Nausea and Vomiting in Adolescents and Adults Rahul Kuver, M.D. , John V. Sheffield, M.D. , and George B. McDonald, M.D. 1.0 Introduction Nausea means feeling "sick to the stomach", a sensation that is associated with the ur ge to vomit. V omiting, the forceful discharge of gastric contents, may be a protective physiologic mechanism that prevents entry of potentially harmful substances into the gastrointestinal tract 1!. ersistent vomiting can lead to dehydration, severe alkalosis, bleeding and rarely esophageal perforation ## irrespective of the cause of vomiting. Vo miting is to be differentiated from retching, regurgitation or rumination. Retchingor dry heaves involves the same physiological mechanisms as vomiting, but occurs aga inst a closed glottis$ there is no e%pulsion of gastric contents. Regurgitationis the return of small amounts of food or secretions to the h ypopharyn% in the conte%t of mechanical obstruction of the esophagus, gastroesophageal reflu% disease or esophageal motility disorders. Ruminationis similar to regurgitation, e%cept small amounts of completely swallowed food are returned to the hypopharyn% from the stomach and is often re#swallowed &!. 'umination is not associated with nausea. (his review of nausea and vomiting is based on a )*+IN* literature search encompassing 1--0#&000, using the )e/ headings Nausea and V omiting with the subheadings omplications, +iagnosis, +rug (reatment, (reatment, *tiology, sychology and 'adiography. ertain articles, including placebo#controlled trials of therapy, comprehensive reviews and other publications deemed seminal, were reviewed and are referenced. ertain articles prior to 1--0 were also reviewed. (he emphasis is placed on articles that provide evidence which can be incorporated into guidelines for diagnosis and management. ertain patients typically present with nausea and vomiting, such as cancer chemotherapy patients, patients recovering from general anesthesia, pregnant women and patients whose symptoms are related to motion. )any of these patients are seen in the primary care setting. In most cases, the history can p oint to the etiology without the need for soph isticated diagnostic testing or referral. In a minority of patients, unusual causes of nausea and vomiting may reuire thorough diagnostic testing and referral to a specialist 1!. 2ssessment of the duration of nausea and vomiting is an important initial point in the histor y . ymptoms present for less than a week may be due to conditions which are separable from those causing symptoms over weeks, months or years. or acute nausea and vomiting, the diagnostic algorithm is !ased on three "e# $uestions %&a!le '(3 &a !le ' )) Ke# $uestions in the evaluation of acute nausea and vomiting 1. Is immedia te th erapy neces sary regar dless of t he c ause4 &. 2re empiric symptom atic tr eatme nt and reassu rance suff icient 4 2. Is the patient a woman of child#bearing age4 5. 2re there symptoms of motion sickness or vertigo4 . 2re symptoms consistent with a viral syndrome4 6. Is e% pediti ous workup reui red t o esta blish the cause4 2. Is abdominal or chest pain present4 5. Is there a history of drug, to%in, or environmental e%posure4 . an a pregnancy#related condition e%plain s ymptoms4 +. 2re Nsymptoms present4 *. an an infection account for symptoms4 7. 2re nausea and vomiting symptoms of a systemic disease4
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7/21/2019 Nausea and Vomiting in Adolescents and Adults
Rahul Kuver, M.D. , John V. Sheffield, M.D. , and George B. McDonald, M.D.
1.0 Introduction
Nausea means feeling "sick to the stomach", a sensation that is associated with the urge to vomit. Vomiting, the forceful discharge
of gastric contents, may be a protective physiologic mechanism that prevents entry of potentially harmful substances into the
gastrointestinal tract 1!. ersistent vomiting can lead to dehydration, severe alkalosis, bleeding and rarely esophageal perforation
## irrespective of the cause of vomiting.
Vomiting is to be differentiated from retching, regurgitation or rumination. Retching or dry heaves involves the same
physiological mechanisms as vomiting, but occurs against a closed glottis$ there is no e%pulsion of gastric contents. Regurgitation is the return of small amounts of food or secretions to the hypopharyn% in the conte%t of mechanical obstruction of
the esophagus, gastroesophageal reflu% disease or esophageal motility disorders. Rumination is similar to regurgitation, e%cept
small amounts of completely swallowed food are returned to the hypopharyn% from the stomach and is often re#swallowed &!.
'umination is not associated with nausea.
(his review of nausea and vomiting is based on a )*+IN* literature search encompassing 1--0#&000, using the )e/
headings Nausea and Vomiting with the subheadings omplications, +iagnosis, +rug (reatment, (reatment, *tiology, sychology
and 'adiography. ertain articles, including placebo#controlled trials of therapy, comprehensive reviews and other publications
deemed seminal, were reviewed and are referenced. ertain articles prior to 1--0 were also reviewed. (he emphasis is placed on
articles that provide evidence which can be incorporated into guidelines for diagnosis and management.
ertain patients typically present with nausea and vomiting, such as cancer chemotherapy patients, patients recovering fromgeneral anesthesia, pregnant women and patients whose symptoms are related to motion. )any of these patients are seen in the
primary care setting. In most cases, the history can point to the etiology without the need for sophisticated diagnostic testing or
referral. In a minority of patients, unusual causes of nausea and vomiting may reuire thorough diagnostic testing and referral to a
specialist 1!.
2ssessment of the duration of nausea and vomiting is an important initial point in the history. ymptoms present for less than a
week may be due to conditions which are separable from those causing symptoms over weeks, months or years.
or acute nausea and vomiting, the diagnostic algorithm is !ased on three "e# $uestions %&a!le '(3
&a!le ' )) Ke# $uestions in the evaluation of acute nausea and vomiting
1. Is immediate therapy necessary regardless of the cause4
&. 2re empiric symptomatic treatment and reassurance sufficient4
2. Is the patient a woman of child#bearing age4
5. 2re there symptoms of motion sickness or vertigo4
. 2re symptoms consistent with a viral syndrome4
6. Is e%peditious workup reuired to establish the cause4
2. Is abdominal or chest pain present4
5. Is there a history of drug, to%in, or environmental e%posure4
. an a pregnancy#related condition e%plain symptoms4
+. 2re N symptoms present4
*. an an infection account for symptoms4
7. 2re nausea and vomiting symptoms of a systemic disease4
8* reflu% disease 'efractory to symptomatic treatment *lective
hronic intractable
nausea:vomiting with
unrevealing workup
*lective
1.1 2ssociated ymptoms
ertain symptoms are typically associated with nausea and vomiting. 2ssociated upper 8I tract complaints such as bloating,
early satiety, dysphagia and odynophagia should be sought. +yspepsia can be associated with nausea. ightheadedness,abdominal or chest pain, cough or hematemesis are symptoms that should prompt an assessment for conditions that may
reuire immediate therapy regardless of the underlying cause of nausea and vomiting. 2 missed menstrual period, vertigo,
arthralgias, low grade fevers and nausea and vomiting associated with motion are clues that suggest a condition that may be
treated empirically . ymptoms that are severe, such as chest or abdominal pain, N symptoms, fever with chills, a history
of an underlying systemic disease or of immunosuppression should prompt a diagnostic workup.
cover anaerobes 4Pen3, or lindamycin5cover 3ram neg aerobes and Staphaureus i7 recent hospitali!ation
spiration Fever, coughDyspnea
Decreased o)ygensaturationIn7iltrates on chest 9:ray
ontrol air8ay ntibiotics as above"ronchoscopy i7 locali!ed 8hee!ing orparenchymal volume loss to remove7oreign body
ntra:abdominal
bleeding
bdominal painypotension, tachycardia
Increasing abd girthDropping T
T abdomenSurgical consultation
Table 2a -- Treatment of volume depletion secondary to Nausea and Vomiting-ild -oderate : Severe
Oral li1uids ::/:; liters2day
Oral electrolyte solutions3atorade, Pedialyte5
IV isotonic 7luids 40<=> saline5 :: +:/ liters over + hr, then based on monitoring o7 vital signs,urine output< onsider central venous or pulmonary capillary 8edge pressure measurementsto guide therapy< -onitor serum electrolytes :: replace ?@ and -g@ as needed<
Table 2b -- Treatment of hypoalemic hypochloremic alalosis
!ondition Treatment
-ild hypokalemia+ m(126 ?@ decrease A /00:;00 m(1 total bodyde7icit
Severe hypokalemia?@*/<Bm(126 A ;00:C00 m(1 total body de7icit
(?3 changes, neuromuscular symptoms
') A ;0:0 m(1 ?I p<o< -onitor serum ?
