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Speaker : Dr omar kamal
 Name: Mrs. Nagalakshmi B D
 Age: 33 yrs
 W/O: Mr. Harish
 IP No.: 98870
 Place : bangalore
 Occupation : Housewife
 Date of Admission :18/10/13
 Date of surgery 18/10/13
Chief complaints :
 h/o 8 months of amenorrhoea
 h/o Swelling of B/l lower limbs since 15 days
 HOPI :
Patient with 8 months of amenorrhea appreciating fetal
movements well, was apparently normal 15 days back, when
she started noticing swelling of both lower limbs, aggravated
by work , no diurnal or postural variation, present through
out day
No H/o headache, blurring of vision, epigastric pain,
bowel/bladder disturbances, fever, rashes, bleeding
 Obstetric History: ML: 12 years NCM G2P1L1
 1st Pregnancy: in 2006 , FTVD of live male baby of
weight 2.5kg at Bangalore hospital. No antenatal/
Intrapartum/Postpartum complications . Breast fed for
6 months . H/o using male barrier contraception .
 2nd pregnancy: Present pregnancy, spontaneous
conception
 1st Trimester : Pregnancy diagnosed by UPT ; +ve after
5 week of LMP. Started on Folic acid supplementation .
Blood investigations and scan done on 17/4/13
showed SLIUG . No H/o fever, rashes, excessive
vomiting, pain abdomen, bleeding/spotting PV.
 2nd trimester: Quickening felt at 4th month of
gestation. Continued folic acid. Started on
Iron/Calcium supplementation. Immunised with 2
doses of Inj.T.T. Scan on 14/6/13 showing SLIUG of
18+2 weeks at 18+2 weeks by LMP, fetal doppler
normal.
 3rd trimester: Appreciates fetal movements well,
continued iron/calcium/ folic acid. Patient had
increased readings of BP since 30 weeks .Tab.
Methyldopa 250 mg BD started.
 now referred to hospital with above complaints for
further management
 Menstrual History: PMC: 3-4/ 24-25 days, regular,
normal flow, no clots
 LMP- 8/2/13 EDD- 15/11/13
POG- 36 wks
 Past History : No H/o Diabetes/hypertension/
Tuberculosis/ epilepsy/ Thyroid disorders.
 Family History: No H/o Diabetes/ Tuberculosis/
epilepsy/ Thyroid disorders.
O/E
Moderately built and nourished. conscious and
cooperative
Vitals :
PR 88/min and regular
BP 150/90 mmHg measured in sitting position
Afebrile
B/l pedal edema
No pallor ,icterus cyanosis ,clubbing or
lymphadenopathy
Facies No abnormality
Upper incisors no loose or protruding teeth
Nose both nares patent no nasal airflow obstruction
Mallampati Class 2
Thyromental distance >3fingers
Mouth opening adequate
Movement at atlanto occipetal joint normal
No obvious external pathology
RS : B/L air entry equal NVBS
CVS : S1S2 heard, no murmur
P/A-Uterus 32-34 size, relaxed, cephalic lower pole ,
non tense, non tender , FHS+ 148 bpm regular
PROVISIONAL DIAGNOSIS
33 yrs female, G2P1L1 with 36 wks of gestation with
SLIUG, with mild pre eclampsia
 In 2000, National High Blood Pressure Education Program
classified hypertensive disorders complicating pregnancy
as:
Gestational hypertension
Preclampsia- eclampsia
chronic hypertension
chronic hypertension with superimposed preeclampsia
 Blood Pressure ≥ 140/90 on two or more occasions
- in a previously normotensive
patient
- after 20 weeks gestation
- without proteinuria
- returning to normal 12 weeks
after delivery
 Almost half of these develop preeclampsia
syndrome
 Blood Pressure ≥ 140/90 before 20 weeks of
gestation
Or
 Persistence of hypertension beyond 12 weeks after
delivery
 New-onset proteinuria ≥ 300 mg/24 hours in
chronc hypertensive women but no proteinuria
before 20 weeks gestation
 A sudden increase in proteinuria or blood pressure
or platelet count <1 lakh/mm3 in women with
hypertension and proteinuria before 20 weeks’
gestation
 New onset of hypertension & proteinuria in a previously
normotensive woman
 after 20 weeks of gestation
 Returning to normal after 12 weeks of delivery.
 Edema not a part of diagnosis now.
Eclampsia :
 New onset of seizures or unexplained coma during
pregnancy or postpartum period in patients with pre-
existing preeclampsia and without pre-existing
neurological disorder
 The NHBPEP has recommended that clinicians
consider the diagnosis of preeclampsia in the absence
of proteinuria when any of the following findings are
present:
1) Persistent epigastric or right upper quadrant pain,
2) Persistent cerebral symptoms,
3) Fetal growth restriction,
4) Thrombocytopenia,
5) Elevated serum liver enzyme concentrations
• Preconception
- Partner related
 Nulliparity
 limited exposure to paternal sperms
 Partner who fathered a preeclamptic pregnancy in
another women
-Non partner related
 History of Preeclampsia in previous pregnancy
 Advanced maternal age
 Family history of Preeclampsia
 History of placental abruptio, IUGR, fetal death
-Maternal disease related
 Obesity, BMI>35 doubles the risk
 Hypertension
 Diabetes
 Thrombotic vascular diseases
-Behaviour-
 Smoking :
-Pregnancy associated-
 Multiple gestation
 Molar pregnancy
 Exact mechanism unknown, disease of theories.
