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Discussion Starter · #1 ·
There's something I don't understand. How come we give Magnesium Sulfate to pregnant women with severe preeclampsia. Isn't MgSO4 a tocolytic! Tocolysis is absolutely contraindicated in severe preeclampsia.

Anyone there can explain for me please
 

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In the context of SEVERE pre-eclampsia/eclampsia (PE/E) at any gestational age (and mild pre-eclampsia if >=36wks of gestation?), MgSO4 is administered in order to PREVENT further eclamptic seizures (i.e. NOT ablate current ones!).

MgSO4 is also administered in the context of PRETERM labor as a tocolytic. I conjecture that once birth has begun, magnesium has no effect.

Now, a little conversation... PE/E is a condition where decidual-vascular interface is interrupted; VEGF and sFlt (a circulating analogue of the placenta with action identical to VEGF receptor) are major cytokines involved in the pathophysiology of PE/E. In normal pregnancy, VEGF mediates the remodeling of placental vessels, acting on the endothelium and rendering the vessels of low resistance/high blood flow. This remodeling is essential for the proper administration of nutrients and oxygen to the feto-placental unit. This beneficial effect of VEGF is ablated in PE/E, because circulating sFlt binds to VEGF and cancels its effects before it acts on the endothelium. In brief (and with a little extrapolation), eclampsia is a condition of systemic inflammation and SYSTEMIC VASCULAR CONTRACTION. This systemic vasular contraction is believed also to cause cerebral hypoperfusion, leading to hypoxia and, in turn, to the ignition of eclamptic seizures.

Magnesium's mechanism of action in the context of PE/E is still under discussion, but according to recent data, it exerts a "selective ability to improve cerebral vascular perfusion, thus reducing epileptogenic
local ischemia" (NEJM 348;4 & Lancet 2002; 359:1877-89). Direct inhibition of calcium effects on the CNS are also another proposed mechanism, but it has been proved that magnesium is more effective in eclampsia as an anticolvusant than other causes of seizures (e.g. epileptic ones).

On the contrary, during preterm labor magnesium exerts its effect directly on the smooth muscle of the myometrium (NEJM 356:271-283), by inhibiting the influx of calcium and thus the organized contractions of the myometrium that lead to parturition. In other words, this selectivity is evident BEFORE parturition begins. Once labor is in process, magnesium has not been shown to inhibit it.

I hope this proves helpful, at least to initiate a constructive discussion!
 

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Discussion Starter · #3 ·
Still not clear

Thank you for the detailed comprehensive answer with references. I admire your scientific approach and they way you analyze stuff.

One misconception still in my mind. If MgSO4 is inhibiting Calcium influx then I see no reason why it cannot stop a contracting already-in-labor uterus?
 

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Discussion Starter · #4 ·
It will be nullified by Oxytocin

The use of MgSO4 in PE/E is primarily to avoid seizures. Its tocolytic effects are quickly nullified by the IV Oxytocin that we "always" give right after it.
So your misunderstanding is valid and a good point but remember the Oxytocin.
 
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