Esophagus and Stomach Notes

B. Belingon – Notes from case session & case session slides, Anna’s notes (Dr. Esterl), Becky’s notes (Dr. Sideman)

 o

Omeprazole or protonics 40 mg/d & bring back in 4-6 wks (real world)

Surgery  

Does patient in this case need surgery? NO. Indications 

Lifelong PPI use (pt wishes to stop meds)



Failure of medical therapy





Complications of GERD not responding to medical therapy (esophagitis, stricture, barrett’s) Paraesophageal hernia assoc w GERD

Pedi indications: FTT, pulm compromise Anti-reflux procedures: Lap Nissen fundoplication (take greater curve behind esophagus to create a short, loose wrap; goal = re-establish length of intra-abdominal esophagus by creating Nissen) 



A 42 year old male with a long history of gastroesophageal reflux disease presents to your office with persistent epigastric pain. He has been on OTC Zantacs for several months with little improvement in pain. The vital signs are stable. On physical examination his abdomen is soft, obese and nondistended with normal bowel sounds. The rectal exam shows no masses but is occult blood positive. You perform a barium swallow which reveals gastroesophageal reflux. You perform 24 hour pH monitoring in the distal esophagus which confirms gastroesophageal reflux disease. You perform esophagoduodenoscopy which shows long standing esophagitis. You perform multiple biopsies in the distal esophagus which reveal mild intestinal dysplasia. 







Dx: Barrett’s esophagus Change in esophageal mucosa with replacement of the squamous epithelium by columnar o epithelium. (METAPLASIA) Dysplasia - Histologic changes that occur before neoplastic Barrett’s cells become malignant o Classified as low grade dysplasia versus high grade dysplasia  Can lead to ulcers and strictures; untreated  adenocarcinoma of distal esophagus o Cancer risk is significantly higher in patients with high grade dysplasia o Rate of cancer development for patients with high grade dysplasia in Barrett’s esophagus  is 4-6% (Overall cancer risk in patient with Barrett’s esophagus is 0.5% per year)  Workup Mult biopsies along whole extent of esophagus  results: mild esophageal dysplasia = Barrett’s o esophagitis (intestinal columnar metaplasia) Treatment of high grade dysplasia Must confirm by 2 pathologists; esophagectomy if surgical candidate; if not good surgical o candidate — q3 month surveillance until carcinoma identified (cancer dev in ~50% pts during f/u) vs mucosal ablative techniques (can poss miss seeing adenocarcinoma) Treatment of low grade dysplasia Q6-12 mo surveillance; tx w PPI +/- fundoplication o Double-dose PPI (omeprazole 40 mg x 2 per day) (H2 blockers don’t have best response  for typical GERD or Barrett’s) Repeat upper endoscopy & mult biopsies  Fundoplication (can do early in disease process) + max dose PPI therapy can halt or  reverse Barrett’s and prevent progression to adenocarcinoma

A 42 year old female describes a 2 month history of progressively worsening dysphagia. She denies any previous medical or surgical history. She has no cardiac symptoms. She takes no OTC or prescription


medications. The vital signs are stable. The lungs are clear. The heart has a regular rate and rhythm with no gallops, rubs or clicks. The abdomen is soft and nondistended with no masses or hernias. The bowel sounds are normal. 





Next step? Barium swallow (results = sigmoid-shaped esophagus that ends o in “bird’s beak”; air-fluid level can indicate sm bowel obstruction) Least invasive, least expensive  Potential for perforation if don’t do barium swallow  first; use gastrografin Dx: Achalasia Failure of the LES to relax o Progressive esophageal dilation and dysphagia (liquids then solids) o Typically middle-aged women w no other history o Dx with manometry o Hypertensive LES, failure of LES to relax, esophageal aperistalsis, elevated lower  esophageal baseline pressure What infectious dz process can cause exact same pathology? Chagas’ (Trypanosoma cruzi) o

Workup o

EGD  



Goal to rule out cancer or pseudoachalasia, ensure no masses causing compression Don’t actually need endoscopy to rule in achlasia

Treatment Pneumatic dilation of LES (slight balloon through scope and inflate) o Botox injection o Heller myotomy *surgery of choice* - longitudinal incision thru muscle of L chest, tight Oo shaped circle, makes a C, can’t contract as before; minimally invasive Medications don’t usually work (nitrates, CCB) o

A 55 year old male with a long history of alcohol disease presents to the Emergency Department with left chest pain and upper abdominal pain after a severe episode of violent vomiting. The vital signs are temp 103, P 130, RR 34 and BP 90/60. The neck and left chest wall have crepitus. The left chest is dull to percussion with decreased breath sounds and vocal fremitus. The abdomen is soft, distended and slightly tender with decreased bowel sounds. 

