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_______________________________________________________________ #3316 Hyperemesis Gravidarum

CME Resource Sacramento, California Phone: 800 / 232-4238 FAX: 916 / 783-6067 1

Hyperemesis Gravidarum

Mention of commercial products does not indicate endorsement.A complete Works Cited list begins on page 22.

Faculty

Sandra Msics, CNM, MSN, RN, is a native o Beth-lehem, Pennsylvania. She attended Penn State Univer-sity where she graduated with a BS in Psychology. In1983, she moved to Miami, Florida where she earneda BS degree in Nursing at Barry University, graduatingmagna cum laude.

Ms. Mesics worked as an RN in Labor & Delivery,postpartum, and newborn nursery at Mount SinaiMedical Center, Miami Beach, FL and started workon her Masters degree in 1994. She became a certiednurse-midwie in 1997, and was the rst nurse-midwiegranted privileges at Mount Sinai Hospital o GreaterMiami.

In 2001, Ms. Mesics returned to Bethlehem, PA toaccept a aculty position teaching maternity nursingat St. Lukes School o Nursing. She also maintainsprivileges at St. Lukes Hospital, providing nurse-midwiery care in the womens health clinic. In 2004,Ms. Mesics became director o the School o Nursing.She is a member o Sigma Theta Tau Nursing HonorSociety, the American College o Nurse-Midwives,and the Association o Womens Health, Obstetric,and Neonatal Nurses, as well as the National Leagueor Nursing. She served on the advisory committee oretal bronectin.

Copyright 2008 CME Resource

CouRSe #3316 5 CoNTACT HouRS Release Date: 09/01/08 expiRationDate: 08/31/11

Faculty Disclosure

Contributing aculty, Sandra Mesics, CNM, MSN, RN,has disclosed no relevant nancial relationship with anyproduct manuacturer or service provider mentioned.

Division Planner

Jane Norman, RN, MSN, CNE, PhD

Division Planner Disclosure

The division planner has disclosed no relevant nancialrelationship with any product manuacturer or serviceprovider mentioned.

AudienceThis course is designed or all nurses, especially thoseworking in obstetrics and maternal/child nursing.

Accreditation

CME Resource is accredited as a provider o continuingnursing education by the American Nurses CredentialingCenters Commission on Accreditation.

Designation of Credit

CME Resource designates this continuing educationactivity or 5 ANCC contact hours.

CME Resource designates this continuing educationactivity or 6 hours or Alabama nurses.

AACN Synergy CERP Category A.

Individual State Nursing Approvals

In addition to states that accept ANCC, CME Resourceis approved as a provider o continuing educationin nursing by: Alabama, ABNP0353 (valid throughDecember 12, 2013); Caliornia, CEP9784; CaliorniaBVNPT Provider #V10662; Florida Provider #50-2405;Iowa, #295; Kentucky, 7-0054, Kentucky Board oNursing approval o an individual nursing continuing

education provider does not constitute endorsement oprogram content; Texas, ANCC/Type I Provider.

HoW To ReCeIVe CReDIT

Read the enclosed course.

Complete the questions at the end o the course.

Return your completed Evaluation to CMEResource by mail or ax, or complete online atwww.NetCE.com. (I you are a Florida nurse or abehavioral health proessional, please return theincluded Answer Sheet.) Your postmark or acsimiledate will be used as your completion date.

Receive your Certicate(s) o Completion by mail, ax, or email.

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#3316 Hyperemesis Gravidarum _______________________________________________________________

2 CME Resource November 29, 2010 www.NetCE.com

About the Sponsor

The purpose o CME Resource is to provide challengingcurricula to assist healthcare proessionals to raise theirlevels o expertise while ullling their continuingeducation requirements, thereby improving the qualityo healthcare.

Our contributing aculty members have taken care toensure that the inormation and recommendations areaccurate and compatible with the standards generallyaccepted at the time o publication. The publisherdisclaims any liability, loss or damage incurred as aconsequence, directly or indirectly, o the use and appli-cation o any o the contents. Participants are cautionedabout the potential risk o using limited knowledgewhen integrating new techniques into practice.

Disclosure Statement

It is the policy o CME Resource not to accept commer-cial support.

Course Objective

Practitioners commonly treat nausea and vomiting inearly pregnancy, regardless o whether the patient tsall the criteria o a diagnosis o hyperemesis gravidarum.The purpose o this course is to increase the awarenesso hyperemesis gravidarum and present guidelines ornursing management o the condition.

Sections marked with this symbol includeevidence-based practice recommendations.The level o evidence and/or strengtho recommendation, as provided by theevidence-based source, are also included

so you may determine the validity or relevance o theinormation. These sections may be used in conjunc-tion with the course material or better application toyour daily practice.

Learning Objectives

Upon completion of this course, you should be able to:

Dene hyperemesis gravidarum, and1.distinguish it rom the normal nauseaand vomiting o pregnancy.List the potential eects o hyperemesis2.

gravidarum on the etus and mother.Compare the various theories o etiology3.o hyperemesis gravidarum.

Identiy the populations at risk or4.hyperemesis gravidarum.Describe dietary interventions or5.treatment o hyperemesis gravidarum.

Describe pharmacological agents used in6.the management o hyperemesis gravidarum.

Describe the role o intravenous therapy7.in treating hyperemesis gravidarum.

Outline nonpharmacologic interventions8.to treat hyperemesis gravidarum.

Explain the nursing assessment and9.related diagnosis and interventions orthe patient with hyperemesis gravidarum.

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INTRoDuCTIoN

Between 50% and 80% o pregnant womenexperience nausea and vomiting beginning at aboutthe ourth week and ending at about the twelthweek o gestation. In act, nausea and vomiting areconsidered a presumptive sign o pregnancy, andor about 20% o pregnant women, these symptomsmay persist throughout the whole pregnancy [38].While nausea and vomiting are common occur-rences, hyperemesis gravidarum is rare, occurringin about 0.1% to 0.2% o all pregnancies [35].

In the United States, more than 50,000 women arehospitalized annually or hyperemesis gravidarum,with an average hospital stay o our days [14].The nancial burden on the United States health

system has been estimated to be about $130 millionper year, not including physician ees or the loss oproductivity at home and in the workplace [38].

DefINITIoN of

HypeReMeSIS GRAVIDARuM

There is some variation in the literature as to theexact denition o hyperemesis gravidarum. It isoten dened as intractable nausea and vomiting

during pregnancy severe enough to require hospital-ization [2]. Moreover, the condition appears duringthe rst trimester and is unassociated with othermedical conditions, such as cholestasis, hepatitis,preeclampsia, viral syndrome, Menieres disease,or infuenza [45].

The most commonly accepted denition is thathyperemesis gravidarum is a severe orm o nauseaand vomiting with weight loss greater than 5% oprepregnancy body weight, dehydration, acidosis

rom starvation, alkalosis rom loss o hydrochloricacid, hypokalemia, ketosis, acetonuria, andptyalism (excessive salivation) [2]. In most cases,the onset o symptoms is between 4 and 10 weeksgestation and the symptoms usually subside by 20weeks gestation.

Clinically, practitioners commonly treat nauseaand vomiting in early pregnancy, regardless owhether the patient ts all the criteria o a diag-nosis o hyperemesis gravidarum.

effeCTS of HypeReMeSISGRAVIDARuM

feTAl effeCTS

There is some debate in the literature as to whetherhyperemesis gravidarum is associated with lowinant birth weight. Zhang and Cai ound a modestassociation between severe nausea and vomiting inpregnancy and etal growth restriction [61]. Chinound a signicantly lower mean birth weight orbabies born to women with hyperemesis gravi-

darum than in women with either mild nausea andvomiting in pregnancy or no nausea in pregnancy[9]. Gross, Librach, and Cecutti ound intrauterinegrowth restriction (IUGR) and signiicantlylower birth weights or women with hyperemesisgravidarum [25]. This study ound that a maternalweight loss o greater than 5% was the criticalactor in etal growth restriction.

Animal studies have shown that unbalancedmaternal nutrition exposes the etus to excess

glucocorticoids, which restrict etal growth andprogram permanent alterations in cardiovascular,endocrine, and metabolic syndromes, resulting inhypertension, dyslipidemia, insulin resistance, andtype 2 diabetes [75]. This eect in humans remainsto be determined.

