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Surgery > Esophagus > Flashcards

Esophagus Flashcards

1
Q

Where does the esophagus begin?

A

lower border of C6 (pharynx)

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2
Q

Muscle types in esophagus

A

Superior third = striated

Middle third = Both striated and smooth

Lower third = smooth

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3
Q

What are the 3 areas of narrowing?

A

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

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4
Q

Where is the LES?

A

T11

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5
Q

What is the distance of the GEJ from incisor teeth?

A

40cm - important for endoscopy

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6
Q

T8 vs T10 vs T12

A

T8 = IVC

T10 = Esophagus

T12 = Aorta

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7
Q

Achalasia definition

A

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

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8
Q

Signs/symptoms of achalasia

A

Triad = Dysphagia, regurgitation, weight loss

Dysphagia for solids and liquids

Severe halitosis

May feel knot or ball of food getting stuck

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9
Q

Achalasia dx

A

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

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10
Q

Achalasia tx

A

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

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11
Q

Complications of achalasia

A

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

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12
Q

Diffuse esophageal spasm definition

A

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

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13
Q

Signs/symptoms of DES

A

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)

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14
Q

DES dx

A

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

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15
Q

Tx for DES

A

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.

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16
Q

Nutcracker esophagus

A

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

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17
Q

Esophageal diverticula definition

A

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

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18
Q

Zenker’s diverticulum

A

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

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19
Q

Esophageal varices pathophys

A

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)

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20
Q

Signs/symptoms of esophageal varices

A

Painless hematemesis

Unprovoked (not postemetic)

Hemodynamic instability common

Risk for rebleeding high

Peripheral stigmata of liver disease

21
Q

Treatment of esophageal varices

A

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

22
Q

Esophageal stricture definition

A

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

23
Q

Risk factors and causes of esophageal stricture

A

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

24
Q

Signs/symptoms of stricture

A

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

Odynophagia may or not be there

25
Q

Dx of stricture

A

Initial eval via barium swallow

Esophagoscopy is needed always since it should be evaluated for malignancy and to determine the right treatment

26
Q

Tx of stricture

A

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

27
Q

Esophageal perf or rupture - general info

A

Trauma to esophagus may result in leakage of air and esophageal contents into mediastinum

Surgical emergency

50% mortality

28
Q

Causes of esophageal perf/rupture

A

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

29
Q

Signs/symptoms of esophageal perf/rupture

A

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

30
Q

How do you treat ANY GI bleed?

A

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

31
Q

Dx of esophageal perf

A

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)

32
Q

Esophageal perf tx

A

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

33
Q

Caustic injury of esophagus - definition

A

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

34
Q

Signs/symptoms of caustic injury

A

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

35
Q

Tx of caustic injury

A

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

36
Q

GERD pathophys

A

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

37
Q

Signs of GERD

A

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

38
Q

Dx of GERD

A

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

39
Q

Tx of GERD

A 
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

40
Q

Barrett’s esophagus def

A

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

41
Q

Barrett’s signs

A

Usually similar to GERD

Bleeding, hematemesis

Signs of esophageal perf

42
Q

Barrett’s dx

A

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

43
Q

Barrett’s tx

A

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

44
Q

Esophageal carcinoma - Epi

A

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

45
Q

Risk factors for esophageal carcinoma

A

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
46
Q

Alarm symptoms of esophageal carcinoma

A

Dysphagia (progressive)
Odynophagia
Weight loss

Dysphagia doesn’t usually develop until 60% of lumen is obstructed

47
Q

Esophageal cancer dx and tx

A

Barium swallow first then EGD with bx to confirm

Stage with CT (TNM) and resection

48
Q

Schatzki’s ring

A

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

49
Q

Plummer-Vinson

A

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

Surgery (27 decks)

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