Definition

• Nausea refers to the imminent desire to vomit and often precedes or

Nausea and Vomiting accompanies vomiting.

De Los Reyes, Michelle | Isorena, Nicole Ericka | Mathiyas, Aishwarya | Nebres-
Alday, Julianne Arantxa | Nuñez, Justine Marie | Pavericio, Maria Chelo |
Rustique, Mark Edmon | Sounder-Rajan, Deepak | Yago, Brian Jr.
GROUP 5
Dr. Jean Louise C. Vitualla
Professor
• Vomiting refers to the forceful expulsion of gastric contents through the
mouth.
• Retching refers to labored rhythmic respiratory activity that precedes emesis.
• Regurgitation refers to the gentle expulsion of gastric contents in the absence
of nausea and abdominal diaphragmatic muscular contraction.
• Rumination refers to the regurgitation, rechewing, and re swallowing of food
from the stomach.

Pathophysiology
•Gastric contents are propelled into the esophagus when there is relaxation of the
gastric fundus and gastroesophageal sphincter followed by a rapid increase in
intraabdominal pressure produced by contraction of the abdominal and diaphragmatic
musculature.
•Increased intrathoracic pressure results in further movement of the material to the
mouth.
•Reflex elevation of the soft palate and closure of the glottis protect the nasopharynx
and trachea and complete the act of vomiting.
•Vomiting is controlled by two brainstem areas, the vomiting center and chemoreceptor
trigger zone.
•Activation of the chemoreceptor trigger zone results in impulses to the vomiting
center, which controls the physical act of vomiting.
 ETIOLOGY
INTRAPERITONEAL
Nausea and vomiting are not diseases, but rather
are symptoms of many different conditions, such as: ENTERIC INFECTIONS
OBSTRUCTION DISORDERS
- Viral
- Pyloric obstruction - Bacterial
- Small bowel obstruction
- Colonic obstruction
- Superion mesenteric artery syndrome

INTRAPERITONEAL
EXTRAPERITONEAL

• INFLAMATORY DISEASES • ALTERED SENSORIMOTOR

FUNCTION • CARDIOPULMONARY • LABYRINTHINE
- cholecystitis • PHYCHIATRIC
- Gastroparesis DISEASES DISEASE ILLNESS
- pancreatitis - Cardiomyopathy - Motion sickness
- Intestinal pseudoobstruction - Anorexia and
- appendicitis - Myocardial infarction - Labyrithitis bulimia nervosa
- Gastroesophageal reflux - Malignancy
- hepatitis - Depression
- Chronic idiopathic nausea
- Function vomiting
• BILLARY COLIC
- Cyclic vomiting sundrome
• ABDOMINAL IRRADIATION
- Cannabinoid • INTRACEREBRAL
DISORDERS
- Hyperemesis syndrome
- malignancy
- Rumination syndrome - hemorrhage
- abscess
- Hydrocephalus

• POSTOPERATIVE
VOMITING
 MEDICATIONS/METABOLIC DISORDERS

• DRUGS • ENDOCRINE/ METABOLIC

- Cancer chemotheraphy DISEASE
- Antibiotics - Pregnancy
- Cardiac Antiarrhythics - Uremia
- Digoxin - Ketoacidosis
- Oral hypoglycemia
- Oral cotraceptives
- Thyroid and parathyroid
disease
Evaluation of nausea and vomiting
- Antidepressants - Adrenal insufficiency
- Smoking cessatation agents - Systemic effects of cancer
- Parkinson’s disease treatments • Toxins
- Liver failure
- ethanol

