Use of a prenatal risk screen to predict maternal traumatic pregnancy-associated death: program and policy implications.

BACKGROUND: Motor vehicle crashes, homicide, suicide, and drug abuse are among the leading causes of pregnancy-associated deaths. To prevent such deaths, identifying women for intervention is required. The universally offered Florida Healthy Start Prenatal Risk Screen was evaluated to identify women at increased risk for traumatic pregnancy-associated death. METHODS: Florida's Enhanced Maternal Mortality Reporting Database for 1999 through 2005 was linked with Florida's Healthy Start Prenatal Risk Screen to identify traumatic pregnancy-associated death as the outcome. Distribution of Healthy Start risk scores among women who died were compared with the screened population. Traumatic death estimates per 100,000 births were drawn for each risk score, along with estimates of the relative risk (RR) of traumatic death for each score. The RR of women with scores greater than or equal to 4 were compared with the risk of women scoring 0 to 3. FINDINGS: Almost 20% of the 620,959 women who did not die of traumatic death had a risk score of 0, compared with only 3% of the 144 women who did die of traumatic death. As risk scores increased, the chance of traumatic deaths sharply increased. A woman with a score of 4 had 11.78 times (confidence interval [CI], 4.63-29.69) the risk of traumatic death compared with a woman with a risk score of 0. CONCLUSIONS: The implementation of prenatal risk screening to identify women at increased risk for traumatic pregnancy-associated death would help to ensure that policies to reduce infant risk factors also address maternal risk factors.

Nitric oxide and cyclic GMP levels in sickle cell patients receiving hydroxyurea.

Recent studies suggest that nitric oxide (NO) may partly be responsible for the beneficial effect of hydroxyurea (HU) in sickle cell disease (SCD) patients. NO stimulates cyclic guanosine monophosphate (cGMP) production, which mediates vasodilatation. We investigated the association between NO, cGMP and fetal haemoglobin (HbF) levels after HU administration. Our data showed that chronic HU significantly increased NO, cGMP, and HbF levels in SCD. Recently it was shown that HbF production was stimulated by cGMP-dependent protein kinase. Our results suggest that NO stimulates cGMP production, which then activates a protein kinase and increases the production of HbF.

Arterialization of peripheral venous blood in sickle cell disease.

Arterialization of the venous blood is thought to be indicative of cutaneous shunting, and occurs in patients with sickle cell disease (SCD) during vaso-occlusive crisis (VOC). We performed the present study to quantify the amount of shunting that occurs in sickle cell patients presenting at the Howard University Sickle Cell Center, Washington, D.C., as outpatients and for hospitalizations associated with sickle cell crisis. Peripheral venous blood was drawn anaerobically into heparinized syringes from 9 normal control subjects (NC), 24 outpatients (steady-state group), and 14 inpatients during crisis (VOC group). Spectrophotometric measurements were made for the following species of hemoglobin (Hb): oxy-Hb (O2Hb), reduced Hb (RHb), carboxy-Hb (COHb), and met-Hb (MHb). In addition, fetal hemoglobin (HbF) was measured by high-pressure liquid chromatography (HPLC). The O2Hb saturations of the steady state group were not significantly different than those of the NC group (55 +/- 4% vs. 40 +/- 6%). However, the O2Hb saturations of the VOC group were 73 +/- 3%, and this value was found to be significantly greater than those of both the steady-state and the NC groups (p < 0.05). Reduced hemoglobin saturations were inversely related to the O2Hb values, as expected. Compared to the NC group, the steady-state, and VOC groups had greater dyshemoglobin (COHb and MHb) levels (p < 0.05). These findings suggest that the percentages of venous O2Hb and dyshemoglobins may be increased in sickle cell disease even in the absence of VOC. Therefore, the venous O2Hb saturation may be a useful biochemical marker for the arteriovenous shunting and hemodynamic adaptations associated with sickle cell disease.