Acute Gastrointestinal Hemorrhage

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
“Learning without thinking is useless. Thinking without learning is dangerous.” - Confucius

Definition and Terminology I> Upper gastrointestinal hemorrhage (UGIH) : Bleeding upon the ligament of treitz Hematemesis : vomiting for fresh blood shown active/ massive bleeding

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

II> Lower gastrointestinal hemorrhage (LGIH): bleeding below ligament of Treitz Hematochezia: means fresh blood, clot, or current jelly stool

FIGURE 46-1D. Rotation of the intestine
FIGURE 46-1D. Rotation of the intestine. A, The intestine after a 90-degree rotation around the axis of the superior mesenteric artery, the proximal loop on the right, and the distal loop on the left. B, The intestinal loop after a further 180-degree rotation. The transverse colon passes in front of the duodenum. C, Position of the intestinal loops after reentry into the abdominal cavity. Note the elongation of the small intestine, with formation of the small intestine loops. D, Final position of the intestines after descent of the cecum into the right iliac fossa. (From Podolsky DK, Babyatshy MW: Growth and development of the gastrointestinal tract. In Yamada T [ed]: Textbook of Gastroenterology. Philadelphia, JB Lippincott, 1995, vol 2, chap 23, with permission. Adapted from Sadler TW [ed]: Langman’s Medical Embryology, 5th ed. Baltimore, Williams & Wilkins, 1985).

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

FIGURE 48-6. Arterial supply of the colon
FIGURE Arterial supply of the colon. (From Gordon PH, Nivatvongs S [eds]: Principles and Practice of Surgery for the Colon, Rectum and Anus, 2nd ed. St. Louis, Quality Medical Publishing, 1999, p 23.)

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

Upper gastrointestinal hemorrhage(UGIH)
variceal bleeding - Cirrhosis and portal hypertension - Endoscopic diagnosis and management - Surgical management

Lower gastrointestinal hemorrhage ( LGIH)
- Relate Surgical Anatomy of small and large intestine - Guideline for approach and treatment - Group of diseases cause LGIH and specific consideration - Historical background of investigation for localization and surgical management for LGIH

PERIOD I …

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

FIGURE 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.) 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.)

NERVE SUPPY TO THE STOMACH
FIGURE Vagal innervation of the stomach. The line of division for truncal vagotomy is shown and is above the hepatic and celiac branches of the left and right vagus nerves, respectively. The line of division for selective vagotomy is shown and occurs below the hepatic and celiac branches. (From Mercer D, Liu T: Open truncal vagotomy. In Operative Techniques in General Surgery 5:8-85, 2003.)

FIGURE 45-5. Gastric mucosa surface
FIGURE Gastric mucosa surface. The normal distribution of gastric glands is depicted on the left. The glands are gray and the gastric pits are black (ื17). (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

GASTRIC GLAND FIGURE Cells residing within a gastric gland. (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

FIGURE Diagrammatic representation of resting and stimulated parietal cell. Note the morphologic transformation between the nonsecreting parietal cell and the stimulated parietal cell with increases in secretory canalicular membrane surface area. (From Mulholland MW: Anatomy and physiology. In Greenfield LJ, Mulholland MW [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993.)

FIGURE The central role of the enterochromaffin-like (ECL) cell in regulation of acid secretion by the parietal cell is shown. As demonstrated, ingestion of a meal stimulates vagal fibers to release acetylcholine (cephalic phase). Binding of acetylcholine to M3 receptors located on the ECL cell, parietal cell, and G cell results in the release of histamine, hydrochloric acid, and gastrin, respectively. Binding of acetylcholine to M3 receptors on D cells results in the inhibition of somatostatin release. Following a meal, G cells are also stimulated to release gastrin, which interacts with receptors located on ECL cells and parietal cells to cause the release of histamines and hydrochloric acid (gastric phase). Release of somatostatin from D cells decreases histamine release and gastrin release from ECL cells and G cells, respectively. In addition, somatostatin inhibits parietal cell acid secretion (not shown). The principal stimulus for activation of D cells is antral luminal acidification (not shown). (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

