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1. Role of the Anesthesiologist in management of PIHDr. C.K. DuaDir.Prof., & HeadDeptt. of AnaesthesiologyM.A.M.C. www.anaesthesia.co.inanaesthesia.co.in@gmail.com

2. What are the different types of Hypertension during pregnancy? • P.I.HPreeclampsia(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. Pregnancy > 20 weeks B.P. > 140/90mmHgat least twice > 6 hrs apart Systotic / Diastolic > 30/15mmHg M.A.P. >105mmHg or >20 mmHg above baseline. Wt gain >2.5 Kg./wk (1st sign of impending P.I.H.) Proteinuria >0.3gm/dNot essential for diagnosis(appears late) Non-dep.Odema (not a reliable sign). P.I.H. : Range of disorders collectively & formerly known as toxemias of pregnancy. Pre-eclampsia

5. EclampsiaConvulsions : 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 factorsAge, parity, Family h/o P.I.H.Partner related factorsPregnancy associated factors : Multiple pregnancies, congenital anomalies Antepartum urinary tract infectionExogenous 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/PAI–2 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 <1,50,000/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• BlindnessLiver • 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 > 0.3 gm/24hrs.Severe pre-eclampsia • B.P.  160/110 • Proteinuria  5 gm /24 hrs • S. Creatinine >1.6. • Oliguria < 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 < 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) BP>10mmHg Rise during and after placement of icepack on forehead for 3min • Roll over test >30mmHg Severe 20-29 mmHg Mild <20mmhg 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 daysRapid weight gain - > 8 Kg. In 3 wks.Generalised swelling - 2 daysVisual disturbances - 2 daysOn Examination :B.P. 166 / 114 mm HgGeneralised 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 treatmentDelivery 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 <170/110 & >130/90 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 occurSodium nitroprusside SNP 0.25 µg/kg/min. High dose of SNP;Cyanide 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 cerebralautoregulation 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 patient’s 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 < 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 (>100 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 arrestTreatment - 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 reflexEdemaAirway assessmentDetailed CVS & resp. examinationObstetric & 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?