1. ABNORMAL PLACENTATION
 Stage1: failure of trophoblastic invasion into
myometrium
Penetrates only decidua
superficial placentation  ↓placental
perfusion
 stage2 : endothelial damage
systemic manifestations of Preeclampsia
 Family history of pre eclampsia: genetic origin
 Mutations in Complement Regulatory Protein gene
 Genes assoc.:
 MTHFR, F5 leiden, AGT, HLA, NOS3, F2(prothrombin), ACE
 Exposure to sperms of different partner
 long term exposure to paternal antigen in
sperms of same partner- protective
 activated auto antibodies to angiotensin
receptor-1 AA-AT1activate AT1
receptorsincreased sensitivity to angiotensins
 hypertension
 ↑ plasma Homocystiene
 ↑ serum sFlt1(soluble fms-like tyosine kinase)
 ↓serum and urinary Platelet Growth Factor
 ↓ Vascular Endothelial Growth Factor
1. Respiratory
 Airway is edematous;
 ↓ internal diameter of trachea due to capillary
engorgement
 Pharyngolaryngeal edema visualization difficult
 Subglottic edema – airway obstruction
 CNS manifestations include:
headache,
visual disturbances,
hyperexcitability, hyperreflexia,
coma, seizures
Cause: cerebral edema and hypoperfusion
 Vasospasm and exaggerated responses to
catecholamines
 Characteristically, blood pressure and SVR are
elevated
 Severe preeclampsia is usually a hyperdynamic
state
 Pulmonary edema is a severe complication – 3 %
 Plasma colloid osmotic pressure is diminished and
increased vascular permiability influences PE

T3 POST PARTUM
NORMAL 22 17
PRE ECLAMPSIA 18 14
 Hemoconcentration
 Thombocytopaenia  most common
 Platelet count correlates with disease severity and
incidence of abruptio placentae
 DIC due to activation of coagulation
cascadeoverconsumption of coagulants and
platelets spontaneous haemorrhage
 HELLP syndrome
 Periportal haemorrhage
 subcapsular bleeding
 hepatic rupture: 32% maternal mortality
Decreased GFR 34 % than normal
- oliguria
- renal failure
- uric acid, creatinine is elevated
Glomerulopathy
- proteinuria
 The characteristic renal histologic lesion is
glomerular capillary endotheliosis
 Uteroplacental insufficiency
 Fetal complications:
- hypoxia
-IUGR
-Prematurity
-IUD
-Placental abruptio
No screening test is really helpful
Various screening methods are:
 Diastolic notch at 24weeks by doppler ultrasonography
 Absence or reversal of end diastolic flow
 Average mean arterial pressure ≥ 90 mmHg in second
trimester
 Angiotensin infusion test: angiotensin infusion required to
raise the blood pressure >20 mm Hg from baseline
 Roll over test: rise in blood pressure >20 mmHg from
baseline on turning supine at 28-32 weeks gestation is
positive.
 Regular Antenatal checkup:
rapid gain in weight
rising blood pressure
edema
proteinuria/deranged liver or renal profile
 Low dose Aspirin in High risk group: ↑PGs and↓TXA2
 Calcium supplementation: no effects unless women
are calcium deficient
 Antioxidants- Vitamin C and E
 Nutritional supplementation: zinc, magnesium, fish
oil, low salt diet
Maternal
 Gestational age 38 weeks*
 Platelet count <100,000/mm3
 Progressive deterioration in hepatic function
 Progressive deterioration in renal function
 Suspected placental abruption
 Persistent severe headaches or visual changes
 Persistent severe epigastric pain, nausea, or
 vomiting
Fetal
 Severe intrauterine growth restriction
 Nonreassuring fetal status
 Oligohydramnios
Obstetric Management
. Maternal evaluation :
Hemoglobin and hematocrit
platelet count : decreased, if < 1 lakh
coagulation profile
LFTs : indicated in all patients
KFTs : raised (S.urea creatinine is
decresaed in Normal pregnancy)
Urine Routine : proteinuria
Fetal evaluation :
 Daily fetal movement count
 Ultrasound
 Doppler ultrasound for fetal blood flow
 Velocimetry
. Seizure Prophylaxis
Routinely used in severe PE
Magnesium sulphate: most commonly used
Initiated with onset of labor till 24h postpartum
For caesarean, started 2hrs before the section till
12hrs postpartum
Delivery
 The only definitive treatment
 Preeclamptic patients divided into 3 categories
A- Preeclampsia features fully subside
B- partial control, but BP maintains a steady
high level
C- persistently increasing BP to severe level
 Gp A: can wait till spontaneous onset of labor
don’t exceed Expected Date of Delivery
 Gp B: >37wk terminate w/o delay
<37wk, expectant management at least
till 34wks
 Gp C: terminate irrespective of POG,
start seizure prophylaxis and
steroids if<34wks
Anaesthetic management
 Is the diagnosis correct
 Condition of mother before the start of
anaesthetic
 Evidence of end organ damage
 Airway
 Haemodynamic monitoring
 Fluid status: volume depleted patients
 BP control
 Coagulation status
 Choice of anesthetic technique for LSCS
 Evidence of recent bleeding causing hemodynamic
instability.
 Drug history and status of the fetus
Laboratory investigations
 Hematocrit
 Platelet count /PT/PTT
 Abnormal liver enzymes
 Signs of Hemolysis (elevated LDH, Bilirubin)
 Uric acid, Urea , Creatinine ,Proteinuria
MEDICAL
General Measures-
Good rest , Salt restricted diet in severe cases,regular
follow up ,identification of risk factors and use of
predictors.