IV ?6 +0 to ;0 m(12hr depending on severity4+0 m(12hr normally, ;0m(12hr i7 ?*/5
ontinuous (?3 monitoring, check serum ? 1;h
Severe lkalosis 4p.E<BB5 heck "3s and serum electrolytes 1;h<In renal 7ailure pts, hemodialysis can correct alkalosis cid therapy ::use 8ith cautionalculate @ de7icit 4m(15 A 0<B ) lean body 8t 4kg5 ) 4measuredOG5 : 4desired OG5H<'eplace hal7 the de7icit over +/hr, remainderover ne)t /;hr l solution A +B0ml l in + liter sterile /O<
If vomiting has been severe and protracted, intravascular volume depletion may have occurred, leading to orthostatic
h#-otension and renal insufficiency. 1#-o"alemic h#-ochloremic al"alosis results from loss of gastric hydrochloric acid,
ncreased /B loss due to renin#angiotensin#aldosterone and volume contraction. In these situations, intravascular access should be
established and fluid resuscitation instituted prior to diagnostic studies.
• Vomiting or retching can cause mucosal in=ury and bleeding
*ither vomiting or retching can lead to mucosal in=ury e.g. Mallor#)2eiss tear!, evident as hematemesis and:or melena$
e%cessive blood loss may contribute to intravascular volume depletion. In the case of 8I bleeding with a significant drop in
hematocrit or signs of intravascular volume depletion, consultation for upper endoscopy should be obtained. In certain situations,
depending on the findings on endoscopy and the effectiveness of endoscopic therapy, surgical consultation may be necessary.
Gey uestions can help identify conditions that can be treated empirically. ertain presentations and etiologies are sufficientlycharacteristic as to be identifiable as self#limited. In these situations, no specific treatment is necessary, or, if specific therapy is
available, the benign nature of the condition precludes the need for an e%tensive diagnostic evaluation. 2 ma=ority of patients seen
n the ambulatory care setting falls into this category.
&.&.1 +arl# -regnanc#
If the patient is a woman of child#bearing age, a pregnancy test should be done. regnanc#)related nausea and vomiting is
common, reported in F0#-0E of pregnancies 11!1&6!. 'ising estrogen and progesterone levels during pregnancy have beenmplicated, as has maternal serum prostaglandin *& levels 1&@!. (he onset is usually shortly after the first missed menstrual
period, and symptoms may begin before the woman recogni9es that pregnancy has occurred. ymptoms typically begin by four to
si% weeks of gestation, peaking in severity by eight to twelve weeks, and resolving spontaneously by the &0th week 11!. Nausea,
sometimes accompanied by vomiting, is noted especially in the morning. In one prospective study of 1D0 pregnant women,
however, "morning sickness" occurred in only 1.CE, whereas C0E reported nausea lasting all day 1&A!. ymptoms usually
disappear by the fourth month of pregnancy, although they may persist into the third trimester. 5abies born to a mother with
nausea and vomiting of pregnancy have birth weights similar to babies born to mothers without these symptoms. (hus, the
prognosis for mother and baby is generally e%cellent. /owever, in one study a higher than normal incidence of antepartum
hemorrhage was noted 1&!. Vomiting during pregnancy is not teratogenic 16!.
If pregnancy#related nausea and vomiting are not characteristic of morning sickness for e%ample, has its onset in the second or
third trimester and is severe!, then other potentially more serious conditions such as hyperemesis gravidarum, acute fatty liver of
pregnancy, and /* syndrome need to be considered.
In general, referral to an obstetrician for management of nausea and vomiting of pregnancy is indicated for these more serious
conditions.
&reatment of regnanc#)related nausea and vomiting
7or typical pregnancy#related nausea and vomiting, reassurance is often all that is needed, although an anti#emetic may be
necessary. (raditionally, dietary advice such as dry toast in the morning and avoiding fatty foods was offered. 2ntacids for reflu%
symptoms associated with nausea and vomiting may be used. If an anti#emetic is necessary, then antihistamines may be used andare considered safe for use during pregnancy. (he efficacy or safety of phenothia9ines or metoclopramide have not been
established for nausea and vomiting of pregnancy in controlled trials despite their widespread use 11!.
linical trials assessing the efficacy of anti#emetic therapy are of varialbe uality. 2n analysis of such trials showed that anit#
histamines, pyrido%ine, and D acupressure appeared to reduce the freuency of nausea in early pregnancy 1&D!. 2 risk#benefit
assessment of drug therapy for nausea and vomiting of pregnancy show that controlled trials demonstrated the safety and efficacy
of dicyclomine, anti#histamine /1 receptor antagonists, and phenothia9ines 1&F!. (he pooled data, however, were not
homogenous.
2 prospective trial comparing pregnancy outcomes in women given metoclopramide in the first trimester for the treatment of
nausea and vomiting in pregnancy compared to women who received nonteratogenic drugs, showed no increased risk of fetal
malformations, spontaneous abortions, or decreased birth weight of the infants in the metoclopramide group 16A!.
(he effectiveness of pyrido%ine vitamin 5D! for nausea and vomiting of pregnancy has been studied in a randomi9ed, double#
blind placebo#controlled trial. atients in the treatment group received 60 mg:day of pyrido%ine hydrochloride for A days. 2
significant decrease in post#therapy nausea in the treatment group was noted 1@!. imilar results were noted for vomiting in
another study over a 6#day duration 1A!. Acu-ressure at the D point located on the wrist has also been studied in a randomi9ed,
double#blind placebo#controlled study and found to reduce nausea, but not vomiting, in pregnant patients 1D!. i%ty women were
assigned to two treatment groups3 one to a group receiving D acupressure, and a control group receiving pressure at another
anatomic location. ymptom scores after A#F days of treatment were used to =udge efficacy. Nausea scores improved over time in
both groups, achieving statistical significance in the acupressure group. In another study, 1D1 pregnant symptomatic women were
assigned to three groups3 D acupressure treatment, placebo acupressure band placed in an inappropriate location! or control.
Improvement in nausea and vomiting or retching was noted in all three groups, with no statistically significant differences noted
n the acupressure group 1F!.
&.&.& Vertigo
Nausea or vomiting associated with vertigo suggests another set of causes. Vertigo is a sensation of the environment spinning
around, often described as di99iness by the patient. *valuation of the di99y patient begins with a thorough history, which can
dentify the cause in many patients. If a characteristic change in head position brings on vertigo, benign positional vertigo is
usually the cause, which does not usually lead to nausea and vomiting. 2ssociated aural symptoms such as hearing loss, fullness in
the ears and tinnitus should be ascertained. Neurologic symptoms such as headache, visual changes or loss of sensation are
mportant to determine. oss of consciousness associated with vertigo should be determined.
eripheral causes of vertigo, such as !enign -ositional vertigo, vesti!ular neuronitis, Meniere4s disease and acoustic neuroma
need to be distinguished from central causes of vertigo, such as multiple sclerosis, brainstem ischemia and central nervous systemtumor. (he physical e%amination is often helpful in determining whether a peripheral or central cause of vertigo is present. 2
complete head and neck e%am including e%amination of the tympanic membranes is advised. ranial nerves should be tested,
ncluding assessment of e%traocular muscle function. Nystagmus can aid in diagnosis. N#stagmus of peripheral origin is rotatory
or hori9ontal. Vertical nystagmus is pathognomonic for brain stem disease, as is nystagmus that is more pronounced in one eye.
N#stagmus may be tested by having the patient look ahead, then 60 degrees to the left and to the right. ausing at each position
allows evaluation of nystagmus. Induced nystagmus is done by rapidly changing the position of the head. (he /allpike#+i% or
Nylen#5arany! maneuver is performed by making the patient undergo a rapid change from the erect sitting position to a supine
position with the head hanging to the left, right or center. 2 positive test is present when paro%ysmal nystagmus is induced after a
brief delay. 2 positive test is diagnostic for either benign positional vertigo, which is seldom associated with nausea and vomiting$
or a central nervous system disorder. In order to distinguish the two, the following characteristics of nystagmus are noted. 7or
benign positional vertigo, a 6#&0 second latency, rotatory nystagmus and adaptation i.e. less response to repeat testing! is seen.
7or a central nervous system cause, no latency is seen, the nystagmus can be vertical or hori9ontal and can last longer than D0
seconds and there is no adaptation.
5alance testing such as the 'omberg test and assessment of the gait should also be performed. Vertigo can also be an early
symptom in multiple sclerosis. esions in the lower midbrain and pons produce internuclear ophthalmoplegia. (his is checked for
by having the patient follow the finger of the e%aminer from side to side hori9ontally. In this type of nystagmus the eye on the side
to which the ga9e is directed participates strongly with a hori9ontal nystagmus, whereas the opposite eye will show less
nystagmus and weakness of internal rotation. 2 careful cardiac e%amination is also necessary, as arrhythmias can produce
symptoms which are confused with vertigo 1C!.
