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Acute Gastrointestinal Hemorrhage Sirikan Yamada, M.D., F.R.C.S.T Assistant Professor Department of Surgery Faculty of Medicine, CMU Chiang Mai, Thailand

Acute Gastrointestinal Hemorrhage

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Acute Gastrointestinal Hemorrhage. Sirikan Yamada, M.D., F.R.C.S.T Assistant Professor Department of Surgery Faculty of Medicine, CMU Chiang Mai, Thailand. “Learning without thinking is useless. Thinking without learning is dangerous.”. - Confucius. Acute Gastrointestinal Hemorrhage. - PowerPoint PPT Presentation

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Page 1: Acute Gastrointestinal Hemorrhage

Acute Gastrointestinal Hemorrhage

Sirikan Yamada, M.D., F.R.C.S.TAssistant ProfessorDepartment of SurgeryFaculty of Medicine, CMUChiang Mai, Thailand

Page 2: Acute Gastrointestinal Hemorrhage

“Learning without thinking is useless.

Thinking without learning is dangerous.”

- Confucius

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Acute Gastrointestinal Hemorrhage

Definition and TerminologyI> Upper gastrointestinal hemorrhage (UGIH): Bleeding upon the ligament of treitz

•Hematemesis : vomiting for fresh blood shown active/ massive bleeding

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Acute Gastrointestinal Hemorrhage

Definition and Terminology (cont)

•Coffee ground: blood+gastric secretion shown resent subside UGIH

•Melena: Hb+acid= acid hematin, since 50cc of blood 1000cc of blood caused melena persist For 5-7 days, and occult blood can be positive for 21 days

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Acute Gastrointestinal Hemorrhage

II> Lower gastrointestinal hemorrhage(LGIH): bleeding below ligament of Treitz

Hematochezia: means fresh blood, clot, or current jelly stool

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Divisions of the stomach  (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

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Upper gastrointestinal hemorrhage(UGIH)

*** Guideline for approach and management

non-variceal bleeding- Related Surgical Anatomy and

pathophysiology of Stomach and Duodenum

- Group of diseases caused UGIH and specific consideration

- Endoscopic and surgical management for UGIH

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Upper gastrointestinal hemorrhage(UGIH)

variceal bleeding- Cirrhosis and portal hypertension- Endoscopic diagnosis and managem

ent- Surgical management

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Lower gastrointestinal hemorrhage( LGIH)

- Relate Surgical Anatomy of small and large intestine

- Guideline for approach and treatment- Group of diseases cause LGIH and sp

ecific consideration- Historical background of investigatio

n for localization and

surgical management for LGIH

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PERIOD I …

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Why we have to learn …..

Over all mortality rate is still high in upper GI hemorrhage,

about 5-8%

Dudnick R, Martin P, Friedman LS; management of bleeding ulcer. Med Clin North Am 75:948,1991

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Blood supply to the stomach and duodenum with anatomical relationships to the spleen and pancreas. The stomach is reflected cephalad. (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

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NERVE SUPPY TO THE STOMACH

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GASTRIC GLAND

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Risk Factor for Peptic Ulcer Hemorrhage

Aspirin (ASA) : since 1899Non-steroidal antiinflammatory drug ( N-SAID) :

has both Cyclooxygenase-1 and 2: COX - 1(house keeping enzyme) & COX 2( Co-

enzyme) Selective COX- 2 inhibitor: 1999 EX: Clelcoxib, Rofecoxib

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COX theory ASA – inhibit COX- 1, decrease Thromboxane&

decrease prostaglandin caused of lost of protection for gastric mucosa, and decrease hemostasis

N-SAID- inhibits both COX-1 and COX-2 :results like in ASA user. Increase risk of complication in PU patients =6.1 (relative risk) and in recent GI bleeding patients= 13.5 (relative risk)

Selective COX-2 inhibitor: results more protection for gastric mucosal barrier, and hemostasis

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Acute Gastrointestinal Hemorrhage

IDENTIFICATION SOURCE OF BLEEDING AND SPECIFIC THERAPY

RESUSCITATIONand STABILIZATION INTENSIVE MONITORING

INITIAL ASSESSMENT

** Initial evaluation and treatment of patients

with acute gastrointestinal hemorrhage

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Initial AssessmentInitial ResuscitationCritical care and monitoringDefinite diagnosis and management

UPPER GI HEMORRHAGE

Evidence based critical care, Paul Ellis Marick , 2001

How should surgeons deal with and step up this complicated problem ?