Dx: Boerhaave’s syndrome Spontaneous rupture of esophagus o Present w acute onset chest pain, fevers, o usually after episode of retching/vomiting Physical exam finding: crepitus of chest or o neck (may be the only phys finding) o

Dx w CXR (pneumomediastinum or L pleural effusion d/t disruption of mediastinal pleura) or contrast esophagram (use water sol contrast = gastrografin =/= barium) Can also give secondary findings  (atelectasis)






Patient is unstable: hypotension, tachycardia, fever (indicates SIRS or early septic shock  once have a source can call septic shock); source? Ruptured esophagus secondary to significant episode of retching/vomiting ABC’s o

o

o

o

 

Listen to breath sounds (decr breath sounds, vocal fremitus, dull to percussion), can get a CXR but this is an acute setting, can put chest tube in OR Resuscitate for shock (large bore IV, 1-2L fluids for septic shock; can give pressors as support but appropriate only if have enough volume (preload!!!) How do you know when adequately resuscitated? CVP (Nl 4-6) — incr until about 711 or so; can also put in Foley to monitor UOP Can also give early intervention (pre-op) w broad-spectrum Abx (shown to decr mortality) to cover mouth flora  feed thru jejunostomy

Labs: CBC chem, LFTs, amylase/lipase (alcoholic hx), T & C for blood Treatment Surgical emergency!!! o 15% mortality w/i 24 hrs, 45% mortality > 24 hrs   

Die from mediastinitis d/t leakage into mediastinum MCC of perforation? Iatrogenic; perforates in L chest b/c of esophageal shift

After 24 hrs, tissue is too friable to handle sutures so divert (gastrostomy, spit fistula, chest tube) Mucosal injury may be larger than muscle injury  primary closure of mucosal  injury; staple off cardia of stomach; esophagus doesn’t seal well (b/c lacks serosa)  buttress w any tissue nearby; drain widely (if you think you need 1 chest tube, put in 2; if you think you need 5 chest tubes, put in 10) Drainage, debridement (may have intense inflammatory response from contaminated saliva in other organs in chest/stomach), repair, diversion If pt presents 48 hrs post perforation  lots of inflammation  unable to stent Take to OR and resect distal esophagus, give spit fistula on neck for saliva; staple off  cardia of stomach; stabilize  Reconstruct esophagus in 1 yr using stomach or colon for reconstruction 

o

o

A 27 year old otherwise healthy male presents to your clinic with a history of regurgitation of undigested food. He sometimes wakes from sleep with uncontrollable coughing spells. His girlfriend states that he has worsening bad breath. The vital signs are stable. The lungs are clear. The heart has a regular rate and rhythm. The abdomen is soft, nondistended and nontender with normal bowel sounds. 

Dx: Zenker’s Diverticulum Dysfunction of the cricopharyngeus leads to mucosal herniation o Sx: Dysphagia, regurgitation of undigested food, halitosis, possibly aspiration and pneumonia o o Food stasis in diverticulum w bacterial overgrowth


o

 



Diagnosed with modified barium swallow (anatomical study b/c anatomical problem!) Diverticulum usually on L side  Don’t need manometry or upper  endoscopy (scope may get stuck or perforate)

Is this a typical Zenker’s pt? No, usually they’re older Treatment Diverticulectomy o Cricopharyngotomy o o Proximal myotomy  done on constrictors  separate distal muscle as far down as possible Vs. achalasia  distal myotomy 

**Compare & contrast Zenker’s w epiphrenic diverticulum

A 55 year old male with a history of 2 DUI offenses is required by the court to attend an outpatient alcoholic support group for 1 year, to perform 40 hours of community service and to take antabuse to avoid al cohol consumption. He relapses, consumes alcohol while on antabuse and develops acute violent emesis. With his fourth episode of emesis he develops massive painless hematemesis. He has never had a previous history of hematemesis. His vital signs include temp 100, P110, RR 22 and BP 110/70. He appears malnourished. The lungs are clear. The heart shows mild tachycardia but no gallops, rubs or clicks. The abdomen is soft and nondistended with no masses or hernias. The bowel sounds are normal. There are no signs and symptoms of cirrhosis. You place supplemental oxygen and 2 large bore IV catheters into the upper extremities. 