One classic study by Depue et al. ound a correla-tion between central nervous system disorders andskeletal malormations in babies born to womenaected by hyperemesis gravidarum [13].

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Despite the act that hyperemesis gravidarum maybe associated with poor etal growth and outcome,epidemiological evidence has shown that womenwho have normal nausea and vomiting in earlypregnancy have a statistically decreased risk omiscarriage in the rst 20 weeks o gestation than

do those who t the diagnosis o hyperemesis gravi-darum [25]. This nding implies that normal nauseaand vomiting in the rst trimester o pregnancy isprotective against miscarriage. This evidence wassupported by a large epidemiological study thatshowed women who experienced vomiting in earlypregnancy had a decreased risk o miscarriage [58].The authors conclusion is that any vomiting inearly pregnancy is protective. However, althoughthe sample was large (903 women), the authors didnot investigate how many vomiting episodes these

women reported.MATeRNAl effeCTS

Prior to the modern understanding o fuid andelectrolyte balance, hyperemesis gravidarumcould be a lie-threatening event. In many cases,pregnancy termination was advocated. Today,while this condition is rarely atal, several lie-threatening complications may occur, commonlyinvolving the central nervous system [14].

Wernickes encephalopathy results rom a de-ciency o thiamine (vitamin B1) and is mani-ested by conusion, gait ataxia, ophthalmoplegia(paralysis o the eye muscles), or convulsions.Typically, thiamine is initially lost by prolongedvomiting and when intravenous fuid replace-ment containing dextrose is given. The bodysmetabolism o the dextrose quickly consumes theremaining thiamine. Thereore, the cause is usuallynot the hyperemesis itsel but is instead due tofuid replacement without thiamine supplements.

More than 20 cases have been reported in recentyears, with permanent morbidity or mortality in80% o the cases [43]. Also, a rapid correction osevere hyponatremia (sodium deciency) by intra-venous inusion may cause osmotic demyelinationsyndrome, an uncommon disorder.

Rare reports have included esophageal rupture,spontaneous pneumomediastinum (presence o airor gas in the mediastinum), vasospasm o cerebralarteries, rhabdomyolysis (disintegration o stri-ated muscle bers with excretion o myoglobin inthe urine), peripheral neuropathy due to vitaminB6 and B12 deciency, and coagulopathy due tovitamin K deciency.

Hyperemesis gravidarum imposes a physical,emotional, and nancial burden on women and

their amilies. Nearly 50% o employed womenbelieve that their eectiveness at work is impairedby this problem, and 25% o women must taketime away rom work [38]. Approximately 50% owomen with nausea and vomiting in pregnancyreport that the condition has adverse eects ontheir spousal relationships. More than one-hal oaected women eel depressed. Some women mayactually choose to terminate pregnancies aectedby hyperemesis. One survey ound that out o 1100women with hyperemesis, 17 reported terminatinga pregnancy due to hyperemesis and 42 women hadconsidered doing so [66].

Presence o hyperemesis gravidarum has beenshown to signicantly aect a womans quality olie. One study indicated that women experiencingsevere nausea and vomiting had decits in theeight measured domains o quality o lie, includingphysical unctioning, role limitations (physical andemotional), bodily pain, general health, vitality,social unctioning, and mental health [4].

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THeoRIeS of eTIoloGy

No single cause or hyperemesis gravidarum hasbeen ound. Theories o causality include hypo-thyroidism/thyrotoxicosis, gestational hormones,hepatic dysunction, gastric dysunction, inection,autonomic nervous system dysunction, nutritionaldeciencies, and psychological actors [2]. Each othese theories will be discussed in some detail. Itis likely, however, that hyperemesis gravidarum isa multiactorial syndrome, with no single etiologybeing responsible [15].

HypeRTHyRoIDISM/ THyRoToxICoSIS

In normal pregnancy, the thyroid gland enlarges50% and thyroxine (T4) secretion increases due to

increased levels o human chorionic gonadotropin(hCG) and human chorionic thyrotropin (hCT),which are secreted by the placenta. The hCGmolecule is a glycoprotein molecule that containsthe structural characteristics required or interac-tion with the thyroid stimulating hormone (TSH)receptor and activation o the membrane adenylatecyclase that regulates thyroid cell unction. ThehCT molecule is also a glycoprotein molecule withproperties similar to TSH; it increases the secre-tion o thyroid hormone and stimulates the incor-

poration o inorganic phosphate into the thyroid.The increase in thyroid hormone levels occurs inthe rst trimester and continues throughout preg-nancy. Estrogen levels also increase during preg-nancy. The increase in estrogen causes an increasein thyroxine-binding globulin (TBG) productionin the liver. About 80% o thyroid hormones arebound to TBG, resulting in serum T4 concentra-tions in the hyperthyroid range.

Pregnancy is characterized by adaptation o thyroid

hormone economy to the rise in TBG concen-tration [35]. During the rst trimester, there is agradual rise in serum protein-bound iodine, whichis dependent on the increase in estrogen levels.There is also a small increase in ree T4 and adecrease in thyroid stimulating hormone during

early pregnancy [29]. This suggests that thyroidhormones are stimulated by something other thanTSH.

The normal rise in serum T4 that occurs in preg-nancy may be due to the eects o hCG. As TSHand hCG share the same common a-subunit, it

has been suggested that hyperemesis may be due toelevated hCG levels [60]. Support or this hypoth-esis comes rom a study by Goodwin, Montoro, andMestman [22].

However, Kennedy, Darne, Davies, and Priceconducted an in vitro study o thyroid activity inve hyperemesis patients and did not nd supportor the hypothesis that hCG stimulates thyroidactivity [30]. Wilson et al. studied thyroid hormonelevels in 10 patients with hyperemesis gravidarum

and ound that, while individual patients wereound to have some abnormal thyroid unctiontests, the group as a whole showed no dierencesin thyroid hormone levels rom a group o healthyrst trimester pregnant women [60]. Levels o hCGwere also normal in the hyperemetic patients. Theauthors suggest that hyperemesis gravidarum maybe caused by some circulating stimulator not yetidentied. Abell and Riely suggest that there is acirculating hormone or hormone-like substancethat may stimulate the thyroid gland and renderit temporarily unresponsive to the control o thepituitary [2]. When this substance subsides in laterpregnancy, both the hyperemesis gravidarum andthe hyperthyroidism resolve.

There is an increased incidence o transient hyper-thyroidism in hyperemesis patients [11]. Goodwin,Montoro, and Mestman studied 67 patients withdiagnosed hyperemesis gravidarum and ound that66% had biochemical hyperthyroidism [22]. Thesigns and symptoms o hyperthyroidism include

tachycardia, diarrhea, nausea and vomiting,hyperkinesia, atigue, irritability, and weight loss.In addition, one investigation also ound a greatermean arterial pressure and pulse in pregnantpatients with hyperthyroidism. Laboratory resultsshow marked elevation o thyroid hormones andsuppression o thyroid-stimulating hormone [22].

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There is some debate in the literature regardingwhether the severity o the nausea and vomitingin pregnancy is related to the degree o hyper-thyroidism. While some investigators, includingGoodwin, Montoro, and Mestman, ound asignicant association between the severity o

vomiting and the degree o hyperthyroidism, otherstudies showed no correlation [17; 22]. Goodwin,Montoro, and Mestman speculate that vomitingmight induce thyroid stimulation but add thatthere is no evidence to support such an eect. Theybelieve that the source o the hyperthyroidism islinked to the cause o the vomiting, but it is notcausative in and o itsel [22].

Kimura et al. measured triiodothyronine (T3),T4, THS, hCG, and thyroid-stimulating activity(TSA) in 51 pregnant women [31]. The womenwere divided into three groups: those withoutemesis (n=9), those with emesis (n=19) and thosewith hyperemesis gravidarum (n=8). While theresearchers ound no signicant dierence in thehCG levels among the three groups, they ound thatT4 levels were signicantly higher in the emesis andhyperemesis groups than in the non emesis group.Also, TSA levels were unexpectedly high in thegroup with hyperemesis. The study ound thatclinical symptoms o thyrotoxicosis were ound

to be correlated to levels o T4. The patients withthyrotoxicosis were ound to have T4 levels twicethe upper limit o normal. The authors suggesta new diagnosis o gestational thyrotoxicosisbecause the symptoms are dierent than classicalGraves disease and clear up in the latter hal opregnancy [31].