Specific Measures
Antihypertensive drug therapy
 To establish & maintain hemodynamic stability (control
hypertension & avoid hypotension)
 To provide excellent labor analgesia
 To prevent complications of preeclampsia
 To be able to rapidly provide anesthesia for Caesarean
Section
 Neuraxial analgesia:
Lumbar Epidural-
gradual onset of sympathetic blockade
cardiovascular stability
↓ stress response
maintains uteroplacental circulation
avoids neonatal depression
extended analgesia if cesarean required
excellent post op analgesia
Combined Spinal Epidural Analgesia
Advantages
(1) provision of high-quality analgesia, which
attenuates the hypertensive response to pain
(2) reduction in levels of circulating catecholamines
(3) improvement in intervillous blood flow
(4) Provision of anesthesia through catheter for
emergency cesarean delivery
Disadvantage
 epidural catheter function cannot be fully evaluated until
after resolution of the intrathecal analgesia
 special considerations in pre eclampsia
(1) assessment of coagulation status,
(2) intravenous hydration prior to the epidural
administration of LA
(3) treatment of hypotension,
(4) use of an epinephrine-containing LA solution
Acid aspiration prophylaxis given
1. H2 blockers
2. non particulate antacid
3. metoclopramide
Routine
 Heart rate ,
 Blood pressure ,
 Pulse oximetry ,
 Temperature monitoring ,
 Urine output ,
 Neuromuscular monitoring and
 Capnography
 Invasive central blood pressure monitoring not
routinely indicated
 Does not improve patient outcome
 Indications:
-Oliguria patients
-Unresponsive or refractory hypertension
-Persistent arterial desaturation
-Pulmonary edema
- massive hemorrhage
-frequent ABG measurement
 Begins with the securing of a good IV access and
 rapid fluid administration , An 18G is provided .
 Choice of fluid should be isotonic saline or isotonic
solution containing electrolytes.
 Only dextrose containing solutions should be avoided
as oxytocin infusions are known to have an antidiuretic
effect and can result in water intoxication
 Patient transfers should be in left lateral position and
positioned same on table
 Spinal anaesthesia
 Epidural anaesthesia
 Combined Spinal Epidural Anaesthesia
 General anaesthesia
 Spinal anesthesia is a generally preferred anesthetic
technique in emergency
 Simple to perform, provides rapid onset and a dense
block
 spinal anesthesia can be safely used with 0.5 %
bupivacaine (5 – 10mg) along with 20 micg fentanyl
 Epidural anesthesia considered the optimal
anesthetic technique for cesarean delivery
Advantages
 relatively stable maternal BP
 Increased uteroplacental blood flow
 ability to titrate the administration of LA and
intravenous fluids
 reduce the possibility of fluid overload and pulmonary
edema.
 post op analgesia
 Extension of an existing continuous lumbar epidural
aneshesia
 Injection of 8 to 10 ml of 1.5 to 2 % lidocaine with
epinephrine 1 : 200000, 0.5 % bupivacaine , or
0.5 % ropivacaine provides level of T 10 analgesia
 Addition of 25 – 50 micg fentanyl to LA will
• speed up the onset of block
• improve the quality and duration
• decrease visceral discomfort associated with uterine
exteriorization, interiorization, peritoneal retraction
 platelet count lower than 50,000/mm3 precludes the
administration of neuraxial anesthesia.
 For women with a platelet count between 50,000/mm3
and 80,000/mm3, the risks and benefits of neuraxial
anesthesia must be weighed against the risks of
general anesthesia
 A platelet count of 75,000/mm3 to 80,000/mm3 for
epidural catheter removal
Indications
- coagulopathy
-sustained fetal bradycardia with reassuring
maternal airway
- severe ongoing maternal hemorrhage
- patients refusal
- contraindications to neuraxial technique
1.Difficult intubation-
-smaller size tube
-difficult airway cart ready
2. Exaggerated and prolonged hypertensive response to
laryngoscopy and intubation: -risk of intracranial
hemorrhage.
-labetalol(10 mg),
esmolol( 2mg/kg ),
nitroglycerine (0.1 mg/kg/min),
nitroprusside(0.5mcg/kg/min)
remifentanyl (1mcg/kg)
3.MgSO4 prolong action of both depolarising and
NDMR , as it inhibits calcium facilitated
presynaptic transmitter release
4. Impairs uterine and intervillous blood flow
5. Acid aspiration prophylaxis followed
1. Induction :
 Denitrogenation for 3 mins of 100 % oxygen
 rapid sequence induction
 induced with thiopentone(4-5 mg/kg) and
Sch(1-1.5mg/kg)
2. Intubation :
 small size cuffed ETT 6 to 6.5
 difficult airway cart should be ready
3. Maintenance :
 Maintained with 50 % N20 in O2 and volatile
halogenated agent ( isolflurane, desflurane )
 after delivery, inhalational agent decreased
 ratio of N2O: O2 increased to 70 : 30
 narcotics, BZD administered
4. Extubation :
 exaggerated CVS response should be avoided by pre
treating with lignocaine or esmolol
5. Post operative pain relief :
 Intravenous or epidural opioids like fentanyl
Neonate of PIH mother is at higher risk for
 prematurity
 SGA
 asphyxiation
 drug depression
 meconium aspiration
Immediate complications in neonate
 respiratory distress
 instability of body temperature
 poor feeding
 hypoglycemia
 hypocalcemia
Severely PIH prone to
 pulmonary edema
 convulsions within 24 hrs of delivery
1. Analgesia
2. Fluid balance - strict I/O chart,restrict intake 75ml/hr
3. Haemodynamic control
4. MgSO4 - atleast 24 hrs postpartum or until
diuresis ( 200 ml/hr for atleast 3 hrs )
 CVA: main leading cause of death in pts with PE
 Pulmonary edema, pleural effusion, ARDS
 laryngeal edema
 Placental abruptio’
 Renal failure: oliguria most common
 Liver:
Subcapsular liver hematoma
HELLP Syndrome,
hepatic rupture with shock
 DIC
 Eclampsia
 Maternal death
Diagnosis:
1. Hemolysis:
 Peripheral smear - schistocytes, burr cells, and
echinocytes
 ↑bilirubin >1.2mg/dL,
 LDH>600 IU/L
1. Elevated liver enzymes:
 SGOT> 70 IU/L
 LDH>600 IU/L
2. Low platelets: <1 lakh /mm3
 Immediate hospitalisation
 Stabilise mother
 antihypertensives
 anti seizure prophylaxis
 correct coagulation abnormalities
 Assess fetal condition- FHR, doppler ultrasound,
biophysical profile
 Ultimate goal:
 >34 wks gestation deliver
 <34wks expectant management if stable maternal
and fetal conditions
 Platelet transfusion if: <40,000/mm3 before cesarean
<20,000/mm3 before delivery
 Rupture of a subcapsular hematoma of the liver is a
life-threatening complication of HELLP syndrome
 manifest as abdominal pain, nausea and vomiting, and
headaches
 pain worsens over time and becomes localized to the
epigastric area
 Hypotension and shock typically develop, and the
liver is enlarged and tender
 Treatment consisting of intravascular volume
resuscitation, blood and plasma transfusions, and
emergency laparotomy
Eclampsia
 Is the new onset of seizures or unexplained coma during
pregnancy or postpartum period in patients with pre-
existing PE and without pre-existing neurological disorder.
