SURGICAL COMPLICATIONS OF PUD md 5 july.pptx

1. SURGICAL COMPLICATIONS
OF PUD
DR OMAR.M .MWAKITSANGA( RESD SEM2)
DR ZEPHANIA(RESD SEM6)
FACILITATOR: DR LUTEGE.

2. Outlines
• Anatomy of the stomach
• Venous drainage and its innervation
• Peptic ulcer disease
• Etiopathogenesis
• Clinical features
• Diagnosis
• Complication
• Treatment

3. Anatomy
The stomach is divided into:
• Cardia
• Fundus
• Body
• Antrum
• Pylorus

9. Anatomy…
•Microscopic Anatomy
• Glandular portions of stomach
• Lined by simple columnar epithelium
• This luminal surface is interrupted at intervals
by gastric pits
• Opening into these gastric pits are one or more
gastric glands that have functional significance
• Mucosa has three types of gastric glands
(locations)
-Cardiac
-Gastric
-Pyloric

10. • Parietal cells
• Location- neck of gastric pit
• Stimulated by Ach, Histamine and Gastrin
• Secretes HCl + Intrinsic Factor
• Chief Cells
• Location- base of gastric pit
• Stimulus- Vagal
• Secretes Pepsinogen (eventually leads to pepsin- digestive
enzyme)

11. Anatomy…
• Pyloric Glands
• Gastrin cells
• Location- mucosa of distal stomach
• Stimulus- amino acids
• Secretion- Gastrin (stimulates HCl production by way of parietal cells)
• Somatostatin
• Location- mucosa of distal stomach + Duodenum
• Stimulus- HCl or low pH in duodenum
• Actions- Inhibits gastric emptying, Pancreatic secretions, and gallbladder contraction

12. INTRODUCTION
PUD
oBreak or defect in the mucosa within the GIT exposed to ACID-PEPTIC
activity
oExtends beyond the muscularis mucosa
oAssociated with an acute or chronic inflammatory response

13. Classification
1.Lesser curve
(at or near incisura
2. Combined
-GU: body or incisura
+ DU (high acid output)
3. Prepyloric
(<3cm of pylorus: high acid)
4. Proximal (high lesser curve)
5. NSAIDs induced

14. Modified Johnson classification of peptic
ulcers

15. Duodenal Ulcer
Types
l. 1st. part or bulb*
2. Post bulbar –
2nd part
3. Pyloric Channel

16. Curling’s and Cushing’s Ulcers
• Curling’s ulcer is thought to result from stress-induced elevation of
gastric acid secretion due to severe burns.
• Cushing’s ulcer results from stress-induced elevation of gastric acid
secretion due to head trauma.
• Most commonly they are observed in the acid-producing portions of
the stomach (fundus and body).

17. Etiology
• Peptic ulcers are caused by increased aggressive factors, decreased
defensive factors, or both.
• This in turn leads to mucosal damage and subsequent ulceration.

18. Defensive (protective) factors
 mucosal bicarbonate secretion
 mucus production,
blood flow
 growth factors,
cell renewal
endogenous prostaglandins.
Damage (aggressive) factors
H. pylori infection
NSAIDs
hydrochloric acid secretion
pepsins
ethanol ingestion
Smoking
duodenal reflux of bile
 ischemia
hypoxia

19. The Role of Helicobacter pylori
• Adhesins: facilitate attachment to gastric
epithelial cells.
• Urease: produces ammonia from urea.
• Ammonia helps to alkanize the pH of the
surroundings and can also damage epithelial cells.

20. The Role of Helicobacter pylori…
• Proteases and phospholipases that break down
the glycoprotein lipid complex of the mucous gel.
• This reduces the efficacy of the mucosal defense.
• Surface factors that are chemotactic for
neutrophils and monocytes, which in turn
contribute to epithelial cell injury.

21. The role of NSAIDs
•In synthesis of prostaglandins, the rate-
limiting step is under the enzyme
cyclooxygenase (COX).
•NSAIDs inhibits COX-1.

22. The role of NSAIDs…
•Interruption of prostaglandin synthesis
results into;
• Increased acid secretion,
• Decreased mucin and bicarbonate secretion,
• Decreased surface active phospholipid
secretion,
• Decreased epithelial cell proliferation.

23. The role of NSAIDs…
• Injury to the mucosa also occurs as a result of the
topical encounter with NSAIDs.
• NSAIDs are weak acids and remain in a non-ionized
lipophilic form when found within the acid
environment of the stomach.
• Once trapped intracellularly in an ionized form they
cause cell injury.

24. The Role of Cigarette Smoking
•Smoking appears to
decrease healing
rates, impair response
to therapy, and
increase ulcer-related
complications such as
perforation.

