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![Management of Massive Haemorrhage
• Preparation
– Identify patients at risk
– Large bore IV access x 3
– Blood available [Type specific; O neg]
– Avoid caval obstruction; supplemental O2
– Foetal monitoring, change indicative of massive
bleed
• Search for evidence of DIC
- Peripheral blood smear
- PT, PTT, Platelet counts, Fibrinogen level; D-dimer
level
- ? Specific factor analyses
- Bedside coagulation testing (TEG)](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-62-2048.jpg)
![*Immediate aggressive volume replacement
*Crystalloid until blood available [warming+]
*Consider PRBC once blood loss > 2,000mL
*Anticipate need early
*Unmatched type specific or Type O blood available if
required
*Dilutional coagulopathy once >80% of blood volume replaced
*Platelets - if < 20,000/mm3 or higher if bleeding persisting
*FFP only to correct measured clotting abnormalities
*Cryoprecipitate
Volume Replacement](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-63-2048.jpg)
![*Uterine atony
* Uterine Massage; Oxytocin
* Ergometrine [post delivery]; Prostaglandins [Intra-Endometrial]
* U/S to detect retained products
*Surgical exploration to repair lacerations, ligate arteries, perform hysterectomy
*Angiography
* Selective embolization of Uterine, internal iliac or internal pudendal artery with slowly
absorbable gelatin sponge
*Consider prophylactic placement of embolectomy catheters in internal iliac
arteries of patients at high PPH risk.
*Factor VIIa
* Rescue therapy in severe haemorrhage
Specific Therapies](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-64-2048.jpg)
![IV Antihypertensives
*Nicardipine
* Onset action 10mins; duration 4 – 6hrs
* Initial infusion 5mg/hr; increase by 2.5mg/hr every 5min; max 10mg/hr
* Potential for NM blockade interaction with Magnesium
*Nitroglycerin
* Titrate to MAP
* Less effective in severe Hypertension
* b Blockers
* Atenolol [IUGR]
* Esmolol [Foetal Bradycardia]](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-75-2048.jpg)
![Severe Pre-Eclampsia
*Cardiorespiratory
* Diastolic dysfunction; LV Failure; Pulmonary Oedema
* Increased alveolar-capillary permeability; ALI/ARDS
* SBP generally ≥150mmHg; DPB ≥ 110
*Renal
* Glomeruloendotheliosis [Proteinuria >5g/d];
* Oliguria; Renal Impairment
*Hepatic
* Epigastric Pain; ↑Bilirubin; ↑Transaminases
* Subcapsular Haematomas; Hepatic Lacerations
*Neurologic
* Headaches; Visual Disturbances; Focal neurologic deficits
* Hyperreflexia ± Clonus; Cerebral Oedema; CNS irritability ± Seizures
*Haematologic
* Thrombocytopenia; DIC; Haemolysis](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-78-2048.jpg)
![Management of severe Preeclampsia
*Early diagnosis; close monitoring; aggressive BP control
*Indication for immediate delivery [curative in most cases]
*Evidence of cerebral irritability may herald imminent onset of Seizures
*Magnesium
* Questionable value in mild Preeclampsia
* Associated with improved maternal outcome in severe Preeclampsia
*Steroids
* ? Role for high-dose steroid regimen (dexamethasone 10 mg 12-hourly)](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-80-2048.jpg)
![Venous Thromboembolism
* Pregnancy and puerperium a hypercoagulable state
* Incidence
* Clinically symptomatic venous TE in 1-2 per 1000 pregnancies
* 3 times more common in Postpartum period
Risk Factors
* Maternal age [>40yrs]
* Ethnic and genetic factors
* Caesarean section [3 – 16 times increased risk]
Clinical signs
Investigations
* ABG, ECG
* D-Dimers less useful
* Radiographic testing [V/Q scan; CT-PA]
* Require less than the 5 rads associated with teratogenesis
Begin therapy immediately if high index of suspicion
* Heparin [Fractionated or Unfractionated] versus Warfarin
* APTT 2 – 2.5; Anti-Factor Xa 0.6 – 1.1; INR 2.5 – 3
* Continue therapy for 6 – 8 weeks post delivery](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-94-2048.jpg)
![Amniotic Fluid Embolism
* Catastrophic complication
* 1 case per 8,000-30,000 pregnancies in US
* amniotic fluid, fetal cells, hair, or other debris enter maternal circulation
* Usually occurs in Labour; Trauma; Abortion
* possible anaphylactic reaction to fetal antigens
* Clinical Features
* Severe respiratory distress; ALI/ARDS
* Cardivascular collapse
* DIC – may be major clinical manifestation
* Treatment is supportive
* Emergent C/S in unresponsive Cardiac Arrest [5min CPR]
* Outcome
* Mortality 60 to 80%
* Most survivors have permanent neurologic impairment.
* Neonatal survival is 70%.
* No evidence increased AFE risk in future pregnancies.](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-95-2048.jpg)
![Epidemiology
*Most common non-obstetric cause of Maternal Death
*46% of deaths among pregnant women in one US series
*57% homicides; 9% suicides; 21% RTA’s
*Patterns and mechanisms of injury same as in nongravid patients
*Causes of Maternal Death from Trauma
*Head Injury
*Haemorrhage
*Causes of Foetal death from Trauma
*Placental abruption [shear forces]
*Head injury [Pelvic fracture]
*Compromised Uteroplacental Circulation](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-97-2048.jpg)
![Management Principles - I
*Optimal management of Mother is best for Foetus
*Initial assessment and resuscitation should follow standard protocols
*U/S; FAST(Focussed assessment with sonography with trauma); DPL(Diagnostic
peritoneal lavage)
*Targeted Radiographic studies
*Uterine shielding where possible
*Highest foetal risk at 8 – 15/40
*Exposure less than 1RAD low risk
*Plain x-ray 0.2 RAD; CT 0.5RAD per slice
*Avoid supine Hypotension Syndrome [Left Lateral tilt]
*Foetal monitoring and Obstetric consultation once foetus potentially viable](https://image.slidesharecdn.com/obsanaesthesia-170904022321/75/Obs-anaesthesia-98-2048.jpg)
Uploaded byManu Gupta
Obs anaesthesia
This document discusses maternal mortality rates globally and the leading causes of pregnancy-related deaths. It notes that 99% of maternal deaths occur in developing countries, where rates are over 400 deaths per 100,000 live births compared to less than 15 deaths in developed countries. The leading specific causes of death are embolism, hypertensive disorders, haemorrhage, infection, and anesthesia complications. Effective strategies to reduce mortality include increasing the use of neuraxial anesthesia techniques and improving airway management skills.
