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1. Dr Mekuanint D. (OBGY year II Resident )
Modulator: Dr Tizita (OBGY Consultant)
Yekatit 12 HMC/Abebech Gobena /
April,2021
Management of preeclampsia and
Eclampsia

2. Outline
 Introduction
 Incidence
 Classification
 Risk factors
 Etiopathogenesis
 Management
 Eclampsia
2

3. INTRODUCTION
 Preeclampsia is a multisystem, progressive disorder
characterized by
 new onset of hypertension and proteinuria or
 hypertension and end-organ dysfunction with or without
proteinuria in the last half of pregnancy
 A key focus of routine prenatal care is monitoring
pregnancies for signs and symptoms of preeclampsia.
3

4. Incidence
 Most common medical complications of pregnancy
 5% and 10%
 5 percent in white, 9 percent in Hispanic, and 11 percent in
African-American women
4

5. Classification
 Preeclampsia and eclampsia syndrome
 Chronic hypertension of any etiology
 Preeclampsia superimposed on chronic hypertension
 Gestational hypertension
5

6. Diagnosis
6

7. Indicators of Severity
7

8. Risk Factors
High risk
8
 >= 1
 Low dose Asprine

9. Moderate risk
9
 More than one
 Consider low dose
Asprine

10. Low risk
10
 Previously uncomplicated
full term delivery
 Asprine is Not
recommended

11. ETIOPATHOGENESIS
Develop in women with the following characteristics:
 exposed to chorionic villi for the first time
 exposed to a superabundance of chorionic villi, as with twins or hydatidiform
mole
 preexisting conditions associated with endothelial cell activation or
inflammation,
 diabetes,
 obesity,
 cardiovascular or renal disease,
 immunological disorders, or
 hereditary influences
 genetically predisposed to hypertension developing during pregnancy.
11

12.  A fetus is not a requisite for preeclampsia to develop.
 although chorionic villi are essential, they need not be
intrauterine.
12

13. …Etiology
 Placental implantation with abnormal trophoblastic invasion of
uterine vessels
 Immunological maladaptive tolerance between maternal,
paternal (placental), and fetal tissues
 Maternal maladaptation to cardiovascular or inflammatory
changes of normal pregnancy
 Genetic factors including inherited predisposing genes and
epigenetic influences.
13

14. 14

15. …Pathogenesis
 Regardless of precipitating etiology,
 cascade,
 systemic vascular endothelial damage with resultant
 vasospasm,
 transudation of plasma,and
 ischemic and
 thrombotic sequelae
15

16. Management
 Management varies depending
 gestational age
 severity
 Preeclampsia with features of severe disease
 <28 week –Termination
 28-34 week-expectant management is recommended
 34-37 week--expectant management may be recommended
16

17. …
17
 Preeclampsia without features of severe disease
 <37 week-- expectant
 ≥37 weeks —termination

18. Treatment of hypertension
 Severe hypertension should be treated to prevent maternal
vascular complications (eg, stroke, heart failure)
 systolic pressure is ≥160 mmHg or diastolic pressure is ≥105
to 110 mmHg
18

19. Choice of drug and dose
 two settings
 Acute management of severe hypertension, which may require
parenteral therapy, and
 Longer-term blood pressure control during expectant
management of severe preeclampsia
19

20. Acute therapy
 intravenous labetalol or hydralazine as first-line agents
 Nifedipine
20

21. Labetalol
 effective, has a rapid onset of action, and a good safety
profile.
 Begin with 20 mg intravenously over 2 minutes followed at
10-minute intervals by doses of 20 to 80 mg up to a
maximum total cumulative dose of 300 mg, if blood pressure
remains above target level
 A constant infusion of 1 to 2 mg/min can be used
 The fall in blood pressure begins within 5 to 10 minutes and
lasts from 3 to 6 hours
21

22. Hydralazine
 5 mg intravenously over 1 to 2 minutes
 If a total dose of 30 mg does not achieve optimal blood
pressure control, another agent should be used.
 The fall in blood pressure begins within 10 to 30 minutes and
lasts from 2 to 4 hours.
22

23.  Calcium channel blockers
Nifedipine
 30 mg sustained release tablet
Nitroglycerin
 hypertension associated with pulmonary edema
 It is given as an intravenous infusion of 5 mcg/min and
gradually increased every 3 to 5 minutes to a maximum dose of
100 mcg/min.
23

