Eclampsia Flashcards

1
Q

Definition of eclampsia

A

RCOG define eclampsia as a condition which causes women to experience convulsions similar to an elliptic fit in pregnancy, labour or postnatal. Usually follows presentation of pre-eclampsia but not always.

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2
Q

Incidence rate

A

Eclampsia is rare and affects 2.7 in 10,000 pregnancies according to Baston and Hall. Less common in the UK due to good antenatal care and monitoring throughout pregnancy.

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3
Q

Death rate?

A

6/225 women who have eclampsia die

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4
Q

Risk factors

A
Primip
>35 or <20 years old
Multiple pregnancy
Infection
Diabetes
Obesity
Hypertension
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5
Q

Cause?

A

Unknown but thought to be due to abnormal implantation of the placenta. Shown with IUGR/ SGA.

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6
Q

Physiology of implantation

A

Trophoblast implants and spiral arteries form to allow for perfusion from placenta to baby > in eclampsia the serial arteries become fibrous and narrowed> this leads to production of proinflammatory proteins> these enter maternal blood stream causing inflammation in endothelial cells and vasoconstriction > poor perfusion

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7
Q

Kidneys?

A

Poor perfusion to kidneys damages the glomerulus > this slows the filtration rate causing proteinuria and oligouria > also leads to retained salts and therefore hypertension.

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8
Q

Liver?

A

Reduced blood flow > hypoxia > damage to tissues> causes swelling > elevated ALTs and liver capsule stretches causing epigastric pain

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9
Q

Retinas?

A

Reduced blood flow to retinas> hypoxia> Scotoma> are of vision becomes worse. Women experience blurred vision and flashing lights.

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10
Q

Endothelial cells

A

Damage> clot formation which uses platelets damage to red blood cells > haemolysis > DIC (low platelets) > vessels become more permeable and leaky causing oedema.

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11
Q

Oedema?

A

Oedema is likely to occur globally and therefore cerebral oedema will cause headaches, confusion and seizures.

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12
Q

What can Eclampsia evolve to?

A

HELLP. Haemolysis. Elevated Liver Enzymes. Low platelets. 10-20% of eclamptic women. If unrecognised/ untreated > eclamptic fit.

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13
Q

Signs of tonic-clonic seizures?

A

eye-rolling, twitching, skin cyanosed, jerking movements, facial swelling, unresponsive.

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14
Q

Aim of eclampsia management?

A

Stabilise condition. Control seizures and blood pressure. Deliver baby? eliminate fluids and oxygenate.

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15
Q

Initial Management

A

Ensure safe zone. Into left lateral to ensure patent airway and reduce aortocaval compression. Check for obstructions.
Commence 02 15l/min non rebreathe mask.
Continuous obs with dynamap, at least every 10 minutes.
CTG
Venous access (2x 16 G cannulas)
Catheterise with consent (foley indwelling with urometer) Aim for UO of previous hour + 30 mls.
Fluid restriction to avoid pulmonary oedema.
Medical Review

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16
Q

What bloods for eclampsia?

A

FBC (Hb - haemorrhage? PLT -DIC & HELLP?
Us&Es - Kidney function (increased creatinine if poor)
LFTs- Liver function (increased ALTs if damaged)
Group and Save to crossmatch for transfusion and transfer to theatre.
Clotting bloods- DIC & HELLP

17
Q

Mag sulphate?

A

4g bolus IV over 15 minutes.
2- 4g further bolus if still convulsing over 5-15 mins
1g hourly maintenance dose

18
Q

Signs of magnesium sulphate toxicity

A
Absent patella reflexes
UO <20ml/ hour
Resps< 14
SATS< 95%
STOP INFUSION IF SIGNS OF TOXICITY
19
Q

How to treat the hypertension?

A

Magnesium sulphate can reduce blood pressure so monitor closely.
Labetalol orally 200mg (not for asthmatics) OR Nifedipine 20mg orally
IV labetalol 20mg over 2 minutes can double with 10-minute intervals but not exceed 50mg hourly.
IV hydralazine (5 mg every 20 mins until 20 mg) for asthmatics.

20
Q

After care

A

Strict fluid restriction so close monitoring of UO.
Repeat bloods at 6-24 hours and monitor Magnesium levels.
? Hypo pathway for baby due to potential compromise and IUGR/ Maternal drugs and cord gases.
PN care TWOC, VTE adjusted.
Document, DATIX, debrief.