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Obs anaesthesia
- 1. Moderator - Dr.Vatsala Aggarwal Presenter – Dr. Shalini Patidar *
- 2. * Global Maternal MortalityRates(MMR)- 400/100,000 live births Significant inequality between developed and developing countries with 99% maternal deaths in developing countries. MMR in developed country <15/100,000 live births.
- 3.
- 4. ●Although anaesthesia hasbecome the 7th cause of pregnancy related mortality , the predisposing factors are similar Inexperienced anaesthesia personnel Airway problems lack of appropriate monitoring lack of resuscitation equipment ●Maternal mortality can be reduced by increasing the use of neuraxial anaesthesia improving airway management skills Simulation of anaesthesia techniques for education purpose
- 5. * *Overview of maternalphysiology *Anesthesia concerns in the parturient-recent changes in clinical practice *Management of complicated pregnancies *Regional anesthesia in PIH *Use of supraglottic airway devices in obstetric patient. *CPR in pregnant patients
- 6. * Almost all thechanges seen are due to high levels of progesterone and include: *35% Total Blood Volume * heart rate 15 beats/min *40% CO *30% SV *15% SVR *500ml/min blood flow to uterus * venous return from legs *AORTOCAVAL COMPRESSION (mechanical)
- 7. * *Patients with pre-existingcardiac disease may decompensate either during labor or immediately post delivery. This corresponds to the time of maximal CO *Approx. 400 – 600ml blood loss occurs at delivery *Supine hypotensive syndrome
- 8.
- 9. * * oxygen consumption~ 20% (100% in labor) due to increased metabolic rate * minute ventilation ~ 50% (due to increased tidal volume) * arterial pCO2 * FRC causing a decrease in oxygen reserves
- 10. * *Uptake of inhalationalagents is faster *Decreased FRC and increased oxygen consumption increase the risk of hypoxia with apnea *Preoxygenation prior to GA less effective
- 11. * *Venous engorgement ofairway mucosa *Edema of airway mucosa *Worsening of Mallampati score in labor
- 12. * *Trauma to upperairway with suctioning, intubation *Increased incidence of difficult/failed intubation x10 *Require smaller ETT
- 13. * *Decrease in MACby 25 – 40% *Decreased dose of Local Anesthetic requirement for regional techniques *More rapid onset of neural blockade
- 14. * *Decreased inhalation anestheticagent requirements *Decreased dose of local anesthetic for same effect *Increased risk of local anesthetic toxicity
- 15. * *Increased gastric fluidvolume *Increased gastric fluid acidity *Decreased competency of lower esophageal sphincter
- 16. * *Increased risk ofaspiration *All parturients are “full stomach” *Aspiration prophylaxis recommended for C/S i.e. *0.3M Sodium citrate 30 mls po *Ranitidine 50mg iv *Metoclopramide 10mg iv
- 17. * *Where is thepain coming from? *Is pain bad in labor? *Analgesic options
- 18. * Nociceptive pathways involved T10 – L1during labour plus S2-S4 for delivery
- 19. * ●Psychological stress cancause: -increased levels of catecholamines -hyperventilation These may result in decreased uterine blood flow leading to hypoxia and acidosis in the fetus
- 20. * *Mental preparation *Family support *Medicalsupport *Cultural expectations *Underlying mental status *Parity *Size and presentation of the fetus *Maternal pelvic anatomy *Duration of labor *Medications
- 21.
- 22. * *Breathing exercises *Autohypnosis *Acupuncture * Music *Massage/walking *TENS *Water bath
- 23. * *Nitronox: 50:50 mixtureof oxygen and nitrous oxide *Low dose desflurane(0.2%),enflurane, Isoflurane(0.2-0.25%),Sevoflurane(0.8%) in oxygen Advantages: on demand delivery, relatively safe Disadvantages: variable efficacy, nausea, drowsiness, loss of airway reflexes and unconciousness with volatile analgesics .
- 24. * *Narcotics: meperidine, morphine,fentanyl Advantages: relatively good analgesia Disadvantages: nausea, vomiting, sedation, neonatal depression (max. 2 hours after meperidine dose), short duration of action.
- 25. * *Epidural, spinal, combinedspinal-epidural Advantages: excellent pain control, minimal impact on progress of labor with low doses, less drug transfer to fetus, improved uterine blood flow, decrease in birth trauma e.g. use of forceps, minimal neonatal depression Disadvantages: invasive technique, side effects (hypotension, headache, itching, nausea, urinary retention, limited mobility), nerve damage, infection
- 26. * *General considerations ofthe parturient undergoing surgery *Obstetric surgery
- 27. * *Altered physiology asmentioned *Risks to the fetus: *Effect of the disease process/therapies *Possible teratogenicity of anesthetic agents *Intraoperative effects on uteroplacental blood flow *Increased risk of preterm labor/ risk of abortion
- 28. * *Altered physiology *Altered responseto anesthesia *Decrease in MAC *Increased sensitivity to neuraxial agents *Decreased plasma cholinesterase *Decreased protein binding (more free drug) *Limited drug information in parturients
- 29. * *Teratogenicity: *Limited information dueto impracticality of conducting trials with sufficient power *Guidelines based on a) effects on reproduction in animals; b) epidemiological surveys of OR personnel; c) studies of pregnancy outcomes in parturient undergoing ante partum surgery
- 30. *Nitrous oxide hasbeen shown to have a teratogenic effect in rats during the first trimester *No anesthetic agent is a proven teratogen in humans *Anesthetic agents deemed safe include: thiopental,morphine, meperidine,fentanyl, succinylcholine, NDMRs *Limiting nitrous oxide use but only if hypotension secondary to volatiles can be avoided
- 31. Avoidance of hypoxemia Avoidanceof hypotension Avoidance of acidosis Maintain PaCO2 in the normal range for the parturient Minimize effects of aortocaval compression *
- 32. * *The rate ofcesarean delivery has increased(4.5% in 1965 to 31.1% in 2006) * One of the most common surgical procedure *As more patients become high risk, anaesthetic challenges also Increase Despite increasing complexity including obesity, congenital heart disease and other chronic diseases,anaesthesia related maternal mortality has decreased over the past 50 years from 36 per 100,000 Caesarean deliveries to one per 100,000 cesarean deliveries.
