PUD management

1. PEPTIC ULCER DISEASE

2. PEPTIC ULCER DISEASE
• Peptic ulcers are erosions in the GI mucosa that extend through the muscularis mucosae.
• most common symptom-dyspepsia, majority- asymptomatic.
• complicated by bleeding, gastric outlet obstruction, fistulization, and perforation.
• predominant causes- H. pylori and NSAIDs.
• less common mechanisms-ZES, other medication and infectious exposures, radiation therapy,
gastric bypass surgery.
• The incidence and prevalence in developed countries-declining in recent decades, as has the
progression to complicated PUD.
• due to a combination of increased detection and eradication of H. pylori infection, more rational
NSAID use, and environmental factors.
• The lifetime prevalence of PUD is estimated to be 5% to 10%, with an annual incidence of 0.1% to
0.3%

3. Pathogenesis
• decreased defensive factors, increased aggressive factors, or both.
• Protective (or defensive) factors include mucosal bicarbonate
secretion, mucus production, adequate blood flow, growth factors,
cell renewal, and endogenous prostaglandins.
• Damaging (or aggressive) factors include hydrochloric acid secretion,
pepsins, ethanol ingestion, smoking, duodenal reflux of bile, ischemia,
NSAIDs, hypoxia, and, most notably, H. pylori infection.

4. Helicobacter pylori Infection
• Marshall and Warren in Australia in 1984. Nobel Prize in Medicine in 2005.
• It is estimated that half of the world’s population is affected by H. pylori.
• Previously, 80% to 95% of duodenal ulcers and approximately 75% of gastric ulcers were
associated with H. pylori infection – fallen to 50% to 75% in developed countries more
recently with improved diagnosis, treatment, and prevention.
• H. pylori is a spiral-shaped, flagellate, gram-negative bacteria that resides in gastric-type
epithelium within or beneath the mucus layer.
• Mucolytic enzymes both facilitate passage through the mucus layer and protect the bacteria
from mucin’s antibiotic effects.
• Urease-urea into ammonia and bicarbonate, creating an alkaline microenvironment
• The bacteria attach to the gastric epithelial cells by binding to surface adhesions.
• Microaerophilic and can live only in gastric epithelium.
• Heterotopic gastric mucosa in the proximal esophagus, Barrett esophagus, gastric metaplasia
in the duodenum, within a Meckel diverticulum, and in heterotopic gastric mucosa in the
rectum.

5. potential mechanisms
• Production of toxic products that cause local tissue injury-breakdown products from
urease activity (e.g., ammonia), cytotoxins, mucinase, phospholipases, and platelet-
activating factor
• Induction of a local mucosal immune response- attract neutrophils and monocytes,
which then produce numerous proinflammatory cytokines and reactive oxygen
metabolites.
• Increased gastrin levels and changes in acid secretion-basal and stimulated gastrin
levels are significantly increased, secondary to a reduction in somatostatin release
from antral D cells because of infection with H. pylori.
• Gastric metaplasia occurring in the duodenum. protective response to decreased
duodenal pH,allows for H. pylori to colonize these areas of the duodenum, which
causes duodenitis

6. Invasive Tests
Urease assay.
• Endoscopic biopsy specimens should be taken from the gastric body and the antrum and are then tested for
urease.
• Sensitivity> 90%, and specificity is 95% to 100%,
• sensitivity lowered in patients who are taking PPIs, H2 -receptor antagonists, or antibiotics.
Histology.
• histologic visualization of H. pylori using either routine hematoxylin-eosin stains or special stains (e.g., silver,
Giemsa, Genta stains).
• Sensitivity is approximately 95% and specificity is 99%, making histology slightly more accurate than the
urease assay testing.
Culture.
• sensitivity is approximately 80%, and specificity is 100%.
• diagnosis requires 3 to 5 days.
• provide opportunity to perform antibiotic sensitivity testing