24. Long-term oral therapy
 Nifedipine
 Alpha methyldopa
•Administer 250-750 mg every six to eight hours.
 The maximum dose is 3000 mg per 24 hours
24

25. Seizure prophylaxis
 Candidates for seizure prophylaxis
 Intrapartum and postpartum seizure prophylaxis to all women
with preeclampsia,
 Drug of choice:
 Magnesium sulfate
25

26. Dosing
 loading dose of 6 g of a 10 percent solution intravenously
over 15 to 20 minutes followed by 2 g/hour as a continuous
infusion
 5 g of a 50 percent solution intramuscularly into each
buttock (total of 10 g) followed by 5 g intramuscularly every
four hours
 therapeutic range of 4.8 to 8.4 mg/dL (2.0 to 3.5 mmol/L)
26

27.  Renal insufficiency
 Magnesium sulfate is excreted by the kidneys.
 Women with renal insufficiency should receive a standard
loading dose
 Reduced maintenance dose.
 1 g/hour if the serum creatinine is >1.2 and <2.5 mg/dL
 no maintenance dose if the serum creatinine is ≥2.5 mg/dL or
magnesium toxicity is suspected
27

28. Timing of Magnesium sulfate
 at the onset of labor or induction, or prior to a cesarean
delivery
 while they are being considered for conservative
management.
 Prolonged antepartum therapy??
28

29. Side effects
 Rapid infusion of magnesium sulfate causes peripheral
vasodilation and a drop in blood pressure.
diaphoresis
flushing, and
warmth
Nausea
vomiting
29
headache
muscle weakness
visual disturbances, and
palpitations

30.  Transient reduction of total and ionized serum calcium
concentration due to rapid suppression of parathyroid
hormone release
30

31. Toxicity
 Magnesium toxicity is uncommon in women with good renal
function
 loss of deep tendon reflexes occurs at 7 to 10 mEq/L
 respiratory paralysis at 10 to 13 mEq/L
 cardiac conduction is altered at >15 mEq/L
 cardiac arrest occurs at >25 mEq/L
31

32. When to check magnesium levels
 every six hours
 A seizure while receiving magnesium sulfate
 Clinical signs/symptoms suggestive of magnesium toxicity
 Renal insufficiency (creatinine >1.2 mg/dL [106 micromol/L)
32

33.  Antidote
 Calcium gluconate
33

34. Preterm pregnancies:
 Conservative management
 the risks of serious sequelae from disease progression need to
be balanced with the risks of preterm birth
34

35. Indications for Delivery in Women <34
Weeks
 Uncontrolled severe hypertension
 Eclampsia
 Pulmonary edema
 Disseminated intravascular coagulation
 Placental abruption
 Nonreassuring fetal status
 Fetal demise
35

36. Corticosteroid—Delay Delivery 48 hr
 Preterm ruptured membranes or labor
 Thrombocytopenia <100,000/μL
 Hepatic transaminase levels twice upper limit of normal
 Fetal-growth restriction
 Oligohydramnios
 Reversed end-diastolic Doppler flow in umbilical artery
 Worsening renal dysfunction
36

37. Algorithm for severe preeclampsia at <34
37

38. 38

39. 39

40. Eclampsia :
40
 Development of convulsions or unexplained
coma during pregnancy or postpartum in
patients with signs and symptoms of PE.
 Excluding other posible cause of convulsion

41. Incidence
41
 1 in 2000 to 1 in 3448 pregnancies.
 2-3 % in PE with SF
 0.6% in PE without SF
 higher in
 tertiary referral centers
 Multifetal gestation
 in those without prenatal care

42. Pathophysiology
42
 The precise cause of seizures in preeclamptic women is not
clearly understood.
1. hypertension causes a breakdown of the autoregulatory
system of the cerebral circulation,
 hyperperfusion,
 endothelial dysfunction, and
 vasogenic and/or cytotoxic edema.

