33 yr, G2 L1 (nvd), GA 35 w 3 to 4 days vomiting, diarrhea epigastric pain and

headace Bp 110/80 150/100 Emergency unite Bp 200/100 + headace and

vomiting Hb 14 and plt 187000 4 gr magnesium sulfate and cs

After cs LDH 670 972 Hb 13 Plt 172000 Ast 54 72 Alt 30 32 Cr 1.2 1.44 1.7 1.6 1.2

7 days later7 days later

Bp 180/100 190/100 Bp 180/100 190/100 Magnesium sulfate 4 gr stat and 1 gr/h INF S TNG Serum TNG captopril 25 mg stat

4 50 AM i l i i 4:50 AM, tonic-clonic seizure Magnesium sulfate 20%, 2gr Phenytoin

Lab dataLab data

Hb: 12 3 Hb: 12.3 PLT: 280000 UA: Pr (+++)( ) Cr: 1.2 1 LFT: normal UR AC: 6

Neurologic consultNeurologic consult

Brain MRI : hypoxi ischemic change Brain MRI : hypoxi ischemic change Brain MRV: normal Brain MRA: normal Suggestion : continue magnesium sulfate phenytoin Cardiology consult: Enalapril 50mg BD amlodipine daily

INTRODUCTIONINTRODUCTION

EclampsiaEclampsia

The occurrence of one or more generalized convulsions

and/or coma in the setting of preeclampsia and in the

absence of other neurologic conditions

INCIDENCE AND EPIDEMIOLOGYINCIDENCE AND EPIDEMIOLOGY

occurs in 2 to 3 percent of severely preeclamptic womennot receiving anti-seizure prophylaxis

between 0 and 0.6 percent in women with preeclampsiawithout severe features

Risk factors Risk factors NulliparityPreeclampsia in a previous pregnancyAge >40 years or <18 yearsFamily history of preeclampsiay y p pChronic hypertensionChronic renal diseaseAntiphospholipid antibody syndrome or inherited thrombophiliaVascular or connective tissue diseaseVascular or connective tissue diseaseDiabetes mellitus (pregestational and gestational)Multifetal gestationHigh body mass indexBl kBlack raceMale partner whose mother or previous partner had preeclampsiaHydrops fetalisUnexplained fetal growth restriction

Male partner whose mother or previous partner had preeclampsia

Woman herself was small for gestational ageFetal growth restriction, abruptio placentae, or fetal demise in a previous pregnancyProlonged interpregnancy intervalPartner related factors (new partner, limted sperm exposure [eg, previous use of barrier contraception])

Hydatidiform moleSusceptibility genes

Peak incidencePeak incidence

teenage years and low twenties

women over 35 years of age

Timing

A t t

Timing

Antepartum

intrapartum

postpartum

E l i i t 20 k fEclampsia prior to 20 weeks of gestation is rare

molar pregnancy molar pregnancy

ti h h li id d antiphospholipid syndrome

Timingg

Approximately one half of all cases of Approximately one-half of all cases ofeclampsia occur prior to term

Just over one-third of cases occur atterm, intrapartum or within 48 hours of, pdelivery

Late postpartum eclampsiaLate postpartum eclampsia

eclamptic seizures developing greater than 48 eclamptic seizures developing greater than 48hours, but less than four weeks postpartum

one-quarter of all postpartum cases

PATHOGENESIS OF SEIZURESPATHOGENESIS OF SEIZURES

Cerebral overregulation in response to high

systemic blood presure

vasospasm of cerebral

t iunderperfusion of the brainsystemic blood presure arteries

localized ischemia/infarction, and cytotoxic (intracellular) edemacytotoxic (intracellular) edema

PATHOGENESIS OF SEIZURESPATHOGENESIS OF SEIZURES

Loss of autoregulation

hyperperfusion, endothelial damage, and vasogenic edema

autoregulation

CLINICAL MANIFESTATIONS AND DIAGNOSIS

one or more generalized convulsions and/or coma

the absence of other neurologic conditionsthe absence of other neurologic conditions

tonic-clonic seizures

almost always self-limiting

l d i 60 75 d usual duration 60 to 75 seconds

In the hours before the seizureIn the hours before the seizure

persistent frontal or occipital headaches persistent frontal or occipital headaches thunderclap headaches visual disturbances right upper quadrant or epigastric paing pp q p g p altered mental status shortness of breath shortness of breath

Postpartum eclampsiaPostpartum eclampsia

The diagnosis may be delayed because prodromalg y y p

symptoms are nonspecific and severe signs and

symptoms, such as severe hypertension and severe

headache, may be intermittent.y

A large retrospective cohort study (2012)

152 patients with preeclampsia/eclampsiap p p pThe most common presenting symptom headache (70%) headache (70%) shortness of breath blurry vision nausea or vomiting, edemag, neurological deficit epigastric pain epigastric pain

Bilateral facial palsy is a rare entity inpregnancy that may be the first sign ofp g y y gpreeclampsia and suggests increased severityof disease, warranting close monitoring., g g

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS

In general, women with typical eclamptic seizures

who do not have focal neurologic deficits or

l d d t i di ti l tiprolonged coma do not require diagnostic evaluation

with either electroencephalographic or cerebral

imaging studies . If cerebral imaging is performed,

magnetic resonance imaging is the optimal studymagnetic resonance imaging is the optimal study.

