Nausea and Vomitting

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NAUSEA and VOMITTING

current_medical_diagnosis_treatment

Nausea & Vomiting

Nausea is a vague, intensely disagreeable sensation of sickness or "queasiness" that may or

may not be followed by vomiting and is distinguished from anorexia. Vomiting often follows,

as does retching (spasmodic respiratory and abdominal movements). Vomiting should be

distinguished from regurgitation, the effortless reflux of liquid or food stomach contents; and

from rumination, the chewing and swallowing of food that is regurgitated volitionally after

meals.

The medullary vomiting center (which contains histamine H1-receptors and muscarinic

cholinergic receptors) may be stimulated by four different sources of afferent input: (1)

Afferent vagal and splanchnic fibers from the gastrointestinal viscera are rich in serotonin 5-

HT3receptors; these may be stimulated by biliary or gastrointestinal distention, mucosal or

peritoneal irritation, or infections. (2) Fibers of the vestibular system, which have high

concentrations of histamine H1and muscarinic cholinergic receptors. (3) Higher central

nervous system centers; here, certain sights, smells, or emotional experiences may induce

vomiting. For example, patients receiving chemotherapy may develop vomiting in

anticipation of its administration. (4) The chemoreceptor trigger zone, located outside the

blood-brain barrier in the area postrema of the medulla, which is rich in opioid, serotonin 5-

HT3, neurokinin 1 (NK1) and dopamine D2receptors. This region may be stimulated by drugs

and chemotherapeutic agents, toxins, hypoxia, uremia, acidosis, and radiation therapy.Although the causes of vomiting are many, a simplified list is provided in Table 141.

Table 141. Causes of nausea and vomiting.

Visceral afferent

stimulation

Infections

Mechanical obstruction

Gastric outlet obstruction: peptic ulcer disease, malignancy,

gastric volvulus

Small intestinal obstruction: adhesions, hernias, volvulus,

Crohn's disease, carcinomatosis

Dysmotility

Gastroparesis: diabetic, medications (metformin, acarbose,

pramlintide, exenatide), postviral, postvagotomy

Small intestine: scleroderma, amyloidosis, chronic intestinal

pseudo-obstruction, familial myoneuropathies

Peritoneal irritation

Peritonitis: perforated viscus, appendicitis, spontaneousbacterial peritonitis


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Viral gastroenteritis: Norwalk agent, rotavirus

"Food poisoning": toxins fromBacillus cereus, Staphylococcus

aureus, Clostridium perfringens

Hepatitis A or B

Acute systemic infections

Hepatobiliary or pancreatic disorders

Acute pancreatitis

Cholecystitis or choledocholithiasis

Topical gastrointestinal irritants

Alcohol, NSAIDs, oral antibiotics

Postoperative

Other

Cardiac disease: acute myocardial infarction, congestive heart

failure

Urologic disease: stones, pyelonephritis

CNS disorders Vestibular disorders

Labyrinthitis, Meniere's syndrome, motion sickness, migraine

Increased intracranial pressure

CNS tumors, subdural or subarachnoid hemorrhage

Migraine

Infections

Meningitis, encephalitis

Psychogenic

Anticipatory vomiting, bulimia, psychiatric disorders

Irritation of chemoreceptor

trigger zone

Antitumor chemotherapy

Drugs and medications

Calcium channel blockers

Opioids

Anticonvulsants

Antiparkinsonism drugs

-Blockers, antiarrhythmics, digoxin

Nicotine

Oral contraceptives

Cholinesterase inhibitors

Radiation therapy

Systemic disorders


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Diabetic ketoacidosis

Uremia

Adrenocortical crisis

Parathyroid disease

Hypothyroidism

Pregnancy

Paraneoplastic syndrome

NSAIDs, nonsteroidal anti-inflammatory drugs; CNS, central nervous system.

Complications of vomiting include dehydration, hypokalemia, metabolic alkalosis, aspiration,rupture of the esophagus (Boerhaave's syndrome), and bleeding secondary to a mucosal tear

at the gastroesophageal junction (Mallory-Weiss syndrome).

Clinical Findings

Symptoms and Signs

Acute symptoms without abdominal pain are typically caused by food poisoning, infectious

gastroenteritis, drugs, or systemic illness. Inquiry should be made into recent changes in

medications, diet, other intestinal symptoms, or similar illnesses in family members. The

acute onset of severe pain and vomiting suggests peritoneal irritation, acute gastric or

intestinal obstruction, or pancreaticobiliary disease. Examination may reveal fever, focal

tenderness or rigidity, guarding, or rebound tenderness. Persistent vomiting suggestspregnancy, gastric outlet obstruction, gastroparesis, intestinal dysmotility, psychogenic

disorders, and central nervous system or systemic disorders. Vomiting that occurs in the

morning before breakfast is common with pregnancy, uremia, alcohol intake, and increased

intracranial pressure. Vomiting immediately after meals strongly suggests bulimia or

psychogenic causes. Vomiting of undigested food one to several hours after meals is

characteristic of gastroparesis or a gastric outlet obstruction; physical examination may reveal

a succussion splash. Patients with acute or chronic symptoms should be asked about

neurologic symptoms that suggest a central nervous system cause such as headache, stiff

neck, vertigo, and focal paresthesias or weakness.

Special Examinations

With vomiting that is severe or protracted, serum electrolytes should be obtained to look for

hypokalemia, azotemia, or metabolic alkalosis resulting from loss of gastric contents. Flat

and upright abdominal radiographs are obtained in patients with severe pain or suspicion of

mechanical obstruction to look for free intraperitoneal air or dilated loops of small bowel. If

mechanical small intestinal or gastric obstruction is thought likely, a nasogastric tube is

placed for relief of symptoms. The cause of gastric outlet obstruction is best demonstrated by

upper endoscopy, and the cause of small intestinal obstruction is best demonstrated with

abdominal CT imaging. Gastroparesis is confirmed by nuclear scintigraphic studies or 13C-

octanoic acid breath tests, which show delayed gastric emptying and either upper endoscopyor barium upper gastrointestinal series showing no evidence of mechanical gastric outlet


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obstruction. Abnormal liver function tests or elevated amylase or lipase suggest

pancreaticobiliary disease, which may be investigated with an abdominal sonogram or CT

scan. Central nervous system causes are best evaluated with either head CT or MRI.

Treatment

General Measures

Most causes of acute vomiting are mild, self-limited, and require no specific treatment.