- 33. The current levelof safety of cesarean delivery has been achieved * Dynamic changes in the training and practice of obstetric anaesthesia * Use of High-fidelity simulators *Widespread use of neuraxial anaesthesia
- 34. * * Preparation *Preventing complications *Choiceof Anesthetic technique *Effects on the fetus
- 35. * *Premeds: antacid (sodiumcitrate) *IV access and fluid bolus within 30 minutes of operating (avoid glucose containing fluids) *Left lateral tilt with wedge under right pelvis *Routine Monitors: ECG, NIBP, pulse oximeter, fetal monitoring *Additional monitors for GAs: ETCO2, nerve stimulator, temp probe
- 36. * *Aspiration prophylaxis *Detailed airwayassessment *Fluid resuscitation/left lateral tilt to prevent hypotension *Safe practice for placement of neuraxial blocks
- 37. * *Local infiltration bysurgeon *Regional anesthesia: spinal, epidural, combined spinal-epidural *General anesthesia
- 38. * *Rarely performed *Patient usuallyin extremis *Surgery must be done via midline incision, gentle retraction, no exteriorization of the uterus *Usually done to supplement a regional technique if local anesthetic toxicity not a concern
- 39.
- 40. * These include withdrawalof *0.75% bupivacaine from obstetrics, * widespread use of test doses, * fractionation of epidural injection *the use of dilute solutions by continuous infusion.
- 41. * Simple to perform Rapidonset Single shot technique Profound neural block Technique of choice for uncomplicated elective caesarean sections and in many emergency caesarean sections
- 42. * *Potential Complications: *Hypotension *Headache (rare~1:100) *Backache (temporary ~24hrs) *Nausea/vomiting (secondary to BP, narcotics) *Neurological damage (very rare) *Anaphylaxis (very rare)
- 43. *Incidence of Hypotensionafter spinal anaesthesia for Caesarean section - 80% (without prophylactic management) *Preventive measures include fluid preload, lateral tilt, and use of vasopressors.
- 44. * *Ephedrine has been recommended. *Potential complications -supraventricular tachycardia, -tachyphylaxis -fetal acidosis. Equivalent dose of ephedrine and phenylephrine in the prevention of post-spinal hypotension in Caesarean section: S. Saravanan1, M. Kocarev2,* R. C. Wilson2, E. Watkins2, M. O. Columb3 and G. Lyons2 Oxford Journals, Medicine, BJA, Volume 96, Issue 1, Pp. 95- 99) *Phenylephrine - better fetal acid–base status -similar efficacy in blood pressure control Potential complications -bradycardia -serial dilution for i.v. administration is a source of error. phenylephrine is more potent than ephedrine by a factor of 80 for equivalent maternal blood pressure control
- 45. * *More technically challenging *Sloweronset *Used when already placed for labor analgesia *Useful in parturient where a slow, controlled onset of block is needed *Allows prolongation of block should surgery be complicated
- 46. * Potential Complications: *Hypotension *Headache (approx1:100) *Transientbackache~24hrs *Urinary retention *Unintentional spinal injection *Intravascular injection of local anesthetic *Neurological damage *Infection
- 47. * *Used when requirethe speed and density of a spinal anesthetic with the flexibility of prolonging the block by supplemental increments of local anesthesia via the epidural catheter *Complications: as mentioned for spinals and epidurals *However, high block with delay in recognizing and treating its cardiorespiratory consequences, as well as lack of appropriate resuscitation equipment and drugs continue to result In maternal injury.
- 48. * *Used when *Patient refusesregional technique *Regional technique is contraindicated *Emergency C/S when there is inadequate/absent regional analgesia and to delay will cause undue risk to the fetus / mother
- 49. * *Complications: *Failed intubation *Failed ventilationcausing death or neurological injury *Awareness *Aspiration pneumonia
- 50. * *Avoid hypotension, hypoxia,acidosis, hyperventilation *Limit time between uterine incision and delivery to less than 3 minutes *Infants exposed to GA have lower Apgar at one minute but no difference at 5 mins *No significant alteration in neurobehavioral scores with regional techniques
- 51. * *Supraglottic airway devices- laryngeal mask airway (LMA) & LMA Proseal-TM have been used successfully in obstetric patients undergoing GA. * LMA Proseal-TM incorporates a second tube intended to permit continuity with the gastrointestinal tract and isolation from the airway, minimizing gastric insufflations during positive-pressure ventilation. *The LMA Proseal-TM has been used successfully as a rescue device during failed rapid sequence induction in obstetric patients and has been incorporated in the obstetric difficult airway algorithm .
- 53. * *A prospective cohortstudy involving 1,067obstetric patients concluded that the LMA is effective and probably safe in most elective caesarean deliveries. SAFE use of SGD requires *Proper Patient selection *Proper airway assessment, *Adequate fasting *Non-obese parturients. *An anaesthetist with proficient regular use of LMA. Effective airway was obtained in 99% of the parturients and only seven parturients required intubation. There were no reported episodes of aspiration, gastric insufflations, hypoxia, layrngospasm or bronchospasm.
- 54.
- 55. * Focus onMaternal ‘driven’ emergencies *Need to consider 2 patients rather than 1 *Role of Physiologic Alterations of Pregnancy *Impact of pathologic conditions related to Pregnancy *Delivery of the Foetus may abrogate pregnancy induced conditions *Outcome *Generally Good…. *Obstetric ‘disasters’ every anaesthetists nightmare! Key Points
- 56. * *Maternal Age <15 & > 35. *Parity Factors - 5 or more - great risk. PP hemorrhage if new pregnancy within 3 months *Medical-Surgical Hx - hx of previous uterine surgery &/or uterine rupture, DM, cardiac dis, lupus, HTN, PIH, HELLP, DIC etc.