7. Noninvasive Tests
Urea breath test.
• The carbon-labeled urea breath test is based on the ability of H. pylori to hydrolyze urea as a result of its
production of urease.
• Both sensitivity and specificity are greater than 95%.
• It is recommended that patients discontinue antibiotics for 4 weeks and PPIs for 2 weeks to ensure optimal
test accuracy.
• The urea breath test is less expensive than endoscopy and samples the entire stomach. .
Stool antigen.
• H. pylori bacteria are present in the stool of infected patients
• stool antigen testing is likely the most cost-effective method for assessing treatment efficacy.
Serology.
• enzyme-linked immunosorbent assay tests for the presence of IgG antibodies to H. pylori
• Antibody titers can remain high for 1 year or longer after eradication; consequently, this test cannot be used
to assess response to therapy.

8. Nonsteroidal Antiinflammatory Drugs
• NSAIDs, including aspirin, are absorbed through the stomach and small intestine and
function as inhibitors of the cyclooxygenase enzymes.
• Cyclooxygenase enzymes - rate-limiting step of prostaglandin synthesis in the GI
tract.
• Prostaglandins (including thromboxane A2) promote gastric and duodenal mucosal
protection from luminal acid and pepsin - increasing mucin and bicarbonate
secretion, increasing blood flow to the mucosal endothelium and promoting
epithelial cell proliferation and migration to the luminal surface.
• NSAID-induced ulcers are more often found in the stomach. Gastritis is not frequently
found with NSAID-induced ulcers. When NSAID use is discontinued, the ulcers usually
do not recur.

9. Gastric Ulcers
• The modified Johnson anatomic classification system for gastric ulcers
60%
15%
20%
10%
5%
• peak incidence occurs in
individuals 55 to 65 years old.
• lower socioeconomic class
• predisposing factors-chronic
alcohol intake, smoking, long-term
corticosteroid therapy, infection,
and intra arterial therapy.
• Ulcer formation is more likely due
to an inflammatory response to
the bacterial infection itself.

10. Clinical Manifestations
• Clinical challenge- differentiation between gastric carcinoma and a benign ulcer.
• This is in contrast to duodenal ulcers, in which malignancy is extremely rare.
• Similar to duodenal ulcers- recurrent episodes of quiescence and relapse.
• They also cause pain, bleeding, and obstruction and can perforate.
• Occasionally, benign ulcers have also been found to result in spontaneous gastrocolic fistulas.
Surgical intervention is required in patients who develop complications from gastric ulcer disease.
• Most frequent - perforation.
• Most perforations occur along the anterior aspect of the lesser curvature.
• In general, older patients have increased rates of perforations, and larger ulcers are associated with higher
morbidity and mortality.
• Similar to duodenal ulcers, gastric outlet obstruction can also occur in patients with type II or III gastric ulcers.
However, one must carefully differentiate between benign obstruction and obstruction secondary to
carcinoma.

13. Duodenal Ulcer
The only requirements are acid and pepsin secretion in combination with infection by
H. pylori or ingestion of NSAIDs.
Clinical Manifestations
• Abdominal pain.
• Mid epigastric,well localized
• frequently relieved by food.
• may be episodic, worse during periods of emotional stress.
• When the pain becomes constant, this suggests that there is deeper penetration of
the ulcer.
• Referral of pain to the back is usually a sign of penetration into the pancreas
• diffuse peritoneal irritation is the result of free perforation.

14. Diagnosis
• laboratory studies include complete blood count, liver chemistries, serum creatinine, serum amylase, and
calcium levels.
• A serum gastrin level should also be obtained in patients with ulcers that are refractory to medical therapy or
require surgery.
Upper gastrointestinal radiography
• barium within the ulcer crater, usually round or oval and may or may not be surrounded by edema. location
and depth of penetration of the ulcer and the extent of deformation from chronic fibrosis.
Flexible upper endoscopy.
• Endoscopy is the most reliable method for diagnosing gastric and duodenal ulcers.
• ability to sample tissue to evaluate for malignancy and H. pylori infection.
• therapeutic purposes in the setting of GI bleeding or obstruction.
• Larger ulcers and ulcers with irregular or heaped-up edges are more likely to harbor cancers.
• Multiple biopsy-all four quadrants if possible.
• Helicobacter pylori testing. Gold standard for diagnosis of H. pylori is mucosal biopsy performed during upper
endoscopy.

