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). Persistent 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 expulsion of gastric contents. Regurgitation is the return of small amounts of food or secretions to the hypopharynx in the context of mechanical obstruction of the esophagus, gastroesophageal reflux disease or esophageal motility disorders. Rumination is similar to regurgitation, except small amounts of completely swallowed food are returned to the hypopharynx from the stomach and is often re-swallowed (2). Rumination is not associated with nausea.

This review of nausea and vomiting is based on a MEDLINE literature search encompassing 1990-2000, using the MeSH headings Nausea and Vomiting with the subheadings Complications, Diagnosis, Drug Treatment, Treatment, Etiology, Psychology and Radiography. Certain articles, including placebo-controlled trials of therapy, comprehensive reviews and other publications deemed seminal, were reviewed and are referenced. Certain articles prior to 1990 were also reviewed. The emphasis is placed on articles that provide evidence which can be incorporated into guidelines for diagnosis and management.

Certain 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. Many 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 require thorough diagnostic testing and referral to a specialist (1).

Assessment of the duration of nausea and vomiting is an important initial point in the history. Symptoms present for less than a week may be due to conditions which are separable from those causing symptoms over weeks, months or years.

For acute nausea and vomiting, the diagnostic algorithm is based on three key questions (Table 1):

Whether immediate therapy is needed due to the consequences of nausea and vomiting regardless of the underlying cause
Whether empiric treatment and reassurance are sufficient
Whether expeditious work-up is required to establish the cause.
For chronic nausea and vomiting, the diagnostic algorithm is based on history and physical exam findings that point to the organ system involved: the gastrointestinal tract, the nervous system or the endocrine system. Psychogenic causes are an important additional category to consider in chronic nausea and vomiting. A subset of patients will have no cause identified despite extensive diagnostic testing. This group of patients may benefit from referral to specialized centers. Certain presentations prompt referral to a gastroenterologist (Table 12).

1.1 Associated Symptoms

Certain symptoms are typically associated with nausea and vomiting. Associated upper GI tract complaints such as bloating, early satiety, dysphagia and odynophagia should be sought. Dyspepsia can be associated with nausea. Lightheadedness, abdominal or chest pain, cough or hematemesis are symptoms that should prompt an assessment for conditions that may require immediate therapy regardless of the underlying cause of nausea and vomiting. A 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 . Symptoms that are severe, such as chest or abdominal pain, CNS symptoms, fever with chills, a history of an underlying systemic disease or of immunosuppression should prompt a diagnostic workup.

1.2 Physiology of nausea and vomiting

The vomiting reflex is triggered by stimulation of chemoreceptors in the upper GI tract and mechanoreceptors in the wall of the GI tract which are activated by both contraction and distension of the gut as well as by physical damage. A coordinating center in the central nervous system controls the emetic response. This center is located in the parvicellular reticular formation in the lateral medullary region of the brain. Afferent nerves to the vomiting center arise from abdominal splanchnic and vagal nerves, vestibulo-labyrinthine receptors, the cerebral cortex and the chemoreceptor trigger zone (CTZ).The CTZ lies adjacent in the area postrema and contains chemoreceptors that sample both blood and cerebrospinal fluid. Direct links exist between the emetic center and the CTZ. The CTZ is exposed to emetic stimuli of endogenous origin such as hormones associated with pregnancy and to stimuli of exogenous origin such as drugs (3). The efferent branches of cranial nerves V, VII, and IX, as well as the vagus nerve and sympathetic trunk produce the complex coordinated set of muscular contractions, cardiovascular responses and reverse peristalsis that characterizes vomiting (4).

The area postrema is rich in dopamine receptors and is a target for the antagonists haloperidol, metoclopramide and the phenothiazines. Histamine-1 and muscarinic cholinergic receptors are present in the nucleus ambiguus and lateral vestibular nucleus. 5-hydroxytryptamine (5HT) receptors are present within the area postrema. 5HT can activate dopamine release. The new 5HT3 receptor antagonists have demonstrated efficacy against cytotoxic chemotherapy-induced emesis (5). Drugs effective against motion sickness–such as promethazine, diphenhydramine and scopolamine–have little effect against cytotoxic drug-induced emesis.