43. Pathophysiology…
43
2. hypertension causes activation of the autoregulatory system,
leading to vasoconstriction of cerebral vessels
 hypoperfusion,
 localized ischemia,
 endothelial dysfunction, and
 vasogenic and/or cytotoxic edema

44. CLINICAL PRESENTATION AND FINDINGS
44
 generalized tonic-clonic seizure or coma
 premonitory signs/symptoms
 Hypertension (75 percent)
 Headache
 Visual disturbances (27 percent)
 Right upper quadrant or epigastric pain (25 percent)
 Asymptomatic (25 percent)

45. Diagnosis
45
 convulsions
 hypertension,
 proteinuria, and
 However
 16% of cases, hypertension may be absent
 14% of the cases proteinuria may be absent

46. Diagnosis …
46
 Several clinical symptoms are potentially helpful
 persistent occipital or frontal headaches,
 blurred vision,
 photophobia,
 epigastric or right upper quadrant pain, and
 altered mental status.

47. Time of Onset
47
 Antepartum …
 Intrapartum
 postpartum period.
 first 48 hours
 beyond 48 hours
 extensive neurologic evaluation may be required to rule out the
presence of other cerebral pathology

48. Time of Onset …
48
 Almost all cases of eclampsia (91%) develop in the third
trimester (≥28 weeks).
 21 and 27 weeks’ gestation (7.5%)
 before 20 weeks’ gestation (1.5%)

49. MANAGEMENT
49
 maintaining airway patency and preventing
aspiration
 The woman should be rolled onto her left side.
Prevention of maternal hypoxia and trauma
Treatment of severe hypertension
Prevention of recurrent seizures
Evaluation for prompt delivery

50. Treatment of hypertension
50
 To prevent stroke, which accounts for 15 to 20 percent of
deaths from eclampsia.
 diastolic pressures greater than 105 to 110 mmHg or
 systolic blood pressures ≥160 mmHg
 Drugs
 Hydralazine
 Labetalol
 Nifidipine

51. 51
Diuretics
 Potent loop diuretics can further compromise placental
perfusion.
 before delivery, diuretics are not used to lower blood
pressure

52. Prevention of recurrent seizures
52
 Treatment is primarily directed at prevention of recurrent
seizures and the possible complications
 10 percent of eclamptic women will have repeated seizures
 The anticonvulsive drug of choice is magnesium sulfate.

53. 53
Loading dose
 4 to 6 g intravenously are commonly used
 5 g intramuscularly into each buttock for a total of 10 g;
 the onset of a therapeutic effect will be slower and
intramuscular injection is painful.
 These loading doses may be given safely to patients with
renal insufficiency.

54. 54
Maintenance dose
 1 to 3 g/hour are commonly used.
 5 g can be given intramuscularly every four hours;
 a lower dose maintenance regimen (2.5 g intramuscularly
every four hours)
 The maintenance phase is given only if a
 patellar reflex
 respirations are greater than 12 per minute, and
 urine output is over 100 mL in four hours

55. Management of persistent seizures
55
 Additional bolus of 2 g magnesium sulfate over 5 to 10
minutes
 Frequent monitoring for signs of magnesium toxicity
 If two such boluses do not control seizures, then other drugs
should be given.
 Diazepam or lorazepam is a common choice

56. Response to therapy
56
 Women who do not improve within 10 to 20 minutes
following control of hypertension and seizures and
 those with neurologic deficits
 should be evaluated by a neurologist
may have ongoing nonconvulsive seizures or
underlying structural pathology,
 such as hemorrhage

57. Evaluation for prompt delivery
57
 Contraindication to expectant management
 The definitive treatment for eclampsia
 prompt delivery;After maternal stabilization,

58. 58
 mode of delivery
 gestational age
 cervical status
 whether the patient is in labor, and
 fetal condition and position

59. complications of seizure
59
 Neuronal death
 Rhabdomyolysis
 Metabolic acidosis
 Aspiration pneumonitis
 Neurogenic pulmonary edema
 Respiratory failure

60. Prevention
60
 use of antihypertensive
 timely delivery, and
 prophylactic use of magnesium sulfate during labor and
immediately postpartum in those considered to have PE

61. Reference
61
 William’s obstetrics, 25th
ed.
 Gabbe obstetrics, 7th
ed.
 Up to date 2018
 ACOG PRACTICE BULLETIN
 MANAGEMENT PROTOCOL ON
SELECTED OBSTETRICSTOPICS FOR
HOSPITALS, Ministry of Health Ethiopia,2020

62. Thank you !!!
62
HAPPY ESTER!

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