1 / 40

Pre-eclampsia

Pre-eclampsia. Amanda Baric The Northern Hospital, Australia. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Hypertensive disorders. Pre-eclampsia syndrome of multisystem endothelial dysfunction Eclampsia convulsion in pregnancy H emolysis E levated L iver enzymes L ow P latelets.

varden
Télécharger la présentation

Pre-eclampsia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Pre-eclampsia Amanda Baric The Northern Hospital, Australia www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. Hypertensive disorders... • Pre-eclampsia • syndrome of multisystemendothelial dysfunction • Eclampsia • convulsion in pregnancy • HemolysisElevatedLiver enzymesLowPlatelets proteinuria hypertension

  3. Pathophysiology • Multi-system disorder • May be due to an imbalance of placental prostaglandins • thromboxane compared with prostacyclin vasoconstriction, platelet aggregation, uterine irritability, uteroplacental hypoperfusion

  4. Pathophysiology Abnormal placental perfusion trophoblast serotonin widespread endothelialdysfunction

  5. Pathophysiology • Uterus releases renin which catalyses the conversion of angiotensinogen to angiotensin I widespread arteriolar vasoconstriction. • Aldosterone secretion causes renal reabsorption of sodium and water

  6. Epidemiology • Pre-eclampsia 1-4% of primigravidae (>20 weeks) 1% multiparas • Eclampsia 1:2000 deliveries (UK); half postpartum • HELLP 1:3000 deliveries; 4-12% of severe pre-eclampsia • Pre-eclamsia and eclampsia account for 50,000 maternal deaths per year world-wide.

  7. Diastolic BP >110 mmHgon any one occasion >90 mmHg2 occasions, 4 hr apart Proteinuria>300 mg/24h BP 160/110 mmHg Proteinuria >5 g/24h Oliguria <500 ml/24h Pulmonary oedema Cerebral/visual disturbances Epigastric pain Coagulopathy/HELLP Pre-eclampsia: diagnostic criteria Severe Gestation >20 weeks

  8. Risk factors for pre-eclampsia • Chronic hypertension • Renal disease • Positive family history • Twin pregnancy • Maternal age over 40 years • Nulliparity • Diabetes

  9. Cardiovascular hypertension,cardiac failure Renal hyperuricaemia + proteinuria Cerebral ischaemia  convulsions Stroke Haematological thrombocytopaenia, DIC Hepatic HELLP, hepatic or splenic infarction Pulmonary oedema Placental foetal compromise Organ system involvement

  10. Renal • Renal blood flow and glomerular filtration rate reduction due to arteriolar vasoconstriction • Reduced urea and creatinine concentrations are increased • Proteinuria contributes to a reduction in serum albumin • Hyperuricaemia • Oliguria after delivery is common for up to 6 hours and does not necessarily mean hypovolaemia • ATN is rare

  11. Central nervous system • Headache, visual disturbances, hyperreflexia indicate cerebral irritability • Seizures in late pregnancy represent eclampsia until proven otherwise • Eclampsia may occur as a result of cerebral vascular obstruction or vasospasm • Cerebral oedema and hypertensive encephalopathy can occur • Cerebral haemorrhage accounts for 40% of deaths due to pre-eclampsia

  12. Coagulation • Normal pregnancy results in a hypercoagulable state. • In pre-eclampsia a drop in platelet count and function can occur. A count less than 100,000/ml indicates more severe disease. • Consumptive coagulopathy is rare unless there has been abruption or HELLP is present

  13. Circulatory changes • Circulating blood volume is not as expanded as in a normal pregnancy. • Capillary permeability is increased leading to oedema and a low oncotic pressure. • Pulmonary oedema may occur in up to 2% of severe pre-eclamptics due to ventricular dysfunction, low colloid osmotic pressure, increased intravascular hydrostatic pressure or increased pulmonary capillary permeability.

  14. Hepatic dysfunction • The cause of hepatic dysfunction in pre-eclampsia is not clear. • Periportal hepatic necrosis • Subcapsular haematoma • Fibrin deposition in hepatic sinusoids • Spontaneous liver rupture is a rare but life threatening complication. • Acute fatty necrosis • HELLP syndrome

  15. HELLP • Haemolysis, Elevated Liver enzymes, Low Platelets • Complicates 0.3% of all pregnancies and 4-20% of those with severe pre-eclampsia. • High maternal (24%) and foetal (33%) mortality. • Usually occurs at less than 36 weeks

  16. HELLP (2) • Characterised by malaise, epigastric pain, proteinuria, jaundice, hypertension, nausea and vomiting and a flu-like illness. • May lead to haematuria, disseminated intravascular coagulation, liver and renal failure. • Platelet count is <100,000/ml

  17. HELLP (3) • Treatment is by delivery • Platelet transfusion is recommended if the count is less than 20,000/ml for a vaginal delivery and less than 50,000/ml for caesarean delivery. • Postpartum intravenous dexamethasone hastens recovery and reduces the severity of the disease. (10mg every 12 hours)

  18. Assessment of the pre-elcamptic patient • Cardiovascular system • BP, hydration, pulmonary oedema • Central nervous system • Reflexes, cerebral irritablity • Renal system • Urine output, proteinuria • Hepatic system • Epigastric pain, jaundice • Haematological system • Evidence of bleeding, haemolysis • Airway

  19. Think laryngeal oedema!

  20. Laboratory testing • Full blood count • Coagulation studies if there is a low platelet count • Liver function tests • Uric acid • Urea, creatinine and electrolytes

  21. Management • Definitive management is delivery of the foetus and placenta • Need to stabilize the mother before delivery • Aims of therapy • Avoid eclampsia (Magnesium) • Restore normal haemodynamics (fluids, antihypertensive agents) • Treat coagulopathy

  22. Analgesia for labour and delivery • Lumbar epidural analgesia • Restore circulating blood volume • Control BP • Check platelet count • Epidural or spinal analgesia for caesarean delivery • Concern about fall in BP • General anaesthesia • Low platelet count, maternal haemorrhage. • Concern about difficult intubation and pressor response to intubation, interaction of magnesium with NMB.