- 57. *Obstetric Haemorrhage *Hypertension/ Pre-Eclampsia *Embolism *Sepsise.g. Chorioamnionitis *Trauma Common complicated Obstetric Emergencies
- 58. *Obstetric Haemorrhage *Hypertension/ Pre-Eclampsia *Embolism *Sepsis *Trauma Commoncomplicated Obstetric Emergencies
- 59. *Leading cause ofmaternal death worldwide *2 – 55% of deliveries complicated by PPH *Regional variation marked *Characteristically massive and swift *Blood flow to uterus late pregnancy 10% of CO *Haemorrhage may be concealed *Usual signs of hypovolaemia late or disguised Size of the Problem
- 60. *Late Pregnancy *Placenta Praevia *PlacentalAbruption *Spontaneous uterine rupture *DIC e.g. due to Amniotic Fluid Embolism *Trauma *Postpartum *Uterine Atony *Surgical Trauma *Retained Placenta *DIC Causes
- 61. *Incidence 0.1% ofPregnancies *Causes *Placental Abruption *HELLP syndrome *Intra-uterine Foetal Death *Acute fatty Liver of Pregnancy *Amniotic Fluid Embolism *Clinical Features * Oozing from IV or skin puncture sites, mucosal surfaces, surgical site *Dramatic decrease in Fibrinogen level Disseminated Intravascular Coagulation
- 62. Management of MassiveHaemorrhage • Preparation – Identify patients at risk – Large bore IV access x 3 – Blood available [Type specific; O neg] – Avoid caval obstruction; supplemental O2 – Foetal monitoring, change indicative of massive bleed • Search for evidence of DIC - Peripheral blood smear - PT, PTT, Platelet counts, Fibrinogen level; D-dimer level - ? Specific factor analyses - Bedside coagulation testing (TEG)
- 63. *Immediate aggressive volumereplacement *Crystalloid until blood available [warming+] *Consider PRBC once blood loss > 2,000mL *Anticipate need early *Unmatched type specific or Type O blood available if required *Dilutional coagulopathy once >80% of blood volume replaced *Platelets - if < 20,000/mm3 or higher if bleeding persisting *FFP only to correct measured clotting abnormalities *Cryoprecipitate Volume Replacement
- 64. *Uterine atony * UterineMassage; Oxytocin * Ergometrine [post delivery]; Prostaglandins [Intra-Endometrial] * U/S to detect retained products *Surgical exploration to repair lacerations, ligate arteries, perform hysterectomy *Angiography * Selective embolization of Uterine, internal iliac or internal pudendal artery with slowly absorbable gelatin sponge *Consider prophylactic placement of embolectomy catheters in internal iliac arteries of patients at high PPH risk. *Factor VIIa * Rescue therapy in severe haemorrhage Specific Therapies
- 65. *Obstetric Haemorrhage *Hypertension/ Pre-Eclampsia *Embolism *Sepsise.g. Chorioamnionitis *Trauma Maternal Obstetric Emergencies
- 66. * •Most common medicalproblem encountered during pregnancy •8% of pregnancies •4 categories: *Chronic Hypertension *Pregnancy Induced hypertension *Preeclampsia-eclampsia *Preeclampsia superimposed on chronic HTN *Hypertensive disorder in pregnancy may cause an increase in maternal and fetal morbidity and remains a leading source of maternal mortality*
- 67. * Pregnancy InducedHypertension * (Gestational Hypertension without Proteinuria) * After 20th gestational week; Longterm risk * Essential Hypertension * Before 20/40; Persists after delivery * Secondary Hypertension * consider if SPB consistently > 200mmHg * Primary Hyperaldosteronism * Cushings Syndrome * Phaeochromocytoma * Renal Artery Stenosis * Coarctation of Aorta * Pre-Eclampsia * Gestational Hypertension with Proteinuria Differential Diagnosis
- 68. *Perinatal mortality increasedif severe sustained Maternal BP elevation * Outcome effect in less severe hypertension less clear * Intra-Uterine Growth Retardation * Caution: Effects on uteroplacental perfusion * Increased maternal mortality and end organ damage *Treatment recommended if SBP ≥ 160mmHg of DBP ≥ 110mmHg * Treat lower BP’s if patient symptomatic *Treatment Options * PO: -methyldopa and Labetalol * IV: Labetalol, Hydralazine, Sodium Nitroprusside Treatment Recommendations
- 69.
- 70. Clinical Features *SBP generally≥ 150mmHg; DPB ≥ 110 with *Hypertensive Encephalopathy *Confusion; Papilloedema; Retinal Haemorrhages *Other end-organ dysfunction e.g. Nephropathy, Neuropathy, Retinopathy *Uteroplacental hyperperfusion, placental abruption, haemorrhage *Maternal Catastrophe e.g. Intracranial Haemorrhage *Severe Maternal Hypertension *SBP ≥ 240mmHg; DPB ≥ 140 *ICU management irrespective of presence of clinical sequelae
- 71. Clinical Features *SBP generally≥ 150mmHg; DPB ≥ 110 with *Hypertensive Encephalopathy *Confusion; Papilloedema; Retinal Haemorrhages *Other end-organ dysfunction e.g. Nephropathy, Neuropathy, Retinopathy *Uteroplacental hyperperfusion, placental abruption, haemorrhage *Maternal Catastrophe e.g. Intracranial Haemorrhage *Severe Maternal Hypertension *SBP ≥ 240mmHg; DPB ≥ 140 *ICU management irrespective of presence of clinical sequelae
- 72. Investigation and Management *Investigations *Bloodsincl U+E, Coagulation, CBC, LFT’s *Toxicology *Urinalysis *ECG, CXR; CT Brain *Monitoring *Maternal non-invasive monitoring *Foetal telemetry post viability threshold *Arterial Line + CVC *Treatment Goal *To reduce DBP to just below 100mmHg
- 73. Therapeutic Strategies –Oral * Labetalol PO *Dose 200-400mg BID -methyldopa *BID/TID to max 4g/d *ACEI’s and AT II Blockers *C/I antepartum *Nifedipine *Rapid effect; increases CI; Uteroplacental flow *10mg capsule PO, repeat every 15 – 30mins to max 30mg
