Does the Limb Swell after Revascularisation by Percutaneous Transluminal Angioplasty?

Transcription

1 Eur J Vasc Endovasc Surg 9, (1995) Does the Limb Swell after Revascularisation by Percutaneous Transluminal Angioplasty? S, P. K. Payne 1'2, K. Jones 2, D. Painter 2, R, B. Galland 2 and J. Collin 1. 1Nuffield Dept of Surgery, University of Oxford, John Radcliffe Hospital, Headington, Oxford, and 2Dept of Surgery, Royal Berkshire Hospital, London Road, Reading, U.K. Objective: To discover if limb swelling occurs after successful revascularisation by percutaneous transluminal angioplasty (PTA). Design: Prospective Study. Setting: Vascular Laboratory. Materials: Twenty-five patients with occlusive arterial disease of the lower limb revascularised by percutaneous transluminal angioplasty were studied. Chief Outcome Measures: The ankle/brachial pressure index and foot volumes measured by water displacement plethysmography were measured before and after PTA. Main Results: The volume of the revascularised limb increased by 2% on the first day postangioplasty (p = 0.009) and 4% on the 7th day (p < 0.001) compared with the contralateral leg. Conclusions: Leg swelling is a consequence of revascularisation of the ischaemic limb and occurs in the absence of damage to the lymphatic drainage of the limb. Key Words: Angioplasty; Limb swelling; Oedema; Revascularisation. Introduction Successful revascularisation of the lower limb by femoropopliteal or distal bypass is often associated with postoperative swelling of the limb. This swelling may restrict mobility and can contribute to a compartment syndrome which may threaten limb viability. The mechanism of post-revascularisation limb swelling is not fully understood. Damage to lymphatic drainage vessels during dissection and the hyperaemic response of revascularised chronically ischaemic tissue are regarded as the two most plausible explanations for this swelling) -11 Phlebothrombosis has largely been discounted as a contributory factor.4,6,8,10a2,13 If limb swelling after operative revascularisation was solely due to lymphatic damage then limbs revascularised by percutaneous transluminal angioplasty (PTA) would not be expected to swell after revascularisation. The aim of this study was therefore Please address all correspondence to: S. P. K. Payne, Nuffield Department of Surgery, St George's Hospital, Kogarah, Sydne3~ New South Wales, Australia. to discover if limb swelling occurs after successful revascularisation by PTA. Patients and Methods Twenty-five patients undergoing successful PTA for symptomatic occlusive arterial disease of the lower limb were studied. The indication for revascularisation was intermittent claudication in 17 cases and rest pain or gangrene in the remaining eight. Most patients had already been investigated with intravenous digital subtraction angiography before admission to hospital. The median age of the patients was 59 years (range 51-86), 13 men and 12 women were studied, three diabetics were included. Patients were admitted to hospital on the day of angioplasty. In the morning before PTA the ankle/ brachial pressure index ~4 (ABPI) was measured using a hand held continuous wave Doppler and mercury sphygmomanometer. The volume of both legs was measured using water displacement plethysmography (Fig. 1). The bath was filled with warm water (temperature C) to the level of the overflow /95/ $08-00/ W. B. Saunders Company Ltd.