According to Goodwin, Montero, and Mestman,the degree o thyroid stimulation correlated signi-cantly with hCG levels [22]. They also ound that

in hyperemesis gravidarum, hyperthyroidism didnot persist ater resolution o vomiting. In all cases,the hyperthyroidism was sel-limiting and resolvedwithin 1 to 10 weeks.

The American College o Obstetriciansand Gynecologists (ACOG) recommendsthat in patients with hyperemesisgravidarum who also have suppressedthyroid-stimulating hormone levels,

treatment o hyperthyroidism should not be undertakenwithout evidence o intrinsic thyroid disease (including

goiter and/or thyroid autoantibodies).(http://www.guidelines.gov/summary/summary.aspx?doc_id=10939. Last accessed July 16, 2008.)

lv evidnc: A (Based on good and consistentscientic evidence)

GeSTATIoNAl HoRMoNeS

Human chorionic gonadotropin has been suspectedas the cause o hyperemesis gravidarum based

chiefy on the observation that its peak concen-tration in pregnancy coincides with the peak onausea and vomiting [23]. In a study o 57 womenwith hyperemesis gravidarum, Goodwin et al.ound that when compared with a control groupo non-hyperemesis patients, the hyperemesispatients had signicantly higher levels o hCG[23]. Moreover, the amount o hCG correlatedwith the degree o thyroid stimulation and thedegree o emesis. These researchers believe thathCG is the causative actor or both hyperemesis

and hyperthyroidism in pregnancy.Another suggestion or the causative role o hCGin hyperemesis gravidarum is the associationbetween increased levels o hCG and hyperemesisin cases o hydatidiorm molar pregnancies [32].

Depue et al. conducted a study o serum hormonelevels in the irst trimester o pregnancy andconcluded that the high estrogen levels secreted bythe placenta accounted or hyperemesis gravidarum[13]. This study ound no association betweenhyperemesis gravidarum and hCG levels.

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Another hormone possibly responsible or hype-remesis gravidarum is 17-hydroxyprogesterone, asteroid hormone produced by the corpus luteumduring pregnancy [2]. However, a study by Gadsby,Barnie-Adshead, and Jagger ound that the risinglevels o progesterone in pregnancy act to suppress

nausea and vomiting by inhibiting prostaglandinE-2, which is released rom decidual cells andmacrophages o the decidua basalis [19].

It has been postulated that the position o thecorpus luteum aects nausea and vomiting duringpregnancy [50]. Theoretically, a corpus luteumarising rom the right ovary results in a highconcentration o sex steroids draining directlyinto the inerior vena cava and portal system,overwhelming the liver and causing hyperemesis.However, a case report by Thorp, Watson, andKatz reutes this theory [54]. A woman with severehyperemesis underwent excision o a right-sidedcorpus luteum at 12 weeks gestation. Her symptomsdid not improve ater the surgery.

HepATIC DySfuNCTIoN

In pregnancy, there are ew changes in livermorphology, but there are alterations in liver unc-tion. During the rst trimester, serum albumin andprotein concentration all, although intravascular

protein is increased due to the increase in plasmavolume. Most globulin ractions rise during preg-nancy due to placental hormone production, andthe albumin-globulin ratio decreases because o thedilution o albumin.

Hepatic dysunction has been reported in patientswith hyperemesis gravidarum [2]. Liver enzymeabnormalities have been documented in 25% ocases o hyperemesis gravidarum, as well as hyper-bilirubinemia and retention o bromsulphalein

sodium [39]. It is postulated that because theliver is the major site o inactivation o steroidhormones, hyperemesis may be due to either thelivers inability or slowness in inactivating theincreased hormonal load during pregnancy. Onestudy showed signicantly increased estriol andsex hormone binding globulin in patients with

hyperemesis [13]. Hyperestrogenism can inducevomiting, which can lead to dehydration andinadequate nutrition, thus producing liver enzymeabnormalities.

Goodwin, Montoro, and Mestman examined boththyroid unction and liver unction in 67 hyper-

emesis gravidarum patients and ound that thehyperemesis patients with hyperthyroidism weresignicantly more likely to have abnormalities inelectrolyte levels and liver unction studies, andconversely, those patients with the most severealterations in these parameters demonstrated thegreatest degree o biochemical hyperthyroidism[22].

However, liver unction abnormalities are arrom universal in hyperemesis gravidarum. One

study revealed abnormal liver unctions in only50% o patients with the condition [57]. Becauseliver dysunction does not occur universally withhyperemesis gravidarum and it resolves spontane-ously with the condition, liver dysunction may besecondary to hyperemesis gravidarum.

GASTRIC DySfuNCTIoN

The role o gastric unctioning in hyperemesis grav-idarum has also been studied. During pregnancy,increased levels o progesterone cause relaxation

o the esophageal sphincter, not only resultingin heartburn but in nausea and vomiting as well.Also, as a result o progesterone, gastric emptyingis delayed and small bowel motility is reduced.

The mechanical activity o the stomach iscontrolled by myoelectrical activity that propagatesslow waves that move ood rom the proximal bodyo the stomach to the distal antrum at 3 cyclesper minute. The electrogastrogram (EGG) is atest that measures gastric myoelectrical activity.

It was rst used in 1922 and is mainly utilized asa research tool in gastroenterology. At this time,it is not commonly used as a clinical or diagnostictool. Changes in EGG activity have been associ-ated with clinical syndromes such as dyspepsia,diabetes mellitus, anorexia nervosa, and nauseaand vomiting in pregnancy [1].

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Riezzo et al. used the EGG to study gastric activityin pregnant women and ound abnormal EGGactivity in nine women with severe nausea andvomiting in the rst trimester when compared withtheir EGG activity ater voluntary terminationo the pregnancy [46]. The women with nausea

also had abnormal EGG activity when comparedwith a control group o pregnant women o similargestational age but without nausea and vomiting.The study also ound delayed gastric emptying inwomen with hyperemesis gravidarum.

INfeCTIoN

Inection with Helicobacter pylori, a gram-negativespiral bacterium, has been implicated in gastriculcers and has been investigated as a cause ohyperemesis gravidarum. In a study by Frigo et al.,

the investigators ound that 90.5% o pregnantwomen with hyperemesis gravidarum were sero-positive or H. pylori, as opposed to 46.5% o thepregnant control group [18]. Case reports havealso suggested that eliminating H. pylori inectionmay cure hyperemesis gravidarum [14]. This is apromising eld or urther research.

AuToNoMIC NeRVouSSySTeM DySfuNCTIoN

It is speculated that the changes in gastric unc-

tioning may be related to changes in autonomicnervous system unction, particularly sympatheticadrenergic unction [2]. Other changes in auto-nomic unction related to physiologic changesduring pregnancy include increased basal meta-bolic rate, glomerular ltration rate, blood volume,body temperature, and heart rate. Wallstedt, Riely,and Shaver ound that autonomic unction testvalues were blunted in individuals with hyperem-esis gravidarum [57].

NuTRITIoNAl DefICIeNCIeS

Very ew studies on nutritional deciencies ascausal actors or hyperemesis gravidarum havebeen cited in the literature. The research relatedto nutrition that has been published has ocused ontrace elements, notably zinc and copper. However,an association between hyperemesis gravidarum

and deciency states o these elements has not beenound [2]. This is an area o research that requiresmore attention.

pSyCHoloGICAl fACToRS

Most o the literature regarding a psychological

causation or hyperemesis was published prior toand during the 1970s. One could conclude thatthis is not an active area o research. However,psychological actors should not be entirelydiscounted because there is a denite relationshipbetween psychological actors and eating disorders[52]. Moreover, the cause and eect relation-ship between hyperemesis and psychopathology,including social anxiety, anxiety, insomnia, ordepression, is not clear. A 2004 study ound a highdegree o psychopathology among women with

hyperemesis, but the cause and eect is not clear.It is hypothesized that an underlying psychopa-thology may cause or exacerbate hyperemesis symp-toms, or hyperemesis could cause or exacerbate thepsychopathology [73].

