Ruy Jorge Cruz

Increases in fines and driver licence withdrawal have effectively reduced immediate deaths from trauma on Brazilian roads: first-year report on the new traffic code

Road accidents are a major cause of death in Brazil, with rates increasing steadily for years. Our objective here is to report the impact of the new Brazilian Traffic Code, introduced in 1998. Its main new features include a large increase in fines and a rigid penalty scoring system that leads to driver license withdrawal. Speed limits have actually been raised on many roads, but adherence to the rules has been monitored more closely. We compare the incidence of injured patients and immediate deaths in road accidents and emergency room admissions to a level I trauma centre in downtown São Paulo between January and December 1998 with corresponding data from between January and December 1997. There was an overall 21.3% reduction in the number of accidents and a 24.7% reduction in immediate deaths, saving 5962 lives on Brazilian highways. Tickets issued fell by 49.5% (601977 during 1997 to 304785 during 1998). Motor vehicle accident-related emergency room admissions decreased by 33.2%. We conclude that very costly tickets and threatened driver licences have proved very effective in decreasing immediate deaths from trauma. Further advances in educational programmes associated with road and vehicle safety measures are likely to provide the much needed further reduction in the still high trauma mortality on Brazilian roads and streets.

Small volume of hypertonic saline as the initial fluid replacement in experimental hypodynamic sepsis

IntroductionWe conducted the present study to examine the effects of hypertonic saline solution (7.5%) on cardiovascular function and splanchnic perfusion in experimental sepsis.MethodsAnesthetized and mechanically ventilated mongrel dogs received an intravenous infusion of live Escherichia coli over 30 minutes. After 30 minutes, they were randomized to receive lactated Ringers solution 32 ml/kg (LR; n = 7) over 30 minutes or 7.5% hypertonic saline solution 4 ml/kg (HS; n = 8) over 5 minutes. They were observed without additional interventions for 120 minutes. Cardiac output (CO), mean arterial pressure (MAP), portal and renal blood flow (PBF and RBF, respectively), gastric partial pressure of CO2 (pCO2; gas tonometry), blood gases and lactate levels were assessed.ResultsE. coli infusion promoted significant reductions in CO, MAP, PBF and RBF (approximately 45%, 12%, 45% and 25%, respectively) accompanied by an increase in lactate levels and systemic and mesenteric oxygen extraction (sO2ER and mO2ER). Widening of venous-arterial (approximately 15 mmHg), portal-arterial (approximately 18 mmHg) and gastric mucosal-arterial (approximately 55 mmHg) pCO2 gradients were also observed. LR and HS infusion transiently improved systemic and regional blood flow. However, HS infusion was associated with a significant and sustained reduction of systemic (18 ± 2.6 versus 38 ± 5.9%) and mesenteric oxygen extraction (18.5 ± 1.9 versus 36.5 ± 5.4%), without worsening other perfusional markers.ConclusionA large volume of LR or a small volume of HS promoted similar transient hemodynamic benefits in this sepsis model. However, a single bolus of HS did promote sustained reduction of systemic and mesenteric oxygen extraction, suggesting that hypertonic saline solution could be used as a salutary intervention during fluid resuscitation in septic patients.

Effects of volume resuscitation on splanchnic perfusion in canine model of severe sepsis induced by live Escherichia coli infusion