2.0 Acute nausea and vomiting

Symptoms present for less than a week are defined as acute. The causes of nausea and vomiting of short duration are often separable from etiologies leading to more chronic symptoms. In the initial evaluation of a patient presenting with acute nausea and vomiting, assessment regarding the need for immediate therapeutic intervention regardless of the underlying cause is important. If immediate therapeutic intervention to correct the consequences of vomiting are not necessary, or has been performed, then the important questions are whether empiric treatment of nausea and vomiting and reassurance are sufficient, and whether expeditious diagnostic work-up to determine the underlying cause is necessary. These latter two questions are linked, and key historical points can help determine the most appropriate diagnostic testing and therapy. Referral for additional diagnostic tests and/or management needs to be considered for a variety of situations.

2.1 Immediate therapeutic intervention is necessary regardless of the cause.

Vomiting with intravascular volume depletion requires immediate intervetion
Certain consequences of vomiting require immediate treatment regardless of the cause. The diagnosis and treatment of conditions described in this section are outlined in (Table 2). If vomiting has been severe and protracted, intravascular volume depletion may have occurred, leading to orthostatic hypotension and renal insufficiency. Hypokalemic hypochloremic alkalosis results from loss of gastric hydrochloric acid, increased H+ 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 injury and bleeding
Either vomiting or retching can lead to mucosal injury (e.g. Mallory-Weiss tear), evident as hematemesis and/or melena; excessive blood loss may contribute to intravascular volume depletion. In the case of GI 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.

Vomiting can lead to aspiration
Vomitus may be aspirated, leading to respiratory compromise which may be severe enough to require endotracheal intubation and mechanical ventilation. A corollary to this is the development of aspiration pneumonitis or pneumonia. In the case of aspiration and hypoxemia, ensuring a patent airway is of paramount importance. The management of such patients requires a multidisciplinary approach, and may include the services of an intensivist, gastroenterologist and primary care physician.

Vomiting or retching can lead to esophageal rupture
Vomiting or retching may cause rupture of the esophagus (Boerhaave syndrome), a surgical emergency. Boerhaave syndrome deserves special consideration because a high index of suspicion is required to make a timely diagnosis and surgical intervention is necessary. Spontaneous rupture of the esophagus is an intrathoracic disaster if left untreated. As noted in a recent review of all published cases in the literature since 1980 and 18 additional cases (6), non-specific symptoms such as chest and abdominal pain can lead to mistaken diagnoses such as pulmonary embolus, myocardial infarction, aortic dissection, spontaneous pneumothorax, pancreatitis or perforated peptic ulcer. Forty percent of patients had a history of alcoholism, and 41% had peptic ulcer disease. Pain (83%) and vomiting (79%), often associated with dyspnea (39%) and shock (32%), were the major symptoms. Physical exam may detect crepitus due to air in the soft tissues of the neck and thorax. Chest and abdominal X-rays may show subcutaneous emphysema, pneumothorax, pneumomediastinum, pleural effusion and free mediastinal air. However, up to a third of patients have normal routine X-rays initially (7). Esophagograms with water-soluble contrast agents are diagnostic in most cases. Thoracic CT scans may reveal mediastinal air or pleural fluid even when the esophagogram shows no leak and should be obtained when there is a high degree of suspicion. In the series cited, the mortality rate was 31%, an improvement on the 50% mortality rate noted prior to 1980.