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I. Initial Assessment

A: General assessment and Scoring to categorize the patients - Active or ongoing/ massive/ continue/ or intermittent bleeding

B:Hx and PE (Cirrhotic patient or Non cirrhotic patient )

C:NG tube should be inserted to confirm the level of bleeding

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A. General Assessment Hemodynamic assessment : BP, pulse, postural changes, peripheral perfusion The presence of co morbid diseases Estimation of blood loss by nasogastric tube intubation and hemodynamic response to fluid challenge** remarked that - to use 2 L of crystalloid to stabilize v/s , blood loss is about 15-30% - If BP raises but fall again, blood loss is about 30-40% - If BP continues to fall, blood loss is more than 40%

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Category of Hypovolemic Shock

Class I:Impending (< 10% of blood volumn loss)

no symptom,pulse > 90-100 , BP normalClass II: mild (10-20% of blood volumn loss) fainting, pallor, cool skin, BP drop, pulse>120Class III:modurate(20-30% of blood volumn

loss): urine output -oliguriaClass IV: severe ( >40% of blood volumn loss) may caused unconcious and cardiac arrest

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Category and scoring of patients

To evaluate and predict further ulcer hemorrhage

To select the method of management

“ It is dictated by the rate of bleeding”

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Clinical bleeding

1.Trace heme-positive stools and without severe anemia ( OPD) of cases

2.Visible blood, coffee ground, melena ( IPD/ further evaluation)

1+ 2 = 80 % of cases Fleischer D, et al Gastroenterology, 1983

3.Persistent or massive bleeding / referred due to rebleeding with hemodynamic instability (ICU)

** Massive/ ongoing bleeding is defined as loss of > 30% of estimated blood volume or bleeding required blood transfusion > 6 U/ 24 hours

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Scoring to categorize the patients

Forrest classification severe, moderate, mild Lancet 1974 Rockall Risk Scoring Gut 1996 New Scoring System by Blatchford Lancet 2000 Modified Rockall Score for both Non-variceal and Variceal bleeding AJG 2002

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Rockall Scoring Age Shock Co morbid disease ( cancer diseases) Endoscopic diagnosis Stigmata of recent hemorrhagePre-endoscope score 0-7Post –op endoscope score 0-11 * this scoring system is good to predict for the mortality rate much than rebleeding 0-3 : mortality rate = 0 – 11% 4-7 : mortality rate = 24- 27% > 8 : motality rate = > 40%

Rockall TA et al GUT 1996; 38: 316-21

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New Scoring System by Blatchford

Admission HbBUNPulseSystolic BPFainting or melena as chief complaintLiver disease or cardiac disease

• to predict the need for clinical interventions• But it is in only one study

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High Risk ~Criteria Host Factors- Age >60yr- Co-morbid conditions e.g. renal failure, cirrhosis,

cardiovascular disease, COPD- Hemodynamic instability; mod to severe shock- Coagulopathy include drug-related Bleeding character ; Active continue red blood

from NG after irriagtion and red blood per rectum

Patient course; massive blood transfution> 4-6 units to maintain Hb in 24 hr , re-bleeding in 72 hr , return to have hemodynamic instability

2004 Concensus for Clinical Practice Guideline for the Management of

Upper GI bleeding; สมาคมโรคทางเดิ�นอาหารแห�งประเทศไทย

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I. Initial Assessment

A: General assessment and Scoring to categorize the patients - Active or ongoing/ massive/ continue/ or intermittent bleeding

B: Hx and PE (Cirrhotic patient or Non cirrhotic patient )

C: NG tube should be inserted to confirm the level of bleeding

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B. Take Hx and PE (Cirrhotic patient or Non cirrhotic patient )

- History taking of previous medication and underlying diseases/ anticoagulant usage.

- Esophageal varices is more suspicious

for 60% - 80% in severe upper GI bleeding with history of advanced liver disease or a history of previous variceal bleeding.

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Prediction of UGI bleeding etiology Incidence(%) Duodenal ulcer 24.3 Gastric erosions 23.4 Gastric ulcer 21.3 Esophageal varices 10.3----------20% (in cirrhosis) Malorry-Weiss tear 7.2 Esophagitis 6.3 Duodenitis 5.8 Neoplasm 2.9 Marginal( stomal) ulcer 1.8 Esophageal ulcer 1.7 Miscellaneous 6.8 Silverstein FE, Gilbert DA, Tadeseo FJ, et al, The national ASGE Survey on upper gastrointestinal bleeding Gastrointestinal Endoscopy, 1981

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I. Initial Assessment

A: General assessment and Scoring to categorize the patients - Active or ongoing/ massive/ continue/ or intermittent bleeding

B: Hx and PE (Cirrhotic patient or Non cirrhotic patient )

C: NG tube should be inserted to confirm the level of bleeding

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C. NG tube placement

Should perform in all UGI hemorrhage to confirmation that it is the upper GI

bleeding , monitoring of bleeding and , decompressed the stomach

No report that it may potentiate bleeding in case of esophageal varices, just careful in patients who had severe coagulopathy.