 0.1- 5.5 per 10,000 pregnancies
 Antepartum(50%): mostly in third trimester
 Intrapartum(30%):
 Postpartum(20%): usually within 48hours
Maternal age less than 20 years
Multigravida
Molar pregnancy
Triploidy
Pre-existing hypertension or renal disease
Previous severe Preeclampsia or Eclampsia
Nonimmune hydrops fetalis
Systemic Lupus Erythematosus
 Eclamptic convulsions are epileptiform and consist of four
stages
 Premonitory stage: twitching of muscles of face, tongue,
limbs and eye. Eyeballs rolled or turned to one side, 30s
 Tonic stage: opisthotonus, limbs flexed, hands clenched,
30s
 Clonic stage: 1-4 min, frothing, tongue bite, stertorous
breathing
 Stage of coma: variable period.
 Sustained rise in blood pressure
 Tachycardia, Tachyponea
 Rales
 Mental status changes
 Hypereflexia
 Clonus
 Papilloedema
 Oliguria or anuria
 Right upper quadrant or epigastric abdominal tenderness
 Generalized edema
 Small fundal height for the estimated gestational age
 Loss of normal cerebral auto regulatory mechanisms
 cerebral hyperperfusion
 Edema & ↓cerebral blood flow
 Early detection and judicious treatment with termination
of pregnancy in Preeclamptic patients
 Adequate sedation, Anti hypertensives and prophylactic
Anticonvulsant in peripartum period
 Observe for 24-48 hrs postpartum
1. Prevention of seizures
2. Control of seizures
3. correction of hypoxia and acidosis
4. Blood pressure control
5. Delivery after maternal stabilization
 MgSO4 therapy:
DOC for prophylaxis of eclamptic convulsions
M.O.A:
blocks Ca2+ ion influx into neurons leading to cerebral VD
Other actions: -lowers endothelin-1 levels
- ↑ production of PG I2
- tocolytic action
- attenuates the release of Ach and
sensitivity to Ach at myoneuronal junction
 Turn patient head to one side,
- apply jaw thrust if airway compromised
- nasopharyngeal airway
- Adequate oxygenation
- ensure adequate breathing , bag and mask ventilation
- secure an i.v line
- Drugs- Antiepileptics
Antihypertensives
- Delivery
1. Zuspan or sibai regime( iv regimen )
 4-6 gm i.v over 15 min f/b infusion of 1-2 gm/hr
2. Pritchard regime( im regimen)
 4 gm i.v over 3-5min f/b 5 gm in each buttock ( 14 gm
total )
 maintenance of 5 gm i.m in alternate buttock 4 hrly
 Normal Serum levels- 1.7- 2.4 mg/dl
 Therapeutic range- 5- 9mg/dl
 Patellar reflex lost- >1omg/dl
 Respiratory depression- 15-20 mg/dl
 Cardiac arrest- >25 – 30 mg/dl
 Stop infusion
 Intravenous Calcium 10 ml 10% over 10 minutes
 Endotracheal intubation in respiratory depression
o MgSO4 potentiate and prolong the action of both
depolarizing non-depolarizing muscle relaxants
o At higher doses Mg2+ rapidly crosses the placental barrier,
has been found to significantly ↓ FHR variability
o given cautiously with Ca2+ as may antagonize the
anticonvulsant effect of MgSO4
o cautious use in patients with renal impairment
o May ↑ the possibility of hypotension during regional block
Indications for cesarean section -
Fetal distress
Placental abruption
Extreme prematurity
Unfavorable cervix
Failed induction of labor
Recurrent seizures
 Neuraxial: -
indications
- seizures controlled
- no coagulopathy
- patient cooperative
 GA: -
Indications
-seizures not controlled
-coagulopathy
-reassuring airway
-uncooperative patients
 Preeclampsia is a multisystem disorder.
 Management is supportive, delivery is the only definitive.
 Preeclampsia patients: High risk for difficult intubation.
 Hypertensive response to laryngoscopy intracranial
hemorrhage.
 Spinal Anaesthesia not contraindicated in severe
Preeclampsia
 Eclampsia can be prevented by prophylactic MgSO4
therapy
 Eclamptic patients should be monitored for at least 24 hrs
post partum.