15. Medical Treatment
Antiulcer drugs fall into three broad categories—
• drugs targeted against H. pylori,
• drugs that reduce acid levels by decreasing secretion or chemical neutralization,
• drugs that increase the mucosal protective barrier.
• In addition to medications, lifestyle changes, such as smoking cessation, discontinuing NSAIDs and aspirin, and avoiding coffee and alcohol, help promote
ulcer healing.
Antacids-oldest form of therapy.
• reduce gastric acidity by reacting with hydrochloric acid, forming a salt, and raising the gastric pH. Antacids differ greatly in their buffering ability, absorption,
and side effects.
• Magnesium antacids-best buffers, significant diarrhea,
• phosphorus can occasionally result in hypophosphatemia and sometimes constipation.
• Aluminum hydroxide can bind growth factors and may increase their delivery to injured mucosa.
Sucralfate.
• aluminum salt of sulfated sucrose that dissociates under the acidic conditions in the stomach. sucrose polymerizes and bindsto the ulcer crater to produce a
protective coating that can last for 6 hours.
H2 -receptor antagonists.
• inhibit H 2 receptors on parietal cells.
• All undergo hepatic metabolism and are excreted by the kidney.
• Famotidine is the most potent
• cimetidine is the weakest.
• duodenal ulcer healing rates of 70% to 80% after 4 weeks of therapy and 80% to 90% after 8 weeks.

16. Proton pump inhibitors
• most potent antisecretory agents are PPIs.
• irreversibly bind and inhibit the hydrogen-potassium ATPase on the
parietal cell.
• provide a more complete and prolonged inhibition of acid secretion
than H2 receptor antagonists.
• PPIs require an acidic environment within the gastric lumen to
become activated.
• Maintenance PPI therapy is considered in patients with large (>2 cm)
ulcers, refractory or frequent PUD, those with failed H. pylori
eradication, or patients requiring continued NSAID use.

17. Treatment of Helicobacter pylori infection.
• Current therapy is twofold in its approach, combining antibiotics against H.
pylori with acid-reducing medications.
• The primary goal of the PPIs is to promote short-term healing by reducing
pathologic acid levels and improve symptoms.
• H. pylori eradication helps with initial healing, but its primary efficacy is in
preventing recurrence.
• Eradication rates- decreasing, due to increased prevalence of antibiotic-
resistant strains of H. pylori
• 20% of patients fail initial therapy.
• monitoring for infection eradication with a urea breath test, stool antigen, or
repeat endoscopy with biopsy at 4 to 6 weeks after therapy

18. • 14 day course of triple therapy
• 10- to 14-day course of bismuth quadruple
therapy.
• Side effects-diarrhea, nausea and vomiting,
rash, and altered taste.
• For the 20% with refractory disease, new
antibiotics, metronidazole and tetracycline
• quadruple therapy with the addition of
bismuth is recommended if not previously
used.
• Levofloxacin and rifabutin triple therapies are
also salvage therapeutic options.