Patients should ingest clear liquids (broths, tea, soups, carbonated beverages) and small

quantities of dry foods (soda crackers). For more severe acute vomiting, hospitalization may

be required. Patients unable to eat and losing gastric fluids may become dehydrated, resulting

in hypokalemia with metabolic alkalosis. Intravenous 0.45% saline solution with 20 mEq/L

of potassium chloride is given in most cases to maintain hydration. A nasogastric suction tube

for gastric decompression improves patient comfort and permits monitoring of fluid loss.

Antiemetic Medications

Medications may be given either to prevent or to control vomiting (see above). Combinations

of drugs from different classes may provide better control of symptoms with less toxicity in

some patients. All of these medications should be avoided in pregnancy. (For dosages, see

Table 142.)

Table 142. Common antiemetic dosing regimens.

Dosage Route

Serotonin 5-HT3antagonists

Ondansetron 832 mg or 0.15 mg/kg once daily IV

8 mg twice daily PO

Granisetron 1 mg or 0.01 mg/kg once daily IV

2 mg once daily PO

Dolasetron 100 mg or 1.8 mg/kg once daily IV

100 mg once daily PO

Palonosetron 0.25 mg once as a single dose 30 min before start of

chemotherapy

IV

Corticosteroids

Dexamethasone 820 mg once daily IV

420 mg once or twice daily PO

Methylprednisolone 40100 mg once daily IV

Dopamine receptor antagonists

Metoclopramide 1020 mg or 0.5 mg/kg every 68 hours IV

1020 mg every 68 hours PO


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Prochlorperazine 510 mg every 46 hours PO, IM, IV

25 mg suppository every 6 hours PR

Promethazine 25 mg every 46 hours PO, PR, IM,IV

Trimethobenzamide 250 mg every 68 hours PO

200 mg every 68 hours IM, PR

Sedatives

Diazepam 25 mg every 46 hours PO, IV

Lorazepam 12 mg every 46 hours PO, IV

IV, intravenously; PO, orally; IM, intramuscularly; PR, per rectum.

Serotonin 5-HT3-receptor antagonists

Ondansetron, granisetron, dolasetron, and palonosetron are effective in preventing

chemotherapy- and radiation-induced emesis when initiated prior to treatment. Single-dose

administration schedules are as effective as multiple-dose regimens. Although serotonin

antagonists are effective for the prevention of postoperative nausea and vomiting, less

expensive alternatives (eg, dexamethasone or droperidol) are equally effective.

Corticosteroids

Corticosteroids (eg, dexamethasone) have antiemetic properties, but the basis for these effects

is unknown. These agents enhance the efficacy of serotonin receptor antagonists for

preventing acute and delayed nausea and vomiting in patients receiving moderately to highly

emetogenic chemotherapy regimens. For the prevention of postoperative nausea and

vomiting, corticosteroids, serotonin antagonists, and droperidol have efficacy; however,

combinations of these agents have additive benefit.

Neurokinin receptor antagonists

Aprepitant is a highly selective antagonist for NK1-receptors in the area postrema. It is used

in combination with corticosteroids and serotonin antagonists for the prevention of acute and

delayed nausea and vomiting with highly emetogenic chemotherapy regimens. Combinedtherapy with aprepitant prevents acute emesis in 8090% and delayed emesis in > 70% of

patients treated with highly emetogenic regimens.

Dopamine antagonists

The phenothiazines, butyrophenones, and substituted benzamides have antiemetic properties

that are due to dopaminergic blockade as well as to their sedative effects. High doses of these

agents are associated with antidopaminergic side effects, including extrapyramidal reactions

and depression. These agents are used in a variety of situations. Cases of QT prolongation

leading to ventricular tachycardia (torsades de pointes) have been reported in several patients

receiving droperidol, hence electrocardiographic monitoring is recommended before and afteradministration.


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Antihistamines and anticholinergics

These drugs (eg, meclizine, dimenhydrinate, transdermal scopolamine) may be valuable in

the prevention of vomiting arising from stimulation of the labyrinth, ie, motion sickness,

vertigo, and migraines. They may induce drowsiness.

Sedatives

Benzodiazepines are used in psychogenic and anticipatory vomiting.

Cannabinoids

Marijuana has been used widely as an appetite stimulant and antiemetic. Pure 9-

tetrahydrocannabinol (THC) is the major active ingredient in marijuana and is available by

prescription as dronabinol. In doses of 515 mg/m2, oral dronabinol is effective in treatingnausea associated with chemotherapy, but it is associated with central nervous system sideeffects in most patients.

The_Washington_Manual_of_Medical

Nausea and Vomiting

GENERAL PRINCIPLES

Etiology

Nausea and vomiting may result from side effects of medications, systemic illnesses,central nervous system (CNS) disorders, and primary GI disorders.

Vomiting that occurs during or immediately after a meal can result from acute pyloricstenosis (e.g., pyloric channel ulcer) or from functional disorders.

Vomiting within 30 to 60 minutes after a meal may suggest gastric or duodenalpathology.

Delayed vomiting after a meal with undigested food from a previous meal can suggestgastric outlet obstruction or gastroparesis.

Symptoms lasting longer than 1 month in duration are considered chronic(Gastroenterology 2001;120:261).

P.585

DIAGNOSIS

Clinical Presentation

History

Bowel obstruction and pregnancy should be ruled out. Medication lists should be scrutinized, and systemic illnesses (acute and chronic)

should be evaluated as etiologies or contributing factors.

TREATMENT


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Correction of fluid and electrolyte imbalances is an important supportive measure. Oral intake should be withheld or limited to clear liquids. Many patients with self-

limited illnesses require no further therapy.

NG decompression may be required for patients with bowel obstruction or protractednausea and vomiting of any etiology.

Patients with protracted nausea and vomiting may sometimes require enteral feedingthrough jejunal tubes, or rarely even total parenteral nutrition.

Medications

Empiric pharmacotherapy is often initiated while investigation is in progress, or when the

etiology is thought to be self-limited.

