Medical and surgical management of peptic ulcer diseases. With complications of surgical management.

1. Management of PUD
DR MAHESH MANI ADHIKARI
General Surgery Resident
DH KUSMS

2. Diagnosis
• Routine laboratory studies
• Complete blood count
• Liver chemistries;
• Serum creatinine, serum amylase, and calcium levels.
• Serum gastrin level -refractory to medical therapy or require surgery
• Erect chest radiograph - ruling out perforation.
• The two principal means of diagnosing duodenal ulcers are
• Upper GI radiography
• Flexible upper endoscopy

3. • Flexible upper endoscopy
• Most reliable method
• Ability to sample tissue to evaluate for malignancy
and H. pylori infection
• Therapeutic purposes in the setting of GI bleeding
or obstruction
• Visual diagnosis of more than 90% of peptic ulcers
• Multiple Biopsy is recommended
• Larger ulcers and ulcers with irregular or heaped
edges are more likely to harbor cancers

5. Helicobacter pylori testing
• Gold standard for diagnosis- mucosal biopsy
performed during upper endoscopy
• Invasive Tests
• Urease assay
• Sensitivity >90%, and specificity is 95%
- 100%,
• Rapid urease test kits are commercially
available and can detect urease in
gastric biopsy specimens within 1 hour
with a similar level of diagnostic
accuracy

6. • Histology.
• Sensitivity ~95% and specificity 99%,
slightly more accurate than the urease
assay testing
• Culture.
• Gastric mucosa obtained at endoscopy
• Not widely available, and is relatively
expensive, and diagnosis requires 3 to 5
days
• Opportunity to perform antibiotic
sensitivity testing on isolates,

7. • Noninvasive Tests
• Serology.
• Presence of IgG antibodies to H. pylori.
• 90% sensitivity , specificity rate between 76% and 96%,
• Urea breath test.
• 13c isotopes
• Sensitivity and specificity >95%.
• It is recommended that patients discontinue antibiotics for 4 weeks and PPIs for
2 weeks to ensure optimal test accuracy.
• In evaluating treatment efficacy, best to perform this test 4 weeks after therapy
is completed to avoid false-negative results

8. • Stool antigen
• Use monoclonal antibodies to H. Pylori antigens
• Sensitivities >90% and sensitivities of 86% to 92%
• Likely the most cost-effective method for assessing treatment efficacy.

9. • Upper gastrointestinal radiography.
• demonstration of barium within the ulcer crater,
• usually round or oval and may or may not be
surrounded by edema
• single-contrast radiographic techniques- 50% of
duodenal ulcers may be missed
• double-contrast studies, 80% to 90% of ulcer
craters can be detected.
• CT scan more sensitive in detecting perforations

10. Treatment
Medical management
• Three broad categories—
• Drugs targeted against H. Pylori,
• Drugs that reduce acid levels by decreasing secretion or chemical neutralization, and
• Drugs that increase the mucosal protective barrier
• The focus of therapy is on eradication of the bacteria.
• In addition to medications,
• Lifestyle changes, such as smoking cessation, discontinuing nsaids and aspirin, and
avoiding coffee and alcohol, help promote ulcer healing

11. • Antacids
• Oldest form
• Reduce gastric acidity by reacting with hydrochloric acid
• Magnesium antacids tend to be the best buffers
• Cause significant diarrhea
• Most effective when ingested 1 hour after a meal because they can be retained in
the stomach and exert their buffering action for longer periods

12. • Sucralfate
• Structurally related to heparin
• Does not have any anticoagulant effects
• Aluminum salt of sulfated sucrose that dissociates under the acidic conditions -
sucrose polymerizes and binds to protein in the ulcer crater to produce a protective
coating
• That can last for 6 hours.
• 4 to 6 weeks results in duodenal ulcer healing

13. • H2 receptor antagonists
• Structurally similar to histamine
• Famotidine is the most potent, and cimetidine is the weakest
• Duodenal ulcer healing rates of 70% to 80% after 4 weeks of therapy and 80% to 90%
after 8 weeks.

