Perioperative changes in exhaled nitric oxide during oesophagectomy.

INTRODUCTION: Oesophagectomy is a major surgical procedure, associated with high rates of postoperative cardiopulmonary morbidity, that is in part due to the frequent requirement for periods of intraoperative one-lung ventilation (OLV). The current pilot study aims to investigate variation in exhaled NO levels during oesophagectomy with emphasis on the response to OLV and correlation to physiological variables and clinical outcomes. METHODS: Breath-to-breath concentrations of NO were analysed in patients undergoing oesophagectomy at various stages of two-lung ventilation. Furthermore, we also analysed the effects of OLV both in the selectively ventilated and collapsed lungs. RESULTS: Twenty-four patients were recruited to the study (17 male, 60.2 ± 12.8 years). Regarding two-lung ventilation, the baseline levels of NO (2.9 ppb), tended to increase after re-inflation of the collapsed lung (3.5 ppb, P = 0. 888) and decreased at 2 h (2.1 ppb, P = 0.022) and 12 h (2.2 ppb, P = 0.733) postoperatively. Compared to baseline, selective measurements of NO at the end of OLV demonstrated a significant reduction of NO levels in the ventilated lung (1.6 versus 3.1 ppb, P = 0.028), whereas re-inflation of the collapsed lung revealed higher levels of NO (3.4 versus 2.7 ppb, P = 0.657). Exhaled NO correlated significantly with systolic blood pressure and lactate (P < 0.007). Exhaled NO levels tended to be higher at all perioperative time points in patients who developed postoperative respiratory complications (P > 0.05). CONCLUSION: This study highlights effects of oesophagectomy and OLV on exhaled concentrations of NO. The observed variations may be related to differential ventilation during OLV altering the complex balance between synthesis and consumption of NO as well as local and generalised tissue injury associated with this surgery. Findings should prompt further larger studies to establish the relationship between exhaled NO and lung injury both during and after oesophagectomy and one-lung ventilation.

The nonsaphenous vein of the popliteal fossa: prevalence, patterns of reflux, hemodynamic quantification, and clinical significance.

BACKGROUND: A large tortuous vein coursing over the posterior aspect of the knee and the upper calf may give rise to a constellation of varicose veins unrelated to the great (GSV) or small (SSV) saphenous veins. Designated the popliteal fossa vein (PFV), it perforates the deep popliteal fascia and empties into the deep system. We examined the prevalence, anatomic reflux patterns, hemodynamic role, and clinical significance of the PFV. METHODS: We examined 543 patients (818 limbs) with venous disease, aged 14 to 94 years (median, 55 years). The study consisted of group A, comprising limbs with a PFV, and group B, formed by the remaining limbs. The history, clinical examination, and venous duplex scan findings were analyzed retrospectively. Venous clinical severity and venous segmental disease scores of group A were compared with those of an equal number of CEAP-, sex-, and age-matched control limbs. In situ venous hemodynamics of the PFV obtained with duplex scan are reported. RESULTS: A PFV was found in 24 (2.93%) of 818 limbs (95% confidence interval [CI], 1.8%-4.1%); 24 (4.4%) of 543 subjects (95% CI, 2.7%-6.2%), 12 men and 12 women aged 23 to 82 years (median, 54 years) had a PFV. CEAP clinical classes in limbs with a PFV were as follows: C2, 15 limbs; C3, 5 limbs; C4, 2 limbs; C5, 1 limb; and C6, 1 limb. Proximal and distal (92%), superficial (100%), perforator (87.5%), and complex-pattern (41.7%) reflux occurred more often in group A (P < .01). Incompetence in the GSV (75%), posterior arch, and posteromedial and saphenous tributaries was also more frequent in group A (P < .05). SSV reflux in group A (29%) matched that in group B. The PFV terminated at the deep system (96% in the popliteal vein) above the SSV (median distance, 1.5 cm; 95% CI, 0.5-2 cm). The odds ratio for a PFV in limbs with prior SSV disconnection was 5.68. Deep reflux was evenly distributed in group A (41.7%) and group B (27%). The prevalence of incompetent perforators was 283% (95% CI, 194%-373%) in group A and 96% (95% CI, 95%-98%) in group B (P < .001). PFV tributaries were distributed at the popliteal area (100%); the posterior (87.5%), medial (62.5%), and lateral (37.5%) upper calf; and the posterior distal thigh (17%), often projecting to the posterior GSV arch (50%). The (median) peak velocity of reflux in the PFV was 82.6 cm/s, the mean velocity was 17.7 cm/s, the duration was 2.4 seconds, the volume flow was 231.5 mL/min, and the expelled volume was 9.3 mL. The median diameter of the PFV at the crossing of the fascia was 0.527 cm. Venous clinical severity (range, 2-17; median, 5.5) and venous segmental disease (range, 0.5-8; median, 2.75) scores in limbs with a PFV exceeded (P