Phenothiazines and related agents. Prochlorperazine (Compazine), 5 to 10 mg PO tid-qid, 10 mg IM or IV q6h, or 25 mg PR bid; promethazine (Phenergan), 12.5 to 25.0

mg PO, IM, or PR q4-6h; and trimethobenzamide (Tigan), 250 mg PO tid-qid, 200 mg

IM tid-qid, or 200 mg PR tid-qid are effective. Drowsiness is a common side effect,

and acute dystonic reactions or other extrapyramidal effects may occur. Dopamine antagonists include metoclopramide (10 mg PO 30 minutes before meals

and at bedtime, or 10 mg IV prn), a prokinetic agent that also has central antiemetic

effects. Drowsiness and extrapyramidal reactions may occur, and a warning has been

issued by the FDA regarding the risk of tardive dyskinesia with high dose or long-

term use; tachyphylaxis may limit long-term efficacy. Domperidone is an alternate

agent that does not cross the blood-brain barrier and therefore has no CNS side

effects; however, it is not uniformly available.

Antihistaminic agents are most useful for nausea and vomiting related to motionsickness, but may also be useful for other causes. Agents used include

diphenhydramine (Benadryl, 25 to 50 mg PO q6-8h, or 10 to 50 mg IV q2-4h),

dimenhydrinate (Dramamine, 50 to 100 mg PO or IV q4-6h), and meclizine (Antivert,

12.5 to 25 mg 1 hour before travel).

Serotonin 5-HT3receptor antagonists. Ondansetron (Zofran, 0.15 mg/kg IV q4h forthree doses or 32 mg IV infused over 15 minutes beginning 30 minutes before

chemotherapy) is effective in chemotherapy-associated emesis. It can also be used in

emesis that is refractory to other medications (4 to 8 mg PO or IV up to q8h),

especially the sublingual formulation. Granisetron (Kytril, 10 mcg/kg IV for one to

three doses 10 minutes apart, or 1 mg PO bid) is also effective.

Neurokinin-1 (NK-1) receptor antagonist. Aprepitant (Emend, 125 mg PO day 1, 80mg PO days 2 and 3) is an alternative agent currently indicated only for

chemotherapy-induced nausea and vomiting.

common_symptoms_guide

Nausea-Vomiting (Pediatric)

HISTORYDESCRIPTORS

GENERAL DESCRIPTORS: refer to inside cover.

CHARACTER: type and amount of vomiting; how frequent.

AGGRAVATING FACTORS: fright; excitement; certain foods (specify); possibility of drugor poison ingestion, or head injury.


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Relieving Factors: burping the infant.

ASSOCIATED SYMPTOMS

Fever; weight loss; headache; earache; sore throat; vomiting blood; abdominal distention;

diarrhea; decrease in bowel movements; crying on urination; dark urine.

MEDICATIONS

Any.

ENVIRONMENTAL HISTORY

Recent contact with others suffering from vomiting, hepatitis.

PHYSICAL EXAMINATIONMEASURE: pulse, weight, height. Compare to growth chart.

EYES: fundi absent venous pulsations, or papilledema.

NECK: stiffness.

ABDOMEN: check for distention, masses, apparent tenderness.P.252

RECTAL: stool for occult blood.

SKIN: turgor; purpura.

SPECIAL: if possible, check vomitus for occult blood.

GENERAL CONSIDERATIONS

Abdominal pain see ABDOMINAL PAIN (PEDIATRIC).

Abdominal trauma see TRAUMA.

DIAGNOSTIC ISSUES -----HISTORY PHYSICAL EXAM

ACUTE

GASTROENTERITIS OR

SYSTEMIC INFECTION(seeDIARRHEA,

ACUTE for other

considerations)

Acute vomiting and fever often

accompanying many childhood

infections (e.g., otitis media,

tonsillitis, kidney infection).Diarrhea may be noted.

Fever is common. Normal

abdominal examination.

Abnormal ear or throat exam

may be present.

HEPATITISAs in acute gastroenteritis above.

Dark urine and a contact with

someone who has had hepatitis may

be noted.

Hepatic tenderness or

enlargement.

GASTROINTESTINAL OBSTRUCTIONHigh bowel obstruction

(pyloric stenosis orduodenal atresia)

Persistent vomiting with large

amounts of food in vomitus. No bilein vomitus. May vomit blood.

Weight loss. Decreased skin

turgor may be noted as well asa flaccid abdomen by


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Usually noted in first 3 months of

life.

examination.

Lower bowel obstruction

(intussusception,

Hirschsprung's disease,

meconium plug)

Green bile in vomitus. Abdominal

distention. Decrease or cessation of

bowel movement. Rare in the child

over 2 years of age.

Abdominal distention and

hyperresonance. Absent bowel

sounds alternating with high

pitched rushes. Stools may bepositive for occult blood.

NORMAL INFANTILE REGURGITATION(gastroesophageal reflux) Variable amount and frequency of

vomiting; common in premature

infants. Often related to excessive

stimulation after feeding. May be

relieved by burping the infant

frequently or changing feeding

schedule.

Normal examination.

CEREBRAL IRRITATION(meningitis, brain tumor,

severe head injury)

Head holding, headache, lethargy, or

projectile vomiting may be noted.

Symptoms progress over hours to

days.

Fever, decreased pulse, and

stiff neck are common.

Bulging fontanels or

papilledema may be noted.

FOLLOWING POISON OR MEDICATION INGESTIONHistory of ingestion may be noted. May be normal.

RESULTING FROM METABOLIC DISEASE (gluten sensitivity,

phenylketonuria)

Newborns may begin vomiting soon

after birth or later in life as certain

foods are introduced.

Weight loss and decreased

skin turgor may be present.

UNCLEARThe older child may vomit from

fright, excitement, or to get

attention.

Normal

Kochar_Clinical_Medicine_for_Students

Nausea and Vomiting

Monica Ziebert

Nausea is the subjective disagreeable sensation of the need to vomit that may or may not

result in vomiting. Vomiting (emesis) is the forcible expulsion of the upper gastrointestinal

contents through the mouth. This is different from regurgitation, which is the passive passage

of the gastric contents into the mouth. Vomiting is controlled by the vomiting center in the

medulla and is triggered by afferent neural pathways from the gastrointestinal (GI) tract in

response to distention, mucosal injury, peritoneal irritation or infection. Other non-GI sources

of input include the cerebral cortex, when noxious thoughts, emotional experiences, sights, orsmells provoke vomiting. The vestibular apparatus signals the vomiting center during motion


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sickness and inner ear disorders. Finally, the chemoreceptor trigger zone within the medulla

provides input to the vomiting center in response to bloodborne stimuli (such as drugs, toxins,

and metabolic disorders) provoke vomiting.

