Preeclampsia is defined as new onset hypertension and proteinuria after 20 weeks of gestation. It can progress to eclampsia, which is characterized by seizures in addition to the symptoms of preeclampsia. Magnesium sulfate is the primary treatment for preventing seizures in women with eclampsia, as it is more effective than other anticonvulsants like diazepam or phenytoin. Care of women with eclampsia involves prevention of seizures, management of hypertension, and evaluation for prompt delivery of the fetus once the mother is stabilized.
Amniotic Fluid Embolism [AFE] Approach to ManagementArun Vasireddy
Amniotic fluid embolism (AFE) is a life threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation.
Steiner and Luschbaugh first described AFE in 1941, after they found fetal debris in the pulmonary circulation of women who died during labor. Data from the National Amniotic Fluid Embolus Registry (USA) suggest that the process is more similar to anaphylaxis than to embolism, and the term anaphylactoid syndrome of pregnancy has been suggested because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE.
The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
Amniotic Fluid Embolism [AFE] Approach to ManagementArun Vasireddy
Amniotic fluid embolism (AFE) is a life threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation.
Steiner and Luschbaugh first described AFE in 1941, after they found fetal debris in the pulmonary circulation of women who died during labor. Data from the National Amniotic Fluid Embolus Registry (USA) suggest that the process is more similar to anaphylaxis than to embolism, and the term anaphylactoid syndrome of pregnancy has been suggested because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE.
The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
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Eclampsia is conclusive and convulsive phase of a wide spectrum disease pre eclampsia. More conclusive RCT are required to assert the efficacy of biomarkers as a sensitive predictability of eclampsia.
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Eclampsia is conclusive and convulsive phase of a wide spectrum disease pre eclampsia. More conclusive RCT are required to assert the efficacy of biomarkers as a sensitive predictability of eclampsia.
Pregnancy induced hypertension introduction
Classification of pregnancy induced hypertension
Preeclampsia -
Definition
Criteria for diagnosis of preeclampsia,
Epidemiology of preeclampsia,
Risk factors of preeclampsia,
Pathogenesis of preeclampsia,
Pathophysiology of preeclampsia,
Course of preeclampsia,
Complications of preeclampsia,
What is HELLP ?
Management of preeclampsia at home, at hospital, during labour, during puerperium,
Management of acute fulminant preeclampsia
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2. PREECLAMPSIA
New onset of hypertension and proteinuria after
20 weeks of gestation in a previously
normotensive woman
Criteria for the diagnosis of preeclampsia
Systolic blood pressure ≥140 mmHg
Or
Diastolic blood pressure ≥90 mmHg
And
Proteinuria ≥0.3 grams in a 24-hour urine
specimen
Sibai b et al. Preeclampsia. Lancet.2005;365:785-799
3. Eclampsia –
Occurrence of one or more generalized
convulsions and/or coma in the setting of
preeclampsia and in the absence of other
neurologic conditions.
Sibai b et al. ACOG. Diagnosis, prevention and mm of eclampsia;.2005;402-410
4. Eclamptic seizure occurs in 2-3 % of
severely preeclamptic women not receiving
anti-seizure prophylaxis;
Incidence of eclampsia in developing
countries varies widely: from 6 to 157 cases
per 10,000 deliveries
5. Approximately one maternal death due to
eclampsia per 100,000 live births
case-fatality rate of 6.4 deaths per 10,000 cases
Geographic variation in the incidence of hypertension in pregnancy. World Health
Organization International Collaborative Study of Hypertensive Disorders of Pregnancy.
Am J Obstet Gynecol 1988; 158:80.
