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(RECITATION)
By time
Indeed, mankind is in loss
Except for those who have believed
and done righteous deeds and
advised each other to truth and
advised each other to patience.
Al- Asr
PRE ECLAMPSIA BY GROUP B2
(GYNAE WARD 3)
BASICS OF
HYPERTENSIVE
DISORDERS IN
PREGNANCY
By NEHA NITYA
HYPERTENSION IN PREGNANCY IS DIVIDED
INTO 4 CATEGORIES:
3. PRE eclampsia-Eclampsia
1. Chronic Hypertension (of any cause)
4. Chronic Hypertension with Superimposed Pre-eclampsia
2. Gestational Hypertension
CLASSIFICATION OF
HYPERTENSIVE DISORDERS
Based on two:
2. 20 Week’s Gestation
BEFORE
AFTER
1. PREOTEINURIA
WITH
WITHOUT
Pregnant woman with Blood Pressure > 140/90
mmHg
Non-PROTEINURIC PROTEINURIC
AFTER 20 WEEK’s
GESTATION
BEFORE 20 WEEK’s
GESTATION
AFTER 20
WEEK’s
GESTATION
BEFORE 20
WEEK’s GESTATION
CHRONIC HTN GESTATIONAL
HTN
RENAL
DISORDERS
PRE
ECLAMPSIA
CHRONIC
HYPERTENSI
ON
Hypertension as defined by
a BP > 140/90 mmHg
BEFORE PREGNANCY/20
WEEK’S GESTATION.
OR
Hypertension first
diagnosed AFTER 20
WEEK’S and persistent
AFTER 12 WEEKS’
Hypertension as
defined by a BP >
140/90 mmHg for
FIRST TIME DURING
PREGNANCY AFTER
20 WEEK’S
GESTATION, which
returns to normal
<12 weeks’
Postpartum and
WITHOUT
PROTEINURIA.
PRE-ECLAMPSIA
The minimum criteria for diagnosis of Pre-Eclampsia are
Blood pressure > 140/90mm Hg recorded on at least two
separate occasions and at least 4hrs apart, presented
AFTER 20 WEEKS’ GESTATION with PROTEINURIA
>300mg/24hr OR >1+ protein with Dipstick.
EDEMA no longer is DIAGNOSTIC criteria for
PRE-Eclampsia
PRE-ECLAMPSIA
SUPERIMPOSED ON
CHRONIC HYPERTENSION:
Superimposed pre-eclampsia on chronic HTN is
characterized by:
New onset Proteinuria (> 300mg/24hr) in a woman
with hypertension but NO PROTEINURIA before.
PATHO PHYSIOLOGY By MUSKAN
There are two stages of pathophysiology of Pre
eclampsia
STAGE 1: Deficient trophoblast invasion
STAGE 2: Endothelial dysfunction and diffuse
vasospasm
STAGE 1: DEFICIENT
TROPHOBLAST INVASION
• Failure of trophoblast invasion of
myometrium segments of spiral arteries
• Results in inadequate blood flow to the
placenta and foetus, resulting in
uteroplacental ischemia
STAGE 2: ENDOTHELIAL
DYSFUNCTION AND VASOSPASM
Due to uteroplacental ischemia, oxidative and
inflammatory stress occurs resulting in
activation of mediators that cause
• Endothelial damage
• Diffuse vasospasm
ENDOTHELIAL DAMAGE
• Progressive inflammation = more endothelial
damage
Results in increased capillary permeability
causing
• HEMOCONCENTRATION
• EDEMA
DIFFUSE VASOSPASM
• Vasospasm increases peripheral vascular resistance
(PVR)
As Blood pressure = Heart rate x Peripheral vascular
resistance
Increased PVR increases Blood pressure
• Note that normal pregnancy is associated with
DECREASED PVR
SEQUELAE OF
PATHOLOGICAL
CHANGES
M. Rayan Younus
WHAT HAPPENS
NEXT ???
SEQUELAE OF ABNORMAL
PLACENTA FORMATION:
Release of inflammatory mediators which cause
endothelial injury, causing:
1. Vasospastic and ischemic damage
2. Oedematous damage
3. Thrombotic damage
ORGAN SYSTEMS INVOLVED
These changes affect the following organ systems
mainly:
1. Cardiovascular system
2. Renal system
3. Hepatic system
4. Haematological system
5. Central nervous system
CARDIOVASCULAR SYSTEM
Generalized vasospasm
Increased peripheral resistance
Increased blood pressure
Oedema
Oozing out of plasma fluid into interstitium
Haemoconcentration
NORMAL HAEMOCONCENTRATI
ON
NORMAL HAEMOCONCENTRATI
ON
RENAL SYSTEM
Glomerular endotheliosis:
Characteristic lesion of pre
eclampsia which results in
endothelial and mesangial cell
swelling.
It causes:
Proteinuria of intermediate
weight proteins such as albumin
and transferrin.
Further exacerbates oedema.
• Decreased GFR which leads to oliguria or anuria in
severe cases.
• Oliguria leads to raised serum creatinine & urea.
HAEMATOLOGICAL SYSTEM
Endothelial injury
Platelet activation and depletion
Coagulopathy can lead to DIC in
severe and complicated cases.