Differential Diagnosis

There are a myriad of causes of nausea and vomiting, which can be included in the

differential diagnosis. They range from mild, quickly resolving illnesses to serious, life-threatening conditions. The causes can be classified according to conditions within the GI

tract and conditions outside the GI tract (Table 21.1).

The history and physical examination provide clinic clues that will narrow the large

differential diagnosis associated with the causes of nausea and vomiting (Table 21.2). The

history should reveal information on symptom characteristics such as severity, duration of

symptoms, frequency, provocative features such as relationship to meals and medications,

and the quality and quantity of vomits. Acute onset of nausea and vomiting in the setting of

severe abdominal pain usually points to a gastrointestinal cause such as obstruction or

peritoneal irritation from one of the inflammatory conditions (appendicitis, cholecystitis, and

pancreatitis). Acute symptoms without abdominal pain can be due to gastroenteritis,

medications, central nervous system (CNS) conditions like hemorrhage and infection, andmyocardial infarction.

Chronic nausea and vomiting can occur in GI conditions associated with impaired motor

function (dysmotility), CNS diseases, and systemic illnesses ranging from malignancy to

endocrinopathies. Intermittent and recurrent symptoms suggest cyclic vomiting syndrome, a

rare disorder of unknown etiology but strongly related to migraine headaches. Nausea and

vomiting that occurs mostly in the morning favors pregnancy, alcohol use, uremia, and

increased intracranial pressure. Provocative features such as knowing the relationship of

symptoms to eating can be helpful. The onset of nausea and vomiting immediately after

eating strongly suggests an eating disorder, whereas postprandial symptom onset can point to

obstruction or gastroparesis. In gastroparesis, patients will also often complain of early

satiety. The vomitus might even contain ingested food from the previous day. Small bowel

obstruction is associated with large volumes of bilious emesis with colicky periumbilical

pain. Other important distinguishing quality features of the vomitus are whether it is feculent

or projectile. A feculent vomitus occurs in a distal small bowel obstruction while projectile

vomiting

P.117

occurs in pyloric (or gastric outlet) obstruction or in intracerebral process causing increased

intracranial pressure. Pyloric obstruction may also produce a sensation of epigastric fullness,

blunt pain, nausea, and weight loss and can lead to the vomiting of food consumed even days

before. Table 21.1 Causes of nausea and vomiting

Conditions within the GI

tract Conditions outside the GI tract

Obstructive

Pyloric obstruction Small bowel

obstruction

Colonic obstruction

Enteric infections

Pregnancy

Hyperemesis gravidarum

Cardiopulmonary disease

Myocardial infarction

Medications

Cancerchemotherapy

Antibiotics Digoxin Oral hypoglycemics Oral contraceptives Nonsteroid anti-


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Viral gastroenteritis Bacterial gastroenteritis Hepatitis

Inflammatory diseases

Cholecystitis Pancreatitis Appendicitis

Impaired motility

Gastroparesis Intestinal pseudo-

obstruction

Functional dyspepsia Gastroesophageal

reflux

Irritable bowelsyndrome

Malignancy

Pancreatic cancer Metastatic disease Radiation therapy

Mucosal injury

Peptic ulcer disease Gastritis Esophagitis

Cardiomyopathy

Labyrinthine diesease

Motion sickness Viral Labyrinthitis Malignancy

Intracerebral disorders (increased

intracranial pressure)

Brain tumor Hemorrhage Abscess Pseudotumor cerebri

Seizure disorders

Demyelinating diseases

Migraine

CNS infections

Meningitis Encephalitis

Cyclic vomiting syndrome

Psychiatric illness

Anorexia and bulimia Depression Anxiety Psychogenic

inflammatory drugs

Beta blockers Opioids Theophylline Iron supplements

Toxins

Ethanol

Endocrine/metabolic disease

Uremia Liver failure Ketoacidosis Thyroid and

parathyroid disease

Adrenalinsufficiency

Nephrolithiasis (renal colic)

Postoperative vomiting

Adapted from Kaspar DL.Harrison's Principles of Internal Medicine,16th ed. New York:

McGraw-Hill, 2004. With permission.

The identification of associated symptoms can be the key to further narrowing the

differential. Neurologic symptoms such as vision changes, headache, photophobia, and

vertigo will point to a CNS or labyrinthine cause. The presence of other GI symptoms like

constipation and diarrhea can be important. For example, diarrhea along with nausea and

vomiting suggests gastroenteritis. The presence of constipation can lead to a consideration of

colon obstruction or pseudo-obstruction. The latter condition is impaired motility of either the

small bowel and colon resulting retention of food residue, abdominal distention, pain, and

altered bowel movements. Pseudo-obstruction can be idiopathic or caused by inheritedconditions or systemic diseases including a malignant or paraneoplastic process.


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Table 21.2 Clinical clues associated with the causes of nausea and vomiting

Clinical clues Possible cause of nausea and vomiting

Duration

Acute onset GI tract:Obstruction

Gastroenteritis

Inflammatory condition

Non-GI tract:Toxins and medications

Meningitis

CNS hemorrhage

Myocardial infarction

QualityBilious Small bowel obstructionFeculent Small bowel obstruction or rarely colonicProjectile Pyloric obstruction or intracerebral conditionHematemesis Peptic ulcer disease, esophageal varices, esophagitis (GERD), Mallory-Weiss tearPartially digested food Gastroparesis or pyloric obstruction

QuantityLarge volumes Small bowel obstruction

Frequency

Only in the morning Pregnancy, intracerebral condition, uremia, and alcohol useRecurrent and intermittent Cyclic vomiting syndrome

Provocative features

Immediately after eating Eating disorder (bulimia)>1 hour after eating Gastroparesis or pyloric obstructionWhile a passenger in car Motion sicknessRecumbent posture Intracranial involving the posterior fossaAfter taking medications MedicationsRecent picnic with potato salad Bacterial gastroenteritis (food poisoning )

Associated symptomsCrampy, colicky pain Obstructive conditionsAbdominal pain relieved with vomiting Pyloric obstruction

Bloating Colonic obstruction or pseudo-obstructionEpigastric pain radiating to back PancreatitisRight upper quadrant abdominal pain CholecystitisRight lower quadrant abdominal pain AppendicitisAbdominal pain radiating to groin Nephrolithiasis (renal colic)Jaundice, dark urine, light stools Hepatitis or choledocholithiasisConstipation Colonic obstruction or pseudo-obstructionDiarrhea, myalgia, headache Viral gastroenteritisChest pain and diaphoresis Myocardial infarctionHeadache Migraine, meningitis, gastroenteritis, or intracerebral process