FIGURE Intracellular signaling events within parietal cell are depicted. As shown, histamine binds to H2 receptors, stimulating adenylate cyclase through a G-protein-linked mechanism. Adenylate cyclase activation causes an increase in intracellular cyclic AMP levels, which in turn activates protein kinases. Activated protein kinases stimulate a phosphorylation cascade with a resultant increase in levels of phosphoproteins that activate the proton pump. Activation of the proton pump leads to extrusion of cytosolic hydrogen in exchange for extracytoplasmic potassium. In addition, chloride is secreted through a chloride channel located on the luminal side of the membrane. Gastrin binds to type B cholecystokinin receptors and acetylcholine binds to M3 receptors. Following the interaction of gastrin or acetylcholine with their receptors, phospholipase C is stimulated through a G-protein-linked mechanism to convert membrane-bound phospholipids into inositol triphosphate (IP3). IP3 stimulates the release of calcium from intracellular calcium stores, leading to an increase in intracellular calcium that in turn activates protein kinases, which activate the H/K-ATPase. ATP, adenosine triphosphate; ATPase, adenosine triphosphatase; cAMP, cyclic adenosine monophosphate; Gs protein, stimulatory guanine nucleotide protein; Gi, inhibitory guanine nucleotide protein; PLC, phospholipase C: PIP2, phosphatidylinositol 4,5 diphosphate. (From Zuidema G: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, WB Saunders, 1995.)

Risk Factor for Peptic Ulcer Hemorrhage
Aspirin (ASA) : since 1899 Non-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

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

** Initial evaluation and treatment of patients with acute gastrointestinal hemorrhage

UPPER GI HEMORRHAGE How should surgeons deal with and step up this complicated problem ? Initial Assessment Initial Resuscitation Critical care and monitoring Definite diagnosis and management Evidence based critical care, Paul Ellis Marick , 2001

A: General assessment and Scoring to categorize the patients
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

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%

Category of Hypovolemic Shock
Class I:Impending (< 10% of blood volumn loss) no symptom,pulse > , BP normal Class II: mild (10-20% of blood volumn loss) fainting, pallor, cool skin, BP drop, pulse>120 Class III:modurate(20-30% of blood volumn loss): urine output -oliguria Class IV: severe ( >40% of blood volumn loss) may caused unconcious and cardiac arrest

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”

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

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

Rockall Scoring Age Shock Co morbid disease ( cancer diseases)
Endoscopic diagnosis Stigmata of recent hemorrhage Pre-endoscope score 0-7 Post –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 = % > 8 : motality rate = > 40% Rockall TA et al GUT 1996; 38:

New Scoring System by Blatchford
Admission Hb BUN Pulse Systolic BP Fainting or melena as chief complaint Liver disease or cardiac disease to predict the need for clinical interventions But it is in only one study

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; สมาคมโรคทางเดินอาหารแห่งประเทศไทย

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

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.

Prediction of UGI bleeding etiology
Incidence(%) Duodenal ulcer Gastric erosions Gastric ulcer Esophageal varices % (in cirrhosis) Malorry-Weiss tear Esophagitis Duodenitis Neoplasm Marginal( stomal) ulcer Esophageal ulcer Miscellaneous Silverstein FE, Gilbert DA, Tadeseo FJ, et al, The national ASGE Survey on upper gastrointestinal bleeding Gastrointestinal Endoscopy, 1981

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

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.

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

Necessary Laboratories
CBC,plt BS, BUN, Cr, electrolyte PT, PTT, bleeding time LFT G/M EKG CxR

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

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

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

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

dosage 40 mg i.v. every 12 hrs. for 5 days
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

SOMATOSTATIN Somatostatin / Octreotide infusion PROSTAGLANDIN ANALOQUE
- In massive UGIH with Hx of advance liver disease is recommended PROSTAGLANDIN ANALOQUE - Cytoprotective agent

Somatostatin causes Splanchnic vasocostriction Reduces Azygos venous blood flow Reduces portal colatteral circulation and decreases portal pressure Octreotide (Somatostatin analoque) 50 microgram i.v.bolus then 50 microgram/ hr for infusion rate for 5 days it can be discontinued without tapering.