 



DDx (upper GI bleed): esophageal varices, perforated ulcer, stress gastritis, submucosal vessel bleeding (Dieulafoy’s lesion), Boerhaave’s Dx: Mallory-Weiss Tear Mucosal tear after vomiting  causes upper GI bleed o (disrupts blood vessels under mucosa vs. Boerhaava’s fullthickness tear) Tear usually almost always at GE junction o Usually self-limited o o Painless hematemesis!

ABC’s: resuscitate!!! w large bore IVs, T&C blood (don’t need H&H) Treatment Most bleeding stops w resuscitation (medical management) o Inject w epi to vasoconstrict, or cauterize o Can have PPI, ocreotide, or somatostatin drip o Endoscopic treatment (for dx or to control bleeding) o Rarely requires surgical treatment (explore stomach, can do blind figure 8 sutures around tears; get o vascular to embolize; or get interventional radiology  angioembolization of any bleeders)

Massive upper GI bleeding from liver dz  variceal hemorrhage  need to intubate, marked resuscitation, full laps, do upper endoscopy; tx = banding, PPI & ocreotide continuously for 12 days If still bleeding w marked hematemesis  do another upper endoscopy, band where appropriate o Still bleeding  control acute hemorrhage w temporizing measures  NG lavage to confirm o upper GI source (SB tube: tube w gastric balloon holding 500 cc w esophageal balloon holding 50 cc)  put down nasogastric groove KUB to make sure balloon below diaphragm to avoid perforation  pressure stops  bleeding




o

NG tube proximal to esophageal tube to collect blood Can do operative procedure (TIPS or porto-caal shunt)  good for pts getting more  definitive procedure later (liver transplant) Best tx = liver transplant

A 45 year old male presents to your office with vague chest “pressure”. The pain is substernal in location and dull in nature with no radiation to the back, neck or arms. He describes frequent early satiety. He describes frequent gaseous eructations, nausea and vomiting. He denies cough. He denies history of gastroesophageal reflux disease. He denies previous cardiopulmonary history. The vital signs are temp 98, P 90, RR 22 and BP 130/70. The lungs are clear to auscultation and percussion. The heart has a regular rate and rhythm with no gallops, rubs or clicks. The abdomen is soft and nondistended but with slight epigastric tenderness. The rectal exam shows no masses but is trace occult positive. 

Dx: Paraesophageal hiatal hernia Types – Confirm type w barium swallow (barium better to see o motility) Type I: Sliding (most common, can move betw abd and  thorax; won’t see on CXR) Type II: Paraesophageal (esophagus in anatomical  position [GEJ in correct location] but par t of stomach herniates adjacent to esophagus; CXR shows large gastric bubble in retrocardiac area/behind heart) Type III: Combo I & II 



 o o



Sx: GERD, epigastric discomfort, post-prandial bloating, dysphagia Complications: ulceration  anemia, strangulation (esp w paraesophageal) Incarceration: something protrudes thru hernia & gets stuck; strangulation: compromised  blood flow

Workup o o o o

Guaiac (+) = ischemia until proven otherwise Upper endoscopy — to reveal degree of ischemia CT scan (look for other organs that herniated) Check blood flow w fluorescence or Doppler




Treatment Surgical emergency b/c complications include stomach becoming ischemic and perforating o o Indications: Symptomatic, or if stomach in chest Laparoscopic paraesophageal hernia repair +/- mesh o Reduce stomach, repair hiatus, add fundoplication; empty stomach contents o Put in G-tube, resect hernia sack, close crura behind stomach, secure diaphragm to prevent repeat o herniation

A 35 year old male attempts suicide by ingestion of the caustic alkaline liquid agent “Drano”. He presents to the Emergency Department at University Hospital with drooling, and substernal chest pain. The vital signs are temp 101, P 110, RR 28 and BP 116/60. He appears uncomfortable and diaphoretic. He has no crepitance in the neck. The heart has tachycardia but no gallops, rubs or clicks. The breath sounds are equal bilaterally. The abdomen is soft and nondistended with no masses. The rectal examination shows no masses but is trace guaiac positive. 



