Observational studies suggest a protective efect of magnesium against the development of cerebral palsy in very-Iowbirthweight newborns (Nelson, 1995; Schendel, 1996). At least ive randomized trials have also assessed neuroprotective efects in preterm neonates. These findings are discussed in detail in Chapter 42 (p. 824). Nguyen and colleagues (2013) expanded this possibility to include term newborn neuroprotection, but data were insuicient to draw conclusions.
Last, in cases of preterm labor, magnesium has been given for several days for tocolysis (Chap. 42, p. 826). Administration in these instances has been associated with neonatal osteopenia (American College of Obstetricians and Gynecologists, 20 16c).
The multinational Eclampsia Trial Collaborative Group study (1995) involved 1687 women with eclampsia randomly allocated to one of three diferent anticonvulsant regimens: magnesium sulfate, diazepam, or phenytoin (Table 40-12). In aggregate, magnesium sulfate therapy was associated with a significantly lower incidence of recurrent seizures (9.7 percent) compared with women given phenytoin (28 percent) or diazepam (17 percent). Importantly, the aggregate maternal death rate of 3.2 percent with magnesium sulfate was signiicantly lower than that of 5.2 percent for the other two regimens.
In their review of more than 9500 treated women, Smith and coworkers (2013) reported the overall rate of absent patellar tendon reflexes to be 1.6 percent; respiratory depression, 1.3 percent; and calcium gluconate administration, 0.2 percent. Only one mother died due to magnesium toxicity. Our experiences are similar. In the more than 60 years of magnesium use at Parkland Hospital, only one woman has died from an overdose (P ri tchard, 1984).
Dangerous hypertension can cause cerebrovascular hemorrhage and hypertensive encephalopathy, and it can trigger eclamptic convulsions in women with preeclampsia. Other complications include placental abruption and congestive heart failure induced by elevated hypertensive afterload.
Because of these serious sequelae, the working group for the National High Blood Pressure Education Program (NHBPEP) (2000) and the 2013 Task Force recommend treatment to lower systolic pressures to or below 160 mm Hg and diastolic pressures to or below llO mm Hg. Martin and associates (2005, 2016) reported provocative observations that highlight the importance of treating systolic hypertension. They described 28 selected women with severe preeclampsia who sufered an associated stroke. Most (93 percent) were hemorrhagic strokes, and all women had systolic pressures > 160 mm Hg before sufering their stroke. By contrast, only 20 percent of these same women had diastolic pressures > 110 mm Hg.
From other observations, it seems likely that at least half of serious hemorrhagic strokes associated with preeclampsia are in women with chronic hypertension (Cunningham, 2005). Long-standing hypertension results in development of CharcotBouchard aneuysms in the deep penetrating arteries of the lenticulostriate branch of the middle cerebral arteries. hese vessels supply the basal ganglia, putamen, thalamus, and adjacent deep white matter, as well as the pons and deep cerebellum. These unique aneurysmal weakenings predispose these small arteries to rupture during sudden hypertensive episodes.