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Sumit Tyagi

This document discusses hypertensive disorders in pregnancy, including their classification, symptoms, pathogenesis, predictors, and management. It classifies hypertensive disorders into gestational hypertension, preeclampsia, eclampsia, preeclampsia superimposed on chronic hypertension, and chronic hypertension. It describes the symptoms and criteria for diagnosing each condition. It discusses the risk factors, preventive measures, pathological alterations, maternal and neonatal complications, and medical management for preeclampsia. The medical management involves monitoring, controlling blood pressure below certain thresholds, and delivering early if certain severe conditions develop.

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HYPERTENSIVE DISORDERS IN PREGNANCY : COMPLICATIONS & MANAGEMENT PRESENTER: DR. SUMIT TYAGI MODERATOR: DR.MANISH GOYAL
CLASSIFICATION GESTATIONAL HYPERTENSION ( PIH / TRANSIENT HYPERTENSION ) PRE-ECLAMPSIA ECLAMPSIA PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION CHRONIC HYPERTENSION
GESTATIONAL HYPERTENSION BP > 140/90 mm Hg for the first-time during pregnancy after 20 weeks but no protein urea. This is transient hypertension and BP becomes normal by 12 weeks postpartum.
PRE-ECLAMPSIA Hypertensive syndrome that occurs in pregnant women after 20 weeks gestation consisting of new onset and persistent hypertension defined as systolic pressure >/= 140 mm Hg or diastolic BP >/= 90 mm HG take on at least 2 occasions >4 hours apart with any of the following : URINE ANALYSIS 1. Proteinuria >300 mg/24 hours or persistentm30 mg/dl (1+ on dip stick ) in 2 random urine samples collected at least 4 hours apart 2. Urine albumin: creatinine ratio > 8mg/dl Systemic involvement yes 1. Renal insufficiency : serum creatinine > 1.1 mg/dl 2. Liver involvement : elevated transaminases, right upper quadrant pain 3. Neurological complications Hematological complications
SEVERE PRE-ECLAMPSIA BP > 160/110 mm Hg Protein urea : 2 gm/24 hours or 2+ on dipstick Serum creatinine : >1.2 mg/dl Platelets < 1 lac/mm3 Microangiopathic hemolysis Elevated SGOT/SGPT persistent headache or visual disturbances persistent epigastric pain due to hepatocellular necrosis, ischemia and oedema leading to stretch in Glissons capsule
CHRONIC HYPERTENSION BP > 140/90 mmHg Before pregnancy or diagnose before 20 weeks gestation or hypertension first diagnosed after 20 weeks gestation and persistent after 12 weeks postpartum
Superimposed Preeclampsia on Chronic Hypertension All chronic hypertensive disorders regardless of their cause predisposed to the development of superimposed Preeclampsia or Eclampsia Preeclampsia is accompanied by proteinuria
ECLAMPSIA Eclampsia is the occurrence of seizures in women with Pre-Eclampsia when seizures cannot be attributed to other causes. seizures are grand mal type May appear before, during or after labour May develop more than 48 hours after delivery and may be encountered up to 10 days postpartum
PATHOGENESIS Failure of normal invasion of trophoblast cells leads to mal adaptation of maternal spiral arterioles Maladaptation of vessels Can interfere with normal villous development leading to placental insufficiency and subsequently hypoxia leading to foetal growth retardation and release of both vasoconstrictors and vasodilators leading to increased perfusion of vascular beds with endothelial damage and hypertension Vascular construction causes resistance to blood flow and accounts for the development of arterial hypertension
PREDICTORS OF PRE-ECLAMPSIA Rollover test : Elevation of 20 mm hg or more in systolic BP after patient assume supine position after lying lateral recumbent Elevated uric acid levels > 5.9 mg/dl Hypocalciuria Decrease urinary kallikrein excretion Increased cellular plasma fibronectin coagulation activation : Thrombocytopenia and platelet aggregation appear to be an integral feature of pre- eclampsia excessive platelet activation has been linked to maternal vasoconstriction, endothelial cell injury placental infarction and transient renal dysfunction thromboxane A2 is released promoting vasospasm further platelet aggregation and endothelial cell injury Immunological factors : TNF- alpha, Growth factors and interleukins increased Placental peptides: Increased corticotropin releasing hormone, ACTIVIN A, INHIBIN A Doppler velocimetry studies of the uterine artery : unreliable screening test as sensitivity is 78% with positive predictive value of 28%
