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Role of the Anesthesiologist in management of PIH Dr. C.K. Dua Dir.Prof.,

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Title: PREGNANCY INDUCED HYPERTENSION Dr. C.K. Dua Dir., Prof., & Head Deptt. of Anaesthesiology M.A.M.C. Author: M.K.DUA Last modified by: Guest – PowerPoint PPT presentation

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Title: Role of the Anesthesiologist in management of PIH Dr. C.K. Dua Dir.Prof.,


1
Role of the Anesthesiologist in management of
PIH Dr. C.K. Dua Dir.Prof., Head Deptt. of
Anaesthesiology M.A.M.C.
www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
2
What are the different types of Hypertension
during pregnancy?
  • P.I.H Preeclampsia(6- 8)
  • Eclampsia (0.05 )
    Gestational Hypertension(6-7)
  • Chronic Hypertension(3-5)
  • Chronic Hypertension with superimposed P.I.H

3
What is P.I.H. how will you
differentiate between gestational
hypertension, chronic hypertension pre-eclampsia
eclampsia?
4
P.I.H. Range of disorders collectively
formerly known as toxemias of pregnancy.
Pre-eclampsia
  • Pregnancy gt 20 weeks
  • B.P. gt 140/90mmHg at least twice gt 6 hrs apart
  • Systotic / Diastolic gt 30/15mmHg
  • M.A.P. gt105mmHg or gt20 mmHg above baseline.
  • Wt gain gt2.5 Kg./wk (1st sign of impending
    P.I.H.)
  • Proteinuria gt0.3gm/d Not essential for
    diagnosis(appears late)
  • Non-dep. Odema (not a reliable sign).

5
Eclampsia Convulsions grand mal,
appears before during or within 48 hrs. after
delivery in patients who fulfill thecriteria of
pre-eclampsia. Gestational Hypertension
Hypertension without proteinuria or generalised
oedema during the last weeks of pregnancy or
immediately after delivery. Chronic
Hypertension Persistent hypertension regardless
of cause before 20 weeks and beyond 6 weeks after
delivery.
Contd.
6
What is the etiology pathogenesis
of P.I.H.?
  • Aetiology unknown
  • Immunological injury
  • uterplacental insufficiency
  • Pathogenesis
  • Central component is maternal endothelial
    cell dysfunction

7
Pathogenesis
  • Abnormal placentation ,?Trophoblastic perfusion
    uterine ischaemia
  • Maternal placental oxidative stress
  • Release of cytotoxic substances
  • Damage to vascular endothelial cells
  • Triggers vasoconstriction (hypertension)
  • Platelet activation aggregation
  • Prostacyclin thromboxane imbalance,? NO
    Activation of
    Renin-Angiotensin ,? Aldosterone
  • Further endothelial cell damage, disruption of
    capillary integrity,
  • Release of trophoblastic material , Fibrin
    deposition, Renal glomerular lesion
    Proteinuria

8
What are the associated risk factors in
patients with pre-eclampsia?
9
Maternal pre-existing condition Chronic
HT,renal disease,Diabetes obesity. Maternal
specific factors Age, parity, Family h/o
P.I.H. Partner related factors Pregnancy
associated factors Multiple pregnancies,
congenital anomalies Antepartum urinary
tract infection Exogenous factors
Cigarette smoking ? incidence Job stress
?risk.
10
What are the latest hypothetical methods of
prevention of P.I.H.?
  • Antiplatelet drugs (Aspirin) inhibits
    cycloxygenase enzyme required for thromboxane A2
    production.
  • Serotinin 2 receptor blocker (Ketanserin)
    with low dose aspirin
  • Fish oil supplemation (?-3 fatty acids,EPA
    DCHA) same met. pathway as arachadonic acid to
    produce PG .