A psychological actor that may play a role inhyperemesis is the womans perception o thepatient-physician relationship. Some studies haveshown that women with hyperemesis encounterphysicians and providers who may doubt, trivi-

alize, or ignore their symptoms. Women were notsatised with physicians who implied that theirsymptoms were caused by psychological actors,stress, or poor coping. In helping a patient sueringrom hyperemesis, it is important or healthcareproviders and patients to explore their belies ocausation and arrive at a mutually agreeable treat-ment plan [71].

Various theories o neurosis have also beenadvanced to explain hyperemesis gravidarum:

stress reaction, a repudiation o emininity, aconscious or unconscious desire not to be pregnant,a subconscious rejection o the etus, a orm osel-punishment, as well as unmarried status andambivalence toward pregnancy [5; 15].

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El-Mallakh, Liebowitz, and Hale presented twocase studies o hyperemesis gravidarum andconcluded that hyperemesis gravidarum ts thecriteria or a conversion disorder (a loss or altera-tion in physical unctioning due to unconsciouspsychological actors) [15]. The authors do not

claim that conversion disorder is the exclusiveetiology o hyperemesis gravidarum but insteadthat it is part o a multiactorial syndrome.

According to Bogen, one o the arguments oeredin support o the psychosomatic theory o hyper-emesis gravidarum is that there is no provenphysiological explanation [5]. Bogen perormed abibliographical analysis o the literature on hyper-emesis rom 1965 to 1991. Using Medline, sheexamined 384 studies on the subject and oundthat 64 were concerned with determining theetiology o hyperemesis gravidarum. O the 64,31 were published in English. Finally, o these 31,only our examined possible psychological causes.Upon urther investigation, these our studieswere ound to suer rom insucient controls. Inaddition, there were no attempts to eliminate thebias o interviewers and hospitalization was usedas a criterion or diagnosis o an illness.

Bogen ound no scientic evidence to suggest thatambivalence towards pregnancy causes nausea andvomiting. She asserts that unexplained illness inwomen was commonly attributed to reproductiveunction in the 19th century. The cure or suchillness was surgery: hysterectomy, ovariectomy, andclitorectomy. Ater psychoanalysis was introducedby Freud, these illnesses in women were attributedto neuroses. In the latter hal o the 20th century,any condition o pregnancy that is not usual isconsidered abnormal. Bogen asserts that whilenausea and vomiting in the rst trimester o preg-

nancy is normal, vomiting beyond that point isconsidered abnormal and thereore pathological.

populATIoN AT RISk

Lazarus used the criteria o weight loss greaterthan 5% during the rst 16 weeks o pregnancyand determined that the incidence o hyperemesisgravidarum as 0.1% to 0.2% o all pregnancies [35].This rate is lower than that ound by Abell andRiely, who estimated the incidence to be 0.3% to1% [2].

Abell cites high body weight and nulliparity(having not given birth to a child) as risk actorsor hyperemesis [1]. Maternal age younger than20 years and twin gestation were also noted asrisk actors [2]. Godsey and Newman studied 140women admitted to a hospital or hyperemesis grav-idarum and ound that a signicant number were

nulliparous [21]. The condition can repeat itselin subsequent pregnancies and is more commonin women with a history o spontaneous abortions[19]. A 2005 study has shown a high risk o recur-rence in second pregnancies, which was somewhatreduced by a change in paternity. For women withno history o hyperemesis, a long interval betweenbirths slightly increased the risk o hyperemesis inthe second pregnancy [72]. Conversely, pregnantwomen older than 35 years o age and those whosmoke cigarettes seem to be less at risk [2].

There is little demographic data relating to hype-remesis gravidarum and little evidence to suggestthat any racial or ethnic group is at increased risk.One study did note an increased risk among PacicIslander (Polynesian) women [8].

A study o antenatal hospitalizations o 1,825enlisted United States servicewomen between1987 and 1990 showed that 5.5% o all admissionswere due to hyperemesis. The study also showed

that the largest percentage (30.2%) o admissionsduring the rst 19 weeks o pregnancy were due tohyperemesis. The same study showed no statisti-cally signicant dierences between black andwhite women [3].

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According to a report summarizing inormationrom the Nationwide Inpatient Sample (NIS), adatabase maintained by the Agency or HealthcareResearch and Quality, excessive vomiting duringpregnancy was the second most common reasonor antepartum hospitalizations in the year 2000,

ranking only behind preterm labor [28]. Hyper-emesis was the admitting complaint or 36,626discharges or antepartum stays, accounting or9.7% o all antepartum hospitalizations. The statis-tics or antepartum hospital stays were not brokendown into individual diagnoses, but the averagelength o hospitalization or all antepartum patientsis 2.8 days. The NIS covers all patients dischargedrom hospitals rom 28 states, which includes about7 million records [28].

In a study o ive women with hyperemesis,Kennedy et al. made the serendipitous ndingthat all ve women in the study were Asian while10% o the clinical population was Asian [30]. Theauthors do not hypothesize, however, that Asianwomen are at higher risk or hyperemesis.

In another study o 67 women with hyperemesispresenting at Los Angeles Womens hospital, 94%were Hispanic [22]. However, the authors do notgive the racial mix o the general population servedby this acility.

INTeRVeNTIoN STRATeGIeS

Intervention strategies or hyperemesis gravidarumare outlined in Table 1. Generally, treatmentis dependent on the severity o symptoms. Mildnausea and vomiting without dehydration may betreated on an outpatient basis with a conservativeapproach. Treatment begins with a modication othe diet and alternative treatments beore utilizing

pharmacological treatment.I nausea and vomiting are accompanied bydehydration, inpatient care may be indicated orrehydration and vitamin and mineral replacementas well as antiemetic therapy. Once ketonuria andnausea and vomiting are resolved, home care might

include antiemetic treatment, either orally or byhome inusion via subcutaneous pump.

Intractable cases may be managed by total paren-teral nutrition (TPN) via a central venous cath-eter or parenteral nutrition via a percutaneousendoscopic gastrostomy (PEG) tube. This may be

continued as long as oral eeding is not tolerated.While treatment strategies to this point haveocused on symptomatic management o womenalready experiencing hyperemesis gravidarum, onestudy shows promise or preemptive treatment orwomen who experienced hyperemesis in a previouspregnancy [69]. In this study, women who hadhyperemesis in a previous pregnancy were assignedto either the treatment group or the control group.Women in the treatment group received a standard

orm o pharmacological therapy prior to the onseto symptoms, while those in the control groupreceived treatment only ater the onset o symp-toms. The authors ound that there was a substan-tial decrease in the symptoms o hyperemesis in thetreatment group versus the control group [69].

DIeT AND beHAVIoR MoDIfICATIoN

Kousen recommends irst treating nausea andvomiting o pregnancy conservatively with dietin the hopes that the problem will not progress to

hyperemesis gravidarum [33]. General recommen-dations include choosing a bland diet, increasingcarbohydrate intake, decreasing at intake,avoiding oensive ood odors, and not takingtablets containing iron. Kousen also advises omit-ting prenatal vitamins containing iron until thenausea resolves.

Specic suggestions oered by Newman, Fullerton,and Anderson are to eat bread or crackers beoregetting out o bed in the morning, when nauseated,

and beore retiring or the night [42]. They alsorecommend eating small meals every 2 to 3 hours;drinking liquids between meals rather than withmeals to avoid gastric distention; eating low-at,high-protein oods; avoiding ried oods; and saltingood to taste.

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A controversial approach by Erick involves eedinghyperemesis patients potato chips and lemonade[16]. The study ound that potato chips were supe-rior to the commonly prescribed saltine crackersin that they supplied more olic acid, vitamin C,

and potassium. Potato chips also drive a thirst,particularly or cold, tart, or sweet liquids. Erickound that lemonade is better tolerated by patientsthan either ginger ale or plain water.

TReATMeNT of HypeReMeSIS GRAVIDARuM

Antimtics

Meclizine (Antivert) 25-50 mg qd PO PregnancyCategoryB

Antihistaminethatdecreasesexcitabilityofmiddleear. Associated with relie o nausea and vomiting.