Risk factors of Pre-eclampsia HIGH RISK FACTORS Hypertension during last pregnancy Chronic renal disease SLE Anti-phospholipid syndrome Diabetes Chronic hypertension
Risk factors of Pre-eclampsia MODERATE RISK FACTORS First pregnancy Assisted reproduction Age 40 years or more Pregnancy interval of more than 10 years BMI of 35 kg per metre square or more Family history of pre-eclampsia Multiple pregnancies Vitamin d deficiency Low dietary calcium
PREVENTIVE MEASURES Aspirin 75 mg daily from 12 weeks of gestation till delivery for patients with 1 high risk factor or >1 moderate risk factors Calcium supplementation >1 g daily during pregnancy may reduce chances in low dietary calcium supplementation Adequate rest in 3rd trimester Reduction of workload and stress Controlled weight loss Exercise
PATHOLOGICAL ALTERATIONS 1. Cardiovascularchanges : Increase in cardiac afterload due to hypertension. 2. Haematological changes: Thrombocytopenia (platelet count less than 1,00,000/mm3), microangiopathichemolysis(due to intense vasospasm),decreased clottingfactors,increasederythrocytedestruction,increasedfibrin degradation products and deficiency of antithrombin III. 3. Endocrine changes: Increase in deoxycorticosteronein third trimesterdue to conversionfrom plasma progesterone causes retention of sodium. 4. Fluid and electrolyte changes: Decreased plasma oncotic pressure which leads to increased extracellular fluid with associated decrease in intravascular volume. 5. Kidney: Oliguria is a result of reduced renal perfusion and glomerularfiltration. Plasma uric acid and serum creatinineare elevated.There is proteinuria> 300 mg per 24 hours or more than 1 + on urinary dipstick test. Acute renal failure and renalcorticalnecrosis may develop in severe cases
PATHOLOGICAL ALTERATIONS 6. Liver: Increased liver enzymes. Epigastric and right hypochondriac pain due to periportal haemorrhagic necrosis, which causeshepatic rupture or subcapsular hematoma. 7. HELLP syndrome: Triad of Haemolysis, elevated liver enzymes and low platelets. 8. Nervous system: Cerebral oedema, hyperaemia, focal thrombosis and haemorrhage , visual disturbances due to retinal artery vasospasm. Increased cerebral perfusion pressure may cause severe headaches. 9. Uterus and placenta: Incompletetrophoblastic invasion of spiral arteries causes reduction in diameter of vessels as compared to normal. In addition, vasospasm decreases placental perfusion leading to Intra Uterine Growth Retardation
MATERNAL COMPLICATIONS Intracranial haemorrhage : leading cause of maternal death DIC Pulmonary oedema Congestive heart failure Placental abruption Acute renal failure Liver rupture Cerebrovascular accident Septic shock
NEONATAL COMPLICATIONS SHORT TERM COMPLICATION OLIGOHYDRAMNIOS FETAL GROWTH RETARDATION PRETERM BIRTH PREMATURITY WITH RESPIRATORY DISTRESS LOW APGAR SCORE NICU STAY & SMALL FORGE MECONIUM ASPIRATION INTRACRANIAL HEMORRHAGE INTRA UTERINE FETAL DEATH
NEONATAL COMPLICATIONS LONG TERM COMPLICATIONS CEREBRAL PALSY LOW IQ HEARING LOSS VISUAL IMPAIRMENT INSULIN RESISTANCE DIABETES MELLITUS HYPERTENSION CAD
MANAGEMENT OF PRE-ECLAMPSIA MEDICAL MANAGEMENT Early prenatal detection and prompt institution of therapy and corrective measures. The timingof prenatal examinations :4 weeks until 28 weeks then every 2 weeks until 36 weeks and weekly thereafter. Hospitalization is considered for women with new-onset hypertension, which is persistent or worsening or development of proteinuria. Detailed systemic examination Daily scrutiny of headache,visual disturbance,epigastricpain and rapidweight gain. Weighton admissionand every day thereafter.
