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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.

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Pre-eclampsia

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  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

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