Esophagus

Question 1

Where does the esophagus begin?

Answer 1

lower border of C6 (pharynx)

Question 2

Muscle types in esophagus

Answer 2

Superior third = striated

Middle third = Both striated and smooth

Lower third = smooth

Question 3

What are the 3 areas of narrowing?

Answer 3

1) At beginning - from the cricopharyngeus muscle
2) Where left mainstem bronchus and aortic arch cross
3) At hiatus of diaphragm

Question 4

Where is the LES?

Answer 4

T11

Question 5

What is the distance of the GEJ from incisor teeth?

Answer 5

40cm - important for endoscopy

Question 6

T8 vs T10 vs T12

Answer 6

T8 = IVC

T10 = Esophagus

T12 = Aorta

Question 7

Achalasia definition

Answer 7

LES cannot relax

Resulting dysphasia due to 3 mechanisms:

• Complete absence of peristalsis in esophageal body
• Incomplete/impaired relaxation of LES after swallowing
• Increased resting tone of LES

This all increases pressure within esophagus, causes dilation, and causes progressive loss of normal swallowing

Question 8

Signs/symptoms of achalasia

Answer 8

Triad = Dysphagia, regurgitation, weight loss

Dysphagia for solids and liquids

Severe halitosis

May feel knot or ball of food getting stuck

Question 9

Achalasia dx

Answer 9

1 = manometry: increased LES tone

Lat upright CXR may show dilated esophagus and presence of air-fluid levels in posterior mediastinum

Barium swallow reveals Bird’s beak sign

Esophagoscopy is indicated to r/o mass lesions or strictures and to get a bx

Question 10

Achalasia tx

Answer 10

Medical = drugs that relax LES - nitrates, ca blockers, antispasmodics

***Surg = Esophagomyotomy (heller’s myotomy) with or without fundoplication - incise tunica muscularis. Divide LES (if all the way add Nissen 360 fundop or partial fundop).

Endoscopic dilation - lower success, more complications (perf)

Botox

Question 11

Complications of achalasia

Answer 11

Risk of SCC up to 10% over 15-25 years

Patients may get pulmonary complications like aspiration, pneumonia, bronchiectasis, asthma due to reflux and aspiration

Question 12

Diffuse esophageal spasm definition

Answer 12

Unknown etiology. Primarily a disease of the esophageal body. Can be primary issue of the muscle or may occur in association with reflux esophagitis, esophageal obstruction, collagen vascular disease, or diabetic neuropathy

Spasm is in distal 2/3 and is caused by uncontrolled large-amplitude rapid contractions of smooth muscle

LES tone is Normal

Question 13

Signs/symptoms of DES

Answer 13

Dysphagia for solids and liquids

Substernal CP, similar to MI. Acute onset may radiate to arms, jaw, back. May happen at rest or may follow swallowing

No regurgitation (unlike achalasia); no water brash (unlike GERD)

Question 14

DES dx

Answer 14

Barium swallow can reveal “corkscrew” appearance of esophagus due to ripples and sacculations from uncoordinated contraction. Barium may be totally normal though. LES appears normal though always.

Manometry shows large, uncoordinated repetitive contractions in lower esophagus. May be normal when asymptomatic though. LES manometry will show normal resting pressure with LES relaxation upon swallowing

Esophagoscopy should be done to r/o mass, stricture, esophagitis

Bc of the cardiac-like complaints, dx is often delayed for cardio workup.

Patients with DES often have other functional intestinal disorders like IBS and spastic colon

Question 15

Tx for DES

Answer 15

Nitrates or Ca blockers to relax smooth muscle

Surg via esophageal myotomy is NOT as succesful in relieving symptoms as it is in achalasia so it’s not recommended unless dysphagia is severe and incapacitating.

Question 16

Nutcracker esophagus

Answer 16

Another hypermotility disorder that is more focal in nature within the esophagus

Question 17

Esophageal diverticula definition

Answer 17

Outpouching of esophageal mucosa that protrudes through a defect in the muscle layer (remember esophagus has no serosa). Often co-existing motility issue.

