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PURPOSE - To evaluate an approach to the treatment of iliofemoral deep vein thrombosis (DVT) that included pharmacomechanical catheter-directed thrombolysis with reteplase and the Helix mechanical thrombectomy device, followed by early stent placement.
MATERIALS AND METHODS - During 3-year period, 23 symptomatic limbs in 18 patients with iliofemoral DVT were treated with reteplase catheter-directed thrombolysis. After an initial infusion of 8 to 16 hours, any residual acute thrombus over a long segment (> 10 cm) was treated by maceration with use of the Helix thrombectomy device. Residual short-segment (< 10 cm) iliac vein thrombus and/or stenosis were treated with stent placement. Technical success, clinical success, complications, thrombolytic infusion time, total thrombolytic agent dose, fibrinogen level changes, and late limb status were retrospectively analyzed.
RESULTS - Technical success was achieved in 23 of 23 limbs (100%). Clinical success was achieved in 22 of 23 limbs (96%). Complete or partial thrombolysis was observed in 19 of 23 limbs (83%). Major bleeding was observed in one patient (6%) and necessitated blood transfusion. Mean per-limb thrombolytic infusion time and total dose were 19.6 hours +/- 8.1 and 13.8 U +/- 5.3 reteplase, respectively. Mean serum fibrinogen nadir and percentage drop in serum fibrinogen were 282 mg/dL +/- 167 and 47% +/- 24%, respectively. Late (mean, 19.8 +/- 11.6 months) modified Venous Disability Scores were 0 (none) for six limbs, 1 (mild) for 10 limbs, 2 (moderate) for two limbs, and 3 (severe) for no limbs.
CONCLUSION - In a preliminary experience, pharmacomechanical catheter-directed iliofemoral DVT thrombolysis with early stent placement was safe and effective.
We examined the impact of infection on hepatic and muscle glucose metabolism in dogs adapted to chronic total parenteral nutrition (TPN). Studies were done in five conscious chronically catheterized dogs, in which sampling (artery, portal and hepatic vein, and iliac vein), infusion catheters (inferior vena cava), and Transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days after surgery, dogs were placed on TPN. After 5 days of TPN, an infection was induced, and the TPN was continued. The balance of substrates across the liver and limb was assessed on the day before infection (day 0) and 18 (day 1) and 42 h (day 2) after infection. On day 0, the liver was a marked net consumer of glucose (4.3 +/- 0.6 mg. kg-1. min-1) despite near normoglycemia (117 +/- 5 mg/dl) and only mild hyperinsulinemia (16 +/- 2 microU/ml). In addition, the majority (79 +/- 13%) of the glucose taken up by the liver was released as lactate (34 +/- 6 micromol. kg-1. min-1). After infection, net hepatic glucose uptake decreased markedly on day 1 (1.6 +/- 0.9 mg. kg-1. min-1) and remained suppressed on day 2 (2.4 +/- 0.5 mg. kg-1. min-1). Net hepatic lactate output also decreased on days 1 and 2 (15 +/- 5 and 12 +/- 3 micromol. kg-1. min-1, respectively). This occurred despite increases in arterial plasma glucose on days 1 and 2 (135 +/- 9 and 144 +/- 9 mg/dl, respectively) and insulin levels on days 1 and 2 (57 +/- 14 and 34 +/- 9 microU/ml, respectively). In summary, the liver undergoes a profound adaptation to TPN, making it a major site of glucose disposal and conversion to lactate. Infection impairs hepatic glucose uptake, forcing TPN-derived glucose to be removed by peripheral tissues.
The effect of a negative arterial-portal venous (a-pv) glucose gradient on skeletal muscle and whole body nonhepatic glucose uptake was studied in 12 42-h-fasted conscious dogs. Each study consisted of a 110-min equilibration period, a 30-min baseline period, and two 120-min hyperglycemic (2-fold basal) periods (either peripheral or intraportal glucose infusion). Somatostatin was infused along with insulin (3 x basal) and glucagon (basal). Catheters were inserted 17 days before studies in the external iliac artery and hepatic, portal and common iliac veins. Blood flow was measured in liver and hindlimb using Doppler flow probes. The arterial blood glucose, arterial plasma insulin, arterial plasma glucagon, and hindlimb glucose loads were similar during peripheral and intraportal glucose infusions. The a-pv glucose gradient (in mg/dl) was 5 +/- 1 during peripheral and -18 +/- 3 during intraportal glucose infusion. The net hindlimb glucose uptakes (in mg/min) were 5.0 +/- 1.2, 20.4 +/- 4.5, and 14.8 +/- 3.2 during baseline, peripheral, and intraportal glucose infusion periods, respectively (P < 0.01, peripheral vs. intraportal); the hindlimb glucose fractional extractions (in %) were 2.8 +/- 0.4, 4.7 +/- 0.8, and 3.9 +/- 0.5 during baseline, peripheral, and intraportal glucose infusions, respectively (P < 0. 05, peripheral vs. intraportal). The net whole body nonhepatic glucose uptakes (in mg . kg-1 . min-1) were 1.6 +/- 0.1, 7.9 +/- 1.3, and 5.4 +/- 1.1 during baseline, peripheral, and intraportal glucose infusion, respectively (P < 0.05, peripheral vs. intraportal). In the liver, net glucose uptake was 70% greater during intraportal than during peripheral glucose infusion (5.8 +/- 0.7 vs. 3.4 +/- 0.4 mg . kg-1 . min-1). In conclusion, despite comparable glucose loads and insulin levels, hindlimb and whole body net nonhepatic glucose uptake decreased significantly during portal venous glucose infusion, suggesting that a negative a-pv glucose gradient leads to an inhibitory signal in nonhepatic tissues, among which skeletal muscle appears to be the most important.