19. Complicated Ulcer Disease
• most patients with ulcers being treated and cured medically.
• The surgeon’s role -hemorrhage, perforation, and obstruction

20. Hemorrhage
• relatively common,with an annual incidence of approximately 19 to 57 cases per 100,000
• present with hematemesis, melena, or both.
• The use of NSAIDs is the major risk factor for peptic ulcer bleeding,
• H. pylori testing can have decreased sensitivity both with active bleeding as well as PPI use
The initial approach
• Large-bore IV access, rapid restoration of intravascular volume with fluid and blood products, and close
monitoring of vital signs
• IV PPI during their initial evaluation.
• The role of nasogastric (NG) lavage- useful as a predictor of high-risk patients and as an aid for later
endoscopic intervention.
Upper flexible endoscopy
• for diagnosis and for therapeutic intervention.
• endoscopy within 24 hours.
• All patients undergoing endoscopic examination should be tested for H. pylori status.

21. For high-risk patients requiring intervention
• endoscopic control-thermal coagulation, hemoclips, or sclerosant injection.
• Epinephrine injection monotherapy is no longer recommended given the high rebleeding rates, but epinephrine can be
added as a second modality to other endoscopic therapies.
• Patients who have a second episode of bleeding after initially successful endoscopic therapy are typically treated with
repeat endoscopy.
• Patients with recurrent bleeding can be considered for interventional angiography with transarterial embolization if
they are hemodynamically stable and those resources are available.
• Embolization can still be useful, especially for patients who are poor surgical candidates based on other medical
comorbidities.
• 5% to 10% of patients have persistent bleeding that requires surgical intervention.

22. Indications for surgical intervention in these patients include:
• failed endoscopic treatment
• hemodynamic instability
• continued slow bleeding with transfusion requirement.
The vessel most likely to be bleeding is the gastroduodenal artery
because of erosion from a posterior ulcer.

23. • Kocher maneuver
• Anterior wall of the duodenal bulb-longitudinally,
• The gastroduodenal artery is oversewn, with a
three-point U stitch technique
• The course of the common bile duct can be
identified by inserting a probe through the ampulla
of Vater transduodenally or performing an
intraoperative cholangiogram.
• The duodenotomy is closed transversely

24. Perforation
• sudden-onset, severe epigastric pain,
• which can lessen a few hours after initial onset as the body tries to wall off the perforation.
• CXR-free air
• localized peritoneal signs on examination.
• Patients with more widespread spillage have diffuse peritonitis.
• If no free air noted on x-ray, CT scan with oral contrast.
• Initial empiric antibiotic therapy should cover enteric gram-negative rods, anaerobes, and
mouth flora and should be based on local susceptibility patterns.
• Perforation complicates 2% to 10% of PUD
• highest mortality rate of any complication of ulcer -30%

26. • The perforation usually can easily be accessed through an upper midline
incision.
• Perforations smaller than 1 cm can generally be closed primarily and
buttressed with a well-vascularized omentum.
• For larger perforations or ulcers with fibrotic edges that cannot be brought
together without tension, a Graham patch repair with healthy omentum is
performed.
• Multiple stay sutures are placed that incorporate healthy tissue on the
proximal and the distal sides of the ulcer.
• The omentum is placed underneath these sutures, and they are tied to secure
it in place and seal the perforation

28. • For very large perforations (>3 cm), control of the duodenal defect can be
difficult.
• The defect should be closed by the application of healthy tissue, such as
omentum or jejunal serosa from a Roux-en-Y type limb.
• In such cases, a pyloric exclusion is typically performed by oversewing the
pylorus using absorbable suture or stapling across it using a noncutting linear
stapler.
• A gastrojejunostomy is created to bypass the duodenum in a Billroth II or
Roux-en-Y fashion.
• Over several weeks, the pyloric exclusion stitches or staples give way,
restoring normal GI anatomy after the perforation site has been given time to
heal.
• Alternatively, a duodenostomy tube can be placed through the perforation
with wide peritoneal drainage. An alternative in this difficult situation is
antrectomy and a Billroth II or Roux-en-Y

30. Gastric outlet obstruction
• Acute inflammation of the duodenum or pylorus can lead to mechanical
obstruction
• Early satiety, anorexia, weight loss, nausea, and vomiting.
• Prolonged vomiting- dehydrated and develop hypochloremic, hypokalemic
metabolic alkalosis secondary to the loss of gastric juice rich in hydrogen and
chloride.
• Chronic inflammation leads to recurrent episodes of injury and healing,
ultimately leading to fibrosis, scarring, and stenosis of the outflow tract.
• The stomach can become massively dilated in this setting and lose its muscular
tone.
• Marked weight loss and malnutrition are common.