14. • Proton pump inhibitors
• Most potent antisecretory agents
• More complete and prolonged inhibition of acid secretion than H2 receptor
antagonists
• More effective during the day
• Healing rate of 85% at 4 weeks and 96% at 8 weeks
• Produce more rapid healing of ulcers than standard H2 receptor antagonists
• Generally replaced H2 receptor antagonists as primary therapy for PUD in the
presence or absence of H. Pylori infection.
• Require an acidic environment within the gastric lumen to become activated

15. • Treatment of helicobacter pylori infection
• Combining antibiotics against H. pylori with antacid medications.
• Eradication of H. pylori has shown recurrence rates of 2%,
• With initial healing rates of 90%.
• Monitoring for infection eradication with
• A urea breath test, stool antigen, or repeat endoscopy with biopsy at 4 to 6
weeks after therapy is important,
• And many patients will require further treatment with alternative regimens.

16. • Treatment of H. Pylori–
positive peptic duodenal
ulcer disease is triple
therapy
• Triple therapy includes a PPI
and two antibiotics,

17. Surgical treatment for Uncomplicated Peptic ulcers
• Rare as medical therapy has become more effective
• Goal - reduce gastric acid secretion
• Accomplished by removing
• Vagal stimulation via vagotomy,
• Gastrin-driven secretion by performing an antrectomy, or both.
• Vagotomy decreases peak acid output by approximately 50%, whereas vagotomy plus
antrectomy decreases peak acid output by approximately 85%.

18. VAGOTOMY
• Rationale - elimination of direct cholinergic stimulation of
gastric acid secretion
• TRUNCAL VAGOTOMY
• Division of the anterior and posterior vagal trunks
after they emerge below the diaphragm.

19. • SELECTIVE VAGOTOMY
• Vagus nerves are carefully isolated from the
esophagus and
• Divided beyond the point where they give
of branches to the liver and to the celiac
ganglion

20. • PROXIMAL GASTRIC VAGOTOMY
• Also known as highly selective vagotomy, selective
proximal vagotomy, or parietal cell vagotomy
• Control the cephalic phase of secretion
• While maintaining
• The celiac branch,
• The hepatic branch, and
• The anterior and posterior nerves of latarjet to
the distal antrum

21. • Vagal denervation - upper two-thirds of the
stomach,
• While innervation is left intact to the lower
third as well as to the biliary tract and small
intestine.
• Dissection is usually started about 6 cm
from the pylorus on the anterior wall of the
stomach

22. DRAINAGE PROCEDURES
• In any patient who undergoes a truncal, selective, or supradiaphragmatic vagotomy
• To facilitate gastric emptying
• Two categories:
• Pyloroplasties and gastrojejunostomy

23. • PYLOROPLASTY
• Heineke-Mikulicz Pyloroplasty

24. • Finney pyloroplasty

25. • GASTROJEJUNOSTOMY
• First performed alone in 1881
• Two problems:
• Marginal ulcers (because no vagotomy was
performed) and
• Vomiting
• Commonly indicated - duodenal obstruction and the
duodenal bulb is so scarred, inflamed, and edematous
that pyloroplasty is not safe or is excessively technically
demanding.
• Procedure of choice when vagotomy and drainage is
being performed laparoscopically.
• To reduce the incidence of marginal ulcers
• Lifelong PPI can significantly reduce this complication
without the morbidity associated with vagotomy

26. GASTRIC RESECTION PROCEDURES
• Common gastric resection performed for intractable duodenal ulcer is antrectomy (40%
distal gastrectomy) that is combined with a TV or an SV
• Reduced by nearly 80%.