Dimenhydrinate (Dramamine) 50-100 mg q4-6h PO PregnancyCategoryB Antihistaminethathasanticholinergicand

antiemetic properties. Decreases vestibular stimulation.

Diphenhydramine (Benadryl)25-50 mg q6-8h PO; not to exceed 400 mg/d10-50 mg q6-8h IV/IM; not to exceed 400 mg/d PregnancyCategoryB Antihistaminewithanticholinergicandsedative

properties. Can be used or vestibular disordersthat may cause nausea and vomiting.

Prochlorperazine (Compazine)

5-10 mg q4-6h IM/PO; not to exceed 40 mg/d25 mg bid by way o the rectum (PR) PregnancyCategoryC

Antidopaminergicdrugthatblocksdopaminereceptors; has an anticholinergic eect.

Promethazine (Phenergan) 12.5-25 mg q8h PO/PR25 mg IM/IV PregnancyCategoryC AnH1 receptor-blocking antihistamine agent

that provides sedative and antiemetic eects.

Metoclopramide (Reglan) 5-10 mg q8h IM/PO/IV/SC PregnancyCategoryB

Blocksthedopaminereceptoragentsinthechemoreceptor zone o the central nervous system;stimulates intestinal motility.

Hydroxyzine (Atarax, Vistaril) 50-100 mg q6h PO PregnancyCategoryC AnH1 receptor-blocking antihistamine agent

that provides sedative and antiemetic eects.

Trimethobenzamide (Tigan) 200 mg q6h PR PregnancyCategoryC Exactmechanismofactionunknown.

Droperidol (Inapsine) 0.625-2.5 mg q3-4h IM/IV PregnancyCategoryC

Neurolepticagentthatblocksdopaminestimulationo the chemoreceptor zone to reduce nausea andvomiting.

*Droperidol has been given a black box warningby the FDA; it has been associated with atal cardiacarrhythmias.

Ondansetron (Zoran) 8 mg q12h PO/IM/SV/IV PregnancyCategoryB Selective5-HT3 receptor antagonist that blocks

serotonin.

Doxylamine Succinate (Unisom)25 mg

PregnancyCategoryBStrids

Methylprednisolone (Medrol) 16 mg q8h IV/PO PregnancyCategoryC Corticosteroid

Atrnativ Tratmnts

Acupressure Hypnosis

Pyridoxine(VitaminB6) 10- 50 mg q8h PO Pregnancy Category A Nutritional supplement

Ginger1gqdx4daysFluid Replacement LactatedRingersorD5LRwith:

Thiamine 100 mg qd Multivitamin supplement

Enternal Nutrition Nasogastrictube Jejunostomy

Percutaneousendoscopicgastrostomy(PEG)

Parenteral Nutrition

Source: [33; 63; 64; 65; 66] Table 1

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Because o the electrolytes lost in vomiting,Newman, Fullerton, and Anderson suggest oodshigh in potassium and magnesium, as well as saltingood, as tolerated, to replace chloride [42]. Theseauthors also suggest chewing one milk o magnesiatablet 2 to 3 times per day to settle the stomach

and replace magnesium stores.Behavioral changes recommended or patients withhyperemesis gravidarum are to take requent rests,get plenty o resh air, avoid sudden movements,avoid brushing teeth immediately ater eating, andsit upright or some time ater meals to reduce therequency o gastric refux. Acupressure wristbands,which are sometimes used by passengers on boats toprevent seasickness, have been ound to be helpulor some women with nausea in pregnancy [26].

Avoiding oensive odors is o special importance.An overly sensitive sense o smell is commonin pregnancy, possibly due to increased estrogenlevels. Oensive odors commonly are ood odorsbut can also be perumes or chemicals. Minimizingodors and increasing resh air are key ways to avoidnausea [16].

In addition, hyperemesis suerers should havepsychological support, including reassurance,perhaps amily and individual counseling, and a

reduction in demands o daily living and environ-mental stimulation [15].

It is important that healthcare proessionals acceptthe patients complaints o nausea and vomitingas a real physical problem and not necessarilypsychological in origin. Women who think thattheir providers do not believe their complaints onausea and vomiting may eel anger, diminishedsel-esteem, and conusion [40]. Acceptance othe patients complaint and the assurance that it

is not all in her head are paramount to establishinga therapeutic relationship.

Nursing assessment should rst include how otenthe vomiting episodes occur. Next, the nurseshould determine any patterns to the nausea andvomiting episodes, such as what time o the day ornight they occur. The nurse should also determinewhat conditions lead to vomiting, such as an empty

stomach or certain smells. Assessment must alsoinclude what, i any, oods seem to make the situ-ation worse or better. And nally, the nurse mustdetermine what measures the patient has alreadytried to alleviate the symptoms.

A dietary plan may be drawn up using most o thediscussed strategies (eating small meals every 2to 3 hours, avoiding an empty stomach, avoidingried or highly seasoned oods, and maintainingadequate hydration). The nurse can suggest thatthe patient keep a log o the type and amount oood consumed, as well as any episodes o nauseaand vomiting. This may help both the patient andthe nurse nd patterns and dietary solutions to theproblem.

Evaluation o a dietary plan should be ongoing atevery prenatal visit. The goal is normal weight gain,ewer episodes o nausea and vomiting, normal vitalsigns, and no ketonuria. The dietary plan is alsoan important adjunct to pharmacological therapyor hyperemesis.

pHARMAColoGICAl MANAGeMeNT

I diet and liestyle changes do not resolve theproblem o nausea and vomiting, drug therapymay be indicated. Despite evidence o saety tothe etus, most antiemetics are contraindicated inpregnancy [36]. The dilemma in treating hyperem-esis gravidarum pharmacologically is that becauseo possible teratogenic eects, both providers andpregnant women are reluctant to use pharmaco-

logical agents, especially in the rst trimester opregnancy. Currently, no drugs are approved bythe U.S. Food and Drug Administration (FDA)or treating morning sickness [27]. However, theantiemetic medications used to treat nausea andvomiting in pregnancy all into two broad classes:antihistamines and phenothiazines.

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Antihistamins

Antihistamines block the eects o histamine atthe H1 receptor and do not block histamine release.Most antihistamines have anticholinergic eects,such as constipation, dry eyes, dry mouth, blurredvision, and sedation. They are used to treat motion

sickness and insomnia as well as allergic conditions[12]. Antihistamines dry the mucous membranes,thus decreasing the excessive salivation associatedwith hyperemesis gravidarum. A meta-analysis ostudies published in the last 30 years shows thatantihistamines are not teratogenic in the rsttrimester o pregnancy and are eective in reducingvomiting [36].

Among the antihistamines used by women ornausea and vomiting during pregnancy is doxy-

lamine succinate, available in an over-the-countersleeping aid (Unisom) and previously in Bendectin(discussed later in this section). It carries an FDApregnancy Category B, which indicates that humanetal risk is relatively unlikely [33].

Dimenhydrinate is also Category B, but it has anoxytocic eect near term, which could inducelabor i used in the last trimester. However, it hasbeen used in the rst trimester with no reports ocongenital malormations [33]. Meclizine has beenused or nausea and vomiting in pregnancy sincethe 1960s, with recommended dosages o 2550mg per day [42]. Diphenhydramine is anotherCategory B antihistamine that has shown someeectiveness in treating nausea and vomiting inpregnancy. Promethazine has been used or sometime as a rst-line pharmacologic treatment orhyperemesis gravidarum, particularly in rectalsuppository orm.

Nursing considerations or these medicationsinclude inorming the patient that the medica-tions may cause drowsiness and to avoid drivingor operating machinery while taking them. Thesemedications may also cause oral dryness, sorequent mouth rinses and good oral hygiene maybe indicated to alleviate these symptoms, providedthey do not trigger vomiting episodes.

phnthiazins

Phenothiazines are dopamine antagonists that acton the chemoreceptor trigger zone to inhibit nauseaand vomiting. Commonly used phenothiazines arechlorpromazine, prochlorperazine, promethazine,and trifuoperazine. As a class, the phenothiazides

have been ound to be non-teratogenic in clinicalstudies, although some anectdotal case reports haveshown some major malormations associated withrst trimester use [36]. Aside rom prochlorperazine,the phenothiazines are not commonly prescribedor treatment o hyperemesis gravidarum [12].

