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Eating and drinking in labor
EATING AND DRINKING IN LABOR A Literature Review
Leslie M. Ludka,
CNM, MSN.
Thepdy of nothing ty mouth (NF0) in labor has become a well-&ahlished routine in many hospitals throughout the United States. The NFJOp&y is a curlolls phenomenon because it is based largely on anewddalltanfomMtiandhasnotbeen supported by research data. Many researchers are now auesUonln~ the practice of mutine f&gin lab& (l5). This Hterahtre review wiIl dixuss
&hktodcdbmisdwfood
and drink during !&or, maternal mort&y statistics, risk factors for anesthesia-related complications. the mvth of the enmtv stomach. antacids.
stwss
related to fcad and fluid dep: rivation, and current research and cUnical implications.
HISTORICAL OVERVIEW Until the 194Os, paiutient women in the United States were encouraged
and Catherine C. Roberts,
CNM,
to eat and drink as a means of malntining their stamkm for the work of labor and delivery. Dr. Joseph DeLee (6) warned that food must be encouraged throughout labor to avoid general A. delayed labor, and serious p&p&urn hemonhage. By the mid-1940s. however, the practice as cUnlcaUy unsound. and it was tirtuaUyabandoned.Thechangecanbe traced to obstebtc aw.thesiolc@ts’ fear of matemal matalky due to ilspit&ion of stomach contents In the 194Os, Mend&m (7). an obskttkian from Com-ell, hypothesized that postanesthetic pneumonia was caused not so!& bv infected ma-
terial but amtrated
rather by stokuh
cwtenti
into the Iunax He believed gasIlk timewas delayed in labor. Mendehon noted that it was not uncommon for a &entto vomit food ingested 2448 hours ~rovmushr(7). He reviewed charts of ;14,016 pqlnandes from 1932-1945 and found that aspkati of stomach contents into the lungs occurred in 0.15% (N = 66). In 1945, Mendel-
thi
emptying
MSN
conducted a seriesof expelmenk that examkted the dfeck of
so”
thattv-mwn-he
pmhihited f&n eatkw and minkirm dutiw bbcx. He be-
cqxmted into anesthesia practice. In addition. skilled anesthetistswere quite rare. Often, the administration of gases was left in the hands of the most member of the anesthetic team. These factorsledtoanestheaiarelated cases of aspiration pneumcnia in the parhxfect. Expanding on Mendelson’s research, further studies on aspiratton pnaumon!afolmdlwokeyfactolstbat predicted an increased risk of maternal mortality and morbidity: the combination of an amirate with a volume of 25 mL or more and--the more lethal factor-a oH lass than 2.5 f8121. The dini& manifestationa‘of pulmonary aspiration. which is now commonly referred to as “Mendelson’s syndrome, ‘I includes intense bronchwpasm. pulmonic congas&m, and exudate pwxk~ction (131. In 1956, Parker (14) undertook a skdytodetermhewhytkrehadbean no maternal deaths while using ganeral anesthesia at home. In Birmingham, England, 100,CKIO births took place in the home behwen 1943 and 1952. During that period, 3,048 farhops delivedas ware completed with no deaths from aspiration pneumonia.TbaseoFeralilJedwara done under gewral anesthesia with an open face mask. The women at home were commonly hamassad down in the litbotomy position and given anesthesiawith no reported fa-
junior
CathedneC. Robed receiwd her B.SN from the Universityof Rhode blond and her M.S.N. and CJ”.M. ,mm We UnluersltySchwl of Nursing.She 19cwendy h &in&al pmtice m N&h Centml Bmnx Hmphl, Nrru York City.
MO
klities At the same time, in the Bw-
that failure to secure a patent akway
mingham Maternity Hospital, 2,200 operative deliveries were performed with four maternal deaths due to aspiration. Speculation was that the fLw&ba&machkleklthehc6pitalwas less safe than the opan mask. Recommendations included that focal anesthesiabe used for simple fordeHvay, and if general an&-&a had to be used, it should be provided by an experienced anesttattst using a cuffed endohacheal tube.
was the prtmay cause of anesthesiarelated maternal deaths. There were no deaths related to ragtonal anastbesia 118). Out of 15 deaths (0.82 per 100,CKX live b+rths),one was k&ad as having bean from aspiration of stomach contents. A study done in New York City from 1981-1983 revealed the matemal mmiality ratio to be 36.1 deaths par 100,WO Uve births (19). Ai,estbesia-related deaths ranked as the third cause,with 13 cases111%). Four ware associated with legally induced aborttons and ono with ectopic prag nancy. There was no specific breakdown for the cause of ihe remaining eight anesthesia-related cases. A recent study by Rooks and colleagues (20) looked at freestanding birth centers, with regard to different varlablas. They revlewd cases from 11,814 women who ate and drank at will. There was no rrported mortal&y or morbidity from aspiration pneuraontaavan~th0awerowomen who required emergency cesarean sectiona Twenty-two parcent of !tw2 had eatan solid foods, yet they had no asplraiion complicatbns.
MATERNAL
MmTALrw
Fasting in labor is believed by many members of the medical communiiy to reduce the risk of maternal marbtdlty and mortality by reducing stomach contents, thereby elimkmtingpr&utsforpulmonaryaspiratkm (7, 11, 13, 15). Howwar. detailed analysts of overaU matemal moxt&y atatiatjcsin the United States reveals inadequate and tncons&tentmethods of c&&g, c&g&zing, and raporting information. Unlike England, where the spa& cause of the maternal death ia repwted, here in the United States aspiration pneumonia is grouped under the broad eatogoty of “compfkxttons of the admlnistmnon of w&h&c or other aedatknl in labm/delivay.” It is one of four subgroups related to the obstetdc anesthetic P&Jam (16, 17). In 1950, the incidence of maternal deathSwaS83per1OLWOlhret4thS. In 1960, itwar37.1 par100,ocniiva biis. The latest *Ii&a for OvaraIl maternal mcftality h 1988 is 8.4 per 1OLWLKllive bhths, which is a statiswlllysisni&antiMBade fmmddper 1cKwciu live births in 1987. In 1989, 320 women died, for a maternal martat@ tate of 7.9 per loo,wo uvabll?hs (161. Matemal mortaiitv IS a rare cccunence. Maternal da&s robted to anesthesia do MCW but it is impassible to pinpoint the exact nature of the comp&a~on. A more data&ad st;ldy, done in Mtchtt from 1972-1984, showed
Joumal of Name.M!dwikry
RISK FACTORS FOR ANESTHESlA.RElATED COMPUCATIONS Fatled Iatubation The ocNmmca of asptratton is directly related to difficult lntabattan during general ane&esia regard&a of the patient’s oral intake Expected ra:as of IntubaUon failure an! rap.xted asonefailureoutGievaIy300caaas raquldng ganeml anesthetics.Difficult intubatfon was a key factor in approximately one-half of the anasthe&-related deaths reported by the ConfidenUal Enquky 1976-1978 (21). Endkr and coworkers (18) specufate that a high rate of failed intubatlon resultsfrom the increaslng numbar of cesoreansecttons.,many of which are done with general aneathesta.
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Vol. 38. No. 4. Juh+Aaa1~41993
In order to avoid failed intubation, experts agree that conect anesthetic care for general anesthesia should be undertaken This includes preopemthw assessment, rapid and safe induction, awake extubation. and postoperative monitoring. The interval from safe inductton of general anesthesia to complete control of the airway by cuffed endotracheal inhlbation presents the greatest risk for aspiration and death (‘2.2). Cricotd prwure. when properly applied by a trained aaistanf has proven to be a safe, reliable method of preventing aspiration during induction of general anesthesia (22-24). Repeated attempts at intubation should be abandoned, because they are rarely suecessful(21-24). Inadequate Abdominal
Anticipation Deliveries
of
Proper asxssment and pleparation of the obstetric patient by anesthesia pascnlnel is hnpemave for the preventin of an&he& problems. This axssment might bean antenatally with the pdmaw prwida notifying the anesthe#st ihat a pardcular pat&M is at high ti for abdomtnai delivery (23-25). It has been suggested that anesth&kgists should mutinelygoonroundsto-~~tential dtfftculttes in the event of abdominal delivery with general anesthesia. A clinical histoy, focusing on signs and and layngea~edema a&&ted with preecfanpsia, is crucial in the care of the otstebtc patient (23.25).
Substandard
Management
There is considerable agreement among experts In anesthesiology that substandard manwtement of anesthe& care isa primary cause of pulmalalv asdlatkxl17. 11. 14.22-W.
regain
patientto cmsctousness and then proceeding -Mb an awake intub&ion or adminbkatton of a re@XMI b&k. If there is an emergency, then general anesthesia with a mask and cricoid pressure sharld be employed. A cricothyroidotomy is used as a last resort (18, 21).
Emergency Cesawzm Secttons and Regional Anesthesia The need for seneml anesthesia in an emergency shim has been pstimated to mnae from 3.5% to 13% (25, 34). In their prospective observation sbldy of 360 comecutive patients deiiverau by emergency cesarcan section. Morgan et al (25, 34) found that 87% of the cesarean set6ms m&l have been addpIed and that general ane3thesta was only needed in 13% of the s&jects. Conklin (35) states that t&as there is an absolute contraindtcation, a re@onal block for cesaean section Is appropdate in most emergency situations. He rasons that, in this way, the partudent can protect her ow atway hum p+Ikmay e5pirdiion (35). Ma& et al i35) l-me clearly shown tbat newbum outcomesalter an emrgency cesarean section were better when re&nal anesthesia was us& Haste is a weU-known factor in crttkal awsthetic inctdents, and it is the parhnient’swell-beingthat shouldbethe first W”cem, tQcause fetal disiTe% is som&mes misdia@cwd (18,21,25, 33,37). Many authors concede that reyional a&_ has little effect on sasti emptykw f14,30,32,3&40). Crawford (39). an En&h physittan who has researched the topic of PO_ tential aspiration in labor, stated that “a matha undergoing a comfortable bbor, with the aid of an optdural analgesi4 da25 wekome refreshment, and alI other things b&q equal, we offer her a lemon sorb& or a cup of tea and a slice of toast Roberts and Shirley (32) state that regional
_”
,lotJmal
of w
.
vol. 38. No. 4. July/Ausust 1993
THEMYIHOFTHEEMPlY STOMACH GasttcEmpty&~
Physioltqy
GasIlk emptyklg isgclwmed mainly bytwfactols l)thevolumoofgasmC contents, and 2) the influence of chzmical and physkxl properties of chymeintbeduc&umandjejunum (411. l-be rate of emptying depends ontbevoklmeoftke~osma~ presswe, and chemical propertier. Gasacemptyingis~testreatestandfajtest at the bqinning of digestion. when the vdume of the stomach ccatents is~~~krgestF~tiStb~mosipavedUl chemical agent In the d&&d diet that SkwJs sastdc motiltty (41. 42). Gastric motility is adversely affected by massive sympatbe& discharges such as pan, nawea, and emotional d&ubances 143). Heavy exerdse does not impede emp&&gof liquids; theyareemptiedaknostlmdMeiy. Solkis, on the other hand. must be !asthan1mmindtameterto~ throl&the~c~Lm~ canrematntntb2stomachaskxgas nine hours. continuing to sttmu!ate g&Tic SecMion (41).
