pregnancy induced hypertension - pre eclampsia
TRANSCRIPT
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 dopplernormal.
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-AT1activate AT1 receptorsincreased 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 hyperdynamicstate
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 cascadeoverconsumption 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 weightrising blood pressureedemaproteinuria/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,regularfollow 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 AnalgesiaAdvantages
(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 deliveryDisadvantage 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 anesthetictechnique 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 neuraxialanesthesia 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, stertorousbreathing
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 gmtotal )
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 hrspost partum.