Intra-abdominal bleeding is a rare complication of vomiting
Intra-abdominal bleeding is a rare complication of vomiting. Hemoperitoneum has been described following vomiting. Splenic laceration secondary to persistent emesis in a pregnant patient was diagnosed at laparotomy (8). Hepatic laceration caused by vomiting leading to massive intra-abdominal hemorrhage was described (9). In both cases, abdominal pain in the context of nausea and vomiting was the chief complaint. Surgical intervention is necessary for diagnosis and treatment. Rectus sheath hematoma, diagnosed by ultrasound or CT, may lead to abdominal pain, and needs to be considered in the patient who is anti-coagulated (10). Anticoagulation or low platelet counts may lead to intramural hematomas of the esophagus after vomiting. The presentation is one of severe substernal or intrascapular pain, hematemesis and dysphagia.

2.2. Empiric treatment and reassurance are sufficient

If the patient does not have complications of vomiting that require immediate attention, and if the underlying cause of the nausea and vomiting as suggested by the history does not require expeditious work-up and therapy, then the patient can be reassured and treated empirically with anti-emetic agents (Table 11). Before such a decision is made, however, symptoms and signs that favor a self-limited illness should be reviewed and compared with findings that favor serious underlying disease. Such a comparison is provided in (Table 3).

Key questions can help identify conditions that can be treated empirically. Certain presentations and etiologies are sufficiently characteristic 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 extensive diagnostic evaluation. A majority of patients seen in the ambulatory care setting falls into this category.

2.2.1 Early pregnancy

If the patient is a woman of child-bearing age, a pregnancy test should be done. Pregnancy-related nausea and vomiting is common, reported in 70-90% of pregnancies (11)(123). Rising estrogen and progesterone levels during pregnancy have been implicated, as has maternal serum prostaglandin E2 levels (124). The onset is usually shortly after the first missed menstrual period, and symptoms may begin before the woman recognizes that pregnancy has occurred. Symptoms typically begin by four to six weeks of gestation, peaking in severity by eight to twelve weeks, and resolving spontaneously by the 20th week (11). Nausea, sometimes accompanied by vomiting, is noted especially in the morning. In one prospective study of 160 pregnant women, however, “morning sickness” occurred in only 1.8%, whereas 80% reported nausea lasting all day (125). Symptoms usually disappear by the fourth month of pregnancy, although they may persist into the third trimester. Babies born to a mother with nausea and vomiting of pregnancy have birth weights similar to babies born to mothers without these symptoms. Thus, the prognosis for mother and baby is generally excellent. However, in one study a higher than normal incidence of antepartum hemorrhage was noted (12). Vomiting during pregnancy is not teratogenic (13).

If pregnancy-related nausea and vomiting are not characteristic of morning sickness (for example, 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 HELLP 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.

Treatment of Pregnancy-related nausea and vomiting

For typical pregnancy-related nausea and vomiting, reassurance is often all that is needed, although an anti-emetic may be necessary. Traditionally, dietary advice such as dry toast in the morning and avoiding fatty foods was offered. Antacids for reflux symptoms associated with nausea and vomiting may be used. If an anti-emetic is necessary, then antihistamines may be used and are considered safe for use during pregnancy. The efficacy or safety of phenothiazines or metoclopramide have not been established for nausea and vomiting of pregnancy in controlled trials despite their widespread use (11).

Clinical trials assessing the efficacy of anti-emetic therapy are of varialbe quality. An analysis of such trials showed that anit-histamines, pyridoxine, and P6 acupressure appeared to reduce the frequency of nausea in early pregnancy (126). A 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 H1 receptor antagonists, and phenothiazines (127). The pooled data, however, were not homogenous.

A 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 (135).

