MANAGEMENT OF PUD
By Biruk Ertiban(GSR III)
Moderator Dr Samuel Tesfaye(GS)
outline
• Introduction
• PUD and types
• Complications of PUD
• Managemant of PUD
Management of PUD
complications(bleeding(UGIB),perforation,obstruction,inter
actablity)
• Summary
• References
Introduction
• the stomach is asymmetrical, pearshaped, most proximal
abdo GI organ then duodenum
• parietal (oxyntic) cells(body,cardia)
Arterial and Venous Blood Supply
of stomach
…cont
Venous drainage
Surgical importance of rich gastric blood
supply
• At least two of the four can be ligated or occluded
• rich venous interconnections in the stomach,
distal splenorenal shunt(splenic vein and lt renal
vein)
effectively decompress esophagogastric varices in portal
hypertension
Innervation
• vagus nerves provide the extrinsic parasympathetic
innervation to the stomach
• Ach
…cont
…cont
Function in stomach
• In the stomach the vagus nerves
• affect secretion (including acid),
• motor function
• mucosal bloodflow
• cytoprotection.
extrinsic sympathetic nerve supply
• originates at spinal levels T5 through T10
• There may be more intrinsic gastric neurons(myenteric
and submucosal plexuses) than extrinsic neurons, but
their function is poorly understood
…cont
• epinephrine is important in the sympathetic nerves,
• Others..
• cholinergic,
• Adrenergic
• peptidergic (e.g., substance P
and somatostatin).
…cont
• Proximal gastric distension stimulates the acid secretion
by vagovagal reflex(which is abolished by truncal or HSV)
• Antral distention also stimulates antral gastrin secretion.
• Acetylcholine stimulates gastrin release
and gastrin stimulates histamine release from ECL cells.
Basal acid secretion
• Interprandial basal acid secretion is 2 to 5 mEq
hydrochloric acid per hour
• 10% of maximal acid output (MAO),
and it is greater at night
• contributes to the relatively low bacterial counts found in
the stomach.
• Basal acid secretion is reduced 75% to 90% by vagotomy
or H2 receptor blockade.
…cont
• H2 receptor knockout mice do not secrete acid in
response to gastrin implies the pivotal role of ECL cells in
acid production
• Somatostatin inhibits histamine release from ECL cells
and gastrin release from antral G cells.
• Helicobacter pylori infection, inhibits D cells and this leads
to an exaggerated acid secretory response (see section
Helicobacter pylori Infection).
Gastric Mucosal Barrier
…cont
• TV and HSV significantly affects receptive relaxation and
gastric accomodiation phases
• result in decreased gastric compliance, shifting the
volume/pressure curve to the left
• Increases liquid emptying rate,
• But increases dumping symptoms after vagotomy
…cont
• Proximal gastric tone also is decreased by duodenal
distention, colonic distention, and ileal perfusion with
glucose (ileal brake)
• vagotomy abolishes phase II of the
gastric MMC but has little influence on phase III(present in
autotransplanted stomach)
MMC(fasting)
• Phase I(about half the length of the entire cycle) is a
period of relative motor inactivity. High-amplitude
muscular contractions do not occur
• Phase II (about 25% of the entireMMC cycle) consists of
some irregular, high-amplitude, generally nonpropulsive
contractions.
• Phase III, a period of intense,regular, (about three per
minute) propulsive contractions, only lasts about 5 to 10
minutes begin in the stomach, and the frequency
approximates that of the myoelectric gastric slow wave.
• Phase IV is a transition period.
PUD
• focal defects in the gastric or duodenal mucosa
that extend into the submucosa or deeper.
• They may be acute or chronic
• imbalance between mucosal defenses and acid/peptic
injury
…cont
Pathophysiology and Etiology
• H. pylori infection and/or NSAID use
• final common pathway to ulcer (“no acid, no ulcer”
remains true).
• The previous thought of all duodenal ucer dueto
hyperacidity and all gastric ulcer dueto loss of mucosal
protection is not true today
…cont
• (beneficially)
 decreased H. pylori infection prevalence ,
better medical therapy
increased outpatient management;
• (detrimentally)
NSAIDs and
aspirin use in aging population
.
…cont
• H.pylori,NSAIDs,cigarette(90% of serious peptic ulcer
complications )
• ZES (gastrinoma),
• antral G-cell hyperfunction and/ or hyperplasia, systemic
mastocytosis,
• trauma,
• Burns
• major physiologic stress
• drugs (all NSAIDs, aspirin, and cocaine),
• Smoking
• psychologic stress
H.pylori
Southern Ethiopia
• Peptic ulcer disease in south Ethiopia is strongly
associated with Hebcobacter pylori
• Helicobacterpylori infection was detected in 93% of 174
patients with a peptic ulcer compared with 63% of 116
patients with normal findings
H.Pylori eradication vs ucer recurrrence
Acid Secretion and Peptic Ulcer
• duodenal ulcer more than gastric ulcer
• There is no correlation between acid
secretion and the severity of the ulcer
disease
• 70% of patients with duodenal ulcers have
an acid output within
the normal range
…cont
• Duodenogastric reflux may play a role weakening the
gastric mucosal defenses(bile, lysolecithin, and
pancreatic juice)
• NSAIDs and aspirin
• Impaired feedback mechanism of gastrin level
• associated with H. pylori infection
• increased rates of gastric emptying
• decreased duodenal bicarbonate secretion(decreases the
buffering capacity
NSAIDS
• Inc. risk of peptic ulcer disease about 5-fold
• Inc. upper GI bleeding about 4-fold
• risk for bleeding and ulceration is proportional to the daily
dosage of NSAIDs
• Complications of PUD (hemorrhage and perforation) are
much more common
…cont
• overall risk of significant serious adverse GI events in
patients taking NSAIDs is more than three times that of
controls
• NSAIDs Vs cyclooxygenase enzymes Vs PGs(rate
limiting)
• NSAID-induced ulcers are more often found in the
stomach
Age more 60 years old(on NSAID)
• risk of complication increases to five times in patients In
elderly patients taking NSAIDs,
• require an operation related to a GI complication is 10
times that of the control group
• will die from a GI cause is about four and half times higher
Smoking
• smokers are twice as likely to develop PUD as
nonsmokers
• increases gastric acid secretion and
duodenogastric reflux
• decreases gastroduodenal prostaglandin production and
pancreaticoduodenal bicarbonate production
Stress
• Both physilogic and psychologic
• Curling ulcer(burn)
• Cushing ‘s ulcer(head trauma)
• Stressful life events increase the occurrence of PUD
comlications
• NB…. Alcohol is commonly mentioned as a risk factor for
PUD, but confirmatory data are lacking
Modified Johnson classification for gastric
ulcer
mortality
• duodenal ulcer was 3.7%
• 2.1% for gastric ulcer of the admitted
• High rates of hospitalization and mortality in elderly
patients for the peptic ulcer complications of bleeding
and perforation.