S-ontaneous and 5nduced N#stagmus and their 6auses
+irection of fast component 2way from side with disease (oward side with disease
or direction changing!
*ffect of visual fi%ation uppressed Not suppressed
<sual anatomical location of
problem
abyrinth or vestibular nerve 5rainstem or cerebellum
5nduced N#stagmus
7eature eripheral 5V! entral
(ime to onset after
uick position change
latency!
6#&0 seconds Immediate
+uration ess than 1 minute ersists longer than 1 minute
7atigability )arked None
Vertigo may be a symptom of a more serious underlying disorder , such as vertebro#basilar vascular insufficiency or a
cerebellopontine#angle tumor. In order to determine which vertiginous patient needs further diagnostic testing and possible
referral, several items in the history are helpful. 2re there associated neurologic symptoms such as headache, visual changes or
oss of sensation and strength, suggesting cortical or brain stem disorders4 Is there a history of sei9ures4 /as the patient lost
consciousness with the episode of vertigo4 Is there antecedent cranial or cervical trauma4 If the answer is affirmative to any of
these uestions, then empiric therapy is not advised.
'eferral to a neurologist and possibly a neurosurgeon may be necessary in patients with N symptoms suggestive of a brain
stem lesion, vertebro#basilar insufficiency or cortical lesions. 2dditionally, in patients with vertigo associated with sei9ures,referral to a neurologist is appropriate. If vertigo is associated with syncope, a thorough cardiac evaluation by a cardiologist may
be indicated to rule out arrhythmias or other cardiac causes.
&.&.&.1 Vesti!ular neuronitis
(he sudden onset of vertigo with nausea and vomiting, increasing in severity over several hours with resolution over a similarspan of time, is characteristic of vestibular neuronitis. atients may awaken from sleep with vertigo. (here is often a history of a
recent or concurrent upper respiratory tract infection, and clusters of cases may be seen. (he etiology is probably viral, and the
condition is often diagnosed in adolescents and young adults. 7ollowing the acute episode, prolonged di99iness similar to motion
sickness may be noted, lasting weeks to months. No new associated auditory deficits, fullness in the ear, or tinnitus are noted.
ersistent nystagmus toward the affected side may be noted. linical and histopathologic studies implicate an isolated lesion of
the vestibular nerve 1-!.
In cases where there is doubt about the diagnosis based on the signs and symptoms, additional diagnostic tests to consider include
audiologic assessment, electronystagmography with caloric testing and head (. 'eferral to an otolaryngologist should be
considered for refractory or atypical cases.
&reatment
(reatment for nausea and vomiting is symptomatic, similar to that for motion sickness %&a!le ''(.
2cute labyrinthitis symptomatically is similar to vestibular neuronitis, e%cept hearing loss on the involved side is also noted. (he
cause may be viral, bacterial or due to a to%in 1C!. 2 history of recent or concurrent upper respiratory tract infection is often
given. )ost patients improve over 1#& weeks, although recurrent episodes have been described. )ost report an upper respiratory
tract illness 1#& weeks prior to the onset of vertigo. everal members of the patientHs family may be affected, and it is seen more
often in spring and early summer. In most cases a viral etiology is likely.
2 subgroup of patients may have herpes 9oster oticus 'amsay#/unt syndrome!, with vertigo and periauricular vesicles or facial
paralysis. Vesicles may be seen on the pinna and on the face in the distribution of the sensory branch of the seventh cranial nerve.
Vertigo may last days to weeks.
&reatment
No specific therapy is recommended. ymptomatic treatment with anti#vertigo medications as for motion sickness may be used if
symptoms are severe %&a!le ''(. If there is suspicion of a bacterial etiology, with fever, chills and a purulent middle ear, then
medical therapy with antibiotics and possibly surgical therapy is indicated to prevent meningitis. In this case, referral to an
otolaryngologist should be considered. 7or the 'amsay#/unt syndrome, acyclovir is effective in the treatment of facial paralysis,
but is ineffective for vertigo 1C!.
&.&.&.6 Meniere4s disease
evere nausea and vomiting may be a manifestation of endolymphatic hydrops, or )eniereHs disease. ymptoms characteristicallynclude episodic aural fullness, tinnitus, hearing loss and vertigo. If vertigo is associated with hearing loss or tinnitus, an
audiogram is needed to diagnose )eniereHs disease or acoustic neuroma. (he onset is abrupt, and usually no precipitating factors
are identified. 2ttacks of vertigo can last a few hours to &@ hours, and subside gradually. /ori9ontal or hori9onto#rotatory
n#stagmus may be observed.
&reatment
(reatment is with restriction of salt intake and anti#vertigo drugs. ymptomatic relief of vertigo can be obtained with
anticholinergic agents e.g. scopolamine orally or by transdermal patch!, or antihistamines e.g. diphenhydramine, mecli9ine or
cycli9ine!. +ia9epam &#A mg orally D#Ch is effective in suppressing the vestibular system %&a!le ''(. In severe cases, referral to
)otion sickness is a form of physiologic vertigo. erspiration, increased salivation, yawning and malaise are described by
patients with motion sickness. /yperventilation can lead to hypocapnia, and venous pooling can predispose to hypotension and
syncope. (he sight and smell of food can e%acerbate nausea. )otion sickness is readily diagnosed by history. (his is a common
syndrome that can occur in an automobile, airplane or at sea. *%aggerated self#generated movement, in fact, can cause motion
sickness by forcing rapid and inappropriate changes of vestibular function &0!.
&reatment
(he treatment of vertigo associated with motion sickness is empirical &1!. (ransdermal scopolamine can prevent motion sickness.
(he patch must be placed several hours prior to the anticipated onset of motion sickness. Anti)histamines such asdymenhydrinate, mecli9ine, cycli9ine, prometha9ine and diphenhydramine can be used
%&a!le ''( (he main side effect of this drug class is drowsiness.
Acu-ressure on the D point located on the wrist, which has been used in traditional hinese medicine to treat nausea and
vomiting of pregnancy, has been evaluated in a randomi/ed, -lace!o)controlled dou!le)!lind stud#. i%ty#four sub=ects were
randomly divided into @ groups D acupressure, dummy#point acupressure, sham D acupressure, and control! and sub=ected to
optokinetic drum rotation which elicits motion sickness in normal volunteers. ub=ects in the D acupressure group reported
significantly less nausea and the incidence of gastric tachyarrhythmia was reduced in this group &&!. In another blinded placebo#
controlled study on 6D patients, however, acupressure provided no protection &6!.
&.&.@ Viral s#ndrome
2cute infections with viruses such as Norwalk agent or other enteric viruses can be accompanied by headache, fever, arthralgias
and non#bloody diarrhea as well as nausea and vomiting. (hese symptoms, suggestive of a viral etiology, are an indication that no
specific diagnostic testing is necessary.
&reatment
*mpiric therapy with liberal fluid intake, anti#emetics and antipyretics may suffice. *mpiric therapy should only be instituted inmmunocompetent patients with symptoms that are mild and typical for a viral syndrome. igns such as protracted fever with
chills, bloody diarrhea and clinically evident fluid depletion should be handled with proper diagnostic studies and appropriate
specific therapy.
2 randomi9ed, double#blind comparison of treatment of uncomplicated nausea and vomiting due to viral gastroenteritis with
prochorpera9ine ompa9ine! or prometha9ine hernergan! was published. (he results showed that prochoropera9ine was
significantly better in terms of symptom relief compared to prometha9ine 11-!.
&.&.A ost)o-erative
ost#operative nausea and vomiting is common, but is unlikely to be encountered in the primary care setting. In a prospective
evaluation of 101 patients admitted for abdominal surgery, the overall incidence of nausea and vomiting was @&E &@!. (hese
symptoms are generally attributed to the general anesthetic agents or analgesics used. In the immediate post#operative setting,
these patients are often treated empirically. /owever, the possibility of other causes of nausea and vomiting must be kept in mind.
Vomiting in the post#operative period following laparoscopy may lead to pneumomediastinum and bilateral pneumothoraces &A!.
ongestion of the eye secondary to phakomorphic glaucoma can lead to intractable nausea and vomiting in the post#operative
state &D!.
