Esophagus Flashcards
Where does the esophagus begin?
lower border of C6 (pharynx)
Muscle types in esophagus
Superior third = striated
Middle third = Both striated and smooth
Lower third = smooth
What are the 3 areas of narrowing?
1) At beginning - from the cricopharyngeus muscle
2) Where left mainstem bronchus and aortic arch cross
3) At hiatus of diaphragm
Where is the LES?
T11
What is the distance of the GEJ from incisor teeth?
40cm - important for endoscopy
T8 vs T10 vs T12
T8 = IVC
T10 = Esophagus
T12 = Aorta
Achalasia definition
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
Signs/symptoms of achalasia
Triad = Dysphagia, regurgitation, weight loss
Dysphagia for solids and liquids
Severe halitosis
May feel knot or ball of food getting stuck
Achalasia dx
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
Achalasia tx
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
Complications of achalasia
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
Diffuse esophageal spasm definition
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
Signs/symptoms of DES
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)
DES dx
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
Tx for DES
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.
Nutcracker esophagus
Another hypermotility disorder that is more focal in nature within the esophagus
Esophageal diverticula definition
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
Zenker’s diverticulum
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
Esophageal varices pathophys
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)
Signs/symptoms of esophageal varices
Painless hematemesis
Unprovoked (not postemetic)
Hemodynamic instability common
Risk for rebleeding high
Peripheral stigmata of liver disease
Treatment of esophageal varices
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
Esophageal stricture definition
Local, stenotic regions within lumen usually a result of inflammatory or neoplastic process
Risk factors and causes of esophageal stricture
1) Long-standing GERD
2) Radiation esophagitis
3) Infectious esophagitis
4) Corrosive/caustic esophagitis
5) Sclerotherapy for bleeding varices
Signs/symptoms of stricture
While small strictures may be asymptomatic, those that obstruct the lumen will induce progressive dysphagia for solids
Odynophagia may or not be there
Dx of stricture
Initial eval via barium swallow
Esophagoscopy is needed always since it should be evaluated for malignancy and to determine the right treatment
Tx of stricture
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
Esophageal perf or rupture - general info
Trauma to esophagus may result in leakage of air and esophageal contents into mediastinum
Surgical emergency
50% mortality
Causes of esophageal perf/rupture
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
Signs/symptoms of esophageal perf/rupture
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
How do you treat ANY GI bleed?
NGT, EGD, 2 large bore IVs, type/cross
Dx of esophageal perf
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)
Esophageal perf tx
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
Caustic injury of esophagus - definition
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
Signs/symptoms of caustic injury
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
Tx of caustic injury
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
GERD pathophys
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
Signs of GERD
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
Dx of GERD
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
Tx of GERD
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
Barrett’s esophagus def
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
Barrett’s signs
Usually similar to GERD
Bleeding, hematemesis
Signs of esophageal perf
Barrett’s dx
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
Barrett’s tx
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
Esophageal carcinoma - Epi
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
Risk factors for esophageal carcinoma
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
Alarm symptoms of esophageal carcinoma
Dysphagia (progressive)
Odynophagia
Weight loss
Dysphagia doesn’t usually develop until 60% of lumen is obstructed
Esophageal cancer dx and tx
Barium swallow first then EGD with bx to confirm
Stage with CT (TNM) and resection
Schatzki’s ring
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
Plummer-Vinson
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
