Predictability of adverse outcomes in hypertensive disorders of pregnancy: a multicenter prospective cohort study.

OBJECTIVES: To explore variables associated with adverse maternal/fetal/neonatal outcomes among pregnant/postpartum patients admitted to ICU for hypertensive disorders of pregnancy (HDP). METHODS: Multicenter, prospective, national cohort study. RESULTS: Variables independently associated with maternal/fetal/neonatal mortality among 172 patients were as follows: Acute Physiology and Chronic Health Evaluation-II (APACHE-II)(OR1.20[1.06-1.35]), gestational age (OR0.698[0.59-0.82]) and aspartate aminotransferase (AST)(OR1.004[1.001-1.006]). Positive likelihood ratio for headache, epigastric pain, and visual disturbances to predict composite adverse outcomes were 1.23(1.16-1.30), 0.76(0.59-1.02), and 1.1(0.98-1.2), respectively. CONCLUSIONS: Maternal/fetal mortality due to HDP was independently associated with severity of illness on admission, gestational age, and elevated AST. Accuracy of clinical symptoms to predict composite adverse outcomes was low.

Characteristics, Outcomes, and Predictability of Critically Ill Obstetric Patients: A Multicenter Prospective Cohort Study.

OBJECTIVE: To evaluate pregnant/postpartum patients requiring ICUs admission in Argentina, describe characteristics of mothers and outcomes for mothers/babies, evaluate risk factors for maternal-fetal-neonatal mortality; and compare outcomes between patients admitted to public and private health sectors. DESIGN: Multicenter, prospective, national cohort study. SETTING: Twenty ICUs in Argentina (public, 8 and private, 12). PATIENTS: Pregnant/postpartum (< 42 d) patients admitted to ICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Three hundred sixty-two patients were recruited, 51% from the public health sector and 49% from the private. Acute Physiology and Chronic Health Evaluation II was 8 (4-12); predicted/observed mortality, 7.6%/3.6%; hospital length of stay, 7 days (5-13 d); and fetal-neonatal losses, 17%. Public versus private health sector patients: years of education, 9 ± 3 versus 15 ± 3; transferred from another hospital, 43% versus 12%; Acute Physiology and Chronic Health Evaluation II, 9 (5-13.75) versus 7 (4-9); hospital length of stay, 10 days (6-17 d) versus 6 days (4-9 d); prenatal care, 75% versus 99.4%; fetal-neonatal losses, 25% versus 9% (p = 0.000 for all); and mortality, 5.4% versus 1.7% (p = 0.09). Complications in ICU were multiple-organ dysfunction syndrome (34%), shock (28%), renal dysfunction (25%), and acute respiratory distress syndrome (20%); all predominated in the public sector. Sequential Organ Failure Assessment (during first 24 hr of admission) score of at least 6.5 presented the best discriminative power for maternal mortality. Independent predictors of maternal-fetal-neonatal mortality were Acute Physiology and Chronic Health Evaluation II, education level, prenatal care, and admission to tertiary hospitals. CONCLUSIONS: Patients spent a median of 7 days in hospital; 3.6% died. Maternal-fetal-neonatal mortality was determined not only by acuteness of illness but to social and healthcare aspects like education, prenatal control, and being cared in specialized hospitals. Sequential Organ Failure Assessment (during first 24 hr of admission), easier to calculate than Acute Physiology and Chronic Health Evaluation II, was a better predictor of maternal outcome. Evident health disparities existed between patients admitted to public versus private hospitals: the former received less prenatal care, were less educated, were more frequently transferred from other hospitals, were sicker at admission, and developed more complications; maternal and fetal-neonatal mortality were higher. These findings point to the need of redesigning healthcare services to account for these inequities.

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

INTRODUCTION: Increased intramucosal-arterial carbon dioxide tension (PCO2) difference (DeltaPCO2) 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 DeltaPCO2. METHODS: In 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 microg/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. RESULTS: In the normal blood flow group, systemic and intestinal oxygen transport and consumption were preserved, but DeltaPCO2 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 DeltaPCO2 (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). CONCLUSIONS: In 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.

Intramucosal-arterial Pco2 gradient does not reflect intestinal dysoxia in anemic hypoxia.

BACKGROUND: An increase in intramucosal-arterial Pco2 gradient (DeltaPco2) might be caused by tissue hypoxia or by diminished blood flow. Our hypothesis was that DeltaPco2 should not be altered in anemic hypoxia with preserved blood flow. METHODS: In 18 anesthetized, mechanically ventilated sheep, oxygen transport was stepwise reduced by hemorrhage (hypovolemia, n = 9) or by hemorrhage and simultaneous dextran infusion (hemodilution, n = 9). RESULTS: Hypovolemia and hemodilution produced comparable decreases in systemic and intestinal oxygen transport and uptake. However, mixed venoarterial and mesenteric venoarterial Pco2 gradients and DeltaPco2 were significantly higher in hypovolemia than in hemodilution (25 +/- 5 vs. 10 +/- 2 mm Hg; 21 +/- 6 vs. 10 +/- 5 mm Hg; and 41 +/- 18 vs. 14 +/- 9 mm Hg, respectively; p < 0.01). CONCLUSION: DeltaPco2 did not reflect intestinal dysoxia during Vo2/Do2 dependency attributable to hemodilution. Blood flow seems to be the main determinant of DeltaPco2.

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

INTRODUCTION: An elevation in intramucosal-arterial PCO2 gradient (DeltaPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, DeltaPCO2 should not be altered. METHODS: In 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 DeltaPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. RESULTS: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. DeltaPCO2 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). DISCUSSION: In this experimental model of hypoxic hypoxia with preserved blood flow, DeltaPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that DeltaPCO2 might be determined primarily by blood flow.