Tasty Morsels of Critical Care 033 | Pre-eclampsia

Welcome back to the tasty morsels of critical care podcast. A meandering monologue through critical care fellowship exam preparation. Today we’re looking at Oh Chapter 64 covering some of the absolute basics of pre eclampsia. ICU level pre eclampsia is rare. In Ireland most of it is managed in separate obstetric hospitals by the obstetricians and the anaesthetists. And given that the definitive treatment is removing the baby from the mother, it turns out that this will typically have been done before we even get involved. Unfortunately its rarity does not get us out of having to know it very well as it is an exam favourite. Firstly some definitions. To have pre eclampsia you’ll need to have * new onset of hypertension with proterinuria OR * new onset of hypertension with end organ damage (inc foetal growth issues) Hypertension here defined as BP >140/90 and proteinuria as >300mg/24hrs or protein +ve on a dipstick. To have eclampsia you simply need to have seizures in addition to the above. To summarise the cause and pathogenesis, the short answer is we don’t know. The longer answer is – we still don’t know but we have lots of science to show it and the medium length, exam appropriate answer answer that I might be able to reproduce is a straight quote from deranged physiology: [pre eclampsia is] a systemic response to placental hypoperfusion, with increased activation of the potent vasoconstrictor endothelin-1, as well as an increased sensitivity to vasoconstrictors in general, and a down-regulation of vasodilatory mechanisms such as nitric oxide synthase. The clinical presentation of pre-eclampsia from a critical care perspective is best split into organ systems * Cardiovascular: hypertension is the main player here. You’ll see increased SVR also * Neurological: early signs can be headache and visual symptoms. You will see hyperreflexia if you look for it and you probably should. But with progression you’ll start seeing seizures, cerebral oedema and even ICH * Renal: protein loss is obvious but the fancy term to pull out is renal endotheliosis which is a form of thrombotic microangiopathy or TMA. A topic that deserves its own post. * Haematologic: low platelets but also impaired function. This might come as part of HELLP syndrome * Hepatic: HELLP syndrome is part of this but the most dramatic complication can be hepatic rupture which as you can imagine is somewhat bleedy While rare you can even get pre eclampsia in the post partum patient and I always liked the quip from Mel Herbert of EMRAP fame, that the usual definitive treatment of pre eclampsia is of course to deliver the baby but if it’s post partum what are we meant to do? put it back in again? We are unlikely to be given the job of ridding the woman of the placenta so we can instead usefully occupy ourselves with supporting the various failing organ systems. The priorities here will be * seizure prevention and treatment. * BP control * maintaining placental perfusion Seizure control here should lead to a brainstem level reflex of magnesium prescription. The indication is described as eclampsia or imminent risk of eclampsia and BP is often in the 160/110 range by this stage. Recommendations are 4g magnesium over 5 mins followed by 1g/hr as an infusion. Any further seizures can be treated with another 2g of magnesium. The NICE guidance on this has a carefully worded phrase t...

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