HEPATIC SYSTEM
Vasospasm and ischemia
Hepatic necrosis
Periportal haemorrhage which
stretches the liver capsule causing
hepatic tenderness.
Increased liver enzymes
CENTRAL NERVOUS SYSTEM
Vasospasm
Cerebral oedema
Release of excitatory neurotransmitters e.g: Glutamate
Seizures and/or coma
RISK FACTORS By PERIH FATIMA
What predisposes a mother to developing HTN and
Preeclampsia?
• Age
• Parity
• Multipara
• Obesity
• Family History
• Hyperplacentosis
• Metabolic Disorders
• Pre-existing Conditions
AGE
PREGNANCY IN EXTREMES OF AGE
BEFORE 20 YEARS
AFTER 40 YEARS
• Studies show that Pre-eclampsia tends to develop in
first pregnancy more than second pregnancy of a
person
• Multipara typically at lower risk for preeclampsia
than nulliparas.
• But multiparas associated with a change in paternity
has the adjusted attributable risk of preeclampsia of
29%.
Why?
• Possibly due to exposure to new set of paternal
PARITY
OBESITY
• BMI of 35 or more
• Leaves mother at risk of developing
various metabolic and systemic disease
FAMILY HISTORY
• Having maternal family history of
preeclampsia was associated with up to a
115% increase in preeclampsia risk, with the
association strongest for early-onset
preeclampsia.
HYPERPLACENTOSIS
Hyperplacentosis is a condition of increased trophoblastic
activity.
Characterized by
⬆️ placental weight and ⬆️ circulating HCG levels
Higher than those associated with normal pregnancy.
• Seen in
- Multiple Pregnancy
- Molar Pregnancy
PRE-EXISTING MEDICAL
CONDITIONS AND
DISORDERS
• Diabetes mellitus
• Homocysteinemia
• Pre-existing Hypertension
• Pre-existing Renal Disease
• Pre-existing Cardiovascular Disease
CONT..
• Thrombophilia
• Autoimmune Disorders :
SLE, rheumatoid arthritis, autoimmune thyroid
disease, and type I diabetes, antiphospholipid
antibody syndrome (APS)
CLINICAL FEATURES By MUHAMMAD SAAD
Visual
disturbances
(due to retinal
arteriolar spasm)
• Blurred vision
• Diplopia
• Scotomas
Frontal
headache
Epigastric and RUQ pain
(due to Liver capsule
stretching)
Lower abdominal pain
(may suggest placental abruption)
Rapid weight gain
(due to fluid accumulation)
Shortness of
breath
General malaise
Signs of
Pulmonary oedema
and hepatic tenderness
Hyperreflexia
Agitation
Generalized Oedema
Due to dec oncotic pressure
SIGNS
Reduced urine
output
CLASSIFICATION OF
HYPERTENSION
MILD HYPERTENSION
SYSTOLIC :140-149 mmHg
DIASTOLIC :90-99 mmHg
MODERATE HYPERTENSION
SYSTOLIC :150-159 mmHg
DIASTOLIC :100-109 mmHg
SEVERE HYPERTENSION
SYSTOLIC: 160 mmHg or
higher
DIASTOLIC: 110 mmHg or
higher
ABNORMALITY MILD SEVERE
Blood pressure Slightly elevated >160/110 mmHg
Proteinuria Trace to 1+ Persistent 2+ or more
Headache  
Visual disturbances  
Upper abdominal pain  
Oliguria  
Pulmonary Edema  
Eclampsia  
MILD VS SEVERE PRE
ECLAMPSIA
DIFFERENTIAL DIAGNOSIS
• Chronic Hypertension
• Pregnancy induced hypertension
• Nephrotic syndrome
• Dissecting aortic aneurysm with hypertension
INVESTIGATIONS By M JUNAID ABDUL
LATHIFF
MATERNAL INVESTIGATIONS
Base line – FBC, Hepatitis B & C, Blood group
Urine analysis
Renal function test
Liver Function Test
Coagulation Profile
Cardiac Biomarkers
BASE LINE INVESTIGATION
Hepatitis B & C
HIV
Blood grouping
FBC- Hemoglobin level- (11-16)
Platelet level- (150-400)
COAGULATION PROFILE
Activated partial thromboplastin
clotting time (APTT), Clot forms
in 25-35 seconds
Fibrin degradation products,
High level indicates DIC
COMPLETE URINE
EXAMINATION
•Proteinuria – defined as >300mg of
protein per 24hr urine collection (Gold
standard method)
•Dipstick reading of +1. (Used only if
other methods are not available)
• Proteinuria is the last
feature to develop in
preeclampsia.
• There may be few
hyaline cyst, epithelial
cells, or even few red
cells
RENAL FUNCTION TEST
• Serum uric acid
• Serum creatinine
LIVER FUNCTION TEST
• Liver enzymes AST/ALT
•Bilirubin
•Lactate dehydrogenase
CARDIAC BIOMARKERS
• To see if the patient is having or already had
a heart attack
• Troponin 1,myoglobin and CK
• B-Natriuretic peptide- higher levels of BNP
indicates possibilities of heart failure.
