First Aid For Surgery - Esophagus

Front 1

Esophagus Anatomy

Back 1

Superior third: striated muscle only; Middle third: both striated and smooth muscle; Inferior third: smooth muscle only; The esophagus does NOT have the serosal layer, so esophageal anastomoses are prone to leaks

Front 2

What are the three areas of esophageal narrowing?

Back 2

(1) Beginning of cricopharyngeus msucle; (2) Where left mainstem bronchus and aortic arch cross; (3) At hiatus of diaphragm

Front 3

Vertebral levels crossing diaphragm

Back 3

T8 = IVC; T10 = Esophagus; T12 = aorta

Front 4

Dysphagia vs Odynophagia

Back 4

Dysphagia is difficulty swallowing; Odynophagia is PAIN on swallowing; may or may not accompany dysphagia

Front 5

Achalasia

Back 5

Failure of LES to relax during swallowing; causes include (1) complete absence of peristalsis in esophageal body; (2) incomplete/impaired relaxation of LES after swallowing; (3) increased resting tone of LES

Front 6

S&S of Achalasia

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(1) Dysphagia for both solids and liquids; (2) Regurgitation of food; (3) Severe halitosis (due to decomposition of stagnant food within the esophagus)

Front 7

Classic triad of achalasia

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(1) Dysphagia + (2) Regurgitation + (3) Weight loss

Front 8

Diagnosis of achalasia

Back 8

(1) Lateral CXR may reveal dilated esophagus and presence of air-fluid levels in posterior mediastinum; (2) Barium swallow will reveal characteristic distal bird's beak sign due to collection of contrast material in proximal dilated segment and passage of a small amount of contrast through narrowed LES; (3) Esophageal motility will confirm nonperistaltic contractions, incomplete LES relaxation, and increased LES tone; (4) Esophagoscopy indicated to r/o mass lesions or strictures and obtain specimens for biopsy

Front 9

Treatment of achalasia

Back 9

(1) Drugs to relax LES: CCB, nitrates, antispasmodics; (2) Surgery: Esophagomyotomy w/ Nissen 360 degree fundoplication; (3) Endoscopic dilatation with balloon or dilators through narrowed lumen to decrease competency of LES

Front 10

Complications of achalasia

Back 10

(1) Risk of Squamous Cell Carcinoma is as high as 10% in patients with long-standing achalasia; (2) Pulmonary complications - aspiration pneumonia, bronchiectasis, asthma 2/2 reflux and aspiration

Front 11

Diffuse Esophageal Spasm

Back 11

May be either a primary disease of the muscle, or may occur in association with reflux esophagitis, esophageal obstruction, collagen vascular disease, or diabetic neuropathy. Spasm occurs in distal 2/3 of esophagus and is caused by uncoordinated large-amplitude rapid contractions of smooth muscle. By definition, LES tone is normal

Front 12

S&S of Diffuse Esophageal Spasm

Back 12

(1) Dysphagia for both solids and liquids; (2) Substernal chest pain, similar to that seen in MI; (3) No regurgitation (unlike achalasia); no water brash (unlike GERD)

Front 13

Diagnosis of Diffuse Esophageal Spasm

Back 13

(1) Barium swallow may reveal characteristic "corkscrew" appearance of esophagus, 2/2 ripple and sacculations that are visible as a result of uncoordinated esophageal contraction. Barium swall may also be entirely normal, however, because the esophagus may not be in spasm at the time of the study. In contrast to achalasia, the LES is of normal diameter; (2) Esophageal manometry studies reveal presence of large, uncoordinated, and repetitive contractions in the lower esophagus; (3) Esophagoscopy to r/o mass lesions, strictures, or esophagitis

Front 14

Treatment for Diffuse Esophageal Spasm

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(1) Nitrates or CCB to relax smooth muscle; (2) Surgical treatment via esophageal myotomy is NOT AS SUCCESSFUL in relieving symptoms as it is for achalasia, and is therefore not recommended unless dysphagia is severe and incapacitating

Front 15

Esophageal Diverticula

Back 15

Outpouching of the esophageal mucosa that protrudes through a defect in the muscle layer. Often occur when there are coexistent motility disorders;

Front 16

Zenker's Pharyngoesophageal Diverticula

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Most common symptomatic esophageal diverticula. Symptoms include dysphagia along with spontaneous regurgitation of undigested food, halitosis, choking, aspiration, repetitive respiratory infections, and, eventually, debilitation and weight loss.

Front 17

Esophageal Varices

Back 17

Caused by portal hypertension, most commonly a result of alcoholic cirrhosis; as elevated portal system pressure imedes the flow of blood through the liver (increased intrahepatic resistance), various sites of venous anastomosis become dilated 2/2 retrograde flow from portal to systemic circulations. Varices are portosystemic collaterals

Front 18

Treatment of esophageal varices

Back 18

Identifying high-risk patients and preventing the first bleeding episode are critical (i.e., screening endoscopy to determine varices in cirrhotic patients). This includes pharmacological therapy to reduce portal pressure and consequently intravariceal pressure—reduce collateral portal venous flow with vasoconstrictors (somatostatin, vasopressin and octreotide-decrease portal flow) and intrahepatic resistance with vasodilators (beta blockers, especially propranolol and nitrates, decrease portal pressure)

Front 19

Esophageal stricture

Back 19

Local, stenotic regions within the lumen of the esophagus; usually result of inflammatory or neoplastic process: RISK FACTORS: GERD, radiation esophagitis, infectious esophagitis, corrosive/caustic esophagitis, sclerotherapy for bleeding varices

Front 20

Treatment of esophageal stricture

Back 20

Endoscopy with bougie dilators carefully passed through the stricture; each successful dilatation is done with a progressively larger dilator; dysphagia is relieved in most cases following adequate dilatation of the esophageal lumen; most feared complication is obviously an esophageal rupture!

