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HDP - eclampsia and preeclamsia
- 1. Hypertensive Disorders in Pregnancy MANOJIT SARKAR MALDAMEDICAL COLLEGE AND HOSPITAL MALDA
- 2. INTRODUCTION It isassociated with severe maternal obstetric complications. Incidence is 5-10%. The most frequent cause of iatrogenic prematurity. Preterm delivery Intrauterine growth restriction (IUGR) Perinatal death Maternal cerebrovascular accidents Placental abruption
- 3. Hypertension in Pregnancy Systolic B.P. ≥ 140 mmHg and/or Diastolic B.P. ≥ 90 mmHg Documented on two occasions At least 6 hours apart Not more than 7 days apart Readings should be confirmed using appropriate measurement technique, and should be remeasured after 10-15 minutes of rest. Other Criteria (Not part of definition currently) SBP increased by 30mmHg DBP increased by 15mmHg Mean Arterial Pressure increased by 20mmHg
- 4. SEVERITY HYPERTENSION Non-severehypertension: SBP 140-159 mmHg or DBP 90-109 mmHg. Mild: SBP 140-149 mmHg or DBP 90-99mmHg. Moderate: SBP 150-160 mmHg or DBP 100-110 mmHg. Severe hypertension: SBP > 160 mm Hg or DBP > 110 mmHg or both.
- 5. How to MeasureBlood Pressure Sitting Position Patient Relaxed Arm well supported Measured in right arm Cuff at heart level Proper cuff size (80% of arm circumference) Slow deflation of bladder (2mmHg/s) From start of Korotkoff I to end of Korotkoff V
- 6. Normal Blood Pressure changesin Pregnancy • Decreases during the first trimester, • Reaching its lowest point at 20 weeks, • Returns to pre-pregnancy levels during the third trimester.
- 7. What is Significant Proteinuriain Pregnancy Total protein in 24 hours urine > 300mg Protein : Creatinine ratio in random sample > 0.1
- 8.
- 9. Classification 2. Pre- eclampsia 4. Eclampsia 3. Preeclampsia superimposed onchronic hypertension 5. Chronic hypertension with pregnancy 1. Gestational hypertension
- 10. GESTATIONAL HYPERTENSION New onsetof hypertension after 20 weeks of gestation without proteinuria or other features of preeclampsia, followed by return of B.P. to normal within 12 weeks post-partum. This terminology replaces the term “Pregnancy Induced Hypertension.”
- 11. Gestational HTN: DIAGNOSIS Determinethe severity of hypertension Measure protein excretion 24-hour urine collection Evaluate for signs/symptoms of severe preeclampsia Perform laboratory evaluation +/- end - organ involvement
- 12. Gestational HTN: DIAGNOSIS CRITERIAFOR MILD GESTATIONAL HYPERTENSION Blood Pressure > 140 to < 160 mm Hg, systolic > 90 to < 110 mm Hg, diastolic Proteinuria < 300 mg per 24-hr collection Platelet count > 100,000/mm3 Liver enzymes Normal Maternal symptoms Absent IUGR / Oligohydramnios Absent
- 13. Gestational HTN: MANAGEMENT Mild Gestational HTN Managed as outpatients (weekly antepartum visits) Daily fetal movement/kick counting NST + AFI OR BPS Fetal growth monitoring every 3-4 weeks No antihypertensive therapy No antenatal corticosteroids Deliver patients no later than their EDD
- 14. Gestational HTN: MANAGEMENT SevereGestational HTN SBP ≥160 mmHg or DBP ≥110 mmHg is treated with antihypertensive agents > 34 wks AOG DELIVER! < 34 wks AOG give steroids
- 16. Gestational HTN: Risk ofProgression to Preeclampsia 15-25% risk Women with early onset of gestational hypertension are more likely to progress to preeclampsia than women with late onset
- 17. Gestational HTN: RECURRENCE Prevalence: 22- 47 % (2nd pregnancy) tends to recur with subsequent pregnancies
- 18. Gestational HTN: LONG-TERM PROGNOSIS associatedwith development of HTN later in life associated with development of diseases related to hypertension (CVD, CKD,DM)
- 19. PREECLAMSIA New onsetof hypertension after 20 weeks of gestation along with properly documented proteinuria or end-organ dysfunction symptoms, followed by return of B.P. to normal within 12 weeks post-partum. Preeclamsia Gestational Hypertension Proteinuria
- 20. Note it…………………….. Preeclampsiacan also occur without proteinuria, with end- organ dysfunction manifestations. Edema is no longer considered a specific diagnostic criterion for preeclampsia.