- 74. IV Antihypertensives *Labetalol * Rapidlydecreases BP (5 mins) but not at expense of Uteroplacental blood flow; no effect foetal HR * Decreases SVR and slows maternal HR *Hydralazine * Direct arterial vasodilator (preferred by Obstetricians) * Care as onset action 10-20 mins; lasts approx 8 hrs * 5 – 10mg boluses every 15-30mins until BP controlled *Na Nitroprusside * Potent, rapid, arterial and venous vasodilator * IV infusion 0.25-0.5mg/Kg/min; max 4mg/Kg/min * S/E’s: Headache, dizziness, flushing, ototoxicity, cyanide toxicity * Foetal Cyanide toxicity not a major issue
- 75. IV Antihypertensives *Nicardipine * Onsetaction 10mins; duration 4 – 6hrs * Initial infusion 5mg/hr; increase by 2.5mg/hr every 5min; max 10mg/hr * Potential for NM blockade interaction with Magnesium *Nitroglycerin * Titrate to MAP * Less effective in severe Hypertension * b Blockers * Atenolol [IUGR] * Esmolol [Foetal Bradycardia]
- 76. Pre-Eclampsia *Incidence *7% of pregnanciesin the US *Generally after 32nd week of gestation *May initially present after delivery as the HELLP syndrome *Primigravida versus older multiparous *Pathogenesis *Multi-system disease *Endothelial cell injury *Placental toxin release *Genetic and immunologic factors *Generalised vasospasm; ?PG/TX imbalance *Microthrombi *Classic Clinical Triad
- 77. * •New onset HTN •After20 weeks of gestation, or •Early post-partum, previously normotensive •Resolves within 48 hrs postpartum •With the following (Renal or other systemic) • Proteinuria > 300 mg/24hr • Oliguria or Serum-plasma creatinine ratio > 0.09 mmol/L • Headaches with hyperreflexia, eclampsia, clonus or visual disturbances • ↑ LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right abdominal pain • Thrombocytopenia, ↑ LDH, hemolysis, DIC •10% in primigravida •20-25% with history of chronic HTN
- 78. Severe Pre-Eclampsia *Cardiorespiratory * Diastolicdysfunction; LV Failure; Pulmonary Oedema * Increased alveolar-capillary permeability; ALI/ARDS * SBP generally ≥150mmHg; DPB ≥ 110 *Renal * Glomeruloendotheliosis [Proteinuria >5g/d]; * Oliguria; Renal Impairment *Hepatic * Epigastric Pain; ↑Bilirubin; ↑Transaminases * Subcapsular Haematomas; Hepatic Lacerations *Neurologic * Headaches; Visual Disturbances; Focal neurologic deficits * Hyperreflexia ± Clonus; Cerebral Oedema; CNS irritability ± Seizures *Haematologic * Thrombocytopenia; DIC; Haemolysis
- 79. * Mild Severe Systolic arterialpressure 140 mm Hg – 160 mm Hg ≥160 mm Hg Diastolic arterial pressure 90 mm Hg – 110 mm Hg ≥110 mm Hg Urinary protein <5 g/24 hr Dipstick +or 2 + ≥5 g/24 hr Dipstick 3+or 4+ Urine output >500 mL/24 hr ≤500 mL/24 hr Headache No Yes Visual disturbances No Yes Epigastric pain No Yes
- 80. Management of severePreeclampsia *Early diagnosis; close monitoring; aggressive BP control *Indication for immediate delivery [curative in most cases] *Evidence of cerebral irritability may herald imminent onset of Seizures *Magnesium * Questionable value in mild Preeclampsia * Associated with improved maternal outcome in severe Preeclampsia *Steroids * ? Role for high-dose steroid regimen (dexamethasone 10 mg 12-hourly)
- 81.
- 82. * *One of themost important advantages of labor epidural analgesia is that it provides a route for rapid initiation of anesthesia for emergency C/S. *In the past there were concerns re: use of regional anesthesia for C/S in preeclamptics *possibility of severe BP secondary to sympathectomy in patient with volume contraction *risk of pulmonary edema due to excessive fluid administration with regional block *risk with use of pressor agents to treat BP
- 83. * *Epidural anesthesia wouldprobably be preferred by many anesthesiologists in a severely preeclamptic pt in a non-urgent setting *For urgent cases it is reassuring to know that spinal is also safe *This allows us to avoid general anesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension
- 84. * *Prior to placingregional block in a preeclamptic it is recommended to check the platelet count. *No concrete evidence at to the lowest safe platelet count for regional anesthesia in preeclampsia *Any clinical evidence of DIC would contraindicate regional *In the absence of such signs, most anesthesiologists would proceed at plt count >100K, many would proceed at 80- 100K, <80K some would proceed (esp. spinal)
- 85. * *When placing aregional block in a patient with a platelet count < 100K, the most important thing is to monitor resolution of block closely *Bleeding time has been discredited as an indicator of epidural bleeding risk and is not indicated. Channing-Rogers, Semin Thromb Hemost 1990;16:;1-30 *Low-dose aspirin is not a contraindication to regional anesthesia in preeclampsia * CLASP study: 1422 women on aspirin received epidurals without any bleeding complications
- 86. * *Airway edema iscommon *Mandatory to reexamine the airway soon before induction *Edema may appear or worsen at any time during the course of disease *tongue & facial, as well as laryngeal *Laryngoscopy and intubation may severe BP *Labetolol & NTG are commonly used acutely *Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine may be given to blunt response
- 87. * *Magnesium sulfate potentiatesdepolarizing & non-depolarizing muscle relaxants *Pre-curarization is not indicated. *Initial dose of succinylcholine is not reduced. *Neuromuscular blockade should be monitored & reversal confirmed.
