Maternal haemorrhage.

Maternal haemorrhage is the leading cause of preventable maternal death worldwide and encompasses antepartum, intrapartum, and postpartum bleeding. This review highlights factors that predispose to severe bleeding, its management, and the most recent treatment and guidelines. Advances in obstetric care have provided physicians with the diagnostic tools to detect, anticipate, and prevent severe life-threatening maternal haemorrhage in most patients who have had prenatal care. In an optimal setting, patients at high risk for haemorrhage are referred to tertiary care centres where multidisciplinary teams are prepared to care for and deal with known potential complications. However, even with the best prenatal care, unexpected haemorrhage occurs. The first step in management is stabilization of haemodynamic status, which involves securing large bore i.v. access, invasive monitoring, and aggressive fluid management and transfusion therapy. Care for the patient with maternal bleeding should follow an algorithm that goes through a rapid and successive sequence of medical and surgical approaches to stem bleeding and decrease morbidity and mortality. With the addition of potent uterotonic agents and the advent of minimally invasive interventional radiological techniques such as angiographic embolization and arterial ligation, definitive yet conservative management is now possible in an attempt to avoid hysterectomy in patients with severe peripartum bleeding. If these interventions are inadequate to control the bleeding, the decision to proceed to hysterectomy must be made expeditiously. Recombinant factor VIIa is a relatively new treatment that could prove useful for severe coagulopathy and intractable bleeding.

Difficult airway in a patient with Coffin-Siris syndrome.

We report on a patient with Coffin-Siris syndrome and consider a potential association between this condition and difficult intubation. Although this inherited condition is extremely rare, anesthesiologists should be aware of its existence and prepare for potential airway management problems whenever it is encountered.

Comparative systemic toxicity of ropivacaine and bupivacaine in nonpregnant and pregnant ewes.

BACKGROUND: Ropivacaine is a new amide local anesthetic, having therapeutic properties similar to those of bupivacaine but with a wider margin of safety. Bupivacaine is probably the most commonly used drug in obstetric epidural analgesia, even though laboratory studies have suggested that pregnancy increases the cardiotoxicity of bupivacaine but not of other local anesthetics. The current study was designed to reevaluate, in a random and blinded fashion, the systemic toxicity of bupivacaine and ropivacaine in nonpregnant and pregnant sheep. METHODS: Chronically prepared nonpregnant and pregnant ewes were randomized to receive an intravenous infusion of ropivacaine or bupivacaine at a constant rate of 0.5 mg.kg-1.min-1 until circulatory collapse. The investigators were blinded to the identity of local anesthetic. Heart rate, arterial blood pressure, and cardiac rhythm were monitored throughout the study. Arterial blood samples were obtained before infusion and at the onset of toxic manifestations, which appeared in the following sequence: convulsions, hypotension, apnea, and circulatory collapse. Serum drug concentrations and protein binding were determined. Blood pH and gas tensions were measured. RESULTS: There were no significant differences between non-pregnant and pregnant animals in the doses or serum concentrations of either drug required to elicit toxic manifestations. In nonpregnant animals, similar doses and serum concentrations of ropivacaine and bupivacaine were associated with the onset of convulsions and circulatory collapse. In pregnant ewes, greater doses of ropivacaine as compared to bupivacaine were required to produce convulsions (7.5 +/- 0.5 vs. 5.0 +/- 0.6 mg.kg-1) and circulatory collapse (12.9 +/- 0.8 vs. 8.5 +/- 1.2 mg.kg-1). The corresponding serum concentrations of ropivacaine were similar to those of bupivacaine. Pregnancy did not affect the serum protein binding of either drug. The proportion of animals manifesting a malignant ventricular arrhythmia as the terminal event was similar among all groups. CONCLUSIONS: The systemic toxicity of ropivacaine or bupivacaine is not enhanced by gestation in sheep. This is in contrast to an earlier study in which the cardiotoxicity of bupivacaine was enhanced during ovine pregnancy. Greater doses of ropivacaine, as compared to bupivacaine, are needed to produce toxic manifestations in pregnant animals.

Effect of ropivacaine and bupivacaine on uterine blood flow in pregnant ewes.