Can be true, which involves all 3 layers of esophagus (midesophageal diverticulum) or false involving mucosa and submucosa only (Zenker)

Characterized by location - Pharyngoesophageal (Zenker), midesophageal, or epiphrenic (terminal third of esophagus)

Pharyngoesophageal and epiphrenic are “pulsion” diverticula bc they are caused by increased esophageal pressure - both are FALSE ones

Question 18

Zenker’s diverticulum

Answer 18

1 = Cervical pharyngocricoesophageal myotomy (incise the cricopharyngeus) - always done when surg is needed

Pharyngoesophageal (Zenker) is the most likely kind of diverticulum to be symptomatic

Dysphagia with spontaneous regurgitation of undigested food, halitosis, choking, aspiration, repetitive respiratory infections, and eventual debilitation and weight loss

Diagnosis with Barium swallow for all types of diverticula. Endoscopy is dangerous due to risk of perf through diverticulum

Tx is to relieve symptoms and prevent complications.

“When Zenker’s causes Zymptoms it requires Zurgery” Asymptomatic only treated if > 2cm in size.

Diverticulopexy - suture diverticulum in inverted position to prevertebral fascia. Added to myotomy for larger diverticula

Diverticulectomy - endoscopic stapling of diverticulum along with myotomy is done in largest ones

Question 19

Esophageal varices pathophys

Answer 19

From portal HTN, usually a result of alcoholic cirrhosis

As elevated portal system pressure impedes the flow of blood through the liver (increased intrahepatic pressure), various sites of venous anastomosis become dilated secondary to retrograde flow from portal to systemic ciruclation. Varices are portosystemic collaterals

Clinically significant portal-systemic sites are cardio-esophageal junction (dilation = esophageal varices), periumbilical region (dilation = caput medusae), and rectum (dilation = hemorrhoids)

Question 20

Signs/symptoms of esophageal varices

Answer 20

Painless hematemesis

Unprovoked (not postemetic)

Hemodynamic instability common

Risk for rebleeding high

Peripheral stigmata of liver disease

Question 21

Treatment of esophageal varices

Answer 21

1) ID high-risk patients and prevent the first bleeding episode! - screening endoscopy to determine varices in cirrhotic patients. This includes pharm therapy to reduce portal pressure - reduce collateral portal venous flow with vasoconstrictors (somatostatin, vasopressin, octreotide) and reduce intrahepatic resistance with vasodilators (B blockers, esp propranolol and nitrates, reduce portal pressure)

Variceal bleeding stops spontaneously in about 50%

2) Manage the ruptured varices that cause acute bleeds
- stabilize hemodynamics: NS or LR with RBCs, NG suction/lavage
- continuous vasopressin/somatostatin/ octreotide to reduce splanchnic blood flow and portal pressure

3) Endoscopic sclerotherapy (inject bleeding vessel with sclerosing agent via catheter) or band ligation (equivalent with fewer complications) for control of ruptured varices has 90% success rate. Patients are usually intubated first to prevent aspiration of blood
4) Balloon tamponade to apply direct pressure and hemostasis to varix with the balloon
5) For refractory acute bleeding, TIPSS (tansjugular intrahepatic portosystemic shunt)
6) Intraoperative placement of portocaval shunt. Surg is considered when there is continued bleed or recurrent rebleeding with poor control
7) Liver transplant

Question 22

Esophageal stricture definition

Answer 22

Local, stenotic regions within lumen usually a result of inflammatory or neoplastic process

Question 23

Risk factors and causes of esophageal stricture

Answer 23

1) Long-standing GERD
2) Radiation esophagitis
3) Infectious esophagitis
4) Corrosive/caustic esophagitis
5) Sclerotherapy for bleeding varices

Question 24

Signs/symptoms of stricture

Answer 24

While small strictures may be asymptomatic, those that obstruct the lumen will induce progressive dysphagia for solids

Odynophagia may or not be there

Question 25

Dx of stricture

Answer 25

Initial eval via barium swallow Esophagoscopy is needed always since it should be evaluated for malignancy and to determine the right treatment

Question 26

Tx of stricture

Answer 26

Esophagus visualized endoscopically and bougie dilators are carefully passed through the stricture. Each successful dilation is done with progressively larger dilator Dysphagia is relieved in most cases following adequate dilation of the lumen Most feared complication is esophageal rupture