IntroductionWe conducted the present study to investigate whether early large-volume crystalloid infusion can restore gut mucosal blood flow and mesenteric oxygen metabolism in severe sepsis.MethodsAnesthetized and mechanically ventilated male mongrel dogs were challenged with intravenous injection of live Escherichia coli (6 × 109 colony-forming units/ml per kg over 15 min). After 90 min they were randomly assigned to one of two groups – control (no fluids; n = 13) or lactated Ringers solution (32 ml/kg per hour; n = 14) – and followed for 60 min. Cardiac index, mesenteric blood flow, mean arterial pressure, systemic and mesenteric oxygen-derived variables, blood lactate and gastric carbon dioxide tension (PCO2; by gas tonometry) were assessed throughout the study.ResultsE. coli infusion significantly decreased arterial pressure, cardiac index, mesenteric blood flow, and systemic and mesenteric oxygen delivery, and increased arterial and portal lactate, intramucosal PCO2, PCO2 gap (the difference between gastric mucosal and arterial PCO2), and systemic and mesenteric oxygen extraction ratio in both groups. The Ringers solution group had significantly higher cardiac index and systemic oxygen delivery, and lower oxygen extraction ratio and PCO2 gap at 165 min as compared with control animals. However, infusion of lactated Ringers solution was unable to restore the PCO2 gap. There were no significant differences between groups in mesenteric oxygen delivery, oxygen extraction ratio, or portal lactate at the end of study.ConclusionSignificant disturbances occur in the systemic and mesenteric beds during bacteremic severe sepsis. Although large-volume infusion of lactated Ringers solution restored systemic hemodynamic parameters, it was unable to correct gut mucosal PCO2 gap.

Short-lasting systemic and regional benefits of early crystalloid infusion after intravenous inoculation of dogs with live Escherichia coli

We investigated the systemic and regional hemodynamic effects of early crystalloid infusion in an experimental model of septic shock induced by intravenous inoculation with live Escherichia coli. Anesthetized dogs received an intravenous infusion of 1.2 x 10(10) cfu/kg live E. coli in 30 min. After 30 min of observation, they were randomized to controls (no fluids; N = 7), or fluid resuscitation with lactated Ringers solution, 16 ml/kg (N = 7) or 32 ml/kg (N = 7) over 30 min and followed for 120 min. Cardiac index, portal blood flow, mean arterial pressure, systemic and regional oxygen-derived variables, blood lactate, and gastric PCO2 were assessed. Rapid and progressive cardiovascular deterioration with reduction in cardiac output, mean arterial pressure and portal blood flow (approximately 50, approximately 25 and approximately 70%, respectively) was induced by the live bacteria challenge. Systemic and regional territories showed significant increases in oxygen extraction and in lactate levels. Significant increases in venous-arterial (approximately 9.6 mmHg), portal-arterial (approximately 12.1 mmHg) and gastric mucosal-arterial (approximately 18.4 mmHg) PCO2 gradients were also observed. Early fluid replacement, especially with 32 ml/kg volumes of crystalloids, promoted only partial and transient benefits such as increases of approximately 76% in cardiac index, of approximately 50% in portal vein blood flow and decreases in venous-arterial, portal-arterial, gastric mucosal-arterial PCO2 gradients (7.2 +/- 1.0, 7.2 +/- 1.3 and 9.7 +/- 2.5 mmHg, respectively). The fluid infusion promoted only modest and transient benefits, unable to restore the systemic and regional perfusional and metabolic changes in this hypodynamic septic shock model.

Systemic and regional effects of supraceliac aortic occlusion during experimental hepatic vascular exclusion

BACKGROUND Supraceliac aortic occlusion (AO) has been recommended to avoid hypotension during hepatic vascular exclusion (HVE). We hypothesized that AO may negatively affect splanchnic perfusion during HVE. METHODS Twenty-six dogs (16 +/- 0.3 kg) were randomly assigned to HVE (n = 13) or HVE+AO (n = 13), during 30 minutes followed by a 60-minute reperfusion period. Cardiac output (CO), mean arterial pressure (MAP), superior mesenteric artery blood flow (SMABF, ultrasonic flowprobe), gastric mucosal PCO(2) (gas tonometry) and PCO(2)-gap were evaluated. RESULTS HVE alone induced decreases in MAP from 115 +/- 5.1 to 26 +/- 1 mm Hg, in CO from 2.0 +/- 0.1 to 0.4 +/- 0.1 L/min and SMABF from 398 +/- 42 to 16 +/- 7.6 mL/min, while PCO(2) gap increased from 4 +/- 3.7 to 52 +/- 5.4 mm Hg. Supraceliac aortic occlusion only avoided severe hypotension. During reperfusion MAP, CO, and SMABF were partially restored, while PCO(2) gap showed no improvements in either group. CONCLUSIONS HVE promotes major systemic and splanchnic perfusional derangement. Concomitant AO may avoid HVE-induced hypotension without producing further deleterious effects.