Lubarsky SL, Barton JR, Friedman SA, et al. Late postpartum eclampsia revisited. Obstet
Gynecol 1994; 83:502
6. Nulliparity
Preeclampsia in a previous pregnancy
Age >40 years or <18 years
Family history of preeclampsia
Chronic hypertension
Chronic renal disease
Antiphospholipid antibody syndrome or inherited
thrombophilia
Vascular or connective tissue disease
Diabetes mellitus (pregestational and gestational)
Multifetal gestationHigh
body mass index
7. Black race
Hydrops fetalis
Unexplained fetal growth restriction
Fetal growth restriction,
abruptio placentae, or fetal demise in a previous
pregnancy
Prolonged interpregnancy interval
Partner related factors (new partner, limted sperm
exposure [eg, previous use of barrier contraception])
Hydatidiform mole
Susceptibility genes
11. Headache- temporal, frontal, occipital, or
diffuse
Generalized hyperreflexia; sustained ankle
clonus may be present.
Visual symptoms - include blurred vision,
flashing lights (photopsia), and scotomata .
Diplopia or amaurosis fugax may also occur.
Cortical blindness is rare .
12. Blindness related to retinal pathology, optic
nerve damage, retinal artery spasm, and
retinal ischemia, may be permanent
Seizures
Posterior reversible leukoencephalopathy
syndrome (PRES)
Stroke leading to death or disability is the
most serious complication
13. Cerebral overregulation results in vasospasm
of cerebral arteries, underperfusion of the
brain, localized ischemia/infarction, and
cytotoxic (intracellular) edema.
Loss of autoregulation of cerebral blood flow
(ie, hypertensive encephalopathy) results in
hyperperfusion, endothelial damage, and
vasogenic (extracellular) edema.
Morriss MC, Twickler DM, Hatab MR, et al. Cerebral blood flow and cranial
magnetic resonance imaging in eclampsia and severe preeclampsia. Obstet
Gynecol 1997; 89:56
14. General principles-
The immediate issues in caring for an
eclamptic woman include:
1. Prevention of maternal hypoxia and trauma
2. Management of severe hypertension, if
present
3. Prevention of recurrent seizures
4. Evaluation for prompt delivery.
15. Maternal assessment should include:–
History and examination: BP, weight gain,
edema, sensorium
–Serial or continuous blood pressure
monitoring
–Urinanalysis for proteinuria
–quantification for degree of severity
16. –Blood test include
•Platelet count and morphology, CBC
•Haemocoagulation system: PT, aPTT
•Uric acid, creatinin, electrolytes for renal
function
•Serum uric acid –useful early and for
progression
•Hepatic enzymes (AST,ALT,GGT)& bilirubin
–Fluid balance –urine output, CVP, SP02 etc
–ECG
17. •Cerebral imaging is not necessary for the
diagnosis and management of most women
with eclampsia.
•Cerebral imaging findings in eclampsia are
similar to those found in patients with
hypertensive encephalopathy.
18. Cerebral imaging is indicated :-
•focal neurologic deficits
•prolonged coma
•atypical presentation for eclampsia:
•onset before 20 weeks of gestation or
•more than 48 hours after delivery
•eclampsia refractory to adequate mgso4 therapy
Sibai BM. Hypertension and Obstetrics. Churchill Livingstone. 2002
19. •Fetal monitoring:–
-Cardiotocography–for acceleration, loss of
variability or decelerations
–Fetal ultrasound -may be useful for fetal size and
morphology, amniotic fluid volume estimation
–Placental and fetal blood flow measurement of
uterine artery and main fetal Doppler
velocimetry(including diastolic flow)
20. Treatment required when:–
Systolic bp> 160 mm Hg or
Diastolic bp> 110 mm Hg
Hydralazine: agent of choice(5-10mg IV
max30)
–Causes direct arteriolar vasodilation
–Improves renal and uteroplacental blood flow
21. •Labetalol: causes rapid decrease in arterial
bp without compromising uteroplacental flow
–May cross placenta but fetal complications
rare
–20-40mg every 30min for a max of 220mg
IV
22. Nifedipine: oral 10-20mg every 30min for a
max of 50mg
-causes direct relaxation of arteriolar smooth
muscle
–Maintains uterine perfusion
–Can cause uterine muscle relaxation
–increase risk of post partum haemorrhage–
Relative contra-indication with use of Mg
23. •Sodium nitroprusside: hypertensive
emergencies but should be avoided due to
safety concern
•Nitroglycerin : useful especially when
pulmonary oedema complicates situation
WHO recommmendations for prevention and treatment of PEC & EC 2011
24. Reasonable goal is systolic BP of 140 to 155
mmHg and diastolic BP of 90 to 105 mmHg.
