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Atypical pet prof.salah 1
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%
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.
12.
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
15.
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↓
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
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 .
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.
30.
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.
34.
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.
38.
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
42.
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
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
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
57.
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).