MANAGEMENT OF PRE-ECLAMPSIA Weight on admission and every day thereafter. Analysis for proteinuria on admission and at least every 2 days thereafter. Four hourly blood pressures monitoring in sitting position. Measurement of serum creatinine, complete blood count (CBC), liver enzymes, plateletsfrequency determined by the severity of hypertension. Frequent foetal monitoring clinically or by USG. Ample but not excessive proteins and calories; and no salt or fluid restriction in the diet
MANAGEMENT OF PRE-ECLAMPSIA ACE inhibitors, ARBs and chlorothiazideshave to stop these drugs and change over to other drugs before they become pregnant as these drugs can cause congenitalmalformations. Blood pressure shouldbe controlledto below 160/110 mm Hg to prevent maternalmorbidity, particularly from intracranial haemorrhage, encephalopathy, myocardial ischemia and failure. Oral antihypertensiveinclude the following drugs: Beta blockers: Labetalol (300 mg to 2400 mg/day). combined留 and 硫 blocker.50 mg over 1 minute f/b 20 mg/hr which can be increased by 20 mg every 20 min to a maximumdose of 160 mg per hour. Methyldopa : It is 留 methylanalogue of dopa, the precursor of dopamine (DA) and NA. The 留 methyl-NAis a selective留2 agonist formed in brain from methyldopaand acts oncentral 留2 receptors to decrease efferent sympathetic activity.Antihypertensive effect develops over 46 hours and lasts 1224 hours. Dose: 0.250.5 g BDQID oral (max 4 g/day).
MANAGEMENT OF PRE-ECLAMPSIA Nifedipine : Calcium channel blocker, it decreases peripheral vascular resistance without compromisingcardiac output. Dose is 10 to 20 mg every 4 to 6 hourly. Hydralazine : 5-10 mg slow iv injection or 200-300 mcg/min then 50-150 mcg/min for maintainence control. Caution : acute porphyria, cor-pulmonale, idiopathic SLE, severe tachycardia. Patient may need Fluid bolus along with titration of antihypertensives. SODIUM NITROPRUSIDE : use in refractory cases. Alternative anti HTN agents : oral clonidine, GTN infusion The target of blood pressure control in uncomplicated chronic hypertension is to keep blood pressure less than 150/100 mm Hg. Do not lower diastolicblood pressure below 80 mm Hg. In pregnant women with target-organdamage secondary to chronic hypertension; aim is to keep blood pressure lower than 140/90 mm Hg.
CONDITIONS MANDATE FOR IMMEDIATE DELIVERY Severe hypertension that persists after 24 to 48 hours of treatment Progressive thrombocytopenia Liver dysfunction Progressive renal dysfunction Premonitory signs of eclampsia Evidence of foetal jeopardy Persistent headache or other neurologic sequelae of pre- eclampsis
Definitive treatment for pre-eclampsia and eclampsia is termination of pregnancy. In uncomplicated pre-eclampsia, if women is near term, pregnancy is allowed to continue under the close observation until the cervix is more suitable for induction. In severe pre-eclampsia, before 34 weeks of gestation glucocorticoids may be tried for lung maturity : betamethasone 12 mg IM 24 HOURS apart in women between 24 and 34 weeks.
SIGNS OF IMPENDING ECLAMPSIA Headache Visual disturbance, such as blurring or flashing before the eyes Epigastric pain Oliguria Vomiting Sudden swelling of the face, hands or feet
Measures taken to prevent seizures Collaborative Eclampsia trial regimen for administration of MgSO4 :- ZUSPAN REGIMEN :- LOADING DOSE : 4-5 gm IV over 5 minutes followed by MAINTAINANCE DOSE : an infusion of 1 gm/hr maintained for 24 hours. If the woman had an eclamptic seizure, the infusion should be continued foe 24 hours after the last seizure and should not be discontinued during delivery. For recurrent seizures, further 2-4 gm MgSO4 given over 5 minutes. Measure serum Mg levels 4-6 hourly & maintain in between 4-7 meq per litre.