Evaluation of nausea and vomiting

1 Nausea and vomiting are an evolutionary strategy against food poisoning
Nausea is an aversive experience that of ten precedes vomiting, but is not
2 simply the result of low-level stimulation that, if stronger, would evoke
the vomiting response
Vomiting response is present in most vertebrates, but apparently
3 absent in several commonly used laboratory animals
Diagnostic and management strategies vary depending on the duration
4 of symptoms.
• In the absence of acute abdominal pain, significant headache, or recent
initiation of certain medications, acute nausea and vomiting is usually
the result of self-limited gastrointestinal infections.
• Nausea and vomiting is also a common adverse effect of radiation
therapy, chemotherapy, and surgical anesthesia.
3
• Chronic nausea and vomiting is defined by symptoms that persist for at
least one month.
• Alarm signs such as dehydration, acidosis caused by an underlying
metabolic disorder, or an acute abdomen warrant additional evaluation
• Patients with risk factors for gastric malignancies or alarm symptoms
should be evaluated with esophagogastroduodenoscopy
 Mallory-Weiss vs. Boerhaave’s Syndrome

Nausea & Vomiting

Complications

Mallory-Weiss vs. Boerhaave’s Syndrome

Dehydration & Malnutrition
MALLORY-WEISS SYNDROME BOERHAAVE’S SYNDROME

Etiology Upper gastrointestinal mucosal tear Esophageal transmural tear

Submucosal arterial or venule plexus bleeding Esophageal air/fluid leakage into nearby areas (e.g. ▪ A prolonged bout of vomiting can cause the body to lose more fluid than it can
Pleura)
take in. The result is dehydration, which occurs when your body doesn’t have the
fluid it needs to function properly.
Clinical Presentation Vomiting, Retching Vomiting, retching, chest & upper abdominal pain ▪ Severe dehydration can cause kidneys to shut down. It can be particularly
Hematemesis
Epigastric pain
Odynophagia, fever, dyspnea
Septic shock can ensue
dangerous in children and the elderly.
Subcutaneous emphysema may be seen
▪ When nausea causes repeated vomiting over time, it can result in serious
malnutrition.
▪ Appetite loss, or not feeling the urge to eat, can accompany nausea, but it can
Laboratory/Imaging Endoscopy confirms diagnosis CT or Contrast Esophagography with Gastrograffin also occur on its own. It may be harder to notice, but it can be even more serious
confirms diagnosis when it leads a person to not consume enough nutrients to maintain health.
Chest Xray: Pneomomediastinum & pleural effusions

Treatment Most tears heal spontaneously Surgery: For thoracic perforation

Endoscopic therapy for continual bleeding
 Dental Caries & Erosions
• Frequent vomiting can have a negative effect on oral health.
• Issues include dryness, sores, redness of the mouth and tongue, chronic sore throats, and
erosion of the enamel that protects the teeth.
• The bile and acids from stomach coming through the mouth can cause damage to teeth, gums,
and throat.
• Erosion increases the risk of decay, causing more cavities and sensitivity of the teeth.
• Over time, more severe cases of erosion can also change the way the lower and upper teeth
come together, and a person could end up losing some of his teeth.
Aspiration Pnuemonitis
• It occurs when food, saliva, liquids, or vomit is breathed
into the lungs or airways leading to the lungs, instead of
being swallowed into the esophagus and stomach.
• It is often caused by a defective swallowing mechanism,
such as a neurological disease or as the result of an injury
that directly impairs swallowing or interferes with
consciousness.
• Signs and symptoms often include fever and cough of
relatively rapid onset.
• Complications may include lung abscess.
• Treatment: Supportive measures such as airway
clearance, oxygen supplementation and positive pressure
ventilation.
Metabolic Alkalosis & Hypokalemia
• Vomiting generates metabolic alkalosis by the loss of
gastric secretions, which are rich in hydrochloric acid
(HCl).
• Severe vomiting also causes loss
of potassium (hypokalemia) and sodium (hyponatremia).
• The kidneys compensate for these losses by retaining
sodium in the collecting ducts at the expense of hydrogen
ions (sparing sodium/potassium pumps to prevent further
loss of potassium), leading to metabolic alkalosis.
Treatment
• Antihistamine (maclizine and dimenhydrinate) - nausea due to inner ear dysfunction
• Anticholinergics (scopolamine) - nausea by motion sickness
• Haloperidol and phenothiazine (prochlorperazine) - controls mild nausea and vomiting.
Side effects includes sedation, hypotension, and parkinsonian symptoms
• Metocloparamide - superior to phenothiazine in treating severe nausea and vomiting,
and useful in treatment of gastroparesis
• IV metocloparamide - effective as prophylaxis against nausea when given before
chemotherapy
• Ondansetron and granisetron, serotonin receptor blockers, and glucocorticosteroids -
nausea and vomiting associated with cancer chemotherapy
• Aprepitant - controls nausea from highly emetic drugs like cisplatin
• Erythromycin - effective in some patients with gastroparesis
 Definition
1 3
Dysphagia Dysphagia - difficulty of moving
food or liquid through the
Globus pharyngeus - sensation
of a lump lodged in the throat.
mouth, pharynx, and esophagus.
-Swallowing is unaffected
Patient senses swallowed
material sticking along the path.