• use of NSAIDs and aspirin in this elderly cohor
• H. pylori infection.
Clinical Manifestations
• 90% of patients with PUD complain of abdominal pain
• Reffered pain signifies penetration into the pancrease
• nonradiating, burning in quality, and located in the epigastrium
• DU pain >>2 to 3 hours after a meal and at night
• pain that awakens them from sleep(2/3rd )
• nausea,
• bloating,
• weight loss,
• stool positive for occult blood,and anemia
…cont
• Duodenal ulcer is about twice as common in men
• incidence of gastric ulcer is similar in men and women
• gastric ulcer patients are older than duodenal ulcer
patients
• GU incidence is increasing in the elderly(NSAID and
aspirin)
Diagnosis of PUD
• In the young patient(clinical Dx)
• empirical PPI therapy for PUD without confirmatory
testing after pt counseling of small possibility of an
alternative diagnosis
.
Routine laboratory studies include
• complete blood count;
• liver chemistries;
• serum creatinine,
• serum amylase
• calcium levels.
• A serum gastrin level(ulcers that
are refractory to medical therapy or require surgery)
• H.pylori(urea breath test, serum,stool Ag).
…cont
• The two principal means of diagnosing duodenal ulcers
flexible upper endoscopy(need to perform a biopsy to R/o
malignancy, upper endoscopy has replaced upper GI
radiography all with
Age > 45 years old, all patients, regardless of age, should
have this study if any alarm symptoms
Biopsy(gastric ulcer)
• >>>H.pylori(urease assay,culture)
• >>> histologic evaluation
• first biopsy >>only a 70% sensitivity
in detecting gastric cancer
• four biopsy specimens increased this yield to 95%
• taking seven specimens increased it to 98%
Medical Treatment of Peptic Ulcer
Disease
• Acid supressants>>>PPIs, high doseH2RAs
• Protective>>>sucralfate
• H.pylori>>> ABCs
• Iv PPIs for admitted patients+ lifelong PPI on discharge
• acid supressive therapy for 3 months(if underlying cause
resolved)
• Avoid alcohol,smoking NSAIDs
• Pt on NSAIDs is a must, always take concomitant PPIs or
high dose H2 receptor blockers
…cont
• Treat documented H. pylori infection
• give eradication Tx if H. pylori testing is negative and
ulcer symptoms persist
• H. pylori eradication will decrease of elective surgical
procedures and decline complications and mortality from
emergent complications
long-term maintenance
PPI
• all patients admitted to hospital with ulcer complications,
• all high-risk patients on NSAIDs
or aspirin (the elderly or debilitated),
• all patients with a history of recurrent ulcer or bleeding
Complications of PUD
• bleeding,
• Perforation
• Obstruction
• Interactablity
• >>>>>>>7% of hospitalized patients need surgery
Bleeding peptic ulcer
• present with melena and/or hematemesis
• NG tube aspirate Is diagnostic
• Abdominal pain is quite uncommon
• Shock could be the presentation
• Early endoscopy is important to diagnose the cause and
manage
…cont
• Three-fourths of the patients who come to the hospital
with bleeding peptic ulcer will stop bleeding with acid
supression ,resuscitation and NPO
• one fourth will continue to bleed or will rebleed after an
initial quiescent period(all mortalities of UGIB)
high-risk group
• Shock,
• hematemesis,
• transfusion requirement exceeding four units in 24 hours
• endoscopic stigmata (active bleeding or visible vessel)
• these patients benefit from
endoscopic therapy to stop the bleeding
…cont
• most common endoscopic hemostatic modalities used
• injection with epinephrine
• Electrocautery
• Clipping
• Persistent bleeding or rebleeding afterendoscopic therapy
is an indication for operation(vs repeat endoscopic
treatment)
…cont
• elective operation even after initially successful
endoscopic treatment in elderly patient, especially if they
have a high-risk ulcer.
high-risk lesions
• Deep bleeding ulcers on the posterior duodenal bulb ()
gastroduodenal vessel erosion
• Bleeding at lesser gastric curvature(left gastric vessels
erosion)
• early operation should be considere since not
amenable for conservative control
classifying the endoscopic
appearance of bleeding ulcers
Causes of upper GI bleeding(up to 70% of
non variceal bleeding(PUD))
High risk groups
…cont
• operation for ulcer perforation is much more common than
operation for bleeding ulcer
• suture ligation of the bleeder;
• Suture ligation and definitive nonresective ulcer operation
(HSV or V +D)
• gastric resection (usually, including vagotomy and ulcer
excision).
• Take biopst of gastric ulcer if not resected.
Surgery indication for bleeding PUD
• similar to the approach to a trauma patient(ABCs)
• massive hemorrhage unresponsive to endoscopic control,
• transfusion requirement of more than four to six units of
blood despite attempts at endoscopic control
• Lack of availability of a therapeutic endoscopist,
• recurrent hemorrhage after one or more
attempts at endoscopic control,
• lack of availability of blood for
transfusion,
…cont
• Age more than 60 years of age
• Shock at presentation,
• more than four units of blood in 24 hours or eight units of
blood in 48 hours,
• rebleeding,
• ulcers >2 cm in diameter
…cont
• repeat hospitalization for bleeding ulcer
• concurrent indications for surgery(perforation or
obstruction)
• Bleeding from posterior duodenal ulcer or lesser curvature
gastric ulcer
surgeries
• oversewing of the ulcer usually without vagotomy
…cont
• initial pyloromyotomy incision allows access to the
bleeding posterior duodenal ulcer
• expeditious Kocher maneuver allows the surgeon to
control the hemorrhage with the left hand .