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

IV. Definite diagnosis and management
Esophagogastroduodenoscope ( EGD for Dx and Rx) Technique of operative intervention

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 hour after onset of bleeding

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

General Complications of EGD
GI perforation Sepsis Pulmonary aspiration Respiratory failure Induce bleeding Ventricular tachycardia Myocardial infarction Death

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%

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,II Active bleeding lesion, oozing Visible vessel, Adherent clot Ulcer location Posterior duodenal bulb Higher lessor gastric curvature, High lying ulcer Ulcer size and character Large and hard edge

Forrest’s Endscopic finding Classification
IA : Active or Spurting IB : Oozing ulcer IIA: Non-bleeding visible vessel IIB: Adherent clot III : other unspecsified

Endoscopic Intervention For PU bleeding
Thermal Techniques ; monopolar/bipolar/heater probe/laser photo coagulation Injection Methods; 3.6% hypertonic saline+1:20,000 adrenalin 9-12 cc or 1:10, cc via gauge needles. 0.5 cc each point Topical Agents; cyanoacrylate tissue glues/ microcrystalline collagen hemostat : * good for diffuse gastric mucosal lesions or adjunct to other modalities Mechanical methods; Hemoclips (1.5mm)/ balloon tamponad Sukawa, et al, Surg Clin of North Amer, 1992

And Heat probe coagulation in acute GU bleeding
Post combind adrenalin injection And Heat probe coagulation in acute GU bleeding

Post injection + Heater probe coagulation
in active DU bleeding

Follow up EGD of DU bleeding 1 month

Dieulafoy’s lesion : Therapeutic Hemoclip via EGD

Complication Perforation ; 1-3 % Necrosis on high dose epinephrine
Induce 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

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)

INTRAVARICEAL INJECTION ( underfluoroscope and venogram)
FIGURE 51-5A. Techniques of endoscopic sclerotherapy. A flexible endoscope is used for intravariceal injection (A), paravariceal (submucosal) injection (B), and combined paravariceal and intravariceal injection (C). (A to C, Modified from Terblanche J, Burroughs AK, Hobbs EF: Controversies in the management of bleeding esophageal varices. N Engl J Med 320: , 1989.)

PARAVARICEAL INJECTION
FIGURE 51-5B. Techniques of endoscopic sclerotherapy. A flexible endoscope is used for intravariceal injection (A), paravariceal (submucosal) injection (B), and combined paravariceal and intravariceal injection (C). (A to C, Modified from Terblanche J, Burroughs AK, Hobbs EF: Controversies in the management of bleeding esophageal varices. N Engl J Med 320: , 1989.)

FIGURE 51-5C. Techniques of endoscopic sclerotherapy
FIGURE 51-5C. Techniques of endoscopic sclerotherapy. A flexible endoscope is used for intravariceal injection (A), paravariceal (submucosal) injection (B), and combined paravariceal and intravariceal injection (C). (A to C, Modified from Terblanche J, Burroughs AK, Hobbs EF: Controversies in the management of bleeding esophageal varices. N Engl J Med 320: , 1989.)

ENDOSCOPIC MUCOSAL VARICEAL BAND LIGATION
FIGURE 51-6A. Endoscopic ligation of esophageal varices. A, The varix is drawn into the ligator by suction. B, An O ring is applied. (A and B, From Turcotte JG, Roger SE, Eckhauser FE: Portal hypertension. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993, p 899.)

FIGURE 51-6B. Endoscopic ligation of esophageal varices
FIGURE 51-6B. Endoscopic ligation of esophageal varices. A, The varix is drawn into the ligator by suction. B, An O ring is applied. (A and B, From Turcotte JG, Roger SE, Eckhauser FE: Portal hypertension. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993, p 899.)

SB- tube FIGURE The modified Sengstaken-Blakemore tube. Note the accessory nasogastric (N-G) tube for suctioning of secretions above the esophageal balloon and the two clamps, one secured with tape, to prevent inadvertent decompression of the gastric balloon. (From Rikkers LF: Portal hypertension. In Goldsmith H [ed]: Practice of Surgery. Philadelphia, Harper & Row, 1981, pp 1-37.)