2
Odynophagia - pain on
swallowing

Pathophysiology Mechanical Obstruction

Mechanical causes of dysphagia can be

• Luminal
Dysphagia is caused by two main e.g., large food bolus, foreign body
mechanisms: • Intrinsic to the esophagus
e.g., inflammation, webs and rings, strictures, tumors, or

1. Mechanical Obstruction or • Extrinsic to the esophagus

e.g., cervical spondy_x0002_litis, enlarged thyroid or
2. Motor Dysfunction mediastinal mass, vascular compression.
 Motor Dysfunction Approach to Patients with Dysphagia

The motor function abnormalities that cause dysphagia may be related to:
Defects in initiating
the swallowing
reflex
e.g., tongue paralysis,
lack of saliva, lesions
affecting sensory
components of
cranial nerves X and
XI
Disorders of the
pharyngeal and
esophageal striated
muscle
e.g., muscle disorders
such as polymyositis
and dermatomyositis,
neurologic lesions
such as myasthenia
gravis, polio, or
amyo_x0002_trophic
lateral sclerosis, and
• The medical history often gives clues as to the site of abnormality in the esophagus
and the underlying cause.
• Difficulty only with solids implies mechanical dysphagia.
Disorders of the
esophageal smooth • Difficulty with both solids and liquids may occur late in the course of mechanical
muscle dysphagia but is an early sign of motor dysphagia.
• Patients can sometimes pinpoint the site of food sticking. Weight loss out of
e.g. achalasia, proportion to the degree of dysphagia may be a sign of underlying malignancy.
scleroderma,
myotonic dystrophy • Hoarseness may be related to involvement of the larynx in the primary disease process
(e.g., neuromuscular disorders), neoplastic disruption of the recurrent laryngeal nerve,
or laryngitis from gastroesophageal reflux.

Approach to Patients with Dysphagia

• Physical examination may reveal signs of skeletal muscle, neurologic, or oropharyngeal

diseases.
• Neck examination can reveal masses impinging on the esophagus.
• Skin changes might suggest the systemic nature of the underlying disease.
• Dysphagia is nearly always a symptom of organic disease rather than a functional
complaint.
• If oropharyngeal dysphagia is suspected, videofluoroscopy of swallowing may be
diagnostic.
• Mechanical dysphagia can be evaluated by barium swallow and esophagogastroscopy
with endoscopic biopsy. Barium swallow and esophageal motility studies can show the
presence of motor dysphagia.
 • Oropharyngeal dysphagia is at term that describes swallowing problems
occurring in the mouth and or the throat.
• These swallowing problems most commonly result from impaired muscle
function, sensory changes, or growths and obstructions in the mouth or throat.
Oropharyngeal Dysphagia • Oropharyngeal dysphagia can commonly result from muscle weakness.
Additionally, a person may have reduced ability to feel food, liquid or saliva that
remains in the mouth or throat after swallowing.
• In some cases, an individual may not be able to feel food, liquid or saliva
entering the windpipe called aspiration.