Duration and amplitude decay of acute arterial leg inflow enhancement with intermittent pneumatic leg compression: an insight into the implicated physiologic mechanisms.

PURPOSE: By acutely enhancing the arterial leg inflow, intermittent pneumatic leg compression (IPC) improves the walking ability, arterial hemodynamics, and quality of life of claudicants. We quantified the duration of acute leg inflow enhancement with IPC of the foot (IPC(foot)), calf (IPC(calf)), or both (IPC(foot+calf)) and its amplitude decay in claudicants and controls in relation to the pulsatility index, an estimate of peripheral resistance. These findings are cross-correlated with the features of the three implicated physiologic mechanisms: (1) an increase in the arteriovenous pressure gradient, (2) suspension of peripheral sympathetic autoregulation, and (3) enhanced release of nitric oxide with flow and shear-stress increase. METHODS: Twenty-six limbs of 24 claudicants with superficial femoral artery occlusion or stenoses (>75%) and 24 limbs of 20 healthy controls matched for age and sex, meeting stringent selection criteria, had their popliteal volume flow and pulsating index (peak-to-peak velocity/mean velocity) measured with duplex scanning at rest and upon delivery of IPC. Spectral waveforms were analyzed for 50 seconds after IPC delivery per 5-second segments. The three IPC modes were applied in a true crossover design. Data analysis was performed with the Page, Friedman, Wilcoxon, Mann-Whitney and chi2 tests. RESULTS: The median duration of flow enhancement in claudicants exceeded 50 seconds with IPC(foot), IPC(calf), and IPC(foot+calf) but was shorter (P < .001) in the controls (32.5 to 40 seconds). Among the three IPC modes, the duration of flow enhancement differed (P < .05) only between IPC(foot) and IPC(foot+calf). After reaching its peak within 5 seconds of IPC, flow enhancement decayed at rates decreasing over time (trend, P < .05, Page test), which in both groups were highest at 5 to 20 seconds, moderate at 20 to 35 seconds, and lowest at 35 to 50 seconds (P < .05, Friedman test). Baseline and peak flow with all IPC modes was similar between the two groups. Pulsatility index attenuation in claudicating limbs lasted a median 32.5 seconds with IPC(foot), 37.5 seconds with IPC(calf), and 40 seconds with IPC(foot+calf); duration of pulsatility index attenuation was shorter in the control limbs with IPC(foot) (30 seconds), IPC(calf) (32.5 seconds), or IPC(foot+calf) (35 seconds), yet differences, as well as those among the 3 IPC modes, were not significant. CONCLUSION: Leg inflow enhancement with IPC exceeds 50 seconds in claudicants and lasts 32.5 to 40 seconds in the controls. Peak flow occurs concurrently with maximal pulsatility index attenuation, within 5 seconds of IPC. Irrespective of group or IPC mode, the decay rate (%) of flow enhancement is highest within 5 to 20 seconds of IPC, moderate at 20 to 35 seconds, and lowest at 35 to 50 seconds. Since attenuation in peripheral resistance terminates with the mid time period (20 to 35 seconds) of flow decay, and nitric oxide has a half-life of <7 to 10 seconds, the study's data indicate that all implicated physiologic mechanisms (1, 2, and 3) are likely active immediately after IPC delivery (0 to 20 sec) and all but nitric oxide are effective in the mid time period (20 to 35 seconds). As the pulsatility index has returned to baseline, the late phase of flow enhancement (35 to 50 seconds) could be attributable to the declining arteriovenous pressure gradient alone.

Prevalence, anatomic patterns, valvular competence, and clinical significance of the Giacomini vein.

