Management of peptic ulcer disease

1. Surgical management of PUD
Vagotomy and Drainage procedures
-Techniques and complications
BY SINTAYEHU A. (GSR III)
MODERATOR: DR. HAILU (ASSISTANT PROF.OF SURGERY)
ADDIS ABABA UNIVERSITY,
ADDIS ABABA, ETHIOPIA

2. Outline
 Introduction
 Epidemiology
 Pathophysiology
 Clinical manifestation
 Diagnosis
 Complications
 Treatment
2

3. Introduction
PUD
 Is a break in the lining of stomach and duodenum that extends into the
submucosa or deeper
 esophagus, at the margin of GJ, jejunum, and a Meckel's diverticulum
 important cause of morbidity and health care costs
 estimated costs $5.65 billion per year in the USA
 natural history: sequence of healing and exacerbation over years
 resolution without intervention to complications
 Identifying and treating the causes decrease relapse
 Distal antral ulcers slower to heal, likely to recur
3

4. Introduction contd,
 From 1950s to 1970s PUD was most common indication for UGI surgery
 Since 1980s, elective operation for PUD in Europe and US reduced by 50-
80%
 Result of effective
 acid suppressive agents (H2RAs,PPI),
 H.pylori eradication therapy and
 endoscopic therapy
 Studies suggest emergency operations for PUD remained similar
4

5. Epidemiology
H.pylori and NSAIDs
 Nearly 50% of the world’s population is estimated to be infected with H.
pylori
 30-40% of persons living in the developed, and
 80-90% of persons living in the developing world
 PUD annual incidence ranged from 0.1 to 0.19 percent, overall prevalence
of 0.12%-1.50%
- relatively common worldwide
 Ulcer incidence increases with age for both DUs and Gus
5

6. Relevant anatomy
 Gross:
 Blood supply:
6

7. Contd. 7
Innervation:
Extrinsic
Vagus: rt & lt
Sympathetic: from coeliac plexus
T5-10
Intrinsic:

8. Pathophysiology
 Duodenal ulcers:
 H.pylori related , mainly result from increase in acid and pepsin load and gastric
metaplasia in duodenal cap
 Gastric ulcers: most commonly associated with NSAIDs ingestion
In both - imbalance between aggressive and cyto-protective factors
 inflammation is the leading cause of the imbalance
8

9. Pathogenesis contd,
 H.Pylori:
 80% to 95% of duodenal ulcers and
 approximately 75% of gastric ulcers are associated
with H. pylori infection
Potential Mechanisms
 Production of toxic products- tissue injury
 Induction of a local mucosal immune response
 Inflammatory reactions
 Increased gastrin and acid levels- decreasing somatoatatin
 Gastric metaplasia in duodenum- allows h.pylori colonization
9

10. contd
 NSAIDs including aspirin, ibuprofen diclofenac, etc.
1, Inhibit PG synthesis by blocking cyclooxygenase
 PGs are responsible for production of mucus and bicarbonate in stomach
 Loss of alkaline buffer zone which protect the stomach mucosa from acid
2, topical irritation and epithelial damage
 implicated in 30% of Gus and small number of H. pylori-negative duodenal
ulcers.
 With H.pylori they have synergistic effects on gastric mucosal damage
10

11. Non-NSAID, non-H. pylori ulcers
 R/o H.pylori and NSAIDs and then consider
 Drugs other than NSAIDs: acetaminophen, glucocorticoids, clopidogrel, etc.
 Zollinger-Ellison syndrome:
 Carcinoid syndrome: histamine secreting
 Antral G cell hyperfunction
 Infections like cmv, hsv, fungal infections
 Radiotherapy
 Inflammatory and infiltrative diseases: Sarcoidosis, CD
 Physiological stress
 Idiopathic
11

12. Duodenal Ulcer
 Most commonly by H.pylori
up to 95%
 4x more common than GUs
 Usual age 25-50 years
 Male to female ratio—4:1
 Genetic link:
 3x more common in 1st degree relatives
 more common in patients with blood group O
12