31. Initial management
• gastric decompression with NG tube placement and correction of fluid and
electrolyte abnormalities.
• Nutritional status should be assessed as these patients often present
malnourished.
Upper endoscopy should be performed to rule out a malignancy and assess for
H. pylori infection.
• Endoscopic dilation (with or without stenting) and
• H. pylori eradication are the mainstays of initial therapy.
• Novel endoscopic techniques, including ultrasound-guided gastric bypass and
peroral endoscopic myotomy, are also being explored.
• Patients with refractory obstruction are best managed with primary
antrectomy and reconstruction along with vagotomy.

33. • Another surgical option, especially when there is significant
inflammation or scarring present, is vagotomy with a drainage
procedure, typically either a Jaboulay gastroduodenostomy or a
gastrojejunostomy.

34. Intractable peptic ulcer disease
• Intractability is defined as failure of an ulcer to heal after an initial trial of 8 to
12 weeks of therapy or if patients relapse after therapy has been discontinued
• it is estimated to occur in 5% to 10% of patients.
• Benign gastric ulcers that persist must be evaluated for malignancy as well as
other less common sources of ulceration such as ZES, Crohn disease, or
sarcoid.
• For any intractable ulcer, adequate duration of antisecretory therapy, H. pylori
eradication, and elimination of NSAID use must be confirmed.
• fasting serum gastrin level should be obtained to rule out gastrinoma.

35. Surgical Procedures for Peptic Ulcers
• Elective operative intervention for PUD has become rare as medical therapy
has improved.
• The goal of operative ulcer therapy is to reduce gastric acid secretion.
This can be accomplished by
• removing vagal stimulation via vagotomy,
• gastrin-driven secretion by performing an antrectomy,
• decreasing the number of parietal-cells with a subtotal gastrectomy, or a
combination procedure.
• Vagotomy decreases peak acid output by approx 50%,
• vagotomy + antrectomy decreases peak acid output by approx 85%

37. Truncal vagotomy
division of the left and right vagus nerves above the hepatic and
celiac branches, just above the GE junction.
Drainage procedures- to avoid gastric
stasis

38. Heineke-Mikulicz pyloroplasty
(Weinberg modification)

39. • When the duodenal bulb is scarred,Finney pyloroplasty or Jaboulay
gastroduodenostomy may be a useful alternative.
• Significant scarring or inflammation may necessitate a
gastrojejunostomy.
• bile reflux may be more common after gastroenterostomy, and
• diarrhea is more common after pyloroplasty.
• The incidence of dumping syndrome is similar for both.

40. Selective vagotomy
• main right and left vagus nerves just distal to the celiac and hepatic
branches,
• pyloric drainage procedure is also performed.
• higher ulcer recurrence rates than truncal vagotomy,
• largely been abandoned.

41. Highly selective vagotomy
• AKA parietal cell vagotomy or proximal gastric vagotomy.
• divides only the vagus nerves supplying the acid-producing portion of the stomach
within the corpus and fundus.
• preserves the vagal innervation of the gastric antrum and pylorus, so there is no need
for routine drainage procedures.
• the nerves of Latarjet are identified anteriorly and posteriorly, and the crow’s feet
innervating the fundus and body of the stomach are divided
• divided up until a point approximately 7 cm proximal to the pylorus, the area in the
vicinity of the gastric antrum.
• Superiorly, division of these nerves is carried to a point at least 5 cm proximal to the
GE junction on the esophagus
• The criminal nerve of Grassi- represents a very proximal branch of the posterior trunk
of the vagus, avoid missing this branch- predisposition for ulcer recurrence

42. Antrectomy
• requires reconstruction of GI continuity that can be accomplished by
a gastroduodenostomy (Billroth I procedure or gastrojejunostomy
(either Billroth II procedure or Roux-en-Y reconstruction).
Partial gastrectomy
• Partial, or subtotal, gastrectomy removes both gastrin-producing and
acid-secreting cells. Reconstruction with Billroth II or Roux-en-Y being
the most commonly used.