FETAL INVESTIGATIONS
• USS
• Cardiotocography
• Doppler of umbilical artery
ULTRA SOUND SCAN
AND
CARDIOTOCOGRAPHY
• To assess feta well being
• To assess fetal distress
• Amniotic fluid volume – adequate
DOPPLER SCAN
• Umbilical artery doppler flow
to assess any blood clot
• We measure pulsatile index,
resistance index and
systolic/diastolic ratio.
SCREENING
• Uterine artery doppler is done in first
trimester, high RI indicates resistance in spiral
artery which leads to hypo perfusion of the
fetus
• Serum placental growth factor, low level
indicates small fetus with significant placental
pathology.
• Mean arterial pressure.
• Provisional Dx- Chronic hypertension
superimposed preeclampsia.
COMPLICATIONS By Muhammad Usama
HELLP
HAEMOLYSIS
ELEVATED LIVER ENZYMES
LOW PLATELETS!
• Complication due to hepatic and
haematologic damage in
preeclampsia.
• Occurs in severe cases.
• CLINICAL FEATURE: Epigastric pain,
nausea, vomiting, liver
tenderness(Right S.C)
CONT..
• Hypertension maybe mild
• Can lead to ascites, hepatic rupture, DIC, placental
abruption, FGR, foetal demise.
• STROKE is most common cause of maternal death.
• TREATMENT: Correct coagulation defects, stabilize
mother, prompt delivery.
ECLAMPSIA (OBSTETRIC
EMERGENCY)
Definition: Tonic- clonic convulsions occurring in a
women with well developed preeclampsia in the
absence of any other(neurological/metabolic) cause.
• It’s an obstetric emergency, life threatening condition
for both, the mother and the foetus.
• Seizures may occur antenatally, intrapartum or post
partum (within 48 hrs; most common).
• Convulsions may lead to spontaneous recovery,
lethargy or into comatose state.
CONT..
• Clinical features: Severe throbbing headache, visual
disturbance, oligo/anuria and hyperreflexia in addition
to other manifestations of preeclampsia.
• Cerebral haemorrhage is the most common cause of
maternal death.
• Investigations: Urine for protein, CBC, coagulation
profile, cross matching for blood, LFT, urea &
creatinine.
OTHER COMPLICATIONS OF
PREECLAMPSIA
• Cerebral haemorrhage
• DIC
• Renal failure
• Placental abruption
MANAGEMENT By MUQADAS MEMON
• Oral: Labetalol (first drug of choice)
• Others: Methyldopa, nifedipine.
• I/V: Hydralazine or Labetalol infusions if severe preeclampsia.
• Contraindications of Labetalol:
• Bronchial asthma
• Severe bradycardia
• Overt cardiac failure.
MNEMONIC
(HYPERTENSIVE DRUGS
SAFE IN PREGNANCY)
New Moms Love Hugs
Nifedipine
Methyldopa
Labetalol
Hydralazine
MNEMONICS FOR
HYPERTENSIVE DRUGS
CONTRAINDICATED IN
PREGNANCY
ADAA
Atenolol
Diuretics
ARBs
ACE
Inhibitors
MILD PRE ECLAMPSIA
(140/90-149/99 mmHg)
• Home care with BP monitoring 4 times a day along
OPD visits for maternal and foetal assessment
• Blood tests (for liver and kidney function) twice a
week.
MODERATE PRE ECLAMPSIA AND
SEVERE PRE ECLAMPSIA
(150/100-159/109mmHg)
• Hospital admission required
• BP monitored 2 hourly, blood tests required thrice a
week
• I/V antihypertensive (Labetalol or hydralazine)
• fluid restriction (80ml/hour)
• In severe preeclampsia to prevent eclampsia I/V
MgSo4 is administered.
(160/110mmHg or higher
along significant
proteinuria)
MGSO4 (ANTICONVULSANT )
Cerebral vasodilator and membrane stabiliser.
• Loading dose: 4gm , maintenance infusion: 1gm/h for
about 24hrs.
• Can be given as a remedy as it decreases further
occurrence of seizure or it can be given as prevention of
seizures in case of severe preeclampsia.
• Has narrow therapeutic range, Monitor respiration,
reflexes, urine output and MgSO4 levels to prevent
toxicity.
10% Calcium gluconate is antidote in toxicity. Dose:
DAY CARE
• To avoid hospital admissions as they add additional
risks to mother and foetus,
• ‘Day care’ could be offered, by midwife of the local
area, near by GP, nearest RHC centre.
• Preventive intervention: Low dose aspirin (75mg daily)
given to women at high risk of preeclampsia.
ADDITIONAL POINTS IN
MANAGEMENT
• If delivery before 34th week(due to any
complication)administer corticosteroid betamethasone
to mother, for foetal lung maturity.
• Monitor closely during 48 hours after delivery as risk
of convulsions.
• After C-section, is risk of thromboembolism and DVT,
so prophylactic S/C heparin and stockings prescribed.
• By 6th week of postpartum Preeclampsia will resolve.
