Analysis of the venous thromboembolic risk associated with severe postpartum haemorrhage in the NOHA First cohort.

Severe postpartum haemorrhages (PPH) are responsible for maternal morbidity/mortality. Their complex management sometimes requires haemostatic supplementation, and therapeutic trials on fibrinogen or activated factor VII, which may add to the thrombotic risk, are currently being considered. Furthermore, there is a risk of venous thromboembolism (VTE) during the postpartum period, hence we studied the relationship between severe PPH and VTE in women during their first pregnancy. Among the 32,463 women enrolled between January 1, 1999 and February 1, 2004 in the NOHA First cohort, 317 developed severe PPH, 11 postpartum VTE and 60 had postpartum superficial vein thrombosis (SVT). In the women with severe PPH, whilst there were no episodes of VTE, there were three episodes of SVT, which occurred 6 weeks postpartum. All of the women with severe PPH received packed red blood cell (RBC) units, 29 (9.1%) platelets units, 51 (16.1%) fresh frozen plasma and 29 (9.1%) fibrinogen concentrates. Three patients with both severe PPH and SVT received only packed RBC. Severe PPH or packed RBC unit transfusion were associated with postpartum SVT (adjusted relative risk: 5.3 (1.6-17) and 4.7 (1.5-15) respectively), independent of caesarean section delivery and low-molecular-weight heparin (LMWH) use in the postpartum, but were not independent indicators of one another. This the VTE and SVT risks associated with severe PPH are low (<1% and <2%, respectively). Severe PPH increases the risk of postpartum SVT, but transfusion with platelet units and plasma supplementation using fresh frozen plasma or fibrinogen concentrates do not markedly modulate the risk of venous thrombosis.

Experimental model for comparative evaluation of pharmacologically induced vasodilation of arterial wall mechanical properties.

Arterial wall compliance (C) and distensibility coefficient (DC) are key factors of pathologic physiology, especially in arteries less than 2 mm in diameter. The aim of this study was to design an experimental model allowing comparative measurement of C and DC during pharmacologically induced vasodilation on small-diameter arteries. Both femoral arteries were exposed in eight New Zealand White rabbits. Diameter (d) and systolic/diastolic diameter changes (deltad) were measured simultaneously, and C and DC were calculated before and after topical application of 1 mL of 4% papaverine on the right side and topical application of 1 mL of 1% lidocaine on the left side. Diameter measurements were performed by echo tracking with 20-MHz implanted microprobes. After papaverine and lidocaine application, respectively, d increased from 1.36 mm to 2.23 mm (P < 0.0001) and from 1.45 mm to 2.4 mm (P < 0.0001), deltad increased from 0.0568 mm to 0.0571 mm (P = 0.34) and from 0.064 mm to 0.077 mm (P < 0.01), C increased from 5.7 x 10(-3) mm/mm Hg to 6 x 10(-3) mm/mm Hg (P < 0.02) and from 6.23 x 10(-3) mm/mm Hg to 8.49 x 10(-3) mm/mm Hg (P < 0.01), and DC decreased from 4.22 x 10(-3) mm Hg(-1) to 2.61 x 10(-3) mm Hg(-1) (P < 0.0004) and from 4.36 x 10(-3) mm/mm Hg to 3.46 x 10(-3) mm/mm Hg (P < 0.005). Papaverine- and lidocaine-induced changes were significantly different for deltad, C, and DC (P < 0.01). These results suggest that, unlike that with papaverine, lidocaine-induced vasodilation leads the artery up to the nonlinear part of its pressure/diameter relationship, with decreased distensibility contrasting with increased diameter and compliance. Our experimental model may be useful to compare the effects of different vasoactive drugs at different concentrations on the mechanical properties of the arterial wall.

Regional blood flows are affected differently by PEEP when the abdomen is open or closed: an experimental rabbit model.

OBJECTIVE: The study of induced circulatory changes requires simultaneous assessment of multiple regional circulations because of interactions and compensatory mechanisms. Positive end expiratory pressure mechanical ventilation (PEEP) is known to cause marked, and potentially deleterious, cardiovascular changes. Our aim was to use a comprehensive approach to assess PEEP-induced circulatory changes in open vs closed abdomen animals. MATERIAL AND METHODS: In the anesthetized rabbit, we used implantable Doppler micro-probes to measure blood flow simultaneously in the ascending aorta, inferior vena cava, portal vein, hepatic artery, common carotid artery, and renal artery. We studied spontaneously breathing animals (Group A), and open (Group B) and closed abdomen (Group C) animals mechanically ventilated at 0 (ZEEP) and 12 cm H(2)O PEEP. RESULTS: In Group A, all biological and hemodynamic variables remained unchanged for three hours at the end of the surgical procedure. In Groups B and C, ZEEP produced no significant hemodynamic change. PEEP induced a decrease in carotid, hepatic, and renal artery blood flow in Groups B and C, a decrease in heart rate and mean arterial blood pressure in Group B, and a decrease in aorta blood flow in Group C. CONCLUSIONS: These experimental results demonstrate the usefulness of the comprehensive approach of circulatory changes, and confirm that PEEP may have deleterious effects on regional blood flow, even without significant change in cardiac output, especially when the abdomen is open.