Nurs ing management o patients receivingphenothiazines should include monitoring orurinary retention; dizziness; hypotension; symp-toms o akathisia, a restlessness or desire to keep

moving; and tardive dyskinesia, an uncontrolledrhythmic movement o muscles including the aceand mouth. Assessment or neuroleptic malignantsyndrome is important. It is maniested by ever,respiratory distress, tachycardia, convulsions,diaphoresis, pallor, atigue, and loss o bladdercontrol. The patient should be taught to expectdrowsiness, to change position slowly to avoidorthostatic hypotension, and to avoid sun exposureand extremes in temperature because the medi-cation causes both photosensitivity and impair-

ment o body temperature regulation.othr Mdicatins

Metoclopramide is a dopamine-receptor blockerin the chemoreceptor trigger zone o the centralnervous system. It has an anticholinergic eect andstimulates mobility o the upper gastrointestinal(GI) tract and accelerates gastric emptying. It hasalso been used as a rst-line pharmacologic treat-ment o hyperemesis gravidarum and has beenshown to be eective. While it is commonly avail-able or injection or in oral orm, pharmacists maymake rectal suppositories [12]. Nursing manage-ment must include monitoring or extrapyramidalside eects, tardive dyskinesia, and drowsiness.

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Hydroxyzine is an antianxiety agent that works as acentral nervous system depressant and has anticho-linergic, antihistamine, and antiemetic properties.It is available orally or or intramuscular injection.Because o these properties, nursing implicationsinclude teaching the patient about the common

side eects o drowsiness, dizziness, and dry mouth.I administered intramuscularly, hydroxyzine mustnot be given in the deltoid muscle, but should beinjected by Z-track because it is both painul andcaustic to tissue [12].

Trimethobenzamide is an anticholinergic thathas been used with some success in hyperemesisgravidarum. It is commonly administered via rectalsuppository or by intramuscular injection, thoughit is available in oral orm. A common side eecto this medication is rectal irritation rom thesuppositories.

Droperidol is oten used as a tranquilizer priorto the administration o anesthesia, but it hasalso been used to treat hyperemesis gravidarumas it suppresses nausea and vomiting. It is usedin inpatient settings only and is given parenter-ally. Droperidol may cause cardiac arrhythmias,particularly a prolonged QT interval, so nursesmust obtain a 12-lead electrocardiogram (ECG)in all patients prior to administration. Monitoringmust also include signs o extrapyramidal reactions,hallucinations, hypotension, and tachycardia [12].This drug is classied as a pregnancy Category Cmedication.

Ondansetron is a selective 5-HT3 receptor antago-nist that has been widely used in treatment ochemotherapy-induced nausea and vomiting. Itacts by blocking the eects o serotonin at thereceptors in the vagal nerve terminals and thechemoreceptor trigger zone in the central nervous

system. In the past several years, it has becomethe most widely used drug o its class to be usedin the treatment o hyperemesis. Animal studieshave shown no teratogenicity, and human studieshave shown the same result [36]. It is classied asa Category B medication.

In a double-blind clinical trial that comparedondansetron to promethazine, there was no statis-tical dierence in the relie o nausea, weight gain,or days o hospitalization [34]. This is particularlyrelevant because ondansetron is considerably moreexpensive than promethazine.

Nursing implications or ondansetron includemonitoring or headache, constipation, or diarrhea.Less commonly, side eects may include dizziness,drowsiness, and dry mouth. While it has beenavailable in oral or intravenous orm or some time,more recently it has been used in subcutaneouspumps, which deliver a basal rate o medication,with occasional boluses as needed.

Transdermal scopolamine is an anticholinergicthat has been suggested as a treatment or hyper-

emesis gravidarum; however, there have been noclinical trials o its eectiveness. Like many othermedications used to treat hyperemesis gravidarum,it carries a Category C designation because o itspossible teratogenic eects on the etus, based onanimal studies [49].

Bendectin, the only drug ever approved by the FDAor use in the treatment o nausea and vomiting inpregnancy, was introduced in 1956 and was takeno the market in 1983 [33]. In the 1970s, 30% to

35% o pregnant women were taking this medica-tion [7]. However, case reports and some reportso etal birth deects began to appear, and lawsuitswere brought against the manuacturer. Despite theact that controlled studies ound no increased risko birth deects, these highly publicized lawsuits,involving neonates with severe malormationswhose mothers had taken Bendectin, were judgedunavorably against the manuacturer [42]. By the1980s, insurance premiums exceeded gross sales othe medication, and it was taken o the market.

Unavailability o Bendectin resulted in an increasein admissions to hospitals or nausea and vomitingo pregnancy [7].

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It is interesting to note that ater Bendectin wasremoved rom the market, the incidence o the typeo limb deormities and congenital heart diseaseattributed to the medication did not decrease [7].

The original ormulation o Bendectin included10 mg o dicyclomine hydrochloride, an anti-

spasmodic; 10 mg o doxylamine succinate, anantihistamine; and 10 mg o pyridoxine (vitaminB6). Dicyclomine hydrochloride was removed romthe ormula in 1976 when clinical trials ailed toshow its benets. Bendectin was a delayed-releasetablet, so taking it in the evening beore bedtimereleased the drug early in the morning. The usualdosage was 2 to 4 tablets per day [42].

Pyridoxine, or vitamin B6, is recommended orpatients with hyperemesis gravidarum because a

deciency in the vitamin can lead to nausea andvomiting; it is also essential in protein synthesis.A large, randomized, placebo-controlled studyshowed that 10 mg o vitamin B6 three times aday signicantly decreased nausea, while vomitingdecreased somewhat. The recommended dosage is25 mg every 8 hours or three days [56].

Thus, the individual components o Bendectinhave been available in both over-the-counter andprescription orms and have not demonstrated to

be teratogenic. Moreover, a orm o Bendectinhas remained available in the United Kingdomas Debendox and in Canada as Diclectin. This,along with the act that Bendectin has not beenconclusively shown to be teratogenic, has initiateda move to reintroduce the medication [7].

A 1953 report indicated that cortisone relievedchemotherapy-related nausea and vomitingand hyperemesis gravidarum. However, only in2000 did randomized clinical trials support the

use o steroids as treatment. Corticosteroids arethought to aect a chemoreceptor trigger zonein the brain to reduce nausea and vomiting. Analternative explanation is that corticosteroidscorrect an adrenal insuciency that is caused byincreased adrenal demands during pregnancy [14].

A controlled study compared treatment o hyper-emesis gravidarum with oral methylprednisoloneto oral promethazine. The methylprednisolone wasgiven or three days and then tapered or 2 weeks,while the dosage o promethazine remained thesame. The study showed that methylprednisolone

was more eective at three days than treatmentwith promethazine [48]. Another study, however,demonstrated that oral promethazne improvednausea and vomiting more rapidly, being moreeective in the irst 48 hours. Prednisoloneimproved symptoms ater the rst two days, withlow side eects [67].

It is recommended that steroid therapy, either oralor intravenous, be used or those patients whosehyperemesis does not respond to conventionalantiemetics and intravenous hydration. Nurseswho are monitoring patients receiving steroidtherapy must pay particular attention to glucosecontrol, as the use o glucocorticoids increasesblood glucose levels [67].

It is once again important to note that none othe discussed medications, with the exception oBendectin, which was taken o the market in the1980s, have been approved by the FDA to treatmorning sickness or hyperemesis gravidarum.The drugs have been used with some success asdescribed, but these are o-label uses and are notFDA approved.

INTRAVeNouS THeRApy

Intravenous therapy is designed to replace fuidand electrolyte levels while resting the GI tract.An inusion o Ringers solution with 5% dextrose(D5RL) is recommended over 5% dextrose innormal saline (D5NS) because D5RL suppliessome potassium and calcium, whereas D5NS

does not [42]. Blood levels o sodium, potassium,magnesium, and calcium should be obtainedbeore initiating intravenous therapy so that anymissing minerals can be added to the standardormation. Vitamins, particularly those that arewater-soluble, should also be added to the ormula-tion. In cases o hyponatremia, rapid replacemento sodium levels may result in conusion, spastic

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quadriplegia, horizontal gaze paralysis, delirium,brain damage, or death. This is known as centralpontine myelinolysis [14].

