Esophageal Disorders

upper 1/3 is striated and lower is smooth. Outer is longitudinal and inner is circular

UES is comprised of at least three groups of striated muscles: the distal portion of the inferior pharyngeal constrictor muscle, the cricopharyngeus muscle, and muscle of the proximal esophagus. By remaining closed in its basal state, the UES prevents air from entering the gastrointestinal tract during inspiration, and protects the airway by preventing the reflux of material from the esophagus into the pharynx. 

esophagus to stomach

The striated muscle of the proximal esophagus is supplied by somatic efferent fibers carried in the vagus nerve.  The cell bodies of these somatic efferent fibers are located in the nucleus ambiguus, and the fibers terminate in motor end plates on the striated muscle.  Note that there are no intermediate neurons.  The somatic efferents innervate the striated muscle directly through cholinergic, nicotinic receptors.  The innervation of the smooth muscle in the distal esophagus is more complex.  To the distal esophagus, the vagus nerve carries preganglionic fibers whose cell bodies lie in the dorsal motor nucleus.  The preganglionic fibers release acetylcholine, and supply at least two important types of postganglionic effector neurons located within the wall of the esophagus.  One type of effector neuron excites the smooth muscle by releasing acetylcholine.  The other type of postganglionic effector neuron inhibits the smooth muscle by releasing non-cholinergic, non-adrenergic inhibitory neurotransmitters.  Nitric oxide (NO) and, perhaps, vasoactive intestinal polypeptide (VIP) function as inhibitory neurotransmitters.

Food reaches the pharynxSwallowing center activatedCranial nerves 5, 7, 9, 10, & 12Tongue raisesNasal airway closesEpiglottis closesUES relaxesPharyngeal muscles contract

With the initiation of swallowing (panel 1), the anterior portion of the tongue rises to make contact with the hard palate. A posterior, rolling motion of the tongue thrusts the ingested bolus into the oropharynx.  At the same time, the soft palate and the posterior pharyngeal wall come together (panel 2), thereby sealing the nasopharynx and preventing nasal regurgitation. Several factors contribute to protect the airway during deglutition (panel 3).  Contraction of the suprahyoid muscles pulls the hyoid bone and the attached larynx upwards and forwards.  This movement, combined with contraction of the thyrohyoid, aryepiglottic, and thyroepiglottic muscles causes the epiglottis to flip downward.  More important than these features in protecting the airway is the laryngeal closure that accompanies swallowing.  Laryngeal closure is accomplished by approximation of the vocal cords, and by the approximation of the arytenoids that seal the lower portion of the laryngeal vestibule.  The upper esophageal sphincter relaxes and is pulled open by the anterosuperior movement of the hyoid bone-larynx complex, and the bolus is propelled into the esophagus. Normally, swallowing clears the bulk of the ingested bolus from the oropharynx (panel 4), and little residual material remains behind.

Food reaches the proximal esophagus
Vagal afferents are activated
Peristalsis begins by activation of the intrinsic esophageal nerves (myenteric plexus)
LES relaxes
Peristalsis proceeds from proximal to distal esophagus

Dysphagia
Odynophagia- painful swallowing
Heartburn (“pyrosis”)
Regurgitation
Chest Pain (noncardiac)

Transfer problem – inability to initiate the act of swallowing or inability to transfer the bolus from the pharynx to the upper esophagus

Associated symptoms:
Food sticking in throat
Repetitive swallows
Nasal regurgitation
Coughing
Aspiration

Structural: Zenker’s diverticulum, cricopharyngeal bar, webs, tumors
CNS: Stroke, tumors, trauma
Other neurologic: Parkinson’s, multiple sclerosis, amyotrophic lateral sclerosis
Myopathy: Myasthenia gravis, polymyositis, mixed connective tissue disease

structural reason for oropharyngeal dysphagia

The patient feels that the food bolus stops somewhere in the chest, from the suprasternal notch to the xiphoid process.
If the food bolus is regurgitated, it consists of bland chewed food or swallowed liquids, and does not have a bitter or acidic taste, and does not contain the yellow or green fluid of gastric or biliary secretions.