STATISTICS By MUSHK ZEHRA SHAH
THESE STATISTICS ARE
BASED ON DATA
COLLECTED FROM 120
PATIENTS DURING LAST 6
MONTHS IN GYNAE WARD 3
10%
55.8 %
11.7%
21.7%
0.8%
42.5%
17.5%
40%
42.5%
10%
30.8%
16.7%
CLINICAL CASE By NAHL NIZAMANI
BIODATA:
NAME: Naseem w/o Gul Nabi
AGE:45yrs old
G12 P9+2
RELIGION: ISLAM
OCCUPATION: Embroidery worker
ADDRESS: Tando Mohd Khan
DOA: 15/June/2022
MOA: Emergency
1) h/o of chronic hypertension since her previous
pregnancy 3 years ago.
2) Gestational amenorrhea since 8 months
3) Shortness of breath since 1 month
4) headache since 5 days
5) palpitations and blurring of vision since 01 day.
PRESENTING COMPLAIN:
OBSTETRIC HISTORY
IST TRIMESTER:
• complains of nausea and vomiting
• u/s done at 12 wks.
• no complain of any vaginal discharge or bleeding PV or spotting
• adequate use of folic acid
• no history of fever, flu rash or UTI
• Captopril was replaced by Methyldopa.
2ND TRIMESTER
• quickening felt at 17 wks. for the first time
• satisfactory fetal movements
• adequate and regular use iron and calcium supplements
• no any regular antenatal visits
• anomaly scan not done
• no c/o pv bleeding fever rash raised sugar or abdominal pain
DRUG HISTORY
She had been taking ACE INHIBITOR and
aspirin for her raised blood pressure which is
now substituted with methyldopa because of
her pregnancy.
3RD TRIMESTER
• regular and satisfactory fetal movements
• Un-booked case
• tetanus vaccine not done
• h/o chronically raised bp and urinary urgency problems, no h/o disturbed sugar levels Pv
bleeding or abdominal pain
• last u/s done at 32 wks.
• restricted salty food intake
OBSTETRICAL HISTORY
Booked / Un booked / TT Vaccine
Married Since: 25 years
Husband relation: None
Gravida: 12 Parity: 9 + 2 LCB:3 years
ago
Early Abortion: 2 Late Abortion: None Ectopic:
None
LMP: NSOD EDD: 24 July
Gest Age: 32 w By LMP--------- By USS-----

S NO: Year Place Gender Gest:
Age & Wt.
MOD Delivery
Vaginal/CS
Alive/ IUD/
ENND
Complications
Antepartum/intrapart
um/ PN
Vaccination/ Breast
feeding
1
2003 Home Male 38 weeks and
4.5 kg
NVD Alive None Yes/yes
2
2010 home female 39 wks and 4
kg
NVD alive none yes/yes
3 2012 home male 38 wks and
3.8kg
NVD alive none yes/yes
4 2013 home female 39 wks and
3.9 kg
NVD alive none yes/yes
5 2014 home male 37 wks and
3.8 kg
NVD alive none yes/yes
6 2015 home female 38 wks and 4
kg
NVD alive none yes/yes
7 2017 home male 39 wks and
3.9 kg
NVD alive none yes/yes
8 2017 home unknown unknown NVD IUD none no/no
9 2018 home female 37wks and 4
kg
NVD alive none yes/yes
10 2019 home female 37 wks and 4
kg
NVD alive none yes/yes
11 2020 home unknown unknown NVD IUD none no/no
GYNAECOLOGICAL HISTORY
A.O.M: NSOD
M/C: Regular
IMB: None
DYSM: None
PCB: None
Vaginal Discharge: None
MF/: Regular
LMP: NSOD
DYSP: None
Pap Smear: None
PAST MEDICAL/ SURGICAL HISTORY: Chronic history
of HTN. No any significant past surgical Hx
PERSONAL HISTORY: Everything normal except for
urinary urgency
H/O ALLEGRY: None
BLOOD TRANSFUSION HISTORY: 2 bottles during 2nd
child and 1 bottle during the 1st child
SOCIOECNOMIC CONDITION: poor socioeconomic
status
CONT..
O/E her vitals were the following:
BP: 200/120 mmHg
Pulse: 94 bpm
Temp: 98oF
RR: 20 breaths per min
Sub vitals: pitting edema +ve
Anemia +ve
CONT..