• Heavy suture material
• figure-of-eight sutures or U-stitch to securethe bleeding
vessel at the base of the posterior duodenal ulcer.
• Multiple sutures are usually necessary
…cont
• Vagotomy+antrectomy
Perforated PUD
• second most common complication of peptic
ulcer
• a more common indication for operation
than bleeding
• sudden onset of the excruciating abdominal pain
• Previous Hx of PUD
• Phases of peritonitis
chemical peritonitis develops from the gastric and/or
duodenal secfretions
bacterial peritonitis supervenes within hours
Clinical examination
• marked involuntary guarding
• Rebound tenderness is evoked by a gentle examination
• Upright chest X-ray shows free air in about 80% of
patients
Management approach
• NGT insertion
• Analgesic
• Antibiotic
• Resuscitation with isotonic flids
• Take to OR
surgery
• Supraumblical incision
• 1st portion of duodenum
• Those <1 cm can generally be closed primarily
• buttressed >>>wellvascularized omentum.
…cont
• larger perforations or ulcers ,a Graham patch repair
with a tongue of healthy omentum is performed.
• stay sutures are placed that incorporate a bite of healthy
tissue on the proximal and the distal side of the ulcer.
• The omentum is placed underneath these sutures,
Grahm’s patch
…cont
• very large perforations (>3 cm)
Primary closure is difficult
The defect should be closed by the application of healthy
tissue(omentum or jejunal serosa from a Rouxen-Y type
limb)
bypass the duodenum (Billroth II or
Roux-en-Y fashion)
several weeks, the pyloric exclusion stitches or staples
give way
…cont
• simple patch closure
• patch closure and HSV
• Patch closure and V + D
• biopsy
• Simple patch closure, currently the most
commonly performed
• laparoscopy appears to be the superior approach in
patients with duodenal perforations who are
hemodynamically stable
…cont
• should be done in patients with hemodynamic instability
and/ or exudative peritonitis signifying a perforation >24
hours old
• Vagotomy procedures are ommited this days even in
stable patients because of the availablity of PPIs
• Perforation has the highest mortality rate of any
complication of ulcer disease, approaching 15%
Post OP care
• 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
• A routine contrast radiograph
• H. pylori–positive patients should undergo eradication
with appropriate triple-therapy
Nonoperative management
of perforrated PUD
• Surgery is a rule
• objective evidence that
the leak has sealed (i.e., radiologic contrast study)
• The absence of clinical peritonitis
perforation in an inopportune location
• Patch closure with biopsy
• local excision and closure
• biopsy (for gastric ulcers if not resected)
• closure
• truncal vagotomy and drainag
Gastric outlet obstruction
• 5% of patients with PUD
• due to duodenal or prepyloric ulcer disease,
• may be acute (from inflammatory swelling
and peristaltic dysfunction) or chronic (from cicatrix)>>do
not need surgery
• Significant obstruction from chronic ulceration will require
some sort of more substantial intervention(baloon
dilitation,surgery)
presentation
• nonbilious vomiting
• hypokalemic hypochloremic metabolic alkalosis
• Pain
• Wt loss
• Suction splash
…cont
• Other causes of GOO must be ruled out(pancreatic,
gastric, or duodenal malignancy)
• ulcer disease is now less common than obstruction from
cancer
operation for obstructing PUD(GOO)
• Most managed with endoscopic dilitation
• Surgery is for refractory cases
• Vagotomy and antrectomy.
• vagotomy and gastrojejunostomy(difficult duodenal
stump)
• HSV and gastrojejunostomy (curable gastric or duodenal
cancers can be missed)
Intractable or Nonhealing Peptic Ulcer
• failure of an ulcer to heal after an initial trial of 8 to 12
weeks of therapy
• patients relapse after therapy has been discontinued
• unusual indication for peptic ulcer operation
• The surgeon should review the differential diagnosis of
nonhealing ulcer before any
consideration of surgery
Endoscopic and UGI radiography
features that suggest malignancy
• Intraluminal location
• Irregularity and nodularity
• Surrounded by asymmetric mass
• Clubbed mucosal fold
• Ulcers in the fundus(rare but malignant if they present)
• Larger ulcers
• irregular or heaped edges
…cont
• With single-contrast radiographic techniques, 50% of
duodenal ulcers missed
• double-contrast studies, 80% to 90% of ulcer craters can
be detected
Surgical Treatment of Peptic Ulcer
Disease
• The indications for surgery in PUD
bleeding,
perforation,
Obstruction
intractability or nonhealing
Non compliant to medical Tx
Refractory H.pylori inf.