- 88. * *Usually reserved forpatients with complications *oliguria unresponsive to modest fluid challenge (500 cc LR X 2) *pulmonary edema *refractory hypertension *may have increased CO or increased SVR *Poor correlation between CVP and PCWP in PIH *However, at most centers anesthesiologists would begin with CVP & follow trend *not arbitrarily hydrate to a certain number *If poor response, change to PA catheter
- 89. HELLP(can progress toDIC) * A severe variant of the preeclamptic spectrum of diseases * 0.3% of deliveries * 30% post partum * Syndrome may develop without substantial BP changes * Clinical Features and Diagnosis * Microangiopathic Haemolytic anaemia (H) * Consumptive coagulopathy * Elevated Liver enzymes (EL); Low Platelets (LP) * Presenting Symptoms * Usually non-specific * 20% present with epigastric/RUQ pain, nausea + vomiting * Complications * Acute renal failure; nephrogenic DI * ALI/ARDS * Haemorrhage incl Liver lacerations, subcapsular haematoma * Hypoglycaemia; Hyponatremia * Outcome * Maternal mortality up to 24% in some series * Perinatal mortality 8 – 60%
- 90. Coma / Seizures *Neurologicinvolvement in 50% of critically ill obstetric patients *Coma * GCS score independent predictor of maternal mortality * Diverse aetiology including Vascular, Infective, Metabolic, Intracranial Mass lesions, Toxic, Preeclampia *Seizures * Commonest cause pre-existing Epilepsy * Presence of hypertension increases likelihood of Preeclampsia * Fulminant Hepatic Failure due to acute fatty liver of Pregnancy *Eclampsia * Seizures or coma in presence of Preeclampsia or gestational hypertension * Potentially lethal phase * 50 –75% have occipital/frontal headaches * 20-30% visual symptoms * Cerebral oedema
- 91. Coma / SeizureManagement *Management * A, B, C * Left lateral position * Increase uterine blood flow * Minimize aspiration risk *Initial Seizure control * Lorazepam / Diazepam * IV MgSO4 *Prevention of recurrent seizures * MgSO4 superior to Phenytoin or diazepam * Initial dose 4 – 6g, plus infusion of 2g/hr * Mg levels after 6hrs (therapeutic level 4 – 8mEq/L) * Check for patellar reflexes; muscle weakness; arrythmias (Ca gluconate) * BP Control
- 92. * *Preeclampsia is aserious multi-organ system disorder of pregnancy that continues to defy our complete understanding. *It is characterized by global endothelial cell dysfunction. *The cause remains unknown. *There is no effective prophylaxis.
- 93. *Obstetric Haemorrhage *Hypertension/ Pre-Eclampsia *Thrombosis/Embolism *Sepsise.g. Chorioamnionitis *Trauma Maternal Obstetric Emergencies
- 94. Venous Thromboembolism * Pregnancyand puerperium a hypercoagulable state * Incidence * Clinically symptomatic venous TE in 1-2 per 1000 pregnancies * 3 times more common in Postpartum period Risk Factors * Maternal age [>40yrs] * Ethnic and genetic factors * Caesarean section [3 – 16 times increased risk] Clinical signs Investigations * ABG, ECG * D-Dimers less useful * Radiographic testing [V/Q scan; CT-PA] * Require less than the 5 rads associated with teratogenesis Begin therapy immediately if high index of suspicion * Heparin [Fractionated or Unfractionated] versus Warfarin * APTT 2 – 2.5; Anti-Factor Xa 0.6 – 1.1; INR 2.5 – 3 * Continue therapy for 6 – 8 weeks post delivery
- 95. Amniotic Fluid Embolism *Catastrophic complication * 1 case per 8,000-30,000 pregnancies in US * amniotic fluid, fetal cells, hair, or other debris enter maternal circulation * Usually occurs in Labour; Trauma; Abortion * possible anaphylactic reaction to fetal antigens * Clinical Features * Severe respiratory distress; ALI/ARDS * Cardivascular collapse * DIC – may be major clinical manifestation * Treatment is supportive * Emergent C/S in unresponsive Cardiac Arrest [5min CPR] * Outcome * Mortality 60 to 80% * Most survivors have permanent neurologic impairment. * Neonatal survival is 70%. * No evidence increased AFE risk in future pregnancies.
- 96. *Obstetric Haemorrhage *Hypertension/ Pre-Eclampsia *Embolism *Sepsise.g. Chorioamnionitis *Trauma Maternal Obstetric Emergencies
- 97. Epidemiology *Most common non-obstetriccause of Maternal Death *46% of deaths among pregnant women in one US series *57% homicides; 9% suicides; 21% RTA’s *Patterns and mechanisms of injury same as in nongravid patients *Causes of Maternal Death from Trauma *Head Injury *Haemorrhage *Causes of Foetal death from Trauma *Placental abruption [shear forces] *Head injury [Pelvic fracture] *Compromised Uteroplacental Circulation
- 98. Management Principles -I *Optimal management of Mother is best for Foetus *Initial assessment and resuscitation should follow standard protocols *U/S; FAST(Focussed assessment with sonography with trauma); DPL(Diagnostic peritoneal lavage) *Targeted Radiographic studies *Uterine shielding where possible *Highest foetal risk at 8 – 15/40 *Exposure less than 1RAD low risk *Plain x-ray 0.2 RAD; CT 0.5RAD per slice *Avoid supine Hypotension Syndrome [Left Lateral tilt] *Foetal monitoring and Obstetric consultation once foetus potentially viable
- 99. Specific Pregnancy Complicationsduring trauma * Foetomaternal Haemorrhage * 1 in 4 gravid Trauma pts * Kleihauer test * Abruptio Placentae * Amniotic Fluid Embolism * Premature Labour * Uterine rupture * Foetal Demise * Cardiac Arrest * Standard algorithms initially+ CPR * Consider open cardiac massage * Caesarean section
- 100.
- 101. GOALS 1. To understandand perform basic and advance life support in pregnant patients 2. Understand the adaptations of CPR 3. Understand the importance of early defibrillation when appropriate 4. Understand the need to perform perimortem cesarean section
- 102. *ANATOMICALAND PHYSIOLOGICAL CHANGES IN PREGNANCY CARDIOVASCULARSYSTEM Uteroplacental blood flow Maternal blood volume Arterial pressure Cardiac output Increases 30 – 45% 20th week of gestation Maternal heart rate increases 10- 15 beats/min SBP and DBP First two trimesters – decreases by 10 – 15 mm hg Returns to baseline by term
- 103. Supine pregnant patient Graviduterine pressure Compression of IVC Decreased venous return Decreased cardiac output – 10 – 30%
- 104. Poor venous flow Compromises infradiaphragmatic i.vsites Femoral / saphenous routes Not recommended for i.v access During resuscitation
- 105. *RESPIRATORY SYSTEM Increased Tidal Volume Progesterone stimulated hyperventilation Increasedminute ventilation Chronic respiratory alkalosis Decreased Functional Residual Capacity – 20% Rapid decrease in arterial oxygen content during arrest Right side shift of oxyhemoglobin curve during arrest state Maintain maternal PO2 of >60 mm hg in arrest state
- 106. Delayed Gastric emptying inpregnancy (progesterone like effects of placental hormones) Increased acidity of stomach contents cardiac sphincter relaxation causes regurgitation of stomach contents Increased chance of aspiration and vomiting *GASTO-INTESTINAL SYSTEM
- 107. *AIRWAY AND VENTILATION CONSIDERATION IN PREGNANCY Decreasedtolerance for hypoxia and apnoea Tongue, mucosa, supraglottic edema & friability Difficult mask ventilation • Low FRC • Elevated diaphragm • Raised intra-abdominal pressure Mallampatti class 3 airway Weight gain & obesity • Increased neck folds • Foreshortened neck Increased risk of aspiration • Increased gastric emptying time • Decreased lower esophageal sphincter tone
- 108. * Key Interventions toPrevent Arrest * Place the patient in the full left-lateral position to relieve possible compression of the inferior vena cava. Uterine obstruction of venous return can produce hypotension and may precipitate arrest in the critically ill patient. * Give 100% oxygen. * Establish intravenous (IV) access above the diaphragm.