13. C/P:
Epigastric Pain:
1. 2-5 hrs after meals (food emptied after 2-3hrs but stimulated acid stays 3-
5hrs)
2. b/n about 11 PM and 2 AM (maximal circadian acid stimulation),
 No weight loss
 Complications:
 Commonly haemorrhage,
 perforation, sometimes obstruction, is observed.
13

14. Gastric ulcer
 Less common than DU
 Usually beyond 6th decade
 Less related to H.pylori- about 75%
 Male to female ratio—2:1 , more BG A
 Disruption of mucus barrier most important factor.
 In NSAIDs users: 3-4-fold increase in risk of gastric ulcer
 10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
14

15. Contd.
 C/P:
 pain immediately after meal, vomiting is common, associated with weight
loss, No night pain,
 Complications:
 Perforation,
 haemorrhage and at
times obstruction, are common.
 Malignant transformation 10% in giant ulcers
15

16. Diagnosis
,
 History and P/E = sn and sxs, risk factors, patient condition
 Patient <50yrs and no alarming signs - initial approach noninvasive test and treatment
 H.Pylori test
1.Non Invasive
 Urea Breath test,C13,14
 Fecal H.Pylori antigen test
 Serology
2.Invasive (endoscopy) : detect ulcer
 Rapid urease test
 Culture biopsy, Histology,
 Polymerase chain reaction of gastric biopsy specimen
 Barium meal: limited role in detecting ulcers
16

17. Management
 Medical treatment:
 smoking cessation, discontinuing NSAIDs and aspirin,
and avoiding coffee and alcohol,
 Acid atisecrnetory agents
 helicobacter pylori eradition
17

18. Treatment Regimens for
H. pylori Eradication
 Triple Therapies
 Proton pump inhibitor BID +
 Amoxicillin 1000mg BID +
 Clarithromycin 500mg BID
or
 PPI bid +
 Metronidazole 250mg QID +
 Tetracycline 500mg QID
 Quadruple Therapy
 Bismuth subsalicylate 525mg QID +
 Proton pump inhibitor BID +
 Metronidazole 250mg QID +
 Tetracycline 500mg QID
18

19. Surgical Treatment of PUD
 Indications restricted to
 Bleeding
 Perforation
 Intractability
 Obstruction
19

20. Bleeding
PUD is
Frequent cause of upper gastrointestinal bleeding
 Estimated to account for approximately 40–46%
 Patients with gastric ulcer bleeding, their ulcers tend to be on the lesser
curvature
 Patients with duodenal ulcer bleeding, their ulcers tend to be on the
posterior wall of the duodenum
20

21. Be Alarmed
 Risk factors associated with higher mortality in bleeding ulcer are:
 Increasing age(>60)-not tolerate prolonged bleeding
 Presence of shock on presentation
 RBC transfusion>6 unit
 Severe comorbidity
 laboratory evidence of severe bleeding (hemoglobin/hematocrit
 Re-bleeding
 Severe coagulopathy
21

22. Approach
 ABC of life, check v/s, aggressive
management of hypovolemic shock
 Hx: previous pud hx, dyspepsia, recent
alcol/anagesics, severe vomiting, CLD,
complete hx
 NGT flush stomach with 50ml N/S and
aspirate
 fresh blood indicates active or a very
recent hemorrhage
 coffee ground – recent bleeding which
has stopped
 clean aspirate or bile – no recent
hemorrhage.
 Do PR
 fresh blood or juicy soft melena indicates
active or very recent bleeding
 dry and solid melena signifies a non-
recent bleeding
 Investigations
 CBC, OFT, Coagulation profile
 Blood type and cross-match
22

23. Contd.
 Group III: elective investigation, no operation
 Group II: resuscitate, emergency endoscopy
 Group I: serious bleeders
 If previous history of portal hypertension or clinical stigmata of chronic liver disease
- variceal bleeding
 Take to critical care
 Sedate, intubate ,gastric lavage(facilitate endoscopy, prevent aspiration)
 Endoscopy
 If no varices proceed with surgery
23

