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pregnancy induced hypertension ppt uploaded on 2-3-12
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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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Recommended