PREGNANCY-INDUCED HYPERTENSION

BY

MUHAMMAD OMER AJMAL

INTRODUCTION

bull Hypertensive disorders of pregnancy are responsible for significant maternal and perinatal morbidity and are the second leading cause after embolism of maternal mortality

bull Hypertensive disorders of pregnancy complicate approximately 12 to22 of all pregnancies and are directly responsible for 176 of maternal deaths in the united states (high risk pregnancy 3rd edi)

DEFINITIONSbull Hypertension ndash sustained systolic BP gt 140mmHg or diastolic BPgt

90mmHg

bull Chronic Hypertension ndash hypertension which predates pregnancy or is diagnosed before 20wks gestation

bull PIH ndash hypertension diagnosed after 20 weeks gestation in a patient without a history of chronic hypertension and is defined as a systolic BP greater than 140mmHg or diastolic BP greater than 90mmHg OR alternatively as a consistent uarrin systolic or diastolic BP by 30mmHg and 15mmHg respectively above the Pts normal base line

bull Pre-eclampsia ndash PIH in association with renal involvement causing proteinuria (gt300mg24h or 2+ on dipstick

Preeclampsia

bull A Mild

bull B severe (HELLP SYNDROME)bull Multiorgan disease characterized by development of hypertension

with Proteinuria after the 20th week of gestationbull Disorder of unknown etiology with most cases occurring in the first

pregnancybull Proteinuria is defined as 300 mg or more of protein in a 24- hour

urine collectionbull Edema may manifest as a recent rapid weight gain

bull

bull Severe Pre-eclampsia ndash pre-eclampsia in association with any ofndash Sustained BP gt 160110ndash Proteinuria gt5g24hrs or 3+ on dipstickndash Urine output lt400ml24hrsndash Pulmonary oedema or evidence of pulmonary

compromisendash Epigastric or RUQ painndash Hepatic rupturendash Platelet count lt100 x 109Lndash Evidence of cerebral and visual complicationsndash Intrauterine growth delay (oligohydramnios)

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

INTRODUCTION

bull Hypertensive disorders of pregnancy are responsible for significant maternal and perinatal morbidity and are the second leading cause after embolism of maternal mortality

bull Hypertensive disorders of pregnancy complicate approximately 12 to22 of all pregnancies and are directly responsible for 176 of maternal deaths in the united states (high risk pregnancy 3rd edi)

DEFINITIONSbull Hypertension ndash sustained systolic BP gt 140mmHg or diastolic BPgt

90mmHg

bull Chronic Hypertension ndash hypertension which predates pregnancy or is diagnosed before 20wks gestation

bull PIH ndash hypertension diagnosed after 20 weeks gestation in a patient without a history of chronic hypertension and is defined as a systolic BP greater than 140mmHg or diastolic BP greater than 90mmHg OR alternatively as a consistent uarrin systolic or diastolic BP by 30mmHg and 15mmHg respectively above the Pts normal base line

bull Pre-eclampsia ndash PIH in association with renal involvement causing proteinuria (gt300mg24h or 2+ on dipstick

Preeclampsia

bull A Mild

bull B severe (HELLP SYNDROME)bull Multiorgan disease characterized by development of hypertension

with Proteinuria after the 20th week of gestationbull Disorder of unknown etiology with most cases occurring in the first

pregnancybull Proteinuria is defined as 300 mg or more of protein in a 24- hour

urine collectionbull Edema may manifest as a recent rapid weight gain

bull

bull Severe Pre-eclampsia ndash pre-eclampsia in association with any ofndash Sustained BP gt 160110ndash Proteinuria gt5g24hrs or 3+ on dipstickndash Urine output lt400ml24hrsndash Pulmonary oedema or evidence of pulmonary

compromisendash Epigastric or RUQ painndash Hepatic rupturendash Platelet count lt100 x 109Lndash Evidence of cerebral and visual complicationsndash Intrauterine growth delay (oligohydramnios)

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

DEFINITIONSbull Hypertension ndash sustained systolic BP gt 140mmHg or diastolic BPgt

90mmHg

bull Chronic Hypertension ndash hypertension which predates pregnancy or is diagnosed before 20wks gestation

bull PIH ndash hypertension diagnosed after 20 weeks gestation in a patient without a history of chronic hypertension and is defined as a systolic BP greater than 140mmHg or diastolic BP greater than 90mmHg OR alternatively as a consistent uarrin systolic or diastolic BP by 30mmHg and 15mmHg respectively above the Pts normal base line

bull Pre-eclampsia ndash PIH in association with renal involvement causing proteinuria (gt300mg24h or 2+ on dipstick