24. Endoscopic therapy
-diagnostic + treatment
Injection Therapy
adrenalin, hypertonic saline and adrenalin
Endoscopic hemoclips
Laser coagulation
Electrocoagulation
Thermo-coagulation
Angiographic embolization
24

25. Indications for surgery
 Hemodynamic instability despite vigorous resuscitation (>3 unit transfusion)
 Failure of endoscopic techniques to arrest hemorrhage
 Recurrent hemorrhage after initial stabilization (with up to two attempts at
obtaining endoscopic hemostasis)
 Shock associated with recurrent hemorrhage
 Continued slow bleeding with a transfusion requirement exceeding three units
per day
 Preop
 Iv crystalloid, blood , Catheter, Iv PPI
25

26. Operative Management
 Endoscopy(preferably by surgeon)
 Source of bleeding
 Exploration: Upper midline , transverse chevron
 Look for external visual or palpable features of chronic ulceration
 from the duodenum to the gastric cardia
 Duodenal “Kocherization” will be necessary to reveal the sporadic postbulbar
ulcer in the second portion of the duodenum
 If no external evidence of pathology and you did’t scope before surgery:
1. Proceed according to preop endoscopy
2. Intraoperative endoscopy
3. Surgical exploration- pyloroduodenotomy
26

27. Surgical options
 GUs:
 Suture ligation of the bleeder (and biopsy for gastric ulcer)
 Suture ligation and definitive nonresective ulcer operation (HSV or V and D) –
not required
 Gastric resection (usually including vagotomy and ulcer excision)- giant ulcer, pt
not cooperative with acid reducing drugs
 DUs:
 Pyloroduodenotomy – inspect duodelal bulb ald antrum
 suture ligature of the bleeding vessel and/or by ligating the GDA at the superior,
and inferior aspect of the ulcer and medial branch
 Optionally if patient is fit Pyloroplasty and vagotomy
27

28. Perforation
 Duodenal perforation accounts for approximately 60% of peptic
perforation
 Duodenal 60
 antral/pyloric 20
 gastric body ulcers 20
 Mortality rate for perforated ulcer is higher in the elderly and is higher after
gastric than after duodenal perforation
 ranges from 10-40%
 delay in operative treatment is a primary determinant of morbidity,
mortality, and cost
28

29. Perforation
 C/P:
1st phase (within 2hrs of onset)
 Sudden severe epigastric pain, quickly
generalize
 2nd phase(2-12hrs of onset)
 Abdominal pain may lessen, generalized
&worsen on mov’t
 Regidity
 3rd phase(>12hrs of onset)
 increasing abdominal distention
 abdominal pain, tenderness, and rigidity
may be less evident
 Temperature elevation and hypovolemia
 Investigation:
 CBC,OFT, serum amylase
 Imaging:
 CXR-free air, 70%
 CT with oral contrast
 Contrast study: leakage of gastrograffin
29

30. Contd,
 Initial management:
 NGT, IV volume replacement, IV PPI, and broad spectrum intravenous
antibiotics
 Test for H.pylori status if unknown
 Non-operative Rx:
 Perforated ulcer that is sealed by omentum or surrounding tissue, patient
hemodynamically stable and with other serious illness when the risk of surgery
is prohibitive
1. Late presenter
2. Severely sick
 NPO,NGT,iv fluid,IV abxs, iv PPI or H2RAs with close monitoring
30

31. Contd,
surgical options
 DUs;
 Simple patch closure
 Definitive surgery
 Patch closure and HSV
 Patch closure and TV/D
 Special problem
 “Kissing” ulcers
31
 BP>90 mmHg,
 operation within 48 hrs of perforation, and
 lack of associated medical illnesses
 APACHE II score<11
 Skilled gastroduodenal surgeon

32. Contd.
 Gus;
 high over all mortality rate (older & have comorbidities)
 Principles:
 Remove the ulcer
 Remove gastrin secreting antrum
 partial gastrectomy due to risk of malignancy,
 unless the patient is at unacceptably high risk( advanced age, comorbid disease,
intraoperative instability, or severe peritoneal soilage)
 Patch closure alone-associated post op GOO and biopsy of the ulcer is
necessary when performed
32

