We report the results of adapting medical therapy to the monitoring of hemodynamic response in the prevention of a first variceal bleeding or rebleeding in patients with cirrhosis. Hepatic venous pressure gradient (HVPG) was measured before and after propranolol was initiated. The patients were considered responders if HVPG decreased below 12 mm Hg or at least 20% as compared with baseline value. If patients were not responders, isosorbide-5 mononitrate (I-5MN) was added, and a third hemodynamic study was performed. Thereafter, the patients were followed for a mean of 28 months. Thirty-four consecutive patients were treated to prevent a first bleeding episode in 20 patients and a rebleeding in 14 patients.H W G value was initially 19.8 2 4.6 mm Hg and decreased to 17.6 +-5.7 mm Hg (P < .05) after propranolol alone. Thirteen patients (38%) were responders to propranolol. I-5MN improved hemodynamic response in 7 cases. Among these 20 (59%) hemodynamic responders, only 2 (10%) experienced variceal bleeding, as compared with 9 of 14 (64%) nonresponders (P c .05). Using multivariate analysis, only hemodynamic response was found to have an independent predictive value for the risk of variceal bleeding. In conclusion, hemodynamic response to drug therapy identifies patients who are efficiently protected from variceal bleeding as well as nonresponders in whom an alternative treatment should be T rebleeding has been demonstrated by multiple studies and metaanalyses.'J However, some of the patients still experience bleeding while undergoing treatment. Should such a subgroup be identified, the patients could be offered alternative treatment.It was shown more than 25 years ago that hepatic venous pressure gradient (HVPG) has to be higher than 12 mm Hg for variceal bleeding to occur. Toulouse, 31059, France. E-mail. BUREAU. C@cbu-toulouse.j;j%x: (33) -9139/02/3606-0010$3~. OO/O doi:lO. 1053-9139/02/3606-0010$3~. OO/O doi:lO. (ihep.2002 several studies have demonstrated that, whenever drug therapy reduces HVPG below 12 mm Hg4 or by 20% or more of its pretreatment value,5-7 bleeding risk is very effectively prevented. This can be achieved with propran-O I O I ,~>~J the effects of which can be increased by adding isosorbide-5 mononitrate (I-5MN) .h.8,9 Furthermore, the Reston Consensus Conference recommended the monitoring of HVPG in patients with cirrhosis, who need to be treated to prevent either bleeding or rebleeding.'O To our knowledge, the results of such an approach have never been reported. We considered that those recommendations should be followed to improve the results of medical management of portal hypertension and hereby report our preliminary experience. 0270
The aim of this study was to investigate the influence of different strategies of blood volume restitution in the outcome of portal hypertension-related bleeding in anesthetized cirrhotic rats. Gastrointestinal hemorrhage was induced by sectioning a first order branch of the ileocolic vein in 38 cirrhotic rats (common bile duct ligation and occlusion). The subsequent hypovolemic shock was treated with no transfusion (n ؍ 17), moderate transfusion (50% of expected blood loss, 5 mL, n ؍ 11), and total transfusion (100% of expected blood loss, 10 mL, n ؍ 10). At the end of the blood transfusion period (minute 15), mean arterial pressure (MAP) partially recovered in rats receiving moderate transfusion or no transfusion but decreased in the 10-mL transfusion group (212 ؎ 43%, P < .05 vs. no transfusion and 5 mL transfusion). After transfusion, groups given no or 5 mL transfusion remained hemodynamically stable. However, rats receiving 10 mL transfusion continued to deteriorate with persistent bleeding and progressive fall in MAP (265 ؎ 12%; P < .05 vs. no transfusion and 5 mL transfusion). Collected blood loss was significantly greater in the 10-mL group (20.0 ؎ 1.5 g) than in groups given 5 mL (15.9 ؎ 2.8 g; P < .05) or no transfusion (13.2 ؎ 2.1 g; P < .05 vs. 10 mL and 5 mL transfusion). Survival in the no transfusion group was 47%. Rats given 5-mL transfusion had 64% survival. The worst survival was observed in the 10-mL transfusion group (0% survival; P < .05). We concluded that a transfusion policy aimed at completely replacing blood loss worsens the magnitude of bleeding and mortality from portal hypertensive-related bleeding in cirrhotic rats. On the contrary, moderate blood transfusion allowed hemodynamic stabilization and increased survival. Bleeding from esophageal varices is a frequent and severe complication of portal hypertension in patients with cirrhosis. An important part of the treatment of variceal bleeding is the general management of hypovolemic shock, in which blood volume replacement represents a crucial step. 1 However, there is little information on how blood volume restitution should be done. There is a general concern as to avoiding over transfusion, 1,2 since it is known that plasma volume expansion increases portal pressure in patients with portal hypertension. [3][4][5] The blood volume dependency of portal pressure is further illustrated by the fact that depletion of blood volume during hemorrhage or lymph drainage lowers portal pressure. 6 In addition, studies in portal hypertensive rat models have shown that blood volume restitution following a hemorrhage produces an increase of portal pressure beyond baseline values, which is not observed in normal rats, 4,5,7 suggesting that total blood volume restitution, even if not causing an expansion of the blood volume above prehemorrhage values, may have detrimental effects when correcting hypovolemia in portal hypertensive animals.The present study addressed these issues by investigating the effects of different schedules of blood volu...
We report the results of adapting medical therapy to the monitoring of hemodynamic response in the prevention of a first variceal bleeding or rebleeding in patients with cirrhosis. Hepatic venous pressure gradient (HVPG) was measured before and after propranolol was initiated. The patients were considered responders if HVPG decreased below 12 mm Hg or at least 20% as compared with baseline value. If patients were not responders, isosorbide-5 mononitrate (I-5MN) was added, and a third hemodynamic study was performed. Thereafter, the patients were followed for a mean of 28 months. Thirty-four consecutive patients were treated to prevent a first bleeding episode in 20 patients and a rebleeding in 14 patients. HVPG value was initially 19.8 +/- 4.6 mm Hg and decreased to 17.6 +/- 5.7 mm Hg (P <.05) after propranolol alone. Thirteen patients (38%) were responders to propranolol. I-5MN improved hemodynamic response in 7 cases. Among these 20 (59%) hemodynamic responders, only 2 (10%) experienced variceal bleeding, as compared with 9 of 14 (64%) nonresponders (P <.05). Using multivariate analysis, only hemodynamic response was found to have an independent predictive value for the risk of variceal bleeding. In conclusion, hemodynamic response to drug therapy identifies patients who are efficiently protected from variceal bleeding as well as nonresponders in whom an alternative treatment should be considered.
We studied the incidence of gastro-oesophageal reflux (GOR) during general anaesthesia with the laryngeal mask airway (LMA) in a paediatric population with two ventilatory regimes: spontaneous breathing and controlled mechanical ventilation (CMV). Thirty children between 6 months and 15 years, ASA I-II, for routine surgery, were randomly assigned in two groups: spontaneous ventilation (n=14), and CMV (n=16). A pH probe was situated in the central third of the oesophagus. Some 66% of the patients breathing spontaneously had GOR episodes vs. 92% of the patients with CMV (P < 0,01). Reflux took place mainly after LMA removal (21% vs. 68%; P < 0,01) and in the Postanaesthetic Care Unit (PACU) (29% vs. 43%; P < 0,05). There was a high incidence of GOR during general anaesthesia and in the PACU in paediatric patients anaesthetized with the LMA. GOR episodes were significantly more evident in the CMV group, mainly after LMA removal, but without clinical significance.
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