PIH

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Pregnancy-induced Hypertension : 

1 Pregnancy-induced Hypertension ANISH JOSHI

Preeclampsia Hypertension Proteinuria 1. Greater than 300 mg in 24 hour period2. Greater than 100 mg/dl dipstick (sustainable)Edema After the twentieth week of gestation ,Although the signs and symptoms may appear earlier with H.mole.Resolving within 48 hours after deliveryEclampsia Seizures + preeclampsia. : 

2 Preeclampsia Hypertension Proteinuria 1. Greater than 300 mg in 24 hour period2. Greater than 100 mg/dl dipstick (sustainable)Edema After the twentieth week of gestation ,Although the signs and symptoms may appear earlier with H.mole.Resolving within 48 hours after deliveryEclampsia Seizures + preeclampsia.

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3 Classification : 1. Mild : Bp ≥140/90mmHg or a rise of 30mmHg systolic pressure or 15 mmHg diastolic pressure over the prepregnant level,with or without trace proteinuria or edema. 2. Severe : BP > 160/110 mmHg Proteinuria > 5 gm/24hr, > ++ Azotemia/oliguria (< 400 mL/24 hr) Microangiopathic hemolysis Thrombocytopenia End organ symptoms: 1. CNS 2. Visual 3. Hepatic Intrauterine growth delay (oligohydramnios?) Roll over test: increase of >20mmHg of DBP on turning from left lateral position to supine position

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4 TYPES- 1) PIH 2) CHRONIC HYPERTENSION ESSENTIAL / RENAL / Others MOSTLY OBESE, ELDERLY, PAROUS & LIKELY TO BE ON ANTIHYPERTENSIVE DRUGS USUALLY PREEXISTS / APPEARS EARLY (<20WKS) & PERSISTS POSTPARTUM END ORGAN DAMAGE MAYBE PRESENT A) COINCIDENTAL - sustained high BP throughout pregnancy & postpartum B) AGGRAVATED BY PREGNANCY - I) SUPERIMPOSED PREECLAMPSIA II) SUPERIMPOSED ECLAMPSIA

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5 Nulliparity Young or elderly gravidas Family history Chronic HTN Renal disease Antiphospholipid syndrome Diabetes Multiple gestation Angiotensinogen gene T235 (?) Previous severe PIH before 28 weeks Risk Factors

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6 Normal Preeclampsia 3rd trimester

Etiology :1. Utero-placental ischaemia : Abnormal development of the placental bed vessels / shallow trophoblast invasion in spiral arteries 2. Endothelial cell activation/dysfunction:Cytotoxic factors : oxygen free radicals /lipid peroxidation / VLDL /fibronection / platelet derived growth factor( PDGF) / TNF-α /IL-6 / anti-vascular endothelial factor /endothelial inhibitive factor 3. Immunity ;Failure to express HLA-G mRNA or protein .4. Genetics :Recessive trait . : 

7 Etiology :1. Utero-placental ischaemia : Abnormal development of the placental bed vessels / shallow trophoblast invasion in spiral arteries 2. Endothelial cell activation/dysfunction:Cytotoxic factors : oxygen free radicals /lipid peroxidation / VLDL /fibronection / platelet derived growth factor( PDGF) / TNF-α /IL-6 / anti-vascular endothelial factor /endothelial inhibitive factor 3. Immunity ;Failure to express HLA-G mRNA or protein .4. Genetics :Recessive trait .

Pathology : 1.    Placenta : (1)   premature aging of villi (2)   hemorrhage (3) necrosis 2.    Kidney (1)   swelling of endothelial cells because of deposition of amorphous materials (2)   swelling of the glomerular capillarities.3.   Liver : periportal areas 4. Brain :cortical /subcortical areas 5. Heart :increase of cardiac afterload , prelod may  or . 6. Hematological: Hypercoagulation status, HELLP : 

8 Pathology : 1.    Placenta : (1)   premature aging of villi (2)   hemorrhage (3) necrosis 2.    Kidney (1)   swelling of endothelial cells because of deposition of amorphous materials (2)   swelling of the glomerular capillarities.3.   Liver : periportal areas 4. Brain :cortical /subcortical areas 5. Heart :increase of cardiac afterload , prelod may  or . 6. Hematological: Hypercoagulation status, HELLP

Clinical finding : Headache Visual disturbances Tightness of chest Convulsion : 

9 Clinical finding : Headache Visual disturbances Tightness of chest Convulsion

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10 Maternal complications Liver Jaundice HELLP Hepatic rupture Coagulation DIC Microangiopathic haemolysis HELLP CNS Eclamptic convulsions Cerebral haemorrhage Cerebral oedema Cortical blindness Retinal detachment Renal Cortical necrosis Tubular necrosis Pulmonary oed. Electrolyte disturbances

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11 LOOK FOR APPEARANCE OF OMINOUS FEATURES DAILY- RECORD B.P 4 TIMES, MONITOR U.O & TEST FOR PROTEINURIA QUALI. / QUANT ALT.DAY- BODY WEIGHT EVERY 4TH DAY- URIC ACID, PLATELET COUNT, L.F.T. (LDH) WEEKLY- CREATININE MONITORING MATERNAL Refractory HTN Unresponsive oliguria Unresponsive pulmonary edema PAC/CVC

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12 DAILY -FHS, FUNDAL Ht. ABDOMINAL GIRTH, LIQUOR, FOETAL MOVEMENT COUNT, USG - ON ADMISSION & THEN 3 WEEKLY FOR FOETAL BIOPHYSICAL PARAMETERS, PLACENTA AND LIQUOR VOLUME DOPPLER USG FOR PLACENTAL BLOOD FLOW VELOCITY EVERY 4TH DAY MONITORING FOETAL

