1. Atypical PET&Eclapmsia
DR. SALAH ROSHDY,MD
PROFESSOR.OF
OBSTETRICS/GYNECOLOGY
QASSIM COLLEGE OF MEDICINE
Sohag University,Egypt

2. PRE: History
Eclampsia - Preeclampsia Prenatal Care
 2200 BC Egypt: pregnant women  New concept in the 20th
with fits century
 Eclampsia: Greek word: suddenly,
flash  1902: Ballantyne. Pro-
 1619: Varardus: first use of word
maternity clinic.
eclampsia  1910: USA. Nursing visits at
 1843: Lever. Proteinuria. Swelling home.
and convulsions: Nephritic  1920: Prenatal visits: check
toxemia
for hypertension, swelling,
 1897: Vaquez. Hypertension proteinuria to detect :
 1899: Strogonov: treatment, Preeclampsia
sedation
 1900s: prenatal care,
preeclampsia

3. Maternal Mortality: A Global Tragedy
 Annually, 585,000
women die of
pregnancy related
complications Cur
rent
 99% in developing App
roa
ch
world to
Re
 ~ 1% in developed duc
tion
countries of
Mat
ern
al
Mor
talit
3 y

4. Maternal Death Watch
 380 women become
Every Minute... pregnant
 190 women face
unplanned or unwanted
pregnancy
 110 women experience a
pregnancy related
complication
 40 women have an
unsafe abortion
 1 woman dies from a
pregnancy-related
complication
4

5. Global Causes of Maternal
Mortality
Hemorrhage 24.8%
Infection 14.9%
19.8 24.8
Eclampsia 12.9%
7.9
Obstructed Labor
6.9%
14.9 Unsafe Abortion
12.9 12.9%
6.9 12.9 Other Direct Causes
7.9%
Indirect Causes
19.8%

6. Maternal Mortality
 USA: 15/100,000 live births
 Mali: 800/100,000 live births
 Hemorrhage
 Embolism
 Preeclampsia
 Infection

7. Hypertensive Disorders of Pregnancy
6-8% of
all
gestations Chronic Hypertension
Pregnancy Induced (pre-existing or
Hypertension undiagnosed prior to
pregnancy))
PIH Preeclampsia
(no (PIH with
proteinuria) proteinuria)
Severe HELLP
Preeclampsia Eclampsia Syndrome AFLP

8. National High Blood Pressure Education Program
Classification ( NHEP) 2000
1-Gestational hypertension.
2-Preeclampsia (mild, severe)
3-Eclampsia.
4-Superimposed preeclampsia upon chronic
hypertension.
5-Chronic hypertension with pregnancy.

9. Risk Factors for Pre-eclampsia
 Nulliparity  Chronic renal disease
 Maternal age <16 or  Antiphospholipid
>40yrs syndrome (APLS)
 Multiple pregnancy  Diabetes mellitus
 Family history of pre-  Angiotensin gene T235
eclampsia or eclampsia
 Chronic (pre-existing)
hypertension

10. PREECLAMPSIA
 Only occurs in humans
 Incidence 5 % of pregnancies.
 200,000 Moms in USA
6 million World wide
 Leading cause of death & disability mothers and infants.
70,000 maternal deaths World wide every year
 Characterized by new onset of proteinuria and hypertension
after 20 weeks of pregnancy
 Cause of Preeclampsia remains unknown.

11. PREECLAMPSIA
 No clinically useful screening test
 Antihypertensive therapy lowers the blood pressure but
does not improve the fetal outcome.
 The only “cure” is delivery of the
placenta.

13. The placenta – perhaps as
as a result of ischemia –
secretes a factor into the
maternal circulation
which
produces systemic
endothelial dysfunction

14. ENDOTHELIAL DYSFUNCTION LEADS TO :
 Hypertension - disturbed endothelial control of vascular tone
 Proteinuria - increased glomerular vascular permeability
 Coagulopathy – abnormal expression of pro & anti coagulants
 Liver Dysfunction – ischemia & vasoconstriction

16. BIOMARKERS OF PLACENTAL DYSFUNCTION
 sVEGF R1
 Soluble Vascular Endothelial Growth Factor Receptor 1
 Also known as soluble fms-like tyrosine kinase 1 (sFlt-1)
 Anti-angiogenic protein
 Elevated in preeclampsia

17. BIOMARKERS OF PLACENTAL
DYSFUNCTION
 PlGF
 Placental Growth Factor
 Angiogenic protein, promotes angiogenesis
 Binds to VEGF Receptor (VEGF R1 and sVEGF R1)
 Free PlGF is reduced in preeclampsia