- 22. Risk Factors Genetic Age &parity Partner factors Pregnancy Factors Underlying Medical Conditions Others Risk Factors
- 23. Risk Factors: Cont. Genetic Genetic Predisposition FamilyHistory Race & Ethnicity More Common in black & Asians Pregnancy by ovum donation Age &Parity Teenage pregnancy <18yrs Age>35 yrs Long interval between pregnancy>10 years Nulliparity Partner Factors Change of partner Limited sperm exposure Pregnancy by donor insemination Partner fathered an eclamptic pregnancy
- 24. Risk Factors: Cont. PregnancyFactors Multiple pregnancy Hydatiformmole Hydropsfetalis Fetalchromosomal anomaly (trisomy13) Underlying MedicalDiseae Chronic hypertension Diabetes mellitus Renal Disease Cardiovascular disease Hyperthyroidism Metabolic Syndrome Others ObesityBMI> 35 kg/m2 Psychological stress & strain Smoking Previous history ofpreeclamsia • Hyperhomocysteinemia , • Autoimmune disease • Antiphospholipid antibodies, • Thrombophilia
- 25.
- 26. 2 stage modelfor preeclampsia Stage 2 Maternal syndrome (HTN, proteinuria, Endothelial dysfunction) Stage1 Reduced placental implantation ???
- 27. Reduced placental implantation –Stage-1 PREDISPOSINGFACTORS: Abnormal implantation Association with microvascular diseases (diabetes, hypertension etc.) Association with large placentas (hydrops, multiple gestation, hydatidiform mole)
- 30. Net effect Replacement ofendothelial lining & muscular arterial wall by trophoblast cells Distended tortuous spiral arteries Lowresistence, low pressure, high flow system
- 31. ETIOLOGICAL FACTORS Placental hypoxia Immunologicalfactors Placental enzymes Genetic factors (MTHFR, F5,) Oxidative stress
- 32. What causes maternal syndrome Stage2 Maternal syndrome (HTN, proteinuria, Endothelial dysfunction) Stage1 Reduced placental implantation What gets into maternal circulation
- 33. Maternal Syndrome stage-II Not justhypertension and proteinuria But also involves different end organs
- 34. Physiology of maintain uteroplacentalflow in Normal pregnancy Placenta releases angiotensinase destruction of angiotensin-II(a potent vasoconstrictor) BP stabilized Vascular synthesis of PGI-2 and NO in excess vasodilation BP stabilized & uteroplacental flow maintains Release of VEGF restores uteroplacental flow
- 35. Normal balance ofagonist & anta-gonistic factors: 1.vasodialator & vasoconstrictor 2. angiogenic and antiangiogenic factors
- 36. 1.vasodialator & vasoconstrictor vasodialator NO PGI-2 vasoconstrictor Angiotensin- II Endothelin-I ThromboxaneA2 placenta Syncytiotrophoblast & endothelium
- 37. 2. angiogenic and antiangiogenicfactors Angiogenicfactor •VEGF •TFG-beta •PlGF Antiangiogenicfactor • sFlt-1 • sEng
- 39.
