Pre-eclampsia and eclampsia slide

1. Pre-eclampsia recognition,
Pathophysiology
and Management
Krishna Bahadur Sodari
Smriti Dahal
Subhadra Kumari Shah

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3. Pre-eclampsia
• Multisystem disorder characterized by development of
HTN to the extent of 140/90 mm Hg or more with
proteinuria after 20th
week in previously normotensive
and nonproteinuric woman
• Diagnostic criteria
▪ Hypertension
▪ Edema
▪ Proteinuria
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4. Risk factors
▪ Primigravida
▪ Family history
▪ Placental abnormalities
– Hyperplacentosis
– Placental ischaemia
▪ Obesity
▪ Preexisting vascular disease
▪ Thrombophilias (antiphospholipid
syndrome, Protein C, S def)
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5. Etiology
• Involves a number of maternal, placental, and fetal
factors which include
o Failure of trophoblast invasion
o Vascular endothelial damage
o Inflammatory mediators
o Immunological intolerance between maternal and
fetal tissues
o Coagulation abnormalities
o Increased free radical
o Genetic predisposition
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6. Trophoblast invasion and
uterine vascular changes
• Invasion of endovascular trophoblast
into the walls of spiral arteriols
– In the 1st trimister- upto decidual
segment
– In the 2nd trimister- upto
myometrial segment
• Endothelial lining replaced by fibrinoid
formation
• Spiral artery becomes distended and
funnel shaped
• Low resistance, low pressure and high
flow system spiral atrery
• 2nd wave of artery migration is absent
in preeclampsia so reduction of blood
supply to the fetoplacenta unit
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7. In pre-eclampsia
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8. Etiopatogenesis
▪ Hypertension
– endothelial dysfunction due to oxidative stress
and inflammatory mediators
– vasospasm due to imbalance of vasodilators (
PGI2, NO)and vasoconstrictors( angiotensin
II TXA2 and endothelin)
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9. ▪ Edema
– Increased oxidative stress⭢ endothelial injury ⭢
increased capillary permeability ⭢edema
▪ Proteinuria
– Spasm of glomerular arteriole⭢ anoxic change in
the endothelium of glomerular tuft⭢ increased
capillary permeability⭢ increased leaking of
protein
– Decreased tubular reabsorption
– Albumin constitutes 50-60% and globulin 10-15%
of total protein excreted in the urine
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10. • HELLP syndrome
– Hemolysis
– Elevated liver enzymes (AST and ALT>70
IU/l, LDH >600 IU/l, bilirubin (>1.2mg/dl)
– Low platelet count (<100000/mm3)
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11. Types
• Mild
– Blood pressure
>140/90 mmHg
– Systolic <160
mmHg
– Diastolic <110
mmHg
– No significant
proteinuria
• Severe
– Systolic >=160 mmHg or
diastolic>=110 mmHg
– Proteinuria >5gm/24 hr
– Oliguria (˂400ml/24hr)
– Platelet count <100000/mm3
– HELLP syndrome
– Cerebral or visual disturbances
– Retinal hemorrhage, exudatea
or papilledema
– Epigastric pain
– IUGR
– Pulmonary edema 11