18. Normal Pregnancy Preeclampsia
sVEGF R1
PlGF sVEGF R1
PlGF
Healthy endothelial cell Endothelial cell injury
•Maintains vascular tone •Hypertension
•Maintains glomerular filtration •Proteinuria
•Maintains blood-brain barrier •Cerebral edema
•Maintains anti-coagulant state •Coagulation/liver function
abnormalities
Anti-angiogenic state: anti↑ / pro↓

19. The Constant Pathophysiological
Changes
Is
Vascular endothelial:
Damage +Dysfunction
+ Spasm

20. Possible mechanisms in Preeclampsia
Friedman and Lindheimer,1999

22. Multisystem Features Of Preeclampsia
Hypertension Proteinuria
Systemic blood vessels Kidneys
Multi-organ
Cerebral vessels disease Liver
Eclampsia HELLP syndrome
Fetus
Intra-uterine growth

23. Severe pre-eclampsia: symptoms, signs & diagnosti
criteria
Headaches
Visual Disturbances
Pulmonary Oedema
Hepatic Dysfunction
RUQ or Epigastric Pain
Oliguria
Elevated Creatinine
Proteinuria of 5 g or more in 24 hrs
Systolic BP > 160 to 180 mm Hg
Diastolic BP > 110 mm Hg
Thrombocytopaenia or haemolysis

24. Clinical Course of Neglected Severe Pre-eclampsia
CNS
Eyes Seizures
Arteriolar Spasm Intracranial Haemorrhage
Retinal Haemorrhage CVA
Papilloedema Encephalopathy
Transient Scotomata
Pancreas
Respiratory System Ischaemic Pancreatitis
Pulmonary Oedema
ARDS Kidneys
Acute Renal Failure
Liver
Subcapsular Haemorrhage Uteroplacental Circulation
Hepatic Rupture IUGR
Abruption
Haematopoietic System Fetal Compromise
HELLP Syndrome Fetal Demise
DIC

26. Case 1
 A 20-year-old primigravida was hospitalized at 37
weeks with regular contractions. She had had irregular
antenatal visits, which revealed no abnormality.
 She had a blood pressure (BP) between 130/80 and
100/60 mmHg on admission.
 Laboratory findings were unremarkable , with a trace of
proteinuria in the urinalysis.
 She had no prodromes suggestive of hypertensive
disease.
 She delivered a healthy female baby vaginally a few
hours later, uneventfully.

27. Case 1
 At 4 h after delivery, she developed a generalized
convulsion, lasting 23 min, despite being
normotensive,and soon after this she had two
other seizures.
 MgSO4 was given .
 Following the seizures, her BP ranged between
140/90 and 100/60 mmHg .
 Slight increases in the liver function tests and LDH
values and slight decreases in hemoglobin and
platelets were detected .

28. Case 1
 hemoglobin 10.3 mg/dL,
 hematocrit 31.5%,
 platelets 91,000/mm3,
 alanine aminotransferase (ALT) 35 U/L,
 aspartate transaminase (AST) 66 U/L,
 lactate dehydrogenase (LDH) 932 U/L).

29. Case 1
 Computed tomography (CT) was completely
normal. Subsequently, she had three more
seizures and another
 2-g bolus of MgSO4 was infused over 35 min
and continued for the following 24 h, during
which she suffered no further convulsion.
 The next day, a 24 h urine sample revealed
330 mg proteinuria;
 cranial magnetic resonance imaging (MRI)
showed no abnormality.

31. Case 2
 A 20-year-old nulligravida was admitted with
regular contractions at 37 weeks gestation.
 All her prenatal visits had been normal,
including BP, which was recorded as 120/80 to
110/70 mmHg.
 There was no prodrome of hypertensive disease
and no laboratory abnormality, including
platelet count, liver enzymes, LDH,
electrolytes, and glucose, although proteinuria
(3+) on dipstick was noticed on admission.

32. Case 2
 She delivered a 2800-g male fetus vaginally,
uneventfully.
 Following the delivery, her BP increased
suddenly to 150/100 to 140/100 mmHg.
 Then, she had a generalized seizure lasting
5-10 s. Then, 2 h later, she developed sudden
blindness, an occipital headache, and
myoclonic seizures, particularly involving
the right upper extremity.

33. Case 2
 The postictal BP was around 160/120 mmHg.
 MgSO4 was given for 24 h as the patient
seemed to have atypical eclampsia.
 She had no seizure subsequently. Her BP
remained high for a few days, ranging
between 150/100 and 140/90 mmHg and
normalized on postpartum day 3, with 930
mg/dL proteinuria in the 24 h urine collected
postpartum.
 Cranial MRI was unremarkable.