- 40. Basic mechanism ofdifferent organ damage Increased vasoconstriction Decreased organ perfusion Increased endothelial dysfunction – capillary leak, oedema, Pulmonary oedema, proteinuria. Activation of coagulation: DIC, low platelets Haemoconcentration
- 42. Multisystem Features Of Preeclampsia HypertensionProteinuria Eclampsia HELLP syndrome Intra-uterine growth restriction Multi-organ disease Cerebral vessels Fetus Liver Systemic blood vessels Kidneys
- 43. Organ Damage utero-placenta IUGR HematologicalEpistaxis, DIC like features, hemoconcentration CNS Cerebral edema, cerebral hge seizures Heart Subendothelial hge , focal necrosis & hge, cardiomyopathy, heart failure Lungs Pulmonary edema, hemorrhagic brochopneumonia Kidneys glomerular endotheliosis, oliguria liver Subcapsular hge, ischaemiaperiportal necrosis, HELLP
- 44. CVS involvement: •↑afterload ↑edperipheral resistance •↓preload↓edpregnancy inducedhypervolumia • Pulmonary leak edemaalveolar endothelial damage & ↓edplasma oncoticpr • hemoconcentration& ↑edhematocrit ↓edblood volume than normal pregnancy(16%vs50%): Heart failure ↓cardiac output
- 45. Hematological system Thrombocytopenia& other PLabnormality: •↑edPL activation & degranulation, •↓ed life span. •Corelateswellwthdisease severity. Intravascular hemolysis •endothelial damage & altered fluidity of erythrocyte membrane d/t change in serum lipid content → ↑edLDH, spherocytosis,reticulocytosis •microangiopathichemolysis ↑edcoagulation & fibrinolysis •Feature like DIC •Release ofthromboplastin •↓fibrinogen •AT-III •plasminogen
- 46. Renal system involvement: ↓ed renal perfusion :(d/t ↓ed blood volume & ↑ed afferent arteriolar pr.) ↓ed GFR : d/t glomerular capillary endotheliosis Endothelial dysfunction + mesangial swelling + BM disruption (but podocyte disruption minimal) Oliguria ↑ed creatinine level ↑ed uric acid
- 47.
- 48. Brain involvement: Acute severeHTN cerebrovascular overregulation Vasospasm Parenchymal ischemia Cytotoxic edema sudden ↑↑SBP exceeds normal range of cerebrovascular autoregulation Forced vasodilation +hyperperfusion Vasogenicedema
- 49. Lungs involvement: High SBP ↑edarteriolarpr ↑edextravasationof blood into alveoli + rupture of arteriole Pulmonary edema, hemorrhagicbrochopneumonia
- 50. PREECLAMPSIA PREDICTION Thereare many test during early pregnancy— or across pregnancy—of various biological, biochemical, and biophysical markers implicated for preeclampsia prediction. The most predictive investigative procedures are cumbersome, time-consuming and with poor sensitivity and with poor positive predictive value for preeclampsia. The efficacy of the preventive methods is questionable too Currently, no screening tests are predictably reliable, valid, and economical (Kleinrouweler, 2012).
- 51. Endothelial Dysfunction/Oxidant Stress Feto-Placental unitEndocrine Dysfunction RenalDysfuntion Misc Placental Perfusion/ Vascular Resistance related Tests Uterine Artery Doppler Velocimetry AT- III ANPFree fetal DNA Adapted from Conde-Agudelo and associates (2009)
- 52. Trials of differentpreventive methods and their outcomes Sibai et al. Lancet 365:785-99, 2005.
- 53. Provocative Pressure Tests Three testshave been extensively evaluated to assess the blood pressure rise in response to a stimulus.
- 54. 1.Roll-over test After restingin the left lateral position turning to a supine position induces a rise in diastolic pressure of 20 mmHg or more is a positive test indicative of tendency to develop pre-eclampsia. Perform at 28 to 32 weeks pregnancy.
- 55. 2.Hand-grip test Isometric(sustained) contraction of striated muscles is known to cause general sympathetic activation and hence increase systemic arterial pressure in healthy adults. The patient compresses an inflated sphygmomanometer cuff for a 3-minutes period at maximal and then at 50% of maximal voluntary contraction. An increase in diastolic pressure >20 mmHg at 28-32 weeks’ gestation is associated with an increased incidence of GHTN and eclampsia.