25. Other Possible Causes
• Steroid use?
• Psychological stress?
• Alcohol?
• Diet?

26. Clinical features
Symptoms
• Acute peptic ulcers
• Symptoms of short duration
• Ulcers recognized when they cause hematemesis
• May perforate
• May progress to an ulceration.
• Chronic peptic ulcers
• Main symptom: Pain in upper abdomen.

27. Complications of PUD
• Acute complications
1. Perforation
2. Bleeding
• Chronic complications
1. GOO
2. Penetration
3. Carcinoma of the stomach
4. Hour glass contracture of stomach
5. Teapot deformity

28. Bleeding PUD
• Hemorrhage from peptic ulcer can be chronic which causes anemia.
• Acute bleeding resulting in massive hematemesis and melena.
• Precipitating factors for bleeding are
Chronicity of the disease destructing stomach layers exposing blood
vessels
Atherosclerosis→ vessels do not contract
Sudden, severe acid peptic digestion brought about by irritants such
as alcohol and drugs

29. Clinical presentation of bleeding PUD
• Previous hx of PUD
• Hx of abdominal pain
• Hx of hematemesis or melena
• Features of hemorrhagic shock

30. diagnosis
• Emergency upper OGD is done to confirm the diagnosis
• Forrest classification when OGD is done
la Spurting, bleeding
lb Nonspurting, active bleeding
lla Visible vessel
llb Non-bleeding ulcer with overlying clot
llc Ulcer with hematic-covered (black) base
lll Clean ulcer base

32. Management of bleeding PUD
• Resuscitation
• Aim: Prevent cardiovascular collapse
Evaluate for continuing losses
Locate site of bleeding
Arrest hemorrhage.

33. Non surgical Rx
• Transfusion of blood and its products
• Anti-acids
• Lesser coagulation
• Sclerotherapy
• Haemoclip application
• Bipolar electro-coagulation

34. Surgical management
Indications for surgery in bleeding PUD
 Failure of endoscopic hemostasis
 Re-bleeding in the hospital (re-bleeding is more common in gastric
ulcer patients).
 Bleeding requiring massive transfusion
 Elderly patients with re-bleeding.
 Massive hemorrhage leading to shock or cardiovascular instability.
 Recurrent hemorrhage requiring hospitalization.

35. SURGERY
DU. 1. Under sewing + Vagotomy and pyloroplasty.
2. Under sewing + HSV.
• All patients should be given H. pylori eradication
therapy.

36. GU. 1. Partial gastrectomy & Billroth I or
2. Excision of ulcer
+ Truncal vagotomy and drainage
3. Excision of ulcer and HSV

37. PERFORATION
• ?Acute or Chronic Ulcer. Presents with ‘peritonitis’
• Diagnosis : Chest X-ray: Air under diaphragm 75%

38. Classical CXR in perforation
10% have no demonstrable gas on an erect chest x-ray

42. Duodenal perforation

43. SURGERY:
• DU. 1. Closure +/- omental patch (Graham)
& TV+P in an early case with “chronic” ulcer
(H. Pylori eradication after closure)
• GU. 1. Partial Gastrectomy & Billroth I.
2. Excision of ulcer (biopsy)
& Truncal vagotomy + Drainage.
Eradicate H- pylori

44. 3. GASTRIC OUTLET OBSTRUCTION.
(Pyloric stenosis)
Persistent pain and vomiting.
Visible peristalsis and succussion splash
Hypochloremic, hypokalaemic, alkalosis
• Diagnosis : Gastroscopy / Barium meal.
SURGERY:
• DU. 1. Truncal vagotomy + Antrectomy.
2. Truncal vagotomy + Gastrojejunostomy.
• GU. “Hour-glass” 1. Truncal vagotomy + Antrectomy

45. • Common surgical procedures done for GOO related to PUD are
vagotomy and antrectomy, vagotomy and pyloroplasty, truncal
vagotomy and gastrojejunostomy or pyloroplasty,
• Of these, vagotomy and antrectomy with Billroth II reconstruction
(gastrojejunostomy) seems to offer the best results.

47. Complication of PUD surgery
• Complications seen after surgery for PUD are related primarily to the
extent of the anatomical modification performed.
• Minimal alteration (HSV) is associated with higher rates of ulcer
recurrence and less gastrointestinal disturbance.
• More aggressive surgical procedures have a lower rate of ulcer
recurrence but a greater incidence of gastrointestinal dysfunction.
• Overall, morbidity and mortality related to these procedures are
quite low

48. Cont. ….
Complications can be;
1. Non specific : Cardiac. Pulmonary. Thromboembolic etc.
2. Specific:
a. Early. Hemorrhage, Stomal obstruction, Duodenal fistula.
b. Late. Recurrent ulcer, Anastomotic ulcer, Gastro-jejuno-colic fistula
i. Post-gastrectomy Syndromes:
Early dumping (circulatory).
Late dumping (hypoglycemic).
Alkaline reflux / billous vomiting.
ii. Nutritional: Weight loss, steatorrhoea, diarrhoea ,anaemia: Iron, B 12
deficiency, Calcium deficiency, osteomalacia, Malabsorption.