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

TIPS( Transcutaneous-jugular intrahepatic portosystemic shunts)
Non-operative shunt Use in stage of cirrhosis with liver failure In 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 )

FIGURE 51-7. Transjugular intrahepatic portosystemic shunt
FIGURE Transjugular intrahepatic portosystemic shunt. A needle is advanced from a hepatic vein to a major portal vein branch (top left) and a guide wire is placed (top right). A hepatic parenchymal tract is created by balloon dilation (middle left), and an expandable metal stent is placed (middle right), thereby creating the shunt (bottom). (From Zemel G, Katzen BT, Becker GJ, et al: Percutaneous transjugular portosystemic shunt. JAMA 266:390, 1991.)

FIGURE Algorithm for definitive therapy of variceal hemorrhage (see text). TIPS, transjugular intrahepatic portosystemic shunt. (Modified from Rikkers LF: Portal hypertension. In Levine BA, Copeland E, Howard R, et al [eds]: Current Practice of Surgery, Vol. 3. New York, Churchill Livingstone, 1995.)

Topic of interest….. Video capsule Endoscopy Intraoperative endoscopy
Rare causes of upper gastrointestinal hemorrhage from an obscure source; small intestine above ligament of treiz that EGD could not exam, new scope was developed

FIGURE There is a large benign-appearing gastric ulcer protruding medially from the lesser curvature of the stomach (arrow) just above the gastric incisura. (Courtesy of Agnes Guthrie, M.D., Department of Radiology, University of Texas Medical School-Houston.) Gastric Diverticulum

FIGURE Distribution of 95 duodenal diverticula within the four portions of the duodenum. (From Eggert A, Teichmann W, Wittmann DH: The pathologic implication of duodenal diverticula. Surg Gynecol Obstet 154:62-64, 1982, with permission.)

FIGURE Large diverticulum arises from the second portion of the duodenum. (Courtesy of Melvyn H. Schreiber, M.D., The University of Texas Medical Branch.)

FIGURE Algorithm for the management of upper gastrointestinal bleeding. NSAID, nonsteroidal anti-inflammatory drug; PPI, proton-pump inhibitor; LGIB, lower gastrointestinal bleeding; AGML, acute gastric mucosal lesions; OR, operating room.

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.

Type of GASTRIC ULCER GU ( Johnston’s criteria)
Acute or Chronic Type I: at Lessor curvature Type II: GU anywhere with DU Type III: at Prepylorus( prepyloric ulcer) Type IV: in 5 CM below EG junction (high lying GU) Type V - ?

FIGURE 45-10A. A, Location of type 1 gastric ulcer
FIGURE 45-10A. A, Location of type 1 gastric ulcer. B, Location of type 2 gastric ulcer. C, Location of type 3 gastric ulcer. D, Location of type 4 gastric ulcer. (From Kauffman G Jr, Conter R: Stress ulcer and gastric ulcer. In Greenfield LJ, Mulholland MW [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993.)

FIGURE 45-10B. A, Location of type 1 gastric ulcer
FIGURE 45-10B. A, Location of type 1 gastric ulcer. B, Location of type 2 gastric ulcer. C, Location of type 3 gastric ulcer. D, Location of type 4 gastric ulcer. (From Kauffman G Jr, Conter R: Stress ulcer and gastric ulcer. In Greenfield LJ, Mulholland MW [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993.)

FIGURE 45-10C. A, Location of type 1 gastric ulcer
FIGURE 45-10C. A, Location of type 1 gastric ulcer. B, Location of type 2 gastric ulcer. C, Location of type 3 gastric ulcer. D, Location of type 4 gastric ulcer. (From Kauffman G Jr, Conter R: Stress ulcer and gastric ulcer. In Greenfield LJ, Mulholland MW [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993.)

FIGURE 45-10D. A, Location of type 1 gastric ulcer
FIGURE 45-10D. A, Location of type 1 gastric ulcer. B, Location of type 2 gastric ulcer. C, Location of type 3 gastric ulcer. D, Location of type 4 gastric ulcer. (From Kauffman G Jr, Conter R: Stress ulcer and gastric ulcer. In Greenfield LJ, Mulholland MW [eds]: Surgery: Scientific Principles and Practice. Philadelphia, JB Lippincott, 1993.)