&reatment
hile post#operative nausea and vomiting is unlikely to be encountered in the primary care setting, treatment regimens have been
studied in this patient population. (herefore, it is useful to be aware of this literature. 7or e%ample, the efficacy, safety and cost#
effectiveness of ondansetron @ mg intravenously! was compared to dro-eridol 0.D&A mg or 1.&A mg intravenously! in a
randomi9ed, double#blind placebo#controlled trial for the prevention of postoperative nausea and vomiting after outpatient
gynecologic surgery in 1D1 women. +roperidol 0.D&A mg iv provided antiemetic prophyla%is comparable to that of ondansetron @
with ondansetron, tropisetron, granisetron or metoclopramide was studied. ;ndansetron prophyla%is resulted in a lower incidence
of post#operative nausea and vomiting compared to metoclopramide or placebo. (here were no statistically significant differences
among the three 7)1&3 rece-tor antagonists&C!. 2 review of published controlled trials comparing A#/(6 receptor antagonists
to traditional anti#emetic agents including metoclopramide, perphena9ine, prochlorpera9ine, cycli9ine and droperidol! for
prophyla%is of postoperative nausea and vomiting showed the A#/(6 receptor antagonists to be superior 1&C!.
&.6 Diagnostic 0or"u- re$uired
*%perienced physicians triage patients based on the patients history and presentation as well as on clinical instincts that factor in
severity of illness and familiarity with the patient %&a!le 3(. )ost causes of acute vomiting are self#limited illnesses, but nausea
and vomiting can be symptoms of conditions that reuire e%peditious diagnostic workup and treatment %&a!le 8(. 8uidelines for
referral are included in each section.
&.6.1 2bdominal or chest pain
2 history of pain may indicate that nausea and vomiting is a conseuence of a pathophysiologic process in the thoracic cavity or
abdomen. 2bdominal pain preceding nausea and vomiting indicates an organic lesion. ain following vomiting may be due to
tenderness of the abdominal musculature, an abdominal wall or esophageal hematoma, especially in patients who are anti#
coagulated! or esophageal perforation.
&.6.1.1 oronary artery disease
2cute and chronic myocardial ischemia, as well as myocardial infarction, may present with nausea and vomiting. (hese symptoms
may be accompanied by abdominal bloating or fullness. ;ften, concomitant substernal chest pain is present, or the patient may
give a history of angina pectoris. *ven in the absence of classic signs and symptoms of myocardial ischemia, the physician must
keep an open mind to the possibility of a cardiac source of symptoms. 2t a minimum, an electrocardiogram should be obtained in
such patients. 7urther diagnostic evaluation and therapy depend on the clinical impression. ardiac en9ymes to rule out
myocardial infarction and electrocardiographic monitoring may be necessary. )anagement in consultation with a cardiologist
should be considered.
&.6.1.& Intra#abdominal inflammation
2 variety of inflammatory conditions within the abdomen may present with nausea and vomiting including cholecystitis,
appendicitis, pancreatitis, inflammatory bowel disease, cholangitis and peritonitis. (he duration, location, uality, radiation and
pattern of abdominal pain, and factors that e%acerbate or ameliorate the pain, may help distinguish between these possibilities. 2
history of biliary colic or gallstones suggests cholecystitis or gallstone pancreatitis. ain in the periumbilical area which moves to
the right lower uadrant over time classically suggests appendicitis. ;n physical e%am, certain findings are suggestive of aparticular diagnosis. )urphyHs sign tenderness and inspiratory arrest with palpation in the right upper uadrant of the abdomen!
may be elicited in acute cholecystitis. 'ebound tenderness on abdominal e%am suggests peritonitis, and in the conte%t of free air
on ?#ray, warrants laparotomy. In acute pancreatitis, diffuse tenderness to palpation of the abdomen may be elicited, making this
diagnosis a difficult one to make on physical findings alone &-!. Nausea and vomiting in the conte%t of intra#abdominal
nflammation are symptoms that should respond to treatment of the underlying inflammatory process.
'eferral to a gastroenterologist should be considered in severe cases of pancreatitis, in those whom choledocholithiasis is
suspected as a cause of pancreatitis or cholangitis, and in cases where the diagnosis is uncertain. 7or patients with inflammatory
bowel disease I5+! presenting with nausea and vomiting, symptoms may be due to a flare of I5+ or the presence of bowel
obstruction see below!. )anagement of I5+ with the aid of a gastroenterologist should be considered. 'eferral to a general
surgeon is warranted in cases of acute cholecystitis, appendicitis or peritonitis.
&.6.1.6 G5 tract o!struction
;bstruction of the stomach or intestine can present with nausea, vomiting and abdominal pain. hen abdominal pain precedes
nausea and vomiting, obstruction of the 8I tract should be strongly considered. Gastric outlet o!struction may be due to peptic
ulcer disease in the pyloric channel or duodenal bulb, or benign or malignant gastric tumor. atients may complain of early satiety
and bloating. 2bdominal pain is generally postprandial. ymptoms may be worse after a solid meal compared to a liuid one.
(hese symptoms may be resolved with vomiting as the stomach is decompressed. (he volume of gastric contents e%pelled may be
arge. (he vomitus may be foul#smelling, containing food ingested more than 1& hours previously. /eartburn due to reflu% of
acidic gastric contents may be a complaint. hysical e%am findings include a distended abdomen with tympany and, in some
cases, epigastric tenderness. 2 succussion splash heard with the stethoscope after gently rocking the patient from side to side
mplicates retention of liuid contents in the stomach.
+iagnostic tests include upright abdominal ?#rays showing an enlarged gas#filled stomach, contrast radiographs and endoscopy.
ater soluble contrast ?#rays are helpful when a gastric !e/oar is suspected, or when a tight stenosis is present. *ndoscopy is inmany cases the procedure of choice, as histologic diagnosis and in some cases therapy can be provided. 'eferral to a
gastroenterologist is appropriate in cases of acute nausea and vomiting suspected to be due to gastric outlet obstruction.
In the small bowel, a history of prior abdominal surgery may predispose to small !o0el o!struction caused by adhesions. *ightypercent of small bowel obstructions are due to post#operative adhesions. ;ther etiologies include primary or metastatic carcinoma,
benign tumor, internal and e%ternal hernias and rohns disease. ess commonly, prior abdominal radiation, intussusception,
endometriosis, volvulus and congenital abnormalities can lead to small bowel obstruction. (he patient can present with intestinal
colic, which may be intermittent initially, progressing to sustained abdominal pain centered in the midline of the abdomen at or
cephalad to the umbilicus. Vomiting is a cardinal feature, with complete obstruction leading to vomiting of liuid material which
may be feculent if the obstruction is in the distal small intestine. hysical findings include a distended abdomen$ dilated, palpable
oops of bowel$ and high#pitched, intermittent bowel sounds.
2n important aspect of the diagnostic evaluation is the differentiation of incomplete from complete small !o0el o!struction.
omplete obstruction should be considered if the patient is not able to pass flatus. 2bdominal radiographs supine and upright
views! should be obtained. omplete obstruction is suggested by dilated loops of small bowel with air#fluid levels without gas in
the large bowel. In partial obstruction, gas is noted in the colon and rectum, although air#fluid levels and dilated loops of small
bowel are present. If the differentiation between partial and complete obstruction is still uncertain, contrast radiography may help
differentiate these conditions and rule out a paralytic ileus.
7/21/2019 Nausea and Vomiting in Adolescents and Adults
*%cessive alcohol intake may cause severe nausea and vomiting. Mallor#)2eiss tears are directly caused by vomiting or retching
and can be encountered in the patient who has been drinking alcohol. 2cute pancreatitis may be present and leads to nausea,
vomiting and abdominal pain. Intracranial hemorrhage secondary to head trauma from a fall in an inebriated patient can cloud the
clinical presentation, as increased intracranial pressure can itself be a cause of nausea and vomiting. 2lcoholic hepatitis can also
present with nausea and vomiting. Nausea and vomiting in the patient with a history of alcohol use therefore reuires vigilance for
these associated conditions. 2 history obtained from family members or witnesses, a careful abdominal e%am,
head:eyes:ears:nose:throat e%am and neurological e%am, measurement of blood alcohol levels, hematocrit, coagulation profile,
transaminases 2(:2(! and serum amylase and lipase should be obtained in a patient suspected of heavy alcohol use who
presents with severe nausea and vomiting. 2ncillary diagnostic tests such as chest and abdominal ?#rays and a head ( scan may
be necessary to rule out the wide variety of associated conditions that can lead to nausea and vomiting in the patient who presents
after heavy alcohol consumption %&a!le :(.
&.6.&.@ *nvironmental toins and e%posures
*%posure to certain environmental to%ins can lead to nausea and vomiting as prominent symptoms. 6ar!on monoidentoication presents in a non#specific manner. /eadache, di99iness, fatigue and nausea and vomiting are common @0!. In
addition, disturbed =udgment and diminished visual acuity may be seen. 5lood carbo%yhemoglobin levels of @0#D0E are
associated with tachypnea, tachycardia, ata%ia, syncope and sei9ures. (he *G8 may show ( segment changes, conduction
blocks and atrial or ventricular arrhythmias. herry#red coloration of the lips or skin is rare.