- 56. 3. Angiotensin IIsensitivity Sensitivity to infused angiotensin II: is increased may be due to alteration in vascular smooth muscle A II receptors. Sensitivities of all above three tests to range from 55 to 70 percent, and specificities approximated 85 percent. (metaanalysis, Conde-Agudelo and associates 2014)
- 57. • is mostpromising, but currently, none of them is completely suitable for clinical use. (Conde- Agudelo, 2014; Kleinrouweler, 2012; Myatt, 2012a). • These have value for fetal-growth restriction but not preeclampsia (ACOG, 2013a). • As a result of these trials, some methods to prevent Preeclampsia have been theorized… Uterine Artery Doppler Velocimetry (abnormal flow resistance/ diastolic notch in 2nd/ 3rd trimester)
- 58. uterine artery DOPPLER Inpreeclamptic mother: Showing early diastolic NOTCH Decreased EDF (due to high resistance) In normal mother
- 59. Urinary assays a. Micro-albuminuria:detected by radioimmunoassay before albuminuria can be detected by the ordinary methods. The drawback is that not all proteinuric pre- eclampsia are preceded by this phase. Sensitivities ranging from 7 to 90% and specificities between 29 and 97 % (Conde- Agudelo,2014). b. 24 hours urinary calcium excretion: is lower in women with pre-eclampsia than normotensive pregnant women.
- 60. Urinary assays c.Kallikrein/creatinine ratio:is reduced in patients who develop PIH later on if compared to the increased ratio in normal pregnancy. Kallikrein is a blood pressure reducing agent. d. Prostaglandins metabolites: The end metabolite of prostacyclin is decreased while thromboxane B2 (the metabolite of thromboxane A2) is increased in urine of pre-eclamptic women.
- 61. Blood tests a.Plasma urate: serial increase is a warning of PIH before appearance of other clinical features. b.Platelet count: a reduction occurs early in pre-eclampsia. c. Anti-thrombin - III activity: begin to decline as much as 13 weeks prior to the development of clinical manifestations of pre-eclampsia.
- 62. PREVENTION Prepregnancy • Weightloss to ideal BMI • Control of glucose in diabetes • Control of BP in CHTN (diet, exercise) Low dose aspirin 75 mg in High risk patient (from 12 wks) once a day Calcium 500mg twice a day. Not recommended • Vitamins C & E • Dietary salt restriction • Anti-HTN therapy to prevent preeclampsia
- 63. History -special points •Patient Particulars: Age young or >35 yrs, nulliparity, low SES -risk factors • Chief Complaints: Swelling of legs or other parts of body (face, abdominal wall, vulva, or whole body and tightness of the ring on the finger.) Severe disease -Headache, visual changes, nausea, vomiting, abdominal or epigastric pain, and oliguria, insomnia, vaginal bleeding, seizures. • Present Obstetric History: Onset, Duration, Severity of Htn/Proteinuria and H/o drug intake • Past Obstetric History: H/o any hypertensive disorder of pregnancy with week of onset. Also note the interval since last pregnancy, gestational age at delivery. Any foetal complications. • Past History: of pre-existing hypertension, renal disease, diabetes, thrombophilia, or thyroid disorder. • Family History: of Htn, Preeclampsia, Diabetes, CVD
- 64. Physical Examination: ● Obesity/BMI>35 kg/m2 ● Weight (serial measurements): Gain in wt at the rate of >500gs a week or 2.5kgs a month in the later months of pregnancy may be the earliest sign of preeclampsia. ● Oedema (all sites): has to be pathological, meaning visible pitting edema demonstratable over the ankles after 12 hrs bed rest. ● Pulse ● B.P.: ○ right arm, sitting/supine, arm at level of heart, cuff length=1.5 times of arm circumference, diastolic BP is the disappearance of Korotkoff sounds (phase V) ○ taken on 2 occasions at least 6 hrs apart for confirmation of diagnosis. ● CVS examination: auscultation for heart rate, rhythm, splitting of S2, murmurs. ● Ophthalmic examination: retinal haemorrage, nicking of veins, arteriole/vein ratio 3:1 from 3:2, papilloedema ● Deep tendon reflexes: hyperreflexia/presence of clonus
- 65. Obstetric Examination: Nothing specialis found except features of IUGR, oligohydramnios in some cases.