DUODENAL ULCER (DU) Acute or Chronic Post bulbar Kissing ulcer
Aortoenteric fistula

FIGURE 45-12. A to E, Heineke-Mikulicz pyloroplasty
FIGURE A to E, Heineke-Mikulicz pyloroplasty. (A-E, From Soreide JA, Soreide A: Pyloroplasty. Operative Techniques in General Surgery 5:65-72, 2003.)

FIGURE 46-24A. A, Technique of short strictureplasty in the manner of a Heineke-Mikulicz pyloroplasty. B , For longer diseased segments, strictureplasty may be performed in a manner similar to Finney pyloroplasty. (Adapted with permission from Alexander-Williams J, Haynes IG: Up-to-date management of small-bowel Crohn’s disease. In Advances in Surgery. St. Louis, Mosby, 1987, pp )

FIGURE 46-24B. A, Technique of short strictureplasty in the manner of a Heineke-Mikulicz pyloroplasty. B , For longer diseased segments, strictureplasty may be performed in a manner similar to Finney pyloroplasty. (Adapted with permission from Alexander-Williams J, Haynes IG: Up-to-date management of small-bowel Crohn’s disease. In Advances in Surgery. St. Louis, Mosby, 1987, pp )

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)

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

Technicques for suture and tissue handling
Do not forget to pack the spleen before mobilization of stomach Hanging suture should be used Atraumatic non-absorable suture should be used Babcock 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.

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

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)

Acid Reducing and Drainage Precedure
VAGOTOMY : reduce acid secretion in cephalic phase - TV ; resect vagus n. both ant. and post. trunk And 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)

TV FIGURE 44-2A. Truncal vagotomy and parietal cell vagotomy. A , During truncal vagotomy, both vagal trunks are divided at the esophageal hiatus. The vagal branches to the gastric cardia, fundus, antrum, and pylorus are divided, as are the hepatic and celiac branches. A gastric-emptying procedure, either pyloroplasty or gastrojejunostomy, is required because pyloric opening is impaired. B , Parietal cell vagotomy denervates only the parietal cell mass. Innervation of the antropyloric region and the hepatic and celiac branches is preserved. Parietal cell vagotomy preserves normal gastric emptying, but the procedure requires considerably longer operative time and should be used only in stable patients who do not have significant risk factors for poor outcome. (A and B From Mulholland MW: Duodenal ulcer. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice, 2nd ed. Philadelphia, Lippincott-Raven, 1997, p 766.)

FIGURE Anterior view of the stomach and the anterior nerve of Latarjet. The dotted line represents the line of dissection for parietal cell or highly selective vagotomy. Note that the last major branches of the nerve are left intact and that the dissection begins 7cm from the pylorus. At the gastroesophageal junction, the dissection is well away from the origin of the hepatic branches of the left vagus. (From Kelly KA, Teotia SS: Proximal gastric vagotomy. In Baker RJ, Fischer JE (eds): Mastery of Surgery. Philadelphia, Lippincott, Williams and Wilkins, 2001.)

HSV FIGURE 44-2B. Truncal vagotomy and parietal cell vagotomy. A , During truncal vagotomy, both vagal trunks are divided at the esophageal hiatus. The vagal branches to the gastric cardia, fundus, antrum, and pylorus are divided, as are the hepatic and celiac branches. A gastric-emptying procedure, either pyloroplasty or gastrojejunostomy, is required because pyloric opening is impaired. B , Parietal cell vagotomy denervates only the parietal cell mass. Innervation of the antropyloric region and the hepatic and celiac branches is preserved. Parietal cell vagotomy preserves normal gastric emptying, but the procedure requires considerably longer operative time and should be used only in stable patients who do not have significant risk factors for poor outcome. (A and B From Mulholland MW: Duodenal ulcer. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice, 2nd ed. Philadelphia, Lippincott-Raven, 1997, p 766.)