Neck stiffness, photophobia, altered mental status Meningitis

Vertigo and ataxia LabyrinthitisVertigo and tinnitus Mnire's disease


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Altered mental status CNS infection or toxin ingestionMissed menstrual period Early pregnancy

Associated comorbid conditions

Diabetes Ketoacidosis or gastroparesis

History of abdominal surgery Small bowel obstructionHeart disease Myocardial infarctionKidney disease UremiaPeptic ulcer disease Pyloric obstructionPregnancy Hyperemesis gravidarum, acute fatty liver, HELLP syndromeMigraine headaches Cyclic vomiting syndromePhysical exam findings

Fever Infection or inflammatory conditionsQuiet bowel sounds Pseudo-obstructionHigh-pitched bowel sounds Mechanical obstructionSuccussion splash Pyloric obstruction

Tympanic abdomen Obstructive conditionsRebound and guarding Inflammatory disordersPapilledema Intracerebral disorders

Nystagmus Labrynthine disorderKernig and Brudzinski signs MeningitisTachycardia, gallops, edema CardiomyopathyDental enamel erosion BulimiaAdapted from Tierney LM, Henderson M. The Patient History: Evidence-based approach.

New York: McGraw-Hill, 2004.

Nausea and vomiting are also associated with many medications and co-existing medical

conditions ranging from pregnancy to diabetes mellitus. Pregnancy is associated with

hyperemesis gravidum, severe nausea, and vomiting occurring in the first trimester. Two

other conditions associated with nausea and vomiting and pregnancy, acute fatty liver and

HELLP (hemolysis, elevated liver tests, low platelets) syndrome, occur in the second and

third trimester. Diabetics are prone to an impaired motility disorder known as gastroparesis or

chronic delayed gastric emptying.

Pyloric (or gastric outlet) obstruction in adults is most commonly associated with peptic ulcer

disease.

The physical examination should be guided by the information from the history. If a GI tract

cause is suspected, then a focused abdominal and rectal exam will be essential. For example,bowel sounds may be quiet or absent in patients with a pseudo-obstruction, whereas high-

pitched bowel sounds could suggest an early mechanical bowel obstruction. A distended and

tympanic abdomen suggests a bowel obstruction. Tenderness to palpation with rebound or

guarding raises the strong possibility of an inflammatory disorder with associated peritoneal

signs. A succussion splash can be heard during auscultation of the abdomen in patients with a

gastric outlet obstruction or gastroparesis when the patient is passively shaken. Rectal

examination can reveal melena or hematochezia to suggest GI hemorrhage from a specific

cause like peptic ulcer disease (PUD) or gastritis or from a complication of vomiting like a

Mallory-Weiss tear. If a non-GI tract cause is suspected, then the physical examination

findings should complement the history. For example, in patients with a suspected

intracerebral condition caused by increased intracranial pressure, the neurologic examinationP.120


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may reveal papilledema, focal neurologic deficits, or visual field cuts. For example,

pseudotumor cerebri is a condition affecting obese young women and characterized with

intracranial hypertension not caused by a mass. Patients present with headache, nausea, and

pulsatile tinnitus. On examination, they will universally have papilledema and many will

have a sixth nerve deficits.

EvaluationThe evaluation of nausea and vomiting begins with an assessment of the acuity and severity

of symptoms and any immediate complications. Certain causes and complications of nausea

and vomiting are emergencies and as such must be recognized immediately in order that

urgent diagnostic tests and therapy are provided. These conditions include obstruction, intra-

abdominal perforation, peritonitis, myocardial infarction, CNS infection, intracranial

hemorrhage, toxic ingestion, aspiration, and gastrointestinal hemorrhage.

Severe or protracted nausea and vomiting can present with orthostatic hypotension and

lethargy secondary to dehydration and electrolyte disturbances such as hypokalemia,

azotemia, or metabolic alkalosis. These also must be addressed as soon as possible.In the nonurgent presentation of nausea and vomiting, the findings from the thorough history

and examination will point to a gastrointestinal or nongastrointestinal cause and guide the

selection of appropriate tests such as routine hematologic tests, biochemical screening, drug

levels, toxicology, imaging (plain abdominal radiograph, ultrasounds, computed tomography

scans, magnetic resonance imaging), gastric emptying studies, and endoscopy.

Sleisenger_2010

Nausea, retching, and vomiting may occur separately or together. When they occur together

they are often in sequence, as manifestations of the various physiologic events that

integrate the emetic reflex. Vomiting is a complex act that requires central neurologic

coordination, whereas nausea and retching do not imply activation of the vomiting reflex.

When nausea, retching, or vomiting manifest as isolated symptoms, their clinical

significance may differ from the stereotypical picture of emesis.[1,2]

Nausea is an unpleasant subjective sensation that most people have experienced at some

point in their lives and usually recognize as a feeling of impending vomiting in the

epigastrium or throat.

Retching consists of spasmodic and abortive respiratory movements with the glottis closed.

When part of the emetic sequence, retching is associated with intense nausea and usually,

but not invariably, culminates in the act of vomiting.

Vomiting is a partially voluntary act of forcefully expelling gastric or intestinal content

through the mouth. Vomiting must be differentiated from regurgitation, an effortless reflux

of gastric contents into the esophagus that sometimes reaches the mouth but is not usually

associated with the forceful ejection typical of vomiting (see Chapter 12).

PATHOPHYSIOLOGY


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The mechanism of vomiting has been well characterized in experimental animals and

humans (Fig. 14-1).[3] Neurologic coordination of the various components of vomiting is

provided by the emetic center (or vomiting center) located in the medulla, specifically in the

dorsal portion of the lateral reticular formation in the vicinity of the fasciculus solitarius. The

afferent neural pathways that carry activating signals to the emetic center arise from manylocations in the body. Afferent neural pathways arise from various sites along the digestive

tractthe pharynx, stomach, and small intestine. Afferent impulses from these organs are

relayed at the solitary nucleus (nucleus tractus solitarius) to the emetic center. Afferent

pathways also arise from nondigestive organs such as the heart and testicles. Pathways from

the chemoreceptor trigger zone (CTZ) located in the area postrema on the floor of the

fourth ventricle activate the emetic center. Despite its central location, the CTZ is outside, at

least in part, the blood-brain barrier and serves primarily as a sensitive detection apparatus

for circulating endogenous and exogenous molecules that may activate emesis. Finally,

pathways arise from other central nervous system structures, including the cortex,

brainstem, and vestibular system, via the cerebellum.