EfkctofGesIathandLabolcm
-Emptyins Gasklc emptying ttmein
the hbaing wmanvariesaccGfdtngtokldivtdual reports. Acc.xdtng to Anerthesia @r Obstehics (151, aspkaLtoIl risk facton r&ted to d&yea g&k emptying include &aialai age rpeater than 34 weeks, labor, be&bum (which is indicaaw of gaoaqlhageal refw, &ess, narcoti, andsedatives. Other studies show a decrw& WC emptytng time in labor, but the d&y was r&ted to the adminisfmtion of w,rcottm and sedattves (10.40.44, 455). Acco1dklg to obst&ic anestbest& qisis, it is the @c contents that
201
Tayfor et al MS) lnwsttgated the pH and volume of gastric contents in anesthesia115). Asstated, the routine p&y of NPO in labor was initited in the hop?. of decreasing or eliiirating stomach contents thereby lmkg httlo or nothing to asptrate. Yet, studies have repeatedly shown thatthaefsnosuchth@asanemp+ stomach,qardksscdthetimeofthe last meal 110, 44, 46-49). Labwing wanen who have taken nothing orally have been found to secretewayins amounts of Mstric iukes containhydnaak-4 withdangem& low pH values (32,471. Fasting does notetbnMestcmachcontenk,ttwlly inwases the concentration of hydrcchbrk add (501. Therefore. dqivin&e mother of foodand fltidurii labor may achmliy fraease the risk of maternal mortalitu and mabldity fromacid aspiratio;. Hkshetmer et al’s (511 serial x-m” studies alter a bat& ihI show& that there was no cawkmt or charadnIstic alteration of ga5It.z evacuation in prk-dgmvidas dudng labor. Changes that did occur were atbibukdtofunctkmalandneummuscular rather than mechanical causes. How aer, raJlson et at (52) concluded, based on gas& fluids that were aipirated from a nasaf gastxk tube insertedearly in labor, that gasbic emptying time was defayed in labor. Each patWent had 750 ml inserted into the stomach; at 1Omtnute. intewafs, the stomach contents were aspirated and assessed.They found that each patient had rapid emptying over the first 10 minutes and then the volume decreased by aknost one-third. They ackncwledged thd the depressanteffect on gastrfcmobility might be due to anxiety and excitement Simpson and Stakes (43) looked at gashic emptying in rektkm to anxfely levels in patients undergoing
ins
-g!J=Jww~.Tluqr fowdthatgaicempvia$skw? in patknts who had ralow predispodti to awkty. Patknk with a tendency toward high anxiety did not show a delay in gasbic emptying.
the pH. They found that the volume of gastriccontents varied markedly. They concluded that every pa&dent should be assumed to have a full stomach of hifhly acid ffutd contents. Hester and Heath (53) noted that 32% of patknk who had been NPO fvrp&ngalp&dshadgfeaterthan 40 mL of gastdc contents. Over half of them had a gastdc aspkate of less thon pfi 2.5. A&dyLyR&edsandShkfq(11) showed that the lntewal since the last meal to delivery did not guarantee a low valume of gasmc juice in the stomach. They concluded that all patients should be assumed to have a fullstomach, regardlessofthe interal since their last oral intake. ANTACIDS
Asdted&,
t&&k&s study (7) wport~ that anesthesia deaths were duetohydmch!odcaddaqir&mand not to neutral aspirates. In an &xl to make the stomach contents less acidic, antaads (30 mL) have mutin+ teen adminirtered. Particulate antactds such as magnesium hydmxide and megnedum tdsflkxte were gtveven at w but they have r!aw been shown to cause sevew pufmonaty damage when aspirated (22,54,.55). Cohen’sstudy (54) shaved that there is no evidence that edmfnieattcm of
Today, sodium &ate. which contains “0 parikufate matter, is often wed for rapid neuwtion of the stomach contents. It has an tmmedtate onset of antacid action, but it also has a wide variation in offtcan, and duration of action. sodium citmkn&,&es&dimmediakk,,but the cdlical factor that its duration of act&n is the gastric emp rates(56). Therefore. analgesics that prolong gashic emptying also pfolong the antacid’s efficiency. or-
influences
tying
doumd of Nune.Mklw&y
nwzano et al (56) found that sodium cl&ate was not always efftcient in increasing gastric pH to greater than 2.5, especially by the time of extw bation. They demonstrated that effervescent cimeiidine-sodium cltiate k effecthrein Increasing gastdc pH to more than 2.5 at intubation and extubation. Cimitidtne. which is an HZreceptor blmker, increasesgasmc pH by inhibiting gastric acid production for four to eight hours However, It must be noted that the volume (30 mL) of antacld wed is above that crftkalwlumepedictiveofkxraeddsk of maternal mortality should aspkation ocC”I:
FASlffVG. NUTRITION. ENERGY UllLfZATlON
AND
The hydration and energy needs of the woman in labor have been compared to the needs of the athlok in competition (4). Food and fluid dwdvaKon dudng this cdtical time n&y impact directly on labor progrw and outcome. Bid glucoseand muscle glyco9en, major sources of enemy for the mother and the fetus, are&xnpmm&d in the pregnant woman during Mng. Animal studies have shown that there is an immedtate and conffnuous decline In makmal and fetal blood gk~case levels during fasting (57). A direct relaUonshii has hen found between matemal glucose few els and fetal well-being as tndkated by fetal breathing movemenk and general fetal activity (58,591. Fetuses of fasted mothers show less overall activity than fetuses of fed mothers. Stimukting ktal activity dudng fetal nonstress tests Is often accomplished by feeding the mothers (59). When blood gkxose is not available to the mother for energy use, tbe body draws on ik fat supplies. As Q raft!ageqllantilje3ofr~~tiy& are oxidfzed, ultimately increadng the quantiites of ketone In the blood and tissues.Thii accumufatin of ketone (p-hydmxybutydc add, amlnwcetk acid) in the body Is known as k&c&.
*
Vol. 38. No. 4, :ufyAuawt
1993
Excessive production of ketone may lead to their excretion in the urine, referred to as ketonuda. Ketosis may progress to ketoacidosis, which is a” accumulation of ketone in the body, accompanied by a metabolk xldtis. Ketoecidosis can be life threatening. However, ketonuria and ketmis are not the sane as ketoaddosis. It is uncertain whether either k&c& 01 ketonuM is actually harmful to the pregMnt or laboring wcnnen 01 her fetus. Ketosls wcurs in the normal adult human body in response to exeriio” and fasting, both of which may be experienced by the labming woman. Pregnant women in general are more prone to ketosts due to increased fetal demands, increased fat uiilttiio”, and pregnancy-induced hormone changes (4, 601. Studies have shown that preg“anqeqgelatesa”dacceIela~the body’s resq~nse to fasang (61. 62). During delivery. blood levels of ketone, free fatty acids, and gtycerol fise to meet energy doman&. Ketone bodtes and free fatty acids stgnifica& illcrease in the blood after only 12 to 18 houm of f&ng in the third mmeskr (63). A.xwa”g to I-!ale (4). “I” laba this tendency toward ketosts ls accentuated by imxased muscu!ar actltity and imposed ltmitation of oral intake.” It is tnteresttng to note that the amcunt of ketone in the blood of mothers who conswned fcod during tabor has been shown to be sig”tficantiy t&w that of fasted mothers (64.65). Ketonuria may be a misleading guidotothe”eedfortlutda”dcarbohydratere$xwM~KetoMlh~ bfze” shown to cccur in nomlal !&or as we!l as in the normal antqutum @lent (59. 60, 63, 66). It is often determined by a ketosiix, which has been shown to report a hiih falsep&tive reading when the blood acetoaeetato level h wttht” “0”“al range (67). Keton-e t&es, when excreted in the wine. take lag+ ~uantiaes oi sodium and patesstun with them, whtch may decrease the blood PH. The”? dws seem to be some reta-
Jcemal d Nume.MldwUery.
tionship between marked ketonuria and prokqed !&xx, but whkh comes first is unclear (601. Some researchers date that as ketone bodies increase in the mother. they cross the placental barrier and increase in the fetus WI. 65. 681. others disagree, Ileef&y adds and ketone &dies do not readily cm55 the placenta (69). Glucose is the minciwl fuel of the fetus, but the r&cat iiterature supportsthet&fthatketonebGdks”ny save es alternative fuel during fetal life (70, 71). Animal studtes have shown ketone bulks 19 be precursors to lipid synthesis. as well as fuel for the fetal brain. liver, and lung in vitro (71). As menti”ed earlier, ketone and lactic add do lower the b&d PH. Lowered pH in the fetus during tabor has been cause for eta”“. It has bee” related to cardiac atiythmtas and considered to be a” indkatbn of fetal anoxta. However, in a recent study, 72% of infants whose cord pH indic&dtbeywesevoroh/actdoacworo born in a vigorous state, with a” Apgar score of greater than 7 at one minute (72). Essential atim, acids gradually dedine when the preqant woman k deprived of food. After only 12 hours of fwd dqxivatto”, 10 cut of 19 matemal amino acid levels were stg”iEca”uyb&w”o”pregrant!+wkva. Amtno adds waxy cross the placerP ial barTier, and levek I” tbe a”mtaa tlti are affected during maternal t&i”g. A decrease in the esse”tid ami”owtda!ainekshoumtobeof primary path&& signifkance in ketotic hypogtycemia of infavzy (62). Thtisistmportanttobthefetusand the “ewbom becaw glucagw, a hormone that stimulates the CMIVOTsiarofg&qFaltog!+xwt”thettveT. onnot permeate the placenta in the prrzmce of hypoglycemia: however, admintskation of aknin to WOW I” labor i”creanes the glucagml levels of cord b!+xl in the human fetus, tbaetydenemingtherkkofneo~tal ketottc hwemia (62).