On PA examination, following points were
noted:
Symphysio fundal height: 30cm
Fetal lie: longitudinal
Fetal presentation: cephalic 5/5
Fetal movements: +ve
Fetal heartbeat: 140 bpm, REGULAR
Uterine contractions: -ve
INVESTIGATION AND
MANAGEMENT OF
OUR PATIENT
By NIDA KHAN
REPORT OF PATIENT
RINE ANALYSIS
LFT
BNP
USS
Creatinine 0.31 mg/dl
(0.5-0.9)
Urea 19 mg/dl
(20-40)
MY PATIENT’S MANAGEMENT
PLAN:
(She arrived with B.P of 200/120mmHg classified as severe
preeclampsia)
• Maintain I/V line
• Send all labs
• Arrange and cross match blood
• CTG
• Consent (written and informed high risk consent + LSCS
consent + termination)
• Injection MgSo4 (Prophylactically)
• I/V Labetalol
• Catheterise the patient
• FMM
• The goal was to deliver baby at 37th gestational week but due to
severely raised BP, baby was delivered at 34 weeks
• Inj Dexa
•LSCS on 23 June 2022
•ABB of 2.1 kg
•APGAR SCORE 10/10
•Contraception by TUBAL LIGATION
•BOTH MOTHER AND BABY DISCHARGED IN SATISFACTORY CONDITION 
THANK
YOU 
SCAN ME 

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PRE ECLAMPSIA Presentation in Clincial Pathological Conference in Hyderabad LUMHS

  • 2. By time Indeed, mankind is in loss Except for those who have believed and done righteous deeds and advised each other to truth and advised each other to patience. Al- Asr
  • 3. PRE ECLAMPSIA BY GROUP B2 (GYNAE WARD 3)
  • 5. HYPERTENSION IN PREGNANCY IS DIVIDED INTO 4 CATEGORIES: 3. PRE eclampsia-Eclampsia 1. Chronic Hypertension (of any cause) 4. Chronic Hypertension with Superimposed Pre-eclampsia 2. Gestational Hypertension
  • 6. CLASSIFICATION OF HYPERTENSIVE DISORDERS Based on two: 2. 20 Week’s Gestation BEFORE AFTER 1. PREOTEINURIA WITH WITHOUT
  • 7. Pregnant woman with Blood Pressure > 140/90 mmHg Non-PROTEINURIC PROTEINURIC AFTER 20 WEEK’s GESTATION BEFORE 20 WEEK’s GESTATION AFTER 20 WEEK’s GESTATION BEFORE 20 WEEK’s GESTATION CHRONIC HTN GESTATIONAL HTN RENAL DISORDERS PRE ECLAMPSIA
  • 8. CHRONIC HYPERTENSI ON Hypertension as defined by a BP > 140/90 mmHg BEFORE PREGNANCY/20 WEEK’S GESTATION. OR Hypertension first diagnosed AFTER 20 WEEK’S and persistent AFTER 12 WEEKS’
  • 9. Hypertension as defined by a BP > 140/90 mmHg for FIRST TIME DURING PREGNANCY AFTER 20 WEEK’S GESTATION, which returns to normal <12 weeks’ Postpartum and WITHOUT PROTEINURIA.
  • 10. PRE-ECLAMPSIA The minimum criteria for diagnosis of Pre-Eclampsia are Blood pressure > 140/90mm Hg recorded on at least two separate occasions and at least 4hrs apart, presented AFTER 20 WEEKS’ GESTATION with PROTEINURIA >300mg/24hr OR >1+ protein with Dipstick. EDEMA no longer is DIAGNOSTIC criteria for PRE-Eclampsia
  • 11. PRE-ECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION: Superimposed pre-eclampsia on chronic HTN is characterized by: New onset Proteinuria (> 300mg/24hr) in a woman with hypertension but NO PROTEINURIA before.
  • 13.
  • 14. There are two stages of pathophysiology of Pre eclampsia STAGE 1: Deficient trophoblast invasion STAGE 2: Endothelial dysfunction and diffuse vasospasm
  • 15. STAGE 1: DEFICIENT TROPHOBLAST INVASION • Failure of trophoblast invasion of myometrium segments of spiral arteries • Results in inadequate blood flow to the placenta and foetus, resulting in uteroplacental ischemia
  • 16.
  • 17.
  • 18.
  • 19. STAGE 2: ENDOTHELIAL DYSFUNCTION AND VASOSPASM Due to uteroplacental ischemia, oxidative and inflammatory stress occurs resulting in activation of mediators that cause • Endothelial damage • Diffuse vasospasm
  • 20. ENDOTHELIAL DAMAGE • Progressive inflammation = more endothelial damage Results in increased capillary permeability causing • HEMOCONCENTRATION • EDEMA
  • 21. DIFFUSE VASOSPASM • Vasospasm increases peripheral vascular resistance (PVR) As Blood pressure = Heart rate x Peripheral vascular resistance Increased PVR increases Blood pressure • Note that normal pregnancy is associated with DECREASED PVR
  • 22.
  • 25. SEQUELAE OF ABNORMAL PLACENTA FORMATION: Release of inflammatory mediators which cause endothelial injury, causing: 1. Vasospastic and ischemic damage 2. Oedematous damage 3. Thrombotic damage
  • 26. ORGAN SYSTEMS INVOLVED These changes affect the following organ systems mainly: 1. Cardiovascular system 2. Renal system 3. Hepatic system 4. Haematological system 5. Central nervous system
  • 27. CARDIOVASCULAR SYSTEM Generalized vasospasm Increased peripheral resistance Increased blood pressure Oedema Oozing out of plasma fluid into interstitium Haemoconcentration
  • 29. RENAL SYSTEM Glomerular endotheliosis: Characteristic lesion of pre eclampsia which results in endothelial and mesangial cell swelling. It causes: Proteinuria of intermediate weight proteins such as albumin and transferrin. Further exacerbates oedema. • Decreased GFR which leads to oliguria or anuria in severe cases. • Oliguria leads to raised serum creatinine & urea.