PRITCHARD REGIMEN :- Loading dose : 4 gm of 20 % MgSO4 slow IV followed by 5 gm of 50 % IM in each buttock , total dose : 14 gm. Maintainance dose : 5 gm 50 % IM in alternate buttock 4 hourly. SIBAI REGIMEN :- LOADING DOSE : 6 gm MgSO4 IV over 20 minutes MAINTAINANCE DOSE: 2 gm/hour IV infusion
Monitoring & Management of MgSO4 Toxicity In therapeutic doses magnesium sulphate is associated with muscle weakness due to decrease in the amount of acetylcholine released at motor nerve endings, decreased action of acetylcholine on the motor end plate and reduction of excitability of motor fibre membrane. Therefore, it increases the sensitivity of the mother to both the depolarizing as well as non-depolarizing muscle relaxants. When a patient is started on MgSO4 it is necessary to monitor: Patellar reflex (disappears when plasma magnesium level reaches 10 mEq/L; warning impending Mg toxicity) Rate and depth of respiration (depressed at level above 10 mEq/L, respiratory paralysis and arrest occurs above 12 mEq/L)
Monitoring & Management of MgSO4 Toxicity Urine output (Mg is cleared totally by renal excretion, when there is renal insufficiency, plasma magnesium level needs to be checked 4-6 hourly and dosage adjusted accordingly). Uterine effects: In high concentration MgSO4 depresses myometrial contractility secondary to inhibition of intracellular free Ca++ concentration in the uterine cell (seen at serum Mg level of 810 mEq/L). Neonatal effects: Magnesium crosses the placenta to achieve equilibrium in foetal serum. Magnesium sulphate is associated with a minimal risk of intracranial bleed and irregular bone deposits. It can cause a transient reversible change in foetal heart rate and should not be considered as a sign of foetal distress. The neonate may be depressed only if there is severe hypermagnesemia at delivery.
Treatment Withhold MgSO4 Administer Calcium gluconate, 1 g intravenously. For severe respiratory depression and arrest, prompt tracheal intubation and mechanical ventilation is life-saving
Management of a patient with eclampsia on MgSO4 with foetal distress who is posted for emergency LSCS Aspiration prophylaxis :- Pre-induction administration of nonparticulate antacid such as 0.3 M sodium citrate, 30 mL. Intravenous administration of histamine receptor blocking agent 40 minutes before induction. Eg Ranitidine 100 mg Administration of metoclopramide 4 mg to decrease gastric volume 3060 minutes before induction. Pre-oxygenation and denitrogenation with 100% oxygen over 3 minutes is preferred technique; however, if not feasible; patient can be advised to take 8 vital capacity breaths of 100% oxygen in one minute. If blood pressure is high, rapid control of blood pressure can be achieved by: Hydralazine (5 mg IV aliquots up to a maximum of 20 mg) Labetalol (510 mg IV every 10 min) Oral nifedipine (sublingual nifedipine can cause rapid changes in placental circulation which may compromise foetal condition) In resistant cases of Hypertension, sodium nitroprusside and glyceryl trinitrate can be used with continuous arterial BP monitoring.
Management of a patient with eclampsia on MgSO4 with foetal distress who is posted for emergency LSCS Crystalloid fluid bolus of 500 ml to prevent sudden hypotension CVP is indicated in patient with persistent oliguria and presence of pulmonary oedema for fluid management in antepartum and postpartum period Anticipate difficult airway and keep small size tubes, gum elastic bougie, laryngeal mask airway and difficult airway set ready plan for attenuation of response to laryngoscopy Crash induction with thiopentone sodium or propofol and succinylcholine after checking the ability to ventilate if BP is high Use atracurium for maintenance of relaxation it is preferable to use a peripheral nerve stimulator in intraoperative period. Use 2/3rd of the Mac value of inhalational agent to ensure adequate depth of anaesthesia Watch for hemodynamic changes during delivery and removal of placenta. continue magnesium sulphate during intraoperative and post operative.
HELLP SYNDROME HELLP syndrome is a severe form of pre-eclampsia characterizedby: H-Hemolysis (abnormalperipheralblood smear, and an increasedbilirubinlevel of 1.2 mg/dL or greater) EL - elevated liverenzymes (SGOT > 70 U/L, LDH > 600U/L) LP - low platelets (< 1, 00,000/mm It can occur antepartum or postpartum. Delivery represents the only definitive treatment of HELLP syndrome. Patient with HELLP syndrome have a high incidenceof seriousmaternal complicationsincluding disseminatedintravascular coagulation, placentalabruption,need for bloodtransfusion, pleural effusion, acute renal failure, and wound infection. After deliveryof placenta,recovery from HELLP syndrome can be expected to start within 2448 hours. These patients shouldbe monitored in the ICU or HDU. Steroids have no role in management of HELLP syndrome
NEED FOR PLATELET TRANSFUSION IN HELLP SYNDROME For a platelet count of 20K to 49K per mm3 with hemolysis, elevated liver enzymes and low platelet syndrome, platelet transfusion is recommended before LSCS. For a platelet count of 20K to 49K per mm3 with hemolysis, elevated liver enzymes and low platelet syndrome, platelet transfusion should be considered prior to vaginal delivery if there is : 1. Excessive active bleeding 2. Known platelet dysfunction 3. Rapidly falling platelet count 4. coagulopathy
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HTN IN PREGNANCY.pptx

  • 1. HYPERTENSIVE DISORDERS IN PREGNANCY : COMPLICATIONS & MANAGEMENT PRESENTER: DR. SUMIT TYAGI MODERATOR: DR.MANISH GOYAL
  • 2. CLASSIFICATION GESTATIONAL HYPERTENSION ( PIH / TRANSIENT HYPERTENSION ) PRE-ECLAMPSIA ECLAMPSIA PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION CHRONIC HYPERTENSION
  • 3. GESTATIONAL HYPERTENSION BP > 140/90 mm Hg for the first-time during pregnancy after 20 weeks but no protein urea. This is transient hypertension and BP becomes normal by 12 weeks postpartum.