Vel. 38. No. 4. JehdAwud
stating~that
1993
Routkwadminishationofanin~ ve”aBi”fwiontogrewnta”dtreat dehydwa, ketoa, ar&e eloctrolyteimba!ancecanno!+mgerbeconstdered.c.o”+t&safesu~te for food and t&ids t” labor (4, 73, 74). I”~glucosein~tothe
.
to ind-
F$z$2zbeen show” i”thefetus,followd byhypc&attintbenewbo”l. H~k~tiaUyhamdul to the mpidty devetotalg brain of the fetwandthC”ewban.Deleterious effects may indude acid&s, increased c&o” m0ti.z kvek, increa?edl&icactdkvek,andnecr&al jaundice (75-78). Hvposlycemia may result in in+ “?&t&e re@&ory daess, apnea, cyanosis, and setares (78). Sir& (79) reported that term infants of mothers who recetved intravemw giwost?thempyd”rtngtbecourseof sporl~ or oxytocin-ind”ced hbmsbowd”~tbwaingd muscle tone and &!a~ haUhmtt=x tovadcC¶%muiiatoneandlwoholas of age.” study infants had a three tt”wbttt”cidweof~ cm+ (79). Awidi”g excess inha(76). zzJTzzz:~~w I”anotherSt&,Si”ghtotal@O~ reputedthatt”fu5i”g5%gtucoseto thetabmt”gwo”?an~ila* “ificant t”aeae intheincidsncoof hytmMmmb and subzque”t ha”&ttachyp”eainthenavb+x”infantTheretsarebttonsh@txtxw” COIdSlUtMdi~levehiIlnewbom
infzmk a”d matomal i”~nouS tbempy duri”g labor (81). The sodtum fovols of infants whae mother had5%datmsewasr~!wthatofm&erswhohadorathydratto”.Ako,t”fa”tsd”mtheTswho had dext”xe lnhlskm had St&icantly”wev.wtgbtkssi”thefkst48 hvwsthanthosei”fa”kof”wdWS [email protected]”l levekinthemo(hersandinfantswere way sknilar. When hypoaakemia is
203
kducDd in the mother, it will affect the baby by a netbansfer offluid to the Infant. Fluid overload and hypmmtremia can be sodous complicattons for mother and infant (74. 81). Morton et at (74) state, “k SeenIs tuo@al to sum.vess the comentratio” of ketci& at expense of increasing other “manic a&is which place a greakr on the buffering capacity of the blood.” Maternal hyponatmmia may cause cerebral edema. COIM, convulsions, headache, vomiting, lethargy,, confusion, mood changes,and postpattal psychosis(60,81). Hypanatremia in infants may cause co”wlstons$ apnea, cyanotic spells, neonatal @I”dkx, respiratory dtstxess,feeding dtff&&,and&X&bk-~~kSS after birt!? (60. 80, 81). intravenous therapy, oxytoxtcs, toco& drugs, and endotmcheal intub&to” have atI been seen to adws?iyaffectpuk”aaytlutdbaknee, whffh fsakeadyaltered by pregnancy l73.82). A normal healthy woman at term already has a” abundance of kcdy water. with at least 2 L stored in the extfavascular spacea. DumouIt” et al (60) state that t”tmve”0”s therapy is not rwtinely needed, es@ally in the titi 12 hours of labor. A study by Cotton et al (83) showed that the ordered r&e of inkavenous tlufds was often exceeded by hvtce the amount If inbavenou3 therapy is cli”tcaUy warranted because of the wmnan’s high-risk status,then mettculous intake and output monitoring should be maintained.
the
siain
STRESS Reduction of stressin labor may be asswtated with lesspain, lessanxiety, shorter labors, and fewer pednatal prob!env (84-86). Stress during labor increases the Pmdu@ion of makmal catecholamines. Increarod catecholamkw may affect labor by shunting blood away from the uterus and the placenta, and by lengthening labor. These effects “lay lead to pm-
24M
Ion& fetal hypoxia, as ddenced by abnormal fetal heart tiactngs and abnormal scalp pH samplez @4,87). Laboring women are often subjected to procedures that conbibute to thefr sbesslevel. Stresson imposed during labor may cause compllcations and may conbtbute to the need for awIossive intelventtmls 188). Fastin~k a known stressor.Sin&~ (88). in assessingstressful childbhth events, repotted that 27% of wwne” rated resmctk?”of food I” labor to be mcderatefy to most stre&ul. Ftftyseven percent of women found resbicti~1 of tlutds in !&or to be moderately most0lmLdul (88). The stn?ssre5pow of the fetus is to imrease the pmdution of catecholaminos in order to tncrease norepinephdne. This response dws not manlf&ititithanlnaeaseinbkod f!cw 01 a” incloare in heart rate as see” in the adult. Instead, stress in the fetus initiates a wgus nerve reqwsethatcausssadropi”fetalbeai rate in older to consewe oxygen (84, 86. 89). Sane fetal catechdamine production, however, ts normal. Fetal catecholamines have been show” to conbibute to prosta$andf” syntbests, preparing for onset of labor (86).
to
CURRENT
STUDIES
Avattable Me&we on the oral intake of the laboring wana” focuses primadly on why the womzl” should be kept NF’O. Many authors conrider fasting as a “lewls of reducing “latemalmortalftv Maststudtesfccuso” intenrenttons -used to replenish hydration and energy needs of the kboring wo”Ian. Howaver, a recent study at Jubilee Maternity Hospttal in Belfast, Northem Ireland, conducted by midwife Angela Flanagan, in ass&alto” with Dr. K&an Fikpatrtck, a” anesthetist, looked at outcomes of infants and
four labodng w&e” were en& aged to take Ught foods such as eggs, toast, sandwiches, ice cream, yogurt,
JeUler, and fresh kutt. As a control group, 22 won~e” were permitted intake according to the usual p&y of toast and tea in very early labor with stpaof water thereafter. Ms. Flanagan q&d the f&xvi”g w.u,k. Women who ate required less pain relief and less Pitc&, and the length of labor was shortened on the average by about 90 minutes. In addition, Apgar sso:esd babies in the fed group were hither than in the control group. As a direct result of this study, Intake retictio~ have been overturned in Juhileo Maternity Hospltat, and Ms. Flanagan is cunently undertaktng a repltcation study with 1,OOLIexpected subjeci5 (personal co”l”l”“icatton, A”& Flanagan. Febnmty 21,1993). We studied the eating and &linking @terns of labadng women (unpublished master’s thests, Yale University, 1991). The sample con&ted of 76 women who were observed until they de&red or until they received nwdtcation or intravenous therapy. Women uwe netthor encouri& “or dtscwa&frmn.nalt”takentakebutwere simply &sewed in settings &d self&ection of intake. All of the wornon drank at some point in their hbor and 85.6% ate. More women ate kuSef pmtto”s eartier I” uEirlabws.tap&gafft”&PJwpbase
thatper-
tiembysecondstage. Ddnktng also decreased as cavical di!atkm inerased. with sips dominatinginkteacttwandrecondstsge. It was a!sa noted that the peak Inddence of nausea and vomiting occurredfrom6to8nnratharthan9 to 10 cm as commonly thought Women continued to eat and ddnk after a” eptsode of nausea, although they only drank after vomiting. Women tended to eat at comma” mealtlnws.
Literature from anesthesia and obstetdcs have repeatedly show” that there is no cm”p2ul”g scte”titlc rationale for the maintenance of routine institutional NPO poUctes.These po-
dmmmt of N,,me.Mtdwthrv
.
Vol. 38. No. 4, JufylAuw
1993
need exka e”couragemo”t to provent dehydration and prwide the caon currentscientific research. Elkinglories needed to “rat the stlenuow ton 13) points out that “these p&zips demands of labor and delivery. Naumay persiston the basis of anecdotal expedeme, institutional iwrtia to palsea and vomiting are part of labor for a certain Percentage of wornen. changesbegun in the 19405, com‘Women can continue with their i”. pmmise with anesthesia depaltmentalpoBcytoensule&qutedoquatocovemgo.take after being nauseatedwithout intuning further episcdes. ewwrated notions of risk, or fears of litigation.” Researchers agree that every parFUTURE RE%.ARCH huient should be regarded as having a full stomach with hi&ly acidic fluid What is the best diet for the laboring rwardless of how long she has been woman? Would food and fluids dwNh. With this in And, why limit ing a serial induckn help with labor their intake? We found that lababw prcgre&on? Should a woman who women self-regulated intake. 0”~; is comfortable with an epiduml anactI’ve labor began, women usually al@a be permitted to eat and drink? preferred liquids. Dces~“ofaooda~~ Several studies looked at the efkba? To a”swer these questions, fects of skess on labor. finding that mndomized clinical studies should be labor misht be prolonged and could undertake” whereby women admitinvite intervention. Intravenous fluids ted to labor and deliwy are assig”ed are”&areamn?&subs6kltefororal to one of two groups: an eatfluids for the healthy parhuient I?i”&“k&g~a”da”NFogmup. nally, it is worthwhile to consider the A”&h&a,~miduriferv,a”d psychcio#al importance of food and nting departme”!z should be influids to the iabodng woman. Fbod cluded in the de&n of the studs from and ddinknot only pmvide hydration, thestart nutrition, and increased comfort, but American wanen and few are they also giw the woman a feeling of being subjected to policies based 0” control in labor. Choices have bee” a boiief systen~plasued with inaccurhdegrd in the movement of modem a&s, cut&ted research. and “I&Iobatrlcs. 1nslimno”al policies reformation. The cunent policy of IOUgrading eating and drinking in !&or tine fasnng I” normal labor “lust be shculd be reexamined in the fiqht of reevaluated. It is based on anecdotal mlslnfmma~o”. itituI%maJ inertia
icy
CLINICAL
lMPLllxnoNs
lends
Thiiuterature review support to @ns women the choice to eat and drink in normal labor. There is no such thi”g r~ a” empty sto”mch. re~dless of tims from the fast intake, and to arsumo M could be deadly. In most cases, Me~&ko”‘s syw drome on be prevented by appmpaate anesthesia technique. General a”esth&a should be avoided and re@onafanestb&asubstitutedasmuch as uasible. Women should be enccwa~toosatanddrinkastheys.z=z fit. If a woman is !&a&g in the eariy morning hours, however, she may
wintlodud IO the medical cornmunily and the conwner based on current sound scientific rosoarch.