(reatment consists of supportive care and 100E o%ygen. arbo%yhemoglobin levels should be measured every two to four hours,
and o%ygen continued until blood levels are less than 10E. /yperbaric o%ygen 6 atm! is recommended for patients who present
with neurologic signs or symptoms, *G8 changes consistent with ischemia, shock, severe metabolic acidosis and pulmonary
edema.
2cute arsenic -oisoning can present with nausea and vomiting @1!. 2cute fluoride -oisoning from a public water system
produced a clinical syndrome characteri9ed by nausea, vomiting, diarrhea, abdominal pain and paresthesias @&!. esticidee%posure can present with an%iety, vertigo, nausea, vomiting, tearing and weakness @6!. *lemental mercury vapor to%icity
presented with nausea, headache, lumbar pain and shortness of breath at rest @@!. In each of these e%amples, nausea and vomiting
were present in the ma=ority of cases but the presenting symptom comple%es were non#specific.
ood -oisoning due to pre#formed bacterially#derived to%ins can present with nausea and vomiting in association with abdominal
pain and diarrhea. taphylococcal food poisoning typically presents with nausea, vomiting, cramping abdominal pain and diarrhea
between two and four hours after ingestion of food contaminated by the enteroto%in produced by Staphylococcus aureus . ;ften, a
cluster of cases is identified. (reatment is symptomatic. (he illness is short, rarely lasting more than &@ hours.
Vibrio parahemolyticus poisoning is associated with the consumption of raw or improperly refrigerated seafood. (he incubation
period is between 1& and &@ hours, and patients present with e%plosive watery diarrhea, nausea, vomiting and abdominal cramps.
(reatment is supportive, although in protracted cases, antibiotic therapy with tetracycline or ampicillin may be used. ;ther
bacterial causes of food poisoning such as Clostridium perfringens type 2 and Bacillus cereus cause nausea and vomiting as
predominant symptoms in a minority of patients.
&oin e%posure can occur by consumption of seafood or e%posure to marine to%ins. combroid poisoning by the consumption of
spoiled fish of the dark meat varieties can present with skin rash, diarrhea, palpitations, headache, nausea, abdominal cramps,
paresthesias, an unusual taste sensation and breathing difficulties. atients respond to anti#histamines as the to%in is histamine @A,
@D!. igatuera poisoning, seen predominantly in tropical areas, presents with nausea, abdominal pain, vomiting and diarrhea.
eripheral neuropathic symptoms are also characteristic, including paresthesias, dental discomfort and confusion of peripheral hot
and cold sensation. (reatment is symptomatic.
2lthough not to%ins, certain foods can cause hypersensitivity reactions which present with nausea, vomiting, abdominal pain anddiarrhea @F!.
ertain envenomations can present as nausea and vomiting. S-ider !ites, particularly by the female black widow spider or brown
recluse spider, can present with nausea and vomiting. ikewise, scorpion stings and snake bites can present with nausea and
vomiting. In all of these cases, pain, erythema and swelling at the site of the bite is usually evident. <nusual e%amples of
envenomations which present with nausea and vomiting are those due to the bite of the 8ila monster @C! and the sting of the
;nce this diagnosis is established, early delivery is indicated to prevent maternal and fetal death AA!. )anagement by an
obstetrician, and referral to a center speciali9ing in high#risk obstetrics should be considered.
&.6.6.6 1+;; S#ndrome
2 syndrome of hemolysis, elevated liver en9ymes and low platelet count can complicate pre#eclamptic:eclamptic patients. atients
typically present in the third trimester with epigastric or right upper uadrant pain and nausea and vomiting. (hey may present
with no signs of pre#eclampsia hypertension, proteinuria, or edema!, and therefore a non#obstetric diagnosis may be entertained
AD!.
&reatment
)anagement in con=unction with an obstetrician is recommended, and referral to a center speciali9ing in high#risk obstetrics
should be considered.
&.6.@ N symptoms
/eadache, pro=ectile vomiting often in the morning without antecedent nausea, a history of migraine, transient ischemic attacks,
vertigo, photophobia or neck stiffness are elements of the history which should direct the clinician to a N e%planation fornausea and vomiting.
/eadache may be due to migraine, increased intracranial pressure or cerebral vascular hemorrhage. (he clinical diagnosis of
migraine is based on headache characteristics and associated symptoms, particularly nausea and vomiting. (he treatment of
migraine has been recently reviewed AF!. (reatment strategies include A#hydro%ytryptamine agonists, ergotamine tartrate,
sumatriptan, dihydroergotamine, N2I+s and opiates. umatriptan, a selective serotonin receptor agonist, is particularly effective
and well#tolerated AC! A-!. (reatment with oral sumatriptan has been studied in a randomi/ed dou!le)!lind -lace!o)controlled
stud#, and found to be effective D0!.
/eadache in the presence of fever and neck stiffness suggests meningitis D1!. Nausea and vomiting may be a feature of
meningitis. erebral cysticercosis can present with positional headache and nausea and vomiting D&!11D!.
rimary intraventricular hemorrhage presented with nausea and vomiting in F1E of cases in a review of 1@ cases. /eadache and
mental status changes were noted in an eual number of cases D6!. 'eferral to a neurologist or neurosurgeon may be necessary.
Vertebrobasilar vascular insufficiency is a common cause of vertigo in the elderly. Vertigo is abrupt in onset, lasts several minutes
and is often associated with nausea and vomiting. 2ssociated symptoms due to ischemia in the territory of the posterior circulation
nclude visual hallucinations, drop attacks, diplopia, headache and visual field defects. ( scans are usually normal, as symptoms
are transient. 2ngiography may be helpful, but carries a risk of arterial spasm and stroke. 'eferral to a neurologist should be
considered.
Vertigo with nausea and vomiting may also accompany infarction of the lateral brain stem or cerebellum or both. Gey findings are
an acute onset of symptoms, clear cerebellar signs such as e%tremity and gait ata%ia and ga9e#evoked n#stagmus. (hese patients
must be carefully observed for the development of progressive brain stem dysfunction due to edema at the site of infarction.onsultation with a neurologist should be obtained.
erebellopontine#angle tumors, such as acoustic neuroma, meningioma and epidermal cysts grow slowly, so that acute vertigo
with associated nausea and vomiting are rarely presenting symptoms. ;ccasionally, acute onset of vertigo may be present.
<nilateral, progressive hearing loss is present, identified by an abnormal brain#stem auditory evoked response. *valuation by
magnetic resonance imaging )'I! is the most sensitive study. *very patient with vertigo and a unilateral hearing loss or tinnitus
must be assumed to have a retrocochlear lesion until radiographically proven otherwise 1C!. (reatment is surgical removal, so
that referral to an otolaryngologist or neurosurgeon is indicated.
&.6.A 5nfections as a 6ause of Nausea and Vomiting
Infections may present with nausea and vomiting, especially if viral in origin. Nausea and vomiting accompanied by diarrhea and
fever suggests viral gastroenteritis. ;ften, this is self#limited, and patients recover with supportive care. ;ccasionally, volume
depletion is severe, and may reuire volume replacement. 5lood in the stool and fever warrants further investigation and may
ndicate inflammatory bowel disease or bacterial enteritis or colitis.
ertain other infections of the upper 8I tract of non#viral etiology, although rare, should be considered. *sophageal infections are
more commonly seen in immunocompromised patients, and can present with nausea and vomiting alone, although most patients
will develop esophageal symptoms such as dysphagia and odynophagia. 7or immunocompromised patients, the most common
pathogens are andida, )V and /V D@!.
8astric syphilis has become an uncommon disease, with only &@ cases reported in the literature in the past & decades. (he most
common symptoms in a review of F cases were abdominal pain, nausea, and vomiting, with signs of syphilis present in A patients.(he diagnosis was established by identification of spirochetes on mucosal biopsy in D patients. (he diagnosis should be
considered in patients at risk for se%ually transmitted disease who complain of nausea, vomiting and abdominal pain and in whom
unusual gastric lesions or ulcers are refractory to therapy DA!.
<nusual infections such as 'ocky )ountain potted 7ever can present with nausea and vomiting, along with fever, headache,
myalgia and anore%ia. (hese symptoms can be difficult to distinguish from self#limited viral infection. 2 rash may appear later in
the course, but is not pathognomonic DD!.
/epatic abscess presented with nausea and vomiting in @0E of cases in a review of 6A patients. (wenty#nine patients had bacterial
abscesses, and D had amebic abscesses. 7ever was present in -AE and right upper uadrant pain in D6E of patients DF!.