  • 4. PRE-ECLAMPSIA Hypertensive syndrome that occurs in pregnant women after 20 weeks gestation consisting of new onset and persistent hypertension defined as systolic pressure >/= 140 mm Hg or diastolic BP >/= 90 mm HG take on at least 2 occasions >4 hours apart with any of the following : URINE ANALYSIS 1. Proteinuria >300 mg/24 hours or persistentm30 mg/dl (1+ on dip stick ) in 2 random urine samples collected at least 4 hours apart 2. Urine albumin: creatinine ratio > 8mg/dl Systemic involvement yes 1. Renal insufficiency : serum creatinine > 1.1 mg/dl 2. Liver involvement : elevated transaminases, right upper quadrant pain 3. Neurological complications Hematological complications
  • 5. SEVERE PRE-ECLAMPSIA BP > 160/110 mm Hg Protein urea : 2 gm/24 hours or 2+ on dipstick Serum creatinine : >1.2 mg/dl Platelets < 1 lac/mm3 Microangiopathic hemolysis Elevated SGOT/SGPT persistent headache or visual disturbances persistent epigastric pain due to hepatocellular necrosis, ischemia and oedema leading to stretch in Glissons capsule
  • 6. CHRONIC HYPERTENSION BP > 140/90 mmHg Before pregnancy or diagnose before 20 weeks gestation or hypertension first diagnosed after 20 weeks gestation and persistent after 12 weeks postpartum
  • 7. Superimposed Preeclampsia on Chronic Hypertension All chronic hypertensive disorders regardless of their cause predisposed to the development of superimposed Preeclampsia or Eclampsia Preeclampsia is accompanied by proteinuria
  • 8. ECLAMPSIA Eclampsia is the occurrence of seizures in women with Pre-Eclampsia when seizures cannot be attributed to other causes. seizures are grand mal type May appear before, during or after labour May develop more than 48 hours after delivery and may be encountered up to 10 days postpartum
  • 9. PATHOGENESIS Failure of normal invasion of trophoblast cells leads to mal adaptation of maternal spiral arterioles Maladaptation of vessels Can interfere with normal villous development leading to placental insufficiency and subsequently hypoxia leading to foetal growth retardation and release of both vasoconstrictors and vasodilators leading to increased perfusion of vascular beds with endothelial damage and hypertension Vascular construction causes resistance to blood flow and accounts for the development of arterial hypertension
  • 10. PREDICTORS OF PRE-ECLAMPSIA Rollover test : Elevation of 20 mm hg or more in systolic BP after patient assume supine position after lying lateral recumbent Elevated uric acid levels > 5.9 mg/dl Hypocalciuria Decrease urinary kallikrein excretion Increased cellular plasma fibronectin coagulation activation : Thrombocytopenia and platelet aggregation appear to be an integral feature of pre- eclampsia excessive platelet activation has been linked to maternal vasoconstriction, endothelial cell injury placental infarction and transient renal dysfunction thromboxane A2 is released promoting vasospasm further platelet aggregation and endothelial cell injury Immunological factors : TNF- alpha, Growth factors and interleukins increased Placental peptides: Increased corticotropin releasing hormone, ACTIVIN A, INHIBIN A Doppler velocimetry studies of the uterine artery : unreliable screening test as sensitivity is 78% with positive predictive value of 28%
  • 11. Risk factors of Pre-eclampsia HIGH RISK FACTORS Hypertension during last pregnancy Chronic renal disease SLE Anti-phospholipid syndrome Diabetes Chronic hypertension