REFERENCES l.!&wchJ,NewtcaN.FaDda”d lwamges in l&r. Part 1: cms5&tuml andh!st&?Jpracla.Bktb1998;15:815. 2. D&on C, Gudgeon CW. For feeding di;dng k&or. Med J Aurt 1987:147:625-6. 3. Elki@o” K At the wat& +2: where &iemCr and an&b&a obstet Gy”~~1991;71:304.
6. DeLee JR c?bseba for ““r$Qe. 5ul ed PhuadelPhta: samien, 1918. 7. Me”d.?lsuIcL.Tbe8s#aw”of rtornachccntent,intothelu~dt& obstewanosthsriaA”lJobstetA”orth 1946:52:191205. 8. JamerC,ubbsC.BannerT.Pmt-
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ofvohMearnlpHi”&laiAneslhnsmAnalg 1984;6336668. 10. Hddswxth J, Fumsa R. Rwkto”RAccm~of~N”ea”d stwMchiubesforan~“g!3rzsto”wch before~ai”*.& J Ames61 1974;46:526-9. 11. Rob&R,3h&yMRedud”g!he rkkofaddxpim&sndudngcmrean & Ar?sth A&g 197*53%9-68. 12. Tpabpaut d. Appitagon of garm mntenk-anexi&me&study.AmJ PathophysioLq, 1952;28:51-67. 13. WiIuams J. warm OLstekk Now& fcD: A&ton, 1989.
14.P&RBMatemaldeatbfmm aspiration q4yxia. b l&d J 1956 JuiyKL9. 15. Shnider SM G.ason G. Levison &ule&aa ,saaka.2nded.Bdkale: wil2L vakins, 1989. 16. Natkmal Center for He& Statistla.Advawd?epmtofl%laltlMz5iy statirties.l98%mOnthlyVitd~rrpat kd. 40, MI. 8, ruti 2). HwttMk (MD): Pub&cHealth spnico. 1992 17. Kau”iw#hi,Hu$,esH.GtimesG. CawsofmatPmdmaayintheu.s. Am J ObstetG~lnecol1985;163605-12. 18. El&rGC,MarkmaFGSRf, stwensar LB. AI@h&a-relati mater“&“WIt&~i”Mkh@“.A”lJObS&t ~1988;159:1@-93. 19. Dorkna” SF. Maternal“i&&y in New York Cii, 1981-1%?3. ObstetGywsd 1981-19?%76(3 Pt 1):317-23. zo.Ro&sJP,WeatheibyME”wt EK, Septeton DR. Rose”ReldA. Gut-
!Mn
conwe of care In birth centers: the Mti bkth center rtudy. N End J Med 1989;321:16c4-11. 21. Lyons G. Failed intubatian. Ane&b& 1985;40:759-62. 22 Gibbs C. Gesbic aspiration: preventton and be&men,. Clin Anoesth 19%4,1):47-62. 23. D&es JM. Weeks 5, Crone IA rxffkult intubabbn in the pzetlutent Can J Aneeeth 198%36:6&S-74. 24. Selliik 8. Cdcofd gresrure to contrd qurgttation of stomach contents cktdng induction of generel aneesthesia. Lancet 1961;2:4c4-6. 25. Morgen BM. Megni V. Goro+znulk T. Anxsthesla for ememenw tee -se&m. BrJAneestb 1983:5%3%9. 26. Eichom JH, CcqerJB. Cutlen D. Stan&r& for patient monitortng dudng general anesthesia et Harvard Medical &hod. JAM4 1986:256:1017-20. 27. Gibbs C. Rolbln S. Norman P. &use and prevention at maternal espfration. Anesthesiology 1984:61:111-2. 28. HunterA. Moir D. Confidentlelenquhy into maternal deaths. Br J Anaesth 1983;55:367-9. 29. Moman J. Pathophysiology of gas_ btc esptretion. Int Anertheriot Clhl 1977;15:1-11. 30. Morgan J. Anaesthetic contrtbubon to maternal mortality. Br J Anaesth 1987;59:84265. 31. Philfips 0. Tke role of anesthesfa in obstebic mortality. Int Anesthe5tol Cltn 196%6:847-73. 32. Roberts R. Shirley M. The obstet&km’s role in reducing the dsk of esptreixm pneumonia. Am J Obstet Gynecol 1975:124:611-7. 33. Tunstall M. Anesthesia tot obsietric patients. Cltn Obrtet Gyoaol 1960; 7:&65-95. 34. Moqn BM. Aukikh JM, &rker JP. Anaesthetic morbidity following ceeween section under epiduml or general anz&bPsia. Lencet 1984;1:32?-30. 35. Conkltn KA. Con anesthetic-rehted maternal mortality be reduced I!&terl. Am J Obstet Gynecol1990:163 (1 Pt 1):263-4. 36. Marx GP, Luy WM, Cohen S. Fetat-neonatal swus tollarim caesarean xctton for fetal d&trees. B; J Anaesth 1984%1009-21.
206
37. SykpsGS, Molloy PM, Johnson P. Stknt GM, Tombull AC. Fetal d‘%rw and the condttlon of the newborn Intent. Br Med J 1983:287:943-5. 38. Nimmo W. Further stttdfes of gas_ bk emptying during bbor. Anxstbesia 1977;32:1w. 39. Crawford JS. Commentary: setti”gthereuxdsta@bt819&%1623@3 40. Wtlron J. GasWc emptytng In laboor: some recent flndtngs and their dinicel stgntftcence. J Int Med Res 1978;6 fSUppll:%-62 41. Davenport H. Physiolosy of the d&e&e hati Cht: Yearbook Medical Publtshen, 1982. 42. Johnson L. Gastmfntesttnel physidogj. Boston: uosby Year !3ouk 1991. 43. Simpson K, Stakes A Effect of anxiety on garhic emptytng in preoperawe~~.BrJAnweth1%7;5954& 4. 44. Merk L, Marx G, Henry E, Joffe S. The “full stomach”-e continotng problem h an&he& menegemont NY State J Med 1964 Mayll14-5.
end labor. J Obet Gyneool Br Cornmonw 197@77:37-41. 63. Hester JB. Heath ML Pufmonmy add aspketlon syndrome: should prophyitir be routine? Br J Anaeatk 1977;49:595-9. 54. Cohen S. Aspiration syndromes in 7”’ Ar&hestokqy 1979;51:37555. Heaney G, Jones H. Asptrenon syndromes in pregnancy. Br J Aneesth 19’; ;;51:26&7. 56. Onnezzeno X. FrencotsTP. Viaud J-Y, et al. Asptmtton pneomonttis pro phyfaxir
in
&stetiic
a”a&heria:
mm-
&son of effetvessent ctmltidlne-s&urn &ate mixture and sodium cibate. Br J Anaesth 1990;~~6. 57. Stmmons M, Meschia G, Makowski E. B&t&a F. Fetal met&&f reto mzlt&alst?ma!!0”. Pedleb Re% i974;a:mb.
$Qnse
58. Nat& R, Pat&k J, Rfchardron R ELcbothumanmatemetveno~pphsma &%=e conce*etto”D on fetal breathtng movements. Am J Obstet Gynecol 1978;132:36-41.
45. Nffo W, Wilson J. Prexott L. Narcotic analgesks and delayed gastrfc emptytrq during f&x Lancet 1975: l:t3913. 46. Ccdeman D. Dev B. Amwthesie
59. Mllier FM, Skiba H. Klapholz H. The effect of maternal b!cad sugar levels on tetel ectttity. Obstet Gynecof 1978;62:662-5
47. Holdsworth J. Funws R. Routston R. A compettson of epomorphlne end stomech tubes for emptying the stomach before generef ane&esta in obstebics. Br J Aneestb 1974%526-9. 48. TeykxG,Pyse-DavtesJ.Theprophylecttcuseot anteddsfn the preventfan of the acid-pulmonaly-esptrnon syndmme IMeodelmn’s syndrome). Lencet 1966;1:288-91. 49. Row R, Shirley M. Asplmtton dudng vegtnaf delwey. A.-,-on, 1974;40:317.
61. Felfq P, Lynch V. Statvatton in human pregnancy: hypoglycemte. hypoinsullnemte, end hyperketonemte. Sdence 1970:170:990-2.
50. Shay H. Sun D. Shsss and gastdc secretton in men: 1. a study of the mechanb,n inwIved in insulin hyQo&emia Am J Med Sci 1954:22%6%-42. 51. Htrshetmer A, Januay DA, Dew etsa JJ. An x-rev stud” of w&k function lab-x -Am j O&t Gynecd 1938;3~671-3.
dumg
52. Davison JJ. Davison M, Hay D. Gestdc emptying time in fate pregnenw
Journal of Nuw..Mtdwifery
60. -n J, Foulkes J. Ketonwte dudno lebm lcommentetvl. Br J Obstet Gy&col 19&91:97-&~
62. Felig P, Ktm Y. LylKh V. Hen&r R. Amino ecfd meteboliim doting starvation and pwgnancy. J Clfn Invest 1972;51:1196-202. 63. M-r B, Raefnker V, Vtletsis R, FretnkelN. Acceleratedstatvattonandtbe sk@ed btw&fest In kte normal pregnancy. Lancet 1982;1:%9%92. 64. Sabeta V, Novak M, M&her V. Oulhn-u?lntbfc&utiuaah!kemkmnmem potmy za p&k. -&ch &wcol 1963$%152. 65. Sabate V, Wolf H. Lawmann S. The role of free f&y a&s, glycerol, ketone boG!es and glucose in the energy metetim of the mother and fetus during delivery. BtoI Neonatal 196&13:717. 66. Bench-,! F, Srmonds
.