Question 27

Esophageal perf or rupture - general info

Answer 27

Trauma to esophagus may result in leakage of air and esophageal contents into mediastinum Surgical emergency 50% mortality

Question 28

Causes of esophageal perf/rupture

Answer 28

#1 = iatrogenic following endoscopy, dilation, tamponade tubes. Usually in cervical esophagus near cricopharyngeus muscle Boerhaave (15% of cases). Spontaneous perf and FULL THICKNESS tear. Usually in L pleural cavity or just above GEJ/ L lateral wall due to transmission of abdominal pressure to the esophagus. Can be from forceful vomiting, retching coughing, labor, lifting, trauma Mallory-Weiss: Partial thickness mucosal tear. Usually in R posterolateral wall of distal esophagus. Causes bleeding that generally goes away on own. Due to forceful vomiting. Foreign body ingestions (14% of cases) - objects lodge near anatomic narrowing and then perforate through near UES, aortic arch, LES

Question 29

Signs/symptoms of esophageal perf/rupture

Answer 29

Severe, constant cervical, substernal or back pain Dysphagia Dyspnea SubQ emphysema (requires full thickness) Mediastinal emphysema heard as "crunching" sounds (Hamman's sign) - also requires full thickness Sepsis/fever Pneumothorax

Question 30

How do you treat ANY GI bleed?

Answer 30

NGT, EGD, 2 large bore IVs, type/cross

Question 31

Dx of esophageal perf

Answer 31

CXR - L sided pleural effusion; mediastinal, cervical, or subQ emphysema; mediastinal widening Esophagogram with water soluble contrast (gastrograffin) - shows extravasation of contrast in 90% of patients Other studies - EGD, CT, thoracentesis (check fluid for low pH and high amylase)

Question 32

Esophageal perf tx

Answer 32

Resuscitation and stabilization of patient Primary surg closure of full thickness tears within 24h =80-90% survival rate Drain the contaminated mediastinum Monitor for recovery from sepsis

Question 33

Caustic injury of esophagus - definition

Answer 33

Caused by acid (in household cleaning agents) or alkali (lye, NaOH tablets) Alkali is worse than acidic - acid substances usually burn the mouth immediately are less frequently swallowed. Acids also cause coag necrosis which limits their penetration. Alkali cause injury deep into tissue as they dissolve the tissue Caustic injury has acute phase - controlling immediate tissue injury and perf potential - and a chronic phase - managing structures and wallowing issues that have developed Acute damage is dependent on nature of substance, amount ,and time in contact with tissue

Question 34

Signs/symptoms of caustic injury

Answer 34

Oral and substernal pain in initial phase; pain on swallowing and dysphagia Hypersalivation Fever - strongly linked to esophageal lesion Vomiting and hemoptysis Systemic hypovolemia and acidosis Laryngospasm, laryngedema Dysphagia reappears in chronic phase due to fibrosis, retraction, and narrowing of esophagus. Strictures develop in 80% of patients within 2 months

Question 35

Tx of caustic injury

Answer 35

Inspect oral cavity and esophagus - appearance of one does not rule out injury to the other Early esophagoscopy (less than 24h) to establish presence of esophageal injury - extra caution not to perf Limit burn by giving neutralizing agents in first hour: Lye/alkali can be neutralized with half-strength vinegar, lemon juice, orange juice; acid with milk, egg white or antacid (controversial) Broad spectrum antibiotics to prevent infectious complications Controversial** bougie dilation Extensive necrosis leading to perf is best treated with resection. If esophagus is viable, an intraluminal stent may work EMETICS ARE A NO NO

Question 36

GERD pathophys

Answer 36

Loss of normal GE barriers results in reflux Can be from structurally defective LES; hiatal hernia; transient loss of GE barrier with normal LES secondary to gastric weirdness like distention with air/food; delayed gastric emptying; increased intra-abdominal pressure Prolonged exposure to low pH from stomach will cause irritation of esophageal mucosa (also respiratory epithelium) and the development of complications including esophagitis, stricture, Barret's and risk of aspiration