&.6.D S#stemic disease as a cause of nausea and vomiting
2cute nausea and vomiting may be the manifestation of a definable disease process. hile diseases such as diabetes mellitus,
endometriosis and renal insufficiency are chronic in nature, acute e%acerbations may lead to presentations that include nausea and
vomiting.
*ndocrine emergencies can present with nausea and vomiting. Dia!etic "etoacidosis can present with vomiting, along with
polyuria, polydypsia, abdominal pain and changes in mental status. Ninety percent of patients are known diabetics. (he smell of
acetone on the patientHs breath, and the deep#breathing pattern of GussmaulHs respiration aid in the diagnosis DC!. ikewise,
severe vomiting and abdominal pain are central clinical features of alcoholic "etoacidosis. 2s in diabetic ketoacidosis, severe
dehydration can lead to GussmaulHs respiration and mental status changes D-!.
Acute adrenal insufficienc# usually presents with nausea, vomiting, severe hypotension and dehydration F0!. Nausea and
vomiting are common in the uremic patient F1!.
Intestinal endometriosis can present with abdominal pain and nausea and vomiting. In a review of &D cases, abdominal pain was
the main presenting feature in &0, with associated nausea and vomiting in 1&. *stablishing the diagnosis preoperatively was
difficult in patients without a known history F&!.
(he immunosuppressed patient can be considered in a separate category because such patients deserve a thorough diagnostic
workup even if signs and symptoms initially point to a benign self#limited condition as the cause.
(he classic situation is the patient with A5DS, although immunosuppression due to drugs and severe illness need to be considered.
hile the cause of nausea and vomiting may be similar to those seen in immunocompetent patients, several other etiologies need
to be considered. hiefly, opportunistic infections of the upper 8I tract, such as andida esophagitis, )V or /V infection F6!
may be present. hile nausea and vomiting are rarely the sole symptoms seen in these situations, other more typical symptoms
such as odynophagia or dysphagia, hematemesis and weight loss may be accompanied by nausea and vomiting. 7or these patients,
referral to a gastroenterologist for endoscopy to establish the diagnosis should be considered, especially if an empiric trial of
therapy e.g. flucona9ole for presumptive andida esophagitis! is unsuccessful.
&.6.C =nusual causes and conse$uences
(here can be unusual causes or conseuences of nausea and vomiting. (his uestion should be asked by the e%aminer if the
patient does not fit a typical profile in terms of symptoms, or if an unusual complaint arises as a conseuence of vomiting.
(here are several conseuences of nausea and vomiting which are rare but should be considered. Visual floaters may be due tovitreous hemorrhage and retinal vein rupture caused by emesis F@!. tress fracture of the hyoid bone caused by induced vomiting
has been described FA!. (ooth surface enamel loss may occur with repeated emesis FD!. 5enign retropneumoperitoneum can be
nduced by vomiting FF!.
ikewise, unusual causes of nausea and vomiting have been described. S#stemic mastoc#tosis can present with nausea due to
mast cell infiltration of the gastric mucosa FC!. Visually induced paro%ysmal nausea and vomiting can be the presenting
manifestation of multi-le sclerosis F-!. 2cuired or hereditary angioedema can present with gastrointestinal complaints
ncluding episodic nausea C0!. 8astric outlet obstruction may occur due to a giant duodenal gallstone. (his condition is called
Bouveret4s s#ndrome, and often indicates the presence of a cholecystoduodenal fistula C1!. *mesis of gallstones has been
described, indicative of a fistula between the gallbladder and the stomach or duodenum C&!.
6.0 6hronic nausea and vomiting
hronic nausea and vomiting is defined as the presence of symptoms for over a week. (he patient may describe intermittent
symptoms lasting months or years. 2 number of different conditions may be responsible for such symptoms, and a thorough
history and physical e%am are invaluable in pointing to the correct diagnosis.
6.1 (he cause is known from prior workup
In certain situations of chronic or recurrent nausea and vomiting, the cause has been established on previous diagnostic workup. In
these situations, treatment may be instituted without e%tensive diagnostic workup, although the physician must keep an open mind
regarding alternative etiologies. If the patient does not respond to specific therapy, further diagnostic studies should be initiated.
6.& (he cause is not known
If no prior diagnosis or underlying etiology is evident, the patient with chronic or recurrent nausea and vomiting reuires a
diagnostic work#up. onditions such as the post#gastrectomy state, diabetes mellitus leading to gastroparesis and prior abdominal
;ther causes of nausea and vomiting involving the 8I tract include esophageal lesions such as achalasia or esophageal masses that
may cause obstruction to the passage of food. 'egurgitation of undigested food, rather than true vomiting, may be the presenting
complaint. +ysphagia, with or without odynophagia, is usually part of the patientHs complaints. 'eferral to a gastroenterologist for
endoscopy, biopsy and management is indicated for these disorders.
6.&.1.& ;ther 8I causes
ertain situations where 8I causes of nausea and vomiting are present without evidence of mechanical obstruction also need to be
considered.
hronic intractable nausea can be the primary symptom of gastroeso-hageal reflu disease. In a study of 10 outpatients with this
symptom, acid reflu% was the cause of intractable nausea in all patients. In this group of three men and seven women, the average
duration of nausea was & years, with a range of 6 months to D years. None had responded to empiric therapies for nausea. *ither
upper endoscopy or &@ hour esophageal p/ studies showed gastroesophageal acid reflu% in all patients. *sophagitis was
documented on upper endoscopy in A patients$ and in the D patients who had esophageal p/ testing, abnormally increased acid
reflu% was documented. (reatment included omepra9ole, ranitidine or cisapride$ one patient who did not respond to high dose /&blocker or proton pump inhibitor therapy underwent Nissen fundoplication. (reatment of gastroesophageal reflu% led to symptom
resolution in all patients CA!. ith a mean follow#up of D months, all patients reported no recurrence of nausea.
hronic peptic inflammation due to -e-tic ulcer, gastritis or ?ollinger)+llison s#ndrome can present with nausea and vomiting.
Helicobacter pylori infection leads to chronic gastritis and has been associated with gastric and duodenal ulcers. Nausea and
vomiting can be associated symptoms of ulcer disease. atients with recurrent vomiting and suspected peptic ulcer disease should
undergo endoscopy to evaluate this possibility. (he diagnosis of H pylori infection can be established via several methods. H
pylori serology provides evidence of e%posure to the organism. 5reath testing and a stool antigen test are available to non#
nvasively determine whether active infection is present. *ndoscopy with biopsy of the antrum to demonstrate the organism is the
gold standard, and should be considered in cases where peptic ulcer disease is a diagnostic consideration. 2 rapid urease en9yme
test may be used concurrently with biopsy. ;nce the presence of the organism has been established, and the symptoms and clinical
picture are deemed suitable for treatment, several drug combinations are available.
+osino-hilic gastroenteritis is characteri9ed by peripheral eosinophilia, eosinophilic infiltration of the 8I tract and symptoms
referable to the 8I tract including abdominal pain, nausea, vomiting, diarrhea, anemia and protein#losing enteropathy. eripheral
eosinophilia is not an invariable finding. In a review of C patients, the diagnosis was established by endoscopic mucosal biopsy in
A and by laparotomy with full#thickness biopsy in the remainder. atients were treated with prednisone with response in all
patients CD, CF!.
Infiltrative lesions of the stomach linitis -lastica! can present with early satiety and nausea and vomiting. ancreatic cancer can
ead to gastroparesis and nausea and vomiting.
Nausea and vomiting may be caused by disorders of gastric motility without obstruction or evidence of inflammation.
Gastro-aresis is the most common of these motility disorders. In most cases, the diagnosis is made clinically, in the absence of
mechanical lesions causing obstruction of the 8I tract. cintigraphic gastric emptying studies are the gold standard CC, C-!. In
difficult to treat cases, the patient may be referred to a gastroenterologist at a tertiary care center. *soteric tests such as
antroduodenal motility tests and electrogastrography may be used to document slowed gastric muscular activity. (reatment of
gastroparesis includes dietary measures, such as maintaining adeuate hydration, eating small freuent meals, and avoiding fatty
foods and indigestible solids. harmacologic therapy includes antiemetics as well as prokinetic agents. ro"inetic agents such as
metoclopramide and cisapride have been used to treat this disorder -0!. +omperidone has also been shown to enhance gastric
emptying. *rythromycin in low, prokinetic doses &A0 mg ; (I+ 60 minutes before meals! may also be tried. <sually prokinetic
agents are given 1A to 60 minutes prior to meals to enhance the effect on gastric emptying at mealtime. 2 bedtime dose may help
n emptying the stomach of indigestible solids and thereby prevent be9oar formation.