Front 21

Esophageal perforation or rupture

Back 21

Trauma to the esophagus that may result in leakage of air and esophageal contents into the mediastinum - SURGICAL EMERGENCY! - carries 50% mortality

Front 22

Etiology of esophageal rupture

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(1) MCC is iatrogenic during endoscopy, dilatation, tamponade tubes, etc. (2) Boerhaave syndrome - spontaneous perforation and FULL-THICKNESS tear in area of left pleural cavity or just above the GE junction 2/2 transmission of abdominal pressure to the esophagus. Can result from forceful vomiting, retching, coughing, labor, lifting, or trauma; (3) Mallor-Weiss syndrome - a partial thickness mucosal tear, usually occuring in the right posterolateral wall of the distal esophagus and results in bleeding that generally resolves spontaneously 2/2 forceful vomiting

Front 23

Hamman's mediastinal crunch

Back 23

Mediastinal emphysema heard as a "crunching" sound associated with esophageal rupture and air leakage into mediastinum

Front 24

Diagnosis of esophageal rupture

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(1) CXR: left-sided pleural effusion; mediastinal, cervical, or subcutaneous emphysema; mediastinal widening; (2) Esophagogram with water-soluble contrast (Gastrograffin) shows extravasation in 90% of patients

Front 25

Alkali vs acid burns

Back 25

Alkali burns are worse than acidic, as acid substances usually burn the mouth immediately and are less frequently swallowed; alkaline substances are more frequently ingested. Acidic substances also cause coagulative tissue necrosis, which limits their penetration, whereas alkaline substances cause injury deep into the tissue as they dissolve the tissue

Front 26

GERD

Back 26

Causes include a structurally defective sphincter; hiatal hernia; transient loss of the GE barrier (with a structurally normal LES) secondary to gastric abnormalities such as distention with air or food; delayed gastric emptying; and increased intra-abdominal pressure

Front 27

Chronic GERD

Back 27

Prolonged exposure to a low pH from gastric contents (acid, pepsin, and duodenal contents, including biliary and pancreatic secretions) will cause irritation of the esophageal mucosa (as well as the respiratory epithelium) and the development of complications including esophagitis, stricture, Barrett’s esophagus and risk of aspiration.

Front 28

Gold-standard for dx of GERD

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24-hr pH monitoring of the esophagus! A probe with pH electrodes is inserted into the patient’s esophagus for 24 hours. The probe continuously records the esophageal pH; useful in determining the severity of reflux (gold standard for diagnosing GERD).

Front 29

Barrett's Esophagus: Definition

Back 29

Condition in which distal portion of the tubular esophagus becomes lined by columnar epithelium as opposed to the normal squamous epithelium - histologic appearance of intestinal metaplasia [appearance of Goblet cells]. This new region is susceptible to ulceration, bleeding, stricture, and adenocarcinoma formation

Front 30

Diagnosis of Barrett's Esophagus

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Endoscopy for evaluation. Suspect when there is difficulty visualizing the squamocolumnar junction in the lower esophagus or an appearance fo a redder mucosa; multiple biopsies should be taken for tissue diagnosis

Front 31

Management of Barrett's Esophagus

Back 31

Same as those patients with GERD - require lone-term PPI therapy for symptom relief and management of esophageal mucosal injury; monitor and prevent disease progression to malignany risk (1%/yr risk); antireflux surgery when there are associated complications and surgery to result refractory cases with high-grade dysplasia

Front 32

Epidemiology of Esophageal Cancer

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More than 90% are squamous cell carcinomas (SCCs) and adenocarcinomas. The increasing prevalence of adenocarcinomas (due to Barrett’s) as compared to what was mostly SCCs is shifting the epidemiology of esophageal cancer. Other tumors of the esophagus are less common (including leiomyomas, melanomas, carcinoids, lymphomas).

Front 33

Risk Factors for Esophageal Cancer

Back 33

(1) Environmental: tobacco, EtOH, food additives like nitrates; (2) Esophageal disorders: GERD/Barrett's, achalasia, damage from caustic ingestion/strictures; (3) Chronic esophagitis, Plummer-Vinson syndrome; (4) Hx of radiation to the mediastinum

Front 34

S&S of Esophageal Cancer

Back 34

(1) Gradual development of dysphagia (74% of patients) due to invasion of serosal layer, first for solids and later for both solids and liquids (mechanical dysphagia), may be present as well. (2) With advanced disease, the patient will appear cachectic; supraclavicular lymphadenopathy may be present, as may signs of distant metastasis. May develop symptoms depending on local invasion (stridor, coughing, aspiration pneumonia, hemoptysis, vocal cord/recurrent laryngeal nerve paralysis).

Front 35

Schatzki's Ring

Back 35

A thin, submucosal circumferential ring in the lower esophagus often associated with a hiatal hernia. Some believe it to be congenital, others due to infolding of redundant esophageal mucosa, and others due to stricture result from infl ammation from chronic reflux.

Front 36

Plummer-Vinson syndrome

Back 36

An uncommon clinical syndrome characterized by dysphagia, atrophic oral mucosa, spoon-shaped and brittle fingernails, and chronic iron deficiency anemia. More common in perimenopausal women of Scandinavian origin. (1) An esophageal web, which is usually the cause of dysphagia was often thought to be a main component of the syndrome, but evidence has shown that it develops as a response to ingesting ferrous sulfate for the treatment of the anemia. Ferrous sulfate has been known to cause esophageal injury. (2) The web is usually below the cricopharyngeus muscle. Treatment consists of dilatation and iron therapy