Preeclampsia

bull A Mild

bull B severe (HELLP SYNDROME)bull Multiorgan disease characterized by development of hypertension

with Proteinuria after the 20th week of gestationbull Disorder of unknown etiology with most cases occurring in the first

pregnancybull Proteinuria is defined as 300 mg or more of protein in a 24- hour

urine collectionbull Edema may manifest as a recent rapid weight gain

bull

bull Severe Pre-eclampsia ndash pre-eclampsia in association with any ofndash Sustained BP gt 160110ndash Proteinuria gt5g24hrs or 3+ on dipstickndash Urine output lt400ml24hrsndash Pulmonary oedema or evidence of pulmonary

compromisendash Epigastric or RUQ painndash Hepatic rupturendash Platelet count lt100 x 109Lndash Evidence of cerebral and visual complicationsndash Intrauterine growth delay (oligohydramnios)

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Preeclampsia

bull A Mild

bull B severe (HELLP SYNDROME)bull Multiorgan disease characterized by development of hypertension

with Proteinuria after the 20th week of gestationbull Disorder of unknown etiology with most cases occurring in the first

pregnancybull Proteinuria is defined as 300 mg or more of protein in a 24- hour

urine collectionbull Edema may manifest as a recent rapid weight gain

bull

bull Severe Pre-eclampsia ndash pre-eclampsia in association with any ofndash Sustained BP gt 160110ndash Proteinuria gt5g24hrs or 3+ on dipstickndash Urine output lt400ml24hrsndash Pulmonary oedema or evidence of pulmonary

compromisendash Epigastric or RUQ painndash Hepatic rupturendash Platelet count lt100 x 109Lndash Evidence of cerebral and visual complicationsndash Intrauterine growth delay (oligohydramnios)

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Severe Pre-eclampsia ndash pre-eclampsia in association with any ofndash Sustained BP gt 160110ndash Proteinuria gt5g24hrs or 3+ on dipstickndash Urine output lt400ml24hrsndash Pulmonary oedema or evidence of pulmonary

compromisendash Epigastric or RUQ painndash Hepatic rupturendash Platelet count lt100 x 109Lndash Evidence of cerebral and visual complicationsndash Intrauterine growth delay (oligohydramnios)

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

What is HELLP syndrome

bull HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy) It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy It usually develops before delivery but may occur postpartum (after delivery) as well HELLP syndrome consists of the following problems

bull hemolysis - red blood cells break downbull elevated liver enzymes - damage to liver cells cause

changes in liver function lab testsbull low platelets - cells found in the blood that are needed to

help the blood to clot in order to control bleeding

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

What causes HELLP syndrome

bull The cause of HELLP syndrome is unknown Some conditions may increase the risk of developing HELLP syndrome including the following

bull preeclampsia during pregnancy

bull previous pregnancy with HELLP syndrome

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

What Is Eclampsia

bull Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated

bull In addition to the previously mentioned signs of preeclampsia women with eclampsia often have seizures

bull Eclampsia can cause coma and even death of the mother and baby and can occur before during or after childbirth

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Predisposing factors for PE Syndrome

ndash First pregnancy ndash New partnerpaternity ndash Age younger than 18 years or older than 35 years ndash History of preeclampsia ndash Family history of preeclampsia in a first-degree

relative ndash Black race ndash Obesity (BMI sup3 35) ndash Interpregnancy interval less than 2 years or more

than 10 years

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

ndash Chronic hypertension especially secondary causes of chronic hypertension such as hypercortisolism hyperaldosteronism pheochromocytoma or renal artery stenosis

ndash Preexisting diabetes (type 1 or type 2) especially with microvascular disease

ndash Renal disease ndash Systemic lupus erythematosusndash Protein S deficiencyndash Activated protein C resistance ndash Obesity ndash Thrombophilia

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Placentalfetal risk factors for preeclampsia ndash Multiple gestations ndash Hydrops fetalis ndash Gestational trophoblastic disease ndash Triploidy

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Aetiology

bull Unknown

bull Theoriesndash Toxaemiandash Immunological and genetic factorsndash Reduced levels of nitric oxidendash Imbalance of thromboxane and prostacyclin ndash

favours vasoconstriction

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Aetiology

1048766 Pre-eclampsia is mainly a disease of primigravidabull

bull Thus it seems that exposure to past pregnancy or paternalfetal antigens has a protective effect

bull Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells rarr immunosuppression of fetoplacental unit

bull Failure of immunosuppression results in placental damage with release of trophoblasts andor immune complexes to initiate a number of cascades