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UGI LGI Melena Hematemasis or coffee ground Maroon stool * Red stool ** * Guaiac test ( can positive more 2 weeks after bleeding stopped)

* Bile was seen via NG tube** Massive bleeding

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Necessary Laboratories

CBC,pltBS, BUN, Cr, electrolytePT, PTT, bleeding timeLFTG/MEKGCxR

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II. Initial Resuscitation

How to do for good resuscitation?When will we give blood transfusion ? Which medication will be used?

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Large- bore intravenous lines or central lines NG tube aspiration (by hand) to decompress clot

in stomach Volume expansion with colloid or crystalloid Transfusion of blood immediately if patient has

hemodynamically unstable

* Blood products are the most efficient volume expanders** It take about 72 hours for Hct to reach its nadir; therefore, a normal or moderate low Hct does not exclude significant bleeding*** Conversely, minimally falling of Hct also

represent fluid disequilibrium much rather than continued bleeding

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If patients have coagulopathy, they should be corrected.

- PTT prolong > 1.5 times - Platelet < 50,000/ mm3

- FFP should be given after 6 unit of PRC and plt should add after 10 unit of PRC Monitoring V/S, urine out put /hour Airway protection in those who have alteration of consciousness or endotracheal intubations may

facilitate to investigate and give treatment in these patients

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Recommendation for empiric Acid- suppression therapy Traditionally treated, even before the cause is

determined, with acid suppression therapy. Medications are extremely safe, although the efficacy of this practice has not been proven conclusively.

Kupfer, et al Gastroenterol Clin of North Amer, 2000

I.V. Proton pump inhibitor is more effective than

I.V. H 2 blocker in increasing intragastric pH Vasopressin should not be used due to its systemic side effect

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High dose omeprazole significantly reduces the frequency of further bleeding and of surgery in patients with bleeding ulcer.

dosage 40 mg i.v. every 12 hrs. for 5 days Saltzman JR, N Engl J Med, 1997

NEW GENERATION PPI

- Lanzoplazole- Pantoprazole- Rabeprazole - Esomeprazole

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SOMATOSTATIN

Somatostatin / Octreotide infusion

- In massive UGIH with Hx of advance liver disease is recommended

PROSTAGLANDIN ANALOQUE - Cytoprotective agent

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Somatostatin causes - Splanchnic vasocostriction- Reduces Azygos venous blood flow- Reduces portal colatteral circulation and

decreases portal pressureOctreotide (Somatostatin analoque) 50 microgram i.v.bolus then 50 microgram/ hr for infusion rate for 5

days it can be discontinued without tapering.

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III. Critical care and monitoring

ICU is needed, when?

- Massive/ continue or on going bleeding with or without coagulopathy - High Rockall scoring patients ( high risk of morbidity & mortality due to continue or rebleeding - Severe co-morbid disease

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IV. Definite diagnosis and management

Esophagogastroduodenoscope

( EGD for Dx and Rx)Technique of operative intervention

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Endoscogastroduodenoscope ( EGD for Dx and Rx)Indication and Timing - In high score patients ( > 3) - Shock Category II, III - Promptly as a double set up in active /massive bleeding - Under specialist to perform endoscopic therapy for hemostasis or localized potential angiographic or surgical therapy

* Initial diagnostic procedure of choice should be performed in first 6- 24 hour after onset of bleeding

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Precaution and contraindication

Absolute contraindication - GI perforation - Acute uncontrolled unstable angina - Severe untreated coagulopathy - uncontrolled respiratory decompensation - unexperience endoscopist and patient agitation and uncooperation* Intraoperative endoscopy ( on ET-tube and G/A ) in selected cases or shift the intervention to surgery or conservative only

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General Complications of EGD

GI perforationSepsisPulmonary aspirationRespiratory failureInduce bleedingVentricular tachycardiaMyocardial infarctionDeath

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Prediction of further ulcer hemorrhage

The most important endoscopic predictor of persistent or recurrent bleeding is active bleeding( arterial spurting or oozing) at the time of endoscopy

The rate of rebleeding is approximately

3 % in the low risk group

25% in the high risk group Number of blood transfusion units

> 5 units = 57% needing Surgery, mortality = 43%

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Adverse Prognostic Factors in UGIH Endoscopic criteria for endoscopic intervention because of high rate of continue or re-bleeding