E. Ketone
Vol. 38, No. 4. Jely/Augeet
1993
balksin fetal and matema, b&d during parhnitlon. Aurt N Z Obstet Gynecd 1972;12:176.
hamrds of maternal hydm‘ion with 5% dextrrne before -wan sec%n. Lance! 1982:1:116&2.
67. Ccehee E. Jacksa, M. Kekmuria in pregnancy: special reference to calode resmcted food intake in obese dlabeacs Diabetes 1980;29:177-81.
76. Mendida J. Gy!xk L, ScanIon J. The effects of intrapa*m maternal giucme infustonon ‘he nwnd fet,s and newborn. Anesth Analg 1982;61:32-6.
68. Kim Y, Felg P. Maternal and amniotic fluid subsbate levels during caloric deprivation in human pregnancy. Metabolism 1972:21:507-12.
77. Robi”ard J. Se&o, C, Kennedy R, Smith F. Metabdic effects of constant hypztank glucose infusion in well-oxygenated fetuses Am J Obstet Gynecd
84. Ledemmn R, Ledennan D, Work 8, “c&n” D. Anxiety and epinephdne in multiparolM u,vm.m in kbor r&&w shiitoduratkxoffaborandfetdhearf ratepatkmsAmJG%&tGynecol
69. Fisher D. Perkrdal iwulin, gfuc?wn. and carbahydmte metabolism. Per-
1978.1~2a3.
1%%153%70.
inatofogr Endocdnolw Sympaium. Lengky Be&. Mead Johnson. 1973. 70. Rudolf M. Maternal ketosis and irS Clin Endccdnol Metab
effect on the fetus 1983;12:41%28
71. Leiwque A. Hauguel J. Revelli J. Fetal gl”Cose “laiitkm in respDnse to maternal stawation and acute hyperketonemia. Am J PhysWll989:6:699-703 72. &ten B, Johnson T. Nekon J. “mbif cord pH and Apgar xmes as an index of neonatal health. Am J 0bste.t Gy”ecol1%~157:e43aB. 73. Lind T. Fhdd balance dudng labor D revfew. J R Sw Med 1983;76:870-5. 74. Morton K, Jadwn M, Gfffmer M. A compaison of the effec‘s of four YIItdions for the tteatient of ketc.nuM in bbx. &JO&et Gynwoll9L?4+2.4739. 75. Kenepp NB. Fetal and neonatal
78. G&k L. To maintain perinataf glucase,insulin homeaw. Contemp Obsw Gunecd 1983:113-21.
during k2b-x. & 19t!@87:130-1.
J
obsl‘zl
c~incdfofdosmc&pressure.Am J Gbste! G,wcd 1984;149:174-6.
85. Ledemxan E. !.edemmn R, Work
79. Singhi S. Effed of maternal in-paxturn ghtcox thaapy on neonatal b!wd g,ucose levels and neurobehatiom, status of hyp.&ycemic term newborn infants. J
be&hstafa.AmJObsietGyMcd 1%31;13w56.
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femafanx+wplarmac,~
80. Singhi S. Choobng
E, Half J. Kaf-
ghati S. fabwentc neonataf and maternal huwnatremia ,o”owim oxu,ccin and
Gqnaecd
83. COUC+IDB. G&k B. Sp!lknan T. DmmanKInfrqrhnntoportpzaNm
86. Ledennan R, Ledemmn E, Work B, McCann D. The re!&onship of ma-
pbsmacortisdtoprogreosinbbnr.Am J obnet Gvnecd 1978;78:495. 87. Fox-H.
The effee& of catechd-
?,mim and dlug keabnent on the fehu and ne\ubom &Fan 81. Tamw-Mardi
W. Shw
J. Lul D,
Gardner D, Fiynn F. lattcaenlc hypona_ tremia of the newborn due to fldd overload a pmrpective study Br Med J 19Bl;2B3639-42. 82. brook bled fnfanb
Dahfenburg G, Bwneff R, Bray R. The rehhbnship between cad sawn scdfum levels in newborn and maternal inbwenou therapy
J 1979.6:157-65.
BB. Sknpkfn P. S&s, pain, and catechdamkra in labor: pad 2. stress asO_ .&,,a, with childbirth event% a pibt wVW of new mcfbea Birth 1986;13:234-
40-. 89. philime M. Fetal catechdamines Am J ObsleI 1983:146:840. 90. London linws. Gffns birth on an eSg.1992Doe.17. -
HOME STUDY PROGRAM IJF’OAlEB
1
JNM’s 1992 Home St”dy Pmgam. which feat”res “The New&“” lh!arch/Apaill992 SUP plemerd). wflf be v&J for 0.9 CEUs through Apiu 30.1994. The fee is $100. Pfeare note the fdfcwing change Payment and study materials should be sent m to May Ann Shah. JNM Editor, 67 Tany HIU Road, Tarrytaun. NY 10591. JNM’s 1993 Home Study Program, which feabires “Advanced Nursa-Mfdwikry Ractke” (March,Apd, 1993 Suppfmnent), tiff be v&d for 1.0 CELk +hro@ Aplu 30.1995. The fee ir $75 for submissions p&marked by Aug.ut 31, 19%. and $100 tkrealter. PleasD note the fdkJ!#i~ conections: Page 7s: Post-test question X 18 should be feR b!ank on the Answer sheet
I
F’agz33-5: Cdumn Lpamgraph2 senhnceXS-“ThePi~kgond~introducedlhrC& the cervical OS and up into the uterine fundus. much like the techn&w used to sound the ute,,,s p&r to lnhauterine d&e ins.ezta.“--rhodd have been -t ivm sentewes e=rk=% Itkhopedlhatnoreaderws.oxfusedbythkmispinL JNM’s 1994 Home Study Pagmm. wti wlU feature “Ofxtehk C~i@kam,” is wdf undemay. It will ,,a p&shed as a Sprins Su&ment and wi” offa 1.0 CEUS to pattkipanb. Prefimfnay preparafions are ixginnbq for the 1995 Home Study Pmgmm. It is anticipakd that its foeus wiu be “Comprehenskw Hoalfh dent” please w&h fhQ Jcumal for fmtha ,nfonw,bbn and for ‘A Call tot Absbacis.”
JwmdofNunc-Mkiwuay . Vd.38,No.4. July/Augusl1999
207
Leslie M. Ludka,
CNM, MSN.
Thepdy of nothing ty mouth (NF0) in labor has become a well-&ahlished routine in many hospitals throughout the United States. The NFJOp&y is a curlolls phenomenon because it is based largely on anewddalltanfomMtiandhasnotbeen supported by research data. Many researchers are now auesUonln~ the practice of mutine f&gin lab& (l5). This Hterahtre review wiIl dixuss
&hktodcdbmisdwfood
and drink during !&or, maternal mort&y statistics, risk factors for anesthesia-related complications. the mvth of the enmtv stomach. antacids.
stwss
related to fcad and fluid dep: rivation, and current research and cUnical implications.
HISTORICAL OVERVIEW Until the 194Os, paiutient women in the United States were encouraged
and Catherine C. Roberts,
CNM,
to eat and drink as a means of malntining their stamkm for the work of labor and delivery. Dr. Joseph DeLee (6) warned that food must be encouraged throughout labor to avoid general A. delayed labor, and serious p&p&urn hemonhage. By the mid-1940s. however, the practice as cUnlcaUy unsound. and it was tirtuaUyabandoned.Thechangecanbe traced to obstebtc aw.thesiolc@ts’ fear of matemal matalky due to ilspit&ion of stomach contents In the 194Os, Mend&m (7). an obskttkian from Com-ell, hypothesized that postanesthetic pneumonia was caused not so!& bv infected ma-
terial but amtrated
rather by stokuh
cwtenti
into the Iunax He believed gasIlk timewas delayed in labor. Mendehon noted that it was not uncommon for a &entto vomit food ingested 2448 hours ~rovmushr(7). He reviewed charts of ;14,016 pqlnandes from 1932-1945 and found that aspkati of stomach contents into the lungs occurred in 0.15% (N = 66). In 1945, Mendel-
thi
emptying
MSN
conducted a seriesof expelmenk that examkted the dfeck of
so”
thattv-mwn-he
pmhihited f&n eatkw and minkirm dutiw bbcx. He be-
cqxmted into anesthesia practice. In addition. skilled anesthetistswere quite rare. Often, the administration of gases was left in the hands of the most member of the anesthetic team. These factorsledtoanestheaiarelated cases of aspiration pneumcnia in the parhxfect. Expanding on Mendelson’s research, further studies on aspiratton pnaumon!afolmdlwokeyfactolstbat predicted an increased risk of maternal mortality and morbidity: the combination of an amirate with a volume of 25 mL or more and--the more lethal factor-a oH lass than 2.5 f8121. The dini& manifestationa‘of pulmonary aspiration. which is now commonly referred to as “Mendelson’s syndrome, ‘I includes intense bronchwpasm. pulmonic congas&m, and exudate pwxk~ction (131. In 1956, Parker (14) undertook a skdytodetermhewhytkrehadbean no maternal deaths while using ganeral anesthesia at home. In Birmingham, England, 100,CKIO births took place in the home behwen 1943 and 1952. During that period, 3,048 farhops delivedas ware completed with no deaths from aspiration pneumonia.TbaseoFeralilJedwara done under gewral anesthesia with an open face mask. The women at home were commonly hamassad down in the litbotomy position and given anesthesiawith no reported fa-
junior
CathedneC. Robed receiwd her B.SN from the Universityof Rhode blond and her M.S.N. and CJ”.M. ,mm We UnluersltySchwl of Nursing.She 19cwendy h &in&al pmtice m N&h Centml Bmnx Hmphl, Nrru York City.