33. Difficult perforated PUD
Giant ulcer perforation:
 a full thickness perforation of peptic ulcer which are 2cm or more in diameter
 Standard technique of omentopexy is associated with high morbidity and
mortality
Different authors have recommended varied surgical options
 Partial gastrectomy with BI or BII
 conversion of the perforation into a pyloroplasty
 pedicled graft of the jejunum
 Omental plugging
 closure of the perforation using a serosal patch
33

34. GASTRIC OUTLET OBSTRUCTION
 Most cases are associated with duodenal or pyloric channel ulceration,
 gastric ulceration accounting for only 5 percent of cases
 As peptic ulcer become less frequent, malignancy has emerged as a
prominent cause
 C/P: Progressively increasing early satiety
 Bloating
 Indigestion
 Anorexia
 Nausea , Vomiting, Epigastric pain
 weight loss
34

35. Contd
 C/P……
 Dehydrated, Malnourished,
 succession splash
 visible peristalsis at epigastric area
that moves from lt. to rt
 Investigations
 CBC, Serum electrolytes, OFTs,
 Barium UGI series
 atonic, dilated, fluid-filled stomach
 UGI endoscopy and biopsy
 to exclude malignancy, diagnose ulcer
disease, and determine if H. pylori is
present.
35
Medical Rx: correct fluid and electrolyte,
acid suppressing agents,

36. Contd.
 Surgical management
 In the past failed 3days of NGT suction
 in cases where the cause can be reversed (eg, H. pylori or use of NSAIDs) more
conservative approach
 Delay surgery
 until patient stable, fluid & electrolyte restored
 If nutritional status is compromised(ALB<2.8g/dl poor surgical outcome)
 if the stomach is markedly dilated( post op atony)
36

37. Contd.
 Antrectomy and vagotomy
 favored to relieve the obstruction and definitively rule out malignancy
 vagotomy and gastrojejunostomy, preferably with biopsy of the ulcer
 When inflammation and scarring may
prevent safe resection and/or closure
of the duodenal stump
37

38. Vagotomy and antrectomy
 Antrectomy: resection of distal 1/3rd of the stomach( 35-50%)
 For ulcers( refractory, complicated, recurrent)
 Performed with bilateral TV
 Reduces acid secretion by reduction of acetylcholine stimulus of the vagus
nerve and gastrin production of the antrum
 reduces acid the most, lowest recurrence rate.
38

39. Operative steps
-first assess duodenum: B I vs B II vs GJ
1 Vagal trunks identified and vagotomy done
2 Kocher maneuver to mobilize duodenum
3 Division of gastrocolic omentum or lesser sac
Assess posterior wall
4, Division of Rt gastroepiploic vessels
5, Division of Rt gastric vessels &lesser omentum
dissection, ligation of lt gastric artery
-extent of dissection
6, duodenum is circumferentially dissected
2cm beyond pylorus and gently divided
7, stomach wall clamped and divided
39

40. Billrith I
 Closure of stomach wall
 Gastroduodenostomy in two layers
at lower end, E_E or E to side
40

41. Billroth II
 Duodenal stump closed
 Mobilization & tension free closure
 Jejunal loop at 10-15cm from
ligament of treitz anastomsed to stomach
side to end
 Anastomosis on caudal and
posterior stomach wall
 Can be retro/antecolic
41

42. Vagotomy
 vagal nerve transection, thus interrupting sensory and motor impulses to the
stomach and GI tract
 Elimination of direct cholinergic stimulation to acid secretion
 Also makes the parietal cells
 less responsive to histamine and gastrin and
 abolishes the vagal stimulus for release of antral gastrin.
 Three basic types
 truncal, selective, and highly selective
42