Stigmata of recent hemorrhage: Forrest classification I,IIActive bleeding lesion, oozingVisible vessel, Adherent clot Ulcer locationPosterior duodenal bulbHigher lessor gastric curvature, High lying ulcerUlcer size and characterLarge and hard edge

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Forrest’s Endscopic finding Classification

IA : Active or Spurting IB : Oozing ulcerIIA: Non-bleeding visible vesselIIB: Adherent clotIII : other unspecsified

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Endoscopic Intervention For PU bleeding

1) Thermal Techniques ; monopolar/bipolar/heater probe/laser photo coagulation

2) Injection Methods; 3.6% hypertonic saline+1:20,000 adrenalin 9-12 cc or 1:10,000 10 cc via 23-25 gauge needles. 0.5 cc each point

3) Topical Agents; cyanoacrylate tissue glues/ microcrystalline collagen hemostat : * good for diffuse gastric mucosal lesions or adjunct to other modalities

4) Mechanical methods; Hemoclips (1.5mm)/ balloon tamponad

Sukawa, et al, Surg Clin of North Amer, 1992

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Post combind adrenalin injectionAnd Heat probe coagulation in acute GU bleeding

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Post injection + Heater probe coagulation in active DU bleeding

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Follow up EGD of DU bleeding 1 month

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Dieulafoy’s lesion : Therapeutic Hemoclip via EGD

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Complication

Perforation ; 1-3 % Necrosis on high dose epinephrineInduce acute and delayed hemorrhage

5-30% in visible vv. those treated by thermal therapy or injection therapy

* most common is cardiopulmonary in nature or related to sedation given

** Prophylaxis antibiotic should be applied

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Endoscopic Intervention

For Esophageal varices : 1) Endoscopic band ligation combind

2) Endoscopic sclerosing therapy: 1% Ethoxyscleral solution 0.5-1cc /point

3) Combined Ballon Tamponad for temporary control after fail endoscopic intervetion control ( Senstaken Blakemore tube preparation)

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INTRAVARICEALINJECTION( underfluoroscope and venogram)

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PARAVARICEALINJECTION

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ENDOSCOPICMUCOSAL VARICEAL BAND LIGATION

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SB- tube

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Complication

Prophylaxis antibiotics cover gram negative bacteria such as ciprofoxacin, levofloxacin, ceftacidime, amoxicillin-culvulanic acid,and aztreonam are appropriate choices

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TIPS( Transcutaneous-jugular intrahepatic portosystemic shunts)

Non-operative shuntUse in stage of cirrhosis with liver failureIn non-randomize trial : Less effective to

stop GI bleeding than operative shunt, but less invasive.

Technique need radiointervention ( described by Zemel G, Katzen B T, Becker G J, et al

TIPS, JAMA, 266:390,1991 )

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Topic of interest…..

Video capsule EndoscopyIntraoperative endoscopyRare causes of upper gastrointestinal

hemorrhage from an obscure source;

small intestine above ligament of treiz that EGD could not exam, new scope was developed

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Gastric Diverticulum

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Post operative EGD to follow up

For non-definite surgical procedure cases ; after 2 week post operation (in Japan)

To check for malignant potential and adjunct medical treatment including H.pylori eradication in some case

* There is a report of unnecessary management to eradicate H.pylori at the time of hemorrhage occurrence.

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Type of GASTRIC ULCERGU ( Johnston’s criteria)

Acute or ChronicType I: at Lessor curvatureType II: GU anywhere with DUType III: at Prepylorus( prepyloric ulcer)Type IV: in 5 CM below EG junction

(high lying GU)

Type V - ?

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DUODENAL ULCER (DU)

Acute or ChronicPost bulbar Kissing ulcerAortoenteric fistula

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Operative intervention

To stop bleeding by suture in emergency situation or failure bleeding control by endoscopic intervention 1-2 times.

To definite treatment for the cause of bleeding

High risk patient, massive and no time, no blood( rare blood group AB, Rh negative , no skillful endoscopist)

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Operative Finding

Do not forget to palpate and look for the scar at stomach and duodenum both anterior and posterior wall.

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Technicques for suture and tissue handling

Do not forget to pack the spleen before mobilization of stomach

Hanging suture should be usedAtraumatic non-absorable suture should

be usedBabcock preferred to use for temporary

handling stomach incision edge Incision should start at anterior stomach

wall longitudinally or at place that EGD suspected the cause of bleeding.

