Héctor Canales

Incidence and clinical effects of intra-abdominal hypertension in critically ill patients

Objective:The objective of this study was to determine the epidemiology and outcomes of intra-abdominal hypertension in a heterogeneous intensive care unit population. Design:This was a prospective cohort study. Setting:This study was conducted at a medical-surgical intensive care unit in a university hospital. Patients:Study patients included all those consecutively admitted during 9 months, staying >24 hrs, and requiring bladder catheterization. Measurements and Main Results:On admission, epidemiologic data and risk factors for intra-abdominal hypertension were studied; then, daily maximal and mean intra-abdominal pressures (IAPmax and IAPmean), abdominal perfusion pressure, fluid balances, filtration gradient, and sequential organ failure assessment score, were registered. IAPs were recorded through a bladder catheter every 6 hrs until death, discharge, or along 7 days. Intra-abdominal hypertension was defined as IAP ≥12 mm Hg. Abdominal compartment syndrome was defined as IAP ≥20 mm Hg plus ≥1 new organ failure. Main outcome measure was hospital mortality. Of 83 patients, considering IAPmax, 31% had intra-abdominal hypertension on admission and another 33% developed it after (23% and 31% with IAPmean). Main risk factors were mechanical ventilation, acute respiratory distress syndrome, and fluid resuscitation (relative risk, 5.26, 3.19, and 2.50, respectively). Patients with intra-abdominal hypertension were sicker, had higher mortality (53% vs. 27%, p = .02), and consistently showed higher total and renal sequential organ failure assessment score, daily and cumulative fluid balances, and lower filtration gradient. Nonsurvivors had higher IAPmax, IAPmean, and fluid balances and lower abdominal perfusion pressure. Abdominal compartment syndrome developed in 12%; 20% survived. Logistic regression identified IAPmax as an independent predictor of mortality (odds ratio, 1.17; 95% confidence interval, 1.05–1.30; p = .003) after adjusting with Acute Physiology and Chronic Health Evaluation II and comorbidities (odds ratio, 1.15; 95% confidence interval, 1.06–1.25; p = .001; and odds ratio, 2.68; 95% confidence interval, 1.27–5.67; p = .013, respectively). Models with IAPmean and abdominal perfusion pressure also performed well. Areas under receiver operating characteristic curves were .81 and .83. Conclusions:Intra-abdominal hypertension, diagnosed either with IAPmax or IAPmean, was frequent and showed an independent association with mortality. Intra-abdominal hypertension was significantly associated with more severe organ failures, particularly renal and respiratory, and a prolonged intensive care unit stay.

Clinical Characteristics and Outcomes of Obstetric Patients Requiring ICU Admission

OBJECTIVES To review a series of critically ill obstetric patients admitted to our ICU to assess the spectrum of disease, required interventions, and fetal/maternal mortality, and to identify conditions associated with maternal death. DESIGN Retrospective cohort. SETTING Medical-surgical ICU in a university-affiliated hospital. PATIENTS Pregnant/postpartum admissions between January 1, 1998, and September 30, 2005. INTERVENTIONS None. MEASUREMENTS AND RESULTS We studied 161 patients (age, 28 +/- 9 years; mean gestational age, 29 +/- 9 weeks) [mean +/- SD], constituting 10% of 1,571 hospital admissions. APACHE (acute physiology and chronic health evaluation) II score was 14 +/- 8, with 24% predicted mortality; sequential organ failure assessment score was 5 +/- 3; and therapeutic intervention scoring system at 24 h was 25 +/- 9. Forty-one percent of patients required mechanical ventilation (MV). ARDS, shock, and organ dysfunction were present in 19%, 25%, and 48% of patients, respectively. Most patients (63%) were admitted postpartum, and 74% of admissions were of obstetric cause. Hypertensive disease (40%), major hemorrhage (16%), septic abortion (12%), and nonobstetric sepsis (10%) were the principal diagnoses. Maternal mortality was 11%, with multiple organ dysfunction syndrome (44%) and intracranial hemorrhage (39%) as main causes. There were no differences in death rate in patients admitted for obstetric and nonobstetric causes. Fetal mortality was 32%. Only 30% of patients received antenatal care, which was more frequent in survivors (33% vs 6% nonsurvivors, p = 0.014). CONCLUSIONS Although ARDS, organ failures, shock, and use of MV were extremely frequent in this population, maternal mortality remains within an acceptable range. APACHE II overpredicted mortality in these patients. Septic abortion is still an important modifiable cause of mortality. Efforts should concentrate in increasing antenatal care, which was clearly underprovided in these patients.