27. • PARTIAL GASTRECTOMY WITH
BILLROTH I RECONSTRUCTION
• Antrectomy removes the acid-secreting
portion of the stomach, which contains
the G cells that are responsible for
secreting gastrin.
• 35% of the distal stomach should be
removed
• Removing 45% of the lesser curve
(approximately 7 cm from the pylorus

28. • PARTIAL GASTRECTOMY WITH A BILLROTH II
RECONSTRUCTION

29. • PARTIAL GASTRECTOMY WITH A ROUX-EN-Y
RECONSTRUCTION
• Reconstruction with the roux-en-y
gastrojejunostomy is performed by
• Dividing the jejunum approximately 40 cm
distal to the ligament of treitz.
• Mesentery is divided in a straight line down to
the origin to allow more mobility of the roux
limb.
• A 50- to 70-cm roux limb is created and a side-
to-side jejunojejunal anastomosis is constructed

30. Sequelae of Peptic Ulcer Surgeries
• Recurrent ulceration
• Small stomach syndrome
• Early and Late Dumping Syndrome
• Nutritional consequences
• Afferent loop syndrome
• Efferent loop syndrome
• Malignant Transformation
• Gall stone formation

31. Early and Late Dumping Syndrome
EARLY DUMPING SYNDROME LATE DUMPING SYNDROME
Abdominal and vasomotor symptoms Reactive hypoglycemia
~10% patients of gastrectomy/ vagotomy and drainage ~5%
Precipitated and aggravated by carb high food with
fluids
Precipitated by food high in carbohydrate,
exacerbated by exercise
T/t: dietary manipulation, small regular meals with
low carb and high fat and protein
Somatostatin analogue before meals
Occasionally- revision surgery: ge take diwn, repair
pyloropasty, antrectomy with Roux-En- Y
T/T: octretide very effective

32. Afferent Loop Syndrome
• Partial obstruction of the afferent limb
• Pancreatic and hepatobiliary secretions accumulate within the limb, resulting in its
distention,
• Causes epigastric discomfort and cramping
• Eventually - empty the contents into the stomach, resulting in bilious vomiting that offers
immediate relief of symptoms
• If present for a long time, it can also be aggravated by the development of the 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, with the development of
megaloblastic anemia.

33. • Failure to visualize the afferent limb on upper endoscopy is suggestive of the diagnosis.
• Radionuclide studies imaging the hepatobiliary tree have also been used with some
success in diagnosing this syndrome
• Surgical correction is indicated
• Long afferent limb is usually the underlying problem
• Remedies include
• Conversion of the billroth II construction into a billroth I anastomosis,
• Enteroenterostomy below the stoma, and creation of a roux-en-y procedure.
• Marginal ulceration from the diversion of duodenal contents from the gastroenteric
stoma is a potential complication of the roux-en-y conversion

34. Efferent Loop Obstruction
• Rare; may occur at any time
• >50% of cases do so within the first postoperative month
• Initial complaints
• left upper quadrant abdominal pain – colicky
• bilious vomiting, and
• abdominal distention
• diagnosis - GI contrast study of the stomach -failure of oral contrast to enter the efferent
limb
• Operative intervention is almost always necessary, 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.

35. Alkaline Reflux Gastritis
• After gastrectomy - a billroth II anastomosis, reflux of bile is common
• Severe epigastric abdominal pain accompanied by bilious vomiting and weight loss
• HIDA scans usually demonstrate biliary secretion into the stomach and sometimes into
the esophagus
• Upper endoscopy demonstrates friable, beefy red mucosa.
• Therapy is directed at relief of symptoms- medical therapies
• 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 more than 40 cm.

36. Gastric Atony
• Gastric emptying is delayed after truncal and selective vagotomies
• But not after a highly selective or parietal cell vagotomy
• Patients lose their antral pump function and have a reduction in the ability to empty
solids
• Emptying of liquids is accelerated because of loss of receptive relaxation in the proximal
stomach, which regulates liquid emptying.
• Persistent gastric stasis that results in retention of food within the stomach for several
hours
• Rarer cases, it may be associated with a functional gastric outlet obstruction
• Diagnosis - scintigraphic assessment of gastric emptying

37. • Other causes of delayed gastric emptying
• Diabetes mellitus, electrolyte imbalance, drug toxicity, and neuromuscular disorders,
• A mechanical cause of gastric outlet obstruction,
• Postoperative adhesions, afferent or efferent loop obstruction, and internal
herniations, must be ruled out.
• Endoscopic examination - to rule out any anastomotic obstructions
• Functional gastric outlet obstruction and documented gastroparesis- pharmacotherapy
is generally used.
• The agents most commonly used are prokinetic agents such as
• Metoclopramide and erythromycin.
• In rare cases of persistent gastric atony refractory to medical management, gastrectomy
may be required.