thin or marginally nourished individual(relative C/I)
Goal of surgical therapy
• to reduce gastric acidsecretion
vagotomy,
gastrin-driven secretion >>antrectomy
Vagotomy decreases peak acid output by
approximately 50%
vagotomy plus antrectomy decreases>> 85%
Surgical options
• Highly selective vagotomy(HSV)
• vagotomy and drainage (V+D),
• vagotomy and distal gastrectomy
• Taylor procedure(posterior truncal vagotomy and anterior
seromyotomy)
…surgical options
Depends on
• Typeofulcer(duodenal,gastric,recurrent,marginal)
• condition of the patient,
• surgeons experience
• Superimposed lesions(duodenal scarring/inflammation,
adhesions,
or difficult exposure),
…surgical options
• the ulcer diathesis status of the patient,
• H. pylori infection
• NSAID therapy, previous treatment
• future compliance with
Indications for surgery
• nonhealing or intractable PUD
• multiple recurrences,
• large ulcers (>2 cm),
• complications
• Obstruction
• perforation,
• Hemorrhage
• suspected malignancy
Surgery types for interactable ulcers
• lesser operation
• avoid truncal vagotomy and/or distal gastrectomy
• HSV with or without gastrojejunostomy
• distal gastrectomy (to include the ulcer)
• don’t add a vagotomy in patients with type I or type IV
(juxta-esophageal) gastric ulcers
• Type IV gastric ulcers may be difficult to resect as part of
a distal gastrectomy,special procedures are used
summary
Stomach is a pear shaped,1st intra abdominal organ of
the digestive tract followed by duodenum
It has its own protective mechanism from its own acid
secretion
PUD occurs when the protective mechanism fail to control
the stress usually dueto the undelying
causes(H.pylori,NSAIDs,ASA)
…summary
• PUD can complicate if its not treated
Bleeding
Perforation
GOO
Interactablity
• The need for admission and surgery comes when it
complicates
• Surgery is the last(not the first) management for PUD
References
1. Schwartz principle of surgery,10th Ed, P1050-1090
2. Sabiston text book of surgery,20th Ed, P1200-1240
3. Harrison’s prinsiple of Internal medicine,19th edition
4. Uptodate 20.1
5. Netter Atlas Of Human anatomy,6th Edition
THANKYOU

Management of pud

  • 1.
    MANAGEMENT OF PUD ByBiruk Ertiban(GSR III) Moderator Dr Samuel Tesfaye(GS)
  • 2.
    outline • Introduction • PUDand types • Complications of PUD • Managemant of PUD Management of PUD complications(bleeding(UGIB),perforation,obstruction,inter actablity) • Summary • References
  • 3.
    Introduction • the stomachis asymmetrical, pearshaped, most proximal abdo GI organ then duodenum • parietal (oxyntic) cells(body,cardia)
  • 4.
    Arterial and VenousBlood Supply of stomach
  • 5.
  • 6.
  • 7.
    Surgical importance ofrich gastric blood supply • At least two of the four can be ligated or occluded • rich venous interconnections in the stomach, distal splenorenal shunt(splenic vein and lt renal vein) effectively decompress esophagogastric varices in portal hypertension
  • 8.
    Innervation • vagus nervesprovide the extrinsic parasympathetic innervation to the stomach • Ach
  • 9.
  • 10.
    …cont Function in stomach •In the stomach the vagus nerves • affect secretion (including acid), • motor function • mucosal bloodflow • cytoprotection.
  • 11.
    extrinsic sympathetic nervesupply • originates at spinal levels T5 through T10 • There may be more intrinsic gastric neurons(myenteric and submucosal plexuses) than extrinsic neurons, but their function is poorly understood
  • 12.
    …cont • epinephrine isimportant in the sympathetic nerves, • Others.. • cholinergic, • Adrenergic • peptidergic (e.g., substance P and somatostatin).
  • 13.
    …cont • Proximal gastricdistension stimulates the acid secretion by vagovagal reflex(which is abolished by truncal or HSV) • Antral distention also stimulates antral gastrin secretion. • Acetylcholine stimulates gastrin release and gastrin stimulates histamine release from ECL cells.
  • 14.
    Basal acid secretion •Interprandial basal acid secretion is 2 to 5 mEq hydrochloric acid per hour • 10% of maximal acid output (MAO), and it is greater at night • contributes to the relatively low bacterial counts found in the stomach. • Basal acid secretion is reduced 75% to 90% by vagotomy or H2 receptor blockade.
  • 15.
    …cont • H2 receptorknockout mice do not secrete acid in response to gastrin implies the pivotal role of ECL cells in acid production • Somatostatin inhibits histamine release from ECL cells and gastrin release from antral G cells. • Helicobacter pylori infection, inhibits D cells and this leads to an exaggerated acid secretory response (see section Helicobacter pylori Infection).
  • 16.
  • 17.
    …cont • TV andHSV significantly affects receptive relaxation and gastric accomodiation phases • result in decreased gastric compliance, shifting the volume/pressure curve to the left • Increases liquid emptying rate, • But increases dumping symptoms after vagotomy
  • 18.
    …cont • Proximal gastrictone also is decreased by duodenal distention, colonic distention, and ileal perfusion with glucose (ileal brake) • vagotomy abolishes phase II of the gastric MMC but has little influence on phase III(present in autotransplanted stomach)
  • 19.
    MMC(fasting) • Phase I(abouthalf the length of the entire cycle) is a period of relative motor inactivity. High-amplitude muscular contractions do not occur • Phase II (about 25% of the entireMMC cycle) consists of some irregular, high-amplitude, generally nonpropulsive contractions. • Phase III, a period of intense,regular, (about three per minute) propulsive contractions, only lasts about 5 to 10 minutes begin in the stomach, and the frequency approximates that of the myoelectric gastric slow wave. • Phase IV is a transition period.
  • 20.
    PUD • focal defectsin the gastric or duodenal mucosa that extend into the submucosa or deeper. • They may be acute or chronic • imbalance between mucosal defenses and acid/peptic injury
  • 21.
  • 22.
    Pathophysiology and Etiology •H. pylori infection and/or NSAID use • final common pathway to ulcer (“no acid, no ulcer” remains true). • The previous thought of all duodenal ucer dueto hyperacidity and all gastric ulcer dueto loss of mucosal protection is not true today
  • 23.
    …cont • (beneficially)  decreasedH. pylori infection prevalence , better medical therapy increased outpatient management; • (detrimentally) NSAIDs and aspirin use in aging population .
  • 24.
    …cont • H.pylori,NSAIDs,cigarette(90% ofserious peptic ulcer complications ) • ZES (gastrinoma), • antral G-cell hyperfunction and/ or hyperplasia, systemic mastocytosis, • trauma, • Burns • major physiologic stress • drugs (all NSAIDs, aspirin, and cocaine), • Smoking • psychologic stress
  • 26.
  • 27.
    Southern Ethiopia • Pepticulcer disease in south Ethiopia is strongly associated with Hebcobacter pylori • Helicobacterpylori infection was detected in 93% of 174 patients with a peptic ulcer compared with 63% of 116 patients with normal findings
  • 30.