The effectiveness of pyridoxine (vitamin B6) for nausea and vomiting of pregnancy has been studied in a randomized, double-blind placebo-controlled trial. Patients in the treatment group received 30 mg/day of pyridoxine hydrochloride for 5 days. A significant decrease in post-therapy nausea in the treatment group was noted (14). Similar results were noted for vomiting in another study over a 3-day duration (15). Acupressure at the P6 point located on the wrist has also been studied in a randomized, double-blind placebo-controlled study and found to reduce nausea, but not vomiting, in pregnant patients (16). Sixty women were assigned to two treatment groups: one to a group receiving P6 acupressure, and a control group receiving pressure at another anatomic location. Symptom scores after 5-7 days of treatment were used to judge efficacy. Nausea scores improved over time in both groups, achieving statistical significance in the acupressure group. In another study, 161 pregnant symptomatic women were assigned to three groups: P6 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 in the acupressure group (17).

2.2.2 Vertigo

Nausea or vomiting associated with vertigo suggests another set of causes. Vertigo is a sensation of the environment spinning around, often described as dizziness by the patient. Evaluation of the dizzy patient begins with a thorough history, which can identify 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. Associated 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 important to determine. Loss of consciousness associated with vertigo should be determined.

Peripheral causes of vertigo, such as benign positional vertigo, vestibular neuronitis, Meniere’s disease and acoustic neuroma need to be distinguished from central causes of vertigo, such as multiple sclerosis, brainstem ischemia and central nervous system tumor. The physical examination is often helpful in determining whether a peripheral or central cause of vertigo is present. A complete head and neck exam including examination of the tympanic membranes is advised. Cranial nerves should be tested, including assessment of extraocular muscle function. Nystagmus can aid in diagnosis. Nystagmus of peripheral origin is rotatory or horizontal. Vertical nystagmus is pathognomonic for brain stem disease, as is nystagmus that is more pronounced in one eye.

Nystagmus may be tested by having the patient look ahead, then 30 degrees to the left and to the right. Pausing at each position allows evaluation of nystagmus. Induced nystagmus is done by rapidly changing the position of the head. The Hallpike-Dix (or Nylen-Barany) 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. A positive test is present when paroxysmal nystagmus is induced after a brief delay. A 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. For benign positional vertigo, a 3-20 second latency, rotatory nystagmus and adaptation (i.e. less response to repeat testing) is seen. For a central nervous system cause, no latency is seen, the nystagmus can be vertical or horizontal and can last longer than 60 seconds and there is no adaptation.

Balance testing such as the Romberg test and assessment of the gait should also be performed. Vertigo can also be an early symptom in multiple sclerosis. Lesions in the lower midbrain and pons produce internuclear ophthalmoplegia. This is checked for by having the patient follow the finger of the examiner from side to side horizontally. In this type of nystagmus the eye on the side to which the gaze is directed participates strongly with a horizontal nystagmus, whereas the opposite eye will show less nystagmus and weakness of internal rotation. A careful cardiac examination is also necessary, as arrhythmias can produce symptoms which are confused with vertigo (18).

Spontaneous and Induced Nystagmus and their Causes

Spontaneous Nystagmus
Symptom/Sign Peripheral Central
Direction Usually horizontal-rotatory
Never purely vertical Any direction
May be purely vertical
Direction of fast component Away from side with disease Toward side with disease
(or direction changing)
Effect of visual fixation Suppressed Not suppressed
Usual anatomical location of
problem Labyrinth or vestibular nerve Brainstem or cerebellum

Induced Nystagmus
Feature
Peripheral (BPV)
Central
Time to onset after
quick position change
(latency)

3-20 seconds Immediate
Duration Less than 1 minute Persists longer than 1 minute
Fatigability Marked 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. Are there associated neurologic symptoms such as headache, visual changes or loss of sensation and strength, suggesting cortical or brain stem disorders? Is there a history of seizures? Has the patient lost consciousness with the episode of vertigo? Is there antecedent cranial or cervical trauma? If the answer is affirmative to any of these questions, then empiric therapy is not advised.

Referral to a neurologist and possibly a neurosurgeon may be necessary in patients with CNS symptoms suggestive of a brain stem lesion, vertebro-basilar insufficiency or cortical lesions. Additionally, in patients with vertigo associated with seizures, 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.