1-Reversible posterior leukoencephalopathyd (RPLS)syndrome (RPLS)

posterior reversible encephalopathy syndrome(PRES)

common clinical syndromey headaches, seizures, confusion, and visual

disturbances with characteristic neuroimagingfindings

resulting from a number of different causes such ashypertension eclampsia & immunosuppressivetherapy

Reversible posterior leukoencephalopathysyndrome (RPLS)y ( )

Some experts suggest that RPLS is an indicatorp gg

of eclampsia, even when features of

preeclampsia (hypertension, proteinuria) are not

presentpresent .

RPLS in eclampsia settingsRPLS in eclampsia settings

Blood pressures lower than in patients who develop Blood pressures lower than in patients who develop

RPLS in other settings

Th h d h i i ll l li d The headache is typically constant, nonlocalized,

moderate to severe, and unresponsive to analgesia

(thunderclap headache).

2- Use of illicit drugs

Cocaine intoxication presenting as preeclampsia and l ieclampsia

If a patient presents in the third trimester with hypertension andIf a patient presents in the third trimester with hypertension and

clinical symptoms of preeclampsia that rapidly improve shortly

ft d i i i i t i ti h ld b id dafter admission, cocaine intoxication should be considered as

the possible source

3-Infection4-Hypertensive disease4-Hypertensive disease .

5-Space-occupying lesions of the central nervous system

(brain tumor, abscess).

6 Metabolic disorders (hypoglycemia uremia6-Metabolic disorders (hypoglycemia, uremia,

inappropriate antidiuretic hormone secretion resulting in

water intoxication).

7-Stroke

8- Thrombotic thrombocytopenic purpura or

thrombophiliap

9-Cerebral vasculitis.

10- idiopathic epilepsy

evaluation and treatment of noneclampticseizures

seize in the first half of pregnancyseize in the first half of pregnancy focal neurologic deficitsprolonged comaatypical eclampsiayp p

General principlesGeneral principles

maintenance of airway patency

prevention of aspiration

MANAGEMENTMANAGEMENT

Prevention of maternal hypoxia and trauma

Management of severe hypertension, if presentManagement of severe hypertension, if present

Prevention of recurrent seizures

Evaluation for prompt delivery

Treatment of hypertensionTreatment of hypertension

Strokes account for 15 to 20 percent of deaths fromeclampsia

risk of stroke th d f l ti i t li d di t li the degree of elevation in systolic and diastolic pressures maternal age

Aggressive antihypertensive therapy for BP ≥160/105 to 110BP ≥160/105 to 110

treatment of hypertensive crisistreatment of hypertensive crisis

Hydralazine

L b t l lLabetalol

nifedipine nifedipine

treatment of mild hypertension is not

recommended, as neither maternal nor fetal

b fi h b d dbenefits have been demonstrated.

Treatment of convulsionsTreatment of convulsions

Approximately 10 percent of eclamptic women will have Approximately 10 percent of eclamptic women will haverepeated seizures if managed expectantly

magnesium sulfateg Phenytoin diazepam diazepam

i lf tmagnesium sulfate

t l i i l th Ph t i & di recurrent convulsions is less than Phenytoin & diazepam

less likely to be admitted to an intensive care facility

less likely to develop pneumonia

lower cost

ease of administration (eg, cardiac monitoring is not required)

less sedation

The effects of maternal magnesium sulfate treatment on newborns

Neuro protective effects Neuro protective effects

Hypotonic

lower Apgar scores at birth

Increase NICU admision Increase NICU admision

Increase risk of intubation

FDA announcementFDA announcement

More than 5 -7 days treatment in pregnant women

with magnesium sulfate lead to hypocalcema and

increased risk of osteopenia and bone fracture inincreased risk of osteopenia and bone fracture in

newborns

Management of persistent convulsionsManagement of persistent convulsions

magnesium sulfate (2 f i lf t 15 t 20 magnesium sulfate (2 grams of magnesium sulfate over 15 to 20minutes)

Diazepam (0.1 to 0.3 mg/kg over 60 seconds, maximump ( g g ,cumulative dose 20 mg)

Lorazepam (0.02 to 0.03 mg/kg IV, up to a cumulative dose of 0.1mg/kg)

Sodium amobarbital (250 mg intravenously over three tofive minutes )five minutes )

DeliveryDelivery

The definitive treatment for eclampsia is prompt The definitive treatment for eclampsia is promptdelivery

the mode of delivery

gestational age Bishop score

the mode of delivery fetal condition and

position

Cesarean deliveryCesarean delivery

it is desirable to wait 15 to 20 minutes and until the

mother and fetus show signs of recovery (control ofg y (

convulsions; mother oriented to name, time, and

l f l h i ) b f diplace; fetal heart rate reassuring) before proceeding

to surgery, if possible.

AnesthesiaAnesthesia

Magnesium Therapy in Pre-eclampsia Prolongs Analgesia

Following Spinal Anaesthesia with Fentanyl andFollowing Spinal Anaesthesia with Fentanyl and

Bupivacaine: An Observational Study.

Maternal outcome abruption placentae disseminated intravascular coagulopathydisseminated intravascular coagulopathy acute renal failure hepatocellular injury liver rupture intracerebral hemorrhage transient blindness cardiorespiratory arrest i ti iti aspiration pneumonitis acute pulmonary edema postpartum hemorrhage postpartum hemorrhage

Highest risk of maternal deathHighest risk of maternal death

women with eclampsia prior to 28 weeks of gestation women with eclampsia prior to 28 weeks of gestation

multiple seizures outside of the hospital setting

THANKSTHANKSTHANKS