Persistent villi hypoperfusion explains intramucosal acidosis in sheep endotoxemia.

Objective: To test the hypothesis that persistent villi hypoperfusion explains intramucosal acidosis after endotoxemic shock resuscitation. Design: Controlled experimental study. Setting: University-based research laboratory. Subjects: A total of 14 anesthetized, mechanically ventilated sheep. Interventions: Sheep were randomly assigned to endotoxin (n = 7) or control groups (n = 7). The endotoxin group received 5 &mgr;g/kg endotoxin, followed by 4 &mgr;g·kg−1·hr−1 for 150 mins. After 60 mins of shock, hydroxyethylstarch resuscitation was given to normalize oxygen transport for an additional 90 mins. Measurements and Main Results: Endotoxin infusion decreased mean arterial blood pressure, cardiac output, and superior mesenteric artery blood flow (96 ± 10 vs. 51 ± 20 mm Hg, 145 ± 30 vs. 90 ± 30 mL·min−1·kg−1, and 643 ± 203 vs. 317 ± 93 mL·min−1·kg−1, respectively; p < .05 vs. basal), whereas it increased intramucosal–arterial Pco2 (&Dgr;Pco2) and arterial lactate (3 ± 3 vs. 14 ± 8 mm Hg, and 1.5 ± 0.5 vs. 3.7 ± 1.3 mmol/L; p < .05). Sublingual, and serosal and mucosal intestinal microvascular flow indexes, and the percentage of perfused ileal villi were reduced (3.0 ± 0.1 vs. 2.3 ± 0.4, 3.2 ± 0.2 vs. 2.4 ± 0.6, 3.0 ± 0.0 vs. 2.0 ± 0.2, and 98% ± 3% vs. 76% ± 10%; p < .05). Resuscitation normalized mean arterial blood pressure (92 ± 13 mm Hg), cardiac output (165 ± 32 mL·min−1·kg−1), superior mesenteric artery blood flow (683 ± 192 mL·min−1·kg−1), and sublingual and serosal intestinal microvascular flow indexes (2.8 ± 0.5 and 3.5 ± 0.7). Nevertheless, &Dgr;Pco2, lactate, mucosal intestinal microvascular flow indexes, and percentage of perfused ileal villi remained altered (10 ± 6 mm Hg, 3.7 ± 0.9 mmol/L, 2.3 ± 0.4, and 78% ± 11%; p < .05). Conclusions: In this model of endotoxemia, fluid resuscitation corrected both serosal intestinal and sublingual microcirculation but was unable to restore intestinal mucosal perfusion. Intramucosal acidosis might be due to persistent villi hypoperfusion.