43. Truncal vagotomy
 Indications
 failure of medical therapy,
 GOO due to PUD
 UGI bleeding, perforation
 Operative Steps
 Position-supine
 Midline incision and exposure
 abdominal wall retractor placed
 steep reverse Trendelenburg position
 NGT is advanced into the proximal stomach
 gastrophrenic ligament,esophagophrenic ligament divided
43

44. Contd.
 surgeon's right index finger is passed
posterior-superior into the mediastinum
to encircle the esophagus
 The nerve skeletonized~6-cm length into
the mediastinum
clipped proximally and distally and
a 2-cm section is resected
 Defect in the esophageal hiatus is closed
44

45. Contd.
 Complete skeletonization of the vagus nerves ensures the transection of
small intervening nerve branches.
 Failure to transect these small branches may result in an incomplete
vagotomy and recurrent ulcers
 The Rt vagus must be transected proximal to the origin“criminal nerve” of
Grassi
 In case of reoperation TV can be done via Lt thoracotomy
 TV denervates stomach,biliary tree,liver,midgut,
 Antral pump is lost…..drainage procedure required
45

46. Selective vagotomy
 transection of
 anterior nerve of Latarjet distal to
the hepatic branches, and
 posterior nerve of Latarjet distal to
the celiac branches.
 Only solitary pyloric branch from hepatic
division is preserved
 Antral pump is lost and drainage required
 Rarely performed
46

47. HIGHLY SELECTIVE VAGOTOMY
 transection of the proximal gastric branches of
 Anterior nerve of laterjet and
 posterior nerve of Latarjet, with preservation of the distal branches to the
antrum and pylorus ( crow’s foot)
 Vagal division should terminate 7 cm proximal to the pylorus
 Drainage procedure not required
47

48. Drainage procedures
 HEINEKE-MIKULICZ PYLOROPLASTY:
 dividing the pyloric muscle and reconstructing the pyloric channel to improve
gastric emptying
 A Kocher maneuver is required to perform a pyloroplasty
 peritoneum just lateral to the second portion of the duodenum is incised
 2 traction sutures incorporating pyloric vein placed over anterior surface of
pylorus ~1cm apart
 ~5cm longitudinal incision is made between the traction sutures
 Incision transversely closed using full thickness suture
48

49. FINNEY PYLOROPLASTY
 is essentially a side-to side gastroduodenostomy
 preferred when a longer incision on the duodenum is required to control
bleeding or incase of fibrotic duodenum
 relieves tension on the anterior suture line.
 row of interrupted 3-0 silk sutures are placed to approximate the greater
curvature to the superior portion of the proximal duodenum
 inverted U-shaped incision is made approximately 5 mm from the suture
line
49

50. JABOULAY PYLOROPLASTY
 Is a gastroduodenostomy between the antrum of the stomach and the
duodenum. Pylorus not incised.
 Effectively improves gastric emptying.
 relatively easy exposure and dissection
 Kocher maneuver
 antrum of the stomach and the duodenum are aligned by placing a traction
suture just proximal to the pylorus along the greater curve of the stomach.
 posterior interrupted layer is placed
 stomach and duodenum are then opened
 inner, continuous, absorbable layer is placed and carried anteriorly
50

51. Complications of PUD surgery
 Intraoperative complications:
 Hemorrhage
 Acute ischemia of Left lobe of Liver
(aberrant Left Hepatic artery)
 Injury to Spleen, Pancreas, Common Bile duct.
 Disruption of Ampulla of Vater.
 Early post operative complications
 Atelectasis(12-20%)
 Pneumonia(9%)
 Respiratory Failure(3%)
 Pulmonary Embolism(0.05%)
51
• Venous thrombosis of
Lower limbs
• Wound infection
• Sub-phrenic abscess
• Acute Pancreatitis

52. Late complications
Anastomotic Leak: usually at GJ site
 Sxs : Fever, persistent tachycardia , worsening abdominal pain
 Rx: iv abxs, repair of nastomosis and peritoneal lavage
Duodenal Stump Leak: Billroth II Gastrectomy, Incidence: 3-5%.
Commonest cause:
 Excess dissection of duodenal stump and over suturing( ischemia and necrosis),
 acute afferent loop obstruction ------tension on duodenal stump
 POD 4-5; severe RUQ pain, fever, tachycardia, jaundice, bile-stained discharge from
incision; Biliary Peritonitis
 NGT,iv abxs, Thorough peritoneal lavage, duodenostomy tube
52