- 66. Maternal Investigations: Tests maybe abnormal even when BP elevation is minimal. • Urine dipstick testing for proteinuria o Quantitation by laboratory methods if ≥1+ on dipstick testing o Urinary ACR(albumin-creatinine ratio) to detect significant proteinuria (≥30mg/mmol) o 24 hour urine collection is not necessary in routine clinical management • Routine Blood Examination: TLC, DLC, Peripheral Smear, BT, CT, Hb% • Serum Urea, creatinine, electrolytes including lactate dehydrogenase (LDH) and uric acid. • Liver function tests (LFT) -AST, ALT >70 IU/l • Skiagram of chest –PA view, Pulmonary Capillary Wedge Pressure (PCWP), Brain Natriuretic Peptide (BNP) for detection of pulmpnary oedema
- 67. Diagnosing Preeclampsia-Eclampsia: • Bloodpressure ≥ 140/90 mm of Hg (at or after 20 weeks of gestation) on 2 occasions at least 6 hours apart during bed rest. (160/90 mm of Hg is severe disease) • accompanied by one or more of: o significant proteinuria -urinary dipstick 1+ -random urinary protein/creatinine ratio ≥ 30 mg/mmol -24 hour urine excretion ≥300 mg/24 hrs o renal involvement -serum creatinine ≥ 90 mmol/L or -oliguria (<400 ml in 24 hrs) o haematological involvement -platelet count <1 lakh o liver involvement -raised AST, ALT (>70 IU/l) -severe upper abdominal pain o neurological involvement -severe headache -persistent visual disturbances -hyperreflexia with sustained clonus -convulsions (eclampsia) -stroke o pulmonary oedema o fetal growth restriction o placental abruption
- 68. Foetal Investigations: • Cardiotocograph(CTG) • Ultrasound scan (USS) assessment of: o fetal growth o amniotic fluid volume (AFV) o umbilical artery flow (Doppler)
- 69. Differential Diagnosis Pre-existing hypertension New/gestationalhypertension Pre-eclampsia Eclampsia Exacerbation of underlying renal disease/Superimposed pre-eclampsia- eclampsia SLE
- 70. N.B: Grades ofproteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3, 4+=10 Hypertensive Disorders in Pregnancy Gestational HTN ●BP ≥ 140/90mmHg ●No evidence of underlying cause of HTN ●No associated symptoms ●Comes to normal within 12 wks of delivery Pre- eclampsia Non Severe Severe Eclampsia PreEclamsia + Convulsion ± Coma N.B: Pre-eclampsia is principally a syndrome of signs and when symptoms appear it is usually late.
- 71. Indicators of severityof Pre-eclampsia ABNORMALITIES NONSEVERE SEVERE Blood pressure ≥140/90mmHg but <160/110mmHg ≥160/110mmHg Proteinuria ≤2+ ≥3+ Oliguria Absent <400ml/day Headache Absent Present Visual disturbances Absent Present Platelet count Normal Thrombocytopenia (<100,000/mm3) HELLP syndrome Absent May be present ALT,AST >70 IU/L LDH>600 IU/L Bilirubin >1.2g/L Serum transaminases(AST,ALT) Normal (<40 IU/L) Elevated Serum Creatinine Normal Elevated Epigastric pain Absent Present Fetal growth restriction Absent Obvious Pulmonary oedema Absent present
- 72. MANAGEMENT Definitive treatment: DELIVERY! Basedon: AOG Severity of PE Maternal / Fetal condition
- 73. NONSEVERE PE: MANAGEMENT Deliverat ≥37 weeks of gestation Labor induction encouraged
- 74. For Nonsevere -controlled disease : There afterinduction may be done at termdepending on cervical condition Can bemanaged expectantlytill term athome/hospitaland continuedtill term. 74
- 75. What is EXPECTANTMANAGEMENT? NO YES Neither forced nor restricted
- 76. EXPECTANT ANTEPARTUM MANAGEMENTOF NONSEVERE PREECLAMPSIA Inpatient vs outpatient care Close maternal monitoring upon diagnosis of preeclampsia is important to establish disease severity and the rate of progression Hospitalization is useful for making these assessments and facilitates rapid intervention in the event of rapid progression Outpatient care is a cost-effective option for women with stable mild preeclampsia after initial dx evaluation
- 77. EXPECTANT ANTEPARTUM MANAGEMENT OFNONSEVERE PREECLAMPSIA Laboratory follow – up platelet count, serum creatinine, serum AST 1-2x/wk, assess disease progression Assessment of fetal well-being daily fetal movement count twice weekly fetal NST with AFI or twice weekly BPS UMA Doppler indices evaluation
- 78. EXPECTANT ANTEPARTUM MANAGEMENT OFNONSEVERE PREECLAMPSIA Assessment of fetal growth Sonographic estimation of fetal weight done to look for growth restriction and oligohydramnios at the time of diagnosis of PE , repeated every 3 weeks if the initial examination is normal Antenatal corticosteroids < 34 weeks AOG
- 79. But wait…can antihypertensivesbe used in expectant management??? • In non-severe Pregnancy hypertension – No clear Evidence of benefit other than to reduce The Frequency of Episodes of Severe hypertension • May Adversely Effect Fetal Growthvelocity
- 80.