Pregnancy Induced Hypertension - Pre eclampsia

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Pregnancy Induced Hypertension - Pre eclampsia

  • 1. Speaker : Dr omar kamal
  • 2.  Name: Mrs. Nagalakshmi B D  Age: 33 yrs  W/O: Mr. Harish  IP No.: 98870  Place : bangalore  Occupation : Housewife  Date of Admission :18/10/13  Date of surgery 18/10/13
  • 3. Chief complaints :  h/o 8 months of amenorrhoea  h/o Swelling of B/l lower limbs since 15 days  HOPI : Patient with 8 months of amenorrhea appreciating fetal movements well, was apparently normal 15 days back, when she started noticing swelling of both lower limbs, aggravated by work , no diurnal or postural variation, present through out day No H/o headache, blurring of vision, epigastric pain, bowel/bladder disturbances, fever, rashes, bleeding
  • 4.  Obstetric History: ML: 12 years NCM G2P1L1  1st Pregnancy: in 2006 , FTVD of live male baby of weight 2.5kg at Bangalore hospital. No antenatal/ Intrapartum/Postpartum complications . Breast fed for 6 months . H/o using male barrier contraception .  2nd pregnancy: Present pregnancy, spontaneous conception
  • 5.  1st Trimester : Pregnancy diagnosed by UPT ; +ve after 5 week of LMP. Started on Folic acid supplementation . Blood investigations and scan done on 17/4/13 showed SLIUG . No H/o fever, rashes, excessive vomiting, pain abdomen, bleeding/spotting PV.  2nd trimester: Quickening felt at 4th month of gestation. Continued folic acid. Started on Iron/Calcium supplementation. Immunised with 2 doses of Inj.T.T. Scan on 14/6/13 showing SLIUG of 18+2 weeks at 18+2 weeks by LMP, fetal doppler normal.
  • 6.  3rd trimester: Appreciates fetal movements well, continued iron/calcium/ folic acid. Patient had increased readings of BP since 30 weeks .Tab. Methyldopa 250 mg BD started.  now referred to hospital with above complaints for further management
  • 7.  Menstrual History: PMC: 3-4/ 24-25 days, regular, normal flow, no clots  LMP- 8/2/13 EDD- 15/11/13 POG- 36 wks  Past History : No H/o Diabetes/hypertension/ Tuberculosis/ epilepsy/ Thyroid disorders.  Family History: No H/o Diabetes/ Tuberculosis/ epilepsy/ Thyroid disorders.
  • 8. O/E Moderately built and nourished. conscious and cooperative Vitals : PR 88/min and regular BP 150/90 mmHg measured in sitting position Afebrile B/l pedal edema No pallor ,icterus cyanosis ,clubbing or lymphadenopathy
  • 9. Facies No abnormality Upper incisors no loose or protruding teeth Nose both nares patent no nasal airflow obstruction Mallampati Class 2 Thyromental distance >3fingers Mouth opening adequate Movement at atlanto occipetal joint normal No obvious external pathology
  • 10. RS : B/L air entry equal NVBS CVS : S1S2 heard, no murmur P/A-Uterus 32-34 size, relaxed, cephalic lower pole , non tense, non tender , FHS+ 148 bpm regular PROVISIONAL DIAGNOSIS 33 yrs female, G2P1L1 with 36 wks of gestation with SLIUG, with mild pre eclampsia
  • 11.
  • 12.  In 2000, National High Blood Pressure Education Program classified hypertensive disorders complicating pregnancy as: Gestational hypertension Preclampsia- eclampsia chronic hypertension chronic hypertension with superimposed preeclampsia
  • 13.  Blood Pressure ≥ 140/90 on two or more occasions - in a previously normotensive patient - after 20 weeks gestation - without proteinuria - returning to normal 12 weeks after delivery  Almost half of these develop preeclampsia syndrome
  • 14.  Blood Pressure ≥ 140/90 before 20 weeks of gestation Or  Persistence of hypertension beyond 12 weeks after delivery
  • 15.  New-onset proteinuria ≥ 300 mg/24 hours in chronc hypertensive women but no proteinuria before 20 weeks gestation  A sudden increase in proteinuria or blood pressure or platelet count <1 lakh/mm3 in women with hypertension and proteinuria before 20 weeks’ gestation
  • 16.  New onset of hypertension & proteinuria in a previously normotensive woman  after 20 weeks of gestation  Returning to normal after 12 weeks of delivery.  Edema not a part of diagnosis now. Eclampsia :  New onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre- existing preeclampsia and without pre-existing neurological disorder
  • 17.  The NHBPEP has recommended that clinicians consider the diagnosis of preeclampsia in the absence of proteinuria when any of the following findings are present: 1) Persistent epigastric or right upper quadrant pain, 2) Persistent cerebral symptoms, 3) Fetal growth restriction, 4) Thrombocytopenia, 5) Elevated serum liver enzyme concentrations
  • 18.
  • 19. • Preconception - Partner related  Nulliparity  limited exposure to paternal sperms  Partner who fathered a preeclamptic pregnancy in another women -Non partner related  History of Preeclampsia in previous pregnancy  Advanced maternal age  Family history of Preeclampsia  History of placental abruptio, IUGR, fetal death
  • 20. -Maternal disease related  Obesity, BMI>35 doubles the risk  Hypertension  Diabetes  Thrombotic vascular diseases -Behaviour-  Smoking : -Pregnancy associated-  Multiple gestation  Molar pregnancy
  • 21.  Exact mechanism unknown, disease of theories. 1. ABNORMAL PLACENTATION  Stage1: failure of trophoblastic invasion into myometrium Penetrates only decidua superficial placentation  ↓placental perfusion  stage2 : endothelial damage systemic manifestations of Preeclampsia
  • 22.