Thiamine stores must be restored beore intrave-nous therapy begins, as the dextrose in the solutioncauses the body to metabolize thiamine. As previ-

ously mentioned, thiamine deciency can lead toWernickes encephalopathy. Signs and symptoms oWernickes encephalopathy include visual distur-bances, such as diplopia or nystagmus, as well asdisorientation, delusion, and gait ataxia. Whilethere is no specic regimen, Niebyl and Goodwinrecommend parenteral thiamine 100500 mg dailyor three days and 23 mg a day thereater [43].

According to ACOG, intravenous

hydration should be used or thehyperemesis gravidarum patient whocannot tolerate oral liquids or a prolongedperiod or i clinical signs o dehydration are

present. Correction o ketosis and vitamin deciencyshould be strongly considered. Dextrose and vitamins,especially thiamine, should be included in the therapywhen prolonged vomiting is present.

(http://www.guidelines.gov/summary/summary.aspx?doc_id=10939. Last accessed July 16, 2008.)

lv evidnc: C (Based primarily on consensusand expert opinion)

Nursing assessments should include starting andmaintaining the patency o the intravenous inu-sion, maintaining the inusion rate, and assessingthe IV site or inection or iniltration. Veni-puncture can be dicult in dehydrated patients,but placing the site in a dependent position andwarming the area with warm compresses may causeenough vasodilatation to enable an easy inser-

tion. Warming the rst liter o fuid may preventthe eeling o coldness that dehydrated patientsexperience [20].

Assessments might also include intake and output,as well as assessing or episodes o vomiting. Vitalsigns are one marker o hydration status and shouldbe monitored per protocol. Antiemetic therapy isoten initiated as well as intravenous hydration;thereore, ongoing assessments or side eects

should be included.Shortly ater intravenous therapy is initiated,oral eeding may be resumed. The diet is usuallyinitiated with clear liquids and proceeds to small,requent meals. Nurses should monitor dietaryintake and advance the diet as tolerated. I thediet is not tolerated, enteral eeding may be anoption [6].

Discharge planning should be initiated on admis-sion. The goal is to discharge the patient to home

as soon as dehydration is treated, vomiting hassubsided, and the patient is able to keep ooddown. Discharge planning should include coun-seling regarding diet, as well as educating thepatient regarding her medications, side eects,and warning signs.

Enteral nutrition works in conjunction with anti-emetics and is useul i the patients vomiting is notacute. A standard or small-bore nasogastric eedingtube is used to deliver a continuous, low-volume

inusion (50 ml/hr) o an isotonic ormula [6]. Theinusion is gradually increased to 100 ml/hr, andoods are reintroduced as tolerated. The risk oenteral therapy is that aspiration pneumonia candevelop i vomiting leads to displacement o theeeding tube [42]. A small 2006 study ound thatnasogastric tube eedings led to ewer complica-tions, such as inection, deep vein thrombosis,and IUGR, than the use o a peripherally insertedcentral catheter (PICC) [70].

Percutaneous endoscopic gastrostomy (PEG) tubeshave been used or eedings in intractable hyper-emesis gravidarum patients. Studies comparing thesaety and ecacy o this method as compared toTPN are lacking, however.

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As a last resort, TPN may be indicated or long-term therapy in hyperemesis gravidarum. A centralcatheter (Hickman type) is inserted into thesubclavian vein, and ater verication o place-ment and instructions on care, the therapy can becontinued at home or as an outpatient. A PICC

permits long-term administration o hyperosmolarsolutions without the insertion risks associatedwith central venous access. Greenspoon, Rosen,and Ault report that patients have received hyper-alimentation using this system or up to 137 dayswithout complications [24].

A study o 23 women receiving parenteral nutritionsupport during pregnancy demonstrated it provideda sae means o maintaining maternal nutritionand supported good etal growth during the rsttrimester [62].

With TPN, nurses must assess the insertion site orsigns o inection and change dressings per protocol.Due to the dehydration associated with hyperem-esis as well as the elevated coagulation actorsassociated with pregnancy, these women are athigher risk or catheter-related thromboembolsim.Because TPN is a hyperosmolar solution, it maydamage the walls o blood vessels, urther leading toa risk o thrombosis. During initial administration,the nurse should check or signs o hyperglycemia.Home health nurses provide important care ooutpatient hyperemesis patients, monitoring theinusions, assessing the insertion site, monitoringweight gain and response to treatment, teachingsel-care techniques, and planning or removal oTPN and return to eating normally.

NoNpHARMAColoGIC MANAGeMeNT

Beore beginning a discussion o alternative treat-ments or hyperemesis gravidarum, it should be

mentioned that while they may be adequate or thenormal nausea and vomiting o early pregnancy,they may be inadequate or treatment o hyper-emesis gravidarum. Generally, because o their lowrisks and ew side eects, they may be appropriateas adjunctive therapy.

Massage therapy has been shown to increase sero-tonin and dopamine and decrease cortisol levels,all helpul in relaxation and in decreasing stress.Tactile massage is a orm o sot, slow massage thatcan be given on the hands and eet or on the entirebody. One small study ound that tactile massage

was helpul in promoting relaxation, divertingthoughts o nausea and vomiting, and giving thewoman a eeling that her body is unctioningagain. The authors suggest that tactile massage isa good alternative and complementary therapy orhyperemesis [68].

Acupressure has been used or the treatment omorning sickness, as well as motion sickness andpost-chemotherapy nausea and vomiting. As such,it is the best-studied alternative therapy. Treatmentincludes wearing wristbands that apply pressureto the inner orearm approximately three ngerbreadths proximal to the wrist (Sea-Bands). Arandomized, placebo-controlled study involving60 healthy pregnant women with nausea andvomiting showed a statistically signicant decreasein nausea among women using acupressure [59].While most clinical trials show statistically signi-cant improvement in nausea, ewer studies showimprovement in vomiting [53]. However, many othe studies are fawed, having small sample sizes,

inadequate control groups, and ew blind studies[47].

A similar method is an acustimulation device,commonly worn around the wrist, that transmits anelectrical stimulus to the acupressure point. A studyo 41 women showed some benet in using thisdevice to treat nausea o early pregnancy [51].

Ginger ale has been recommended or many yearsto alleviate the nausea and vomiting in early preg-nancy. In act, ginger is the only herbal remedy

ormally studied or the treatment o morning sick-ness. A single randomized trial o ginger showed asignicant reduction o both nausea and vomiting.Two studies used 250 mg o ginger 4 times a day,and both showed a decrease in nausea and vomitingduring the treatment period [55]. However, gingeris not without risks; it has adverse eects on clot-

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ting actors and may potentiate anticoagulants.In some cases, it may actually exacerbate nauseaand vomiting and associated symptoms, such asheartburn [74]. Red raspberry and wild yam, whilealso herbal remedies or nausea and vomiting, havenot been scientically studied [53].

ACOG asserts that treatment o nauseaand vomiting o pregnancy with gingerhas shown benecial eects and can beconsidered as a nonpharmacologic option.

(http://www.guidelines.gov/summary/summary.aspx?doc_id=10939.Last accessed July 16, 2008.)

lv evidnc: B (Based on limited or inconsistentscientic evidence)

Hypnosis has been shown to be eective in treatingmorning sickness [37]. Nausea and vomiting mayhave a psychological as well as a physiologicalcomponent in that expectations, belies, andconditioning may trigger episodes. Hypnosis mayprove to be o use as adjunctive therapy in treatinghyperemesis gravidarum, particularly because othe lack o side eects or complications rom thetechnique.

NuRSING IMplICATIoNS

NuRSING ASSeSSMeNT

Patients with hyperemesis gravidarum are typicallybetween the 4th and the 10th week o gestationand may complain that they are unable to keepanything down or are vomiting constantly. It isimportant to ascertain how requent the vomitingepisodes are, when they are worse, what the trig-

gers are, and what remedies the patient has alreadytried.

On physical examination, the patient may appearweak, pale, and with dry mucous membranes. Aketotic breath smell may be noted. Inrequently,jaundice might be noted. A weight check mayreveal weight loss, as much as 5 lbs. in a week.Blood pressure may maniest orthostatic changes,

and pulse may be elevated secondary to dehydra-tion.