- 81. Hospitalisation??? • Gestational HTN: only if severe HTN • Preeclampsia : If diastolic pressure≥ 100mm of Hg OR, there is proteinuria OR, there is fetal compromise. 37 completed weeks of gestation.
- 82. INTRAPARTUM MANAGEMENT Intrapartummonitoring Fluids monitored closely to avoid excessive administration, since women with severe disease are at risk of pulmonary edema and significant third-spacing
- 83. DELIVERY CARE • Forany HDP, vaginal delivery should be considered unless a CS is required for the usual obstetric indications. • Antihypertensives : continued throughout labour to maintain BP < 160/110 mmHg . • 3rd Stage : actively managed with 10 units IM, particularly in the presence of thrombocytopenia or coagulopathy. (I-A) • Ergometrine should NOT be given
- 84. PES: MANAGEMENT Deliver regardlessof gestational age if proteinuria ( ≥5 grams) is the only criteria for severe disease managed as nonsevere PE mild fetal growth restriction with reassuring Doppler velocimetry treat conservatively * severe hypertension treat conservatively * NOTE: * remote from term
- 85. For early onsetsevere preeclampsia: • Controversy regarding termination in early onset disease • But there is no beneficial role for mother, as well as perinatal mortality is also high instead of conservative management • So… 85 termination is seriously considered
- 86.
- 88. Acute Management ofPES Set 1: Labetalol first protocol •Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic > 110 mmHg) • Initiate appropriate fetal surveillance • Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Labetalol 40 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Labetalol 80 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then: • Emergency consultation with maternal fetal medicine (MFM), anesthesia, internal medicine, critical care specialist. • Give additional antihypertensive medication per specific order. • Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours. • Institute additional BP timing per specific order.
- 89. Acute Management ofPES Set 2: Hydralazine first protocol • Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic ≥ 110 mmHg) • Initiate appropriate fetal surveillance • Hydralazine 5 or 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then: • Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then: • Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then: • Labetalol 40 mg IV over 2 min and; • Obtain emergency consultation with MFM, anesthesia, internal medicine, critical care specialist. • Give additional antihypertensive medication per specific order. • Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every 15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours • Institute additional BP timing per specific order.
- 90. TARGET BP 130to 150 mm Hg systolic and 80 to 100 mm Hg diastolic OR reduce MAP by no more than 25% over 2hrs Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation.
- 91. WOMEN WHO FAILTO RESPOND TO FIRST LINE AGENTS Emergent consultation with anesthesia, maternal fetal medicine or critical care for second line management decisions, which can include labetalol or nicardipine by infusion pump, and nitroprusside for extreme emergencies.(ACOG 2013) Sodium nitroprusside to be used rarely when other agents fail, at 0.25 μg/kg/min to a maximum of 5 μg/kg/min. Nitroprusside should be used for the shortest amount of time possible, due to the risk of fetal cyanide poisoning and increased intracerebral pressure with worsening cerebral edema.
- 92. Seizure Prophylaxis MgS04 givento mild / severe PE Loading dose: 4-6 g, slow IV push, over 15-20 mins Continuous infusion: 1-2 g/hr OR 5g IM into each buttock (total 10 g) followed by 5 g IM, alternate buttocks ever 4h continued for 24 hours after last convulsion or delivery.