Treatment
• In Oropharyngeal dysphagia, there is difficulty in preparing and transporting There are 3 main ways oropharyngeal dysphagia is managed to make
the food bolus eating and drinking as safe as possible:
• through the oral cavity as well as initiating the swallow.
• This may be associated with aspiration or nasopharyngeal regurgitation.
1 2 3
• Oropharyngeal dysphagia can be difficult to treat if it’s caused by a condition
that affects the nervous system.
Swallowing therapy Dietary changes Feeding tubes
 Esophageal Dysphagia Noncardiac Chest Pain
Food sticks in the mid or lower sternal area; can be associated with
regurgitation, aspiration, odynophagia.
• Non-cardiac chest pain (NCCP) is a term used to
describe chest pain that resembles heart pain (angina)
in patients who do not have heart disease.
Causes the ff for solids only: Causes the ff for solids and • The pain typically is felt behind the breastbone
liquids: (sternum) and is described as oppressive, squeezing or
• lower esophageal ring
(Schatzki’s ring—symptoms • diffuse esophageal spasm pressure-like.
are usually intermittent), (occurs with chest pain and • Patients presenting with chest pain, 30% have an
• peptic stricture (heartburn is intermittent), esophageal source rather than angina.
accompanies this), • scleroderma (progressive • History and physical examination often cannot
• carcinoma, and occurs with heartburn), distinguish cardiac from noncardiac pain.
• lye stricture • achalasia (progressive and
occurs without heartburn)

CAUSES:
-Gastroesophageal reflux disease
-Esophageal motility disorders
-Peptic ulcer disease
-Gallstones
-Psychiatric disease (anxiety, panic
attacks, depression.
EVALUATION:
- Trial of antireflux therapy (omeprazole);
-if no response, 24-h ambulatory luminal pH
monitoring;
-if negative, esophageal manometry may show
motor disorder.
-Trial of imipramine, 50 mg PO qhs, may be ESOPHAGEAL INFLAMMATION
worthwhile.
-Consider psychiatric evaluation in selected cases.

VIRAL ESOPHAGITIS
Cause: Signs and symtoms :
✓ Herpesviruses I and II ✓Odynophagia
✓ Varicella-zoster virus ✓ dysphagia
✓ and CMV ✓ fever
✓bleeding
CANDIDA ESOPHAGITIS
1 2
In immunocompromised hosts,
or those with malignancy,
diabetes, hypoparathyroidism,
hemoglobinopathy, systemic
lupus erythematosus, corrosive
esophageal injury, candidal
esophageal infection may
present with odynophagia,
dysphagia, and oral thrush
(50%).
Diagnosis is made by:
✓endoscopy with biopsy,
brush cytology, and culture.
3
Diagnosis
✓endoscopy by identifying
yellow-white plaques or nodules
on friable red mucosa.
✓Characteristic hyphae are seen
on KOH stain. In pts with AIDS,
the development of symptoms
may prompt an empirical
therapeutic trial.
Treatment
1 3
2
In prolonged cases and in
Treatment: In immunocompetent px : immunocompromised:
Treatment :
✓Disease is usually herpes and varicella ✓ acyclovir, 400 mg PO five times a day for
self-limited in the esophagitis are treated 14–21 days.
immunocompetent with Acyclovir, 200 mg ✓ famciclovir, 500 mg PO tid, valacyclovir 1
person; PO five times a day for g PO tid for 7 days.
7−10 days ✓ CMV is treated with ganciclovir, 5 mg/kg
✓viscous lido-caine
IV q12h, until healing occurs, which may take
can relieve pain;
weeks. Oral valganciclovir (900 mg bid) is an
effective alternative to parenteral
treatment.
✓In non responders, foscarnet, 90 mg/kg IV
q12h for 21 days, may be effective.
Treatment
In immunocompromised hosts:
✓fluconazole, 200 mg PO on day 1 followed by 100 mg
daily for 2–3 weeks, is treatment of choice.
✓itraconazole, 200 mg PO bid, or ketoconazole, 200–400
mg PO daily; long-term maintenance therapy is often
required.
✓ Poorly responsive pts or those who cannot swallow may
respond to caspofungin 50 mg IV qd for 7–21 days.
 PILL-RELATED ESOPHAGITIS EOSINOPHILIC ESOPHAGITIS
• Can induce local inflammation in the
esophagus
• Mucosal inflammation with eosinophils with submucosal fibrosis can be seen
✓ Doxycycline
Treatment
especially in pts with food allergies.
✓ tetracycline
• Withdraw offending • The Diagnosis relies on the presence of symptoms of esophagitis with the
✓ aspirin
drug, use antacids, appropriate findings on esophageal biopsy.
✓ nonsteroidal anti-inflammatory drugs
and dilate any
✓ KCl • Eotaxin 3, an eosinophil chemokine, has been implicated in its etiology. IL-5
resulting stricture.
✓ quinidine
and TARC (thymus and activation-related chemokine) levels may be
✓ ferrous sulfate
elevated.
✓ clindamycin
✓ alprenolol
✓ alendronate .
Predisposing factors include recumbency after
swallowing pills with small sips of water and
anatomic factors impinging on the esophagus
and slowing transit.