- 109. Assess forhypotension : maternal hypotension that warrants therapy has been defined as a systolic blood pressure 100 mm Hg or 80% of baseline. Maternal hypotension can result in reduced placental perfusion. In the patient who is not in arrest, both crystalloid and colloid solutions have been shown to increase preload. Consider reversible causes of critical illness and treat conditions that may contribute to clinical deterioration as early as possible.
- 110. *Resuscitation of thePregnant Patient in Cardiac Arrest MODIFICATIONS OF CARDIOPULMONARY RESUSCITATION Patient Positioning Important strategy to improve the quality of CPR and resultant compression force and output. The pregnant uterus especially of >20 weeks gestation or gravid uterus palpated above the umbilicus, compresses the inferior vena cava, impeding venous return and thereby reducing stroke volume and cardiac output. In non cardiac arrest parturients left-lateral tilt results in improved maternal hemodynamics of blood pressure, cardiac output, and stroke volume and improved fetal parameters of oxygenation, nonstress test, and fetal heart rate.
- 111. Left lateral tilt- 30 degrees using wedge (hard) of predetermined angle. Eg. Cardiff wedge Manual left uterine displacement, with the patient in supine, also relieves aortocaval compression .
- 112. Left uterinedisplacement - patient’s left side with the 2- handed technique The patient’s right side with the 1-handed technique , depending on the positioning of the resuscitation team. If chest compressions remain inadequate after lateral uterine displacement or left-lateral tilt, immediate emergency cesarean section should be considered.
- 113. *AIRWAY and BREATHING Active airway management is the initial consideration. Airway management is more difficult during pregnancy Secure airway early in resuscitation OPTIMAL use of bag-mask ventilation and suctioning, while preparing for advanced airway placement should be done Use small endotracheal tubes, short laryngoscope handles Use an ETT 0.5 to 1 mm smaller in internal diameter than that used for a nonpregnant woman of similar size because the airway may be narrowed from edema Give 100 % oxygen and mainatain good saturation
- 114. *CIRCULATION Chest compressionsshould be performed slightly higher on the sternum than normally recommended to adjust for the elevation of the diaphragm and abdominal contents caused by the gravid uterus. Position is slightly above the centre of the sternum Current recommended drug dosages for use in resuscitation of adults can also be used in resuscitation of the pregnant patient in cardiac arrest.
- 115. *DEFIBRILLATION *Management of ventriculararrhythmias require defibrillation during maternal resuscitation. *There should be no delay if use of defibrillation is indicated *Energy levels are same as ACLS protocol *Before delivering the shock, REMOVE FETAL MONITORING EQUIPMENTS to prevent electrocution injury to patient or rescuer
- 116. *Pregnancy-Related Causes ofMaternal Cardiopulmonary Arrest B- Bleeding(haemorrhage)/ DIC E- Embolism/coronary/pulmonary/amniotic fluid embolism A- anesthetic complications U- Uterine atony C- Cardiac diseases/MI/Ischemia/aortic dissection/cardiomyopathy H- Hypertension / Preclampsia/ Eclampsia O- Others / Diff. Diag of standard ACLS guidelines i.e 5H’s and 5T’s P- Placenta previa/ Abruptio placenta S- Sepsis
- 117. *Reversible Causes Electrolyte abnormalities Tamponade Hypothermia HypovolemiaHypoxia Hypomagnesemia Myocardial infarction Pulmonary embolism Tension pneumothorax
- 118. *Haemorrage *Case of placentaprevia/ abruptio placenta, where bleeding is significant *Fluid resuscitation with RL/ NS *Vasopressor agent - Inj. Ephedrine (5mg every 5 mins till response is seen) , if fluids fail to restore adequate blood pressure.
- 119. *EMBOLISM Pulmonary embolism • Thromboembolicdisease risk increased • Hypoxic/ hemodynamic unstable • Anticoagulation with heparin – currently the treatment of choice • Also , adequate oxygenation and treating hypotension • Elevated D-dimer not a helpful screen in pregnancy • CT scan or VP scan to confirm diagnosis on treatment is stated. • Use of thrombolytics reserved when potential benefits outweighs the risks, emergencies beyond 20 wks gestation, postpartum period Amniotic fluid embolism • Dyspnoea, hypotension associated with pt. is labour/ abortion • Sudden onset breathlessness, air hunger, decreased oxygen saturtion • Develop cardiac arrest within minutes • DIC • Multi- organ failure • Treatment tried : cardiopulmonary bypass, open pulmonary artery thromboembolectomy.
- 120. *Anesthetic complication *Bupivacaine inducedarrythmia – amiodarone is the primary drugin the ACLS arrythmia algorithm. *Early administration of lipid emulsification (20% intralipid) – used in resuscitation of bupivacaine- induced cardiotoxicity. ( lipid rescue therapy : picard J . Anesthesia 2009)
- 121. *Cardiac Disease Themost common causes of maternal death from cardiac disease are myocardial infarction, followed by aortic dissection. Women deferring pregnancy to older ages, increases the chance of having atherosclerotic heart disease. Fibrinolytics is relative contraindication in pregnancy PCI(percutaneous coronary intervention)/coronary angioplasty is the reperfusion strategy of choice for ST-elevation myocardial infarction. illnesses related to congenital heart disease and pulmonary hypertension are the third most common cause of maternal cardiac deaths.