11
  • Ca Supplementation.
  • Salt restriction
  • Zinc therapy.
  • Vitamin C E
  • Antioxidants help protect against free radicals
  • Plasminogen Activator Inhibitor PAI-1/PAI2
    ratio is increased in PIH is of great value.Vit
    C supplementation has been associated with a 21
    ? in the PAI-1 / PAI-2 a significantly ?
    incidence of pre- eclampsia.
  • All these trials need further evaluation

12
What are the systemic manifestations of
pre-eclampsia?
13
CVS
  • Systemic Hypertension
  • High cardiac output
  • ?SVR
  • ? Circulating volume
  • ? left ventricular work
  • ? CVP
  • ? or PCWP
  • ? Response to catecholamines Angiotensin II.
  • ? Circulating volume increased HcT
  • Poor co-relation b/w CVP PCWP in severe
    cases
  • volume expansion LV overloading
    LVF

14
Airway Respiratory System
  • ?Na H2O retention
  • ?colloidal osmotic Pr.
  • leaky capillaries.
  • Laryngeal Facial Oedema
  • Distortion of glottis
  • Friable mucosa ?Trauma
  • Increased risk of P. edema in response to IV
    fluid administration .

Edema
Difficult Airway
15
Hematological Profile
  • ?Blood viscosity
  • Increased Hct.
  • Thrombocytopenia lt1,50,000/cumm
  • Low grade DIC
  • Role of Bleeding Time Controversial
  • ? B.T. does not always parallel the pl counts.
  • TEG Preferred
  • ? F.D.P. ,? fibrinogen, ? PT PTT DIC

16
CNS
  • Cerebral irritation Headache Hyper reflexia
  • Cerebral vasospasm edema Ischemia
  • visual disturbances and seizures
  • ? ICP hypoxia, hypercarbia acidosis
    coma
  • Cerebral Hemorrhage Fatal
  • Relation b/w seizure degree of HT?
  • goal of obstetric anesthesia. Keep maternal BP
    within limits of cerebral auto regulation

17
Renal System
  • Decrease renal blood flow G.F.R.
  • ?S. creatinine,
  • Oliguria
  • Damaged glomeruli Proteinuria
  • Acute tubular necrosis,Renal failure
  • D.I.C., Abruptio placenta
  • ATN ARF

18
Ophthalmic Retinal arteriolar spasm
Retinal edema Bilateral retinal detachment
Blindness Liver Vasospasm
Periportal hmg subcapsula haematomas.
Hepatic swelling Epigastric pain
Altered LFT, increase serum transaminase levels
HELLP
19
Foetoplacental unit
  • Increased placental abruption
  • increase premature labor.
  • PPH (MgSo4 )
  • IUGR IUD
  • Intracranial fetal haemorrhage
  • Premature neonates vulnerable to drug
    depression
  • Increased meconium aspiration

Perinatal Mortality (20-30)
20
What is HELLP Syndrome?
  • Haemolysis, elevated liver enzymes and low
    platelet count seen in 20 cases of severe
    pre-eclampsia.
  • Clinical S/S Epigastric pain, upper abdominal
    tenderness, systemic HT, proteinuria,
    nausea vomitting and jaundice.
  • Complications P.edema, P.effusions, Cerebral
    edema, hematuria, oliguria, acute tubular
    necrosis, panhypopitutirism,
  • D.I.C.

21
How do you clinically grade the
severity of P.I.H.?
22
A.C.O.G Criteria
  • Mild pre-eclampsia
  • B.P. ? 140/90 (2 occasions,6 hrs.Apart)
  • Proteinuria gt 0.3 gm/24hrs. Severe
    pre-eclampsia
  • B.P. ? 160/110
  • Proteinuria ? 5 gm /24 hrs
  • ?S. Creatinine gt1.6.
  • Oliguria lt 500 ml./24 hrs.
  • Thrombocytopenia
  • CerebraL involvement headache, visual
    disturbances
  • Rt. Upper quadrant epigastric pain
  • Elevated liver enzyme(HELLP)
  • Pulmonary edema, CHF
  • Seizures Eclampsia

23
What are the markers for prediction,
diagnosis and progression of the disease?
24
Blood pressure Proteinuria/ urine
output Serum uric acid / S. Creatinine/LFT
Haemotological investigations HCT
HG Platelet count
Coagulation studies. PT, PTT, Fibrinogen,FDP
( Indicated platelet count lt
1,00,000, D.I.C., Abruptio
placenta.) Normal life span of
platelets is ? from 8-10 to 3-5 days in
pre-eclampsia
25
? Uterine artery doppler flow studies
?resistance to flow, ?likelihood of pre-eclampsia
sixfold ? Plasma Fibronectin (early marker) ?
Plasminogen Activator Inhibitor ?PAI-1 to PAI-2
ratio is of greatest value
Contd..
26
Clinical tests
  • Cold pressor test (ve at 16-20wks)
  • BPgt10mmHg Rise during and after placement of
    icepack on forehead for 3min
  • Roll over test gt30mmHg Severe
  • 20-29 mmHg Mild
  • lt20mmhg Negative
  • Oxytocin test 3 uterine contractions with late
    fetal decelerations Positive