ANTRECTOMY FIGURE 44-3A. A, Lines mark limits of gastric resection for antrectomy. For patients with more proximal gastric ulcers, the proximal line of resection can be extended or tailored to include the ulcer in the resection. B, Billroth I reconstruction with gastroduodenostomy. Note that truncal vagotomy is included in the procedure. (A and B, From Sabiston DC Jr: Atlas of General Surgery. Philadelphia, WB Saunders, 1994, pp )

FIGURE 45-14A. Hemigastrectomy with Billroth 1 (gastroduodenal) anastomosis. (From Dempsey D, Pathak A: Antrectomy. Operative Techniques in General Surgery 5:86-100, 2003.)

BILLROTH I FIGURE 45-14B. Hemigastrectomy with Billroth 1 (gastroduodenal) anastomosis. (From Dempsey D, Pathak A: Antrectomy. Operative Techniques in General Surgery 5:86-100, 2003.)

BILLROTH I WITH TV FIGURE 44-3B. A, Lines mark limits of gastric resection for antrectomy. For patients with more proximal gastric ulcers, the proximal line of resection can be extended or tailored to include the ulcer in the resection. B, Billroth I reconstruction with gastroduodenostomy. Note that truncal vagotomy is included in the procedure. (A and B, From Sabiston DC Jr: Atlas of General Surgery. Philadelphia, WB Saunders, 1994, pp )

BILLROTH II FIGURE 45-20A. A, Total gastrectomy with a Roux-en-Y anastomosis. B, Subtotal gastrectomy with a Billroth II anastomosis.

FIGURE 45-20B. A, Total gastrectomy with a Roux-en-Y anastomosis
FIGURE 45-20B. A, Total gastrectomy with a Roux-en-Y anastomosis. B, Subtotal gastrectomy with a Billroth II anastomosis.

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 options 1) Suture bleeding point & TV/SV with pyloroplasty 2) Suture bleeding point & HSV 3) Antrectomy with TV or SV In GI hemorrhage – To stop bleeding is the main aim ****

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”

LOCAL PostOp COMPLICATION Re-bleeding Mediastinitis Leakage Post
gastrectomy syndrome FIGURE Causes of afferent loop syndrome.

FIGURE Algorithm for the management of acute hemorrhage due to portal hypertension. TIPS, transjugular intrahepatic portosystemic shunt. (From Rikkers LF: Portal hypertension. In Levine BA, Copeland E, Howard R, et al [eds]: Current Practice of Surgery, Vol. 3. New York, Churchill Livingstone, 1995.)

FIGURE 51-1. The extrahepatic portal venous circulation
FIGURE The extrahepatic portal venous circulation. (From Rikkers LF: Portal hypertension. In Goldsmith H [ed]: Practice of Surgery. Philadelphia, Harper & Row, 1981, pp 1-37.)

FIGURE Portosystemic collateral pathways develop where the portal venous and systemic venous systems are in close apposition. (From Rikkers LF: Portal hypertension. In Miller TA [ed]: Physiologic Basis of Modern Surgical Care. St. Louis, CV Mosby, 1988, pp )

FIGURE 51-3. A three-dimensional reconstruction of a CT angiogram
FIGURE A three-dimensional reconstruction of a CT angiogram. The portal vein (PV), superior mesenteric vein (SMV), splenic vein, and left renal vein are clearly demonstrated. The ready availability of these scans has decreased the need for more invasive techniques such as visceral angiography.

Emergency Surgery for EV Bleeding
PURPOSE 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)

FIGURE Nonselective shunts completely divert portal blood flow away from the liver. (From Rikkers LF: Portal hypertension. In Moody FG, et al [eds]: Surgical Treatment of Digestive Disease. Chicago, Year Book Medical, 1986, pp )

FIGURE A small-diameter (8- to 10-mm) interposition portacaval shunt partially decompresses the portal venous system and may preserve hepatic portal perfusion. (From Sarfeh IJ, Rypins EB, Mason GR: A systematic appraisal of portacaval H-graft diameters: Clinical and hemodynamic perspectives. Ann Surg 204: , 1986.)