2.2.2.1 Vestibular neuronitis

The sudden onset of vertigo with nausea and vomiting, increasing in severity over several hours with resolution over a similar span of time, is characteristic of vestibular neuronitis. Patients may awaken from sleep with vertigo. There is often a history of a recent or concurrent upper respiratory tract infection, and clusters of cases may be seen. The etiology is probably viral, and the condition is often diagnosed in adolescents and young adults. Following the acute episode, prolonged dizziness similar to motion sickness may be noted, lasting weeks to months. No new associated auditory deficits, fullness in the ear, or tinnitus are noted. Persistent nystagmus toward the affected side may be noted. Clinical and histopathologic studies implicate an isolated lesion of the vestibular nerve (19).

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 CT. Referral to an otolaryngologist should be considered for refractory or atypical cases.

Treatment

Treatment for nausea and vomiting is symptomatic, similar to that for motion sickness (Table 11).

2.2.2.2 Acute labyrinthitis

Acute labyrinthitis symptomatically is similar to vestibular neuronitis, except hearing loss on the involved side is also noted. The cause may be viral, bacterial or due to a toxin (18). A history of recent or concurrent upper respiratory tract infection is often given. Most patients improve over 1-2 weeks, although recurrent episodes have been described. Most report an upper respiratory tract illness 1-2 weeks prior to the onset of vertigo. Several members of the patient’s family may be affected, and it is seen more often in spring and early summer. In most cases a viral etiology is likely.

A subgroup of patients may have herpes zoster oticus (Ramsay-Hunt 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.

Treatment

No specific therapy is recommended. Symptomatic treatment with anti-vertigo medications as for motion sickness may be used if symptoms are severe (Table 11). 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. For the Ramsay-Hunt syndrome, acyclovir is effective in the treatment of facial paralysis, but is ineffective for vertigo (18).

2.2.2.3 Meniere’s disease

Severe nausea and vomiting may be a manifestation of endolymphatic hydrops, or Meniere’s disease. Symptoms characteristically include episodic aural fullness, tinnitus, hearing loss and vertigo. If vertigo is associated with hearing loss or tinnitus, an audiogram is needed to diagnose Meniere’s disease or acoustic neuroma. The onset is abrupt, and usually no precipitating factors are identified. Attacks of vertigo can last a few hours to 24 hours, and subside gradually. Horizontal or horizonto-rotatory nystagmus may be observed.

Treatment

Treatment is with restriction of salt intake and anti-vertigo drugs. Symptomatic relief of vertigo can be obtained with anticholinergic agents (e.g. scopolamine orally or by transdermal patch), or antihistamines (e.g. diphenhydramine, meclizine or cyclizine). Diazepam 2-5 mg orally q 6-8h is effective in suppressing the vestibular system (Table 11). In severe cases, referral to an otolaryngologist is appropriate.

2.2.3 Motion sickness

Motion sickness is a form of physiologic vertigo. Perspiration, increased salivation, yawning and malaise are described by patients with motion sickness. Hyperventilation can lead to hypocapnia, and venous pooling can predispose to hypotension and syncope. The sight and smell of food can exacerbate nausea. Motion sickness is readily diagnosed by history. This is a common syndrome that can occur in an automobile, airplane or at sea. Exaggerated self-generated movement, in fact, can cause motion sickness by forcing rapid and inappropriate changes of vestibular function (20).

Treatment

The treatment of vertigo associated with motion sickness is empirical (21). Transdermal scopolamine can prevent motion sickness. The patch must be placed several hours prior to the anticipated onset of motion sickness. Anti-histamines such as dymenhydrinate, meclizine, cyclizine, promethazine and diphenhydramine can be used
(Table 11) The main side effect of this drug class is drowsiness.