12. Clinical Features
• Mild symptoms:
– Slight swelling over the ankles
– Gradually swelling extend to face,
abdominal wall, vulva and whole body
• Alarming symptoms:
– Headache
– Disturbed sleep
– Diminished urinary output
– Epigastric pain
– Eye symptoms (blurring, dimness of
vision)
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13. • Signs
– Abnormal weight gain
– Increased blood pressure
– Edema
– Pulmonary edema
– Placental insufficiency
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14. Investigations
• Urinalysis
– Protein
– Cast (red cell, epithelial)
• Opthalmoscopic examination
• Blood values
– Serum uric acid level >4.5 mg/dl and
– Serum creatinine level >1 mg/dl
– Abnormal coagulation profile
• Antenatal fetal monitoring:
– Fetal kick count, USG for fetal growth and liqour ,
cardio-tocography, umbilical artery flow, etc.
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15. Complications of Preeclampsia
• Immediate
– Maternal
• During pregnancy: Eclampsia, accidental hemorrhage,
dimness of vision, preterm labor, HELLP syndrome,
cerebral hemorrhage,ARDS
• During Labor: Eclampsia, postpartum hemorrhage
• Puerperium: Eclampsia, shock, sepsis
– Fetal
• Intrauterine death, IUGR, asphyxia, prematurity
• Remote
• Residual HTN, Recurrent pre-eclampsia, Chronic renal
disease
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16. Prevention of Preeclampsia
• Regular ANC
• Anti-thrombin agents
– Low dose aspirin 60 mg daily
• Heparin or LMWH
• Ca supplementation
• Balanced diet (rich in protein)
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17. management
Objectives:
• To stabilize hypertension
• To prevent complications
• To prevent eclampsia
• Delivery of a healthy baby in optimal time
• Restoration of health of mother in
puerperium
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18. Therapeutic Measures
• Rest
– Helps by
•Increasing renal blood flow – ⭢ diuresis
•Increases uterine blood flow - ⭢ placental
perfusion
•Reduces BP
• Diet
– Adequate daily protein (100 g)
– Total calorie intake approx. 1600 cal/day
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19. Therapeutic Measures
• Diuretics
– Not preferred as:
• ⭢ placental perfusion
• cause electrolyte imbalance
– Indications
• Cardiac failure
• Pulmonary edema
• Along with selective anti-HTN causing fluid retention
• Massive edema
– Furosemide x PO X 40 mg x 5 days in a week
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20. Therapeutic Measures
• Antihypertensives
– Limited use
– Indications
• Persistent rise in BP associated with proteinuria
• In severe preeclampsia to bring down the BP
• Commonly used anti-HTNs
– Methyl dopa (250-500 mg TDS)
– Labetalol (100 mg TDS/QID)
– Nifedipine (10-20 mg BD)
– Hydralazine (10-25 mg BD)
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21. Management of Severe
Preeclampsia
(hypertensive crisis)
• Labetalol
– (10-20 mg IV every 10 min)
• Hydralazine
– (5 mg IV every 30 min)
• Nifedipine
– (10-20 mg PO every 30 min)
• Short term (when others have failed)
– Nitroglycerin (5 μg/min IV)
– Sodium nitroprusside (0.25 – 5 μg/kg/min IV)
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22. Progress Chart
• Daily clinical evaluation for symptoms
• Blood Pressure (4xday)
• State of edema and Daily weight record
• Fluid intake and urine output
• Urine RE
• Blood (Hct, Plt, Uric acid, Cr, LFT once a wk)
– Coagulation profile if Platelet ≤ 100,000/ml
• Ophthalmoscopic exam on admission
• Fetal wellbeing assessment (USG, Biophysical
profile, amniotic fluid level)
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23. Duration ofTreatment
• Definitive treatment
– Termination of pregnancy (delivery of fetus)
– Continue pregnancy without affecting maternal prognosis
until fetus becomes mature enough to survive in
extrauterine environment (≥ 37 wks)
• Duration of treatment depends on
– Severity of pre-eclampsia
– Duration of pregnancy
– Response to treatment
– Materna and fetal evaluation report
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24. Grouping of Patients
• Group A
Pre-eclamptic features subside and HTN is mild
• Group B
Partial control of features but BP is high and
steady
• Group C
Persistently increasing BP to severe level despite
use of anti-HTN with additional features
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25. Methods of delivery
• Induction of labor
• Cesarean section
Indication are:
1. urgent termination and unripe cervix
2. Severe pre-eclampsia
3. Complicating factors such as elderly primi ,
contracted pelvis, malpresentation
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26. Management during Labor
• Anti-HTN given if BP becomes high
• Prophylactic MgSO4
– if systole ≥ 160 mmHg
– if diastole ≥ 110 mmHg
– if MAP ≥ 125 mmHg
• Reduce duration of labor by
– 1st stage- Low rupture of membrane
– 2nd stage- Forceps or ventouse delivery
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27. Puerperium
• Observe patient closely for at least 48 hrs
• If BP (systolic ≥ 150 or diastolic ≥ 100)
– continue anti-HTNs
– Oral Nifedipine 10 mg x 6 hourly x until BP below
HTN level for at least 48 hours
• With severe pre-eclampsia/acute fulminant
pre-eclampsia
– MgSO4 for 24 hrs
• Admit until
– BP lowers to safe level and proteinuria disappears
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28. Acute Fulminant Preeclampsia
• Clinical condition where onset of pre-eclamptic
manifestations is acute, occurring de novo or
there is rapid deterioration of the established
pre-eclampsia with severe HTN over a short
period of time
• Treatment
– If detected at home ⭢adequately sedate by
• Pethidine 75-100 mg
• Diazepam 10 mg IM
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29. – Shift gently to hospital setting
– Start prophylactic anticonvulsant therapy
– Start parenteral anti-HTNs
– Monitor BP, Urine output, Blood parameters,
Proteinuria
– If condition fails to improve within 6-8 hrs ⭢ plan
delivery
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30. Induction of Labor
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31. References
• Williams Obstetrics, 24th
edition
• D.C. Dutta,Textbook of Obstetrics, 9th edition
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32. ThankYou
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33. Eclampsia