- 93. MgS04 Toxicity 1. Impairedbreathing(@8-10meq/L) 2. Arrythmia and Asystole ( @10-13 mEq/L) 3. Decreased/absent deep tendon reflex (Hyporeflexia at 4 mEq/L, loss of patellar reflex at 7-10 mEq/L) 4. Shock (>13 mEq/L) • For a maintenance dose following must be present - Serum Mg level 4-7meq/l(twice daily) Having Patellar reflex Urine output >30ml/hr RR>12/min
- 94. WHAT If magnesiumtoxicity is suspected??? Administration of 10mL of 10% calciumgluconate(1 g in total) as a slow intravenous push. Serum magnesium level obtained. Magnesium infusion should be discontinued, supplemental oxygen administered,
- 95. For severe-uncontrolled disease: LUCSORIn case of very severe uncontrolled diseaseelective LUCSmay be done without induction Preinduction Cervical ripeningwithprostaglandinfollowed byinduction Terminationis considered 95 If failed
- 96. Postpartum Management NSAIDs forpain control should be avoided in women with poorly controlled hypertension, oliguria, renal insufficiency, or thrombocytopenia patient controlled fentanyl or remifentanil analgesia or epidural. Monitor VS q 2h while on MgS04 Treat PES
- 97. IMMEDIATE REMOTE MATERNAL FETAL ●IUGR ● IUD ● Asphyxia ●Prematurity During Pregnancy During Labour During puerperium●Eclampsia(2%) (more in acute cases) ●Accidental hemorrhage ●Oliguria ●Diminished vision ●HELLP Syndrome ●Cerebral hemorrhage ●ARDS ● Eclampsia ● Postpartum hemorrhage ●Eclampsia( in < 48hrs of delivery) ●Shock ●Sepsis ●Residual hypertension ●Recurrent pre- eclampsia ●Chronic Renal Disease • Abruptio placentae
- 98. HELLP Syndrome This isan acronym for Hemolysis, Elevated Liver enzymes, and Low Platelet count. It is a rare multisystem disorder that complicates pregnancy with lab evidences of micro- angiopathic hemolysis, hepatic dysfunctioning & thrombocytopenia. It is a complication mostly associated with Pre- eclampsia but can also be diagnosed (rarely though) in the absence of these disorders. Incidence 20% of women with severe preeclampsia.
- 99. HEMOLYSIS (due to passage of RBCs through partially obstructed vessel) s) HEPATIC DYSFUNCTION (dueto intravascular fibrin deposition &sinosoid alobst.) Decreased Liver blood flow HELLP Syndrome THROMBO- CYTOPENIA( due to platelet aggregation &diposit ionin the sites ofendothheli aldamage)
- 100. Diagnosis Hemolysis (Hallmark of thetriad) Elevated Liver Enzymes Low Platelet Count LDH>600IU/L Liver Enzymes (<100,000/cu.mm) Low serum haptoglobin High serum bilirubin (>1.2 mg/dl) High ALT & AST (>70 IU/L) Abnormal PBS (Schistocytes {helmet cells} , burr cells {Echinocytes}) Later-low Hb% • ●Epigastric/Right Upper Quadrant pain • ●Nausea, Vomiting 1. Clinical Features: 2. Lab Investigation:
- 102. HELLP Syndrome Initiate IVDexamethasone: Only for dangerously low platelet counts <50,000/uL The 2013 Task Force does not recommend for HELLP syndrome Antepartum: Dex 10mg q12 hrs Postpartum: Dex 10+10+5+5 @ 0,12,24,36 hrs
- 105. Usual Time ofOnset Relation to delivery Percentage Antepartum 72 Post_partum 28 ≤48 hours 80 >48 hours 20 Gestational Age (Weeks) Percentage 21-27 10 28-36 70 >37 20
- 106. SUPERIMPOSED PREECLAMPSIA ON CHRONICHYPERTENSION New onset proteinuria in hypertensive women but no proteinuria before 20 weeks' gestation A sudden increase in proteinuria or blood pressure or platelet count < 100,000/L in women with hypertension and proteinuria before 20 weeks' gestation
- 107. ECLAMPSIA Generalized tonic-clonicseizure in a patient with Preeclampsia not attributed to any other cause. If seizures occur beyond 48-72 hours postpartum causes may be more likely other than eclampsia. occurs in 2 to 3 percent of severely preeclamptic women not receiving anti-seizure prophylaxis Eclampsia Preeclampsia Seizure/ Convulsion/ Coma
- 108. D/D ECLAMPSIA Epilepsy, Intracranial haemorrhage/thrombosis, Meningitis, Cerebral malaria, Amnioticfluid embolism can mimic eclampsia.