  • 12. Risk factors of Pre-eclampsia MODERATE RISK FACTORS First pregnancy Assisted reproduction Age 40 years or more Pregnancy interval of more than 10 years BMI of 35 kg per metre square or more Family history of pre-eclampsia Multiple pregnancies Vitamin d deficiency Low dietary calcium
  • 13. PREVENTIVE MEASURES Aspirin 75 mg daily from 12 weeks of gestation till delivery for patients with 1 high risk factor or >1 moderate risk factors Calcium supplementation >1 g daily during pregnancy may reduce chances in low dietary calcium supplementation Adequate rest in 3rd trimester Reduction of workload and stress Controlled weight loss Exercise
  • 14. PATHOLOGICAL ALTERATIONS 1. Cardiovascularchanges : Increase in cardiac afterload due to hypertension. 2. Haematological changes: Thrombocytopenia (platelet count less than 1,00,000/mm3), microangiopathichemolysis(due to intense vasospasm),decreased clottingfactors,increasederythrocytedestruction,increasedfibrin degradation products and deficiency of antithrombin III. 3. Endocrine changes: Increase in deoxycorticosteronein third trimesterdue to conversionfrom plasma progesterone causes retention of sodium. 4. Fluid and electrolyte changes: Decreased plasma oncotic pressure which leads to increased extracellular fluid with associated decrease in intravascular volume. 5. Kidney: Oliguria is a result of reduced renal perfusion and glomerularfiltration. Plasma uric acid and serum creatinineare elevated.There is proteinuria> 300 mg per 24 hours or more than 1 + on urinary dipstick test. Acute renal failure and renalcorticalnecrosis may develop in severe cases
  • 15. PATHOLOGICAL ALTERATIONS 6. Liver: Increased liver enzymes. Epigastric and right hypochondriac pain due to periportal haemorrhagic necrosis, which causeshepatic rupture or subcapsular hematoma. 7. HELLP syndrome: Triad of Haemolysis, elevated liver enzymes and low platelets. 8. Nervous system: Cerebral oedema, hyperaemia, focal thrombosis and haemorrhage , visual disturbances due to retinal artery vasospasm. Increased cerebral perfusion pressure may cause severe headaches. 9. Uterus and placenta: Incompletetrophoblastic invasion of spiral arteries causes reduction in diameter of vessels as compared to normal. In addition, vasospasm decreases placental perfusion leading to Intra Uterine Growth Retardation
  • 16. MATERNAL COMPLICATIONS Intracranial haemorrhage : leading cause of maternal death DIC Pulmonary oedema Congestive heart failure Placental abruption Acute renal failure Liver rupture Cerebrovascular accident Septic shock
  • 17. NEONATAL COMPLICATIONS SHORT TERM COMPLICATION OLIGOHYDRAMNIOS FETAL GROWTH RETARDATION PRETERM BIRTH PREMATURITY WITH RESPIRATORY DISTRESS LOW APGAR SCORE NICU STAY & SMALL FORGE MECONIUM ASPIRATION INTRACRANIAL HEMORRHAGE INTRA UTERINE FETAL DEATH
  • 18. NEONATAL COMPLICATIONS LONG TERM COMPLICATIONS CEREBRAL PALSY LOW IQ HEARING LOSS VISUAL IMPAIRMENT INSULIN RESISTANCE DIABETES MELLITUS HYPERTENSION CAD
  • 19. MANAGEMENT OF PRE-ECLAMPSIA MEDICAL MANAGEMENT Early prenatal detection and prompt institution of therapy and corrective measures. The timingof prenatal examinations :4 weeks until 28 weeks then every 2 weeks until 36 weeks and weekly thereafter. Hospitalization is considered for women with new-onset hypertension, which is persistent or worsening or development of proteinuria. Detailed systemic examination Daily scrutiny of headache,visual disturbance,epigastricpain and rapidweight gain. Weighton admissionand every day thereafter.