International study on microcirculatory shock occurrence in acutely ill patients

Objectives:Microcirculatory alterations are associated with adverse outcome in subsets of critically ill patients. The prevalence and significance of microcirculatory alterations in the general ICU population are unknown. We studied the prevalence of microcirculatory alterations in a heterogeneous ICU population and its predictive value in an integrative model of macro- and microcirculatory variables. Design:Multicenter observational point prevalence study. Setting:The Microcirculatory Shock Occurrence in Acutely ill Patients study was conducted in 36 ICUs worldwide. Patients:A heterogeneous ICU population consisting of 501 patients. Interventions:None. Measurements and Main Results:Demographic, hemodynamic, and laboratory data were collected in all ICU patients who were 18 years old or older. Sublingual Sidestream Dark Field imaging was performed to determine the prevalence of an abnormal capillary microvascular flow index (< 2.6) and its additional value in predicting hospital mortality. In 501 patients with a median Acute Physiology and Chronic Health Evaluation II score of 15 (10–21), a Sequential Organ Failure Assessment score of 5 (2–8), and a hospital mortality of 28.4%, 17% exhibited an abnormal capillary microvascular flow index. Tachycardia (heart rate > 90 beats/min) (odds ratio, 2.71; 95% CI, 1.67–4.39; p < 0.001), mean arterial pressure (odds ratio, 0.979; 95% CI, 0.963–0.996; p = 0.013), vasopressor use (odds ratio, 1.84; 95% CI, 1.11–3.07; p = 0.019), and lactate level more than 1.5 mEq/L (odds ratio, 2.15; 95% CI, 1.28–3.62; p = 0.004) were independent risk factors for hospital mortality, but not abnormal microvascular flow index. In reference to microvascular flow index, a significant interaction was observed with tachycardia. In patients with tachycardia, the presence of an abnormal microvascular flow index was an independent, additive predictor for in-hospital mortality (odds ratio, 3.24; 95% CI, 1.30–8.06; p = 0.011). This was not true for nontachycardic patients nor for the total group of patients. Conclusions:In a heterogeneous ICU population, an abnormal microvascular flow index was present in 17% of patients. This was not associated with mortality. However, in patients with tachycardia, an abnormal microvascular flow index was independently associated with an increased risk of hospital death.

Effects of levosimendan and dobutamine in experimental acute endotoxemia: a preliminary controlled study

ObjectiveTo test the hypothesis that levosimendan increases systemic and intestinal oxygen delivery (DO2) and prevents intramucosal acidosis in septic shock.DesignProspective, controlled experimental study.SettingUniversity-based research laboratory.SubjectsNineteen anesthetized, mechanically ventilated sheep.InterventionsEndotoxin-treated sheep were randomly assigned to three groups: control (n = 7), dobutamine (10 μg/kg/min, n = 6) and levosimendan (100 μg/kg over 10 min followed by 100 μg/kg/h, n = 6) and treated for 120 min.Measurements and main resultsAfter endotoxin administration, systemic and intestinal DO2 decreased (24.6 ± 5.2 vs 15.3 ± 3.4 ml/kg/min and 105.0 ± 28.1 vs 55.8 ± 25.9 ml/kg/min, respectively; p < 0.05 for both). Arterial lactate and the intramucosal–arterial PCO2 difference (ΔPCO2) increased (1.4 ± 0.3 vs 3.1 ± 1.5 mmHg and 9 ± 6 vs 23 ± 6 mmHg mmol/l, respectively; p < 0.05). Systemic DO2 was preserved in the dobutamine-treated group (22.3 ± 4.7 vs 26.8 ± 7.0 ml/min/kg, p = NS) but intestinal DO2 decreased (98.9 ± 0.2 vs 68.0 ± 22.9 ml/min/kg, p < 0.05) and ΔPCO2 increased (12 ± 5 vs 25 ± 11 mmHg, p < 0.05). The administration of levosimendan prevented declines in systemic and intestinal DO2 (25.1 ± 3.0 vs 24.0 ± 6.3 ml/min/kg and 111.1 ± 18.0 vs 98.2 ± 23.1 ml/min/kg, p = NS for both) or increases in ΔPCO2 (7 ± 7 vs 10 ± 8, p = NS). Arterial lactate increased in both the dobutamine and levosimendan groups (1.6 ± 0.3 vs 2.5 ± 0.7 and 1.4 ± 0.4 vs. 2.9 ± 1.1 mmol/l, p = NS between groups).ConclusionsCompared with dobutamine, levosimendan increased intestinal blood flow and diminished intramucosal acidosis in this experimental model of sepsis.