Dx: Caustic esophageal injury o Alkalis: cause liquefactive necrosis, deep penetration & perforation (worse than acids) Acids: coagulation necrosis involving eschar formation, limited depth of injury o Escar formation shields deeper tissue from injury  o DO NOT induce vomiting (just re-exposes mucosa to caustic agent) , “dilute” with water o Degree st 1 : mucosal hyperemia and edema  nd 2 : limited hemorrhage, exudate ulceration, pseudomembrane  rd 3 : deep ulcer, perforation, obstruction of lumen, massive bleeding  Workup EGD within 24 hrs admission  if discover full thickness injury, pre-emptively go to surgery o o Gastrografin swallow (assess for perforation even if no clinical suspicion) Give Abx only if suspect esophageal perforation  b/c of nature of injury, can progress to full o thickness involvement of esophagus o



 

Treatment Supportive care o Assess airway – do you need to intubate? Consider intubation if pt has lots of secretions  that can’t clear IV fluids   NG tube (radiologic guided) Large volume resuscitation  TPN vs feeds  Surgery for full thickness necrosis or perforation o Esophagogastrectomy  Esophagostomy  FJC 

Prognosis: good for minor burns; chronic strictures for moderate ingestions (need surgery) Different scenario: suicide attempt w “Drano”; presents w tachycardia, equal breath sounds, no crepitus, mild epigastric pain  could have liquefactive necrosis, looks like Boerhaave’s Tx: resuscitation as much as possible, don’t feed; if necessary, gently put down NG tube; do o gastrografin swallow; resection if perforation (happens w/i hrs); if no perforation  gentle upper endoscopy to see burns & stop when see first major burn (textbook) [real world: scope through to nd 2 portion of duodenum)


o o

Can still progress to perforation  perforation can lead to stricture Dx stricture w upper GI swallow; do upper endoscopy to look for tumor if see stricture (need to r/o)  tx stricture w dilation

A 5 year old male ingested pool cleaner hydrochloric acid accidently one month ago and developed a corrosive esophageal injury that was treated nonoperatively. He now presents to the outpatient pediatric surgery clinic with worsening dysphagia of liquid and solid foods. He has the impression that food “gets stuck” in his chest. The vital signs are temp 99, P 100, RR 22 and BP 118/60. He appears comfortable. The heart has a regular rate and rhythm with no gallops, rubs or clicks. The bilateral breath sounds are equal. The abdomen is soft and nondistended with no masses. The rectal examination shows no masses and is guaiac negative. 





Workup Gastrografin swallow o Imaging shows long stricture  EGD o Mucosa inflamed (chronically)  not  a good salmon pink color Dx: Chronic esophageal injury (stricture) Fibrotic scarring of esophagus from caustic o injury Treatment Bougie dilation o o Surgical resection if: Complete stenosis, marked irregularity on swallow study, severe reaction to dilation  (esophagitis/mediastinitis), fistula formation, unable to dilate st nd rd o Surgical resection w gastric or colonic interposition graft (1 choice stomach, 2 choice colon, 3 choice small bowel (jejunum)

A 65 year old male with a long history of cigarette and whisky use presents to your office with progressive dysphagia for liquid and solid meals. He describes a 20 pound weight loss over 3 months. He describes vague substernal chest pain. He has occasional nausea and vomiting. He denies previous medical or surgical history. The vital signs are stable. He appears quite malnourished. The neck has several shotty supraclavicular lymph nodes. The lungs are clear. The heart has a regular rate and rhythm with no gallops, rubs or clicks. The abdomen is soft and nondistended with no masses or hernias. The bowel sounds are normal. The rectal exam shows no masses but is trace occult positive. 