  • 30. HAEMATOLOGICAL SYSTEM Endothelial injury Platelet activation and depletion Coagulopathy can lead to DIC in severe and complicated cases.
  • 31. HEPATIC SYSTEM Vasospasm and ischemia Hepatic necrosis Periportal haemorrhage which stretches the liver capsule causing hepatic tenderness. Increased liver enzymes
  • 32. CENTRAL NERVOUS SYSTEM Vasospasm Cerebral oedema Release of excitatory neurotransmitters e.g: Glutamate Seizures and/or coma
  • 33. RISK FACTORS By PERIH FATIMA
  • 34. What predisposes a mother to developing HTN and Preeclampsia? • Age • Parity • Multipara • Obesity • Family History • Hyperplacentosis • Metabolic Disorders • Pre-existing Conditions
  • 35. AGE PREGNANCY IN EXTREMES OF AGE BEFORE 20 YEARS AFTER 40 YEARS
  • 36. • Studies show that Pre-eclampsia tends to develop in first pregnancy more than second pregnancy of a person • Multipara typically at lower risk for preeclampsia than nulliparas. • But multiparas associated with a change in paternity has the adjusted attributable risk of preeclampsia of 29%. Why? • Possibly due to exposure to new set of paternal PARITY
  • 37. OBESITY • BMI of 35 or more • Leaves mother at risk of developing various metabolic and systemic disease
  • 38.
  • 39. FAMILY HISTORY • Having maternal family history of preeclampsia was associated with up to a 115% increase in preeclampsia risk, with the association strongest for early-onset preeclampsia.
  • 40. HYPERPLACENTOSIS Hyperplacentosis is a condition of increased trophoblastic activity. Characterized by ⬆️ placental weight and ⬆️ circulating HCG levels Higher than those associated with normal pregnancy. • Seen in - Multiple Pregnancy - Molar Pregnancy
  • 41. PRE-EXISTING MEDICAL CONDITIONS AND DISORDERS • Diabetes mellitus • Homocysteinemia • Pre-existing Hypertension • Pre-existing Renal Disease • Pre-existing Cardiovascular Disease
  • 42. CONT.. • Thrombophilia • Autoimmune Disorders : SLE, rheumatoid arthritis, autoimmune thyroid disease, and type I diabetes, antiphospholipid antibody syndrome (APS)
  • 43. CLINICAL FEATURES By MUHAMMAD SAAD
  • 44. Visual disturbances (due to retinal arteriolar spasm) • Blurred vision • Diplopia • Scotomas Frontal headache Epigastric and RUQ pain (due to Liver capsule stretching) Lower abdominal pain (may suggest placental abruption) Rapid weight gain (due to fluid accumulation) Shortness of breath General malaise
  • 45. Signs of Pulmonary oedema and hepatic tenderness Hyperreflexia Agitation Generalized Oedema Due to dec oncotic pressure SIGNS Reduced urine output
  • 46. CLASSIFICATION OF HYPERTENSION MILD HYPERTENSION SYSTOLIC :140-149 mmHg DIASTOLIC :90-99 mmHg MODERATE HYPERTENSION SYSTOLIC :150-159 mmHg DIASTOLIC :100-109 mmHg SEVERE HYPERTENSION SYSTOLIC: 160 mmHg or higher DIASTOLIC: 110 mmHg or higher
  • 47. ABNORMALITY MILD SEVERE Blood pressure Slightly elevated >160/110 mmHg Proteinuria Trace to 1+ Persistent 2+ or more Headache   Visual disturbances   Upper abdominal pain   Oliguria   Pulmonary Edema   Eclampsia   MILD VS SEVERE PRE ECLAMPSIA
  • 48. DIFFERENTIAL DIAGNOSIS • Chronic Hypertension • Pregnancy induced hypertension • Nephrotic syndrome • Dissecting aortic aneurysm with hypertension
  • 49. INVESTIGATIONS By M JUNAID ABDUL LATHIFF
  • 50. MATERNAL INVESTIGATIONS Base line – FBC, Hepatitis B & C, Blood group Urine analysis Renal function test Liver Function Test Coagulation Profile Cardiac Biomarkers
  • 51. BASE LINE INVESTIGATION Hepatitis B & C HIV Blood grouping FBC- Hemoglobin level- (11-16) Platelet level- (150-400)
  • 52.
  • 53. COAGULATION PROFILE Activated partial thromboplastin clotting time (APTT), Clot forms in 25-35 seconds Fibrin degradation products, High level indicates DIC
  • 54. COMPLETE URINE EXAMINATION •Proteinuria – defined as >300mg of protein per 24hr urine collection (Gold standard method) •Dipstick reading of +1. (Used only if other methods are not available)
  • 55. • Proteinuria is the last feature to develop in preeclampsia. • There may be few hyaline cyst, epithelial cells, or even few red cells
  • 56. RENAL FUNCTION TEST • Serum uric acid • Serum creatinine
  • 57. LIVER FUNCTION TEST • Liver enzymes AST/ALT •Bilirubin •Lactate dehydrogenase
  • 58. CARDIAC BIOMARKERS • To see if the patient is having or already had a heart attack • Troponin 1,myoglobin and CK • B-Natriuretic peptide- higher levels of BNP indicates possibilities of heart failure.