MO
klities At the same time, in the Bw-
that failure to secure a patent akway
mingham Maternity Hospital, 2,200 operative deliveries were performed with four maternal deaths due to aspiration. Speculation was that the fLw&ba&machkleklthehc6pitalwas less safe than the opan mask. Recommendations included that focal anesthesiabe used for simple fordeHvay, and if general an&-&a had to be used, it should be provided by an experienced anesttattst using a cuffed endohacheal tube.
was the prtmay cause of anesthesiarelated maternal deaths. There were no deaths related to ragtonal anastbesia 118). Out of 15 deaths (0.82 per 100,CKX live b+rths),one was k&ad as having bean from aspiration of stomach contents. A study done in New York City from 1981-1983 revealed the matemal mmiality ratio to be 36.1 deaths par 100,WO Uve births (19). Ai,estbesia-related deaths ranked as the third cause,with 13 cases111%). Four ware associated with legally induced aborttons and ono with ectopic prag nancy. There was no specific breakdown for the cause of ihe remaining eight anesthesia-related cases. A recent study by Rooks and colleagues (20) looked at freestanding birth centers, with regard to different varlablas. They revlewd cases from 11,814 women who ate and drank at will. There was no rrported mortal&y or morbidity from aspiration pneuraontaavan~th0awerowomen who required emergency cesarean sectiona Twenty-two parcent of !tw2 had eatan solid foods, yet they had no asplraiion complicatbns.
MATERNAL
MmTALrw
Fasting in labor is believed by many members of the medical communiiy to reduce the risk of maternal marbtdlty and mortality by reducing stomach contents, thereby elimkmtingpr&utsforpulmonaryaspiratkm (7, 11, 13, 15). Howwar. detailed analysts of overaU matemal moxt&y atatiatjcsin the United States reveals inadequate and tncons&tentmethods of c&&g, c&g&zing, and raporting information. Unlike England, where the spa& cause of the maternal death ia repwted, here in the United States aspiration pneumonia is grouped under the broad eatogoty of “compfkxttons of the admlnistmnon of w&h&c or other aedatknl in labm/delivay.” It is one of four subgroups related to the obstetdc anesthetic P&Jam (16, 17). In 1950, the incidence of maternal deathSwaS83per1OLWOlhret4thS. In 1960, itwar37.1 par100,ocniiva biis. The latest *Ii&a for OvaraIl maternal mcftality h 1988 is 8.4 per 1OLWLKllive bhths, which is a statiswlllysisni&antiMBade fmmddper 1cKwciu live births in 1987. In 1989, 320 women died, for a maternal martat@ tate of 7.9 per loo,wo uvabll?hs (161. Matemal mortaiitv IS a rare cccunence. Maternal da&s robted to anesthesia do MCW but it is impassible to pinpoint the exact nature of the comp&a~on. A more data&ad st;ldy, done in Mtchtt from 1972-1984, showed
Joumal of Name.M!dwikry
RISK FACTORS FOR ANESTHESlA.RElATED COMPUCATIONS Fatled Iatubation The ocNmmca of asptratton is directly related to difficult lntabattan during general ane&esia regard&a of the patient’s oral intake Expected ra:as of IntubaUon failure an! rap.xted asonefailureoutGievaIy300caaas raquldng ganeml anesthetics.Difficult intubatfon was a key factor in approximately one-half of the anasthe&-related deaths reported by the ConfidenUal Enquky 1976-1978 (21). Endkr and coworkers (18) specufate that a high rate of failed intubatlon resultsfrom the increaslng numbar of cesoreansecttons.,many of which are done with general aneathesta.
.
Vol. 38. No. 4. Juh+Aaa1~41993
In order to avoid failed intubation, experts agree that conect anesthetic care for general anesthesia should be undertaken This includes preopemthw assessment, rapid and safe induction, awake extubation. and postoperative monitoring. The interval from safe inductton of general anesthesia to complete control of the airway by cuffed endotracheal inhlbation presents the greatest risk for aspiration and death (‘2.2). Cricotd prwure. when properly applied by a trained aaistanf has proven to be a safe, reliable method of preventing aspiration during induction of general anesthesia (22-24). Repeated attempts at intubation should be abandoned, because they are rarely suecessful(21-24). Inadequate Abdominal
Anticipation Deliveries
of
Proper asxssment and pleparation of the obstetric patient by anesthesia pascnlnel is hnpemave for the preventin of an&he& problems. This axssment might bean antenatally with the pdmaw prwida notifying the anesthe#st ihat a pardcular pat&M is at high ti for abdomtnai delivery (23-25). It has been suggested that anesth&kgists should mutinelygoonroundsto-~~tential dtfftculttes in the event of abdominal delivery with general anesthesia. A clinical histoy, focusing on signs and and layngea~edema a&&ted with preecfanpsia, is crucial in the care of the otstebtc patient (23.25).
Substandard
Management
There is considerable agreement among experts In anesthesiology that substandard manwtement of anesthe& care isa primary cause of pulmalalv asdlatkxl17. 11. 14.22-W.
regain
patientto cmsctousness and then proceeding -Mb an awake intub&ion or adminbkatton of a re@XMI b&k. If there is an emergency, then general anesthesia with a mask and cricoid pressure sharld be employed. A cricothyroidotomy is used as a last resort (18, 21).
Emergency Cesawzm Secttons and Regional Anesthesia The need for seneml anesthesia in an emergency shim has been pstimated to mnae from 3.5% to 13% (25, 34). In their prospective observation sbldy of 360 comecutive patients deiiverau by emergency cesarcan section. Morgan et al (25, 34) found that 87% of the cesarean set6ms m&l have been addpIed and that general ane3thesta was only needed in 13% of the s&jects. Conklin (35) states that t&as there is an absolute contraindtcation, a re@onal block for cesaean section Is appropdate in most emergency situations. He rasons that, in this way, the partudent can protect her ow atway hum p+Ikmay e5pirdiion (35). Ma& et al i35) l-me clearly shown tbat newbum outcomesalter an emrgency cesarean section were better when re&nal anesthesia was us& Haste is a weU-known factor in crttkal awsthetic inctdents, and it is the parhnient’swell-beingthat shouldbethe first W”cem, tQcause fetal disiTe% is som&mes misdia@cwd (18,21,25, 33,37). Many authors concede that reyional a&_ has little effect on sasti emptykw f14,30,32,3&40). Crawford (39). an En&h physittan who has researched the topic of PO_ tential aspiration in labor, stated that “a matha undergoing a comfortable bbor, with the aid of an optdural analgesi4 da25 wekome refreshment, and alI other things b&q equal, we offer her a lemon sorb& or a cup of tea and a slice of toast Roberts and Shirley (32) state that regional
_”
,lotJmal
of w
.
vol. 38. No. 4. July/Ausust 1993
THEMYIHOFTHEEMPlY STOMACH GasttcEmpty&~
Physioltqy
GasIlk emptyklg isgclwmed mainly bytwfactols l)thevolumoofgasmC contents, and 2) the influence of chzmical and physkxl properties of chymeintbeduc&umandjejunum (411. l-be rate of emptying depends ontbevoklmeoftke~osma~ presswe, and chemical propertier. Gasacemptyingis~testreatestandfajtest at the bqinning of digestion. when the vdume of the stomach ccatents is~~~krgestF~tiStb~mosipavedUl chemical agent In the d&&d diet that SkwJs sastdc motiltty (41. 42). Gastric motility is adversely affected by massive sympatbe& discharges such as pan, nawea, and emotional d&ubances 143). Heavy exerdse does not impede emp&&gof liquids; theyareemptiedaknostlmdMeiy. Solkis, on the other hand. must be !asthan1mmindtameterto~ throl&the~c~Lm~ canrematntntb2stomachaskxgas nine hours. continuing to sttmu!ate g&Tic SecMion (41).
EfkctofGesIathandLabolcm
-Emptyins Gasklc emptying ttmein
the hbaing wmanvariesaccGfdtngtokldivtdual reports. Acc.xdtng to Anerthesia @r Obstehics (151, aspkaLtoIl risk facton r&ted to d&yea g&k emptying include &aialai age rpeater than 34 weeks, labor, be&bum (which is indicaaw of gaoaqlhageal refw, &ess, narcoti, andsedatives. Other studies show a decrw& WC emptytng time in labor, but the d&y was r&ted to the adminisfmtion of w,rcottm and sedattves (10.40.44, 455). Acco1dklg to obst&ic anestbest& qisis, it is the @c contents that
201
Tayfor et al MS) lnwsttgated the pH and volume of gastric contents in anesthesia115). Asstated, the routine p&y of NPO in labor was initited in the hop?. of decreasing or eliiirating stomach contents thereby lmkg httlo or nothing to asptrate. Yet, studies have repeatedly shown thatthaefsnosuchth@asanemp+ stomach,qardksscdthetimeofthe last meal 110, 44, 46-49). Labwing wanen who have taken nothing orally have been found to secretewayins amounts of Mstric iukes containhydnaak-4 withdangem& low pH values (32,471. Fasting does notetbnMestcmachcontenk,ttwlly inwases the concentration of hydrcchbrk add (501. Therefore. dqivin&e mother of foodand fltidurii labor may achmliy fraease the risk of maternal mortalitu and mabldity fromacid aspiratio;. Hkshetmer et al’s (511 serial x-m” studies alter a bat& ihI show& that there was no cawkmt or charadnIstic alteration of ga5It.z evacuation in prk-dgmvidas dudng labor. Changes that did occur were atbibukdtofunctkmalandneummuscular rather than mechanical causes. How aer, raJlson et at (52) concluded, based on gas& fluids that were aipirated from a nasaf gastxk tube insertedearly in labor, that gasbic emptying time was defayed in labor. Each patWent had 750 ml inserted into the stomach; at 1Omtnute. intewafs, the stomach contents were aspirated and assessed.They found that each patient had rapid emptying over the first 10 minutes and then the volume decreased by aknost one-third. They ackncwledged thd the depressanteffect on gastrfcmobility might be due to anxiety and excitement Simpson and Stakes (43) looked at gashic emptying in rektkm to anxfely levels in patients undergoing
ins
-g!J=Jww~.Tluqr fowdthatgaicempvia$skw? in patknts who had ralow predispodti to awkty. Patknk with a tendency toward high anxiety did not show a delay in gasbic emptying.