    H.Pylori eradication vsucer recurrrence
  • 32.
    Acid Secretion andPeptic Ulcer • duodenal ulcer more than gastric ulcer • There is no correlation between acid secretion and the severity of the ulcer disease • 70% of patients with duodenal ulcers have an acid output within the normal range
  • 33.
    …cont • Duodenogastric refluxmay play a role weakening the gastric mucosal defenses(bile, lysolecithin, and pancreatic juice) • NSAIDs and aspirin • Impaired feedback mechanism of gastrin level • associated with H. pylori infection • increased rates of gastric emptying • decreased duodenal bicarbonate secretion(decreases the buffering capacity
  • 34.
    NSAIDS • Inc. riskof peptic ulcer disease about 5-fold • Inc. upper GI bleeding about 4-fold • risk for bleeding and ulceration is proportional to the daily dosage of NSAIDs • Complications of PUD (hemorrhage and perforation) are much more common
  • 35.
    …cont • overall riskof significant serious adverse GI events in patients taking NSAIDs is more than three times that of controls • NSAIDs Vs cyclooxygenase enzymes Vs PGs(rate limiting) • NSAID-induced ulcers are more often found in the stomach
  • 37.
    Age more 60years old(on NSAID) • risk of complication increases to five times in patients In elderly patients taking NSAIDs, • require an operation related to a GI complication is 10 times that of the control group • will die from a GI cause is about four and half times higher
  • 38.
    Smoking • smokers aretwice as likely to develop PUD as nonsmokers • increases gastric acid secretion and duodenogastric reflux • decreases gastroduodenal prostaglandin production and pancreaticoduodenal bicarbonate production
  • 39.
    Stress • Both physilogicand psychologic • Curling ulcer(burn) • Cushing ‘s ulcer(head trauma) • Stressful life events increase the occurrence of PUD comlications • NB…. Alcohol is commonly mentioned as a risk factor for PUD, but confirmatory data are lacking
  • 42.
  • 43.
    mortality • duodenal ulcerwas 3.7% • 2.1% for gastric ulcer of the admitted • High rates of hospitalization and mortality in elderly patients for the peptic ulcer complications of bleeding and perforation. • use of NSAIDs and aspirin in this elderly cohor • H. pylori infection.
  • 44.
    Clinical Manifestations • 90%of patients with PUD complain of abdominal pain • Reffered pain signifies penetration into the pancrease • nonradiating, burning in quality, and located in the epigastrium • DU pain >>2 to 3 hours after a meal and at night • pain that awakens them from sleep(2/3rd ) • nausea, • bloating, • weight loss, • stool positive for occult blood,and anemia
  • 45.
    …cont • Duodenal ulceris about twice as common in men • incidence of gastric ulcer is similar in men and women • gastric ulcer patients are older than duodenal ulcer patients • GU incidence is increasing in the elderly(NSAID and aspirin)
  • 46.
    Diagnosis of PUD •In the young patient(clinical Dx) • empirical PPI therapy for PUD without confirmatory testing after pt counseling of small possibility of an alternative diagnosis .
  • 47.
    Routine laboratory studiesinclude • complete blood count; • liver chemistries; • serum creatinine, • serum amylase • calcium levels. • A serum gastrin level(ulcers that are refractory to medical therapy or require surgery) • H.pylori(urea breath test, serum,stool Ag).
  • 48.
    …cont • The twoprincipal means of diagnosing duodenal ulcers flexible upper endoscopy(need to perform a biopsy to R/o malignancy, upper endoscopy has replaced upper GI radiography all with Age > 45 years old, all patients, regardless of age, should have this study if any alarm symptoms
  • 49.
    Biopsy(gastric ulcer) • >>>H.pylori(ureaseassay,culture) • >>> histologic evaluation • first biopsy >>only a 70% sensitivity in detecting gastric cancer • four biopsy specimens increased this yield to 95% • taking seven specimens increased it to 98%
  • 53.
    Medical Treatment ofPeptic Ulcer Disease • Acid supressants>>>PPIs, high doseH2RAs • Protective>>>sucralfate • H.pylori>>> ABCs • Iv PPIs for admitted patients+ lifelong PPI on discharge • acid supressive therapy for 3 months(if underlying cause resolved) • Avoid alcohol,smoking NSAIDs • Pt on NSAIDs is a must, always take concomitant PPIs or high dose H2 receptor blockers
  • 54.
    …cont • Treat documentedH. pylori infection • give eradication Tx if H. pylori testing is negative and ulcer symptoms persist • H. pylori eradication will decrease of elective surgical procedures and decline complications and mortality from emergent complications
  • 55.
    long-term maintenance PPI • allpatients admitted to hospital with ulcer complications, • all high-risk patients on NSAIDs or aspirin (the elderly or debilitated), • all patients with a history of recurrent ulcer or bleeding
  • 56.
    Complications of PUD •bleeding, • Perforation • Obstruction • Interactablity • >>>>>>>7% of hospitalized patients need surgery
  • 57.
    Bleeding peptic ulcer •present with melena and/or hematemesis • NG tube aspirate Is diagnostic • Abdominal pain is quite uncommon • Shock could be the presentation • Early endoscopy is important to diagnose the cause and manage
  • 58.
    …cont • Three-fourths ofthe patients who come to the hospital with bleeding peptic ulcer will stop bleeding with acid supression ,resuscitation and NPO • one fourth will continue to bleed or will rebleed after an initial quiescent period(all mortalities of UGIB)
  • 59.
    high-risk group • Shock, •hematemesis, • transfusion requirement exceeding four units in 24 hours • endoscopic stigmata (active bleeding or visible vessel) • these patients benefit from endoscopic therapy to stop the bleeding
  • 60.
    …cont • most commonendoscopic hemostatic modalities used • injection with epinephrine • Electrocautery • Clipping • Persistent bleeding or rebleeding afterendoscopic therapy is an indication for operation(vs repeat endoscopic treatment)
  • 61.