In women with extremely severe
hypertension (≥180/120 mmHg), a diastolic
goal of 100 to 105 mmHg should be achieved
within two to six hours, with the maximum
initial (within 10 to 20 minutes) fall in BP not
exceeding 25 percent of the presenting value
Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000; 356:411.
Ledingham JG, Rajagopalan B. Cerebral complications in the treatment of accelerated
hypertension. Q J Med 1979; 48:25
25. Use of antihypertensive agents to control
mildly elevated blood pressure in the setting
of preeclampsia/eclampsia has not been
shown to alter the course of the disease, nor
to diminish perinatal morbidity or mortality.
Sibai BM. Treatment of hypertension in pregnant women. N Engl J Med 1996; 335:257.
von Dadelszen P, Ornstein MP, Bull SB, et al. Fall in mean arterial pressure and fetal growth
restriction in pregnancy hypertension: a meta-analysis. Lancet 2000; 355:87.
Magee LA, Ornstein MP, von Dadelszen P. Fortnightly review: management of hypertension in
pregnancy. BMJ 1999; 318:1332.
26. •Airway protection
•Maintain oxygenation(O2 inhalation via mask)
•Control of seizures–Continued convulsions may
indicate other cerebral pathology–Management
may involve treatment cerebral oedema
•Delivery of fetus when mother is in stable
condition, even in some situation CS is needed
acutely
27. •Magnesium sulphate: -anticonvulsant of choice
–Action by:
•antagonism of calcium and hence decreased
systemic and cerebral vasospasm
•Increase release of PGI2 by vascular endothelium
–Other effects in parturient include:
•Tocolysis
•Decreased cathecholamine release
•Mild antihypertensive
•Increases renal and uterine blood flow
28. –Renaly excreted–so reduce dose in renal
failure
–Therapeutic level 4-7 mEq/l ; must monitor
for toxicity
–Repeated seizures despite therapeutic levels
need to consider other anticonvulasnts.
29. Regimen Loading Dose Maintenance Dose
Pritchard
(Intramuscular)
4gm IV over 3-5 min
f/b 10gm deep IM(5gm
each buttock)
5gm IM 4 hourly in
alternate buttock
Zuspan or Sibai
(Intravenous)
4gm IV over 15-20
min.
1-2gm/hr IV infusion
4/2/2015Dutta’s. Hypertensive disorder of pregnancy: 17 29
31. An additional benefit of magnesium
sulfate therapy is in women expected to have
a preterm delivery within 24 hours have
consistently demonstrated a decreased risk of
cerebral palsy and severe motor dysfunction
in offspring
Crowther CA, Hiller JE, Doyle LW, et al. Effect of magnesium sulfate given for neuroprotection before
preterm birth: a randomized controlled trial. JAMA 2003; 290:2669.
Rouse DJ, Hirtz DG, Thom E, et al. A randomized, controlled trial of magnesium sulfate for the
prevention of cerebral palsy. N Engl J Med 2008; 359:895.
32. • Additional bolus of 2 grams of magnesium
sulfate over 15 to 20 minutes, with careful
monitoring for signs of magnesium toxicity.
• Phenytoin : effective in pre-eclampsia
–Central anticonvulsant activity
–No effect on uterine tone, fetal HR or neonatal
tone
•Diazepam: effective especially if needed acutely
but causes fetal/ neonatal
complications(depression of muscle tone and
breath centre)
33. The Eclampsia Trial Collaborative Group
conducted two prospective trials
The primary outcome measures were the
rates of recurrent seizures and maternal
death.
Magnesium sulfate was significantly more
effective than either diazepam or phenytoin:
Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial.
Lancet 1995; 345:1455.
34. Additional advantages of magnesium sulfate therapy
include lower cost, ease of administration and less
sedation .
