and increased deposition of fibrin within the vascular bed.
In our study, there was no significant effect of magnesium
sulfate on platelet count. This finding is similar to
Moghadas et al.’s preterm labor study. But, there was no
significant effect of magnesium on bleeding time.
The discrepancy might be resulted from the study designs
[22]. In addition to its antithrombotic effects, MgSO
4
decreases BP, abolishing vasoconstriction induced by
endothelin 1 and peroxides in placental vasculature [23].
We found in this study that magnesium sulfate decreases
each of the systolic and diastolic BP values. Thus, the
systemic use of magnesium sulfate in preeclampsia lowers
the resistance in the peripheral vascular bed. The decreasing
effect of magnesium sulfate on the resistance of the vascular
bed explains the statistical difference of creatinine values
between the pretreatment and post-treatment group.
Having applied 6 g of magnesium sulfate rather than 4 g
as a bolus dose, and checking the magnesium blood level
before it probably had reached the steady state may be
some limiting points in our study. However, the mean of
post-treatment magnesium sulfate value (3.22
+
0.63 mg/
dl) of our study was high enough for treatment.
In conclusion, this practice of administering magnesium
(a 6-g bolus followed by 2 g/h) to patients with severe
preeclampsia did not influence the platelet count at the end
of the second hour, but it prolongs the bleeding time in our
study. We speculated that this can be clinically important if
it is used for a long time or in high doses, in severe
preeclamptic or HELLP cases, worsening this condition
and causing possible complications on bleeding. Larger
studies inspecting dose and time effect of magnesium
infusion are needed to clarify the correlation between
magnesium use and clotting disorders in preeclamptic
cases.
Declaration of interest:
The authors report no conflicts
of interest. The authors alone are responsible for the
content and writing of the paper.