38. Metabolic Disturbances
• Anemia –
• Related to iron deficiency (more common)
• Or impairment in vitamin B12 metabolism
• More than 30%
• Related to a combination of decreased iron intake, impaired iron absorption, and
chronic blood loss
• Iron supplements to the patient’s diet corrects this metabolic problem

39. • Megaloblastic anemia from vitamin B12 deficiency only rarely
• Develops after partial gastrectomy but is dependent on the amount of stomach
removed
• Because of the lack of intrinsic factor.
• Patients undergoing subtotal gastrectomy should be placed on life-long vitamin
b12 supplementation.
• If a patient develops a macrocytic anemia, serum vitamin b12 levels should be
determined and, if abnormal, treated with long-term vitamin b12 therapy.

40. • Osteoporosis and osteomalacia-
• Deficiencies in calcium .
• If fat malabsorption is also present, the calcium malabsorption is aggravated further
because fatty acids bind calcium
• Increases with the extent of gastric resection
• Associated with a billroth II gastrectomy.
• Develops approximately 4 to 5 years after surgery.
• Treatment
• Calcium supplements (1 to 2 g/day) in conjunction with vitamin D (500 to 5000 U
daily).
• 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).

41. Complicated Ulcer Disease
• PERFORATED DUODENAL ULCERS:
• Typically complain of sudden-onset, frequently severe epigastric pain
• Have free air visible on the chest radiograph
• Have localized peritoneal signs on examination.
• More widespread spillage have diffuse peritonitis
• Small subset - the perforation may seal spontaneously;
• However, operative intervention is required in almost all cases

42. • Highest mortality rate of any complication of ulcer disease, approaching 15%.
• And increases by ~2.4% with every hour elapsed from presentation to surgical
intervention.
• Emergent surgical intervention
• First portion of the duodenum
• T/t:
• Adequate resuscitation and analgesia
• Surgery:
• Accessed through an upper midline incision
• Perforations smaller than 1 cm can generally be closed primarily and buttressed
with a wellvascularized omentum.
• Graham patch repair with a tongue of healthy omentum is performed.

43. • 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
• Such cases, a pyloric exclusion is typically performed by oversewing the pylorus using
absorbable suture or stapling across it using a noncutting linear stapler
• Gastrojejunostomy is created to bypass the duodenum in a billroth II or roux-en-y
fashion
• Alternatively, a duodenostomy tube can be placed through the perforation with wide
peritoneal drainage.
• Leakage of gi contents into the drain is likely, but in most cases sepsis will resolve.

44. • An alternative in this difficult situation is
• Antrectomy and a billroth II or roux-en-y reconstruction.
• Perforations can also be treated laparoscopically- who are hemodynamically stable
• For patients - negative for H. Pylori, are taking long-term nsaids that they cannot
discontinue, or have failed medical therapy in the past for their ulcer disease, an acid
reducing procedure can be added at the time of repair

45. • After repair, the stomach is decompressed until bowel activity returns.
• Drains should be kept in place until patients have eaten without a change in drain output
or quality, which would suggest a leak.
• All H. pylori–positive patients should undergo eradication with appropriate triple-therapy
regimens.

46. • PERFORATED GASTRIC ULCERS
• Perforated type I gastric ulcers
• In patients in stable condition, distal gastrectomy with a billroth I anastomosis is
recommended
• Unstable patients, simple patching of the gastric ulcer with biopsy
• And treatment for H. Pylori, if positive, is recommended
• Even if the biopsy is negative, the risk for malignancy still needs to be ruled out;
• Therefore, documentation of healing is required with repeat endoscopy and biopsy.