2 Limb Swelling After PTA 273 The limb being measured was lowered into the bath until the patient stood flat-footed on the bottom of the bath. The subject then stood still until the water level had settled. The volume of water displaced into the bucket was then measured. The coefficient of variation of this measurement was less than 1% on 20 repeated measures. Percutaneous transluminal balloon angioplasty was performed via the femoral route to the common iliac artery (10 cases) or the superficial femoral artery (15 cases). Before discharge from hospital the morning after angioplasty the limb volume and ABPI measurements were repeated. Patients returned to the hospital 6 days later when limb volumes and ABPI were re-measured. At that time all patients were asked whether their symptoms had improved following the PTA. Statistical Analysis The limb volumes were measured in both legs so that the non-treated limb could serve as a control to eliminate the effect of systemic or postural factors on limb volume. The measurements were expressed as a ratio of the volume of the treated limb to the control contralateral limb. Comparisons were made using the non-parametric Wilcoxon test for paired data. Confidence intervals were calculated using the nonparametric Wilcoxon test. Results All angioplasties were technically successful as determined by completion angiography. All patients also reported symptomatic improvement in either rest pain or claudication distance on the 7th post-angioplasty day. Symptom improvement was accompanied by a rise in ABPI after angioplasty in all but three cases. Before revascularisation the median ABPI was 0.6 (95% confidence limits; ). This improved to 0.85 (95% confidence limits; ) 1 day after angioplasty and 0.93 (95% confidence limits; ) 6 days later. The median increase in ABPI on the first post operative day was 0.25 (95% confidence limits; ) and 0.3 (95% confidence limits; ) 6 days later (Fig. 2). These increases are both statistically significant (p < 0.001, Wilcoxon). -Revascularisation by PTA was associated with an increase in the volume of the treated limb. Before revascularisation the median volume ratio (revascularised limb/control limb) was 1.0 (95% confidence limits; ). On the first postoperative day this had increased to 1.02 (95% confidence limits; ) and on the seventh postoperative day the median volume ratio was 1.04 (95% confidence limits; ). Thus the median increase in volume ratio was 2.1% (95% confidence limits; %) on the first postoperative day and 4.3% ( %) at day seven (Fig. 3). These increases are both statistically significant (p = 0.009, p < respectiveln Wilcoxon). Four patients who had themselves noticed limb swelling were investigated after angioplasty to exclude deep venous thrombosis. One patient underwent ascending phlebography and three patients underwent colour Duplex scanning, in none of these four cases was venous thrombosis demonstrated. Fig. 1. Limb volume being measured using the water displacement plethysmograph. The limb is lowered into the water bath displacing water into the bucket. The volume of water displaced is then measured. Discussion Limb swelling following operative revascularisation has previously been noted to be maximal at 7 days

3 274 S.P.K. Payne et al postoperativel3~ decreasing gradually thereafter. 15'16 Oedema often restricts mobility after revascularisation and in some cases may even be severe enough to cause a compartment syndrome threatening the viability of the limb, although this is uncommon in elective arterial reconstruction. Patman reported a frequency of fasciotomy for compartment syndrome of 0.45% in a review of 2000 peripheral arterial reconstructions. 17 We also found that leg swelling was greater on the 7th day than on the 1st day post angioplasty. Four of our patients noted that swelling was restricting mobility (those investigated to exclude deep venous thrombosis) but none developed a compartment syndrome. The mechanism of limb swelling after revascularisation is not fully understood but lymphatic damage during dissection 1-6 and increased capillary filtration 7-11 have both been suggested as explanations. Postoperative limb swelling in patients undergoing distal bypass is greater than in those undergoing bypass to the above knee popliteal artery. 2 This may be related to the more extensive dissection involved in distal bypass surgery, or alternatively it may be because the most ischaemic limbs are more likely to require distal bypass. The use of autogenous vein is associated with more oedema than when a Increase in ABPI synthetic conduit is used. 2 This may also be explained by the more extensive dissection required for vein harvesting, or by the greater use of vein in the most ischaemic limbs. The amount of swelling has been shown by Porter, 1 AbuRahma 6 and Vaughan 4 to correlate with the extent of lymphatic damage demonstrated on lymphangiography. Storen 13 however, found no difference in the amount of lymphatic damage between oedematous and non-oedematous limbs in a series of 14 patients following arterial reconstruction. A"lymphatic sparing" operation, where the lymphatics are carefully avoided during dissection, has been reported to be associated with less postoperative swelling than the "standard" procedure. 4'6 The distribution of oedema has been shown (using magnetic resonance imaging) to be similar to that found in patients with primary lymphoedema. ~5 These findings all favour the theory that post-revascularisation swelling is primarily due to lymphatic damage at the time of surgery. The amount of post-revascularisation limb swelling has also been shown to correlate with the severity of pre-operative ischaemia (as measured by ABPI). 8,10 ' Increase in limb volume ratio (Limb volume ratio expressed as a proportion [%] of the eontralatera! limb. Changes shown are relative to day O) ! ,~ -='~.~ 10 ~'~ 0.6,., "~ 0.4 ~ ~ 0 0.0,o Day 1 Day 7 Fig. 2. Ankle brachial pressure index changes after angioplasty. The scattergram shows the change in ABPI compared with preangioplasty. The bars depict median values and 95% confidence limits. Day 1 Day 7 Fig. 3. Increase in limb volume after angioplasty. The scattergram shows the changes in the ratio of revascularised limb volume to contralateral limb volume compared with pre-angioplasty. The bars depict median values and 95% confidence limits.