43. Zollinger-Ellison syndrome
• clinical triad- gastric acid hypersecretion, severe PUD, and gastrin-producing
neuroendocrine tumors (NETs; gastrinomas).
• The islet cell-gastrin
• Abdominal pain and PUD are the hallmarks - more than 80% of patients.
• diarrhea, weight loss, steatorrhea, and esophagitis.
• Endoscopy -prominent gastric rugal folds, reflecting the trophic effect of
hypergastrinemia on the gastric fundus.
• 20% to 30% of patients have ZES as part of multiple endocrine neoplasia type
1, an autosomal dominant syndrome.
• serum parathyroid hormone, ionized calcium, and prolactin levels

44. Diagnosis
• Most- elevated fasting serum gastrin levels (>200 pg/mL),
• Values higher than 1000 pg/ mL are diagnostic.
• PPI use, H. pylori infection, and renal failure - elevation of fasting serum
gastrin
• In patients with gastrin levels in this equivocal range, the most sensitive
diagnostic test is the secretin-stimulated gastrin level.
• Serum gastrin samples are measured before and after IV secretin
administration. An increase in the serum gastrin level of >200 pg/mL above
basal levels is suggestive of gastrinoma
• The best initial imaging study to localize- triple-phase CT or MR imaging (MRI)
of the abdomen.
• <1 cm in diameter, small liver metastases- somatostatin receptor scintigraphy
or EUS.

45. Treatment
• Acid suppression therapy -high-dose PPI.
• Medical management- indicated preoperatively and for patients with
metastatic or unresectable gastrinoma.
• The next step in management is localization and staging of the tumor.

46. • Localized gastrinomas should be resected- long-term cure rates are only about
50%.
• Once the tumor is located intraoperatively, a resection according to oncologic
principles (rather than a tumor enucleation) with at least 10 lymph nodes
removed.
• Small case series suggest that patients who are not operative candidates-
symptom palliation and slower disease progression with radiation therapy.
• Patients with tumor recurrence or metastatic disease - somatostatin analogs
and/or chemotherapy (streptozocin/doxorubicin or temozolomide-based
regimen).
• For patients with liver metastases- liver-directed therapies (radiofrequency
ablation, cryoablation, embolization, resection, or transplantation)

47. Postgastrectomy syndromes
• numerous physiologic derangements caused by loss of reservoir
function, interruption of the pyloric sphincter mechanism, and vagal
nerve transection.
• The GI and cardiovascular symptoms may result in disorders
collectively referred to as postgastrectomy syndromes.
• Approximately 20% to 25% of patients who undergo surgery for PUD
subsequently develop some degree of postgastrectomy syndrome,
although this frequency is much lower in patients who undergo highly
selective vagotomy.

48. Dumping Syndrome
• combination of both GI and vasomotor symptoms due to rapid postprandial gastric
emptying.
• GI symptoms include abdominal pain, early satiety, nausea/vomiting, diarrhea, and
bloating.
• Vasomotor systemic symptoms include diaphoresis, tachycardia, palpitations,
headache, and syncope.
• more common after partial gastrectomy with the Billroth II reconstruction.
Early dumping
• occurs within 30 minutes of a meal and is a result of rapid passage of high osmolarity
food from the stomach into the small intestine.
• Gastrectomy/interruption of the pyloric sphincter mechanism, prevents the stomach
from preparing its contents and delivering them to the proximal bowel in the
form of small particles in isotonic solution.
• Hypertonic food bolus induces a rapid shift of extracellular fluid into the intestinal
lumen to achieve isotonicity- luminal distention