A urine dipstick analysis should be perormed, withparticular attention to the presence o ketones.Specic gravity will be increased [41].

RelATeD NuRSING DIAGNoSeS,plANS, INTeRVeNTIoNS,AND eVAluATIoNS

Applicable nursing diagnoses are listed below, withsuggested interventions and rationales. These arebased on the North American Nursing DiagnosisAssociation (NANDA) diagnoses as o 2005.

Nasa

Nausea is dened as a subjective unpleasant,wavelike sensation in the back o the throat,epigastrium, or abdomen that may lead to the urgeor need to vomit [44].

Olactory stimulation can sometimes trigger nausea.Interventions include avoiding unpleasant odors

and ood smells, particularly those that trigger thenausea. The patient should avoid ried or greasymeals because these also promote nausea. Thepatient should attempt small, requent meals anddrink fuids in between meals because this helpsto reduce the amount o ood in the stomach andavoid the eeling o ullness that can aggravatenausea. The patient should avoid lying supine orat least 30 minutes ater eating because the supineposition applies pressure on the diaphragm anddigestion is improved by gravity.

The nurse can teach the patient diversion tech-niques, such as taking a whi o isopropyl alcohol.This intervention diverts attention rom thenausea. The nurse can also teach the patient guidedimagery and relaxation techniques or recommendacupressure bands.

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The expected outcome would be a decrease innausea within a given time rame, perhaps 24to 72 hours. However, because nausea is otenaccompanied by vomiting, time is o the essence;dehydration can easily occur in 72 hours [10].

Imaancd Ntritin,lss than bd Rqirmnts

Simply deined, imbalanced nutrition is theinability to meet metabolic needs by nutritionalintake. The recommended daily amount (RDA)or caloric intake in early pregnancy is similar tothe RDA or nonpregnant women: 2200 caloriesper day. Later in the pregnancy, the caloric intakeincreases by 300 calories per day.

Nursing interventions are similar to those ornausea. Nurses may counsel the patient to eatlow-at oods and carbohydrates, such as ruit,breads, cereals, rice, and pasta. These oods providecalories and help prevent hypoglycemia, whichcan cause nausea. Salting oods can help to replacechloride, which is lost in vomiting.

Evaluation o the nursing interventions shouldinclude monitoring or weight gain and monitoringurine or ketonuria. The patient should be askedabout the number and severity o nausea andvomiting episodes or complaints o atigue [10].

Acta r Ris Dhdratin

Dehydration is a state in which an individual is atrisk or or experiencing fuid depletion. The nursingassessment may reveal dry mucous membranes,decreased skin turgor, tachycardia, hypotension,increased body temperature, and ketonuria. Thehemoglobin and hematocrit may be elevated, butsodium, potassium, and chloride may be reduceddue to vomiting.

Because women with hyperemesis gravidarumare unable to maintain oral hydration, inpatienttreatment is initially required to intravenouslyhydrate the patient. Thereore, nursing interven-tions are collaborative and supportive to medicalmanagement. The intravenous site is monitored

or signs o inection and inltration, and site careis provided per institutional policies. Intravenousintake is monitored, as well as output, includingbowel, urine, and vomitus. Normal urinary outputis about 1 ml/kg/hour. A record o bowel elimina-tion may yield inormation as to the eectiveness

o dietary interventions.The nurse may be responsible or administeringparenteral antiemetics and vitamins as well asmonitoring or any adverse reactions to the medi-cations. Daily weight gain may also be monitored,and the patient is assessed or readiness to tolerateoral eedings, with the diet being advanced astolerated.

Discharge planning may involve teaching abouttaking medications, maximizing caloric intake,

and perhaps arranging or home health services orintravenous inusions or subcutaneous antiemetictherapy [10].

Imaird Tiss Intgrit

This nursing diagnosis includes impaired oralmucous membrane integrity, due to both dehy-dration and vomiting. Nursing assessments mightreveal a complaint o dry mouth, bad taste, or evenexcessive salivation. Inspection may reveal dry orcracked mucous membranes, pallor, ulcerations,

edema, coated tongue, or hemangiomas (a networko small blood-lled capillaries near the surace othe skin).

Interventions should include teaching oral hygiene,such as brushing at least 3 times a day, ater eachmeal, or ater each episode o vomiting. The use oa sot-bristle brush is indicated, as bleeding gumsare common in pregnancy and a hard-bristle brushcould urther injure sot oral tissue. An alcohol-reemouthwash should be used, as alcohol-based prod-

ucts can be drying. However, these interventionsmust be evaluated on an individual basis as theymay exacerbate the nausea and vomiting. Treat-ment o dehydration will generally improve oralmucous membrane integrity [10].

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ReSouRCeS foR CARe

Several support groups or hyperemesis gravidarumsuerers have emerged on the Internet.

Th Hrmsis edcatin

and Rsarch (HeR) fndatinAn excellent site, with advice and linkshttp://www.hyperemesis.org

yah! Hrmsis Srt Grhttp://health.groups.yahoo.com/group/Hyperemesis

Hrmsis GravidarmSrvivrs (HGS)

Advice and support rom survivorso hyperemesis gravidarum

http://www.angelre.com/nt/hugsWhile the obstetrician-gynecologist, nurse-midwie, or nurse practitioner is oten the primarycaregiver in instances o hyperemesis gravidarum,i the patient is admitted to a hospital, a teamapproach to care is useul. Such a team approachmight include, in addition to the primary provider,nurses, dietitians, pharmacists, gastroenter-ologists, and perhaps psychological or social worksupport.

CoNCluSIoN

Hyperemesis gravidarum is a serious complicationo pregnancy in the rst trimester. I untreated, itcan lead to IUGR, low birth weight inants, andpossibly neonatal abnormalities. The eects on themother include weight loss, fuid and electrolytedisturbances, dehydration, starvation, Wernickesencephalopathy, esophageal stulas, and in rarecases, death.

There is probably no single etiology or hyperem-esis gravidarum. This disorder has been reerredto as a multiactorial syndrome and may involvepsychological actors as well as physiological andmetabolic disorders. The possible roles o hyper-thyroidism/thyrotoxicosis, gestational hormones,

hepatic dysunction, gastric dysunction, inection,autonomic nervous system dysunction, nutritionaldeciencies, and psychological actors as causes orhyperemesis gravidarum have been explored. Areview o the literature has shown that there aredeciencies o sample sizes, lack o control groups,and variations in how the disorder is diagnosed, andor every study that suggests a connection betweenhyperemesis and a metabolic disorder, anotherstudy reutes it.

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Risk actors are dened, but ethnic and demo-graphic data are lacking. Resources or aectedwomen are scarce. One pharmacological productthat was used successully in the treatment o hyper-emesis gravidarum or more than 20 years was takeno the market because o litigation. The litigious

nature o American society has made it unlikelythat research will be done on other possible phar-macological treatments or the disorder, althoughother, potentially more dangerous pharmaceuticalsare commonly bought over-the-counter and usedor treatment. Conversely, intravenous, enteral,and parenteral eeding o hyperemesis patientshave been quite eective in treatment.

Nurses play a key role in all aspects o the manage-ment o hyperemesis gravidarum. Oten, they arethe rst to hear o the patients complaints onausea and vomiting. Nursing assessment may leadto an initial diagnosis, and nurses are responsible,in inpatient and home visitation settings, or the

administration and monitoring o pharmacologictherapy and fuid replacement therapy. Nursesteach all aspects o the disease process, rom dietaryand alternative methods o management to sideeects o pharmacologic therapy. Ongoing nursingevaluations should monitor treatment and screenor exacerbations o the condition. Nurses providepsychological support or patients and acilitate themobilization o community resources necessary totreat this disorder.

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Evidence-Based Practice Recommendations Citation

American College o Obstetricians and Gynecologists.Nausea and Vomiting of Pregnancy. Washington, DC: American College oObstetricians and Gynecologists; 2004. Summary retrieved rom National Guideline Clearinghouse at http://www.guidelines.gov/summary/summary.aspx?doc_id=10939. Last accessed July 16, 2008.

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