OBJECTIVE: Coursing the posterior thigh as a tributary or trunk projection of the small saphenous vein (SSV), the Giacomini vein's clinical significance in chronic venous disease (CVD) remains undetermined. This cross-sectional controlled study examined the prevalence, anatomy, competency status, and clinical significance of the Giacomini vein across the clinical spectrum of CVD in relation to the SSV termination. METHODS: One hundred eighty-nine consecutive subjects (301 limbs) with suspected CVD (109 men, 80 women; age, 18-87 years [median, 61 years]) underwent examination, clinical class (CEAP) stratification, and duplex ultrasound determination of the sites and extent of reflux >0.5 sec) and Giacomini vein's anatomy. RESULTS: A Giacomini vein was found in 70.4% of limbs (212 of 301; 95% confidence interval, 65%-75.6%). Extent, pattern, and sites of reflux in all named superficial and deep veins were evenly distributed in limbs with and without a Giacomini vein; perforator vein incompetence in thigh and calf was also balanced (all, P > .2). Giacomini vein had no effect ( P > .2) on SSV termination anatomy, displaying a similar prevalence in classes C(0-6) . In 212 limbs, either as a tributary or trunk projection of the SSV, the Giacomini vein ascended subfascially (n = 210) to the lower (8%; n = 17), middle (47.6%; n = 101), or upper (44.3%; n = 94) thigh, and terminated at the deep system (45.3%; n = 96) and/or perforated the fascia (64.2%; n = 136), to join the superficial system. Giacomini vein morphology was not affected by the SSV termination anatomy and CEAP clinical class. Incompetence was detected less often (P < .001) in the Giacomini vein (4.7%; n = 10 of 212) than in the saphenous trunks cumulatively (53.3%; n = 113 of 212). Yet the odds ratio of Giacomini incompetence was 11.94 (7 of 33 over 3 of 169) in the presence of SSV reflux, and 11.67 (6 of 23 over 4 of 179) when both the great saphenous vein (proximal, proximal plus distal) and SSV were incompetent. CONCLUSION: Found in more than two thirds of limbs, the Giacomini vein has a complex anatomy that is linked vastly to the deep or superficial veins of the posteromedial thigh, but is unaffected by the anatomy of SSV termination and CEAP clinical class. Its presence proved insignificant to the extent, pattern, sites, and clinical severity of venous incompetence, yet the Giacomini vein was far less often susceptible to reflux than the saphenous trunks were. Routine Giacomini vein investigation is not justified in view of these findings. Investigation could be considered selectively in limbs with SSV incompetence, with or without great saphenous vein incompetence, supported by the high odds of concomitant Giacomini vein reflux.

Effects of epidural-and-general anesthesia combined versus general anesthesia alone on the venous hemodynamics of the lower limb. A randomized study.