*ndocrine and metabolic causes can lead to chronic nausea and vomiting. (he classic situations are the patient with diabetes
mellitus, the patient with adrenal insufficiency and the patient with hypercalcemia.
6.&.6.1 Dia!etes mellitus
Nausea and vomiting, often accompanied by weight loss and early satiety, are common gastrointestinal symptoms in patients with
diabetes. *pisodes of nausea and vomiting may last days to months or occur in cycles C-!. 2bout half of patients with insulin or
non#insulin#dependent diabetes have delayed gastric emptying diabetic gastro-aresis!. ome complain of epigastric pain,
nausea, vomiting or postprandial fullness. Be/oars may form in the stomach, leading to gastric outlet obstruction e%acerbating the
underlying gastroparesis. +iabetic gastroparesis may contribute to inadeuate glycemic control and impaired absorption of orally
administered drugs. 2lthough less common, gastric emptying rates may be accelerated in diabetics as well -6!.
6.&.6.& Adrenal insufficienc#
2drenal insufficiency presents with nonspecific symptoms such as weakness, fatigue, nausea, vomiting, anore%ia and weight loss.
It should be suspected if the patient has hyperpigmentation, hyponatremia and:or hyperkalemia$ a history of autoimmune disease
such as hypothyroidism or diabetes$ or recent use of corticosteroids F0!. 8astric stasis has been demonstrated in a patient with
primary adrenal insufficiency -@!, and therefore this diagnosis should be considered in patients presenting with chronic nausea
and vomiting. (he short cosyntropin ortrosyn! stimulation test &A0 ug IV or I), with measurement of plasma cortisol 60
minutes later! is diagnostic, with a normal response being stimulated plasma cortisol greater than &0 ug:dl. ith the diagnosis of
adrenal failure, therapy with hydrocortisone 100 mg IV Ch should be given, along with normal saline with AE de%trose until
hypotension is treated. )aintenance therapy with prednisone is reuired.
6.&.6.6 1#-ercalcemia
/ypercalcemic states can alter gut motility and present with nausea and vomiting. 8I symptoms of severe hypercalcemia serum
calcium L 1& mg:dl! includes nausea and vomiting, as well as anore%ia, constipation and abdominal pain. Neurologic symptoms
nclude such as weakness, fatigue, confusion, stupor and coma$ renal effects such as polyuria and nephrolithiasis may be seen.
+ehydration resulting from nausea and vomiting and anore%ia can lead to even more severe hypercalcemia -A!. erum ioni9ed
calcium is a better indicator of true hypercalcemia, as total serum calcium levels are linked to serum albumin levels. rimary
hyperparathyroidism and malignancy are the two most common causes of hypercalcemia. (reatment of the underlying cause, as
well as treatment of the hypercalcemia with e%tracellular volume restoration, saline diuresis and treatment with bisphosphonates
should be instituted when appropriate.
6.&.@ s#chogenic causes
'epetitive vomiting may be a conscious and voluntary act as in patients with !ulimia who vomit in part to control their weight. In
rumination, the patient increases intraabdominal pressure, regurgitates food into the mouth and swallows it again. 2t a more
subconscious level, vomiting may occur in otherwise healthy persons as part of a strong emotional reaction, and in patients as an
e%pression of an underlying psychopathologic condition or as a conversion reaction.
In the diagnostic workup of psychogenic vomiting, a thorough history including a family and social history are important. Volume
depletion and signs of nutritional deficiencies should be sought on physical e%amination. 2 complete neurologic e%am should beperformed. +epression, weight loss and altered perception of body image suggest anoreia nervosa. *%cessive concern with
body weight, loss of dental enamel, parotid hypertrophy, electrolyte disturbances and chronic diarrhea indicate !ulimia -D!.
2lmost A0E of bulimics report nausea and other gastrointestinal symptoms -F!. 7ormal psychiatric testing including inpatient
evaluation and assessments such as the )innesota )ultiphasic ersonality Inventory should be considered. (hese types of tests
may be helpful if an abnormality in the hypochondriasis, depression or hysteria scales is found. 'eferral to a psychiatrist should
;ften, psychogenic causes of nausea and vomiting are diagnoses of e%clusion. 'ecently, however, hypomotility in the gastric
antrum, abnormal gastric electrical activity and delayed gastric emptying have been reported in patients thought to have
psychogenic nausea and vomiting. sychologic stress may in fact lead to vomiting in otherwise normal people -C!. In patients
with functional nausea and vomiting, tricyclic antidepressants at low doses may be of benefit. In a retrospective analysis of 6F
such patients treated with amitriptyline, desipramine, nortriptyline do%epin or imipramine, symptomatic response was documented
n C@E of the patients. +ose at response averaged A0 mg:day, and the outcome was not related to the tricyclic antidepressant used
11F!.
anic disorder has been associated with nausea --!. atients with borderline personality disorder can present with episodic
vomiting 100!. ocial phobia may manifest as nausea and fear of eating in public 101!.
(he c#clic vomiting s#ndrome is characteri9ed by recurrent, self#limited episodes of nausea and vomiting separated by symptom#
free intervals. In a report of F1 cases, the length and symptomatology of episodes were stereotyped and characteristic for each
patient 10&!. (here was a coincident relationship with migraine and irritable bowel syndrome. atients could identify conditions
that precipitated episodes, commonly heightened emotional states and infections 106!. hile all patients in the series were
children, a case in a DA#year old diabetic woman with a 10 year history of recurrent nausea and vomiting was reported 10@!.
*pisodes of vomiting were always characteri9ed by elevations in serum 2(/, serum cortisol and urinary cortisol. /owever,
suppression of these elevations with de%amethasone did not alleviate the clinical symptoms. Intramuscular ketorolac produced
prompt and sustained relief.
2 review of 1F adult patients with cyclic vomiting syndrome who had been treated with tricyclic antidepressants was published
11C!. ymptoms began at age 6A range 1@#F6 years!. (he average duration of each episode was D days range 1#&1 days!. (hesymptom#free interval averaged 6.1 months range 0.A to D months!. 7ewer than a third of the patients reported a prodrome or
triggering events. (ricyclic antidepressant therapy led to complete remission of symptoms in 1F.DE of patients, and partial
response in AC.AE of patients.
6.&.A No cause found despite thorough investigation
7inally, there may be patients in whom no etiology can be determined despite e%tensive diagnostic testing. In this group of
patients, a gastric emptying study should be performed 10A!. If the emptying study is abnormal, a trial of a -ro"inetic agent such
as metoclopramide may be useful. In cases of intractable gastroparesis, placement of gastrostomy tubes and =e=unostomy tubes for
decompression and feeding respectively may be effective 10D!. rior to the institution of these measures, the patient should beconsidered for referral to a tertiary care center for further testing, including electrogastrography and small bowel motility studies.
If the gastric emptying study is normal, then consideration can be given to laparotomy with full thickness biopsy of the small
ntestine to rule out a neuropathic or myopathic disorder. uch an invasive approach should be considered in the rare patient in
whom vomiting is severe and has led to nutritional compromise or to severe disruption of uality of life.
@.0 Drug (herapy for Nausea and Vomiting
@.1 lasses of +rugs
(he following is a brief summary of the drugs used to treat nausea and vomiting, including indications, contraindications and
potential adverse reactions. 7or most of these agents, safety for use in pregnancy has not been established. henever possible, the
potential benefits must be weighed against potential adverse effects. (his is not a comprehensive list of potential uses and adverse
effects. 7or detailed information regarding these drugs, the package insert should be consulted prior to prescribing. 2 summary of
anti#emetic agents is provided in %&a!le ''(.
@.1.1 henothia/ines
rochlorpera9ine and chlorproma9ine are the phenothia9ines used most freuently for nausea and vomiting of various causes.
(hey act at the (> to block dopamine receptors. rochlorpera9ine has good absorption after parenteral and oral administration,
with a serum half#life of F hours. ide effects include hypotension, autonomic responses, hypersensitivity reactions e.g.
cholestatic =aundice! and hormonal dysfunction. 2ntidopaminergic effects include dystonia, dyskinesia and tardive dyskinesia.
Indication is primarily for treatment of motion sickness. ide effects include sedation. It should be used with caution with narrow#
angle glaucoma, stenosing peptic ulcer, pyloroduodenal obstruction and symptomatic prostatic hypertrophy. 2dditive effects with
alcohol and other N depressants occurs.