  • 20. MANAGEMENT OF PRE-ECLAMPSIA Weight on admission and every day thereafter. Analysis for proteinuria on admission and at least every 2 days thereafter. Four hourly blood pressures monitoring in sitting position. Measurement of serum creatinine, complete blood count (CBC), liver enzymes, plateletsfrequency determined by the severity of hypertension. Frequent foetal monitoring clinically or by USG. Ample but not excessive proteins and calories; and no salt or fluid restriction in the diet
  • 21. MANAGEMENT OF PRE-ECLAMPSIA ACE inhibitors, ARBs and chlorothiazideshave to stop these drugs and change over to other drugs before they become pregnant as these drugs can cause congenitalmalformations. Blood pressure shouldbe controlledto below 160/110 mm Hg to prevent maternalmorbidity, particularly from intracranial haemorrhage, encephalopathy, myocardial ischemia and failure. Oral antihypertensiveinclude the following drugs: Beta blockers: Labetalol (300 mg to 2400 mg/day). combined留 and 硫 blocker.50 mg over 1 minute f/b 20 mg/hr which can be increased by 20 mg every 20 min to a maximumdose of 160 mg per hour. Methyldopa : It is 留 methylanalogue of dopa, the precursor of dopamine (DA) and NA. The 留 methyl-NAis a selective留2 agonist formed in brain from methyldopaand acts oncentral 留2 receptors to decrease efferent sympathetic activity.Antihypertensive effect develops over 46 hours and lasts 1224 hours. Dose: 0.250.5 g BDQID oral (max 4 g/day).
  • 22. MANAGEMENT OF PRE-ECLAMPSIA Nifedipine : Calcium channel blocker, it decreases peripheral vascular resistance without compromisingcardiac output. Dose is 10 to 20 mg every 4 to 6 hourly. Hydralazine : 5-10 mg slow iv injection or 200-300 mcg/min then 50-150 mcg/min for maintainence control. Caution : acute porphyria, cor-pulmonale, idiopathic SLE, severe tachycardia. Patient may need Fluid bolus along with titration of antihypertensives. SODIUM NITROPRUSIDE : use in refractory cases. Alternative anti HTN agents : oral clonidine, GTN infusion The target of blood pressure control in uncomplicated chronic hypertension is to keep blood pressure less than 150/100 mm Hg. Do not lower diastolicblood pressure below 80 mm Hg. In pregnant women with target-organdamage secondary to chronic hypertension; aim is to keep blood pressure lower than 140/90 mm Hg.
  • 23. CONDITIONS MANDATE FOR IMMEDIATE DELIVERY Severe hypertension that persists after 24 to 48 hours of treatment Progressive thrombocytopenia Liver dysfunction Progressive renal dysfunction Premonitory signs of eclampsia Evidence of foetal jeopardy Persistent headache or other neurologic sequelae of pre- eclampsis
  • 24. Definitive treatment for pre-eclampsia and eclampsia is termination of pregnancy. In uncomplicated pre-eclampsia, if women is near term, pregnancy is allowed to continue under the close observation until the cervix is more suitable for induction. In severe pre-eclampsia, before 34 weeks of gestation glucocorticoids may be tried for lung maturity : betamethasone 12 mg IM 24 HOURS apart in women between 24 and 34 weeks.
  • 25. SIGNS OF IMPENDING ECLAMPSIA Headache Visual disturbance, such as blurring or flashing before the eyes Epigastric pain Oliguria Vomiting Sudden swelling of the face, hands or feet
  • 26. Measures taken to prevent seizures Collaborative Eclampsia trial regimen for administration of MgSO4 :- ZUSPAN REGIMEN :- LOADING DOSE : 4-5 gm IV over 5 minutes followed by MAINTAINANCE DOSE : an infusion of 1 gm/hr maintained for 24 hours. If the woman had an eclamptic seizure, the infusion should be continued foe 24 hours after the last seizure and should not be discontinued during delivery. For recurrent seizures, further 2-4 gm MgSO4 given over 5 minutes. Measure serum Mg levels 4-6 hourly & maintain in between 4-7 meq per litre.
  • 27. PRITCHARD REGIMEN :- Loading dose : 4 gm of 20 % MgSO4 slow IV followed by 5 gm of 50 % IM in each buttock , total dose : 14 gm. Maintainance dose : 5 gm 50 % IM in alternate buttock 4 hourly. SIBAI REGIMEN :- LOADING DOSE : 6 gm MgSO4 IV over 20 minutes MAINTAINANCE DOSE: 2 gm/hour IV infusion
  • 28. Monitoring & Management of MgSO4 Toxicity In therapeutic doses magnesium sulphate is associated with muscle weakness due to decrease in the amount of acetylcholine released at motor nerve endings, decreased action of acetylcholine on the motor end plate and reduction of excitability of motor fibre membrane. Therefore, it increases the sensitivity of the mother to both the depolarizing as well as non-depolarizing muscle relaxants. When a patient is started on MgSO4 it is necessary to monitor: Patellar reflex (disappears when plasma magnesium level reaches 10 mEq/L; warning impending Mg toxicity) Rate and depth of respiration (depressed at level above 10 mEq/L, respiratory paralysis and arrest occurs above 12 mEq/L)
  • 29. Monitoring & Management of MgSO4 Toxicity Urine output (Mg is cleared totally by renal excretion, when there is renal insufficiency, plasma magnesium level needs to be checked 4-6 hourly and dosage adjusted accordingly). Uterine effects: In high concentration MgSO4 depresses myometrial contractility secondary to inhibition of intracellular free Ca++ concentration in the uterine cell (seen at serum Mg level of 810 mEq/L). Neonatal effects: Magnesium crosses the placenta to achieve equilibrium in foetal serum. Magnesium sulphate is associated with a minimal risk of intracranial bleed and irregular bone deposits. It can cause a transient reversible change in foetal heart rate and should not be considered as a sign of foetal distress. The neonate may be depressed only if there is severe hypermagnesemia at delivery.