Our hypothesis was that, due to its sympatholytic action, epidural anesthesia (EA) administered as part of anesthesia in abdominal surgery would generate a marked venous leg flow enhancement, thus aiding in the prevention of peroperative venous stasis. We studied, and comprehensively quantified the venous haemodynamic changes in the lower limb during and immediately after abdominal surgery performed under EA and general (GA) anesthesia combined, in comparison to GA alone. This is a prospective, randomized, controlled study, stratified for hypertension and smoking, comprising ASA 1-2 patients undergoing elective total abdominal hysterectomy. Those with peripheral vascular or chronic venous disease, prior DVT or BMI>35 were excluded. Eligible recruits received either GA (Group GA) (n = 10; age 36-65, median 50) alone or epidural anesthesia (EA) and GA combined (Group EA/GA) (n = 9; age 32-58, median 46). EA (L(1-2)) was administered using lignocaine 2%. Both groups had GA induced with fentanyl and propofol, maintained with N(2)O and isoflurane; larygoscopy was facilitated with vecuronium; analgesia was provided either with morphine (Group GA) or epidurally with 2% lignocaine boli (Group EA/GA). Hemodynamics were determined at the popliteal vein in the horizontal supine position at baseline (resting prior to anesthesia), post epidural (20 min after delivery of EA), post induction (15 min after laryngeal intubation), surgery (upon uterus removal) and recovery (30 min after extubation). There was no difference in the mean velocity[V(mean)] between the 2 groups at baseline (p = 0.35([Mann-Whitney])), and post induction (p = 0.5([Mann-Whitney])). However V(mean) was significantly higher in Group EA/GA than Group GA, both at surgery (point estimate[PE]: 1.8 cm/s; 95% CI: 0.01, 6.3 cm/s; p <0.05([Mann-Whitney])) and recovery (PE: 2.6 cm/s; 95% CI: 0.4, 5.1 cm/s; p = 0.02([Mann-Whitney])). Volume flow[V(Q)] was similar in the 2 groups at baseline and post induction (both, p >0.1([Mann-Whitney])), but was significantly higher in Group EA/GA at surgery (PE: 54 ml/min; 95% CI: 18, 159 ml/min; p = 0.045([Mann-Whitney])) and recovery (PE: 49 ml/min; 95% CI: 16, 129 ml/min; p=0.0037([Mann-Whitney])). Peak velocity, V(mean) and V(Q) increased significantly post epidural in Group EA/GA. Contrary to the venous leg flow attenuation in elective abdominal surgery under GA and upon its recovery, EA administered as part of GA is associated with a significant enhancement of both V(mean) and V(Q). This beneficial hemodynamic effect of EA at the vulnerable stage of recovery may be critically essential in light of enhanced blood viscosity, fibrinolytic shut-down, endothelial/platelet activation and immobility, acting in synergy with putative cardiorespiratory protection. The results of this study lend support to the preferential selection of combined EA/GA in subjects at high risk for venous thromboembolism, particularly when optimal DVT prophylaxis is practically unattainable due to limitations pertaining to the nature of surgery.

Lower limb venous haemodynamic impairment on dependency: quantification and implications for the "economy class" position.

The role of stasis in venous disease is undisputed, yet surprisingly, its haemodynamic quantitation remains largely undefined. We investigated the phenomenon of venous stasis in the lower limb upon sitting and standing and project its implications to economy class aircraft passengers. 26 normal limbs, 13 subjects, age 29-54, selected after duplex, plethysmography and ABPI, had peak[V(peak)], mean[V(mean)] and minimum[V(min)] velocities, volume-flow[Q(venous)], pulsatility index [PI(venous)] and diameter obtained on horizontal, sitting (as in economy aircraft seats) and standing with duplex, at popliteal, femoral[FV] and common femoral[CFV]veins [differences in median %]. V(peak), V(mean) and Q(venous) decreased from horizontal to sitting in the CFV [57%, 71%, 31%, respectively], FV [51%, 70%, 34%] and popliteal [31%, 58%, 42%] (all, p<.001). V(peak),V(mean) and Q(venous) decreased further from sitting to standing in the CFV [26%, 44%, 25%, respectively], FV [21%, 42%, 27%] and popliteal [14%, 42%, 20%] (all, p <.001). Diameter, V(min) and PI(venous) increased from horizontal to sitting in the CFV [50%, 63%, 38%, respectively], FV [39%, 23%, 66%] and popliteal [21%, 14%, 84%] (all, p <.001)]. Diameter, V(min) and PI(venous) increased further from sitting to standing in CFV [10%, 22%, 19%, respectively; p =.004], FV [12%, 68%, 2%[ns]; p <.001)] and popliteal [14%, 50%, 24%; p =.017]. In all postures: V(peak), V(mean), Q(venous) and diameter at CFV exceeded FV (p <.025) and popliteal (p <.001) ones; also those at FV exceeded the popli-teal ones (p =.003), except for the diameter on horizontal. V(min) in popliteal was higher than in CFV (p =.003) or FV (p <.025), on horizontal and standing. PI(venous) in CFV was lower than in FV or popliteal (p <.025) on sitting. Right to left differences non-significant. [Wilcoxon(+Bonferroni) test: significance at p <.025] A shift from horizontal to sitting generates a most significant attenuation in Q(venous),V(peak) and V(mean) linked to a reciprocal increase in V(min), PI(venous) and vein diameter, with further exacerbation on standing. V(peak),V(mean) and Q(venous) decline with distance from groin enhancing venous stasis in the periphery. By restricting activation of the natural venous pumps, sitting cramped during long flights may protract the status of haemodynamic stagnation sustained on dependency which paired with marked venous dilatation generates a milieu that may promote thrombogenesis.