@.1.6 ro"inetic agents
(hese agents influence 8I motility through one or more of the following pathways3 1. +irectly or indirectly promoting cholinergic
tone$ &. 2ntagoni9ing inhibitory neurotransmitters e.g. serotonin, dopamine!$ or 6. )imicking noncholinergic nonadrenergic
compounds that increase motility e.g. motilin!. rokinetic agents have been used in the treatment of gastroparesis.
)etoclopramide, domperidone and cisapride are effective both in eliminating the symptoms of gastroparesis and in enhancing the
rate of gastric emptying 10F!.
@.1.6.1 holinergic agents
+irect cholinergic agents include bethanechol, which is the most commonly prescribed agonist, and acts by enhancing the
amplitude of contractions throughout the 8I tract, including the lower esophageal sphincter. (hese agents also stimulate the
secretion of saliva and gastric acid. ide effects develop due to enhanced parasympathetic tone, including abdominal cramps,
diarrhea, salivation, flushing, bradycardia and blurred vision.
@.1.6.& ubstituted 5en9amides
(his class of drugs promotes 8I tract motility and increases antroduodenal coordination by indirectly stimulating cholinergic
nerves. (hey cause the release of acetylcholine from enteric neurons. ide effects include a usually transient increase in stool
freuency. +rugs that belong to this class include metoclopramide, cisapride and trimethoben9amide. 2s metoclopramide e%hibitssignificant anti#dopaminergic effects, it is discussed in the following section.
isapride ropulsidM! was used as a prokinetic for conditions in which delayed gastric emptying may be etiologic. 2ntro#
duodenal motility is enhanced by this agent. In contrast to metoclopramide, cisapride e%hibits no anti#dopaminergic activity. It is
also used for gastroesophageal reflu% disease. ardiac arrhythmias such as ventricular tachycardia, ventricular fibrillation, torsade
de pointes and J( prolongation may occur when cisapride is used concurrently with ketocona9ole, itracona9ole, micona9ole,
flucona9ole, erythromycin, troleandomycin and clarithromycin. +ue to these adverse effects, cisapride was withdrawn from the
market, and is only available from the manufacturer under a compassionate use protocol.
(rimethoben9amide (iganM! is used to treat nausea and vomiting. Its side effects include drowsiness. afety in pregnancy is not
established, although based on limited information, the drug appears to be relatively safe.
@.1.6.6 +opamine receptor antagonists
)etoclopramide is the prototype drug of this class, and has both peripheral and central dopamine receptor antagonist effects.
eripherally, it enhances release of acetylcholine from intrinsic cholinergic neurons. It is an effective antiemetic in patients
receiving chemotherapy. ide effects limit the use of metoclopramide, with an incidence between 10#&0E. (he most common are
due to N effects, ranging from mild an%iety, restlessness, depression, nervousness and insomnia, to marked an%iety, confusion,
disorientation and hallucinations. 7atigue and e%trapyramidal side effects such as tremor, akathisia, tardive dyskinesia and
dystonic reactions that mimic arkinsonHs disease are due to its central antidopaminergic properties. 8ynecomastia due to
enhanced prolactin release has been described 10F!. 5ased on limited information, metoclopramide appears to be relatively safe
for use in pregnancy.
+omperidone )otiliumM! is a ben9imida9ole derivative with anti#dopamine effects in the upper 8I tract. 2 distinguishing feature
compared to other substituted ben9imida9ole agents is the lack of cholinergic activity. 2ntro#duodenal motility and coordination is
enhanced specifically by its peripheral anti#dopaminergic effects. 5ecause domperidone does not cross the blood#brain barrier, no
significant central nervous system anti#dopaminergic effects are seen. entral nervous system side effects as seen with
metoclopramide are rare. 7emale patients may develop galactorrhea due to increased prolactin levels.
Indications are nausea and vomiting associated with motion sickness. (he patch should be applied to the skin behind the ear.
rogrammed delivery of 0.A mg of scopolamine over 6 days is provided. It should be used with caution in elderly patients, and in
patients with pyloric obstruction or urinary bladder neck obstruction, or those with intestinal obstruction. It can be used in
pregnancy if the anticipated benefit =ustifies the potential risk to the fetus. 2dverse reactions include dry mouth, drowsiness,
blurred vision and transient dilation of pupils.
@.1.A 7)1&3 rece-tor antagonists
A#/(6 receptors are located both centrally and peripherally, with high concentrations in the 8I tract. 2ntagonists for this receptor
have been evaluated and found to be effective for a variety of conditions, including cancer chemotherapy#induced emesis, emesis
due to total body irradiation 111!, 8I motility disturbances, carcinoid syndrome and nausea and vomiting related to migraine and
an%iety 6!.
@.1.A.1 ;ndansetron
;ndansetron is the prototype drug of this class. It is effective in the control of chemotherapy#induced emesis. (he principal site of
action is in the area postrema, with some gastric prokinetic activity. ;ndansetron is not effective against motion sickness. 8iven
orally, ondansetron can be dosed C#1& hours. ;ndansetron is superior to high#dose metoclopramide in chemotherapy#induced
emesis. ide effects are few, and include constipation, headache and a transient rise in transaminases.
@.1.A.& ;ther 7)1&3 rece-tor antagonists
2dditional A#/(6 receptor antagonists which have been tested clinically are granisetron and tropisetron. omparative studieshave shown similar efficacy for these two agents 11&!. +irect costs of the drugs in this class did vary widely 1&-!. *fficacy is
more pronounced for cisplatin#containing regimens than for less emetogenic regimens. *ffectiveness is greater for acute emesis
than for delayed emesis. Nausea is more difficult to control than emesis by these agents. 8ranisetron Gytril M! is indicated for the
prevention of nausea and vomiting associated with initial and repeat courses of emetogenic cancer therapy, including high#dose
(hese agents can assist in relief of cytoto%ic drug#induced emesis, especially when combined with other antiemetics.
+e%amethasone alone or in combination with ondansetron were shown to be eually efficacious in preventing delayed
chemotherapy#induced nausea and vomiting in patients at low risk for this 161!. 2 meta#analysis of the available randomi9edevidence of the effectiveness of de%amethasone in the treatment of chemotherapy#induced nausea and vomiting was published.
(hirty#two studies met the inclusion critieria. +e%amethasone was superior to placebo or no treatment for complete protection of
acute emesis odds ratio &.&&$ -AE confidence interval lO, 1.C- to &.D0!. 2lso, de%amethasone was superior to placebo or no
treatment for complete protection from delayed emesis odds ratio &.0@$ -AE l$ 1.D6#&.AD! 16&!. In adrenal insufficiency,
treatment of the underlying cortisol deficiency with corticosteroids will ameliorate the symptoms of this disorder, including
nausea and vomiting.
@.1.D.& )egestrol 2cetate
(his is a progesterone used in the treatment of advanced breast cancer, which has appetite#stimulating properties and can improve
the symptoms of nausea from a variety of causes in cancer patients.
@.1.D.6 (etrahydrocannabinol dronabinol! and Nabilone
(he role of delta#-#tetrahydrocannabinol, the active component of mari=uana, and nabilone, a synthetic cannabinoid, is mainly in
cytoto%ic drug#induced emesis 116!. ide effects tend to limit their usefulness. 2lterations in mood, motor coordination,
cognitive function and memory are common. Nabilone has been used successfully for the management of intractable nausea and
vomiting in terminally staged 2I+ patients 11@!.
+ronabinol )arinolM! is an orally active cannabinoid. It is used for prophyla%is of chemotherapy#induced emesis. ombination
treatment with prochlorpera9ine may result in synergistic or additive antiemetic effects and attenuate the to%icities. 2 potential for
abuse e%ists.
@.1.D.@ 5en9odia9epines
(he an%iolytic and amnesic properties of some ben9odia9epines can be beneficial for patients whose nausea and vomiting have a
psychological component. (his is particularly so for the conditioned emesis of cytoto%ic chemotherapy.
@.1.D.A 5ismuth subsalicylate epto#5ismolM!
2lthough usually used for the symptomatic control of diarrhea, associated upper 8I complaints such as nausea may be relieved.
@.1.D.D (ricyclic 2ntidepressants
(he tricyclic antidepressant class of drugs amitriptyline, nortriptyline, do%epin, desipramine, and imipramine! have been used at
ow doses average does A0 mg:day for the treatment of fuctional nausea and vomiting 11F! and cyclic vomiting syndrome 11C!,
with some efficacy.
@.1.D.F 8inger >ingiber officinale!
8inger has been advocated as a treatment for nausea and vomiting. 2 systematic review, however, of the evidence from si%
randomi9ed clinical trials did not show a significant difference from placebo. /owever, individual non#controlled studies have
favored ginger over placebo for the treatment of nausea and vomiting caused by seasickness, early pregnancy and chemotherapy