The distinct clinical profile of chronically critically ill patients: a cohort study

IntroductionOur goal was to describe the epidemiology, clinical profiles, outcomes, and factors that might predict progression of critically ill patients to chronically critically ill (CCI) patients, a still poorly characterized subgroup.MethodsWe prospectively studied all patients admitted to a university-affiliated hospital intensive care unit (ICU) between 1 July 2002 and 30 June 2005. On admission, we recorded epidemiological data, the presence of organ failure (multiorgan dysfunction syndrome (MODS)), underlying diseases (McCabe score), acute respiratory distress syndrome (ARDS) and shock. Daily, we recorded MODS, ARDS, shock, mechanical ventilation use, lengths of ICU and hospital stay (LOS), and outcome. CCI patients were defined as those having a tracheotomy placed for continued ventilation. Clinical complications and time to tracheal decannulation were registered. Predictors of progression to CCI were identified by logistic regression.ResultsNinety-five patients (12%) fulfilled the CCI definition and, compared with the remaining 690 patients, these CCI patients were sicker (APACHE II, 21 ± 7 versus 18 ± 9 for non-CCI patients, p = 0.005); had more organ dysfunctions (SOFA 7 ± 3 versus 6 ± 4, p < 0.003); received more interventions (TISS 32 ± 10 versus 26 ± 8, p < 0.0001); and had less underlying diseases and had undergone emergency surgery more frequently (43 versus 24%, p = 0.001). ARDS and shock were present in 84% and 83% of CCI patients, respectively, versus 44% and 48% in the other patients (p < 0.0001 for both). CCI patients had higher expected mortality (38% versus 32%, p = 0.003), but observed mortality was similar (32% versus 35%, p = 0.59). Independent predictors of progression to CCI were ARDS on admission, APACHE II and McCabe scores (odds ratio (OR) 2.26, p < 0.001; OR 1.03, p < 0.01; and OR 0.34, p < 0.0001, respectively). Lengths of mechanical ventilation, ICU and hospital stay were 33 (24 to 50), 39 (29 to 55) and 55 (37 to 84) days, respectively. Tracheal decannulation was achieved at 40 ± 19 days.ConclusionCCI patients were a severely ill population, in which ARDS, shock, and MODS were frequent on admission, and who suffered recurrent complications during their stay. However, their prognosis was equivalent to that of the other ICU patients. ARDS, APACHE II and McCabe scores were independent predictors of evolution to chronicity.

Intramucosal–arterial PCO2 gap fails to reflect intestinal dysoxia in hypoxic hypoxia

IntroductionAn elevation in intramucosal–arterial PCO2 gradient (ΔPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO2 should not be altered.MethodsIn 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes.ResultsBoth progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO2 increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant).DiscussionIn this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO2 might be determined primarily by blood flow.

Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study.

IntroductionIncreased intramucosal–arterial carbon dioxide tension (PCO2) difference (ΔPCO2) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in ΔPCO2.MethodsIn 19 anesthetized and mechanically ventilated sheep, we measured cardiac output, superior mesenteric blood flow, lactate, gases, hemoglobin and oxygen saturations in arterial, mixed venous and mesenteric venous blood, and ileal intramucosal PCO2 by saline tonometry. Intestinal oxygen transport and consumption were calculated. After basal measurements, sheep were assigned to the following groups, for 120 min: (1) sham (n = 6), (2) normal blood flow (n = 7) and (3) increased blood flow (n = 6). Escherichia coli lipopolysaccharide (5 μg/kg) was injected in the last two groups. Saline solution was used to maintain blood flood at basal levels in the sham and normal blood flow groups, or to increase it to about 50% of basal in the increased blood flow group.ResultsIn the normal blood flow group, systemic and intestinal oxygen transport and consumption were preserved, but ΔPCO2 increased (basal versus 120 min endotoxemia, 7 ± 4 versus 19 ± 4 mmHg; P < 0.001) and metabolic acidosis with a high anion gap ensued (arterial pH 7.39 versus 7.35; anion gap 15 ± 3 versus 18 ± 2 mmol/l; P < 0.001 for both). Increased blood flow prevented the elevation in ΔPCO2 (5 ± 7 versus 9 ± 6 mmHg; P = not significant). However, anion-gap metabolic acidosis was deeper (7.42 versus 7.25; 16 ± 3 versus 22 ± 3 mmol/l; P < 0.001 for both).ConclusionsIn this model of endotoxemia, intramucosal acidosis was corrected by increased blood flow and so might follow tissue hypoperfusion. In contrast, anion-gap metabolic acidosis was left uncorrected and even worsened with aggressive volume expansion. These results point to different mechanisms generating both alterations.