    …cont • elective operationeven after initially successful endoscopic treatment in elderly patient, especially if they have a high-risk ulcer.
  • 62.
    high-risk lesions • Deepbleeding ulcers on the posterior duodenal bulb () gastroduodenal vessel erosion • Bleeding at lesser gastric curvature(left gastric vessels erosion) • early operation should be considere since not amenable for conservative control
  • 67.
  • 68.
    Causes of upperGI bleeding(up to 70% of non variceal bleeding(PUD))
  • 70.
  • 71.
    …cont • operation forulcer perforation is much more common than operation for bleeding ulcer • suture ligation of the bleeder; • Suture ligation and definitive nonresective ulcer operation (HSV or V +D) • gastric resection (usually, including vagotomy and ulcer excision). • Take biopst of gastric ulcer if not resected.
  • 73.
    Surgery indication forbleeding PUD • similar to the approach to a trauma patient(ABCs) • massive hemorrhage unresponsive to endoscopic control, • transfusion requirement of more than four to six units of blood despite attempts at endoscopic control • Lack of availability of a therapeutic endoscopist, • recurrent hemorrhage after one or more attempts at endoscopic control, • lack of availability of blood for transfusion,
  • 74.
    …cont • Age morethan 60 years of age • Shock at presentation, • more than four units of blood in 24 hours or eight units of blood in 48 hours, • rebleeding, • ulcers >2 cm in diameter
  • 75.
    …cont • repeat hospitalizationfor bleeding ulcer • concurrent indications for surgery(perforation or obstruction) • Bleeding from posterior duodenal ulcer or lesser curvature gastric ulcer
  • 76.
    surgeries • oversewing ofthe ulcer usually without vagotomy
  • 77.
    …cont • initial pyloromyotomyincision allows access to the bleeding posterior duodenal ulcer • expeditious Kocher maneuver allows the surgeon to control the hemorrhage with the left hand . • Heavy suture material • figure-of-eight sutures or U-stitch to securethe bleeding vessel at the base of the posterior duodenal ulcer. • Multiple sutures are usually necessary
  • 78.
  • 79.
    Perforated PUD • secondmost common complication of peptic ulcer • a more common indication for operation than bleeding • sudden onset of the excruciating abdominal pain • Previous Hx of PUD • Phases of peritonitis chemical peritonitis develops from the gastric and/or duodenal secfretions bacterial peritonitis supervenes within hours
  • 80.
    Clinical examination • markedinvoluntary guarding • Rebound tenderness is evoked by a gentle examination • Upright chest X-ray shows free air in about 80% of patients
  • 81.
    Management approach • NGTinsertion • Analgesic • Antibiotic • Resuscitation with isotonic flids • Take to OR
  • 82.
    surgery • Supraumblical incision •1st portion of duodenum • Those <1 cm can generally be closed primarily • buttressed >>>wellvascularized omentum.
  • 83.
    …cont • larger perforationsor ulcers ,a Graham patch repair with a tongue of healthy omentum is performed. • stay sutures are placed that incorporate a bite of healthy tissue on the proximal and the distal side of the ulcer. • The omentum is placed underneath these sutures,
  • 84.
  • 85.
    …cont • very largeperforations (>3 cm) Primary closure is difficult The defect should be closed by the application of healthy tissue(omentum or jejunal serosa from a Rouxen-Y type limb) bypass the duodenum (Billroth II or Roux-en-Y fashion) several weeks, the pyloric exclusion stitches or staples give way
  • 86.
    …cont • simple patchclosure • patch closure and HSV • Patch closure and V + D • biopsy • Simple patch closure, currently the most commonly performed • laparoscopy appears to be the superior approach in patients with duodenal perforations who are hemodynamically stable
  • 87.
    …cont • should bedone in patients with hemodynamic instability and/ or exudative peritonitis signifying a perforation >24 hours old • Vagotomy procedures are ommited this days even in stable patients because of the availablity of PPIs • Perforation has the highest mortality rate of any complication of ulcer disease, approaching 15%
  • 89.
    Post OP care •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 • A routine contrast radiograph • H. pylori–positive patients should undergo eradication with appropriate triple-therapy
  • 90.
    Nonoperative management of perforratedPUD • Surgery is a rule • objective evidence that the leak has sealed (i.e., radiologic contrast study) • The absence of clinical peritonitis
  • 91.
    perforation in aninopportune location • Patch closure with biopsy • local excision and closure • biopsy (for gastric ulcers if not resected) • closure • truncal vagotomy and drainag
  • 92.
    Gastric outlet obstruction •5% of patients with PUD • due to duodenal or prepyloric ulcer disease, • may be acute (from inflammatory swelling and peristaltic dysfunction) or chronic (from cicatrix)>>do not need surgery • Significant obstruction from chronic ulceration will require some sort of more substantial intervention(baloon dilitation,surgery)
  • 93.
    presentation • nonbilious vomiting •hypokalemic hypochloremic metabolic alkalosis • Pain • Wt loss • Suction splash
  • 94.
    …cont • Other causesof GOO must be ruled out(pancreatic, gastric, or duodenal malignancy) • ulcer disease is now less common than obstruction from cancer
  • 95.
    operation for obstructingPUD(GOO) • Most managed with endoscopic dilitation • Surgery is for refractory cases • Vagotomy and antrectomy. • vagotomy and gastrojejunostomy(difficult duodenal stump) • HSV and gastrojejunostomy (curable gastric or duodenal cancers can be missed)
  • 96.
    Intractable or NonhealingPeptic Ulcer • failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy • patients relapse after therapy has been discontinued • unusual indication for peptic ulcer operation • The surgeon should review the differential diagnosis of nonhealing ulcer before any consideration of surgery
  • 98.
    Endoscopic and UGIradiography features that suggest malignancy • Intraluminal location • Irregularity and nodularity • Surrounded by asymmetric mass • Clubbed mucosal fold • Ulcers in the fundus(rare but malignant if they present) • Larger ulcers • irregular or heaped edges
  • 99.