  • 30. Treatment Withhold MgSO4 Administer Calcium gluconate, 1 g intravenously. For severe respiratory depression and arrest, prompt tracheal intubation and mechanical ventilation is life-saving
  • 31. Management of a patient with eclampsia on MgSO4 with foetal distress who is posted for emergency LSCS Aspiration prophylaxis :- Pre-induction administration of nonparticulate antacid such as 0.3 M sodium citrate, 30 mL. Intravenous administration of histamine receptor blocking agent 40 minutes before induction. Eg Ranitidine 100 mg Administration of metoclopramide 4 mg to decrease gastric volume 3060 minutes before induction. Pre-oxygenation and denitrogenation with 100% oxygen over 3 minutes is preferred technique; however, if not feasible; patient can be advised to take 8 vital capacity breaths of 100% oxygen in one minute. If blood pressure is high, rapid control of blood pressure can be achieved by: Hydralazine (5 mg IV aliquots up to a maximum of 20 mg) Labetalol (510 mg IV every 10 min) Oral nifedipine (sublingual nifedipine can cause rapid changes in placental circulation which may compromise foetal condition) In resistant cases of Hypertension, sodium nitroprusside and glyceryl trinitrate can be used with continuous arterial BP monitoring.
  • 32. Management of a patient with eclampsia on MgSO4 with foetal distress who is posted for emergency LSCS Crystalloid fluid bolus of 500 ml to prevent sudden hypotension CVP is indicated in patient with persistent oliguria and presence of pulmonary oedema for fluid management in antepartum and postpartum period Anticipate difficult airway and keep small size tubes, gum elastic bougie, laryngeal mask airway and difficult airway set ready plan for attenuation of response to laryngoscopy Crash induction with thiopentone sodium or propofol and succinylcholine after checking the ability to ventilate if BP is high Use atracurium for maintenance of relaxation it is preferable to use a peripheral nerve stimulator in intraoperative period. Use 2/3rd of the Mac value of inhalational agent to ensure adequate depth of anaesthesia Watch for hemodynamic changes during delivery and removal of placenta. continue magnesium sulphate during intraoperative and post operative.
  • 33. HELLP SYNDROME HELLP syndrome is a severe form of pre-eclampsia characterizedby: H-Hemolysis (abnormalperipheralblood smear, and an increasedbilirubinlevel of 1.2 mg/dL or greater) EL - elevated liverenzymes (SGOT > 70 U/L, LDH > 600U/L) LP - low platelets (< 1, 00,000/mm It can occur antepartum or postpartum. Delivery represents the only definitive treatment of HELLP syndrome. Patient with HELLP syndrome have a high incidenceof seriousmaternal complicationsincluding disseminatedintravascular coagulation, placentalabruption,need for bloodtransfusion, pleural effusion, acute renal failure, and wound infection. After deliveryof placenta,recovery from HELLP syndrome can be expected to start within 2448 hours. These patients shouldbe monitored in the ICU or HDU. Steroids have no role in management of HELLP syndrome
  • 34. NEED FOR PLATELET TRANSFUSION IN HELLP SYNDROME For a platelet count of 20K to 49K per mm3 with hemolysis, elevated liver enzymes and low platelet syndrome, platelet transfusion is recommended before LSCS. For a platelet count of 20K to 49K per mm3 with hemolysis, elevated liver enzymes and low platelet syndrome, platelet transfusion should be considered prior to vaginal delivery if there is : 1. Excessive active bleeding 2. Known platelet dysfunction 3. Rapidly falling platelet count 4. coagulopathy