47. • Types II and III gastric ulcers
• Treated with patch closure, with or without truncal vagotomy and pyloroplasty,
• Depending on the medical condition, hemodynamic status, and extent of peritonitis,
• Followed by treatment for H. Pylori if positive.

49. • BLEEDING PEPTIC ULCERS
• Most nonvariceal bleeding (70%) is attributable to peptic ulcers
• Persistent bleeding is associated with a 6% to 8% mortality
• Most commonly used scores are the blatchford and rockall prediction scores
• Blatchford score incorporates the patient’s blood urea, hemoglobin, blood pressure,
and other clinical parameters to predict the need for therapeutic intervention with
transfusion, endoscopy, or surgery

53. • Patients at high risk - on endoscopy to have active bleeding,
• Via an arterial jet or oozing,
• An adherent clot, or
• A visible vessel within the ulcer, are, and intervention is required
• Patients - low risk
• Without active bleeding, no visible vessel, and a clean ulcer base are and do not
require further intervention
• All patients undergoing endoscopic examination should be tested for H. Pylori status

54. • High-risk patients requiring intervention,
• The best initial approach is endoscopic control,
• Primary hemostasis in approximately 90%
• Most common method of control is injection of a vasoconstrictor at the site of
bleeding
• 30% of patients have rebleeding- use of a second vasoconstrictor or sclerosing agent,
thermocoagulation, and placement of clips at the site of bleeding
• All high-risk patients –
• Monitored setting, preferably an intensive care unit, until all bleeding has stopped
for 24 hours
• A PPI administered intravenously, with an initial bolus followed by continuous
infusion or intermittent dosing for up to 72 hours

55. • Despite the use of ppis and improved methods of endoscopic control,
• 5% to 10% of patients have persistent bleeding that
• Requires surgical intervention
• Includes patients who become hemodynamically unstable and patients who continue to
bleed and require ongoing blood transfusions (usually >6 U of packed red blood cells).
• Typical approach is through an upper midline laparotomy,

56. • Kocher maneuver - to mobilize the duodenum.
• The anterior wall of the duodenal bulb is opened longitudinally,
• And the incision can be carried across the pylorus.
• The gastroduodenal artery is oversewn,
• With a three-point u stitch technique, which effectively ligates the main vessel
(superior and inferior stitches) and prevents back-bleeding from any smaller
branches (medial stitch), such as the transverse pancreatic artery
• Avoid incorporating the common bile duct into the stitch.
• After the bleeding has been controlled, the duodenotomy is closed transversely to avoid
narrowing

58. Gastric outlet obstruction.
• Acute inflammation of the duodenum
• Can lead to mechanical obstruction,
• With a functional gastric outlet obstruction manifested by
• Delayed gastric emptying, anorexia, nausea, and vomiting.
• In cases of prolonged vomiting, patients may become dehydrated and develop a
hypochloremichypokalemic metabolic alkalosis secondary to the loss of gastric juice rich
in hydrogen and chloride
• Chronic inflammation of the duodenum may lead to
• Recurrent episodes of healing followed by repair and scarring, - fibrosis and stenosis
of the duodenal lumen

59. • Stomach can become massively dilated - rapidly loses its muscular tone.
• Marked weight loss and malnutrition are also common
• Now less common than obstruction from cancer
• Cancer must be ruled out with endoscopy.
• Endoscopic dilation and H. Pylori eradication are the mainstays of therapy
• Median of five dilations required,
• Patients with refractory obstruction are best managed with primary antrectomy and
reconstruction along with vagotomy.

60. • Intractable peptic ulcer disease
• 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
• Intractable PUD is unusual for duodenal ulcer disease in the H. Pylori era.
• Benign gastric ulcers that persist must be evaluated for malignancy.
• A serum gastrin level should also be determined in patients with ulcers refractory to
medical therapy to rule out gastrinoma.
• Intractable duodenal ulcer should be treated with an acid-reducing operation
• Truncal vagotomy, selective vagotomy, or highly selective vagotomy, with or without
an antrectomy.

61. Thank you!