27
A 35 YEARS OLD PRIMIGRAVIDA AT 34 WKS.
GESTATION WAS ADMITTED TO THE HOSPITAL WITH THE
FOLLOWING COMPLAINTS Severe Headache -
Two days Rapid weight gain - gt 8 Kg. In 3
wks. Generalised swelling - 2 days Visual
disturbances - 2 days On Examination
B.P.
166 / 114 mm Hg Generalised Swelling
Exaggerated patellar reflexes Chest
Clinically
clear
28
Role of Anesthesiologist
  • Vaginal delivery
  • Operative delivery
  • Control of convulsions
  • ICU mangement

29
What are the principles of
management of this case of severe pre-eclampsia?
30
Definitive treatment Delivery of fetus
  • Supportive treatment
  • General management
  • Control of hypertension
  • Prevention of seizures.
  • Correction of intravascular fluid volume
  • Maintenance of urine output.
  • Management of associated maternal complication

31
What is the medical Management of
Hypertension ?
32
Maintain BP lt170/110 gt130/90 mm Hg
Avoid precipitous ? BP I/v fluid for volume
expansion before Rx. Acute treatment
Hydralazine is most commonly used Rapid
onset, short duration direct effect. Dose
5-10 mg i/v every 20-30 min/ infusion. Max
dose 200 mg / day. Max. effect - 20-30
min. Disadv. - Tachycardia, headache, tremors
vomitting
33
Nitroglycerin 10 µg/min i/v
titrated to response. Risk of excessive
hypotension ? UPBF High dose of NTG Meth.
Hb. may occur Sodium nitroprusside SNP
0.25 µg/kg/min. High dose of SNPCyanide
toxicity. Short term admn. Intra-arterial
monitoring Labelatol better
alternative, faster onset,relatively free of
maternal side effects. Advantage of ?-adrenergic
blocking effect on uteroplacental vasculature
Dose 50mcg mg i/v ,100 mg PO , 20-160 mg/hr
infusion. Maximum of 220-300 mg. Use cautiously
in asthmatics
34
Trimethaphan - 1-4 mg i/v bolus or infusion
500 mg/250 ml. of 5 dextrose. Adv Rapid
onset - hydrolysed by pl. cholinesterase No
effect on cerebral autoregulation limited
placental transfer. Disadv Histamine release,
vasodilatation , reduced venous
return,tachycardia, tachyphylaxis , prolonged
action ofscoline due to inhibition of plasm
pseudocholinesterase
35
Rx of chronic rise in B.P. Methyldopa - Most
commonly used agent Labetalol,
Hydrallazine, Clonidine ß adrenergic
antagonists risk of fetal bradycardia
Calcium channel blocker MgSo4 potentiates.
ACE inhibitors not recommended (Teratogenic)
Angiotensin II antagonists fetal risk
Atenolol fetal maldevelopment Diuretic not
preferred -
36
Volume Management
  • Correction of i/v fluid volume before
    antihypertensive
  • Crystalloid solutions 1-2 ml/kg/hr with
    adjustments based on patients clinical
    condition urine output.
  • CVP measurement Pulmonary artery catheter in
    selected cases.
  • Colloid solutions Limited role, - improve
    colloidal osmotic pressure. - Risk of
    increased CVP and P.edema. - No evidence of
    improved outcome

37

Contd
  • Rapid infusions of dextrose containing solutions
    to be avoided - result in maternal hyperglycemia
    neonatal hypoglycemia with hyperbilirubinaemia
  • 7-10 ml/hr of 5 dextrose in 0.45 normal saline
    is well tolerated.
  • Avoid dextrose in water alone if oxytocin is
    added to i/v fluid to prevent water intoxication
    and convulsion (Antidiuretic effect).
  • Transfuse blood when Hct is lt 27.
  • Blood components as per requirement and WHO
    guidelines Platelets, fibrinogen, F.F.P.