Pt’s age, wt loss, RF of smoke/drink, progressive dysphagia (solid then liquids)  cancer until proven otherwise Dx: Esophageal cancer th th Mostly during 5 -7 decade of life o Men > women o o Smoker & drinker = most common contributing factors Progressive dysphagia (solids then liquids) o Wt loss o

Supraventricular LN probably indicates metastatic  biopsy w FNA FNA (+) = metastatic cancer  not resectable b/c it’s spread & stage its reached  not a good o candidate for surgery d/t distal nodal spread  tx w chemo/radiation




Staging o

o o

o 





Barium swallow then EGD + biopsy Imaging shows irregular stricture  Endoscopic ultrasound: determines T stage (depth of invasion) CT abdomen & chest for invasion of structures next to esophagus/metastasis Bone scan if bony pain

Histologic types Squamous cell, adenocarcinoma o Treatment Neoadjuvant chemoradiation (shrink and downstage before surgery) o Surgical resection o Ivory-Lewis esophagectomy (two stage procedure:  laparotomy for gastric mobilization and tubularization, followed by R thoracotomy for esophageal resection & reconstruction) Transhiatal esophagectomy (upper midline laparotomy incision and left neck incision,  pull stomach into the neck; gastric conduit anastomosed to remaining cervical esophagus above level of clavicles) Indication: no evidence of tumor spread (tracheobronchial tree, aorta, RLN), no distant  metastasis, patient fit from cardiopulmonary POV

Diff scenario: female w extra-mucosal obstruction (egg-shaped) in wall of esophagus (non-mucosal, smooth, round lesion)  leiomyoma (MC benign lesion)  don’t do upper endoscopy or biopsy b/c not a mucosal lesion Tx: OR  enuclate lesion (pops out like an egg), close lesion, don’t biopsy o

A 50 year old male presents to your outpatient clinic with a 6 month history of burning epigastric pain. The patient takes over the counter antacids with some improvement in the epigastric pain. The pain is occasionally aggravated by a meat laden diet. The vital signs are stable. The lungs are clear and the heart has a regular rate and rhythm. The abdomen is soft and nondistended with mild epigastric pain on deep palpation and decreased bowel sounds. There are no peritoneal signs. The liver and spleen are not palpable and the liver span is 8 cm. The rectal exam shows no lesions but shows trace occult blood. 



DDx: PUD, biliary  rule out GB: timing of pain (GB typically after fatty or spicy meals), type of pain (GB usually crampy, comes & goes, lasts 20 mins to an hr then goes away) Dx: Peptic ulcer disease (gastric) Imbalance between acid production and acid protection in the o stomach Spectrum of disease from gastritis to ulcer with perforation o Risk factors: H pylori infection >> NSAIDs > stress, o smoking, alcohol use H pylori infection: duodenal >> gastric  o o o

MC complaint: burning epigastric pain Gastric ulcers irritated by high protein diet Types I: gastric body, lesser curve; low acid secretion  II: gastric body & duodenal ulcer; high acid  secretion III: prepyloric region; high acid secretion 


  







IV: high on lesser curvature; low acid secretion V: anywhere; NSAIDs

Workup Obstructive series (if see nonspecific bowel gas pattern  do a swallow) o EGD w biopsy (to r/o malignancy) o If just see chronic inflammation  bring back in 6 wks to repeat upper endoscopy  Test for H Pylori o Treatment Treat the assoc factors o Triple therapy for H pylori: PPI + amoxicillin + clarithromycin, can sub metronidazole  for amox in PCN-allergy Remove risk factors (NSAIDs, ASA, smoking)  Monitor H pylori eradication with breath test o Confirm ulcer resolution w upper endoscopy (if still there  distal gastrectomy) o Complications Bleeding, perforation, obstruction (esp > 3 cm size) o

Diff scenario – Duodenal ulcer  work up is the same (obstructive series to r/o perforation or obstruction; contrast study; EGD), have low likelihood to be cancer, high acid state Tx H pylori w triple therapy for 1 wk, put on PPI o Bring back in 6 wk to ensure sx improving; operate if complications (refractory to tx,  perforation, bleeding, inflammation, or inflammation stricture causing gastric outlet obstruction)

A 75 year old obese diabetic male undergoes a difficult sigmoidectomy and colostomy for perforated sigmoid diverticulitis. He past medical history is significant for coronary artery disease, for which he takes a beta blocker and aspirin 325 mg po daily, and for degenerative joint disease, for w hich he takes ibuprofen 600 mg po daily. He recovers in the surgical intensive care unit after his sigmoidectomy and colostomy. He is on the ventilator and has a radial arterial catheter, a Swan Ganz catheter, a urinary catheter and a nasogastric catheter in position. On the second postoperative day he develops bright red blood from the nasogastric catheter. The vital signs are temp 100.5, P 68, RR 12 and BP 110/80. The lungs have scattered rhonchi bilaterally. The heart has a regular rate and rhythm. The abdomen is soft and slightly distended with mild epigastric tenderness on deep palpation and with decreased bowel sounds. The rectal exam shows no masses but is occult positive. 