  23. The use of magnesium sulphate in obstetrics • First used to prevent eclampsia by Horn in Germany in 1906. • Intramuscular route found to be useful for control of convulsions associated with tetanus, used for eclampsia in 1926 • Intravenous route first used in 1933

  24. Administration of Magnesium • 4 gram bolus given over 15 minutes (8ml of 50% MgSO4 at 32 ml/h for 15 minutes) • Followed by an infusion of 1-2g/h until 24 hours after delivery • Levels need to be checked every 6 hours if using 2g/h or in renal impairment. • Therapeutic level is 1.7-3.5mmol/l • Monitor for signs of toxicity (reflexes) • Treat eclampsia with a 2-4 gram bolus over 5 minutes intravenously.

  25. Intramuscular administration • Intravenous loading dose of 4 gram given over 15 minutes • Followed by 5 gram bolus intramuscularly as a deep injection into each buttock and 5 gram intramuscularly every four hours.

  26. Distribution • Magnesium is distributed rapidly through the extracellular fluid and some is taken up by bone. • Intravenous loading results in an immediate but transient peak level and within 90 minutes, 50% of the loading dose moves into the bones or intracellular • Intramuscular magnesium requires 90-120 minutes to reach peak plasma levels

  27. Plasma levels • Infusions of 1g/h result in plasma levels of less than 1.7mmol/l • 2g/h results in levels between 1.7-3.3mmol/l • Rates of 2g/h are required to reach therapeutic levels • Therapeutic level of 2-4 mmol/l is used but there is no single accepted therapeutic level.

  28. Excretion • Magnesium undergoes renal excretion • 50% of the dose is excreted in the urine after 4 hours • The renal clearance increases linearly with an increase in plasma level • The infusion rate should be reduced and levels monitored if there is renal impairment and oliguria

  29. Toxicity

  30. Treatment of magnesium toxicity • Calcium chloride (5ml or 10%) • Calcium gluconate (10ml of 10%) • Administer as a slow intravenous injection over 10 minutes to avoid hypotension and bradycardia

  31. Contraindications • Myasthenia gravis • Heart muscle damage associated with conduction defects

  32. Effects of magnesium • CNS • Reduces cerebral vasospasm • NMDA receptor blockade • Increased production of prostacyclin • Reduction of MAC of volatile agents • Neuromuscular junction • Reduces acetylcholine release • Prolongs non-depolarizing blockade

  33. Effects of magnesium (2) • Smooth muscle • Relaxation of tone • Placental transfer • Readily crosses the placenta • May cause transient drowsiness, hypoventilation and reduced muscle tone in neonates. • Labour and placental blood flow • Labour outcomes are unaffected • Increases uterine and placental blood flow in animals

  34. Evidence for the use of magnesium • Magpie trial (2000) • RCT by Lucas et al (1995) • MgSO4 or phenytoin for prevention of eclampsia • Collaborative Eclampsia trial (1995) • Compared magnesium, diazepam and phenytoin for prevention of eclampsia

  35. Magpie Trial: Lancet, July 2002 • >10 000 women • world-wide; co-ordinated from Oxford UK • BP 140/90 and + proteinuria (30 mg/100 ml) • 4g Mg i.v. over 10-15 min, 1g/hr for 24 hr • or placebo • Eclampsia:Mg 0.8% (40/5055)vs placebo1.9% (96/5055) • NNT 91 • Maternal deaths: 11 Mg, 20 placebo p = 0.11 • Few attributed to eclampsia

  36. Magpie Trial: Lancet, July 2002 • Mg neither antihypertensive nor tocolytic • No adverse events with nifedipine + Mg • No serum monitoring • tendon reflexes, respiratory rate, urine output • Side effects: • 24% of women on Mg, 5% on placebo • flushing, nausea/vomiting • 5 Mg vs 2 placebo respiratory arrests • 10 Mg vs 6 placebo MI or cardiac failure

  37. Magpie Trial: Lancet, July 2002 • It provides vital missing pieces of information in thepre-eclampsia-magnesium sulphate story, although like all the best stories, it leaves us not entirely sure of thefinal answer. Yentis SM, IJOA 2002; 11: 238

  38. The use of hydralazine • Arterial vasodilator that acts directly on arterial smooth muscle. • Mechanism may be by the release of NO from arteriolar endothelium • Reduces BP but may induce a reflex bradycardia

  39. Hydralazine • 20-30 minute onset • Elimination half life 3 hours • 5-10mg bolus is given over 10 minutes and an infusion of 5 mg per hour is used to keep BP 140-160/90-100mmHg. • Alternatively a 5-10mg bolus can be given every 20 minutes

  40. Side effects of hydralazine • Headache, tremor and vomiting (can be indistinguishable from impending eclampsia) • Severe hypotension, tachycardia, flushing, palpitations, sodium retention, tachyphylaxis to its effect. • Lupus like syndrome with prolonged therapy (months) www.anaesthesia.co.inanaesthesia.co.in@gmail.com

More Related