4 Limb Swelling After PTA 275 Melberg 2~ reported four patients who had no increase in either compartmental pressure or limb circumference when arterial reconstruction had failed. Since the lymphatics of these patients were inevitably damaged in the same manner as patients with successful reconstructions it must be concluded from this study that the revascularisation plays an important role in postoperative limb swelling and that lymphatic damage is of lesser importance. Postoperative phlebothrombosis has been dismissed as the cause of post-revascularisation swelling since no correlation between thrombosis on venography and the degree of swelling has been demonstrated. 4'6'8"1 '12'13 Hamer 22 stands alone in reporting that post-revascularisation oedema correlates with postoperative venous thrombosis based on a series of 21 patients. We found no evidence of deep venous thrombosis in the four cases with most obvious swelling. Revascularisation may cause oxygen derived free radicals to be released. These damage cell membranes by lipid peroxidation and thus increase capillary filtration. Soong et al. 23 have demonstrated a correlation between post-operative oedema and lipid peroxidation. The same group have also shown that inhibition of free radical generation using allopurinol reduces the amount of post-revascularisation swelling. 24 We have shown that the recorded ABPI increased between the first and the 7th postoperative day after angioplasty. The explanation for this observation is not clear but may be related to the swelling of the limb which also increased from days one to seven. As the limb swells so the transmission of pressure from the pneumatic tourniquet to the vessels being compressed will be diminished, and a "falsely" elevated ABPI will result. It is unlikely that percutaneous transluminal angioplasty causes significant impairment of lymphatic drainage from the limb. The methods used to study lymphatic drainage are in any case too crude to permit useful quantitative analysis and are unpleasant for the patient. For these reasons we did not seek to confirm by lymphangiography the absence of lymphatic damage following angioplasty. Nevertheless we believe our study has provided convincing evidence to support the view that limb swelling after revascularisation is a feature of the revascularisation itself and occurs in the absence of damage to lymphatic drainage from the limb. Minimally invasive methods of revascularisation will not therefore eliminate postoperative limb swelling and attention should be directed towards mini- mising the deleterious consequences of revascularisation injury. References 1 PORTER JM, LINDELL TD, LAKIN PC. Leg edema following femoropopliteal autogenous vein bypass. Arch Surg 1972; 105: SCHMIDT KT, WELTER H, PF~IF~R KJ, BECKER HIM. Lypmphangiographische Untersuchungen zum Extremitaten6dem nach rekonstruktiven Gef/isseingriffen im Femoropoplitealbereich. Fortschr Ri~ntgenstr 1978; 128: EICKI-IOFF JH, ENGELL HC. Local regulation of blood flow and occurrence of edema after arterial reconstruction of the lower limbs. Ann Surg 1982; 195: VAUGHAN BF, SLAVOTINEK AH, JEPSON RP. Edema of the