Barium Esophagram
- modified barium swallow with videofluoroscopy single or double contrast
Esophagoscopy (EGD)
Esophageal Manometry

Rings and webs
Peptic stricture
Tumors
Infections
Caustic ingestion
Iatrogenic: Pill-induced esophagitis, radiation, sclerotherapy, NG tube

GERD
Eosinophilic esophagitis (EoE)
Infections
Medications:
tetracycline, KCl, quinidine, alendronate.
chemotherapy: 5-FU, daunorubicin, bleo
Radiation
Caustic ingestion

Clinical symptoms of esophageal dysfunction – usually solid-food dysphagia and food impactions
> 15 eosinophils/ high-power field
Normal 24-hour pH monitoring
No response to high-dose PPI therapy

First case report in 1977
Initially described in children
In adults, 75 % are males
In adults, mean age = 38
50-80 % are atopic – atopic dermatitis, allergic rhinitis, asthma
Most likely food allergens, possibly aeroallergens

A – Concentric rings

B – Linear furrows

C – White plaques
(eosinophilic microabscesses)

D – Food impaction

Acid suppression
Diet – elimination, elemental
Topical steroids – swallowed fluticasone or budesonide
Systemic steroids
Cromolyn, Montelukast
Biologics

painful swallowing
Infectious esophagitis
Fungal (Candida)
Viral – CMV, HSV
Idiopathic.

Corrosive esophagitis
Pill-induced esophagitis

Achalasia
Other spastic motor disorders:
Diffuse esophageal spasm
Nutcracker esophagus
Hypertensive LES.
Scleroderma
Other hypocontractile motor disorders

“Does not relax”
Failure of LES relaxation + loss of peristalsis in distal esophagus
Age range: 25 – 60 years
Gender: Male = Female
Incidence: 0.4 – 0.6/100,000/year
Prevalence: 8/100,000

Typical Sx: dysphagia, regurgitation, chest pain, weight loss.

Atypical Sx: Heartburn, diff belching, globus (sensation of fullness or lump in thraot), hiccups

Net LES tone results from a balance b/w 2 opposing classes of neurotransmitter
those that are Inhibitory--- NO/ VIP
those that are excitatory ---- Ach
Selective loss of Inhibitory neurons in the postganglionic myenteric (located b/w longitudinal & circular muscle layers of the esophagus) plexus leads to unopposed cholinergic excitation which then produces hypertonic LES with failure to relax. The etiology of neural damage is unknown.
on xray you could see air fluid level, large esoph initially then tightening down

Aperistalsis: 100% of cases

Abnormal LES relaxation (absent, incomplete, insufficient duration):
100 % of cases

Elevated LES pressure: 50 % of cases

in achalasia ther is no relaxation

Drugs: botox, nitrates, Ca channel blockers
Pneumatic Dilation-inflate balloon
Myotomy- surgical cutting along muscle

GER = gastroesophageal reflux, which is the effortless movement of stomach contents into the esophagus
GER occurs in almost all people
GERD = GER disease, which is when reflux results in symptoms and/or injury to the esophagus

Key event is reflux of gastroduodenal contents (acid, pepsin, bile) into the esophagus
Acid is the primary mediator of symptoms and damage
Mucosal defenses are overwhelmed

Heartburn, regurgitation, dysphagia, respiratory Sx, chest pain, abdominal pain, nausea, belching

Transient lower esophageal sphincter relaxations (TLESRs)
A hypotensive lower esophageal sphincter (LES)
Anatomic disruption of the gastroesophageal junction, usually associated with a hiatal hernia

on inspiration the diaphragm pinches ait the sphincter

salivation, peristalsis, esophageal bicarb, gravity

Symptoms
Response to empirical trial of acid suppression therapy (PPI)
Endoscopy
24-hour pH monitoring

Ulcer
Stricture
Barrett’s esophagus
Adenocarcinoma

Intestinal metaplasia of the esophagus
Chronic inflammation leads to:
metaplasia -> dysplasia -> carcinoma
No therapy has been proven effective
Consider screening patients over the age of 50 with chronic GERD symptoms
Once identified, routine surveillance is indicated
Esophagectomy for high grade dysplasia or Ca

Reduce or eliminate symptoms

Heal esophagitis

Prevent complications

Improve quality of life

Lifestyle modifications
Antacids
H2-receptor antagonists
Proton pump inhibitors
Antireflux surgery
Prokinetic agents
New endoscopic therapies

Sleep- raise head of bed, avoid melas 3hrs before bed
Diet-avoid fatty and spicy foods, avoid citrusand tomato based foods, avoid chocolate and peppermint
Habits- stop smoking, decrease alcohol intake
Lose weight

Examples: Maalox, Mylanta, Gaviscon, Gelusil
Generally contain ingredients such as aluminum hydroxide, magnesium hydroxide, magnesium trisilicate
Neutralize stomach acid
Work only on a short-term basis

histamine, proton pump, acetylcholine
H2RA, PPI, anticholinergic

All targets are on parietal cell

Tagamet, zantac, axid, pepcid

prilosec, prevacid, aciphex, protonix, nexium, zegerid

PPI's more effective Tx and helps healing

repair hiatal hernia, perform fundoplication. Restore some LES pressure and prevent relaxation