FIGURE Cumulative survival data from four controlled trials of the portacaval shunt versus conventional medical management. (From Boyer TD: Portal hypertension and its complications: Bleeding esophageal varices, ascites, and spontaneous bacterial peritonitis. In Zakim D, Boyer TD [eds]: Hepatology: A Textbook of Liver Disease. Philadelphia, WB Saunders, 1982, pp )

Selective shunt ( distal splenorenal)
FIGURE The distal splenorenal shunt provides selective variceal decompression through the short gastric veins, spleen, and splenic vein to the left renal vein. Hepatic portal perfusion is maintained by interrupting the umbilical vein, coronary vein, gastroepiploic vein, and any other prominent collaterals. (From Salam AA: Distal splenorenal shunts: Hemodynamics of total versus selective shunting. In Baker RJ, Fischer JE [eds]: Mastery of Surgery, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp )

FIGURE The Sugiura procedure combines esophageal transection, extensive esophagogastric devascularization, and splenectomy. The paraesophageal collateral vessels are preserved to discourage re-formation of varices. (Modified from Sugiura M, Futagawa S: Further evaluation of the Sugiura procedure in the treatment of esophageal varices. Arch Surg 112:1317, 1977.)

Gastric Varices Primary
Lessor curvature : common- resolute after Endoscopic intervention for RX of EV Greater curvature: Less common Secondary Isolated Gastric Varices: Fundus, due to splenic vein thrombosis treated by SPLENECTOMY

PERIOD II

Lower gastrointestinal hemorrhage ( LGIH)
- Relate Surgical Anatomy of small and large intestine - Guideline for approach and treatment - Group of diseases cause LGIH and specific consideration - Historical background of investigation for localization and surgical management for LGIH

FIGURE Diagnostic steps in the evaluation of acute lower gastrointestinal hemorrhage. RBC, red blood cell; UGI, upper gastrointestinal. (Modified from Turnage RH: Acute gastrointestinal hemorrhage. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice. Philadelphia, Lippincott-Raven, 1997, p 1158.)

FIGURE 48-2. Anatomy of the colon and rectum: coronal view
FIGURE Anatomy of the colon and rectum: coronal view. The diameter of the right colon is larger than the diameter of the left side. Note the higher location of the splenic flexure, compared with the hepatic flexure, and the extraperitoneal location of the rectum.

FIGURE 48-7. Arterial supply of the rectum
FIGURE Arterial supply of the rectum. (From Gordon PH, Nivatvongs S [eds]: Principles and Practice of Surgery for the Colon, Rectum, and Anus, 2nd ed. St. Louis, Quality Medical Publishing, 1999, p 24.)

FIGURE 48-3. Endopelvic fascia
FIGURE Endopelvic fascia. (From Gordon PH, Nivatvongs S [eds]: Principles and Practice of Surgery for the Colon, Rectum, and Anus, 2nd ed. St. Louis, Quality Medical Publishing, 1999, p 10.)

Approach to Hematochezia
Massive Ongoing Bleeding 10-20% of patients with massive bleeding Major Self Limited Bleeding 80-90% of patients with massive bleeding Minor Self Limited Bleeding

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

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

FIGURE mTc pertechnetate scintigraphy in a child demonstrates a Meckel diverticulum clearly differentiated from the stomach and bladder. (Courtesy of Melvyn H. Schreiber, M.D., The University of Texas Medical Branch.)

FIGURE 48-14. Barium enema with extensive sigmoid diverticulosis.

FIGURE 48-18. CT scan of pelvis shows diverticulitis with abscess.

FIGURE 48-19. CT scan of pelvis
FIGURE CT scan of pelvis. The patient has diverticulitis, and air in the bladder indicates a fistula between the sigmoid and the bladder.

FIGURE 48-16. Colonoscopic view of diverticula.

FIGURE 48-15. Pathogenesis of diverticular disease
FIGURE Pathogenesis of diverticular disease. Diverticula are herniations of the mucosa through the points of entry of blood vessels across the muscular wall. Because the diverticula are formed only by the mucosa rather than by the entire wall of the intestine, they are called false diverticula. Note that the diverticula form only between the mesenteric taeniae and each of the two lateral taeniae. Because there are no perforating vessels, diverticula do not form on the antimesenteric side of the colon.