the pH. They found that the volume of gastriccontents varied markedly. They concluded that every pa&dent should be assumed to have a full stomach of hifhly acid ffutd contents. Hester and Heath (53) noted that 32% of patknk who had been NPO fvrp&ngalp&dshadgfeaterthan 40 mL of gastdc contents. Over half of them had a gastdc aspkate of less thon pfi 2.5. A&dyLyR&edsandShkfq(11) showed that the lntewal since the last meal to delivery did not guarantee a low valume of gasmc juice in the stomach. They concluded that all patients should be assumed to have a fullstomach, regardlessofthe interal since their last oral intake. ANTACIDS
Asdted&,
t&&k&s study (7) wport~ that anesthesia deaths were duetohydmch!odcaddaqir&mand not to neutral aspirates. In an &xl to make the stomach contents less acidic, antaads (30 mL) have mutin+ teen adminirtered. Particulate antactds such as magnesium hydmxide and megnedum tdsflkxte were gtveven at w but they have r!aw been shown to cause sevew pufmonaty damage when aspirated (22,54,.55). Cohen’sstudy (54) shaved that there is no evidence that edmfnieattcm of
Today, sodium &ate. which contains “0 parikufate matter, is often wed for rapid neuwtion of the stomach contents. It has an tmmedtate onset of antacid action, but it also has a wide variation in offtcan, and duration of action. sodium citmkn&,&es&dimmediakk,,but the cdlical factor that its duration of act&n is the gastric emp rates(56). Therefore. analgesics that prolong gashic emptying also pfolong the antacid’s efficiency. or-
influences
tying
doumd of Nune.Mklw&y
nwzano et al (56) found that sodium cl&ate was not always efftcient in increasing gastric pH to greater than 2.5, especially by the time of extw bation. They demonstrated that effervescent cimeiidine-sodium cltiate k effecthrein Increasing gastdc pH to more than 2.5 at intubation and extubation. Cimitidtne. which is an HZreceptor blmker, increasesgasmc pH by inhibiting gastric acid production for four to eight hours However, It must be noted that the volume (30 mL) of antacld wed is above that crftkalwlumepedictiveofkxraeddsk of maternal mortality should aspkation ocC”I:
FASlffVG. NUTRITION. ENERGY UllLfZATlON
AND
The hydration and energy needs of the woman in labor have been compared to the needs of the athlok in competition (4). Food and fluid dwdvaKon dudng this cdtical time n&y impact directly on labor progrw and outcome. Bid glucoseand muscle glyco9en, major sources of enemy for the mother and the fetus, are&xnpmm&d in the pregnant woman during Mng. Animal studies have shown that there is an immedtate and conffnuous decline In makmal and fetal blood gk~case levels during fasting (57). A direct relaUonshii has hen found between matemal glucose few els and fetal well-being as tndkated by fetal breathing movemenk and general fetal activity (58,591. Fetuses of fasted mothers show less overall activity than fetuses of fed mothers. Stimukting ktal activity dudng fetal nonstress tests Is often accomplished by feeding the mothers (59). When blood gkxose is not available to the mother for energy use, tbe body draws on ik fat supplies. As Q raft!ageqllantilje3ofr~~tiy& are oxidfzed, ultimately increadng the quantiites of ketone In the blood and tissues.Thii accumufatin of ketone (p-hydmxybutydc add, amlnwcetk acid) in the body Is known as k&c&.
*
Vol. 38. No. 4, :ufyAuawt
1993
Excessive production of ketone may lead to their excretion in the urine, referred to as ketonuda. Ketosis may progress to ketoacidosis, which is a” accumulation of ketone in the body, accompanied by a metabolk xldtis. Ketoecidosis can be life threatening. However, ketonuria and ketmis are not the sane as ketoaddosis. It is uncertain whether either k&c& 01 ketonuM is actually harmful to the pregMnt or laboring wcnnen 01 her fetus. Ketosls wcurs in the normal adult human body in response to exeriio” and fasting, both of which may be experienced by the labming woman. Pregnant women in general are more prone to ketosts due to increased fetal demands, increased fat uiilttiio”, and pregnancy-induced hormone changes (4, 601. Studies have shown that preg“anqeqgelatesa”dacceIela~the body’s resq~nse to fasang (61. 62). During delivery. blood levels of ketone, free fatty acids, and gtycerol fise to meet energy doman&. Ketone bodtes and free fatty acids stgnifica& illcrease in the blood after only 12 to 18 houm of f&ng in the third mmeskr (63). A.xwa”g to I-!ale (4). “I” laba this tendency toward ketosts ls accentuated by imxased muscu!ar actltity and imposed ltmitation of oral intake.” It is tnteresttng to note that the amcunt of ketone in the blood of mothers who conswned fcod during tabor has been shown to be sig”tficantiy t&w that of fasted mothers (64.65). Ketonuria may be a misleading guidotothe”eedfortlutda”dcarbohydratere$xwM~KetoMlh~ bfze” shown to cccur in nomlal !&or as we!l as in the normal antqutum @lent (59. 60, 63, 66). It is often determined by a ketosiix, which has been shown to report a hiih falsep&tive reading when the blood acetoaeetato level h wttht” “0”“al range (67). Keton-e t&es, when excreted in the wine. take lag+ ~uantiaes oi sodium and patesstun with them, whtch may decrease the blood PH. The”? dws seem to be some reta-
Jcemal d Nume.MldwUery.
tionship between marked ketonuria and prokqed !&xx, but whkh comes first is unclear (601. Some researchers date that as ketone bodies increase in the mother. they cross the placental barrier and increase in the fetus WI. 65. 681. others disagree, Ileef&y adds and ketone &dies do not readily cm55 the placenta (69). Glucose is the minciwl fuel of the fetus, but the r&cat iiterature supportsthet&fthatketonebGdks”ny save es alternative fuel during fetal life (70, 71). Animal studtes have shown ketone bulks 19 be precursors to lipid synthesis. as well as fuel for the fetal brain. liver, and lung in vitro (71). As menti”ed earlier, ketone and lactic add do lower the b&d PH. Lowered pH in the fetus during tabor has been cause for eta”“. It has bee” related to cardiac atiythmtas and considered to be a” indkatbn of fetal anoxta. However, in a recent study, 72% of infants whose cord pH indic&dtbeywesevoroh/actdoacworo born in a vigorous state, with a” Apgar score of greater than 7 at one minute (72). Essential atim, acids gradually dedine when the preqant woman k deprived of food. After only 12 hours of fwd dqxivatto”, 10 cut of 19 matemal amino acid levels were stg”iEca”uyb&w”o”pregrant!+wkva. Amtno adds waxy cross the placerP ial barTier, and levek I” tbe a”mtaa tlti are affected during maternal t&i”g. A decrease in the esse”tid ami”owtda!ainekshoumtobeof primary path&& signifkance in ketotic hypogtycemia of infavzy (62). Thtisistmportanttobthefetusand the “ewbom becaw glucagw, a hormone that stimulates the CMIVOTsiarofg&qFaltog!+xwt”thettveT. onnot permeate the placenta in the prrzmce of hypoglycemia: however, admintskation of aknin to WOW I” labor i”creanes the glucagml levels of cord b!+xl in the human fetus, tbaetydenemingtherkkofneo~tal ketottc hwemia (62).
Vel. 38. No. 4. JehdAwud
stating~that
1993
Routkwadminishationofanin~ ve”aBi”fwiontogrewnta”dtreat dehydwa, ketoa, ar&e eloctrolyteimba!ancecanno!+mgerbeconstdered.c.o”+t&safesu~te for food and t&ids t” labor (4, 73, 74). I”~glucosein~tothe
.
to ind-
F$z$2zbeen show” i”thefetus,followd byhypc&attintbenewbo”l. H~k~tiaUyhamdul to the mpidty devetotalg brain of the fetwandthC”ewban.Deleterious effects may indude acid&s, increased c&o” m0ti.z kvek, increa?edl&icactdkvek,andnecr&al jaundice (75-78). Hvposlycemia may result in in+ “?&t&e re@&ory daess, apnea, cyanosis, and setares (78). Sir& (79) reported that term infants of mothers who recetved intravemw giwost?thempyd”rtngtbecourseof sporl~ or oxytocin-ind”ced hbmsbowd”~tbwaingd muscle tone and &!a~ haUhmtt=x tovadcC¶%muiiatoneandlwoholas of age.” study infants had a three tt”wbttt”cidweof~ cm+ (79). Awidi”g excess inha(76). zzJTzzz:~~w I”anotherSt&,Si”ghtotal@O~ reputedthatt”fu5i”g5%gtucoseto thetabmt”gwo”?an~ila* “ificant t”aeae intheincidsncoof hytmMmmb and subzque”t ha”&ttachyp”eainthenavb+x”infantTheretsarebttonsh@txtxw” COIdSlUtMdi~levehiIlnewbom
infzmk a”d matomal i”~nouS tbempy duri”g labor (81). The sodtum fovols of infants whae mother had5%datmsewasr~!wthatofm&erswhohadorathydratto”.Ako,t”fa”tsd”mtheTswho had dext”xe lnhlskm had St&icantly”wev.wtgbtkssi”thefkst48 hvwsthanthosei”fa”kof”wdWS [email protected]”l levekinthemo(hersandinfantswere way sknilar. When hypoaakemia is
203
kducDd in the mother, it will affect the baby by a netbansfer offluid to the Infant. Fluid overload and hypmmtremia can be sodous complicattons for mother and infant (74. 81). Morton et at (74) state, “k SeenIs tuo@al to sum.vess the comentratio” of ketci& at expense of increasing other “manic a&is which place a greakr on the buffering capacity of the blood.” Maternal hyponatmmia may cause cerebral edema. COIM, convulsions, headache, vomiting, lethargy,, confusion, mood changes,and postpattal psychosis(60,81). Hypanatremia in infants may cause co”wlstons$ apnea, cyanotic spells, neonatal @I”dkx, respiratory dtstxess,feeding dtff&&,and&X&bk-~~kSS after birt!? (60. 80, 81). intravenous therapy, oxytoxtcs, toco& drugs, and endotmcheal intub&to” have atI been seen to adws?iyaffectpuk”aaytlutdbaknee, whffh fsakeadyaltered by pregnancy l73.82). A normal healthy woman at term already has a” abundance of kcdy water. with at least 2 L stored in the extfavascular spacea. DumouIt” et al (60) state that t”tmve”0”s therapy is not rwtinely needed, es@ally in the titi 12 hours of labor. A study by Cotton et al (83) showed that the ordered r&e of inkavenous tlufds was often exceeded by hvtce the amount If inbavenou3 therapy is cli”tcaUy warranted because of the wmnan’s high-risk status,then mettculous intake and output monitoring should be maintained.
