filling defect in the proximal subclavian vein (Fig. 2), consistent with thrombus, but patent axillary and brachial veins. The patient was maintained at complete bed rest with immobilization of his left arm during heparinization. On day 4 of anticoagulation therapy, coumadin therapy was begun and ambulation was permitted. He was discharged on postoperative day 10 in good condition, receiving coumadin 2.5 mglday. His hematocrit at the time of discharge was 28. Comment Many pathogenic mechanisms may be active in the development of upper extremity DVT, some similar to those involved in the genesis of lower extremity DVTs, some different. Stress or effort-induced thrombosis is predominantly a disease of young, healthy, active men. The right side is more commonly affected, presumably because right-handedness is more common.3 Thrombosis usually follows an episode of exer-

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tion. As occurs in many types of activity, e.g., lifting, the shoulder girdle is depressed and the subclavian vein squeezed between the clavicle, first rib, and scalenus anticus muscle (or cervical rib, if present). Blood flow is consequently slowed. In addition, the endothelium of the vein may be injured. Compounding this is the associated Valsalva maneuver which by necessity accompanies most forms of physical exertion. This temporarily, but completely, halts blood flow through the axillary and subclavian veins. Stasis of blood is the net effect and thrombosis the result. These patients are said to have “effort” thrombosis or Paget-Schroetter syndrome. (Paget first described this entity in 1875 and von Schroetter independently in 1884.) Thrombosis in other circumstances may be attributed to one or more of the classic triad of determinants of thrombosis (hypercoagulability, intimal damage, and stasis).” Patients with polycythemia, thrombocytosis, and inherited disorders of the clotting cascade are clearly at increased risk from hypercoagulability. In addition, oral contraceptive use and, theoretically, pregnancy place patients at increased risk for the same reason. The use of indwelling central venous catheters and pacemakers produce intima1 damage that can precipitate the clotting cascade. Indeed, in a review of 44 patients with indwelling pacemakers, Mitrovic et al.” reported thrombosis of the involved vein in 39 (89%). Blood flow characteristics are also altered by the presence of a foreign body, predisposing to platelet aggregation and thrombosis. Patients with congestive heart failure, primary pulmonary hypertension, car pulmonale, or the SVC syndrome secondary to malignancy, all have stasis of blood in the upper extremities. Once stasis reaches a critical level, thrombosis is an inevitable sequela. Pulmonary embolization is a risk whenever phlebothrombosis occurs. It was once thought that embolization from an upper extremity source was uncommon. It is now recognized that pulmonary embolism occurs with an average frequency of 12.4 percent, often after the initiation of adequate anticoagulant therapy. 1*8*10 The most reliable method of diagnosis of upper extremity DVT is venography.2 Horattas, et ~1.‘~ in their review of the literature, similarly concluded that venography is the most accurate diagnostic modality available currently. Doppler ultrasound is less reliable in the upper

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extremities than in the lower extremities. Duplex imaging, however, is more accurate than Doppler scanning alone. Venous plethysmography in axillary and subclavian venous thrombosis is also unreliable, and radionucleotide studies have a high false-negative rate. The optimal form of therapy for upper extremity DVT has not been established because of limited individual experience. Early anticoagulation with heparin is advocated by most authors to prevent propagation of thrombus and maintain patent collaterals, followed by anticoagulation with warfarin, for a period averaging three months. Thrombolytic therapy with its possible complications, is reserved for life-threatening conditions.* Surgical intervention in the form of thrombectomy is advocated by some for individuals with primary upper extremity thrombosis,l” in so far as long-term morbidity (pain, swelling, weakness) is decreased.‘O Ligation of the subclavian vein is performed in those individuals who continue to embolize despite anticoagulation, or when some contraindication to anticoagulation exists. Immediate mortality from pulmonary embolism varies between 3 percent and 60 percent.8 Long-term morbidity from upper extremity DVT is related to the etiology. Thrombosis secondary to “intrinsic” vessel lesions is infrequently associated with long-term sequelae. l However, when “extrinsic” obstruction is causative, 50 percent will have disabling arm swelling and pain. l The cause of the subclavian vein thrombosis in our patient is unclear. With his previous history of left arm swelling, it is possible that the thrombus had been present preoperatively. It is certainly unlikely that his Stage Al prostate cancer was in any way etiologically related. There was no operative trauma to his left arm, except for placement of a 16-gauge intracatheter. The blood pressure cuff was on his right arm and, in any event, was distal to the site of thrombosis. Coagulation studies preoperatively were normal. Of note, the patient had been taking one aspirin per day, and this was stopped

