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
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-AT1activate AT1
receptorsincreased sensitivity to angiotensins
hypertension
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
cascadeoverconsumption of coagulants and
platelets spontaneous haemorrhage
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
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
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
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
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
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
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
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.