    …cont • With single-contrastradiographic techniques, 50% of duodenal ulcers missed • double-contrast studies, 80% to 90% of ulcer craters can be detected
  • 100.
    Surgical Treatment ofPeptic Ulcer Disease • The indications for surgery in PUD bleeding, perforation, Obstruction intractability or nonhealing Non compliant to medical Tx Refractory H.pylori inf. thin or marginally nourished individual(relative C/I)
  • 101.
    Goal of surgicaltherapy • to reduce gastric acidsecretion vagotomy, gastrin-driven secretion >>antrectomy Vagotomy decreases peak acid output by approximately 50% vagotomy plus antrectomy decreases>> 85%
  • 102.
    Surgical options • Highlyselective vagotomy(HSV) • vagotomy and drainage (V+D), • vagotomy and distal gastrectomy • Taylor procedure(posterior truncal vagotomy and anterior seromyotomy)
  • 103.
    …surgical options Depends on •Typeofulcer(duodenal,gastric,recurrent,marginal) • condition of the patient, • surgeons experience • Superimposed lesions(duodenal scarring/inflammation, adhesions, or difficult exposure),
  • 104.
    …surgical options • theulcer diathesis status of the patient, • H. pylori infection • NSAID therapy, previous treatment • future compliance with
  • 105.
    Indications for surgery •nonhealing or intractable PUD • multiple recurrences, • large ulcers (>2 cm), • complications • Obstruction • perforation, • Hemorrhage • suspected malignancy
  • 106.
    Surgery types forinteractable ulcers • lesser operation • avoid truncal vagotomy and/or distal gastrectomy • HSV with or without gastrojejunostomy • distal gastrectomy (to include the ulcer) • don’t add a vagotomy in patients with type I or type IV (juxta-esophageal) gastric ulcers
  • 108.
    • Type IVgastric ulcers may be difficult to resect as part of a distal gastrectomy,special procedures are used
  • 111.
    summary Stomach is apear shaped,1st intra abdominal organ of the digestive tract followed by duodenum It has its own protective mechanism from its own acid secretion PUD occurs when the protective mechanism fail to control the stress usually dueto the undelying causes(H.pylori,NSAIDs,ASA)
  • 112.
    …summary • PUD cancomplicate if its not treated Bleeding Perforation GOO Interactablity • The need for admission and surgery comes when it complicates • Surgery is the last(not the first) management for PUD
  • 113.
    References 1. Schwartz principleof surgery,10th Ed, P1050-1090 2. Sabiston text book of surgery,20th Ed, P1200-1240 3. Harrison’s prinsiple of Internal medicine,19th edition 4. Uptodate 20.1 5. Netter Atlas Of Human anatomy,6th Edition
  • 114.

Editor's Notes

  • #5 the right gastroepiploic artery is second largest artery to the stomach It arises consistently from the gastroduodenal artery behind the first portion of the duodenum. The left gastroepiploic artery arises from the splenic artery together with the right gastroepiploic artery, forms the rich gastroepiploic arcade along the greater curvature
  • #6 Left gastric artery(largest) Right gastric artery Left gastoepiploic artery Right gastroepiploic artery(2nd largest) Short gastric artery
  • #7 veins draining the stomach generally parallel thearteries left gastric (coronary vein) and right gastric veins usually drain into the portal vein, occasionally into the splenic vein. The RGE vein drains into the SMV near the inferior border of the pancreatic neck, left gastroepiploic vein drains into the SMV.
  • #9 From the vagal nucleus in the floor of the fourth cerebral ventricle,through the neck and carotidsheath Mediastinum(gives off the recurrent laryngeal nerve) Then divides into several branches around the esophagus. These branches come together again above the esophageal hiatus and form the left (anterior) and right (posterior) vagal trunks (mnemonic LARP) Near the GE junction the anterior vagus sends a branch (or branches) to the liver in thegastrohepatic ligament, Then the left(ant) vagus continues along the lesser curvature as the anterior nerve of Latarjet posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature. The nerves of Latarjet send segmental branches to the body of the stomach before they terminate near the angularis incisura as the “crow’s foot,” sending branches to the antropyloric region.
  • #10 In 50% of patients, there are more than two vagal nerves at the esophageal hiatus The branch that the posterior vagus sends to the posterior fundus is termed the criminal nerve of Grassi. This branch typically arises above the esophageal hiatus and is easily missed during truncal or highly selective vagotomy (HSV). Most of vagal trunks have afferentnerves(from viscera to brain)
  • #11 Vagal fibers originating in the brain synapse with neurons in Auerbach’s myenteric plexus and Meissner’s submucosal plexus.
  • #13 acetylcholine is an important neurotransmitter mediating vagal function,
  • #21 the start of these trends all predated the use of H2 receptor blockers, or proton pump inhibitors, fiberoptic endoscopy, and highly selective vagotomy decreased hospital admission and death rate(past 30 yrs) but not as dramatically as expected
  • #23 NSAID use causes ulcers predominantly by compromise of mucosal defenses. gastric ulcer was viewed as a disease of An increased understanding of peptic ulcer pathophysiology has blurred this overly simplistic distinction saying increased acid-peptic action causes duodenal ulcer , weakened mucosal defenses causes gastric ulcer
  • #27 The gold standard for diagnosis of H. pylori is mucosal biopsy performed during upper endoscopy, but noninvasive tests offer an effective screening tool and do not require an endoscopic procedure. If endoscopy is to be performed, evaluation of biopsy samples with either a urease assay or histologic examination offers excellent diagnostic accuracy. Evaluation of serum antibodies is the test of choice for initial diagnosis when endoscopy is not required but has the drawback of remaining positive after treatment and eradication of infection. For monitoring treatment efficacy, stool antigen and urea breath testing are better choices.