- 122. *Preeclampsia/Eclampsia Preeclampsia/eclampsia develops afterthe 20th week of gestation and can produce severe hypertension and ultimately diffuse organ-system failure. Magnesium sulphate If untreated, maternal and fetal morbidity and mortality results.
- 123. *Magnesium Sulfate Toxicity Magnesium toxicity present with ECG interval changes: (prolonged PR, QRS and QT intervals) at magnesium levels of 2.5–5 mmol/L AV nodal conduction block, bradycardia, hypotension and cardiac arrest at levels of 6–10 mmol/L. Neurological effects : loss of tendon reflexes, sedation, severe muscular weakness, and respiratory depression are seen at levels of 4–5 mmol/L.
- 124. Others include:gastrointestinal symptoms (nausea and vomiting), skin changes (flushing), and electrolyte/ fluid abnormalities (hypophosphatemia, hyperosmolar dehydration). Patients with renal failure and metabolic derangements can develop toxicity after relatively lower magnesium doses. Iatrogenic overdose is possible in the pregnant woman who receives magnesium sulfate, particularly if the woman becomes oliguric. Administration of calcium gluconate (10 ml of a 10% solution) is the treatment of choice Empiric calcium administration may be lifesaving
- 125. Trauma and drugoverdose *Pregnant women are not exempt from the accidents & mental illnesses *Domestic violence also increases during pregnancy; homicide & suicide are one of the causes of mortality during pregnancy
- 126. *Emergency Cesarean Section inCardiac Arrest *Delivery of the foetus is a part of resuscitation process when applicable. *Despite appropriate modifications – mechanical effect of gravid uterus – decreases venous return from IVC – obstructs blood flow through abd. aorta – decreases thoracic compliance – unsuccessful CPR – increased risk of hypoxia going in for anoxia to mother and foetus BEYOND 4 MINUTES OF ARREST.
- 127. *Why Perform anEmergency Cesarean Section in Cardiac Arrest? Emergency cesarean section in maternal cardiac arrest indicate a return of spontaneous circulation or improvement in maternal hemodynamic status only after the uterus has been emptied. Recent studies indicates ROSC(return of spontaneous circulation) and maternal hemodynamic stability of the mother and normal neurological outcome of the neonate post perimortem casarean. The critical point to remember is that both mother and infant may die if the provider cannot restore blood flow to the mother’s heart.
- 128. *Decision Making forEmergency Cesarean Delivery Gestational age less than 20 weeks Need not be considered because this size gravid uterus is unlikely to significantly compromise maternal cardiac output Gestational age approximately 20 to 23 weeks Perform to enable successful resuscitation of the mother, not the survival of the delivered infant, which is unlikely at this gestational age Gestational age greater than 24 weeks Perform to save the life of both the mother & infant
- 129. *The Importance ofTiming With Emergency Cesarean Section When the maternal prognosis is grave and resuscitative efforts appear futile, moving straight to an emergency cesarean section may be appropriate, especially if the fetus is viable. If emergency cesarean section cannot be performed by the 5-minute mark, it may be advisable to prepare to evacuate the uterus while the resuscitation continues.
- 130. The following canincrease the infant’s survival: Short interval between the mother’s arrest & the infant’s delivery Perimortem caesarean section to be performed within 4 mins of cardiac arrest and delivery of the foetus within 5 mins. No sustained pre arrest hypoxia in the mother Minimal or no signs of fetal distress before the mother’s cardiac arrest Aggressive & effective resuscitative efforts for the mother Delivery to be performed in a medical center with easy access to NICU.
- 131. *Post–Cardiac Arrest Care Post–cardiac arrest hypothermia can be used safely and effectively in early pregnancy without emergency cesarean section (with fetal heart monitoring), with favorable maternal and fetal outcome after a term delivery. No cases in the literature have reported the use of therapeutic hypothermia with perimortem cesarean section. Therapeutic hypothermia may be considered on an individual basis after cardiac arrest in a comatose pregnant patient based on current recommendations for the nonpregnant patient During therapeutic hypothermia of the pregnant patient, it is recommended that the fetus be continuously monitored for bradycardia as a potential complication, and obstetric and neonatal consultation should be sought
- 133. * *Despite recommendations inthe two most recent Confidential Enquiries into Maternal and Child Health (CEMACH) reports, and improvements in patient care using early warning scoring systems (EWS) in the general adult population, no validated system currently exists for the obstetric population. The survey results support CEMACH recommendations for a nationally agreed obstetric EWS. International Journal of Obstetric Anesthesia Volume 18, Issue 3, July 2009, Pages 253–257A national survey of obstetric early warning systems in the United Kingdom R.D.J. Swantona, S. Al-Rawib,M.Y.K. Weea
- 134. * *Assessment and optimisationof the patient during pre- anaesthetic evaluation,robust referral systems,allowing senior staff to refer high risk parturients to senior on call anaesthetists are pre-emptive strategies to avoid requirement of a HDU/ICU admission. *MEWS includes measurement of urine output,deviation of blood pressure,heart rate,oxygen saturation,respiratory rate,temperature and level of consciousness.If threshold score exceeds,it triggers an immediate call for senior consultant and other measures.
- 135. *Pregnancy is nota disease state! *Obstetric emergencies not infrequent *May be associated with serious morbidity *Potential for conflict in regard to Mother vs Foetus overstated *Physiologic Alterations of Pregnancy may play role *Early recognition and decisive intervention Paramount *Need for close cooperation with Obstetric Team *Multi-disciplinary Effort required, incorporating *Anaesthesia Team *Obstetric team *Nurses and Doctors *Outcome *Depends on specific Problem *Generally good when recognised early and managed appropriately Summary
- 136. *REFERENCES *MILLERS ANAESTHESIA 7thEDITION *CURRENT STATUS OF OBSTETRIC ANAESTHESIA: IMPROVING SATISFACTION AND SAFETY-IJA 2009 *ANAESTHESIA FOR LSCS:CHANGING PERSPECTIVES-IJA 2010 *OBSTETRICS ANAESTHESIA:WIDENING HORIZONS-IJA 2010 *COURTESY : UPDATE JUNE 2012 LITERATURE REVIEW *AHA : CIRCULATION 2010 – CARDIAC ARREST IN PREGNANCY *TINTINALLI 7TH EDITION
- 137.