53. Small bowel obstruction
 Internal Hernias through potential mesenteric defects.
 Retrocolic > Antecolic
 Colicky abdominal pain, nausea, vomiting, distension
 Risk of strangulation & perforation
Stomal Obstruction
 Inflammatory adhesions
 Dysphagia, nausea, vomiting, abdominal pain.
 Options:
 -Endoscopic balloon dilatation
 -Surgical release of adhesions
Anastomotic stricture: Progressive dysphagia, vomiting, minimal abdominal pain
 Endoscopic dilation
53

54. Marginal Ulcer Bleeding(MUB)
 Ulceration around gastro-duodenal or gastrojejunal anastomotic site
 Inadequate acid suppression, large retained antrum
 Epigastric pain
 Endoscopy is diagnostic
 PPIs, discontinue NSAIDs
 Endoscopic coagulation or clipping.
Gastrojejunocolicfistula(GJCF)
 result of inadequate resection of stomach or incomplete vagotomy
 symptoms include upper abdominal pain, weight loss, diarrhea,
gastrointestinal bleeding, and fecal vomiting
54

55. POST GASTRECTOMY SYNDROME
- reservoir dysfunction, Vagal denervation, Aberrations in surgical reconstruction
 Dumping Syndrome: early , late
 Frequently attributed to the rapid emptying of gastric content into the small
bowel
 Early: 15’ to 1 hr after a meal
 due to rapid release of hyperosmolar food into small bowel _ rapid shift in
extracellular fluid _ systemic hypotension
 Nausea, vomiting, epigastric fullness, abdominal cramping and diarrhea,
diaphoresis
 Relieved by lying down
55

56. Late dumping syndrome
 1 to 3 hours after a meal
 Carbohydrates absorbed quickly _ blood sugar level rises _ hyper-
insulinemia and consequent hypoglycemia.
 Fainting, tremor, prostration, decreased consciousness
 Relieved by food
56

57. Management
 Conservative:
 Diatery modification
 Low carbohydrate diet
 Avoid some sort of food such as ice cream
 Avoid hyperosmolar liquids
 Anti dumping diet
 Somatostatin analogues; Octreotide100 mcg IV 15-60 minutes before meal to
slow transit time.
57

58. Surgical treatment
 Only small percent require surgery
 For refractory and disabling symptoms
 Pyloric recnstruction ( if pyloroplasty or pyloromyotomy was done)
 Iso/anti peristaltic segment of jejunum interposed between stomach and small
bowel (10-20 cm)
 Conversion of B II to B I
 Conversion to Roux-en-Y gastrojejunostomy
58

59. Metabolic aberration: B II > B I
 Anemia:
Iron Deficiency( reduced absorption)
Fe decreased absorption (Prefered acidic state)
• Rx : Iron supplement
Pernicious anemia( reduced intrinsic factor)
Rx: B12 supplement
Folate deficiency (malabsorption)
Impaired digestion
Malabsorption (duodenum)
• Rx : Folate supplement
59

60. Contd,
 Metabolic Bone disease
 Vit D absorption decreased in fat malabsorption
• Ca decreased absorption (mostly at duodenum)
Rx : Ca and Vit D supplement
Vagotomy diarrhea:
mechanisms: Dumping syndrome, Post vagotomy uncontrolled bowel
movement , rapid gastric emptying time and bacterial overgrowth
 Rx: anti-motility drugs, high fiber diet, acid suppression, antibiotics
- may improve in months to years time
 Severe / refractory- Antiperistaltic jejunal interposition 75-100cm from ligament of
Treutz
60