49.  Post-vagotomy diarrhoea
 Intestinal obstruction:
Adhesions
Internal hernia
Bolus obstruction
Other (Remote)
Carcinoma of gastric remnant
Gall stones.

50. Recurrent ulceration
• The risk of ulcer recurrence is directly related to the
procedure performed. (at the anastomosis -stomal or
marginal ulcer).Progressive epigastric abdominal pain is
the most frequent presenting complaint.
• Reasons for recurrence includes incomplete vagotomy,
retained antrum (measure gastrin level cephalic phase),
and less likely, persistent or recurrent H. pylori infection
NSAID.
• Medical therapy with H2 blockers will heal postoperative
ulceration in 70 to 90% of patients. PPIs role? may have
greater rates of ulcer healing.
• Repeat operation (complete vagotomy, partial
gastrectomy) may be required.

51. Afferent Loop Syndromes
• Two types of afferent loop syndrome.
• Bacterial overgrowth in the afferent limb secondary to stasis most common,
with postprandial abdominal pain, bloating, and diarrhea with concomitant
malabsorption of fats and vitamin B12.
Cases refractory to antibiotics may require surgical revision of the loop.
• The less common afferent loop syndrome can present with severe abdominal
pain and bloating that occur 20 to 60 min after meals. Pain is often followed
by nausea and vomiting of bile-containing material, may improve after
emesis.
 is due to incomplete drainage of bile and pancreatic secretions from partially
obstructed afferent loop Cases refractory to dietary measures may need
surgical revision.

52. • Dumping syndrome (up to 50%, severe 1%)
• Vasomotor and GI signs and symptoms in pts who have undergone vagotomy
and drainage (especially Billroth procedures).
• Two phases; early and late.
 Early dumping; 15 -30 min after meals with crampy abdominal discomfort,
Nausea, Diarrhea, belching, tachycardia, palpitations, diaphoresis, light-
headedness, and, rarely, syncope. Is due to rapid emptying of hyperosmolar
gastric contents into the small intestine, resulting in a fluid shift into the gut
lumen with plasma volume contraction and acute intestinal distention. Release
of vasoactive GI hormones ( neurotensin, motilin) may play a role.

53. The late phase of dumping typically occurs 90 min to 3 h after meals.
Vasomotor symptoms (light-headedness, diaphoresis, palpitations,
tachycardia, and syncope) predominate during this phase. This component of
dumping is thought to be secondary to hypoglycemia from excessive insulin
release.
 Dietary modification is the cornerstone of therapy Small, multiple (six) meals
devoid of simple carbohydrates coupled with elimination of liquids during
meals is important + Antidiarrheals and anticholinergic agents are
complimentary to diet.
The somatostatin analogue octreotide has been successful in diet refractory
cases.

54. Post vagotomy Diarrhea
• Up to 10% of patients, commonly observed after TV, with intermittent
diarrhea 1 to 2 h after meals. May be severe and relentless.
• This is due to a motility disorder from interruption of the vagal fibers
supplying the luminal gut, increased excretion of bile acids, and release of
luminal factors that promote secretion.
• Diphenoxylate or loperamide is often useful in symptom control.
• The bile salt-binding agent cholestyramine may be helpful in severe cases.
• Surgical reversal of a 10-cm segment of jejunum may yield a substantial
improvement in bowel frequency in a subset of patients.

55. Maldigestion and Malabsorption
• Weight loss ( 60%) due to decreased oral intake, mild steatorrhea, Reasons;
decreased gastric acid production, rapid gastric emptying, decreased food
dispersion in the stomach, reduced luminal bile concentration, reduced
pancreatic secretory response to feeding, and rapid intestinal transit.
• ↓B12 levels (intrinsic factor, may be due to competition for the vitamin by
bacterial overgrowth)
• Iron-deficiency anemia may be a consequence of impaired absorption of dietary
iron in patients with a Billroth II gastrojejunotomy.
• FA defiency (↓absorption or intake)
• Malabsorption of vitamin D and calcium resulting in osteoporosis and
osteomalacia is common after partial gastrectomy and gastrojejunostomy
(Billroth II). Osteomalacia can occur as a late complication in up to 25% of post-
partial gastrectomy patients.

56. Gastric Adenocarcinoma
The pathogenesis is unclear but may involve alkaline reflux, bacterial
proliferation, or hypochlorhydria. Endoscopic screening every other
year may detect surgically treatable disease.

57. references
• Schwartz principles of surgery 11th edition
• Sabiston textbook of surgery 20th edition
• Manipal Manual of Surgery 4th Edition
• Bailey and Love Text book of Surgery 27th edition