  • 23.
  • 24.
  • 25.  Family history of pre eclampsia: genetic origin  Mutations in Complement Regulatory Protein gene  Genes assoc.:  MTHFR, F5 leiden, AGT, HLA, NOS3, F2(prothrombin), ACE
  • 26.
  • 27.  Exposure to sperms of different partner  long term exposure to paternal antigen in sperms of same partner- protective  activated auto antibodies to angiotensin receptor-1 AA-AT1activate AT1 receptorsincreased sensitivity to angiotensins  hypertension
  • 28.
  • 29.  ↑ plasma Homocystiene  ↑ serum sFlt1(soluble fms-like tyosine kinase)  ↓serum and urinary Platelet Growth Factor  ↓ Vascular Endothelial Growth Factor
  • 30. 1. Respiratory  Airway is edematous;  ↓ internal diameter of trachea due to capillary engorgement  Pharyngolaryngeal edema visualization difficult  Subglottic edema – airway obstruction
  • 31.  CNS manifestations include: headache, visual disturbances, hyperexcitability, hyperreflexia, coma, seizures Cause: cerebral edema and hypoperfusion
  • 32.  Vasospasm and exaggerated responses to catecholamines  Characteristically, blood pressure and SVR are elevated  Severe preeclampsia is usually a hyperdynamic state
  • 33.  Pulmonary edema is a severe complication – 3 %  Plasma colloid osmotic pressure is diminished and increased vascular permiability influences PE  T3 POST PARTUM NORMAL 22 17 PRE ECLAMPSIA 18 14
  • 34.  Hemoconcentration  Thombocytopaenia  most common  Platelet count correlates with disease severity and incidence of abruptio placentae  DIC due to activation of coagulation cascadeoverconsumption of coagulants and platelets spontaneous haemorrhage
  • 35.  HELLP syndrome  Periportal haemorrhage  subcapsular bleeding  hepatic rupture: 32% maternal mortality
  • 36. Decreased GFR 34 % than normal - oliguria - renal failure - uric acid, creatinine is elevated Glomerulopathy - proteinuria  The characteristic renal histologic lesion is glomerular capillary endotheliosis
  • 37.  Uteroplacental insufficiency  Fetal complications: - hypoxia -IUGR -Prematurity -IUD -Placental abruptio
  • 38.
  • 39. No screening test is really helpful Various screening methods are:  Diastolic notch at 24weeks by doppler ultrasonography  Absence or reversal of end diastolic flow  Average mean arterial pressure ≥ 90 mmHg in second trimester  Angiotensin infusion test: angiotensin infusion required to raise the blood pressure >20 mm Hg from baseline  Roll over test: rise in blood pressure >20 mmHg from baseline on turning supine at 28-32 weeks gestation is positive.
  • 40.  Regular Antenatal checkup: rapid gain in weight rising blood pressure edema proteinuria/deranged liver or renal profile  Low dose Aspirin in High risk group: ↑PGs and↓TXA2  Calcium supplementation: no effects unless women are calcium deficient  Antioxidants- Vitamin C and E  Nutritional supplementation: zinc, magnesium, fish oil, low salt diet
  • 41. Maternal  Gestational age 38 weeks*  Platelet count <100,000/mm3  Progressive deterioration in hepatic function  Progressive deterioration in renal function  Suspected placental abruption  Persistent severe headaches or visual changes  Persistent severe epigastric pain, nausea, or  vomiting Fetal  Severe intrauterine growth restriction  Nonreassuring fetal status  Oligohydramnios
  • 43. . Maternal evaluation : Hemoglobin and hematocrit platelet count : decreased, if < 1 lakh coagulation profile LFTs : indicated in all patients KFTs : raised (S.urea creatinine is decresaed in Normal pregnancy) Urine Routine : proteinuria
  • 44. Fetal evaluation :  Daily fetal movement count  Ultrasound  Doppler ultrasound for fetal blood flow  Velocimetry
  • 45. . Seizure Prophylaxis Routinely used in severe PE Magnesium sulphate: most commonly used Initiated with onset of labor till 24h postpartum For caesarean, started 2hrs before the section till 12hrs postpartum
  • 46. Delivery  The only definitive treatment  Preeclamptic patients divided into 3 categories A- Preeclampsia features fully subside B- partial control, but BP maintains a steady high level C- persistently increasing BP to severe level
  • 47.  Gp A: can wait till spontaneous onset of labor don’t exceed Expected Date of Delivery  Gp B: >37wk terminate w/o delay <37wk, expectant management at least till 34wks  Gp C: terminate irrespective of POG, start seizure prophylaxis and steroids if<34wks
  • 48.
  • 50.  Is the diagnosis correct  Condition of mother before the start of anaesthetic  Evidence of end organ damage  Airway  Haemodynamic monitoring  Fluid status: volume depleted patients  BP control
  • 51.  Coagulation status  Choice of anesthetic technique for LSCS  Evidence of recent bleeding causing hemodynamic instability.  Drug history and status of the fetus
  • 52. Laboratory investigations  Hematocrit  Platelet count /PT/PTT  Abnormal liver enzymes  Signs of Hemolysis (elevated LDH, Bilirubin)  Uric acid, Urea , Creatinine ,Proteinuria
  • 53. MEDICAL General Measures- Good rest , Salt restricted diet in severe cases,regular follow up ,identification of risk factors and use of predictors. Specific Measures Antihypertensive drug therapy
  • 54.
  • 55.