38
Oliguria
  • Normal urine output to be maintained.
  • Persistent oliguria
  • fluid challenge of 500ml crystalloids
  • If no effect
    dopamine infusion
  • Avoid Repetitive unmonitored fluid admn.
  • CVP monitoring

39
Control of seizures
  • MgSo4 commonly used agent for prophylaxis Rx
  • Mech. Of action
  • Both peripheral central effects.
  • Block Ca influx via N-methyl-D asparate
    reverses cerebral vasoconstriction
  • ? Presynaptic release of Ach
  • post junctional receptors sensitivity ?
  • mild relaxant effects on vascular uterine
    smooth muscle
  • decrease fibrin deposition and increase hepatic
    renal circulation

40
- Suggested regime
Initial bolus of 4-6 gm I/v in 20 solution over
5-10 min. or 8-10 ml. of 50 MgSo4 in
100-250 ml. of N.S. over 30-45 min.
followed by infusion of 1-2 g/hr. -
Additional 2-4 gm. given., if required. - If
seizure persist 10 mg diazepam /200 mg of
thiopentone slowly infused.
41
Magnesium levels
Therapeutic range 4-6 meq. / L Normal
levels 1.5 -2 meq. /L Monitoring
Knee jerk Mg. Levels (if possible)
respiration, urine output (gt100 ml. in 4 hrs.).
Toxicity 6-8 meq./ L -
Nausea, Vomitting, diplopia,
somnolense decrease
myometrical
contractility. 5-10 meq./L -
Increase PQ interval, wide QRS 10 meq.
/ L - Loss of deep tendon reflexes.
15 meq./L - SA AV block
respiratory paralysis.
25 meq./L - Cardiac arrest Treatment -
Stop Mg, support ventilation, Ca. ?
42
How to avoid Mg toxicity?
  • Urine flow of at least 100ml during last 4hrs
    before adminstering next dose
  • Patellar reflexes present
  • No Respiratory depression
  • Magnesium levels to be measured 2hrs after start
    of Rx

43
MgSo4 Anaesthetic Management
  • Clinically significant potentiation of both
    depolarising nondep. - Careful
    titration of doses of muscle relaxants.
    - neuromuscular monitoring
  • Potentiates sedatives and opioids, ? Dose
  • Potentiation of Ca channel blockers
  • Post Partum uterine relaxation excessive blood
    loss
  • Neonatal Transient loss of fetal beat to
    beat variability ? Neonatal skeletal Ms tone
    hypoventilation (Ca may be given to
    overcome the problem

44
Pre operative assessment of P.I.H. patients
45
Detailed History Examination
Frequent BP determination.
Fundoscopic examination Neurological
examination for knee reflex Edema
Airway assessment Detailed
CVS resp. examination Obstetric
fetal evaluation. Lab Tests
hematological studies Coagulation
profile Urine studies
K.F.T., L.F.T. Foetal well being
estriol or human placental lactogen,
ultrasound,
46
Role of Anesthesiologist in management of
convulsions in the OT
  • General management
  • Specific management
  • MgSO4
  • Thiopentone Sodium
  • Diazepam
  • Muscle relaxants

47
What is the role of Anesthesiologist in the labor
room for vaginal delivery?
  • Labor analgesia
  • Important considerations
  • Selection of local anesthetic
  • Use of epinephrine
  • Use of test Dose
  • Thrombocytopenia
  • Control of convulsions
  • Airway management

48
What is your choice of anaesthetic
management in this patient scheduled
for L.S.C.S.?
49
Continous lumbar epidural is the technique of
choice provided
  • Coagulation profile is acceptable
  • Circulating volume is maintained adequate
  • Maternal B.P. is controlled
  • Aortocaval compression is avoided
  • No obvious contraindications to R.A
  • ADVANTAGES
  • Protection against pain related maternal foetal
    complications
  • Safeguards against exaggerated hemodynamic
    responses high incidence of difficult / failed
    intubation , P.aspiration related morbidity
    mortality in pre-eclamptic patients with GA.