OTHER CAUSES OF ESOPHAGITIS IN AIDS

Treatment
Involves a 12-week course of swallowed fluticasone (440 μg bid) using Mycobacteria
a metered-dose inhaler. In 30−50% of pts, proton pump inhibitors Cryptosporidium
can reduce eosinophil infiltrates. Pneumocystis
idiopathic esophageal ulcers
giant ulcers
 Esophageal Anatomy
ESOPHANGEAL MOTILITY DISORDERS

Upper Esophageal
Sphincter (UES)

Esophageal Body 18 to 24 cm
(cervical & thoracic)

Lower Esophageal
Sphincter (LES)

NORMAL SWALLOWING
Normal Phases of Swallowing

o Voluntary
Cortical Swallowing Areas
– oropharyngeal phase – bolus is voluntarily moved into the pharynx Frontal cortex
o Involuntary
– UES relaxation
Swallowing Center
– peristalsis (aboral movement)
– LES relaxation Brainstem
o Between swallows Motor Nuclei
– UES prevents air entering the esophagus during inspiration and prevents
esophagopharyngeal reflux
– LES prevents gastroesophageal reflux
– peristaltic and non-peristaltic contractions in response to stimuli Oropharynx & Esophagus
– capacity for retrograde movement (belch, vomiting) and decompression
 ESOPHAGEAL MOTILITY DISORDERS ACHALASIA

o Achalasia means “failure to relax”

o The spectrum of these disorders ranges from the well-defined primary o first clinically recognized esophageal motility disorder
esophageal motility disorders (PEMDs) to very nonspecific disorders that may o dual disorder
play a more indirect role in reflux disease and otherwise be asymptomatic. –LES fails to appropriately relax
o Esophageal motility disorders may occur as manifestations of systemic • resistance to flow into stomach
diseases, referred to as secondary motility disorders. • not spasm of LES but an increased basal LES
o Esophageal motility disorders are less common than mechanical and pressure often seen (55-90%)
inflammatory diseases affecting the esophagus, such as reflux esophagitis, –loss of peristalsis in distal 2/3 esophagus
peptic strictures, and mucosal rings.