49. Late dumping
• occurs 1 to 3 hours after a meal and is less common.
• carbohydrates being delivered rapidly into the proximal intestine.
• they are quickly absorbed- hyperglycemia- the release of large
amounts of insulin to control the increasing blood sugar level.
• An overcompensation - profound hypoglycemia
• hypoglycemia activates the adrenal gland to release catecholamines,
which results in diaphoresis, tremulousness, light-headedness,
tachycardia, and confusion.

50. Tx
• Dietary measures - avoiding foods containing large amounts of sugar,
frequent feeding of small meals rich in protein, fats, and fiber, and
separating liquids from solids during a meal.
• pharmacologic treatments directed at specific symptoms can be
effective, such as tincture of opium or imodium for diarrhea and
meclizine for nausea.
• Anticholinergics can slow gastric emptying and treat spasms.
• Octreotide – increase intestinal transit time and inhibit gastric
emptying

52. Metabolic Disturbances
• most common metabolic -after gastrectomy is anemia.
• Anemia is related to iron deficiency (more common) or impairment in vitamin B12
metabolism. More than 30% have iron deficiency anemia.
• Vitamin deficiency occurs secondary to poor absorption of dietary vitamin B12
because of the lack of intrinsic factor.
• Patients undergoing subtotal gastrectomy should be placed on lifelong vitamin B12
supplementation
• Osteoporosis and osteomalacia- deficiencies in calcium.
• If fat malabsorption is also present, the calcium malabsorption is aggravated further
because fatty acids bind calcium.
• Patients with Billroth II or Roux-en-Y reconstruction that bypasses the duodenum
should also receive supplementation of the fat-soluble vitamins (vitamins A, D, E, and
K).

53. Small Stomach Syndrome
• decreased reservoir present after a large partial gastrectomy.
• Patients experience pain, either abdominal or chest, following ingestion of a meal
and may also suffer from nausea, vomiting, and weight loss.
• decreased distensibility of the proximal stomach. In a patient with a subtotal
gastrectomy, the vagal nerves are transected higher on the stomach which prevents
receptive relaxation of the stomach
• Tx- small frequent feedings. If patients continue to be intolerant of meals, liquid
enteral nutrition can be provided orally, or if need be, through a distal feeding tube.
• In the patients who have a syndrome that is refractory to dietary changes and in the
patients suffering from chronic malnutrition, surgery can be considered to increase
the reservoir size.

55. Afferent Loop Syndrome
• partial obstruction of the afferent limb, which is then unable to empty its contents.
• After obstruction of the afferent limb, pancreatic and hepatobiliary secretions accumulate
within the limb, resulting in its distention, which causes epigastric discomfort and cramping.
• The intraluminal pressure increases enough to empty the contents of the afferent loop
forcefully into the stomach, resulting in projectile bilious vomiting that offers immediate
relief of symptoms.
• obstruction for a long time- blind loop syndrome- bacterial overgrowth occurs in the static
loop, and the bacteria bind with vitamin B12 and deconjugated bile acids; this results in a
systemic deficiency of vitamin B12, fat malabsorption, and deficiency in fat-soluble vitamins.
• Radionuclide studies imaging the hepatobiliary tree have also been used with some success in
diagnosing this syndrome.
• Surgical correction is indicated for this mechanical problem to prevent bowel necrosis or
duodenal stump blowout.

56. • A long afferent limb is usually the underlying problem, so treatment involves the
elimination of this loop. Remedies include conversion of the Billroth II
construction into a Billroth I anastomosis, enteroenterostomy below the
afferent and efferent loops, and conversion to a Roux-en-Y reconstruction.

