PRE ECLAMPSIA Presentation in Clincial Pathological Conference in Hyderabad LUMHS

Gynaecology

1. (RECITATION)

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)

4. Basics of hypertensive disorders in pregnancy By NEHA NITYA

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 HYPERTENSION 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’ POSTPARTUM.

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.

12. PATHO PHYSIOLOGY By MUSKAN

13. There are two stages of pathophysiology of Pre eclampsia STAGE 1: Deficient trophoblast invasion STAGE 2: Endothelial dysfunction and diffuse vasospasm

14. 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

15. 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

16. ENDOTHELIAL DAMAGE Progressive inflammation = more endothelial damage Results in increased capillary permeability causing HEMOCONCENTRATION EDEMA

17. 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 VASOSPASM REDUCES SYSTEMIC PERFUSION which results in END ORGAN DAMAGE

18. Sequelae of pathological changes M. Rayan Younus

19. WHAT HAPPENS NEXT ???

20. Sequelae of abnormal placenta formation: Release of inflammatory mediators which cause endothelial injury, causing: Vasospastic and ischemic damage Oedematous damage Thrombotic damage

21. Organ systems involved These changes affect the following organ systems mainly: Cardiovascular system Renal system Hepatic system Haematological system Central nervous system

22. Cardiovascular system Generalized vasospasm Increased peripheral resistance Increased blood pressure Oedema Oozing out of plasma fluid into interstitium Haemoconcentration

23. NORMAL HAEMOCONCENTRATION NORMAL HAEMOCONCENTRATION

24. 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.

25. HaematologicAl system Endothelial injury Platelet activation and depletion Coagulopathy can lead to DIC in severe and complicated cases.

26. Hepatic system Vasospasm and ischemia Hepatic necrosis Periportal haemorrhage which stretches the liver capsule causing hepatic tenderness. Increased liver enzymes

27. Central nervous system Vasospasm Cerebral oedema Release of excitatory neurotransmitters e.g: Glutamate Seizures and/or coma

28. RISK FACTORS By PERIH FATIMA

29. What predisposes a mother to developing HTN and Preeclampsia? Age Parity Multipara Obesity Family History Hyperplacentosis Metabolic Disorders Pre-existing Conditions

30. AGE Pregnancy in extremes of Age Before 20 years After 40 years

31. 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 antigen. PARITY

32. OBESITY BMI of 35 or more Leaves mother at risk of developing various metabolic and systemic disease

33. 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.

34. Hyperplacentosis Hyperplacentosis is a condition of increased trophoblastic activity. Characterized by ⬆️ placental weight and ⬆️ circulating H CG levels H igher than those associated with normal pregnancy. Seen in - Multiple Pregnancy - Molar Pregnancy

35. Pre-existing Medical Conditions and disorders Diabetes mellitus Homocysteinemia Pre-existing Hypertension Pre-existing Renal Disease Pre-existing Cardiovascular Disease

36. Cont.. Thrombophilia Autoimmune Disorders : SLE, rheumatoid arthritis, autoimmune thyroid disease, and type I diabetes, antiphospholipid antibody syndrome (APS)

37. CLINICAL FEATURES By MUHAMMAD SAAD

38. 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

39. Signs of Pulmonary oedema and hepatic tenderness Hyperreflexia Agitation Generalized Oedema Due to dec oncotic pressure SIGNS Reduced urine output

40. 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

41. 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

42. Differential diagnosis Chronic Hypertension Pregnancy induced hypertension Nephrotic syndrome Dissecting aortic aneurysm with hypertension

43. INVESTIGATIONS By M JUNAID ABDUL LATHIFF

44. Maternal investigations

45. Base line Investigation

46. Coagulation Profile Activated partial thromboplastin clotting time (APTT), Clot forms in 25-35 seconds Fibrin degradation products, High level indicates DIC

47. 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)

48. Proteinuria is the last feature to develop in preeclampsia. There may be few hyaline cyst, epithelial cells, or even few red cells

49. RENAL FUNCTION TEST Serum uric acid Serum creatinine

50. Liver function test Liver enzymes AST/ALT Bilirubin Lactate dehydrogenase

51. 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.

52. Fetal investigations USS Cardiotocography Doppler of umbilical artery

53. Ultra sound scan and Cardiotocography To assess feta well being To assess fetal distress Amniotic fluid volume – adequate

54. Doppler scan Umbilical artery doppler flow to assess any blood clot We measure pulsatile index, resistance index and systolic/diastolic ratio.

55. 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.

56. Complications By Muhammad Usama

57. Hellp H AEMOLYSIS E LEVATED L IVER ENZYMES L OW P LATELETS ! Complication due to hepatic and haematologic damage in preeclampsia. Occurs in severe cases. CLINICAL FEATURE: Epigastric pain, nausea, vomiting, liver tenderness(Right S.C)

58. 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.

59. 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 .

60. 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.

61. other complications of preeclampsia Cerebral haemorrhage DIC Renal failure Placental abruption

62. MANAGEMENT By MUQADAS MEMON

63. 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.

64. Mnemonic (Hypertensive Drugs safe in pregnancy) N ew M oms L ove H ugs N ifedipine M ethyldopa L abetalol H ydralazine

65. Mnemonics for Hypertensive drugs contraindicated in pregnancy ADAA A tenolol D iuretics A RBs A CE Inhibitors

66. 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.

67. 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)

68. MgSO 4 (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: 10ml IV ONLY DEFINITIVE TREATMENT IS DELIVERY

69. 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.

70. 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.

71. STATISTICS By MUSHK ZEHRA SHAH

72. THESE STATISTICS ARE BASED ON DATA COLLECTED FROM 120 PATIENTS DURING LAST 6 MONTHS IN GYNAE WARD 3

73. 10% 55.8 % 11.7% 21.7% 0.8%

74. 42.5% 17.5% 40%

75. 42.5% 10% 30.8% 16.7%

76. Clinical case By NAHL NIZAMANI

77. 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

78. h/o of chronic hypertension since her previous pregnancy 3 years ago. Gestational amenorrhea since 8 months Shortness of breath since 1 month headache since 5 days palpitations and blurring of vision since 01 day. PRESENTING COMPLAIN:

79. 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. 2 ND 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

80. 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. 3 RD 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

81. 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------- 

82. S NO: Year Place Gender Gest: Age & Wt. MOD Delivery Vaginal/CS Alive/ IUD/ ENND Complications Antepartum/intrapartum/ 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

83. 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

84. 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 2 nd child and 1 bottle during the 1 st child SOCIOECNOMIC CONDITION : poor socioeconomic status

85. Cont.. O/E her vitals were the following: BP: 200/120 mmHg Pulse: 94 bpm Temp: 98 o F RR: 20 breaths per min Sub vitals: pitting edema +ve Anemia +ve

86. 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

87. Investigation and management of our patient By NIDA KHAN

88. FBC REPORT OF PATIENT

89. URINE ANALYSIS

90. LFT

91. BNP

92. USS

93. Creatinine 0.31 mg/dl (0.5-0.9) Urea 19 mg/dl (20-40)

94. 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)

95. 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 

96. THANK YOU 

97. SCAN ME 