Intestinal and sublingual microcirculation are more severely compromised in hemodilution than in hemorrhage

The alterations in O2 extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O2 from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco2 (ΔPco2). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution. Our hypothesis was that the unchanged ΔPco2 in hemodilution depends on the preservation of villi microcirculation. For this purpose, pentobarbital-anesthetized and mechanically ventilated sheep were submitted to stepwise hemodilution (n = 8), hemorrhage (n = 8), or no intervention (sham, n = 8). In both hypoxic groups, equivalent reductions in O2 consumption (V̇o2) were targeted. Microcirculation was assessed by videomicroscopy, intestinal ΔPco2 by air tonometry, and V̇o2 by expired gases analysis. Although cardiac output and superior mesenteric flow increased in hemodilution, from the very first step (Hb = 5.0 g/dl), villi functional vascular density and RBC velocity decreased (21.7 ± 0.9 vs. 15.9 ± 1.0 mm/mm(2) and 1,033 ± 75 vs. 850 ± 79 μm/s, P < 0.01). In the last stage (Hb = 1.2 g/dl), these variables were lower in hemodiution than in hemorrhage (11.1 ± 0.5 vs. 15.4 ± 0.9 mm/mm(2) and 544 ± 26 vs. 686 ± 70 μm/s, P < 0.01), and were associated with lower intestinal fractional O2 extraction (0.61 ± 0.04 vs. 0.79 ± 0.02, P < 0.01) but preserved ΔPco2 (5 ± 2 vs. 25 ± 4 mmHg, P < 0.01). Therefore, alterations in O2 extraction in hemodilution seemed related to microvascular shunting, not to fast RBC velocity. The severe microvascular abnormalities suggest that normal ΔPco2 was not dependent on CO2 washout by the villi microcirculation. Increased perfusion in deeper intestinal layers might be an alternative explanation.

Urinary bladder partial carbon dioxide tension during hemorrhagic shock and reperfusion: an observational study

IntroductionContinuous monitoring of bladder partial carbon dioxide tension (PCO2) using fibreoptic sensor technology may represent a useful means by which tissue perfusion may be monitored. In addition, its changes might parallel tonometric gut PCO2. Our hypothesis was that bladder PCO2, measured using saline tonometry, will be similar to ileal PCO2 during ischaemia and reperfusion.MethodSix anaesthetized and mechanically ventilated sheep were bled to a mean arterial blood pressure of 40 mmHg for 30 min (ischaemia). Then, blood was reinfused and measurements were repeated at 30 and 60 min (reperfusion). We measured systemic and gut oxygen delivery and consumption, lactate and various PCO2 gradients (urinary bladder–arterial, ileal–arterial, mixed venous–arterial and mesenteric venous–arterial). Both bladder and ileal PCO2 were measured using saline tonometry.ResultsAfter bleeding systemic and intestinal oxygen supply dependency and lactic acidosis ensued, along with elevations in PCO2 gradients when compared with baseline values (all values in mmHg; bladder ΔPCO2 3 ± 3 versus 12 ± 5, ileal ΔPCO2 9 ± 5 versus 29 ± 16, mixed venous–arterial PCO2 5 ± 1 versus 13 ± 4, and mesenteric venous–arterial PCO2 4 ± 2 versus 14 ± 4; P < 0.05 versus basal for all). After blood reinfusion, PCO2 gradients returned to basal values except for bladder ΔPCO2, which remained at ischaemic levels (13 ± 7 mmHg).ConclusionTissue and venous hypercapnia are ubiquitous events during low flow states. Tonometric bladder PCO2 might be a useful indicator of tissue hypoperfusion. In addition, the observed persistence of bladder hypercapnia after blood reinfusion may identify a territory that is more susceptible to reperfusion injury. The greatest increase in PCO2 gradients occurred in gut mucosa. Moreover, the fact that ileal ΔPCO2 was greater than the mesenteric venous–arterial PCO2 suggests that tonometrically measured PCO2 reflects mucosal rather than transmural PCO2. Ileal ΔPCO2 appears to be the more sensitive marker of ischaemia.