Figure 14-1. Schematic of the proposed neural pathways that mediate vomiting. GI,gastrointestinal; 5-HT, 5-hydroxytryptamine.


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The circuitry of the emetic reflex involves multiple receptors.[4] The following elements are

the most relevant to clinical issues:

1. Stimulation of the 5-hydroxytryptamine3 (5-HT3) serotonin receptor

provokes release of dopamine, which in turn stimulates dopamine D2 receptors in the

emetic center, thereby activating the emetic sequence. This sequence is the basis for the

pharmacodynamic action of antiemetic agents, such as ondansetron, a 5-HT3 receptor

inhibitor that is effective in the treatment of chemotherapy-induced vomiting,[5] and

metoclopramide, a dopamine D2 receptor antagonist.[6]

2. Histamine H1 and muscarinic M1 receptors, which are abundant in the

vestibular center and solitary nucleus, constitute the preferred pharmacologic targets for

inhibiting motion sickness, vestibular nausea, and pregnancy-related emesis.[7]

3. Cannabinoid CB1 receptors in the dorsal vagal complex inhibit the emeticreflex.[8,9] Cannabinoid agonists also modulate 5-HT3 ion channels. Thus, the CB and 5-HT3

receptor systems colocalize and interact in the brainstem.[10]

4. Neurokinin-1 (NK-1) receptors located in the area postrema and the solitary

nucleus bind to substance P and are part of the terminal emetic pathways. NK-1 antagonists

reduce emesis induced by peripherally and centrally acting emetogens. 5-HT3 receptors

appear to be involved to a greater extent in centrally induced emesis than in peripherally

induced emesis. Therefore, NK-1 receptor antagonists appear to be more efficacious than

5HT3 receptor inhibitors and other known antiemetic drugs in reducing vomiting induced by

a variety of causes. Conversely, they may have less potent antinausea effects.[87]

When activated, the emetic center sets into motion, through neural efferents, the various

components of the emetic sequence.[11] First, nausea develops as a result of activation of

the cerebral cortex; the stomach relaxes concomitantly, and antral and intestinal peristalsis

are inhibited. Second, retching occurs as a result of activation of spasmodic contractions of

the diaphragm and intercostal muscles combined with closure of the glottis. Third, the act of

vomiting occurs when somatic and visceral components are activated simultaneously. Thecomponents include brisk contraction of the diaphragm and abdominal muscles, relaxation

of the lower esophageal sphincter, and a forceful retrograde peristaltic contraction in the

jejunum that pushes enteric content into the stomach and from there toward the

mouth.[12] Simultaneously, protective reflexes are activated. The soft palate is raised to

prevent gastric content from entering the nasopharynx, respiration is inhibited

momentarily, and the glottis is closed to prevent pulmonary aspiration, which is a

potentially serious complication of vomiting. Other reflex phenomena that may accompany

this picture include hypersalivation, cardiac arrhythmias, and passage of gas and stool

rectally.


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Current_Pediatric_Diagnosis_Treatment

Vomiting

Vomiting is an extremely complex, poorly understood activity. The centers controlling andcoordinating vomiting are in the paraventricular nuclei of the brain. These nuclei receive

afferent input from many sources: drugs and neurotransmitters in cerebrospinal fluid, the

chemoreceptor trigger zone (CTZ) near the distal fourth ventricle, the vestibular apparatus of

the ear, the GI tract and other abdominal organs, and even from higher cortical areas. Vagal

afferents from gut to brain are stimulated by ingested drugs and toxins, mechanical stretch,

inflammation, and local neurotransmitters. Additionally, local feedback loops in the gut also

appear capable of initiating vomiting.

Vomiting is the presenting symptom of many pediatric conditions. It is the pediatrician's

difficult job to find the underlying cause. The most common cause of vomiting in childhood

is probably acute viral gastroenteritis. However, obstruction and acute or chronicinflammation of the GI tract and associated structures are also major causes. Central nervous

system inflammation, pressure, or tumor may cause vomiting. Metabolic derangements

associated with inborn errors of metabolism, sepsis, and drug intoxication can stimulate either

the CTZ or the brain directly to promote vomiting.

Regurgitation associated with GE reflux of infants should be distinguished from vomiting. In

this instance, spontaneous relaxation of the lower esophageal sphincter creates a common

cavity between the stomach and esophagus. Because the resting pressure of the thorax is

negative, the mildly positive pressure of the abdominal cavity (~ 6 mm Hg) pushes gastric

contents into the esophagus, causing an effortless flow into the mouth. Occasionally,

regurgitated fluid stimulates the pharyngeal afferents and provokes gagging or even acomplete vomiting complex.

Control of vomiting with medication is rarely needed in acute gastroenteritis and should not

be attempted in other patients until the source is clear. Antihistamines and anticholinergics

are appropriate for motion sickness because of their labyrinthine effects. 5-HT3receptor

antagonists (ondansetron, granisetron) are useful for vomiting associated with surgery and

chemotherapy. Benzodiazepines, corticosteroids, and substituted benzamides are also used in

chemotherapy-induced vomiting. Butyrophenones (droperidol, haloperidone) are powerful

drugs that block the D2 receptor in the CTZ and are used for intractable vomiting in acute

gastritis, chemotherapy, and after surgery. Phenothiazines are helpful in chemotherapy, cyclicvomiting, and acute GI infection but are not recommended for outpatient use because of

extrapyramidal side effects.

Cyclic Vomiting Syndrome

Clinical Findings

Cyclic vomiting syndrome (CVS) is characterized by recurrent episodes of stereotypical

vomiting in children usually older than 1 year of age. The emesis is forceful and frequent,

occurring up to six times per hour for up to 72 hours or more. Episode frequency ranges from

two to three per month to less than one per year. Nausea, retching, and small-volume biliousemesis continue even after the stomach is emptied. Hematemesis secondary to forceful


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vomiting may occur. Patients experience abdominal pain, anorexia, and rarely, diarrhea.

Autonomic symptoms, such as pallor, sweating, temperature instability, and lethargy are

common and give the patient a very ill appearance. The episodes end suddenly, often after a

period of sleep. In some children, dehydration, electrolyte imbalance, and shock may occur.

Between episodes, the child is completely healthy.

