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Sri Wahjoeningsih Anestesiologi dan Reanimasi

RSUD dr Sutomo / F. K.UNAIRSURABAYA

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Preeclampsia is

1. Disorder of widespread vascular endothelial malfunction and vasospasm

2. Occurs after 20 weeks’ gestation3. Can present as late as 4-6 weeks’ post partum

Clinically

1. Hypertension and proteinuria, 2. With or without pathologic edema

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Hypertension during Pregnancy

1. Pregnancy-induced hypertension

1. Hypertension without proteinuria/edema2. Preeclampsia

1. Mild2. Severe

3. Eclampsia

2. Coincidental Hypertension: preexisting or persistent

3. Pregnancy-aggravated Hypertension

1. Superimposed preeclampsia2. Superimposed eclampsia

4. Transient Hypertension: occurs in 3rd trimester, mild

Classification

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Preeclampsia used to be called toxemia because it was thought to be caused by toxin in pregnant

women’s bloodstream

This theory has been discarded, possible causes

1. Insufficient blood flow to the uterus

2.Damage to the blood vessels

3.A problem with the immune system

4.Poor diet

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Placenta:

Spiral arteries fail to undergo physiological dilatation and show luminal disease similar to acute atherosis in non-pregnant patients

Kidney:

Glomerular capillary endotheliosus. Might progress to ATN or acute cortical necrosis

Placenta, kidney, brain, and liver show features consistent with chronic ischemia

Pathology

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Vasoconstriction

Primary changes in the vasculature

Impaired endothelial production of prostacylin

Release of platelet-derived factors as thromboxane and serotonin

Release of endothelial procoagulant factors

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Inadequate cellular oxygenation

Low cardiac filling pressures (CVP, PCWP), decreased plasma volume

Vasoconstriction - increased SVR

Low cardiac output

Tissue oxygen extraction impaired

Inadequate oxygen delivery and consumption

Platelet agregationTrombocytopeniaHemolytic anemia

Liver enzyme

Productionof

Vasodilatorysubstance

Vascular Sensitivity toAngiotensin,

norepinephrineand

vasospasme

Glomerularcapillary

permiabilityand

proteinuria

HELLPSensitivity

to vasodilatingsubstances

GFR and RBF

Unknown etiologies

Endothelial damage

Aldosteron escapeSodium and water retention

Edema

Preeclampsia-eclampsia state

Systemic Vascular resistance

Hypertension 8

Endothelium damage Hematological changes?

Humoral factors

Multisystem changes occurring in preeclampsia

Plasma volume SVR and AP

PCWP or CVP

Contractility usually unchanged

HT encephalopathyIschaemia and infarctionVasospasmHaemorrhageOedema

Pulmonary oedemaLeaky capillariesARDS

Proteinurea

GFR Plasma creatinine Glomerulocapillary endotheliosis

Altered LFT Periportal hepatic necrosis Subcapsular haemorrhage Fibrin deposition HELLP

IUGR Preterm delivery Abruptio

placentae9

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Complication of preeclampsia

1.Lack of blood flow to the placenta

2.Placental abruption

3.HELLP syndrome

4.Eclampsia

5.Cardiovascular disease

1. Oliguria (<400 ml/24h)

2. Cerebral signs (headache, blurred vision, altered consciousness)

3. Pulmonary edema, cyanosis

4. Epigastric or right upper quadrant pain

5. Impaired liver function

6. Hepatic rupture

7. Trombocytopenia

8. HELLP syndrome

Symptoms other than hypertension and proteinuria in severe preeclampsia

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Maternal complications of severe pre-eclampsia

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1. Cardiovascular dysfunction (cardiac failure, hypertension)

2. Renal dysfunction (oliguria, reduced GFR, elevated creatinine, acute tubular necrosis, cortical necrosis)

3. Respiratory dysfunction (ARDS, pulmonary edema)

4. Hepatic dysfunction (elevated liver enzymes, subcapsular hematoma, HELLP syndrome)

5. Cerebral dysfunction (encephalopathy, edema, ischemia, hemorrhage, cortical blindness, retinal detachment , infarction, eclampsia)

Fetal complications of severe preeclampsia

• Intrauterine growth retardation

• Premature delivery

• Abruptio placentae

• Fetal distress/fetal demise

Associated maternal risks

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1.Prevent convulsions ( progression to eclampsia)

2.Control blood pressure. The goal is to stabilise the diastolic BP between 90 and 100 mmHg

3.Anticipate and prevent complications

4.Prevent damage to the foetus

Goal management

Obstetric Management

Classically “stabilize and deliver”

Indications for expedited delivery:

Medical management while a waiting delivery:1. Use of steroids X 48 hours if fetus < 34 weeks2. Antihypertensives to maintain DBP < 105-1103. Magnesium sulfate for seizure prophylaxis4. Monitor fluid balance, I/O, daily weights, symptoms,

reflexes, HCT, plts, LFT’s, proteinuria

1. Fetal distress2. BP despite aggressive Rx3. Worsening end-organ function4. Development or worsening of HELLP syndrome5. Development of eclampsia

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Magnesium sulfate has many effects; its mechanism in seizure control is not clear.