34. Eclampsia
▪ Eclampsia refers to the occurrence of one or
more generalized convulsions and/or coma in
the setting of preeclampsia and in the absence
of other neurologic conditions.
▪ Can appear anytime from the second trimester to
the puerperium
▪ More commonly on third trimester
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35. Causes of Convulsion
• Anoxia — spasm of the cerebral vessels- increased
cerebral vascular resistance- fall in cerebral oxygen
consumption- anoxia
• Cerebral edema — may contribute to irritation
• Cerebral dysrhythmia — increases following anoxia
or edema.
• Excessive release of excitatory neurotransmitters
(glutamate)
• Loss of cerebrovascular autoregulation with forced
dilatation and vasospasm
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36. Onset of Fits
• Antepartum (50%)
• Intrapartum (30%)
• Postpartum (20%)
• Intercurrent (Antenatal)
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37. Stages
• Premonitory stage: (30 seconds)
– patient becomes unconscious
– twitching of the muscles of the face, tongue, and limbs
– Eyeballs roll or are turned to one side and become
fixed
• Tonic stage: (30 seconds)
– whole body goes into a tonic spasm
– Respiration ceases and the tongue protrudes between
the teeth
– Cyanosis
– Eyeballs become fixed
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• Clonic stage: (1–4 minutes)
– All the voluntary muscles undergo alternate
contraction and relaxation.
– twitching start in the face then involve one side of the
extremities and ultimately the whole body is involved
in the convulsion
– Biting of the tongue
– Breathing is stertorous and blood stained frothy
secretions fill the mouth
– Cyanosis gradually disappears

39. Stage of coma:
• Following the fit, the patient passes on to the stage
of coma.
• It may last for a brief period or in others deep
coma persists till another convulsion.
• On occasion, the patient appears to be in a
confused state following the fit and fails to
remember the happenings.
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40. Differential Diagnosis
*Absence of previous history of convulsions +
Edema + Hypertension+ Proteinuria+ Fits/Coma
• Epilepsy
• Encephalitis
• Meningitis
• Poisoning
• Cerebral malaria
• Intracranial tumors
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41. Complications
Maternal:
• Injuries
• Pulmonary complications
(Edema, Pneumonia,ARDS,
Embolism)
• Hyperpyrexia
• Cardiac
• Renal failure
• Hepatic
Fetal: Prematurity, Intrauterine asphyxia, effects of drugs,
Trauma
• Cerebral
• Neurologic deficits
• Disturbed vision
• Hematological
(Thrombocytopenia, DIC)
• Postpartum
(Shock, Sepsis, Psychosis)
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42. First AidTreatment andTransport
• Detail maternal records
• Stabilise BP,Arrest Convulsions
• MgSO4 (4g IV loading + 10 g IM)
• Labetalol (20 mg IV)
• Diuretic
• Diazepam (5mg slowly over 1 minute )
• Medical Personnel
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43. General Management
❖ Supportive care
•Prevent serious maternal injury from fall
•Prevent aspiration
•Maintain airway
•Ensure Oxygen
❖ History
❖ Examination
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44. ❖ Monitoring
•Half hourly- pulse, respiration rates and blood pressure
,Hourly- urinary output
❖ Fluid balance:
• Crystalloid solution (Ringer’s solution)
• Total fluids should not exceed the previous 24 hours
urinary output plus 1000 ml (insensible loss through
lungs and skin).
• Rate : 1 ml/kg per hour.
❖ Antibiotic:
• Ceftriaxone 1 gm IV twice daily is given.
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45. SPECIFIC MANAGEMENT
Magnesium sulfate
• acts as a membrane stabilizer and neuroprotector.
• Reduces motor endplate sensitivity to acetylcholine
• blocks neuronal calcium influx
• induces cerebral vasodilatation, dilates uterine
arteries, increases production of endothelial
prostacyclin and inhibits platelet activation
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• Repeat injections are given only if
– knee jerks are present
– urine output > 30 mL/hour
– respiration rate >12 per minute
• Magnesium sulfate is continued for 24 hours after the last seizure
or delivery
• For recurrence of fits, further 2 gm IV bolus is given over 5 min in
the above regimens.
Regimen Loading Dose Maintenance Dose
Intramuscular
(Pritchard)
4 gm IV over 3-5 min
Followed by 10 gm IM (5
gm in each buttock)
5 gm IM 4 hourly in
alternate buttock
Intravenous
(Zuspan or Sibai)
4-6 gm IV over 15-20
min
1-2 gm/hr IV infusion
The therapeutic level of
serum magnesium is 4–7
mEQ/L

47. Detection of magnesium toxicity
• Loss of deep tendon reflexes
• Decreased respiratory rate
• Urine output
• Chest pain, heart block, pulmonary edema
• Oxygen saturation monitoring
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48. • Antihypertensives and diuretics:
– blood pressure > 160/110 mm Hg
• Pulmonary edema
• Heart failure:
• Anuria
- Dopamine infusion (1 macrogm/kg)
• Hyperpyrexia:
• Psychosis: Chlorpromazine or Eskazine (trifluoperazine)
is quite effective
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