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Technicques for suture and tissue handling

Suture bleeding point by Transfixing U stitch it should be performed in acute massive DU

hemorrhage For the difficult large duodenal ulcer and chronic

ulcer, alternative surgical procedures may be added depend on condition of patient

- Ulcerectomy - TV with drainage procedure ( various type of

pyloroplasty, gastrojejunostomy) ** selection for complete diverticulization

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Technicques for suture and tissue handling

Difficult chronic GU ; need tissue ? > 10% of GU > 1 cm are malignant ulcer Chua CL and Jeyaraj PR, Am J Surg; 1992

Difficult type - posterior wall ulcer; ulcerectomy with or

without leaving the ulcer to capsule of pancrease - high lying GU type IV ( Johnston’s type)

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Acid Reducing and Drainage Precedure VAGOTOMY : reduce acid secretion in cephalic

phase - TV ; resect vagus n. both ant. and post. trunkAnd need to do drainage procedure, always - SV ; resect ant. Vagus n. and post. N.of Latajet ( vagus n. after separation of celiac and hepatic branch). Need to do drainage procedue - HSV ; resect only branch of Latajet and preserve branch at Craw foot to preserve function of pylorus ANTRACTOMY : reduce G-cell ( Billroth I, or Billroth II)

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TV

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HSV

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ANTRECTOMY

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BILLROTH I

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BILLROTH I WITH TV

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BILLROTH II

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Operative Procedure for chronic GU and DU

GU Type I ; Antrectomy include ulcer or

ulcer excision GU Type II ; Ulcer excision& TV & pyloroplasty or highly selective vagotomy( HSV) GU Type III and DU ; 3 options1) Suture bleeding point & TV/SV with pyloroplasty2) Suture bleeding point & HSV3) Antrectomy with TV or SV

In GI hemorrhage – To stop bleeding is the main aim ****

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Surgical tecniques for highlying GU( type IV)

Most aggressive distal gastrectomy including portion of ulcer at esophageal wall with roux-en –Y esophagogastrojejunostomy; “ Csendes procedure” Am J Surg; 1978 Antrectomy only with leaving the ulcer in place due to it close to EG junction; “ Kelling- Made- lener procedure” , Maingot ;1997 Greenfield; 1992 For 2-5 cm ulcer at lessor curvature from EG junction; distal gastric resection with a vertical extension( tonque) to include the lesser curvature with end-to-end gastroduodenostomy. “ Pauchet procedure” Shackelford’s; 1991 Wedge of anterior and posterior gastric wall at lessor curvature to include the ulcer, with ligation of left gastric vessels close to stomach wall ; “ Shoe- maker”

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LOCAL PostOpCOMPLICATION

Re-bleeding Mediastinitis Leakage Post gastrectomy syndrome

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Emergency Surgery for EV BleedingPURPOSE Indirect control of bleeding site Do not change the mortality after bleeding EV

in cirrhotic patient

1) Emergency Total or nonselective- Shunt

Operation: Portocaval shunt is the procedure of

choice

2) Non-Shunt Operation: Sugiura’s( Esophageal

transection with devascularizatoion) , Hassab’s

operation(Total devascularization)

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Selective shunt ( distal splenorenal)

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Gastric Varices

PrimaryLessor curvature : common- resolute after

Endoscopic intervention for RX of EVGreater curvature: Less common

Secondary

Isolated Gastric Varices: Fundus, due to splenic vein thrombosis treated by SPLENECTOMY

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PERIOD II

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Lower gastrointestinal hemorrhage( LGIH)

- Relate Surgical Anatomy of small and large intestine

- Guideline for approach and treatment- Group of diseases cause LGIH and sp

ecific consideration- Historical background of investigatio

n for localization and

surgical management for LGIH

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Approach to Hematochezia

Massive Ongoing Bleeding

10-20% of patients with massive bleedingMajor Self Limited Bleeding

80-90% of patients with massive bleedingMinor Self Limited Bleeding

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Diagnosis investigation for LGIH

Nuclear Scintigraphy - Sulfur colloid scan - Technetium 99-m labeled RBC scan

Selective visceral Angiography Colonoscope Barium Enema Ix for small intestine bleeding

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Causes and Treatment of Lower GI Hemorrhage

Colonic Diverticular Disease Arteriovenous Malformation (AVM) Inflammatory Bowel Disease Radiation Injury to Small and Large Bowel Tumor of Colon and Rectum Intussusception Ishemic Colitis Colon and Anorectal Varices Meckel’s and other small intestinal diverticula

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Baron ligation

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Operative Intervention

Exploratory LaparotomyLooking for the cause of bleeding as the information of localization preoperativelyPerform small bowel resection or colonic

resection if localizationIncase of none localization and negative

intraoperative localization, right hemicolectomy may be performed