  • 59. FETAL INVESTIGATIONS • USS • Cardiotocography • Doppler of umbilical artery
  • 60. ULTRA SOUND SCAN AND CARDIOTOCOGRAPHY • To assess feta well being • To assess fetal distress • Amniotic fluid volume – adequate
  • 61. DOPPLER SCAN • Umbilical artery doppler flow to assess any blood clot • We measure pulsatile index, resistance index and systolic/diastolic ratio.
  • 62. SCREENING • Uterine artery doppler is done in first trimester, high RI indicates resistance in spiral artery which leads to hypo perfusion of the fetus • Serum placental growth factor, low level indicates small fetus with significant placental pathology. • Mean arterial pressure. • Provisional Dx- Chronic hypertension superimposed preeclampsia.
  • 64. HELLP HAEMOLYSIS ELEVATED LIVER ENZYMES LOW PLATELETS! • Complication due to hepatic and haematologic damage in preeclampsia. • Occurs in severe cases. • CLINICAL FEATURE: Epigastric pain, nausea, vomiting, liver tenderness(Right S.C)
  • 65. CONT.. • Hypertension maybe mild • Can lead to ascites, hepatic rupture, DIC, placental abruption, FGR, foetal demise. • STROKE is most common cause of maternal death. • TREATMENT: Correct coagulation defects, stabilize mother, prompt delivery.
  • 66. ECLAMPSIA (OBSTETRIC EMERGENCY) Definition: Tonic- clonic convulsions occurring in a women with well developed preeclampsia in the absence of any other(neurological/metabolic) cause. • It’s an obstetric emergency, life threatening condition for both, the mother and the foetus. • Seizures may occur antenatally, intrapartum or post partum (within 48 hrs; most common). • Convulsions may lead to spontaneous recovery, lethargy or into comatose state.
  • 67. CONT.. • Clinical features: Severe throbbing headache, visual disturbance, oligo/anuria and hyperreflexia in addition to other manifestations of preeclampsia. • Cerebral haemorrhage is the most common cause of maternal death. • Investigations: Urine for protein, CBC, coagulation profile, cross matching for blood, LFT, urea & creatinine.
  • 68. OTHER COMPLICATIONS OF PREECLAMPSIA • Cerebral haemorrhage • DIC • Renal failure • Placental abruption
  • 70. • Oral: Labetalol (first drug of choice) • Others: Methyldopa, nifedipine. • I/V: Hydralazine or Labetalol infusions if severe preeclampsia. • Contraindications of Labetalol: • Bronchial asthma • Severe bradycardia • Overt cardiac failure.
  • 71. MNEMONIC (HYPERTENSIVE DRUGS SAFE IN PREGNANCY) New Moms Love Hugs Nifedipine Methyldopa Labetalol Hydralazine
  • 72. MNEMONICS FOR HYPERTENSIVE DRUGS CONTRAINDICATED IN PREGNANCY ADAA Atenolol Diuretics ARBs ACE Inhibitors
  • 73. MILD PRE ECLAMPSIA (140/90-149/99 mmHg) • Home care with BP monitoring 4 times a day along OPD visits for maternal and foetal assessment • Blood tests (for liver and kidney function) twice a week.
  • 74. MODERATE PRE ECLAMPSIA AND SEVERE PRE ECLAMPSIA (150/100-159/109mmHg) • Hospital admission required • BP monitored 2 hourly, blood tests required thrice a week • I/V antihypertensive (Labetalol or hydralazine) • fluid restriction (80ml/hour) • In severe preeclampsia to prevent eclampsia I/V MgSo4 is administered. (160/110mmHg or higher along significant proteinuria)
  • 75. MGSO4 (ANTICONVULSANT ) Cerebral vasodilator and membrane stabiliser. • Loading dose: 4gm , maintenance infusion: 1gm/h for about 24hrs. • Can be given as a remedy as it decreases further occurrence of seizure or it can be given as prevention of seizures in case of severe preeclampsia. • Has narrow therapeutic range, Monitor respiration, reflexes, urine output and MgSO4 levels to prevent toxicity. 10% Calcium gluconate is antidote in toxicity. Dose:
  • 76. DAY CARE • To avoid hospital admissions as they add additional risks to mother and foetus, • ‘Day care’ could be offered, by midwife of the local area, near by GP, nearest RHC centre. • Preventive intervention: Low dose aspirin (75mg daily) given to women at high risk of preeclampsia.
  • 77. ADDITIONAL POINTS IN MANAGEMENT • If delivery before 34th week(due to any complication)administer corticosteroid betamethasone to mother, for foetal lung maturity. • Monitor closely during 48 hours after delivery as risk of convulsions. • After C-section, is risk of thromboembolism and DVT, so prophylactic S/C heparin and stockings prescribed. • By 6th week of postpartum Preeclampsia will resolve.
  • 78. STATISTICS By MUSHK ZEHRA SHAH
  • 79. THESE STATISTICS ARE BASED ON DATA COLLECTED FROM 120 PATIENTS DURING LAST 6 MONTHS IN GYNAE WARD 3
  • 81.