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two weeks before the operation. How this might have played a role in his thrombotic event is unclear. 601 Elmwood Avenue p.0. Box 656 Rochester, New York 14642 (DR. COS) References 1. Donayre CE, White GH, Mehringer SM, and Wilson SE: Pathogenesis determines late morbidity of axillosubclavian vein thrombosis, Am J Surg 152: 179 (1986). 2. Harley DP, White RA, Nelson RJ, and Mehringer CM: Pulmonary embolism secondary to venous thrombosis of the arm, Am J Surg 147: 221 (1984). 3. Prescott SM, and Tikoff G: Deep venous thrombosis of the upper extremity: a reappraisal, Circulation 59: 350 (1979). 4. Weinberg G, and Pasternak BM: Upper-extremity suppurative thrombophlebitis and septic pulmonary emboli, JAMA 240: 1519 (1978). 5. Clagett GP, Thornbury JR, and Penner JA: Upper extremity venous thrombosis with pulmonary embolism, JAMA 227: 187 (1974). 6. Adams JT, and Deweese JA: “Effort” thrombosis of the axillary and subclavian veins, J Trauma 11: 923 (1971). 7. Gloviczki P, Kazmier FJ, and Hollier LH: Axillary-suhclavian venous occlusion: the morbidity of a nonlethal disease, J Vast Surg 4: 33 (1986). 8. Jones JC, Balkcom IL, and Worman RK: Pulmonary embolus after treatment for subclavian-axillary vein thrombosis, Postgrad Med 82: 244 (1987). 9. Gillmer DJ, and Mitha AS: Primary (stress) thrombosis of the upper arm associated with multiple pulmonary embolisms, S Afr Med J 57: 251 (1980). 10. Horattas MC, et ol: Changing concepts of deep venous thrombosis of the upper extremity-report of a series and review of the literature, Surgery 104: 561 (1988). 11. Mitrovic V, Thormann J, Schlepper M, and Neuss H: Thrombotic complications with pacemakers, Int J Cardio12: 363 (1983). 12. Edwards LA, Hilliard JR, and Wood DE: Axillary vein thrombosis and pulmonary embolism possibly due to oral contracention. Can Med Assoc I 100: 78 (1969). -13. Smith-Behn J, Althar R, and-Katz W: Primary thrombosis of the axillary/subclavian vein, Southern Med J 79: 1176 (1986). 14. Warden GD, Wilmore DW, and Pruitt BA; Central venous thrombosis: a hazard of medical progress, J Trauma 13: 620 (1973). 15. Falicov RE, Resnekov L, and Petasnick J: Progressive pulmonary vascular obstruction and car pulmonale due to repeated embolism from axillary vein thrombosis, Ann Intern Med 73: 429 (1970). 16. Hauptli W, et al: Etiology and long-term course of subclavian vein thrombosis with reference to acute therapy (Abstr.), J Suisse Med 119: 647 (1989). 17. Lisse JR, Davis CP, and Thurmond-Anderle ME: Upper extremity deep venous thrombosis: increased prevalence due to cocaine abuse, Am J Med 87: 457 (1989).

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Pulmonary embolism from left subclavian vein thrombus following suprapubic prostatectomy.

Deep venous thrombosis (DVT) of the axillary and subclavian veins accounts for approximately 1-2 percent of all recorded deep venous thrombosis. Pulmo...
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