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OBSTETRICAL EMERGENCIES

OBSTETRICAL EMERGENCIES. Moderator : Dr. Manoj Speaker : Dr. Sandhya. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. OBSTETRICAL EMERGENCIES. Obstetric hemorrhage Fetal compromise Special situations : PIH, pre-eclampsia, eclampsia , HELP syndrome. Difficult airway

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OBSTETRICAL EMERGENCIES

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  1. OBSTETRICAL EMERGENCIES Moderator : Dr. Manoj Speaker : Dr. Sandhya www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. OBSTETRICAL EMERGENCIES • Obstetric hemorrhage • Fetal compromise • Special situations : PIH, pre-eclampsia, eclampsia , HELP syndrome. • Difficult airway • Morbid obesity • Total spinal anesthesia • Maternal cardiac arrest

  3. 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

  4. What is P.I.H. & how will you differentiate between gestational hypertension, chronic hypertension pre-eclampsia & eclampsia?

  5. Pregnancy > 20 weeks Triad – HT , edema & proteinuria 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

  6. EclampsiaConvulsions : grand mal, appears before during or within 48 hrs. after delivery in patients who fulfill the criteria 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…….

  7. 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

  8. What is the etiology & pathogenesis of P.I.H.? Aetiology unknown • Immunological injury • uterplacental insufficiency Pathogenesis • Central component is maternal endothelial cell dysfunction

  9. 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

  10. What are the associated risk factors in patients with pre-eclampsia?

  11. 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.

  12. 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 .

  13. 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

  14. What are the systemic manifestations of pre-eclampsia?

  15. CVS • Systemic Hypertension • High cardiac output • SVR •  Circulating volume •  left ventricular work •  CVP •  or «=»PCWP •  Response to catecholamines & Angiotensin II. •  Circulating volume n vasoconstriction causing hemoconcentration • Poor co-relation b/w CVP & PCWP in severe cases • volume expansion LV overloading LVF

  16. Pulmonary edema –cardiogenic & noncardiogenic. • cardiogenic –impaired LVS or LVDS dysfuntion • Noncardiogenic -↑capillary permeablilty , iatrogenic fluid overload, imbalace bet C0P and hydrostatic pressure.

  17. Airway & Respiratory System Edema • 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 . Difficult Airway

  18. 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

  19. 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

  20. 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

  21. 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

  22. 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%)

  23. What is HELLP Syndrome? • Haemolysis, elevated liver enzymes(AST>70U/L) and low platelet count (<1 L/ mm3)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.

  24. Treatment –urgent delivery of fetus after correction of coagulation profile. CVP and urine output monitoring Blood glucose concentration monitoring(severe hypoglycemia may occur) Choice of anesthesia as per maternal n fetal status

  25. What are the markers for prediction, diagnosis and progression of the disease?

  26. 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

  27.  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…..

  28. 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

  29. What are the principles of management of 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 vol. expansion before Rx.Acute treatment :Hydralazine is most commonly used Rapid onset, short duration & direct vasodilator. It ↓MAP and SVR, ↑ CO & HR no effect on PCWP. 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;Venodilator. It ↓ MAP, PCWP & CI, no effect on CVP , SVR& HR . 10 µg/min i/v titrated to response. Risk of excessive hypotension –  UPBF High dose of NTG – Meth. Hb. may occurSodium nitroprussidePotent arteriolar dialtor SNP 0.5 to 5 µg/kg/min. High dose of SNP; fetalCyanide toxicity. Safely used-acute HT, pulm. Edema and heart failure.

  34. Labelatol ;better alternative, faster onset,relatively free of maternal side effects and has no adverse 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

  35. 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 , It prolongs the action of scoline due to inhibition of plasm pseudocholinesterase

  36. 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

  37. 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

  38. 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.

  39. 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

  40. 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

  41. - 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.

  42. 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, wideQRS 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. ?

  43. 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

  44. 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

  45. Role of Anesthesiologist in management of convulsions in the OT General management Specific management • MgSO4 • Thiopentone Sodium • Diazepam • Muscle relaxants

  46. What is the role of Anesthesiologist in the labor room for vaginal delivery? • Labor analgesia(↓es maternal oxygen requirement n prevents maternal hyperventilation ass. with painful contraction) • ↓es circulating catecholamines levels may entirely blunt the hemodynamic n neuroendocrine response to pain • Appears to protect against eclampsia

  47. Important considerations Selection of local anesthetic(bupivacaine 0.0625%,0.125%, 0.25%) with fentanyl 25mcg Use of epinephrine – generally not advisable as in case of intravascular catheter placement will further↑ BP & can even cause MI. Although most anesthetics are now added with 1:400,000 epinehrine, adverse circulatory effect s have not been reported. Use of test Dose-controversial Thrombocytopenia • Control of convulsions • Airway management

  48. Anesthetic management for LSCS

  49. Continous lumbar epidural is the technique of choice for CS 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?

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