The cause of CVS is unknown; however, a similarity to migraine has long been recognized.

Family history is positive for migraine in 5070% of cases and many patients developmigraine headaches as adults. Research suggests that abnormalities of neurotransmitters and

hormones provoke CVS. About one quarter of patients have typical migraine symptoms

during episodes: premonitory sensation, headache, photophobia, and phonophobia.

Identifiable triggers include infection, positive or negative emotional stress, diet (chocolate,

cheese, monosodium glutamate), menses, or motion sickness.

Differential Diagnosis

Conditions that mimic CVS include drug toxicity, increased intracranial pressure, seizures,brain tumor, Chiari malformation, recurrent sinusitis, choledochal cyst, gallstones, recurrent

small bowel obstruction, inflammatory bowel disease, familial pancreatitis, obstructive

uropathy, recurrent urinary infection, diabetes, mitochondrial diseases, disorders of fatty and

organic acid metabolism, adrenal insufficiency, and Mnchausen syndrome by proxy.

Although tests for GE reflux are often positive in these patients, it is unlikely that GE reflux

and CVS are related.

Treatment

Avoidance of triggers prevents spells in some patients. Sleep can also end a spell although

some children awaken and resume vomiting. Diphenhydramine or lorazepam are used at the

onset of spells in some children to reduce nausea and induce sleep. Early use of antimigraine

medications (sumatriptan), antiemetics (ondansetron), or antihistamines can abort spells in

some patients. Once a spell is well established, intravenous fluids are often required to end it.

With careful supervision, some children with predictable spells can receive intravenous fluids

at home. Several approaches usually are tried before an effective therapy is found. Preventing

spells with prophylactic propranolol, amitriptyline, or antihistamines is effective in some

patients with frequent or disabling spells. Some patients have been successfully treated with

anticonvulsants.

Nelson_Textbook_of_Pediatrics__18th_Edition

VOMITING.

Vomiting is a highly coordinated reflex process that may be preceded by increased salivationand begins with involuntary retching. Violent descent of the diaphragm and constriction of

the abdominal muscles with relaxation of the gastric cardia actively force gastric contents

back up the esophagus. This process is coordinated in the medullary vomiting center, which

is influenced directly by afferent innervation and indirectly by the chemoreceptor trigger zone


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and higher central nervous system (CNS) centers. Many acute or chronic processes can cause

vomiting ( Table 303-1 and Table 303-3 ).

TABLE 303-3 -- Causes of Gastrointestinal Obstruction

ESOPHAGUS

Congenital

Esophageal atresia

Vascular rings

Schatzki ring

Tracheobronchial remnant

Acquired

Esophageal stricture

Foreign bodyAchalasia

Chagas disease

Collagen vascular disease

STOMACH

Congenital

Antral webs

Pyloric stenosis

Acquired

Bezoars/foreign body

Pyloric stricture (ulcer)

Chronic granulomatous disease of childhood

Eosinophilic gastroenteritis

Crohn disease

Epidermolysis bullosa

SMALL INTESTINE

CongenitalDuodenal atresia

Annular pancreas

Malrotation/volvulus

Malrotation/Ladd bands

Ileal atresia

Meconium ileus

Meckel diverticulum with volvulus or intussusception

Inguinal hernia

Intestinal duplication


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Acquired

Postsurgical adhesions

Crohn disease

Intussusception

Distal ileal obstruction syndrome (cystic fibrosis)

Duodenal hematoma

Superior mesenteric artery syndrome

COLON

Congenital

Meconium plug

Hirschsprung disease

Colonic atresia, stenosis

Imperforate anusRectal stenosis

Pseudo-obstruction

Volvulus

Colonic duplication

Acquired

Ulcerative colitis (toxic megacolon)

Chagas disease

Crohn disease

Fibrosing colonopathy (cystic fibrosis)

Vomiting caused by obstruction of the gastrointestinal tract is probably mediated by intestinal

visceral afferent nerves stimulating the vomiting center (see Table 303-1 ). If obstruction

occurs below the 2nd part of the duodenum, vomitus is usually bile stained. Emesis may also

become bile stained with repeated vomiting in the absence of obstruction when duodenal

contents are refluxed into the stomach. Nonobstructive lesions of the digestive tract can also

cause vomiting; this includes diseases of the upper bowel, pancreas, liver, or biliary tree.

CNS or metabolic derangements may lead to severe, persistent emesis.

Cyclic vomitingis a syndrome with numerous episodes of vomiting interspersed with well

intervals. The onset is usually between 2 and 5 yr of age; the frequency of vomiting episodes

is variable (average of 12 episodes per yr) with each episode typically lasting 23 days, withfour or more emesis episodes per hour. Patients may have a prodrome of pallor, intolerance

of noise or light, nausea, lethargy, and headache or fever. Precipitants include infection,

stress, and excitement. Idiopathic cyclic vomiting may be a migraine equivalent (abdominal

migraine),or it may result from altered intestinal motility or mutations in mitochondrial

DNA. The differential diagnosisincludes gastrointestinal anomalies (malrotation,

duplication cysts, choledochal cysts), CNS disorders (neoplasm, epilepsy, vestibular

pathology), nephrolithiasis, cholelithiasis, hydronephrosis, metabolic-endocrine disorders(urea cycle, fatty acid metabolism, Addison disease, porphyria, hereditary angioedema,


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familial Mediterranean fever), chronic appendicitis, and inflammatory bowel disease.

Laboratory evaluationis based on a careful history and physical examination and may

include, if indicated, endoscopy, contrast gastrointestinal radiography, brain MRI, and

metabolic studies (lactate, organic acids, ammonia). Treatment includes hydration and

ondansetron. Prevention may be possible with the antimigraine agent amitriptyline or

cyproheptadine.

Potential complications of emesis are noted in Table 303-4 . Broad management strategies for

vomiting in general and specific causes of emesis are noted in Table 303-5 and Table 303-6 .