  • #33 In the United States, probably more than 90% of serious peptic ulcer complications can be attributed to H. pylori infection, NSAID use, and/or cigarette smoking Pts infected with h.pylori produces more acid with small gastrin stimulation than the normal ones
  • #34 weakening the gastric mucosal defenses, and a variety of components in duodenal juice, including bile, lysolecithin, and pancreatic juice, have been shown to cause injury and inflammation in the gastric mucosa. NSAIDs and aspirin
  • #36 NSAIDs are absorbed through the stomach and small intestine and function as systemic inhibitors of the cyclooxygenase enzymes. Cyclooxygenase enzymes form the rate-limiting step of prostaglandin synthesis in the GI tract
  • #43 Lesser curve, incisura. II. Body of stomach, incisura + duodenalulcer (active or healed). III. Prepyloric. IV. High on lesser curve, near gastroesophageal junction. V. Medication-induced (NSAID/ acetylsalicylic acid), anywhere in stomach Approximately 60% of ulcers are in this location and are classified as type I gastric ulcers. These ulcers are generally not associated with excessive acid secretion and may occur with low to normal acid output. Most occur within 1.5 cm of the histologic transition zone between the fundic and antral mucosa and are not associated with duodenal, pyloric, or prepyloric mucosal abnormalities. In contrast, type II gastric ulcers (approximately 15%) are located in the body of the stomach in combination with a duodenal ulcer. These types of ulcers are usually associated with excess acid secretion. Type III gastric ulcers are prepyloric ulcers and account for approximately 20% of the lesions. They also behave similar to duodenal ulcers and are associated with hypersecretion of gastric acid. Type IV gastric ulcers occur high on the lesser curvature, near the GE junction. The incidence of type IV gastric ulcers is less than 10%, and they are not associated with excessive acid secretion. Type V gastric ulcers can occur at any location and are associated with long-term NSAID use. Finally, some ulcers may appear on the greater curvature of the stomach, but the incidence is less than 5%.
  • #54 Antacids differ greatly in their buffering ability, absorption, taste, and side effects. Magnesium antacids tend to be the best buffers but can cause significant diarrhea, whereas acids precipitated with phosphorus can occasionally result in hypophosphatemia and sometimes constipation. Antacids are 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. If taken on an empty stomach, antacids are emptied rapidly and have only a transient buffering effect. Because of this transient efficacy, the use of buffering antacids has largely been replaced by antisecretory therapy (either H2 receptor antagonists or PPIs) for the treatment of PUD
  • #57 Although intractable disease no doubt exists, its definition is nebulous, and determining exactly when and what type of surgical intervention are required is primarily a matter of judgment. In the current era of excellent treatment options for H. pylori infection and acid suppression, few patients who are truly compliant with medical therapy develop intractable ulcer disease in the absence of malignancy.
  • #61 In a case with exposed vessel, mechanical hemostasis using a clip is useful to control the bleeding
  • #64 which ranges from 0 to 23, with higher scores indicating higher risk
  • #65 which ranges from 0 to 23, with higher scores indicating higher risk
  • #66 Panel B shows the Rockall score, with point values assigned for each of three clinical variables (age and the presence of shock and coexisting illnesses) and two endoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating higher risk. Patients with a clinical Rockall score (Age + Shock + Coexisting illness) of 0 or a complete Rockall score of 2 or less are considered to be at low risk for rebleeding or death.
  • #67 Panel B shows the Rockall score, with point values assigned for each of three clinical variables (age and the presence of shock and coexisting illnesses) and two endoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating higher risk. Patients with a clinical Rockall score (Age + Shock + Coexisting illness) of 0 or a complete Rockall score of 2 or less are considered to be at low risk for rebleeding or death.
  • #68 Forrest classification (Table 48-4), which stratifies the risk of rebleeding based on observed “stigmata of recent hemorrhage.” Lower risk ulcers are much more frequently encountered than actively bleeding ones, even in the setting of inpatients undergoing endoscopy for diagnosis of upper GI bleeding
  • #77 When the mortality for reoperation for rebleeding is considered, the overall mortality is probably comparable for the two approaches. Patients who are in shock or medically unstable should not have gastric resection.
  • #78 Oversewing of the bleeder followed by long-term acid suppression is a reasonable alternative in high-risk or unstable patients.
  • #79 The mortality rate for surgery for bleeding peptic ulcer is around 20%. An initial pyloromyotomy incision allows access to the bleeding posterior duodenal ulcer, and an expeditious Kocher maneuver allows the surgeon to control the hemorrhage with the left hand if necessary. Heavy suture material on a stout needle is used to place figure-of-eight sutures or a U-stitch to secure the bleeding vessel at the base of the posterior duodenal ulcer. Multiple sutures are usually necessary
  • #80 second ulcer or a GI cancer has to be consudered in a patient with perforated and bleeding at a time
  • #81  perforation is their first symptom of ulcer disease Perforation has the highest mortality rate of any complication of ulcer disease, approaching 15%
  • #83 perforation is usually in the first portion of the duodenum and can easily be accessed through an upper midline incision
  • #84 larger perforations or ulcers with fibrotic edges that cannot be brought together without tension, a Graham patch repair with a tongue of healthy omentum is performed. Multiple stay sutures are placed that incorporate a bite of healthy tissue on the proximal and the distal side of the ulcer. The omentum is placed underneath these sutures, and they are tied to secure it in place and seal the perforation
  • #87 there is clearly a trend away from definitive operation for perforated duodenal ulcer, probably because of the ready availability of PPI, and surgeon unfamiliarity with definitive operation in this setting.
  • #91 Vagotomy is usually added for type II and III gastric ulcers. Patch closure with biopsy; or local excision and closure; or biopsy, closure, truncal vagotomy, and drainage are alternative operations in the unstable or high-risk patient, or in the patient with a perforation in an inopportune location. All perforated gastric ulcers, even those in the prepyloric position, should be biopsied if they are not removed at surgery
  • #98 adequate duration of therapy, H. pylori eradication, and elimination of NSAID use must be confirmed. A serum gastrin level should also be determined to R/o gastrinoma
  • #103 Classic truncal vagotomy, in combination with a Heineke-Mikulicz pyloroplasty, is shown in Figure 48-12. When the duodenal bulb is scarred, a Finney pyloroplasty or Jaboulay gastroduodenostomy may be a useful alternative