57. Roux Limb Syndrome
• dysfunctional motility in the roux limb following roux-en-Y reconstructions.
• This dysmotility is actually fairly common after a Rroux-en-Y reconstruction,
occurring in 20% to 40% of the patients. However, only a small portion of
patients actually become symptomatic.
• Patients may present with vomiting, epigastric pain and bloating, and weight
loss.
On upper endoscopy or contrast studies,
• the gastric pouch and roux limb are dilated, but there is no evidence of an
identifiable mechanical obstruction. When the vagus is transected either by
vagotomy or proximal gastrectomy, the duodenal pacer is denervated, thereby
leading to atony of the small bowel as well, which is more prominent in the
roux limb

58. • Patients can respond to prokinetics like erythromycin which works on
the motilin receptors of the small bowel.
• Metoclopramide less effective than erythromycin.
• Behavioral modifications that have some efficacy include the
consumption of small frequent meals, or increasing oral intake of
fluids with meals.
Surgery for unrelenting symptoms.
• conversion to a Billroth II anastomosis, performing a larger gastric
(subtotal) resection, or reconstructing the roux limb either in the
standard fashion or in the uncut or loop bypass procedure

60. Efferent Loop Obstruction
• rare
• more than 50% of cases occur within the first postoperative month.
• left upper quadrant abdominal pain that is colicky in nature, bilious
vomiting, and abdominal distention.
• The diagnosis is usually established by an upper GI series or CT with
oral contrast, with failure of contrast to enter the efferent limb.
• Operative intervention is almost always necessary and consists of
reducing the retroanastomotic hernia if this is the cause of the
obstruction and closing the retroanastomotic space to prevent
recurrence of this condition.

61. Alkaline Reflux Gastritis
• Alkaline Reflux Gastritis After gastrectomy, reflux of bile is common.
• severe epigastric abdominal pain accompanied by bilious vomiting and weight
loss.
• A technetium biliary scan can be used to demonstrate reflux of bile into
the stomach.
• Upper endoscopy demonstrates friable, beefy red mucosa.
• Most patients with Billroth II anastomosis.
• Medical therapies not shown any consistent benefit.
• For patients with intractable symptoms, the surgical procedure of choice is
conversion of the Billroth II anastomosis into a Roux-en-Y gastrojejunostomy,
in which the Roux limb has been lengthened to > 40 cm

62. Gastric Atony
• Gastric emptying is delayed after truncal and selective vagotomies but not after
a highly selective vagotomy.
• With selective or truncal vagotomy, patients lose their antral pump function and
have a reduction in the ability to empty solids.
• In contrast, emptying of liquids is accelerated due to the loss of receptive relaxation
in the proximal stomach.
• feeling of fullness and, occasionally, abdominal pain. In still rarer cases, it may be
associated with a functional gastric outlet obstruction.
• confirmed by scintigraphic assessment of gastric emptying.
• Endoscopic examination of the stomach also needs to be performed to rule out an
anastomotic obstruction.
• prokinetic agents such as metoclopramide and erythromycin.
• In rare cases of persistent gastric atony refractory to medical management,
gastrectomy may be required.

63. Postvagotomy diarrhea
• Diarrhea is seen in varying degrees following vagotomy.
• It is estimated that 30% to 70% of the patients will report an increased frequency of bowel movements
following truncal vagotomy or selective vagotomy
• Bacterial overgrowth- jejunum becomes colonized with aerobic and anaerobic bacteria following vagotomy
due to hypoacidity and stasis’
• Truncal vagotomy denervates the small intestine with a resultant decreased tone in the ileocecal valve or
alters the gastric and duodenal pacemaker.
• Patients present with watery diarrhea, often with significant urgency, with no correlation to meals.
• Patients can subsequently go on to develop hypovolemia, malnutrition, and weight loss.
• In most patients, the diarrhea resolves 3 to 8 months postoperatively. Dietary changes including increasing
soluble fiber, decreasing carbohydrates and lactose consumption, and eliminating caffeine
• Cholestyramine- decreases severity of diarrhea