- 109. PATHOGENESIS OF SEIZURES 1.Cerebral overregulation in response to high systemic blood pressure vasospasm of cerebral arteries underperfusion of the brain localizedischemia/infarction cytotoxic (intracellular) edema
- 110. PATHOGENESIS OF SEIZURES 2.Loss of autoregulation of cerebral blood flow in response to high systemic pressure E.g., hypertensive encephalopathy Hyperperfusion endothelial damage vasogenic (extracellular) edema
- 111. MANAGEMENT Iinitial Mx: Maintenanceof airway patency and prevention of aspiration Gravida rolled onto her left side Protect from trauma Supplemental O2 (8-10L/min via face mask)
- 112. Management of severehypertension, if present Prevention of recurrent seizures Evaluation for prompt delivery definitive treatment of eclampsia is delivery, irrespective of gestational age
- 113. Management of Eclampsia: Prompt delivery of fetus to achieve cure Avoidance of diuretics & hyper osmotic agents Limitation of I.V fluid Intermittent antihypertensive to control BP judiciously Control of convulsion by MgSO4 (IM/IV route) Protection & supporting care during convulsion Protection in a railed cot Protection of airway & prevention of tongue bite Correction of hypoxia & acidosis Managed inEclampsia room. 113
- 114. to control convulsion “Itis the most effective drug to control even recurrent seizures without any central nervous system depression to mother & fetus” 114 Magnesium sulphate
- 115. Dosages →Paralysingagent & Intubation →Amobarbital250mgI.V over 3 min In caseofuncontrolled recurrent seizure(10-15%) : →additional 2-4g of 20% solution IV @ <1g/min →4gm of 20% solution IV slowly(@ <1g/min) +10g of 50% solution deep IM in upper & outer quadrant of buttock by a wide bore needle then 5g of 50% solution IM 4hrly similarly IM regime (Pritchard protocol):1955 →4 gm loadingin100mlof IVFover 15-20 minfollowedby 2- 3g/hr in 100 mlIVF as maintenance I.V regime (Sibaiprotocol):1990 IM doses are as active as IV doses in controlling seizures 115
- 116. • Duration :24 hrs from last convulsion or from delivery which one is longer. 116
- 117. MATERNAL FETAL ●Asphyxia ●Prematurity ●Hypoxia &IUD Injuries Systemic ●Tongue bite ●Injuries due to fall ●Bed sore ●PULMONARY: edema, pneumonia, ARDS, embolism ●CARDIAC: acute left ventricular failure ●RENAL: renal failure ●HEPATIC: necrosis, subcapsular hematoma ●CNS: cerebral hemorrhage, edema(vasogenic) Vision ●Diminished vision due to retinal detachment or occipital lobe ischemia Hematology ●Low platelet count ●Disseminated Intravascular Coagulation Postpartum ●Shock ●Sepsis ●Psychosis
- 118. CHRONIC HYPERTENSION IN PREGNANCY Hypertensionbefore pregnancy / Diagnosed before 20 weeks of pregnancy not due to gestational trophoblastic disease. Hypertension diagnosed after 20 weeks but persistent after 12 weeks postpartum
- 119. Chronic HTN &Pregnancy Etiology : 1. Essential HTN (Most Common) 2. Secondary HTN : 1. Genetic: Glucocorticoid remediable aldosteronism, Liddle Syndrome 2. Renal : Parenchymal, Renovascular 3. Endocrine : Primary hyperaldosteronism, cushing syndrome, Pheochromocytoma 4. Vascular : Aortic coarctation, Estrogen use 5. Others
- 120.