35. Case 3
 A 31-year-old multipara presented with
contractions at 33 weeks gestation with the
cervix 2 cm dilated and 40% effaced.
 Her BP was 110/70 to 110/60 mmHg on
admission.
 Her CBC,routine biochemical tests, and
coagulation studies were normal, but she
had a dipstick proteinuria of 3+.

36. Case 3
 On admission, the intrapartum fetal heart
rate recording revealed poor variability and
late decelerations.
 An emergency Cesarean delivery was
performed for fetal distress and a male fetus
weighing 1900 g was delivered with APGAR
scores of 4 and 6 at 1 and 5 min,
respectively.
 The baby was admitted to the intensive care
unit for respiratory distress syndrome

37. Case 3
 The placenta was atrophic, but not abrupted.
 Then, 2 h postoperatively, the mother became
hypertensive, with a BP of 160/100 to 150/100
mmHg, a severe headache and visual blurring.
 A MgSO4 infusion was started with a loading
dose over 20 minutes, followed by a
maintenance dose of 2 g/h as a continuous
intravenous infusion for 24 h.
 Three days later, she became normotensive and
her complaints resolved.

39. Atypical preeclampsia
Gestational hypertension plus
1 of the following items: Gestational proteinuria
 Symptoms of preeclampsia plus 1 of the following
items:
 Hemolysis  Symptoms of preeclampsia
 Hemolysis
 Thrombocytopenia (  Thrombocytopenia
100,000/mm3)  Elevated liver enzymes
 Early signs and symptoms of
 Elevated liver enzymes (2 times preeclampsia-eclampsia at 20
the upper limit of the normal weeks of gestation
value for  Late postpartum preeclampsia-
aspartate aminotransferase or eclampsia ( 48 hours after
alanine aminotransferase) delivery)

40. Signs and symptoms
 Right upper quadrant pain
Signs and pain
Epigastric symptoms results consistent with
 Retrosternal
preeclampsia chest pain
 Nausea and vomiting
 Shortness of breath/congestive heart failure
 Headaches (not responsive to analgesics)
 Visual changes
 Altered mental status
 Bleeding from mucosal membranes
 Jaundice

41. laboratory test results consistent
with preeclampsia
 Persistent proteinuria( 300 mg/24 h)
 Platelet count ( 100,000/mm3)
 Liver enzymes (aspartate aminotransferase or
alanine aminotransferase) 2 times the upper
limit of normal
 Serum creatinine ( 1.2 mg/dL)
 Lactic dehydrogenase 2 times the upper limit of
normal

43. Hypertension in Pregnancy
Chronic Gestational
Clinical Findings Hypertension Hypertension Preeclampsia
Onset < 20 weeks Third ≥ 20 weeks
trimester
Degree Mild or severe Mild Mild or severe
Proteinuria Absent Absent Usually present
Uric acid > 5.5 mg/dl Rare Absent Usually present
Hemoconcentration Absent Absent Severe disease
Thrombocytopenia Absent Absent Severe disease
Hepatic dysfunction Absent Absent Severe disease

44. CLINICAL CHARACTERISTICS AND LABORATORY TESTS USED TO DISCRIMINATE
PREECLAMPSIA FROM CHRONIC HYPERTENSION
PREECLAMPSIA CHRONIC HYPERTENSION
Age Extremes of age Older (≥30 years)
Parity Nulliparous Often multiparous
Time of diagnosis of After 20 weeks Before 20 weeks
hypertension
Maternal risk factors for Yes No
preeclampsia
Hypertension/preeclampsia Yes Yes
in prior pregnancies
Proteinuria (>300 mg/24hrs) Yes No
Serum uric acid Elevated (≥5.5 mg/dl) Normal to low
Elevated liver enzymes Yes No
Thrombocytopenia Yes No
Headache, blurred vision, Yes No
epigastric abdominal pain
Persistent hypertension No Yes
>12 weeks postpartum

45. 45

47. Frequency of Various Signs and Symptoms
Among Imitators of Pre-eclampsia–
Eclampsia
S&S HELLP AFLP TTP HUS Exce.SLE
Syndrome
Hypertensi 85% 50 % 20-75 % 80-90% 80 %
on
Protenuria 90-95% 30-50% +haemturia 80-90 % 100
%/nephritis
Fever Absent 25-30 % 20-50 % ? Common/fl
are
Jaundice 5-10 % 40-90 % Rare Rare Absent
N& 40 % 50-80 % Common Common Only/APA
Vomiting
Abd/Pain 60-80 % 35-50 % Common Common Only/APA
CNS 40-60 % 30-40 % 60-70 % ? 50%/APA