  • 84.
  • 85.
  • 86.
  • 87. CLINICAL CASE By NAHL NIZAMANI
  • 88. BIODATA: NAME: Naseem w/o Gul Nabi AGE:45yrs old G12 P9+2 RELIGION: ISLAM OCCUPATION: Embroidery worker ADDRESS: Tando Mohd Khan DOA: 15/June/2022 MOA: Emergency
  • 89. 1) h/o of chronic hypertension since her previous pregnancy 3 years ago. 2) Gestational amenorrhea since 8 months 3) Shortness of breath since 1 month 4) headache since 5 days 5) palpitations and blurring of vision since 01 day. PRESENTING COMPLAIN:
  • 90. OBSTETRIC HISTORY IST TRIMESTER: • complains of nausea and vomiting • u/s done at 12 wks. • no complain of any vaginal discharge or bleeding PV or spotting • adequate use of folic acid • no history of fever, flu rash or UTI • Captopril was replaced by Methyldopa. 2ND TRIMESTER • quickening felt at 17 wks. for the first time • satisfactory fetal movements • adequate and regular use iron and calcium supplements • no any regular antenatal visits • anomaly scan not done • no c/o pv bleeding fever rash raised sugar or abdominal pain
  • 91. DRUG HISTORY She had been taking ACE INHIBITOR and aspirin for her raised blood pressure which is now substituted with methyldopa because of her pregnancy. 3RD TRIMESTER • regular and satisfactory fetal movements • Un-booked case • tetanus vaccine not done • h/o chronically raised bp and urinary urgency problems, no h/o disturbed sugar levels Pv bleeding or abdominal pain • last u/s done at 32 wks. • restricted salty food intake
  • 92. OBSTETRICAL HISTORY Booked / Un booked / TT Vaccine Married Since: 25 years Husband relation: None Gravida: 12 Parity: 9 + 2 LCB:3 years ago Early Abortion: 2 Late Abortion: None Ectopic: None LMP: NSOD EDD: 24 July Gest Age: 32 w By LMP--------- By USS----- 
  • 93. S NO: Year Place Gender Gest: Age & Wt. MOD Delivery Vaginal/CS Alive/ IUD/ ENND Complications Antepartum/intrapart um/ PN Vaccination/ Breast feeding 1 2003 Home Male 38 weeks and 4.5 kg NVD Alive None Yes/yes 2 2010 home female 39 wks and 4 kg NVD alive none yes/yes 3 2012 home male 38 wks and 3.8kg NVD alive none yes/yes 4 2013 home female 39 wks and 3.9 kg NVD alive none yes/yes 5 2014 home male 37 wks and 3.8 kg NVD alive none yes/yes 6 2015 home female 38 wks and 4 kg NVD alive none yes/yes 7 2017 home male 39 wks and 3.9 kg NVD alive none yes/yes 8 2017 home unknown unknown NVD IUD none no/no 9 2018 home female 37wks and 4 kg NVD alive none yes/yes 10 2019 home female 37 wks and 4 kg NVD alive none yes/yes 11 2020 home unknown unknown NVD IUD none no/no
  • 94. GYNAECOLOGICAL HISTORY A.O.M: NSOD M/C: Regular IMB: None DYSM: None PCB: None Vaginal Discharge: None MF/: Regular LMP: NSOD DYSP: None Pap Smear: None
  • 95. PAST MEDICAL/ SURGICAL HISTORY: Chronic history of HTN. No any significant past surgical Hx PERSONAL HISTORY: Everything normal except for urinary urgency H/O ALLEGRY: None BLOOD TRANSFUSION HISTORY: 2 bottles during 2nd child and 1 bottle during the 1st child SOCIOECNOMIC CONDITION: poor socioeconomic status
  • 96. CONT.. O/E her vitals were the following: BP: 200/120 mmHg Pulse: 94 bpm Temp: 98oF RR: 20 breaths per min Sub vitals: pitting edema +ve Anemia +ve
  • 97. CONT.. On PA examination, following points were noted: Symphysio fundal height: 30cm Fetal lie: longitudinal Fetal presentation: cephalic 5/5 Fetal movements: +ve Fetal heartbeat: 140 bpm, REGULAR Uterine contractions: -ve
  • 98. INVESTIGATION AND MANAGEMENT OF OUR PATIENT By NIDA KHAN
  • 101. LFT
  • 102. BNP
  • 103. USS
  • 105. MY PATIENT’S MANAGEMENT PLAN: (She arrived with B.P of 200/120mmHg classified as severe preeclampsia) • Maintain I/V line • Send all labs • Arrange and cross match blood • CTG • Consent (written and informed high risk consent + LSCS consent + termination)
  • 106. • Injection MgSo4 (Prophylactically) • I/V Labetalol • Catheterise the patient • FMM • The goal was to deliver baby at 37th gestational week but due to severely raised BP, baby was delivered at 34 weeks • Inj Dexa •LSCS on 23 June 2022 •ABB of 2.1 kg •APGAR SCORE 10/10 •Contraception by TUBAL LIGATION •BOTH MOTHER AND BABY DISCHARGED IN SATISFACTORY CONDITION 