NMDA (N-methyl-D-aspartate) antagonist

Vasodilator

Brain parenchymal vasodilation demonstrated in preeclamptics by Doppler ultrasonography

Increases release of prostacyclin

Potential adverse effects:

Toxicity from overdose (respiratory, cardiac)

Bleeding

Hypotension with hemorrhage

Uterine contractility

Magnesium Sulfate

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1. Renally excreted

2. Preeclamptics prone to renal failure

3. Magnesium levels must be monitored frequently either clinically (patellar reflexes) or by checking serum levels q 6-8 hours

1. Therapeutic level: 4-7 meq/L2. Patellar reflexes lost: 8-10 meq/L3. Respiratory depression: 10-15 meq/L4. Respiratory paralysis: 12-15 meq/L5. Cardiac arrest: 25-30 meq/L

4. Treatment of magnesium toxicity:1. stop MgSO4, 2. IV calcium, 3. manage airway

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Magnesium Sulfate

Antihypertensive therapy aims

To prevent

1. Cerebral hemorrhage

2. Pulmonary edema

3. Other complication of acute hypertension in the mother while preserving or improving placental circulation

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To control an acute hypertensi episodes when

SAP is 170 mmHg or greater

DAP is 110 mmHg or greater

Or both

Hydralazine, labetolol, diaoxide

On admission to the hospital

SAP is greater than 160 mmHg but less than 170 mmHg

DAP is greater than 90 mmHg but less than 110 mmHg

Or both

Metyldopa, oxprenolol, labetolol, clonidin, hydralazine, nifedipine

In more severe crises

Na prusside, glyceryl trinitrate or trimetaphan

To control hypertension

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The aim of fluid therapy is to:

1. Provide an adequate volume to meet daily maintenance requirements and compensate for insensible losses

2. Maintain a satisfactory urine output

3. Act as a conduit for administration of therapeutic agents (e.g magnesium sulfat, hydralazine)

4. Compensate for any reduction in preload and afterload during administration of epidural analgesia

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”Delivery of the fetus and placenta is the definitive management of severe preeclampsia.

Once severe disease has been established and is progressing, delivery of the fetus and placenta must be accomplished to limit maternal risk.”

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Anesthetic Goals of Labor Analgesia in Pre-eclampsia

1. To establish & maintain hemodynamic stability (control hypertension & avoid hypotension)

2. To provide excellent labor analgesia

3. To prevent complications of preeclampsia

1. intracerebral hemorrhage

2. renal failure

3. pulmonary edema

4. eclampsia

4. To be able to rapidly provide anesthesia for C/S22

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Women with severe pre-eclampsia should be encouraged to have

regional anesthesia for Caesarean Section

Regional anesthesia is not contraindicated after an eclamptic fit if the mother has regained consciousness and treatment for seizure and

BP control has been commenced

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If an epidural has already been in place for labour, this can be topped up as long as it has

been effective

If there is no epidural or it is concidered that there is not enough time to top up the epidural, spinal

anesthesia should be provided

The benefit of spinal anaesthesia include provision of rapid, dense and predictable

block suitable for surgery

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There have been concers with spinal anaesthesia and severe pre-eclampsia due to the fear of causing

a sudden and significant drop in BP

Women with pre-eclampsia have high levels of circulating catecholamines which may protect them against a fall in BP as a result of a spinal

induced sympathetic block

If a spinal technique is chosen there should be cautious use of vasopressors as a exaggerated hypertensive response to vasopressors may be

observed

General Anesthesia in Preeclampsia

Airway edema is common1. Mandatory to reexamine the airway soon before induction2. Edema may appear or worsen at any time during the course of

disease tongue & facial, as well as laryngeal

Laryngoscopy and intubation BP3. Labetolol & NTG are commonly used acutely4. Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be

given to blunt response

Magnesium sulfate potentiates depolarizing & non-depolarizing muscle relaxants

5. Pre-curarization is not indicated.6. Initial dose of succinylcholine is not reduced.7. Neuromuscular blockade should be monitored & reversal

confirmed.26

10 preeclamptic patient who

underwent CS, under thiopental-

N20 40% and halothane 0,5%

anesthesia

A

10 preeclamptic patient who

underwent CS, under epidural

bupivacain anesthesia

B

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The laryngoscopy can be obtunded by the following:

1. A short acting opiate bolus (e.g alfentanyl 10-20 mcg/kg or remifentanil 1 mcg/kg)

2. A bolus dose of labetolol 10-20 mg i.v.

3. Bolus of magnesium 40 mg/kg i..v.

4. Bolus of lidocaine 1,5 mg/kg i.v. 3-5 min before induction

If opiates are given prior to delivery, inform the neonatal team of the possibility of neonatal respiratory

depression

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The most concerning possibility is that she has experienced an intracranial event due to excessive hypertension

during intubation.

This should be diagnosed by pupil examination and response and emergency CT scan.

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These are several reasons why she slow to wake up and these include:

1.Effect of excess anaesthetic agents

2.Effect of excess opiates

3. Inadequate reversal of neuromuscular block: magnesium potentiates non-depolarising neuromuscular blocking drugs

4.Respiratory depression due to magnesium toxicity

5.Hypoglycaemia

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After Caesarean section, she should go to a high dependency area for close

observation

Postoperative management

1. Effective postoperative analgesia as this reduces the stress response.

2. Fluid balance. A strict intake/output chart should be maintained for at least 24 hours or until a diuresis develops. A total intake of 75 ml/hr should not be exceeded until the patient begin mobililize her excess extracellular water.

3. Magnesium sulfate. Magnesium sulfat is continued for least 24 hours post partum or until there is evidence of maternal diuresis.

4. Hemodynamic status. It may be necessary to reinstitute antihypertensive therapy to avoid rebound hypertension as the patient begins to experience post operative pain

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Summary

1. Preeclampsia is a syndrome of unknown etiology with multiorgan involvement

2. It presents with a wide spectrum of symptoms

3. It is sometimes difficult to distinguish from other systemic diseases

4. Severe cases may progress to MOF and death

5. Delivery of the child and placenta is the only specific treatment – other lines of teatment are only supportive

6. There are several issues regarding diagnostic techniques and treatment options that need further evaluation

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