FIGURE Barium enema in a patient with a previous attack of diverticulitis. Note stricture in sigmoid colon. Colonoscopy was necessary to exclude cancer.

FIGURE 48-52. Colonoscopic view of sessile polyp
FIGURE Colonoscopic view of sessile polyp. This polyp proved to be a carcinoma after it was removed by segmental resection.

FIGURE Resected right colon containing large benign sessile polyp adjacent to an ulcerated carcinoma.

FIGURE 49-6A. Hemorrhoids. A, Thrombosed external
FIGURE 49-6A. Hemorrhoids. A, Thrombosed external. B, First-degree internal viewed through anoscope. C, Second-degree internal prolapsed, reduced spontaneously. D, Third-degree internal prolapsed, requiring manual reduction. E, Fourth-degree strangulated internal and thrombosed external. (A, to E, By permission of Mayo Foundation.)

FIGURE 49-6B. Hemorrhoids. A, Thrombosed external
FIGURE 49-6B. Hemorrhoids. A, Thrombosed external. B, First-degree internal viewed through anoscope. C, Second-degree internal prolapsed, reduced spontaneously. D, Third-degree internal prolapsed, requiring manual reduction. E, Fourth-degree strangulated internal and thrombosed external. (A, to E, By permission of Mayo Foundation.)

FIGURE 49-6D. Hemorrhoids. A, Thrombosed external
FIGURE 49-6D. Hemorrhoids. A, Thrombosed external. B, First-degree internal viewed through anoscope. C, Second-degree internal prolapsed, reduced spontaneously. D, Third-degree internal prolapsed, requiring manual reduction. E, Fourth-degree strangulated internal and thrombosed external. (A, to E, By permission of Mayo Foundation.)

FIGURE 49-6E. Hemorrhoids. A, Thrombosed external
FIGURE 49-6E. Hemorrhoids. A, Thrombosed external. B, First-degree internal viewed through anoscope. C, Second-degree internal prolapsed, reduced spontaneously. D, Third-degree internal prolapsed, requiring manual reduction. E, Fourth-degree strangulated internal and thrombosed external. (A, to E, By permission of Mayo Foundation.)

FIGURE The band is advanced onto the end of the ligator instrument using a conical attachment (insets). The hemorrhoid is identified at a level proximal to the dentate; this area is tested for sensation before banding. Occluding the suction port of the ligator instrument draws the hemorrhoid into the open end of the ligator, at which time the instrument is fired. The banded hemorrhoid typically sloughs in a week’s time. (By permission of Mayo Foundation.) Baron ligation

FIGURE 49-9A. Closed hemorrhoidectomy
FIGURE 49-9A. Closed hemorrhoidectomy. A, Hemorrhoidal tissues are sharply excised starting just beyond the external component and working proximal, finishing with resection of the internal component. B, The sphincter muscles are preserved by dissecting only the tissues superficial to them. C, The pedicle is transfixed and the defect closed with a running absorbable suture. (A to C, By permission of Mayo Foundation.)

FIGURE 49-9B. Closed hemorrhoidectomy
FIGURE 49-9B. Closed hemorrhoidectomy. A, Hemorrhoidal tissues are sharply excised starting just beyond the external component and working proximal, finishing with resection of the internal component. B, The sphincter muscles are preserved by dissecting only the tissues superficial to them. C, The pedicle is transfixed and the defect closed with a running absorbable suture. (A to C, By permission of Mayo Foundation.)

FIGURE 49-9C. Closed hemorrhoidectomy
FIGURE 49-9C. Closed hemorrhoidectomy. A, Hemorrhoidal tissues are sharply excised starting just beyond the external component and working proximal, finishing with resection of the internal component. B, The sphincter muscles are preserved by dissecting only the tissues superficial to them. C, The pedicle is transfixed and the defect closed with a running absorbable suture. (A to C, By permission of Mayo Foundation.)

Operative Intervention
Exploratory Laparotomy Looking for the cause of bleeding as the information of localization preoperatively Perform small bowel resection or colonic resection if localization Incase of none localization and negative intraoperative localization, right hemicolectomy may be performed

Acute Gastrointestinal Hemorrhage

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