Dx: Stress gastritis Likely a sequence of events in the critically ill with multiorgan failure o Inadequate blood flow to gastric mucosa  Poor formation of mucosal barriers  Mucosal breakdown  Bleeding  ASA/NSAIDs set up for gastritis and/or type V gastric ulcers; can also have stress ulcers after o major surgery Treatment PREVENT – PREVENT – PREVENT (PPI) o NGT lavage o If hemorrhagic stress gastritis – angiographic embolization vs. endoscopic control of hemorrhage o Surgical treatment – vagotomy and drainage, oversewing of bleeders vs. subtotal gastrectomy o (RARELY GETS TO SURGICAL TREATMENT)

Read about stress gastritis!!


A 25 year old male medical student presents to the emergency room with epigastric pain. The pain began approximately 4 hours ago as severe, persistent epigastric pain. The pain is now becoming more diffuse. The patient describes some nausea but no emesis. He has never experienced such pain before. He took OTC Tylenol but there was no relief of pain. He takes no prescribed medication. He smokes a rare cigarette on the weekend and drinks approximately 6-12 beers every week. His past medical history is unremarkable but describes his surgical history is significant for bilateral inguinal herniorraphy at age 2 years. The vital signs are temp 101, P 120, RR 28 and BP 110/60. He looks very uncomfortable and lies motionless in bed. The lungs are clear. The heart shows tachycardia but no gallops, rubs or clicks. The abdomen is rigid, board-like with no bowel sounds. The rectal exam shows no masses but is trace occult positive. 

Rigid board-like abdomen = peritoneal signs of peritonitis



ABC’s  resuscitate!





Dx: Perforated duodenal ulcer Classic presentation o Sudden, severe upper abdominal pain (peritoneal signs) o Onset can be recalled precisely (very sudden) o Severely distressed patient o Rigid abdominal muscles o Duodenal ulcers more prone to perforation than gastric o (duodenal wall more thin than gastric); if gastric ulcer perforation, suspicious of gastric cancer Acute abdominal series (3 films) o Upright CXR – subdiaphragmatic air!!! o







NEED TO

OPERATE Flat and upright KUB

Emergent surgery nd Midline incision [exam will show hole in 2 portion of duodenum w minimal contamination] o If unstable, omental (Graham) patch  use patch of vascularized omentum, swing up and  position over perforation, then suture it down Laparoscopic vs. open repair of perforation (if large, may need to resect area) o Omental patch (if small) o High morbidity & mortality w/o surgery o Treatment Long term use of PPI o Triple therapy against H pylori for 1 wk o o Historically, vagotomy and drainage or parietal cell vagotomy (antrectomy) used to be standard surgical treatment refractory to medical treatment (addresses acid secretion  stimulated by gastrin, histamine, Ach)

Scenario: If pt is bleeding (duodenal ulcer w hemorrhage)  pt presents w pale, clammy skin, melenic bowel movements or hematochezia  tx like shock pt (resuscitate, 2 IVs, T&C for blood); diagnostic test = quick obstructive series to r/o perforation; dx intraluminal hemorrhage w NG tube Upper endoscopy (diagnostic and therapeutic)  see arterial hemorrhage in second part of o duodenum, r/o intra-abdominal perforation, rule in intra-luminal bleeding Tx: triple therapy against H pylori, PPI, control hemorrhage w electrocautery, epinephrine o injection (can do through scope), evacute blood w NG tube o If do electrocautery & bleed again  try electrocautery one more time; after two attempts of electrocautery or epi injection, then operate: pyloroplasty to access, visualize & control hemorrhage; truncal vagotomy and antrectomy are larger, more definitive operations






