Nausea and Vomiting
Nausea and Vomiting
Nausea and Vomiting
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
• POSTOPERATIVE
VOMITING
MEDICATIONS/METABOLIC DISORDERS
1 Nausea and vomiting are an evolutionary strategy against food poisoning • 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 is an aversive experience that of ten precedes vomiting, but is not • Nausea and vomiting is also a common adverse effect of radiation
2 simply the result of low-level stimulation that, if stronger, would evoke therapy, chemotherapy, and surgical anesthesia.
the vomiting response 3
• Chronic nausea and vomiting is defined by symptoms that persist for at
least one month.
Vomiting response is present in most vertebrates, but apparently
3 absent in several commonly used laboratory animals • 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
Diagnostic and management strategies vary depending on the duration should be evaluated with esophagogastroduodenoscopy
4 of symptoms.
Mallory-Weiss vs. Boerhaave’s Syndrome
• Treatment: Supportive measures such as airway • Ondansetron and granisetron, serotonin receptor blockers, and glucocorticosteroids -
clearance, oxygen supplementation and positive pressure nausea and vomiting associated with cancer chemotherapy
ventilation. • 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
The motor function abnormalities that cause dysphagia may be related to: • The medical history often gives clues as to the site of abnormality in the esophagus
and the underlying cause.
Defects in initiating Disorders of the • Difficulty only with solids implies mechanical dysphagia.
Disorders of the
the swallowing pharyngeal and esophageal smooth • Difficulty with both solids and liquids may occur late in the course of mechanical
reflex esophageal striated muscle dysphagia but is an early sign of motor dysphagia.
muscle • Patients can sometimes pinpoint the site of food sticking. Weight loss out of
e.g., tongue paralysis, e.g. achalasia, proportion to the degree of dysphagia may be a sign of underlying malignancy.
lack of saliva, lesions e.g., muscle disorders scleroderma,
affecting sensory such as polymyositis myotonic dystrophy • Hoarseness may be related to involvement of the larynx in the primary disease process
components of and dermatomyositis, (e.g., neuromuscular disorders), neoplastic disruption of the recurrent laryngeal nerve,
cranial nerves X and neurologic lesions or laryngitis from gastroesophageal reflux.
XI such as myasthenia
gravis, polio, or
amyo_x0002_trophic
lateral sclerosis, and
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: EVALUATION:
-Gastroesophageal reflux disease - Trial of antireflux therapy (omeprazole);
-Esophageal motility disorders -if no response, 24-h ambulatory luminal pH
monitoring;
-Peptic ulcer disease
-if negative, esophageal manometry may show
-Gallstones
motor disorder.
-Psychiatric disease (anxiety, panic
attacks, depression.
-Trial of imipramine, 50 mg PO qhs, may be ESOPHAGEAL INFLAMMATION
worthwhile.
-Consider psychiatric evaluation in selected cases.
Treatment
VIRAL ESOPHAGITIS
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
Cause: Signs and symtoms : Diagnosis is made by: self-limited in the esophagitis are treated 14–21 days.
✓ Herpesviruses I and II ✓Odynophagia ✓endoscopy with biopsy, immunocompetent with Acyclovir, 200 mg ✓ famciclovir, 500 mg PO tid, valacyclovir 1
✓ Varicella-zoster virus ✓ dysphagia brush cytology, and culture. person; PO five times a day for g PO tid for 7 days.
✓ and CMV ✓ fever 7−10 days ✓ CMV is treated with ganciclovir, 5 mg/kg
✓viscous lido-caine
✓bleeding 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.
In immunocompromised hosts:
1 2 ✓fluconazole, 200 mg PO on day 1 followed by 100 mg
daily for 2–3 weeks, is treatment of choice.
In immunocompromised hosts, 3
Diagnosis
or those with malignancy, ✓itraconazole, 200 mg PO bid, or ketoconazole, 200–400
diabetes, hypoparathyroidism, ✓endoscopy by identifying mg PO daily; long-term maintenance therapy is often
hemoglobinopathy, systemic yellow-white plaques or nodules
required.
lupus erythematosus, corrosive on friable red mucosa.
esophageal injury, candidal ✓Characteristic hyphae are seen ✓ Poorly responsive pts or those who cannot swallow may
esophageal infection may on KOH stain. In pts with AIDS, respond to caspofungin 50 mg IV qd for 7–21 days.
present with odynophagia, the development of symptoms
dysphagia, and oral thrush may prompt an empirical
(50%). therapeutic trial.
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.
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
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
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.
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