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13 HOSPITALISATION - FOR MONITORING SEDATIVES - DIAZEPAM / PHENOBARBITONE / ALPRAZOLAM ? NUTRITIONAL SUPLEMENTS - PROTEIN, IRON, CALCIUM (1000 MG), VITAMIN E & C, MICRONUTRIENTS STOP - SMOKING & ALCOHOL 1. Antihypertensive drugs: SNP / NTG GENERAL MEASURES TREATMENT

MethylDOPA : 

14 MethylDOPA Centrally acting sympathomimetic It has the longest track record of safety Side effects: failure to control BP, lassitude, depression and immune mediated haematological changes 750 mg to 4 gms daily po, i.v 250-500 mg QID It has a lag period of few hours before it starts to work

Nifedipine : 

15 Nifedipine CCB This has rapid onset of action orally and sublingually (10-15 min) It may cause tachycardia and precipitous fall in BP and headaches Given 4-6 hourly Slow release preparations are given twice daily The tocolytic effect is only theoretical

Labetalol : 

16 Labetalol  &  blocker 100 – 400 mg BD po & i.v 20 mg / hour doubled every 30 minutes It results in gradual fall in BP and has predictable action

Hydralazine : 

17 Hydralazine Arterial dilator 25 - 50 mg BD, iv 50-150 g/min It has a lag period of 20-30 min Severe headaches, & may fail due to tachyphylaxis A lupus like syndrome is quite rarely seen

Magnesium Sulphate : 

18 It probably works by neuronal calcium blocking through the glutamate channel It will nearly always arrest convulsions It does not depress the maternal sensorium The fetus is least affected It is currently the anticonvulsant of choice in eclampsia Magnesium Sulphate

Magnesium Sulphate Protocol : 

19 Magnesium Sulphate Protocol 4 gms IV as 20% soln @ 1 gm/min 10 gms of 50% soln. 5 gms in each buttock If convulsions persist after 15 min give 2 gms IV again as 20 % soln Every 4 hours 5 gms of 50% soln given in alternate buttock Discontinued 24 hours after delivery

Magnesium Sulphate Protocol : 

20 If Mg levels are monitored it muse be between 4 -7 mEq/L If clinical monitoring only The patellar reflex must be present Respiration not depressed Urine output > 100 mL in the last 4 hours Magnesium Sulphate Protocol

Diazepam : 

21 Diazepam It is a very good agent to terminate a fit (10 mg IV repeated if necessary) It is not a good agent to prevent a fit If depresses maternal CNS Doses more than 40 mg must not be used in 24 hours It accumulates in the fetus and results in problems after birth

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22 3 ) ALLYLESTRENOL : - TO PROMOTE FOETAL GROWTH IN DOSES OF 5-10 Mg. 3 - 4 TIMES / DAY DRUGS TREATMENT 4 ) DIURETICS ? : - AVOID ONLY IN PULMONARY OEDEMA, CCF, RENAL HYPERTENSION, SEVERE OLIGURIA / ANURIA. CHLORTHIAZIDE, FRUSEMIDE SHOULD BE STOPPED WELL BEFORE TERMINATION OF PREGNANCY

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23 6 ) GLUCOCORTICOIDS: - <34 WEEKS BETAMETHASONE / DEXAMETHASONE -12 MG, 2 DOSES AT 12 HOURS INTERVAL FOLOWED BY WEEKLY INJ. TILL DELIVERY / 34 WEEKS. DRUGS TREATMENT 5 ) TOCOLYTICS : - ISOXSUPRINE + 7 ) THYROTROPIN RELEASING HORMONE : - ? DOSE - 400 µGm, 8 HOURLY FOR 4 DOSES, TO PROMOTE FOETAL MATURITY IF DELIVERY <34 WEEKS.

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24 1 ) AT 36 WEEKS: - IN ALL CONTROLLED CASES 2 ) AFTER 32 WEEKS: - FOR FOETAL SALVAGE DECREASED FOETAL MOVEMENT SEVERE IUGR WITH OLIGOHYDRAMNIOUS LATE DECELERATION WITH POOR VARIABILITY REVERSED UMBILICAL DIASTOLIC BLOOD FLOW DELIVERY TREATMENT BEST DAY - WHEN ? 3 ) ANY TIME : - IF PROGRESSIVE INSPITE OF TREATMENT, WHEN - BP >160 /100 MM OF HG URINE OUTPUT < 400 ML / 24 HOURS PLATELET COUNT < 50000 / CMM SERUM CREATININE INCREASES PROGRESSIVELY LDH >1000 IU / L

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25 1 ) INDUCTION WITH OXYTOCIN: -After 36 weeks IF FOETAL CONDITION IS GOOD CERVIX IS FAVOURABLE / Cerviprime APPLICATION OF FORCEPS / VENTOUSE DELIVERY TREATMENT BEST WAY - HOW ? 2 ) BY LSCS: - IF TERMINATION BEFORE 36 WEEKS IN CASES OF MATERNAL / FETAL JEOPARDY BEST PLACE - WHERE ?- HIGH-RISK PREGNANCY UNIT / TERTIARY WELL EQUIPED HOSPITAL

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26

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27 Differential Diagnosis - HELLP 1. Sepsis 2. TTP 3. SLE 4. HUS 5. DIC 6. Abruptio placentae 7. Amniotic fluid embolism 8. Drug induced hemolytic anaemia 9. Cholecystitis/ Appendicitis Mississipi Tenessi

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28 Thanks for your attention !