61. Gastroparesis
 Delayed gastric emptying due to a problem with gastric motor function or an
obstruction
 Common after TV
 Epigastric fullness, pain and rarely a functional GOO
 Vast majority improve with time
 If persistent
 Metabolic --> electrolyte abnormalities (K+,Mg++, Ca++), endocrine (hypothyroid),
 medications (opiates, etc.), pre-op GOO --> Functional
 Mechanical --> most common. Stomal edema, adhesions, kinking, hematoma,
intussusception, stricture.
 Rx: partial gastrectomy and B II with Braun entero-enterostomy or R-en-Y
reconstruction
61

62. Bile(alkaline) reflux gastritis
 Reflux of alkaline secretions into gastric remnant
 Commonly occurs after B II gastric reconstruction,
 Occurs late, often >1 year post-op
 Constant burning epigastric pain, often radiating to the back, persistent nausea,
bilious emesis
 Vomiting does NOT relieve pain
 Dx by exclusion=clinical + evidence of bile reflux (scope )
Scope :
 mucosal erythema that involve parastomal region
 bile staining or pooling
 observed enterogastric reflux
62

63. Treatment
 Medical management -rarely help
 PPI and H2 blockers,
 Surgical goal- separate the gastric mucosa from the offending biliary and
pancreatic secretions
 Isoperistaltic jejunal interposition (Henley loop)
 Revision of a B II with a Braun enteroenterostomy, addition of the “uncut” Rouxen-Y
 Conversion to a Roux-en-Y=the procedure of choice, 80% relief
 complete vagotomy and antrectomy
63

64. Afferent Loop Obstruction
 A mechanical problem with partial ob-struction of the afferent limb from kinking,
angulation, stenosis or adhesions.
 Chronic > acute
 risk
 Afferent limb length > 30-40 cm
 Antecolic B II GJ
 Anti-perstaltic GJ
 C/P: diarrhea, Severe postprandial epigastric pain(30-60 mins),projectile vomiting & dramatic clinical relief
after vomiting
Prevention: avoid excess afferent limb
Dx: UGI-dilated limb, EGD
64

65. Treatment
Treatment is always surgical
 Surgical options often depend on causes
 Simple adhesiolysis
 Reduction of internal hernia or volvulus
 Repeated resection and anastomosis
 Conversion of a B II to R-Y
 Conversion of B II to B I
 Shortening afferent limb
 Revision of B II with Braun entero-eterostomy
 Requires a complete vagotomy to prevent marginal ulcer
65

66. Efferent Loop Obstruction
 Much less common
 Can be difficult to distinguish from afferent loop syndrome and bile reflux
gastritis
 Crampy LUQ and epigastric pain, nausea, bilious vomiting
 Usually due to adhesions or internal hernia of the limb behind the GJ in a
right-to left direction.
 Tx : surgical.
66

67. Roux syndrome
 Gastric emptying difficulty in patients who had distal gastrectomy and R-Y
reconstruction in the absence of mechanical obstruction
 present with vomiting, epigastric pain, and weight loss
 Thought to result from atonic roux limb
 Endoscopy may show bezoar formation, dilation of the gastric remnant,
or dilation of the Roux limb
 UGI : delayed gastric emptying
 Medical Rx: (promotality agents)
 Surgical : remove most or all of the gastric remnant, dilated and flaccid
roux limb resected with R-Y reconstruction ,
67

68. References
 MasterTechniques in Surgery , Series Editor: Josef E. Fischer
 Schwartz’s Principles of Surgery 10th edition
 Sabiton text book of surgery 20th edition
 Schackleford’s 6th edition
 Maingot’s ABDOMINAL OPERATIONS 12th edition
 Atlas of Surgical Techniques for the Upper Gastrointestinal Tract and Small
Bowel
 Schein’s Common Sense Emergency Abdominal Surgery 2nd edition
 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #18 Carol Rees Parrish,
R.D., MS, Series Editor
 Japanese Society of Gastroenterology 2016
 Uptodate 21.6
68

69. 69

70. 70
Gastrectomy for PUD………….it is like taking out the
engine to decrease noise in the gear box.”
(Francis D. Moore, 1913–2001)