LSCS is taken, patient shouldbe kept nil per orally (NPO)Methods to increase gastricpHl H 2receptor antagonists likeRanitidine at night and in themorningl Atropine/ glycopyrrolatepremedication is controversialas it decreases oesophagealsphincter tone thusnegative the effect ofmetoclopromidel Sodium citrate orally 30 to 45min preoperativelyFactors that decrease LOSPressure (increased risk ofregurgitation)l Thiopentone, inhalationagents, anticholinergicsl Stomach tube for emptyingthe stomachl Apomorphine to inducevomiting (to reduce gastricvolume)Increase LOS pressure barrierl Metoclopramidel Antacidsl Ranitidinel NeostigmineAnesthesia technique –precaution and carel Timely decision for LSCSl Treat all parturients as fullstomachl Prefer SAB/ epidural block.Avoid GA.l Aspiration prophylaxis in alll Remove gastric tube / Rylestube at induction of anesthesia.l Patient positioning (slighthead up – decreased regurgitation)l Skilled assistance should beavailablel Adequate and appropriateequipment. Proper trolleypreparationl Use of correct cricoid Pressure/ Sellick’s maneuverl Avoid high pressures & volumesfor IPPV before intubationl Familiarize one self with thefailed intubation drilll Care at intubation/ extubationRecommendationsl Withhold oral feeds duringlaborl Regional anesthesia as far aspossiblel Take measures to decreasegastric volume & increase pHl GA by competent anesthetist,with full appreciation of aspirationriskl Well equipped delivery roomsfor administration of safeanesthesiaRapid sequence / Crashinduction of GAAdvantage – decreases risk ofregurgitation & aspirationTechniquel Patient lying supine, in neutralposition, on OT table(parallel to floor)l Pre oxygenation for 3 to 5min, normal tidal breathsl Check for application ofSellick’s maneuverl Precalculated dose of Thiopentone(5-7mg/Kg)l Assistant places thumb & fingeron Cricoid cartilagel Apply Cricoid pressure afterloss of eyelash reflexl Succinyl choline 2mg/Kg IVl Continue oxygen by maskl No Nitrous oxidel No IPPVl Direct laryngoscopy at 1 minafter suxamethonium chloride.Intubate with 7.0 ETTl Once ET in situ, inflate thecuffl Reconnect circuit and ventilatel Release cricoid pressurel Auscultate for equal air entrySellick’s maneuverl Occludes cervical esophagusbetween cricoid cartilage &cervical vertebrael Pressure applied = 40 Newtonforce (100 cm H 2O or 74mm Hg)l Check for pressure to be applied(without discomfort topatient) preoperativelyl Apply pressure with thumb &index fingerl Remove only once ET in situl Double handed modificationl Disadvantage – 50% decreasein LESPAmniotic Fluid Embolism(AFE)-AFE was first reportedby Meyer in 1926. It is the mostdangerous untreatable conditionwith mortality of 80-100%. Itleads to sudden death in theperipartum period (failure to diagnosethe cause & 25% deathsoccur within 1 hour of onset ofsymptoms). It is also termed as“obstetric shock”. Its incidence14Journal of Postgraduate Medical Education, Training & ResearchVol. II, No. 5, September-October 2007
is I: 8,000- 1: 80,000 and contributesto 10% of all maternaldeaths. Average volume of amnioticfluid increases from 50 mlat 12 weeks to 1000 ml at 38weeks of gestation. After this itdecreases. It is hypotonic and isdiluted with fetal urine. The damageto the lungs is irreversiblebecause of the contents of theamniotic fluid.Components of amniotic fluidl p H 6.9 – 7.15l Biochemical mediators – surfactant,endothelin,leukotrienes C4 & D4, IL-1,TNF-a, thromboxane A2,prostaglandin E1, E2, F1a,F2a, arachidonic acid, thromboplastin,collagen and tissuefactor 3, phospholipase A2,PF3.l Electrolytes- Na, K, Mg, Ca,Fe, PO 4, Cl, S, Mn, Znl Nitrogenous products -amino acids, urea, uric acid,creatinine, proteinsl Others–glucose, vitamins,enzymes, steroids, hormones,lipidsl Suspended particles- lanugohair, vernix caseosa, fetalsquames, meconium, fetal gutmucin, trophoblastsAmniotic fluid enters the maternalcirculation through a tear inthe amniotic membranes (spontaneous/manual rupture ofmembranes), or when uterinevessels are abnormally open (placentaaccreta, rupture uterus, placentaabruptio, LSCS, retainedplacenta, trauma from intra uterinemanipulation or instrumentation,uterine or cervical tears).During uterine contractions, apressure gradient develops whichdrives the amniotic fluid intomaternal circulation & to thelungs, causing chemical andphysical damage, anaphylactoidreaction and multi system involvement.Patients at riskl Elderly, multipara, Multiplepregnancyl Commoner with male fetusl Polyhydramniosl Artificial rupture of membranes(ARM), use of oxytocics,tumultuous laborl First trimester curettage abortionsl Second trimester abortionsusing saline, glucose, prostaglandins,urea, hysterotomyl Abdominal trauma, amniocentesisl Placental rupture, Intra uterinedeathl During LSCSl Any time during pregnancy,labor, post delivery - with noobvious causeClinical featuresl No prodromal symptoms (fever,chills, rigor, abdominalpain)l Time course of presentationand symptoms are highly variablel Usual presentation-suddenonset of dyspnea, hypotension,cardio respiratory arrestl Classic triad–hypoxia, hemodynamiccollapse &coagulopathy with no obviouscausel Cyanosis, pallor, altered neurologicalstate, coma- mayoccur in a fewl Grand mal seizures- 10-20%casesl Coagulopathy- DIC, thrombocytopenia-40% cases (decreasedplatelet counts, decreasedfibrinogen, increasedFDP, prolonged PTT & PT)l In 15% cases bleeding fromvagina, stitch line, IV and epiduralcannulae sites, mouthand gumsl Auscultation- bilateralwheeze and crepitationsl In those who survive the initialinsult- non cardiogenicpulmonary edema and renalfailure, multi organ failureoccurs (TEE- RV failure,bulging of interatrial & interventricularseptums fromright to left, severe TR, pericardialeffusion, LV failure)l Increased PCWP, decreasedLVSWI, decreased SVR, increasedPAP, PVR increasedl Signs and symptoms underGA - hypotension, decreasedSpO 2and EtCO 2, arrhythmias,pulmonary vascularspasm & edema, increasedoozing from operative sitel Chest radiography- no findingsor pleura effusion, cardiomegaly,pulmonary edemaPathophysiologyPathogenesis of the disease inAFE is due to –Anaphylacticreaction;Pulmonary vascularreaction;Alveolar membranereaction;Cardiac dysfunction;Coagulation failureAnaphylactic reaction-Fetalcontents of amniotic fluidproduce a reaction similar toanaphylactic shock. Symptomsare not due to histamine (absentJournal of Postgraduate Medical Education, Training & Research15
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