Effects of Intra-Aortic Balloon Occlusion on Intestinal Perfusion, Oxygen Metabolism and Gastric Mucosal PCO2 during Experimental Hemorrhagic Shock

Background: Aortic occlusion has been suggested for the initial treatment of severe uncontrolled hemorrhagic shock. Our objective is to determine the impact of aortic occlusion, during hemorrhagic shock, on splanchnic mucosal perfusion and to correlate these findings with other systemic and regional markers of splanchnic ischemia. Methods: Fourteen dogs (17 ± 1.7 kg) anesthetized with pentobarbital were bled to a mean arterial pressure (MAP) of 40 mm Hg. After 30 min, the animals were randomly assigned to controls (no aortic occlusion, n = 7) and transfemoral aortic occlusion (TAO) at T9 level (n = 7). Superior mesenteric artery blood flow (SMABF, ultrasonic flow probe), gastric mucosal PCO2 (gastric tonometry) and splanchnic oxygen extraction ratio (O2ERsplanc) were evaluated for 120 min. Results:Hemorrhage caused a marked reduction in SMABF and increases in PCO2-gap and O2ERsplanc in both groups. TAO significantly improved MAP and further increased the PCO2-gap and O2ERsplanc, with a decreased SMABF. After reperfusion, SMABF, MAP and O2ERsplanc returned to pre-occlusion values, although the PCO2-gap remained higher in the TAO group. Conclusion: Aortic occlusion promotes blood pressure restoration with an additional insult to mucosal perfusion, which could be adequately predicted by global and/or splanchnic oxygen-derived variables during ischemia, but not during the early reperfusion period.

Gas tonometry for evaluation of gastrointestinal mucosal perfusion: experimental models of trauma, shock and complex surgical maneuvers - Part 1

Evidencias clinicas e experimentais substanciais indicam que o territorio circulatorio mesenterico, principalmente na mucosa intestinal, e altamente vulneravel a reducao na oferta de oxigenio e predisposto a lesao precoce na presenca de alteracoes hemodinâmicas induzidas por trauma, choque, sepse e diversas manobras cirurgicas complexas. A hipoxia ou isquemia intestinal e um dos possiveis mecanismos contribuintes para a disfuncao da barreira gastrointestinal que pode estar associada com o desenvolvimento da resposta inflamatoria sistemica e com a sindrome da disfuncao de multiplos orgaos, causa comum de morte apos trauma, sepse ou cirurgias de grande porte. Monitorar a perfusao intestinal em experimentos pode fornecer dados valiosos quanto a novas intervencoes e tratamentos altamente necessarios para reduzir a morbidade e mortalidade extremamente elevadas no trauma e na sepse. Apresentamos nossa experiencia com a tonometria a gas como monitor da adequacao da perfusao da mucosa gastrointestinal clinica e experimental, em modelos de trauma, sepse, e manobras cirurgicas complexas tais como a oclusao da aorta e a exclusao vascular hepatica.

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

BACKGROUND Acute mesenteric ischemia is a potentially fatal vascular emergency with mortality rates ranging between 60% and 80%. Several studies have extensively examined the hemodynamic and metabolic effects of superior mesenteric artery occlusion. On the other hand, the cardiocirculatory derangement and the tissue damage induced by intestinal outflow obstruction have not been investigated systematically. For these reasons we decided to assess the initial impact of venous mesenteric occlusion on intestinal blood flow distribution, and correlate these findings with other systemic and regional perfusion markers. METHODS Fourteen mongrel dogs were subjected to 45 min of superior mesenteric artery (SMAO) or vein occlusion (SMVO), and observed for 120 min after reperfusion. Systemic hemodynamics were evaluated using Swan-Ganz and arterial catheters. Regional blood flow (ultrasonic flow probes), intestinal O(2)-derived variables, and mesenteric-arterial and tonometric-arterial pCO(2) gradients (D(mv-a)pCO(2) and D(t-a)pCO(2)) were also calculated. RESULTS SMVO was associated with hypotension and low cardiac output. A significant increase in the regional pCO(2) gradients was also observed in both groups during the ischemic period. After reperfusion, a progressive reduction in D(mv-a)pCO(2) occurred in the SMVO group; however, no improvement in D(t-a)pCO(2) was observed. The histopathologic injury scores were 2.7 +/- 0.5 and 4.8 +/- 0.2 for SMAO and SMVO, respectively. CONCLUSIONS SMV occlusion promoted early and significant hemodynamic and metabolic derangement at systemic and regional levels. Additionally, systemic pCO(2) gradient is not a reliable parameter to evaluate the local intestinal oxygenation. Finally, the D(t-a)pCO(2) correlates with histologic changes during intestinal congestion or ischemia. However, minor histologic changes cannot be detected using this methodology.