the
siain
STRESS Reduction of stressin labor may be asswtated with lesspain, lessanxiety, shorter labors, and fewer pednatal prob!env (84-86). Stress during labor increases the Pmdu@ion of makmal catecholamines. Increarod catecholamkw may affect labor by shunting blood away from the uterus and the placenta, and by lengthening labor. These effects “lay lead to pm-
24M
Ion& fetal hypoxia, as ddenced by abnormal fetal heart tiactngs and abnormal scalp pH samplez @4,87). Laboring women are often subjected to procedures that conbibute to thefr sbesslevel. Stresson imposed during labor may cause compllcations and may conbtbute to the need for awIossive intelventtmls 188). Fastin~k a known stressor.Sin&~ (88). in assessingstressful childbhth events, repotted that 27% of wwne” rated resmctk?”of food I” labor to be mcderatefy to most stre&ul. Ftftyseven percent of women found resbicti~1 of tlutds in !&or to be moderately most0lmLdul (88). The stn?ssre5pow of the fetus is to imrease the pmdution of catecholaminos in order to tncrease norepinephdne. This response dws not manlf&ititithanlnaeaseinbkod f!cw 01 a” incloare in heart rate as see” in the adult. Instead, stress in the fetus initiates a wgus nerve reqwsethatcausssadropi”fetalbeai rate in older to consewe oxygen (84, 86. 89). Sane fetal catechdamine production, however, ts normal. Fetal catecholamines have been show” to conbibute to prosta$andf” syntbests, preparing for onset of labor (86).
to
CURRENT
STUDIES
Avattable Me&we on the oral intake of the laboring wana” focuses primadly on why the womzl” should be kept NF’O. Many authors conrider fasting as a “lewls of reducing “latemalmortalftv Maststudtesfccuso” intenrenttons -used to replenish hydration and energy needs of the kboring wo”Ian. Howaver, a recent study at Jubilee Maternity Hospttal in Belfast, Northem Ireland, conducted by midwife Angela Flanagan, in ass&alto” with Dr. K&an Fikpatrtck, a” anesthetist, looked at outcomes of infants and
four labodng w&e” were en& aged to take Ught foods such as eggs, toast, sandwiches, ice cream, yogurt,
JeUler, and fresh kutt. As a control group, 22 won~e” were permitted intake according to the usual p&y of toast and tea in very early labor with stpaof water thereafter. Ms. Flanagan q&d the f&xvi”g w.u,k. Women who ate required less pain relief and less Pitc&, and the length of labor was shortened on the average by about 90 minutes. In addition, Apgar sso:esd babies in the fed group were hither than in the control group. As a direct result of this study, Intake retictio~ have been overturned in Juhileo Maternity Hospltat, and Ms. Flanagan is cunently undertaktng a repltcation study with 1,OOLIexpected subjeci5 (personal co”l”l”“icatton, A”& Flanagan. Febnmty 21,1993). We studied the eating and &linking @terns of labadng women (unpublished master’s thests, Yale University, 1991). The sample con&ted of 76 women who were observed until they de&red or until they received nwdtcation or intravenous therapy. Women uwe netthor encouri& “or dtscwa&frmn.nalt”takentakebutwere simply &sewed in settings &d self&ection of intake. All of the wornon drank at some point in their hbor and 85.6% ate. More women ate kuSef pmtto”s eartier I” uEirlabws.tap&gafft”&PJwpbase
thatper-
tiembysecondstage. Ddnktng also decreased as cavical di!atkm inerased. with sips dominatinginkteacttwandrecondstsge. It was a!sa noted that the peak Inddence of nausea and vomiting occurredfrom6to8nnratharthan9 to 10 cm as commonly thought Women continued to eat and ddnk after a” eptsode of nausea, although they only drank after vomiting. Women tended to eat at comma” mealtlnws.
Literature from anesthesia and obstetdcs have repeatedly show” that there is no cm”p2ul”g scte”titlc rationale for the maintenance of routine institutional NPO poUctes.These po-
dmmmt of N,,me.Mtdwthrv
.
Vol. 38. No. 4, JufylAuw
1993
need exka e”couragemo”t to provent dehydration and prwide the caon currentscientific research. Elkinglories needed to “rat the stlenuow ton 13) points out that “these p&zips demands of labor and delivery. Naumay persiston the basis of anecdotal expedeme, institutional iwrtia to palsea and vomiting are part of labor for a certain Percentage of wornen. changesbegun in the 19405, com‘Women can continue with their i”. pmmise with anesthesia depaltmentalpoBcytoensule&qutedoquatocovemgo.take after being nauseatedwithout intuning further episcdes. ewwrated notions of risk, or fears of litigation.” Researchers agree that every parFUTURE RE%.ARCH huient should be regarded as having a full stomach with hi&ly acidic fluid What is the best diet for the laboring rwardless of how long she has been woman? Would food and fluids dwNh. With this in And, why limit ing a serial induckn help with labor their intake? We found that lababw prcgre&on? Should a woman who women self-regulated intake. 0”~; is comfortable with an epiduml anactI’ve labor began, women usually al@a be permitted to eat and drink? preferred liquids. Dces~“ofaooda~~ Several studies looked at the efkba? To a”swer these questions, fects of skess on labor. finding that mndomized clinical studies should be labor misht be prolonged and could undertake” whereby women admitinvite intervention. Intravenous fluids ted to labor and deliwy are assig”ed are”&areamn?&subs6kltefororal to one of two groups: an eatfluids for the healthy parhuient I?i”&“k&g~a”da”NFogmup. nally, it is worthwhile to consider the A”&h&a,~miduriferv,a”d psychcio#al importance of food and nting departme”!z should be influids to the iabodng woman. Fbod cluded in the de&n of the studs from and ddinknot only pmvide hydration, thestart nutrition, and increased comfort, but American wanen and few are they also giw the woman a feeling of being subjected to policies based 0” control in labor. Choices have bee” a boiief systen~plasued with inaccurhdegrd in the movement of modem a&s, cut&ted research. and “I&Iobatrlcs. 1nslimno”al policies reformation. The cunent policy of IOUgrading eating and drinking in !&or tine fasnng I” normal labor “lust be shculd be reexamined in the fiqht of reevaluated. It is based on anecdotal mlslnfmma~o”. itituI%maJ inertia
icy
CLINICAL
lMPLllxnoNs
lends
Thiiuterature review support to @ns women the choice to eat and drink in normal labor. There is no such thi”g r~ a” empty sto”mch. re~dless of tims from the fast intake, and to arsumo M could be deadly. In most cases, Me~&ko”‘s syw drome on be prevented by appmpaate anesthesia technique. General a”esth&a should be avoided and re@onafanestb&asubstitutedasmuch as uasible. Women should be enccwa~toosatanddrinkastheys.z=z fit. If a woman is !&a&g in the eariy morning hours, however, she may
wintlodud IO the medical cornmunily and the conwner based on current sound scientific rosoarch.
REFERENCES l.!&wchJ,NewtcaN.FaDda”d lwamges in l&r. Part 1: cms5&tuml andh!st&?Jpracla.Bktb1998;15:815. 2. D&on C, Gudgeon CW. For feeding di;dng k&or. Med J Aurt 1987:147:625-6. 3. Elki@o” K At the wat& +2: where &iemCr and an&b&a obstet Gy”~~1991;71:304.
6. DeLee JR c?bseba for ““r$Qe. 5ul ed PhuadelPhta: samien, 1918. 7. Me”d.?lsuIcL.Tbe8s#aw”of rtornachccntent,intothelu~dt& obstewanosthsriaA”lJobstetA”orth 1946:52:191205. 8. JamerC,ubbsC.BannerT.Pmt-
9. 9. JawsC,M&zllJ.GibbsC,Kuck E.R~B.Pulmorw~am&a~““effeck
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HOME STUDY PROGRAM IJF’OAlEB
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JNM’s 1992 Home St”dy Pmgam. which feat”res “The New&“” lh!arch/Apaill992 SUP plemerd). wflf be v&J for 0.9 CEUs through Apiu 30.1994. The fee is $100. Pfeare note the fdfcwing change Payment and study materials should be sent m to May Ann Shah. JNM Editor, 67 Tany HIU Road, Tarrytaun. NY 10591. JNM’s 1993 Home Study Program, which feabires “Advanced Nursa-Mfdwikry Ractke” (March,Apd, 1993 Suppfmnent), tiff be v&d for 1.0 CELk +hro@ Aplu 30.1995. The fee ir $75 for submissions p&marked by Aug.ut 31, 19%. and $100 tkrealter. PleasD note the fdkJ!#i~ conections: Page 7s: Post-test question X 18 should be feR b!ank on the Answer sheet
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F’agz33-5: Cdumn Lpamgraph2 senhnceXS-“ThePi~kgond~introducedlhrC& the cervical OS and up into the uterine fundus. much like the techn&w used to sound the ute,,,s p&r to lnhauterine d&e ins.ezta.“--rhodd have been -t ivm sentewes e=rk=% Itkhopedlhatnoreaderws.oxfusedbythkmispinL JNM’s 1994 Home Study Pagmm. wti wlU feature “Ofxtehk C~i@kam,” is wdf undemay. It will ,,a p&shed as a Sprins Su&ment and wi” offa 1.0 CEUS to pattkipanb. Prefimfnay preparafions are ixginnbq for the 1995 Home Study Pmgmm. It is anticipakd that its foeus wiu be “Comprehenskw Hoalfh dent” please w&h fhQ Jcumal for fmtha ,nfonw,bbn and for ‘A Call tot Absbacis.”
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