  • 56.  To establish & maintain hemodynamic stability (control hypertension & avoid hypotension)  To provide excellent labor analgesia  To prevent complications of preeclampsia  To be able to rapidly provide anesthesia for Caesarean Section
  • 57.  Neuraxial analgesia: Lumbar Epidural- gradual onset of sympathetic blockade cardiovascular stability ↓ stress response maintains uteroplacental circulation avoids neonatal depression extended analgesia if cesarean required excellent post op analgesia
  • 58. Combined Spinal Epidural Analgesia Advantages (1) provision of high-quality analgesia, which attenuates the hypertensive response to pain (2) reduction in levels of circulating catecholamines (3) improvement in intervillous blood flow (4) Provision of anesthesia through catheter for emergency cesarean delivery Disadvantage  epidural catheter function cannot be fully evaluated until after resolution of the intrathecal analgesia
  • 59.  special considerations in pre eclampsia (1) assessment of coagulation status, (2) intravenous hydration prior to the epidural administration of LA (3) treatment of hypotension, (4) use of an epinephrine-containing LA solution
  • 60. Acid aspiration prophylaxis given 1. H2 blockers 2. non particulate antacid 3. metoclopramide
  • 61. Routine  Heart rate ,  Blood pressure ,  Pulse oximetry ,  Temperature monitoring ,  Urine output ,  Neuromuscular monitoring and  Capnography
  • 62.  Invasive central blood pressure monitoring not routinely indicated  Does not improve patient outcome  Indications: -Oliguria patients -Unresponsive or refractory hypertension -Persistent arterial desaturation -Pulmonary edema - massive hemorrhage -frequent ABG measurement
  • 63.  Begins with the securing of a good IV access and  rapid fluid administration , An 18G is provided .  Choice of fluid should be isotonic saline or isotonic solution containing electrolytes.  Only dextrose containing solutions should be avoided as oxytocin infusions are known to have an antidiuretic effect and can result in water intoxication  Patient transfers should be in left lateral position and positioned same on table
  • 64.  Spinal anaesthesia  Epidural anaesthesia  Combined Spinal Epidural Anaesthesia  General anaesthesia
  • 65.
  • 66.
  • 67.  Spinal anesthesia is a generally preferred anesthetic technique in emergency  Simple to perform, provides rapid onset and a dense block  spinal anesthesia can be safely used with 0.5 % bupivacaine (5 – 10mg) along with 20 micg fentanyl
  • 68.  Epidural anesthesia considered the optimal anesthetic technique for cesarean delivery Advantages  relatively stable maternal BP  Increased uteroplacental blood flow  ability to titrate the administration of LA and intravenous fluids  reduce the possibility of fluid overload and pulmonary edema.  post op analgesia
  • 69.  Extension of an existing continuous lumbar epidural aneshesia  Injection of 8 to 10 ml of 1.5 to 2 % lidocaine with epinephrine 1 : 200000, 0.5 % bupivacaine , or 0.5 % ropivacaine provides level of T 10 analgesia  Addition of 25 – 50 micg fentanyl to LA will • speed up the onset of block • improve the quality and duration • decrease visceral discomfort associated with uterine exteriorization, interiorization, peritoneal retraction
  • 70.  platelet count lower than 50,000/mm3 precludes the administration of neuraxial anesthesia.  For women with a platelet count between 50,000/mm3 and 80,000/mm3, the risks and benefits of neuraxial anesthesia must be weighed against the risks of general anesthesia  A platelet count of 75,000/mm3 to 80,000/mm3 for epidural catheter removal
  • 71. Indications - coagulopathy -sustained fetal bradycardia with reassuring maternal airway - severe ongoing maternal hemorrhage - patients refusal - contraindications to neuraxial technique
  • 72. 1.Difficult intubation- -smaller size tube -difficult airway cart ready 2. Exaggerated and prolonged hypertensive response to laryngoscopy and intubation: -risk of intracranial hemorrhage. -labetalol(10 mg), esmolol( 2mg/kg ), nitroglycerine (0.1 mg/kg/min), nitroprusside(0.5mcg/kg/min) remifentanyl (1mcg/kg)
  • 73. 3.MgSO4 prolong action of both depolarising and NDMR , as it inhibits calcium facilitated presynaptic transmitter release 4. Impairs uterine and intervillous blood flow 5. Acid aspiration prophylaxis followed
  • 74. 1. Induction :  Denitrogenation for 3 mins of 100 % oxygen  rapid sequence induction  induced with thiopentone(4-5 mg/kg) and Sch(1-1.5mg/kg) 2. Intubation :  small size cuffed ETT 6 to 6.5  difficult airway cart should be ready
  • 75. 3. Maintenance :  Maintained with 50 % N20 in O2 and volatile halogenated agent ( isolflurane, desflurane )  after delivery, inhalational agent decreased  ratio of N2O: O2 increased to 70 : 30  narcotics, BZD administered 4. Extubation :  exaggerated CVS response should be avoided by pre treating with lignocaine or esmolol 5. Post operative pain relief :  Intravenous or epidural opioids like fentanyl
  • 76.
  • 77.