Question 37

Signs of GERD

Answer 37

Range of symptoms from heartburn to angina-like CP Atypical symptoms = n/v, postprandial fullness, choking, chronic cough, wheezing, hoarseness Minimal or transient refluz may cause asymptomatic esophagitis, while severe reflux may cause severe esophagitis accompanied by laryngitis, aspiration pneumonitis/recurrent pneumonia; idiopathy pulm fibrosis, asthma Presence of dysphagia may indicate peptic stricture formation

Question 38

Dx of GERD

Answer 38

Pts with vague symptoms of chest pain should be evaluated for cardiac and pulm disease (PE, ECG, enzymes) Barium study useful to look for anatomical cause like hiatal hernia. Can also see long-term issues like structures or ulcer 24h ambulatory pH monitoring is best test!! If there are alarm symptoms or PPI fails then EGD with bx

Question 39

Tx of GERD

Answer 39

``` Elevate head of bead Antacids H2 antag (Ranitidine) PPIs Avoid alcohol, chocolate, coffee, peppermint, nicotine (nicotine lowers LES tone) ``` Eat small, freq meals, avoid tight clothing, do not sleep within 3-4 hrs of meal Meds that promote gastric empyting (metoclopramide) Patient undergoes trial of therapy for 6-12w before further investigation. If it fails or patient develops complications like chronic esophagitis or stricture then surgical intervention should be considered. Normal GERD = PPIs Metaplasia = High dose PPI and surveillance for cancer Dysplasia = Cryoablation Adenocarcinoma = Resection Does patient need Nissen? Always consider. May induce pseudo-achalasia

Question 40

Barrett's esophagus def

Answer 40

Distal portion of tubular esophagus becomes lined by columnar epithelium instead of normal squamous - histo appearance of intestinal metaplasia (goblet cells appear) New region susceptible to ulceration, bleeding, stricture, and adenocarcinoma

Question 41

Barrett's signs

Answer 41

Usually similar to GERD Bleeding, hematemesis Signs of esophageal perf

Question 42

Barrett's dx

Answer 42

EGD for evaluation. Suspect when there is trouble visualizing squamocolumnar junction in lower esophagus or an appearance of a redder mucosa Multiple biopsies should be taken for definitive or histo dx

Question 43

Barrett's tx

Answer 43

Same as GERD - requries long term PPI for symptom relief and management of mucosal injury Monitor and prevent disease progression to malignancy (1% per year) Antireflux surgery when associated complications (stricture, ulcer, metaplastic progression) Surg resection for refractory cases with high grade dysplasia

Question 44

Esophageal carcinoma - Epi

Answer 44

More than 90% SCC and adeno Most over 50 yrs old Males more then females 50% of patients have unresectable or metastatic disease at time of presentation 5yr survival is poor (5%) Upper 1/3 = SCC secondary to hot liquids and smoking Lower 2/3 = adeno secondary to GERD

Question 45

Risk factors for esophageal carcinoma

Answer 45

Tobacco Alcohol Food additives (nitrates in smoked and pickled meats) ``` GERD/Barrett's Achalasia Damage from caustic ingestion/strictures Chronic esophagitis Plummer-Vinson History of radiation therapy to mediastinum ```

Question 46

Alarm symptoms of esophageal carcinoma

Answer 46

Dysphagia (progressive) Odynophagia Weight loss Dysphagia doesn't usually develop until 60% of lumen is obstructed

Question 47

Esophageal cancer dx and tx

Answer 47

Barium swallow first then EGD with bx to confirm Stage with CT (TNM) and resection

Question 48

Schatzki's ring

Answer 48

Thin, submucosal circumferential ring in lower esophagus associated with hiatal hernia. Could be congenital, or due to infolding of redundant esophageal mucosa. Or could be from structure Symptoms = brief episodes of dysphagia during hurried ingestion of solids Tx = dilation (usually once) +/- antireflux measures. May also incise ring/excise

Question 49

Plummer-Vinson

Answer 49

Dysphagia, atrophic oral mucosa, spoon shaped/brittle fingernails, chronic Fe deficiency anemia More common in perimenopausal women of scandinavian decent. An esophageal web, which usually causes dysphagia, used to be a main component of the disease, but not anymore. It actually is from ingesting ferous sulfate to treat the disease Web is usually below cricopharyngeus muscle. Tx = dilation and Fe therapy