Scenario: Obstruction  N/V, stricture at duodenum, alkalotic from vomiting Dx: EGD to r/o cancer o Tx for duodenal obstruction d/t ulcer disease = resuscitate, lots of fluid upfront w K+ o supplementation High acid state  pyloroplasty doesn’t help stricture; do vagotomy, antrectomy & Billroth II o reconstruction (for retractability; highly selective vagotomy w vagus n still intact so rest of GI tract works well); Billroth I reconstruction (connect duodenum back to distal stomach) Scenario: Gastritis w type V gastric ulcer  marked hemorrhage, vomiting blood, melenic stools, hx of NSAID use Resuscitate! o o Gastritis: diffuse punctate bleeding all over stomach Tx: discontinue offending agent, r/o H pylori, put on PPI ; if doesn’t resolve  total gastrectomy o Do EGD to ensure not missing anything else o

A 45 year old male with a long standing history of duodenal ulcer disease now presents with nausea and vomiting with every meal. He vomits near totally undigested food. The vital signs are temp 100, P 102, RR 22 and BP 120/70. The abdomen shows some distension and tympany in the left upper quadrant with decreased bowel sounds. There are no peritoneal signs. The laboratory evaluation shows a hyponatremic, hypochloremic metabolic alkalosis. The obstructive series shows a dilated stomach with an air-fluid level. 





Workup [What’s next?] Upper GI series w contrast  confirms obstruction (delineated by contrast) o NG to decompress o o IVF to correct electrolyte abnormality DDx for stricture at level of stomach = gastric cancer (r/o w EGD) o If stricture, then confirm no other assoc findings (on EGD)  Dx: Gastric outlet obstruction Chronic inflammation and recurrent bouts of acute inflammation leads to fibrosis of the pylorus o Fibrotic pylorus limits gastric emptying leading to gastric outlet obstruction o o Antrum contains G cells which stimulate acid secretion from parietal cells (located in fundus) Treatment Goal to relieve obstruction and dysphagia o o Endoscopic dilation Surgical resection (pylorus too scarred to function) o Vagotomy and antrectomy or highly selective vagotomy and gastrojejunostomy 

A 42 year old female with morbid obesity comes to your office wi th complaints of hypertension, back pain, joint aches and diabetes. She has tried multiple diets, exercise programs, biofeedback, psychological counseling and yoga to try to lose weight. Her weight has decreased from 312 to 285 pounds in the last year but her weight interferes with her employment and with her quality of life. She comes to your outpatient clinic for advice. 

Obesity Surgery Morbid obesity assoc illnesses: DJD, Low back pain, HTN, OSA, GERD, Gallstones, Diabetes, o Hyperlipidemia, Asthma, Fatal cardiac arrhythmias, Right sided heart failure, Migraines, Venous stasis ulcers, DVT’s, Stress urinary incontinence, Infertility, Dysmenorrhea, Depression, Increased cancer risk (uterus, breast, colon, prostate) Indications o  BMI > 35 w comorbidities, or BMI > 40


 o

Must have attempted supervised wt loss programs & willing to change lifestyle

BMI   

Normal: 18.5-24.9 Overweight: 25.0-29.9 Obesity 

Mild: 30.0-34.9



Moderate: 35.0-39.9

Severe: > 40 Superobese: > 50  Types of surgery Restrictive: Laparoscopic adjustable  gastric banding, sleeve gastrectomy , vertical banded gastroplasty Malabsorptive: Biliopancreatic diversion, jejunoileal bypass  Combo restrictive & malabsorptive : Roux-en-Y gastric bypass , BPD w duodenal  switch 

o

A 55 year old male presents to your office with vague epigastric pain and fullness. He describes occasional nausea and vomiting. He denies frank hematemesis, melena or hematochezia. He describes anorexia and a 15 pound weight loss over 4 months. The vital signs are stable and his current weight is 65 kg. He denies cigarette or alcohol use. He takes no prescribed medications. He has taken extra strength Tylenol with minimal improvement in epigastric pain. The lungs are clear and the heart has a regular rate and rhythm with no gallops, rubs or clicks. The abdomen is soft and slightly distended with slight epigastric tenderness and with an epigastric mass. The rectal exam shows no masses but is trace positive. 