ACHALASIA
ACHALASIA
• Clinical presentation
– solid dysphagia 90-100% (75% also with dysphagia to liquids)
• Epidemiology
– post-prandial regurgitation 60-90%
– 1-2 per 200,000 population – chest pain 33-50%
– usually presents between ages 25 to 60 – pyrosis 25-45%
– average symptom duration at diagnosis: 2-5 years – weight loss
• Pathology – nocturnal cough and recurrent aspiration
• Diagnosis
– loss of ganglionic cells in the myenteric plexus (distal to proximal)
– plain film (air-fluid level, wide mediastinum, absent gastric bubble,
– vagal fiber degeneration pulmonary infiltrates)
– underlying cause: unknown – barium esophagram (dilated esophagus with taper at LES)
• good screening test (95% accurate)
• autoimmune (antibodies to myenteric neurons in 50% of patients)
– endoscopy (rule out GE junction tumors, esp. age>60)
– esophageal manometry (absent peristalsis, LES relaxation, & resting
LES >45 mmHg)
ACHALASIA
SPASTIC MOTILITY DISOREDRS OF THE ESOPHAGUS
• Treatment - reduce LES pressure and increase emptying
– nitrates and calcium channel blockers • “lumper” approach
• 50-70% initial response; <50% at 1 year – normal
• limitations: tachyphylaxis and side-effects – achalasia
– botulinum toxin (prevents ACH release at NM junction) – spastic motility disorder
• 90% initial response; 60% at 1 year
– pneumatic dilation (disrupt circular muscle) • “splitter” approach (radiology and manometry)
• 60-95% initial success; 60% at 5 years – diffuse esophageal spasm
• recent series suggest 20-40% will require re-dilation – nutcracker esophagus
• risk of perforation 1-13% (usually 3-5%); death 0.2-0.4%
– hypertensive LES
– surgical myotomy (open or minimally-invasive)
– nonspecific esophageal dysmotility
• >90% initial response; 85% at 10 years; 70% at 20 years (85% at 5 years
with min. inv. techniques) • “splitting” has not resulted in a clinical benefit
• <1% mortality; <10% major morbidity
• 10-25% acutely develop reflux, up to 52% develop late reflux

SPASTIC MOTILITY DISOREDRS OF THE ESOPHAGUS SPASTIC MOTILITY DISOREDRS OF THE ESOPHAGUS

• Epidemiology
• Diagnosis
– any age (mean age 40) – manometry
– female > male – barium esophagram
• Symptoms – endoscopy
– dysphagia to solids and liquids – pH monitoring
• intermittent and non-progressive
• present in 30-60%, more prevalent in DES (in most studies) • Treatment
– chest pain – reassurance
• constant % across the different disorders (80-90%) – nitrates, anticholinergics, hydralazine - all unproven
• swallowing is not necessarily impaired – calcium channel blockers - too few data with negative controlled studies in chest pain

• can mimic cardiac chest pain – psychotropic drugs – trazodone, imipramine and setraline effective in controlled studies

– pyrosis (20%) and IBS symptoms (>50%) – dilation - anecdotal reports, probable placebo effect

– symptoms and manometry correlate poorly

Scleroderma Esophagus Scleroderma Esophagus

o Epidemiology
o Scleroderma esophagus is part of a connective tissue disorder, which ▪ Occurs in 75% to 80% of patients
leads to atrophy of esophageal smooth muscle with consequent loss ▪ It most commonly affects woman in the 30- to 50-year age group.
of LES tone and esophageal peristalsis. It is one of the most important
secondary motor disorders to affect the esophagus.

Scleroderma Esophagus Scleroderma Esophagus

o Symptoms
o Diagnosis
▪ The patients may have no symptoms and simply present with features of the connective
▪ confirmed by demonstrating the typical manometric abnormalities.
tissue disorder.
▪ Esophageal involvement leads to reflux symptoms
o Treatment
• including heartburn and acid regurgitation.
▪ proton pump inhibitors
▪ Dysphagia (possibly owing to hypotensive esophageal contractions or non-peristaltic
▪ Esophageal bougienage may also be required.
contractions)
▪ Associated Raynaud's phenomenon