Acupressure on the P6 point located on the wrist, which has been used in traditional Chinese medicine to treat nausea and vomiting of pregnancy, has been evaluated in a randomized, placebo-controlled double-blind study. Sixty-four subjects were randomly divided into 4 groups (P6 acupressure, dummy-point acupressure, sham P6 acupressure, and control) and subjected to optokinetic drum rotation which elicits motion sickness in normal volunteers. Subjects in the P6 acupressure group reported significantly less nausea and the incidence of gastric tachyarrhythmia was reduced in this group (22). In another blinded placebo-controlled study on 36 patients, however, acupressure provided no protection (23).

2.2.4 Viral syndrome

Acute 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. These symptoms, suggestive of a viral etiology, are an indication that no specific diagnostic testing is necessary.

Treatment

Empiric therapy with liberal fluid intake, anti-emetics and antipyretics may suffice. Empiric therapy should only be instituted in immunocompetent patients with symptoms that are mild and typical for a viral syndrome. Signs such as protracted fever with chills, bloody diarrhea and clinically evident fluid depletion should be handled with proper diagnostic studies and appropriate specific therapy.

A randomized, double-blind comparison of treatment of uncomplicated nausea and vomiting due to viral gastroenteritis with prochorperazine (Compazine) or promethazine (Phernergan) was published. The results showed that prochoroperazine was significantly better in terms of symptom relief compared to promethazine (119).

2.2.5 Post-operative

Post-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 42% (24). These symptoms are generally attributed to the general anesthetic agents or analgesics used. In the immediate post-operative setting, these patients are often treated empirically. However, 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 (25). Congestion of the eye secondary to phakomorphic glaucoma can lead to intractable nausea and vomiting in the post-operative state (26).

Treatment

While post-operative nausea and vomiting is unlikely to be encountered in the primary care setting, treatment regimens have been studied in this patient population. Therefore, it is useful to be aware of this literature. For example, the efficacy, safety and cost-effectiveness of ondansetron (4 mg intravenously) was compared to droperidol (0.625 mg or 1.25 mg intravenously) in a randomized, double-blind placebo-controlled trial for the prevention of postoperative nausea and vomiting after outpatient gynecologic surgery in 161 women. Droperidol 0.625 mg iv provided antiemetic prophylaxis comparable to that of ondansetron 4 mg iv without an increased incidence of side effects and in the most cost-effective manner (27). In another randomized, double-blind, placebo-controlled trial conducted on patients undergoing laparoscopic cholecystectomy, prophylactic anti-emetic therapy with ondansetron, tropisetron, granisetron or metoclopramide was studied. Ondansetron prophylaxis resulted in a lower incidence of post-operative nausea and vomiting compared to metoclopramide or placebo. There were no statistically significant differences among the three 5-HT3 receptor antagonists(28). A review of published controlled trials comparing 5-HT3 receptor antagonists to traditional anti-emetic agents (including metoclopramide, perphenazine, prochlorperazine, cyclizine and droperidol) for prophylaxis of postoperative nausea and vomiting showed the 5-HT3 receptor antagonists to be superior (128).

2.3 Diagnostic workup required

Experienced 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 (Table 3). Most causes of acute vomiting are self-limited illnesses, but nausea and vomiting can be symptoms of conditions that require expeditious diagnostic workup and treatment (Table 4). Guidelines for referral are included in each section.

2.3.1 Abdominal or chest pain

A history of pain may indicate that nausea and vomiting is a consequence of a pathophysiologic process in the thoracic cavity or abdomen. Abdominal pain preceding nausea and vomiting indicates an organic lesion. Pain 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.

2.3.1.1 Coronary artery disease

Acute and chronic myocardial ischemia, as well as myocardial infarction, may present with nausea and vomiting. These symptoms may be accompanied by abdominal bloating or fullness. Often, concomitant substernal chest pain is present, or the patient may give a history of angina pectoris. Even 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. At a minimum, an electrocardiogram should be obtained in such patients. Further diagnostic evaluation and therapy depend on the clinical impression. Cardiac enzymes to rule…