The effects of ropivacaine, a new amide local anesthetic, on uterine blood flow and fetal well-being were compared with those of bupivacaine in 10 chronically instrumented pregnant ewes. In random sequence, animals received two intravenous infusions of each drug. The low infusion rate regimens were chosen to result in clinically relevant maternal plasma concentrations of local anesthetics, whereas the more rapid rates of infusions were given to assess the safety of higher maternal drug concentrations. An epinephrine infusion was given to demonstrate the appropriateness of the animal model for the measurement of uterine blood flow. Maternal and fetal heart rates, arterial blood pressure, and the ewe's central venous pressure, intraamniotic pressure, and uterine blood flow were recorded continuously. Arterial blood samples were taken from mother and fetus at frequent intervals to determine acid-base status and local anesthetic concentrations. A total of 39 studies were performed. None of the infusions of either local anesthetic resulted in a significant decrease in uterine blood flow or deterioration in fetal condition. The mean maternal plasma concentrations at the end of infusions were as follows: ropivacaine low dose, 1.60 +/- 0.35 micrograms/mL; bupivacaine low dose, 1.55 +/- 0.15 micrograms/mL; ropivacaine high dose, 2.50 +/- 0.37 micrograms/mL; and bupivacaine high dose, 1.83 +/- 0.19 micrograms/mL. Epinephrine infusion resulted in a 25% decrease in uterine blood flow without adverse fetal effects. We conclude that neither ropivacaine nor bupivacaine, as administered in this study, led to any ill effects on uterine artery blood flow or fetal well-being.

The maternal and fetal effects of milrinone and dopamine in normotensive pregnant ewes.

The safety of milrinone, administered during gestation, was evaluated in seven chronically instrumented pregnant ewes and their fetuses. Each of the following six intravenous regimens was administered in random order: milrinone, 75 micrograms.kg-1, over 1 minute, followed by 240-minute infusions of the drug at a rate of 1, 2, or 4 micrograms.kg-1.min-1; dopamine 5 or 10 micrograms.kg-1.min-1 over 60 minutes; or normal saline solution, 0.5 ml.min-1 for 240 minutes. Maternal and fetal acid-base parameters, heart rate, and blood pressure were monitored as were the ewe's venous and intraamniotic pressures and uterine blood flow. Milrinone concentrations determined in maternal arterial blood samples obtained during 1 and 2 micrograms.kg-1.min-1 infusions were found to be within the human therapeutic range. Bolus injection of milrinone, as well as the lowest drug infusion, resulted in no significant changes in uterine blood flow, whereas 2 micrograms.kg-1.min-1 milrinone infusion led to a 14% to 19% increase in uterine blood flow between 120 and 240 minutes. With the highest milrinone infusion, this increase was approximately 20%. In contrast, with both dopamine infusions, a dose-related decrease in uterine blood flow of 15% to 26% occurred between 15 and 60 minutes. No milrinone could be detected in any fetal plasma samples. Fetal arterial pH and blood gas tensions did not change during milrinone infusions. Dopamine 10 micrograms.kg-1.min-1 led to a progressive decrease in fetal arterial pH and an increase in PaCO2, which may have been related to similar changes in the ewe. It is concluded that milrinone has no adverse effects on uterine blood flow and fetal well-being when administered during ovine pregnancy.

Noninvasive detection of the morphologic and hemodynamic changes during normal pregnancy.

To characterize the morphologic and hemodynamic changes during normal pregnancy, serial echocardiographic measurements (n = 210) of left ventricular (LV) dimensions and mass (M-mode), volumes and ejection fraction (two-dimensional), stroke volume, and cardiac output (Doppler: aortic, apical, and suprasternal) were performed in 15 patients (mean age 30 years) beginning as early as 12 weeks of gestation, at 2-week intervals through delivery, and up to 12 weeks postpartum. Left atrial size increased from 3.4 +/- 0.4 (SD) to 3.8 +/- 0.4 cm near term, decreasing to 3.4 +/- 0.5 cm postpartum (p = 0.006 overall). LV mass changes correlated with increases in body weight. No consistent significant changes in LV volumes and ejection fraction were observed. LV outflow tract cross-sectional area increased significantly from 3.0 +/- 0.2 cm2 at baseline to 3.5 +/- 0.3 cm2 near term, decreasing to 3.2 +/- 0.3 cm2 postpartum (p less than 0.002 for both). Heart rate increased from 70 +/- 7 to 77 +/- 10 beats/min near term decreasing to baseline postpartum (p less than 0.02 for both). Accordingly, cardiac output increased significantly, as detected from both the apical and suprasternal positions averaging from 4.7 +/- 0.6 to 6.5 +/- 1.5 l/min near term, returning to 4.3 +/- 0.6 l/min postpartum (p less than 0.0005 for both). Thus, in normal pregnancy, left atrial size increases significantly without significant changes in LV dimensions, volumes, and ejection fraction. Increased LV mass is related to increased body weight. Cardiac output changes result from increased heart rate and an increase in LV outflow area, which contributes to increased stroke volume.(ABSTRACT TRUNCATED AT 250 WORDS)