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

pathogenesis

bull Immunological Factorsbull Immunological disorders may arise from an abnormal maternal-fetal

antigen- antibody response or from the contents of seminal fluidsbull Spermatozoa may cause antibody formation or prostaglandins may

initiate uterine vasoconstriction

bull Genetic Factorsbull Familial tendency towards preeclampsia exists in some populationbull It may result from a recessive genetic inheritance

bull Endothelial factorsbull Vascular endothelial damage or dysfunction is the common

pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia

bull Endothelial dysfunction lead to hyper reactivitybull Pts with PIH have elevated levels of thromboxane A2 and decrease

prostacycline (PGI2) productionbull TXA2 is a potent vasoconstrictor and promote platelet aggregationbull PGI2 is a potent vasodilator and inhibitor of platelet aggregationbull Endothelial dysfunction may reduce production of nitric oxide and

increase production of endothelin-1 that is also a potent vasoconstrictor and activator of platelets

bull Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role

bull Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Symptomatology

bull Increasing oedema particularly tibial pitting oedema lumbosacral and facial

bull ndash A rise in Blood pressure is insidious and thus asymptomatic

bull ndash Possible symptoms of frontal headache blurring of vision epigastric painrarr impending Eclampsia

bull ndash Signs of cerebral irritation Brisk reflexes clonusbull ndash Placental insufficiency 1048766 Manning score Doppler

studiesIUGR

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

investigations

bull ndash Hypertensionbull MILD- diastolic gt= 90 mmHgbull MODERATE- 95-110 mmHgbull SEVERE- gt110 mmHg

bull ndash Albuminuriabull Significant gt=30 gl

bull ndash Renal function tests deterioratingbull Urea creatinine uric acid decreasing urine output

bull ndash Liver function testsbull Deteriorating enzymes

bull ndash Haematologicalbull Falling platelet count

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Rollover testbull A positive rollover test result is defined as an increase in diastolic

BP of 20mmHg or more when measured 5 minutes after a gravida is ldquorolledrdquo from the lateral to the supine position bw 28-32 weeks gestation

bull 93 of primigravid women with a positive rollover test result later had gestational hypertension and 91 of women who had a negative test result did not have hypertension during that pregnancy

bull However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Angiotensin Testbull A normal pregnant Pt requires mean Angiotensin II doses of 135 to

149 ng kgminute to increase diastolic BP by 20 mmHgbull 91 of women who requires more than 8ng kgmin to achieve this

BP elevation remained normotensive through out pregnancybull Conversely normotensive primigravidae who later had gestational

hypertension responded at doses of less than 8ng kgmin as early as 28-32 weeks gestation

bull 90 of these pts later had overt gestational hypertension

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Complications

bull MATERNALbull Neurologicalbull Headachebull Visual disturbancesbull Hyperexcitabilitybull Seizuresbull Intracranial hemorrhagebull Cerebral edema

bull Pulmonarybull Upper airway edemabull Pulmonary edema

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Cardiovascularbull darr intravascular volumebull uarr arteriolar resistancebull Hypertensionbull Heart failure

bull Hepaticbull Impaired functionbull Elevated enzymesbull Hematomabull rupture

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Renalbull Proteinuriabull Sodium retentionbull Decreased GFRbull Renal failure

bull Hematologicalbull Coagulopathy

ndash Thrombocytopenia

ndash Platelet dysfunction

ndash Prolonged PPT

Microangiopathic hemolysis

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull FETALbull Placental insufficiency rarr1048766 IUGR rarr1048766 Intrauterine

deathbull Premature delivery [iatrogenic] rarr1048766 Neonatal death

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Management

bull Domain of obstetriciansbull Bed restbull Sedationbull Improve intravascular volume bull Control hypertension ndash prevent maternal morbidity

ndash B-blockers in third trimester (labetolol preferred) ndash prolonged use may decrease fetal growth(10-20 mg iv)

ndash Hydralazine ndash for acute reduction(5-10 mg iv increments)

ndash Methyldopa ndash safe in pregnancy(250-500mg) orally

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

ndash Nifedipine(10 mg) orally or sublingually ( tocolytic action)ndash Avoid ACE inhibitors ndash associated with oligohydramnios still

birth neonatal renal failurendash Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered

spray) ndash Nitroprusside( cyanide toxicity more likely if infusion rate exceed

4 ugkgmin over several hours to days) ndash Diuretics - NO PLACE [unless heart failure] SINCE

PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIAndash Invasive arterial central venous and pulmonary artery catheter is

indicated in pts with severe hypertension pulmonary edema persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Treat seizures ndash magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour)Also used to control BP

bull Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy

bull Therapeutic range for serum MgSo4 concentration is bw 4-6 mEqL

bull Urine output respiratory rate patellar reflexes are monitored during magnesium therapy

bull It also crosses placenta so may decreases fetal HR and beat-to-beat variability Neonatal depression can also occur

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Severe pre-eclampsia eclampsiandash ABCrsquosndash Appropriate fetal and maternal monitoring etc

bull Term delivery ideal ndash risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery

bull Aim to stabilise symptoms long enough to mature fetal lungs

In established pre-eclampsia the only definitive treatment is the delivery of the placenta

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

MgSo4 Toxicity

bull If MgSo4 toxicity is suspected MgSo4 infusion should be immediately discontinued

bull IV calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4

bull If respiratory distress occur the Pt may require ETT and mechanical ventilation

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Anaesthetic Implications

bull Pain management during labour

bull Regional anaesthesia for surgical delivery

bull GA for surgical delivery

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Initial laboratory studies should be evaluatedbull Critically ill pts require stabilization before

inductionbull Hypertension should be controlledbull Hypovolemia should be correctedbull A platelet count and coagulation profile should

be checked prior to regional anaesthesia in pts with severe PIH

bull CVP line may be used to guide fluid therapybull Intra arterial BP monitoring is indicated with

severe hypertension

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

bull Epiduralndash Traditionally considered anaesthetic of choicendash Controls excessive surges in BPndash Decreases circulating stress-induced catecholamines

and uterine vascular resistancendash Check platelet countndash Beware of fluid preloading prior to insertion in patients

with pulmonary oedemandash Monitor BP and fetus carefully and treat BP promptly

with ephedrinendash Avoids the increased risk of a failed intubation due to

severe edema of upper airways

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Anaesthetic Implications - Spinal

bull Spinal Anaesthesiandash Evidence based studies limitedndash Use controversial ndash risk of profound maternal

hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS

ndash Theoretical advantage of epidural weighed against known benefits of spinal ie greater reliability less procedural time less epidural vascular trauma

ndash Check platelets reduce preload volume ephidrine etc

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Anaesthetic Implications - GA

bull General Anaesthesiandash Only if regional anaesthesia cotraindicated or

precluded by urgency of need for deliveryndash Endotracheal intubation more difficult in pregnant

population plus oedema of upper airway therefore prepare for difficult intubation

ndash Aspiration prophylaxisndash Preoxygenation with 100 oxygenndash Exaggerated hypertensive response to laryngoscopy

ndash significant morbidity( Labetalol 5-10 mg)ndash RSI

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

ndash Use a small ETT(60 or 65mm) because of airway edema

ndash Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia

ndash If magnesium used ndash expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used)

ndash Normal dose of suxamethonium titrate non-depolarising muscle relaxants

ndash Avoid NSAIDs for post-op analgesia

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Postoperative Management

bull Provide adequate analgesia

bull Maintain strict intake output for at least 24 hours postpartum or until diuresis develops

bull Continue MgSo4 for at least 24 hours postpartum or until evidence of diuresis

bull Maintain hemodynamic control with anti hypertensives if necessary

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message

Take Home Message

bull Usually multi systemic involvementbull Risk of significant obstetric and anaesthetic

complicationsbull Anaesthetic risks reduced by

ndash Early communication and preparationndash Early placement of epidural catheterndash Utilising spinal for urgent C-section if no epidural in

placendash GA only when regional anaesthesia contraindicatedndash Anticipate difficult airwayndash Emphasis on preoperative baseline BP reduction and

blunting hypertensive response to laryngoscopy

• PREGNANCY-INDUCED HYPERTENSION
• INTRODUCTION
• DEFINITIONS
• Slide 4
• Preeclampsia
• Slide 6
• What is HELLP syndrome
• What causes HELLP syndrome
• What Is Eclampsia
• Predisposing factors for PE Syndrome
• Slide 11
• Slide 12
• Aetiology
• Slide 14
• pathogenesis
• Slide 16
• Slide 17
• Symptomatology
• investigations
• Slide 20
• Slide 21
• Complications
• Slide 23
• Slide 24
• Slide 25
• Management
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• MgSo4 Toxicity
• Slide 33
• Anaesthetic Implications
• Slide 35
• Slide 36
• Anaesthetic Implications - Spinal
• Anaesthetic Implications - GA
• Slide 39
• Postoperative Management
• Take Home Message