  • 78. Neonate of PIH mother is at higher risk for  prematurity  SGA  asphyxiation  drug depression  meconium aspiration
  • 79. Immediate complications in neonate  respiratory distress  instability of body temperature  poor feeding  hypoglycemia  hypocalcemia
  • 80. Severely PIH prone to  pulmonary edema  convulsions within 24 hrs of delivery
  • 81. 1. Analgesia 2. Fluid balance - strict I/O chart,restrict intake 75ml/hr 3. Haemodynamic control 4. MgSO4 - atleast 24 hrs postpartum or until diuresis ( 200 ml/hr for atleast 3 hrs )
  • 82.  CVA: main leading cause of death in pts with PE  Pulmonary edema, pleural effusion, ARDS  laryngeal edema  Placental abruptio’  Renal failure: oliguria most common  Liver: Subcapsular liver hematoma HELLP Syndrome, hepatic rupture with shock  DIC  Eclampsia  Maternal death
  • 83. Diagnosis: 1. Hemolysis:  Peripheral smear - schistocytes, burr cells, and echinocytes  ↑bilirubin >1.2mg/dL,  LDH>600 IU/L 1. Elevated liver enzymes:  SGOT> 70 IU/L  LDH>600 IU/L 2. Low platelets: <1 lakh /mm3
  • 84.  Immediate hospitalisation  Stabilise mother  antihypertensives  anti seizure prophylaxis  correct coagulation abnormalities  Assess fetal condition- FHR, doppler ultrasound, biophysical profile
  • 85.  Ultimate goal:  >34 wks gestation deliver  <34wks expectant management if stable maternal and fetal conditions  Platelet transfusion if: <40,000/mm3 before cesarean <20,000/mm3 before delivery
  • 86.  Rupture of a subcapsular hematoma of the liver is a life-threatening complication of HELLP syndrome  manifest as abdominal pain, nausea and vomiting, and headaches  pain worsens over time and becomes localized to the epigastric area  Hypotension and shock typically develop, and the liver is enlarged and tender  Treatment consisting of intravascular volume resuscitation, blood and plasma transfusions, and emergency laparotomy
  • 88.  Is the new onset of seizures or unexplained coma during pregnancy or postpartum period in patients with pre- existing PE and without pre-existing neurological disorder.  0.1- 5.5 per 10,000 pregnancies  Antepartum(50%): mostly in third trimester  Intrapartum(30%):  Postpartum(20%): usually within 48hours
  • 89. Maternal age less than 20 years Multigravida Molar pregnancy Triploidy Pre-existing hypertension or renal disease Previous severe Preeclampsia or Eclampsia Nonimmune hydrops fetalis Systemic Lupus Erythematosus
  • 90.  Eclamptic convulsions are epileptiform and consist of four stages  Premonitory stage: twitching of muscles of face, tongue, limbs and eye. Eyeballs rolled or turned to one side, 30s  Tonic stage: opisthotonus, limbs flexed, hands clenched, 30s  Clonic stage: 1-4 min, frothing, tongue bite, stertorous breathing  Stage of coma: variable period.
  • 91.  Sustained rise in blood pressure  Tachycardia, Tachyponea  Rales  Mental status changes  Hypereflexia  Clonus  Papilloedema  Oliguria or anuria  Right upper quadrant or epigastric abdominal tenderness  Generalized edema  Small fundal height for the estimated gestational age
  • 92.  Loss of normal cerebral auto regulatory mechanisms  cerebral hyperperfusion  Edema & ↓cerebral blood flow
  • 93.  Early detection and judicious treatment with termination of pregnancy in Preeclamptic patients  Adequate sedation, Anti hypertensives and prophylactic Anticonvulsant in peripartum period  Observe for 24-48 hrs postpartum
  • 94. 1. Prevention of seizures 2. Control of seizures 3. correction of hypoxia and acidosis 4. Blood pressure control 5. Delivery after maternal stabilization
  • 95.
  • 96.  MgSO4 therapy: DOC for prophylaxis of eclamptic convulsions M.O.A: blocks Ca2+ ion influx into neurons leading to cerebral VD Other actions: -lowers endothelin-1 levels - ↑ production of PG I2 - tocolytic action - attenuates the release of Ach and sensitivity to Ach at myoneuronal junction
  • 97.  Turn patient head to one side, - apply jaw thrust if airway compromised - nasopharyngeal airway - Adequate oxygenation - ensure adequate breathing , bag and mask ventilation - secure an i.v line - Drugs- Antiepileptics Antihypertensives - Delivery
  • 98.
  • 99. 1. Zuspan or sibai regime( iv regimen )  4-6 gm i.v over 15 min f/b infusion of 1-2 gm/hr 2. Pritchard regime( im regimen)  4 gm i.v over 3-5min f/b 5 gm in each buttock ( 14 gm total )  maintenance of 5 gm i.m in alternate buttock 4 hrly
  • 100.  Normal Serum levels- 1.7- 2.4 mg/dl  Therapeutic range- 5- 9mg/dl  Patellar reflex lost- >1omg/dl  Respiratory depression- 15-20 mg/dl  Cardiac arrest- >25 – 30 mg/dl
  • 101.  Stop infusion  Intravenous Calcium 10 ml 10% over 10 minutes  Endotracheal intubation in respiratory depression
  • 102. o MgSO4 potentiate and prolong the action of both depolarizing non-depolarizing muscle relaxants o At higher doses Mg2+ rapidly crosses the placental barrier, has been found to significantly ↓ FHR variability o given cautiously with Ca2+ as may antagonize the anticonvulsant effect of MgSO4 o cautious use in patients with renal impairment o May ↑ the possibility of hypotension during regional block
  • 103. Indications for cesarean section - Fetal distress Placental abruption Extreme prematurity Unfavorable cervix Failed induction of labor Recurrent seizures
  • 104.  Neuraxial: - indications - seizures controlled - no coagulopathy - patient cooperative  GA: - Indications -seizures not controlled -coagulopathy -reassuring airway -uncooperative patients
  • 105.  Preeclampsia is a multisystem disorder.  Management is supportive, delivery is the only definitive.  Preeclampsia patients: High risk for difficult intubation.  Hypertensive response to laryngoscopy intracranial hemorrhage.  Spinal Anaesthesia not contraindicated in severe Preeclampsia  Eclampsia can be prevented by prophylactic MgSO4 therapy  Eclamptic patients should be monitored for at least 24 hrs post partum.