lower limb after vascular operations. Surg Gynecol Obstet 1970; 131: HANNEQUIN Pt CLI~MENT C, LIEHN JC, EHRARD P, NICAISE Ht VALEYRE J. Superficial and deep lymphoscintigraphic findings before and after femoro-popliteal bypass. Eur I Nucl Med 1988; 14: ABuRAHMA AF, WOODRUFF BA, LUCENTE 13C. Edema after femoropopliteal bypass surgery: Lymphatic and venous theories of causation. J Vasc Surg 1990; 11: STRANDEN E. Transcapillary fluid filtration in patients with leg edema following arterial reconstruction for lower limb atherosclerosis. VASA 1983; 12: MYt-IRE HO, DEDICHEN H. Haemodynamic factors in the oedema of arterial reconstructions. Scand ] Thorac Cardiovasc Surg 1972; 6: SIMEONE FA, HUSNI EA. The hyperemia of reconstructive arterial surgery. Ann Surg 1959; 150: HusNi EA. The edema of arterial reconstruction. Circulation 1967; 35 (suppl 1): JACOBS MJHM, BECKERS RCY, JORNING PJG, SLAAF DW, RENEMAN RS. Microcirculatory haemodynamics before and after vascular surgery in severe limb ischaemia - the relation to postoperative oedema formation. Eur ] Vasc Surg 1990; 4: MYRHE HO, STOREN El, ONGRE A. The incidence of deep venous thrombosis in patients with leg oedema after arterial reconstruction. Scand] Cardiovasc Surg 1974; 8: STOREN EJ, MYHRE HO, STIRIS G. Lymphangiographic findings in patients with leg oedema after arterial reconstructions. Acta Chir Scand 1974; 140: YAO ST, HOBBS JT, IRVINE WT. Ankle systolic pressure measurement in arterial disease affecting the lower extremities. Br ] Surg 1969; 56: HAAVERSTAD Rt NILSEN G, MYHRE H, SAETHER OD, RINCK PA. The use of MRI in the investigation of leg oedema. Eur ] Vasc Surg 1992; 6: PERSSON NH, TAKOLANDER R, BERGQVIST D. Lower limb oedema after arterial reconstructive surgery. Acta Chir Scand 1989; 155: PATMAN RD. Compartmental syndromes in peripheral vascular surgery. Clin Orthop Relat Res 1975; 113: GITLITZ GF. The anterior tibial compartment syndrome. A complication of a femoropopliteal bypass procedure. Vasc Dis 1965; 2: COUPLAND GAE. Anterior tibial syndrome following restoration of arterial flow. Aust NZ J Surg 1972; 41: PERSSON NH, TAKOLANDER R/ BERGQVIST D. Edema after lower limb arterial reconstruction. Influence of background factors, surgical technique and potentially prophylactic methods. VASA 1991; 20: MELBERG PE, STYE J, BIBER B, HASSELGREN PO, KORNER L, SEEMAN T. Muscular compartment pressure following reconstructive arterial surgery of the lower limbs. Acta Chir Scand 1984; 150:

5 276 S.P.K. Payne et al 22 HAMER JD. Investigation of oedema of the lower limb following successful femoropopliteal bypass surgery: The role of phlebography in demonstrating venous thrombosis. Br J Surg 1972; 59: SOONG CV~ YOUNG IS, BLAIR PHB, HOOD JM, ROWCANDS BJ, TRJMBC~ ER, BARROS D'SA AAB. Lipid peroxidation as a cause of lower limb swelling following femoropopliteal bypass grafting. Eur J Vasc Surg 1993; 7: SOONG CV, YOUNG IS, BLAIR PHB, HOOD JM, ROWLANDS BJ, TRIMBLE ER, BARROS D'SA AAB. Reduction of free radical generation minimises lower limb swelling following femoropopliteal bypass surgery. Eur Soc Vasc Surg (Abstract) 1993 Book of Abstracts p 62. Accepted 18 July 1994