TABLE 303-4 -- Complications of Vomiting

COMPLICATION PATHOPHYSIOLOGY

HISTORY, PHYSICAL

EXAMINATION, AND

LABORATORY STUDIES

Metabolic Fluid loss in emesis DehydrationHCl loss in emesis Alkalosis;hypochloremia

Na, K loss in emesis Hyponatremia;hypokalemia

Alkalosis

Na into cells

HCO3loss in urine Urine pH 78

Na and K loss in urine Urine Na , K

HypochloremiaCl conserved

by kidneys

Urine Cl

Nutritional Emesis of calories and nutrients Malnutrition;failure to thrive

Anorexia for calories and

nutrients

Mallory-Weiss tear Retchingtear at lesser curve

of gastroesophageal junction

Forceful emesishematemesis

Esophagitis Chronic vomitingesophageal

acid exposure

Heartburn;hemoccult + stool

Aspiration Aspiration of vomitus,

especially in context ofobtundation

Pneumonia;neurologic dysfunction

Shock Severe fluid loss in emesis or in

accompanying diarrhea

Dehydration (accompanying diarrhea

can explain acidosis?)

Severe blood loss in

hematemesis

Blood volume depletion

From Kliegman RM, Greenbaum LA, Lye PS (eds): Practical Strategies in Pediatric

Diagnosis and Therapy, 2nd ed. Philadelphia, Elsevier, 2004, p 318.

Cl, chloride; HCl, hydrogen chloride; HCO3, bicarbonate; K, potassium; Na, sodium.


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TABLE 303-5 -- Pharmacologic Therapies for Vomiting Episodes

DISEASE/CONDITION

THERAPY-DRUG CLASS: SPECIFIC AGENT/TRADE

NAME (DOSE)

Reflux Dopamine antagonist: metoclopramide (Reglan) (0.10.2 mg/kgqid PO/IV)

Peripheral dopamine antagonist: domperidone (Motilium) (0.20.6 mg/kg tidqid PO)

Gastroparesis Metoclopramide, domperidone; see above

Motilin agonist: erythromycin (24 mg/kg tidqid PO/IV)

Intestinal

pseudoobstruction

Stimulation of intestinal migratory myoelectric complexes:

Octreotide (Sandostatin) (1 g/kg bidtid SC)

Chemotherapy Metoclopramide;see above (0.51.0 mg/kg qid IV, withantihistamine prophylaxis of extrapyramidal side effects)

Serotoninergic 5-HT3antagonist: ondansetron (Zofran) (0.150.3 mg/kg tid IV/PO)

Phenothiazines:(extrapyramidal, hematologic side effects)

Prochlorperazine (Compazine) (0.3 mg/kg bidtid PO)

Chlorpromazine (Thorazine) (>6 mo of age: 0.5 mg/kg tidqidPO/IV)

Steroids:dexamethasone (Decadron) (0.1 mg/kg tid PO)

Cannabinoids:nabilone (tetrahydrocannabinol) (0.050.1 mg/kgbidtid PO)

Postoperative Ondansetron, phenothiazines: see above

Motion sickness; vestibular

disorders

Antihistamine:dimenhydrinate (Dramamine) (1 mg/kg tidqidPO)

Anticholinergic:scopolamine (Transderm Scp) (adults: 1patch/3 days)

Adrenal crisis Steroids:cortisol (2 mg/kg bolus IV followed by 0.20.4mg/kg/hr IV [ 1 mg/kg IM])

Cyclic vomiting syndrome(CVS)

Supportive:

Analgesic:meperidine (Demerol) (12 mg/kg q46h IV/IM)

Anxiolytic, sedative: Lorazepam (Ativan) (0.050.1 mg/kg q6hIV)

Antihistamine, sedative: diphenhydramine (Benadryl) (1.25

mg/kg q6h IV)

Abortive:

Serotoninergic 5-HT3antagonist:

Ondansetron:see above


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DISEASE/CONDITION

THERAPY-DRUG CLASS: SPECIFIC AGENT/TRADE

NAME (DOSE)

Granisetron (Kytril) (10 g/kg q46h IV)

Nonsteroidal antiinflammatory agent (GI ulceration side effect):

Ketorolac (Toradol) (0.51.0 mg/kg q68h IV)Serotoninergic 5-HT1D agonist: sumatriptan (Imitres) (>40 kg;

20 mg intranasally/25 mg PO, one time only)

Prophylactic:(if >1 CVS bout/month;taken daily)

Antimigraine, -adrenergic blocker: propranolol (Inderal) (0.52.0 mg/kg bid PO)

Antimigraine, antihistamine: cyproheptadine (Periactin) (0.250.5 mg/kg/day bidtid PO)

Antimigraine, tricyclic antidepressant: amitriptyline (Elavil)

(0.330.5 mg/kg tid PO, and titrate to maximum of 3.0mg/kg/day as needed; obtain baseline ECG at start of therapy,

and consider monitoring drug levels)

Antimigraine antiepileptic: Phenobarbital (Luminal) (23mg/kg qhs)

Erythromycin:see above

Low estrogen oral contraceptives: consider for catamenial CVS

episodes



bid, twice daily; ECG, electrocardiogram; GI, gastrointestinal; IM, intramuscularly; IV,

intravenously, PO, orally; q46h, every 4 to 6 hours; q6h, every 6 hours; q68h, every 6 to 8hour; qhs, each bedtime; SC, subcutaneously; tid, three times daily; qid, four times daily.

TABLE 303-6 -- Supportive and Nonpharmacologic Therapies for Vomiting Episodes

DISEASE THERAPY

All Treat cause: obstructionoperate; allergychange diet (steroids);

metabolic error

Rx defect; acid peptic disease

H2RAs, PPIs, etc.Complications

Dehydration IV fluids, electrolytes

Hematemesis Transfuse, correct coagulopathy

Esophagitis 2 s, s

Malnutrition NG or NJ drip feeding useful for many chronic conditions

Mecomium ileus Gastrografin enema

DIOS Gastrografin enema; balanced colonic lavage solution (e.g., GoLytely)

Intussusception Barium enema; air reduction enemaHematemesis Endoscopic:injection sclerotherapy or banding of esophageal varices;


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DISEASE THERAPY

injection therapy, fibrin sealant application, or heater probe electrocautery

for selected upper GI tract lesions

Sigmoid volvulus Colonoscopic decompression

Reflux Positioning;dietary measures (infants:rice cereal, 1 tbs/oz of formula)

Psychogenic

components

Psychotherapy;tricyclic antidepressants; anxiolytics (e.g., diazepam: 0.1

mg/kg/tidqid PO)



DIOS, distal intestinal obstruction syndrome; GI, gastrointestinal; H2RAs, histamine2-

receptor antagonists; IV, intravenous; NG, nasogastric; NJ, nasojejunal; PO, orally; PPIs,

proton pump inhibitors; qid, four times a day; tbs, tablespoon; tid, three times a day.

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Nausea and Vomitting