Sustained Gastric Mucosal Acidosis After Hemorrhage in Spite of Rapid Hemodynamic Restoration With Blood or Hypertonic/Hyperoncotic Solution

Splanchnic hypoperfusion has been implicated as the motor of multiple organ dysfunction. Hypertonic saline has shown to benefit microcirculatory blood flow. In hemorrhaged animals, we tested the hypothesis that small-volume 3% NaCl/10% dextran 40 (3%HSD) promotes global and regional improvements, including gastric mucosal acidosis reversal. Seventeen dogs (18.8 ± 1.2 kg) were bled (20 mL/min) to a mean arterial pressure of 40–45 mm Hg, which was maintained at these levels for 15 min. They were randomly assigned to two groups: Blood (n = 9), total shed blood retransfused at 40 mL/min; or a 4-min bolus injection of 3%HSD (n = 8), in a volume equivalent to 25% of total shed blood. All animals were followed for 30 min thereafter. Gastric mucosal PCO2 (gas tonometry), portal vein PCO2, superior mesenteric artery blood flow (SMA, ultrasonic flowprobes), and systemic and regional O2-derived variables were evaluated throughout the protocol. Hemorrhage induced significant reductions of arterial pressure, cardiac output, and SMA blood flow, while portal–arterial and gastric–arterial PCO2 gradients increased. Total shed blood transfusion, as well as 3%HSD bolus injection, promptly restored all parameters, except for the increased gastric–arterial PCO2 gradient. We conclude that persistent gastric mucosal acidosis cannot be adequately predicted by global and splanchnic O2 derived variables in following hemorrhage and resuscitation with total shed blood transfusion or small-volume hypertonic–hyperoncotic solution.

Radioisotope blood volume measurement in uncontrolled retroperitoneal haemorrhage induced by a transfemoral iliac artery puncture

Standard-of-care, large volume crystalloid infusion, in the setting of uncontrolled bleeding, has been challenged and it is not known if fluid resuscitation increases retroperitoneal hemorrhage. We developed an experimental model of retroperitoneal haemorrhage to correlate haemodynamic and metabolic alterations with the blood volume loss. Anaesthetised, spontaneously breathing dogs (17.1+/-0.56 kg) were randomised to unilateral (UL, n=11) or bilateral (BL, n=11) iliac artery puncture, using a metallic device introduced through the femoral arteries and followed for 120 min. Initial and final blood volumes were determined using radioactive tracers, 99mTC and 51Cr, respectively. UL was associated with a stable arterial pressure and a moderate decrease in cardiac output and oxygen delivery. BL induced an abrupt and sustained decrease in mean arterial pressure, from 131.9+/-5.9 to 88.6+/-10.8 mmHg, and a much greater reduction in cardiac output, oxygen delivery and consumption than UL throughout the experiment. Total retroperitoneal blood loss after BL was 36.8+/-3.2 ml/kg, while after UL was 25.1+/-3.4 ml/kg (P=0.0262). We conclude that a transfemoral bilateral iliac artery puncture produces a clinically relevant model of uncontrolled retroperitoneal haemorrhage, with hypotension and low flow state, while a unilateral iliac artery lesion causes a compensated shock state.