48. Lab HELLP AFLP TTP HUS Exce.SLE
Frequency of
Platelet >20,000 Various <20,000 and Symptoms
>50,000 Signs >20,000 >20,000
Haemolysis Imitators of Pre-eclampsia–
Among 50-100% 15-20 % 100 % 100 % 14-23% w/APA
Eclampsia
Anemia <50% Absent 100 % 100 % 14-23% w/APA
DIC <20% 73 % Rare Rare Rare
Hypoglycemia Absent 61% Absent Absent Absent
VW factor
multimers
Absent Absent 80-90% 80% <10%
ADAMTS 13% < 5%
Absent Absent 33-100% Rare Rare
Impaired renal f.
50% 90-100% 30% 100% 40-80%
LDH (IU/L) >600 Variable >1000 >1000 with APA
Elevated ammonia
Rare 50% Absent Absent Absent
Elevated bilirubin 50-60% 100% 100% <10%
Elevated Usually mild† Usually mild†
transaminases
100% 100% with APA

49. Differential diagnosis of eclampsia
 Cerebrovascular accidents
Hemorrhage
Ruptured aneurysm
Arterial embolism or thrombosis
Cerebral venous thrombosis
Hypoxic ischemic encephalopathy
Angiomas
 Hypertensive encephalopathy

50. Differential diagnosis of eclampsia
 Seizure disorders
 Previously undiagnosed brain tumors
 Metastatic gestational trophoblastic disease
 Metabolic diseases
 Reversible posterior leukoencephalopathy syndrome
 Thrombophilia
 Thrombotic thrombocytopenic purpura
 Postdural puncture syndrome
 Cerebral vasculitis

51. Management
Objective
 termination of pregnancy with the least
possible trauma to mother and fetus
 birth of an infant who subsequently thrives
 complete restoration of health to the mother

52. Termination of pregnancy
 Delivery is the cure for preeclampsia
 The prime objectives
 To forestall convulsion
 To prevent intracranial hemorrhage
 To prevent serious damage to vital organs
 To deliver a healthy infant

53. Management of pre-eclampsia
Sibai et al. Lancet 365:785-99, 2005.

54.  Elective cesarean delivery
 Labor induction to effect vaginal delivery has
traditionally been considered to be in the best
interest of the mother
 Several concerns have led some practitioners to
advocate cesarean delivery
 Unfavorable cervix precluding successful induction of
labor
 Perceived sense of urgency because of the severity of
preeclampsia
 The need to coordinate neonatal intensive care

55. LONG-TERM IMPLICATIONS FOR WOMEN WITH
PREECLAMPSIA
Increased incidence of salt-sensitive HTN
(Sibai et al, AJOG 1991, Wilson et al, BMJ 2003)
Increased risk for cardiovascular mortality
(Irgens et al, BMJ 2001, Funai E et al, Epidemiology 2005,
Arnadottir et al, BJOG 2005)
Increased incidence of chronic renal
disease reports of focal sclerosis, increased incidence of
renal biopsies, ESRD- Norwegian study – Vikse et al, JASN
2006, NEJM 2008

56. Why do we need early diagnosis?
For rule-in
Frequent follow-up with MFM specialist
Early measures may help
Steroids for fetal maturation
Specific interventions are under investigation
Aid obstetrician in the decision of when to deliver
(emergency delivery is often needed to save both baby
and mother)
For rule-out
Keep baby in utero
Eliminate unnecessary intervention
Peace of mind for both patient and physician

58. In conclusion
 The absence of hypertension or proteinuria
should not preclude diagnosing
preeclampsia/eclampsia.
 Eclampsia or fetal distress may be an
unusual presenting scenario in atypical cases
before the detection of overt hypertension or
proteinuria.

59. In conclusion
 Even minor clues in diagnoses, such as a
marginally elevated BP or trace proteinuria,
may be critical for appropriate, timely
management.
 Obstetricians should be aware of atypical
presentations,maintain a high level of
suspicion, and be ready to take immediate
steps.

60. Conclusion
 Moreover, valuable time should not be spent
conducting detailed investigations.
 The most common cause of convulsions in
association with hypertension or proteinuria during
pregnancy or immediately postpartum is eclampsia.
 However, late postpartum eclampsia is defined as
eclampsia that occurs more than 48 h, but less than
four weeks, after delivery


61. Conclusion
 All patients with atypical-onset eclampsia
should undergo a neurological evaluation to rule
out the presence of neurologic causes of seizures .
 Cerebral imaging is indicated for patients with
focal neurologic signs, such as hemiparesis, an
unconscious state, and prolonged coma.

62. Conclusion
 Additionally, cerebral imaging may be helpful in
patients who have an atypical presentation of
eclampsia (onset before 20 weeks or more than
48 h after delivery, refractory to magnesium
sulfate therapy, and recurrent seizures).

64. Thank You