Magnesium also appears to selectively increase
cerebral blood flow and oxygen consumption in
women with preeclampsia
Belfort MA, Moise KJ Jr. Effect of magnesium sulfate on maternal brain blood flow in
preeclampsia: a randomized, placebo-controlled study. Am J Obstet Gynecol 1992; 167:661.
36. Most common causes of both ischemic and
hemorrhagic stroke in pregnancy.
The most frequent cerebrovascular disturbance
associated with eclampsia is a reversible
encephalopathy.
Women with preeclampsia are at risk for stroke
and cardiovascular disease well after the
postpartum period and child bearing years. The
relative risks ranged from 1.39 to 5.08.
B. J. Wilson, M. S. Watson, G. J. Prescott et al., “Hypertensive diseases of pregnancy and risk of
hypertension and stroke in later life: results from cohort study,” British Medical Journal, vol.
326, no. 7394, pp. 845–849, 2003
37. -Preeclampsia/eclampsia commonly associated
with ischemic stroke of arterial origin [36
percent])
-Intracerebral hemorrhage [55 percent]) but less
frequently with cerebral venous thrombosis (13
of 136 cases [10 percent])
Cantu-Brito C, Arauz A, Aburto Y, et al. Cerebrovascular complications during pregnancy and postpartum:
clinical and prognosis observations in 240 Hispanic women. Eur J Neurol 2011; 18:819
38. Is a clinical radiologic syndrome of
heterogeneous etiologies that are grouped
together because of similar findings on
neuroimaging studies
RPLS may occur in the setting of preeclampsia
due to impaired cerebral autoregulation from
endothelial damage.
40. Clinical presentation
Headaches
Altered consciousness
Visual disturbances
Seizures - are usually generalized tonic
clonic; they may begin focally.
41. Other risk factors-
Acute and chronic renal failure
Immunosuppressive agents and cytotoxic drugs
Hemolytic and uremic syndrome
Collagen vascular disorders
leukemia
Behcets syndrome
TTP
HIV
Acute intermittent prophyria
Hypercalcemia,hypomagnesmia
Contrast media exposure
Cryoglobulinemia
42. Some suggest that PRES (typical clinical syndrome
and neuroimaging findings) could be considered an
indicator of eclampsia, even when the other
features of eclampsia (proteinuria, hypertension)
are not present.
Br J Obstet Gynaecol 1997 Oct;104(10):1165-72
43. FLAIR images show high signal symmetrically involving bilateral
parieto-occipital, posterior frontal, and temporo-occipital regions
44. The classical presentation of RCVS, also
known as Call Fleming Syndrome, is a
thunderclap headache, with or without
additional neurologic signs.
Diagnostic imaging reveals multifocal
segmental vasoconstriction of the cerebral
arteries, which usually resolves within days to
weeks.
45. Calcium channel blockers may be initiated,
such as nimodipine or verapamil, although
caution should be employed to maintain
cerebral perfusion in watershed regions of a
constricted artery.
The primary difference between RPLS and
RCVS is in the clinical symptoms.
L.H. Calabrese, D.W. Dodick, T. J. Schwedt, and A. B. Singhal, “Narrative review: reversible cerebral
vasoconstriction syndromes,” Annals of Internal Medicine, vol. 146, no. 1, pp. 34– 44, 2007.
46. There is nearly a 4-fold odds of developing
hypertension (OR 3.7, 95% CI 2.70–5.05)
2-fold risk of ischemic heart disease (OR
2.16, 95% CI 1.86–2.52) in women with
preeclampsia.
For fatal and nonfatal stroke, relative risks
ranged from 1.39 to 5.08.
Children may also be at increased risk for
neurological problems and stroke.
47. There was a significant reduction in the rate of
preeclampsia with low dose aspirin started at 16
weeks gestation or earlier in women identified as
moderate or high risk.
Vitamin D deficiency has recently emerged as an
important potentially modifiable risk factor for
both preeclampsia and stroke.
E. Bujold, S. Roberge, Y. Lacasse et al., “Prevention of preeclampsia and intrauterine growth restriction with aspirin started in early
pregnancy: a metaanalysis,” Obstetrics and Gynecology, vol. 116, no. 2 PART 1, pp. 402–414, 2010.