50
What is the status of Spinal
Anaesthesia?
51
Generally not recommended
Limited role in patient with incipient
coagulopathy with very high risk for general
anaesthesia Precautions Avoid sudden
hypotension. Timely Rx of hypotension
Proper dose selection of LA
52
What are the special considerations in
this patient for R.A.?
53
  • All considerations as for any obstetric patient
  • Modest prehydration
  • ?Dose of antihypertensive agent before epidural
    and before each top-up dose
  • Controlled RA to allow admn. Of small boluses of
    i/v fluids ephedrine if reqd.
  • Addition of epidural opioids to reduce LA dose
  • F.H.R. monitoring.
  • Small doses of ephedrine for persistent
    hypotension Increased
    sensitivity to vasopressors
  • Epinephrine addition to L.A. controversial
  • Test dose controversy

54
Platelet count RA
  • gt1,00,000 SAFE
  • gt75,000-80,000 Perhaps Safe
  • 50,000-75000 Significant
  • (grey zone) reluctance
  • lt50,000 Unsafe
  • Clot strength declines rapidly below 80,000/cumm
  • No clear cut association b/w bleeding time
    epidural hematoma

55
What are the anesthetic considerations for
G.A. ?
56
  • Careful pre-anaesthetic evaluation prepn.
  • Exaggerated haemodynamaic responses to lx
    intubation prophylactic admn.of labetolol ,
    fentanyl , lignocaine
  • Rapid sequence induction intubation
  • Defasciculation prior to scholine (not required
    with MgSO4)
  • Airway edema Smaller size ETT
    Gentle instrumentation
  • Titrate the dose of muscle relaxants.
  • Use NM monitor.

57

Contd.
  • Post intubation severe hypertension
    urgent attention ? conc.of volatile anesthetic
    agents
  • Hydrallazine,Trimethaphan, NTG SNP
  • Use low dose (0.67 MAC) of desflurane, sevo,
    enflurane or isoflurane to prevent intraoperative
    HT.
  • Discontinue early to prevent uterine
    relaxation.
  • Avoid hypotension
  • Avoid Drugs that potentiate HT,nephrotoxicity
    hepatotoxicity
  • Continue MgSo4 during intraoperative and post
    operative period
  • Careful extubation ( L. edema )

58
What are the important monitors for perioperative
monitoring of P.I.H. patients?
59
  • N.I.B.P., (I.B.P ), E.C.G, SpO2 ETCO2
  • NM monitoring
  • Temperature monitoring
  • Mg monitoring
  • Uterine Contraction monitoring
  • Continuous FHR monitoring.
  • Coagulation profile monitoring serial estimation
    of platelet
  • Urine output Fluid balance
  • C.V.P - Diastolic gt 105 mmHg with persistent
    oliguria - Extended use of oxytocin
    gt10 mu/min. - Pt. receiving
    antihypertensive Rx Mg. -
    Difficulty in fluid management.
  • PCWP monitoring -P. edema. -
    - chronic HT with impending CHF

60
Should ergometrine / oxytocin be
given to pre-eclamplic patients?
61
Ergometrine not recommended
vomitting, increase in BP
initiate eclampsia. Given only if all
other for uterine atony fail.
Synthetic oxytocin to be given cautiously
Hypersensitive peripheral vasculature.

62
What are the special considerations in the post
partum care of pre-eclamptic patients?
63
  • Continuous post partum monitoring
  • Continue MgSo4 for 24 hrs.
  • Eclamptics for 24 hrs after last post partum
    convulsion.
  • Continue antihypertensive agents.
  • Pain medications to safegaurd against
    convulsions.
  • Epidural narcotic (morphine) can provide
    sustained post operative analgesia.
  • Maintain i/v fluids.
  • Blood transfusion if excessive blood loss.
  • Comfortable quiet environment
  • O2

64
ICU management of PIH patient
  • Pts requiring admission in ICU
  • Severe Hypertension with neurological symp
  • Severe oliguria requiring dialysis
  • Rptd convulsions
  • DIC, HELLP,severe PPH
  • Cerebral Hmg edema
  • Intra abd. Catastropheliver ruopture hematoma
  • Pulmonary edema,CHF

65
Thank You
www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
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