Even if pt had new-onset reflux sx & discomfort in absence of wt loss  consider malignancy b/c of age, could have an early gastric cancer which is not typically symptomatic until more advanced Workup o EGD w biopsy Endoscopic ultrasound (staging) o CT scan o PET scan o Dx: Gastric cancer Poor prognosis because usually diagnosed late o At diagnosis, ~ 50% have disease beyond locoregional confines.  Only half of them can undergo a potentially curative resection  Symptoms – Weight loss, persistent abdominal pain. o Dysphagia – if proximal   Nausea, early satiety (mass effect or poor distensibility of stomach) Gastric outlet obstruction  More prevalent in Asian countries o Must consider in cases of chronic gastric ulcer o Treatment Multimodality o Surgical resection dictated by location o UNRESECTABLE   

Distant metastasis Invasion of major vascular structures - Aorta, encasement or occlusion of hepatic artery, celiac trunk, proximal splenic artery


Involvement of distant lymph nodes (aorto-caval, pancreatic, mediastinal, portal hepatis) Know who benefits from neoadjuvant chemo vs post-op chemo 

o

A 45 year old male underwent a vagotomy and antrectomy with Bilroth II anastomosis for severe duodenal ulcer 2 years ago. He presents to your office with severe epigastric pain and diarrhea. The pain is very similar to his previous ulcer pain. He has taken OTC Zantacs with minimal improvement in pain. The pain improves slightly with meals. The vital signs are stable. The lungs are clear and the heart shows regular rate and rhythm with no gallops, rubs or clicks. The abdomen is soft and distended but has moderate epigastric tenderness on deep palpation. The abdomen shows no hepatosplenomegaly and no hernias. The bowel sounds are decreased. The rectal exam shows no masses but is trace occult positive. He undergoes an upper gastrointestinal barium examination which reveals multiple mucosal ulcerations in the jejunal limbs. 





DDx for numerous ulcerations in atypical location Zollinger-Ellison syndrome caused by gastrinoma o Endocrine tumor that secretes gastrin  Leads to acid hypersecretion and peptic ulcerations  Presenting sx: abd pain, PUD, severe esophagitis  Diagnosis o Serum gastrin level (> 1000 pg/ml is diagnostic) Secretin stimulation test if gastrin level between 200 – 500 o Localize lesion(s) o CT scan If CT scan negative  endoscopic ultrasound (more sensitive than CT) o If EUS negative  Octreotide scan – detects tumors < 1cm [nuclear medicine] o o If scan negative  exploratory laparotomy  palpate for lesions, look in duodenum, can do intraop ultrasound on pancreas Most of the time, gastrinoma located in Passaro’s triangle (gastrinoma triangle)  



3 points that define triangle 1) confluence of cystic and common bile duct o nd rd 2) junction of 2 and 3 portions of duodenum o 3) junction of neck and body of pancreas o

Treatment Take out proximal duodenum and antrum (location of most of acid-producing cells in stomach) o Billroth II: gastrojejunostomy (stomach and sm bowel sewn together), major complications in o 30% of pts  Roux-en-Y more common Post-gastrectomy complications of Billroth II (LIKELY TO SEE ON NBME!!!)  





Dumping syndrome (Efferent loop syndrome) Immediately after eating have to use restroom d/t incr gastric motility o  eat frequent, small meals, limit carb intake, meds Afferent loop syndrome Afferent loop has bile; efferent loop from stomach to intestine; happens o w twist or scar that prevents bile from draining from afferent limb; obstruction of afferent limb usually requires surgery to correct Bile reflux gastritis (from bile washing back into stomach)

Margin ulceration (ulcer at anastomosis of mucosa) Billroth I: pull duodenum and sew onto stomach, doesn’t work well, many times won’t reach 

o 

Diff scenario: Diagnosis if high calcium + gastrinoma? Think PTH


  

st

MEN 1 Syndrome (pituitary, parathyroid, pancreas) (1 MCC – parathyroid adenoma) MEN 2a: Calcitonin, calcium, catecholamines Medullary carcinoma of thyroid, pheochromocytoma, hyperparathyroidism (2 nd MCC) 

rd

3 MCC: cancer (< 1% parathyroid carcinoma)

Esophagus and Stomach Notes

Recommend Documents