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1University of Kentucky UGI BleedObie M. Powell, M.D.Joseph A. Iocono, M.D.Department of SurgeryUniversity of Kentucky
2Mr. Mellenna57 year-old white male with recent history of dark stools presents to the emergency room complaining of a two hour history of vomiting blood and feeling faint.On presentation the patient is pale and lethargic complaining of abdominal pain.
3HistoryWhat other points of the history do you want to know?
4History, Mr. Mellenna Consider the Following Characterization of symptomsTemporal sequenceAlleviating / Exacerbating factors:Pertinent PMH, ROS, MEDS.Relevant family hx.Associated signs and symptoms
5Characterization of Symptoms Un-relenting nausea with associated burning epigastric discomfortPain is steady and rates it as a 5 on a scale of 1-10.
6Temporal Sequence Dark stools off and on for approximately 6 months. Often has some mild epigastric pain to which he pays little attention. This pain has been occurring for the same duration.Today he has been feeling “light headed” for about 3-4 hours, and has been throwing up blood for 2 hours.
7Alleviating / Exacerbating Factors Standing erect worsens his light headedness and laying down improves it.Nothing improves the pain or nauseaIn the past eating food sometimes relieved his abdominal pain.
8PMH HTN MI 3 years prior treated with angioplasty and stenting. COPD The patients past history is significant forHTNMI 3 years prior treated with angioplasty and stenting.COPDOsteoarthritisNo prior abdominal surgery
9PMHMedicationsASA - supposed to be on it but it bothers his stomachMetoprolol 50mg po BIDSimvastatin 10mg po dailyIbuprofen 400mg po QID prn, none in past 2 weeksNKDA
10Family/Social History Family HistoryNon-contributorySocial HistoryMarriedComputer programmerETOH- 6 pack per weekFamily HistoryNon contributorySocial HistoryMarried, computer programmerETOH—6 pack per week
11ROSAs in HPI.The patient denies chest pain, shortness of breath, fever, chills, anorexia, and dysuriaROS should emphasize further characterization of the active disease process AND risk factors that may complicate surgery such as active infection, active CAD, poor exercise tolerance
15Physical Exam What to look for Vital signs: instability, respiratory distress, beware of beta blockadeOverall appearance: signs of anemia, dehydrationAbdominal exam: probe for peritonitisRectal exam: mandatory. Look for perianal causes of bleeding.
16Physical Exam, Mr. Mellenna Vital signs: Temp. 97.8, Pulse 90, BP 95/63 Resp. 30Patient is alert and oriented. Pale skin and dry mucous membranes.During your examination the patient has a large maroon bowel movement
17Physical ExamHead is atraumatic / normocephalic, eyes sunken, pale conjunctivaNeck- No lymphadenopathy, flat neck veins.Oropharynx - dried blood, no active bleeding, dry mucus membranes.CV- Regular rate and rhythm, no murmur, rubs, or gallopsChest- Mild tachypnea, respirations are clear bilaterally no rales, rhonchi, or wheezesAbdomen is scaphoid, soft, mildly tender in mid-epigastrum. Bowel sounds are present and hyperactive.Extremities show no clubbing, cyanosis, or edema.Rectal exam shows gross blood, enlarged smooth prostate, no palpable masses, no hemmorhoids or other peri-anal disease
18Would you like to revise your initial differential diagnosis?
20Laboratory studies: What is necessary? Type and CrossCBC: Do you expect anemia?CMP: evaluate for hepatic dysfunction and renal compromiseCoags: active hemorrhage can cause coagulopathy and requires aggressive replacementABG: probe for acidosis
23Laboratory Values Discussion An elevated BUN to Creatinine ratio can be a sign of upper GI bleed due to the digestion of blood or prerenal azotemia.A patient actively hemorrhaging will show a normal Hgb/Hct prior to being resuscitated. Chronic bleeding presents with typical iron deficiency anemia.
25Interventions to consider ABC’sEnsure adequate airway protection and adequate respirationsStart 2 large bore IV’s.Fluid bolus either NS or LRFoley CatheterNG with gastric lavageSTAT Upper endoscopy
26Endoscopy Upon upper endoscopy the esophagus appears normal. There is a large amount of clot in the stomach, irrigation reveals normal appearing mucosa without signs of ulcer or gastritis.On passing through the pylorus copious gross blood is encountered with a actively bleeding ulcer on the posterior wall of the duodenum.
28EndoscopyAttempt at injecting with epinepherine, and even direct pressure prove unsuccessful with continued brisk pulsatile bleeding.Are there any particular endoscopic findings that suggest a higher risk of failed therapy or re-bleeding?
29What would you do next? Repeat Hct is 18 He is actively bleeding in Endoscopy
30Surgery for Bleeding Ulcers IndicationsPre-operative preparationOperative approachRelevant AnatomyPotential complications
31Operative Indications Duodenal ulcers located on the anterior wall are prone to perforation and present as peritonitis and free air. Those on the posterior wall, which is the more common location, lead to bleeding.The gastroduodenal artery passes just distal to the pylorus and posterior to the duodenum. If it or one of it’s branches are in the ulcer crater they may erode and result in massive bleeding.
32Operative TechniquePatients are explored through an upper midline incision.An incision is made in the anterior duodenum through the pylorus and distal stomach.The site of bleeding is identified. The bleeding can then usually be controlled by placing sutures in 3-4 quadrants around the ulcer base.The gastroduodenal artery may be ligated if necessary
33Operative TechniqueOnce bleeding has been controlled, the horizontal opening through the pyloric channel is closed vertically resulting in a Heineke-Mikulicz pyloroplasty.A truncal vagotomy is then added for long-term ulcer control. Specimens of both vagal trunks are sent to Pathology to document the vagotomy
35Gastrointestinal Bleeding Bleeding can arise anywhere along the GI tract. Bleeding represents the initial symptom of gastrointestinal disease in 1/3 of all patients. The majority of bleeding will stop spontaneously.
36Gastrointestinal Bleeding Hematemesis- Vomiting of blood. Can be either gross blood and blood clots representing rapid bleeding or “coffee-ground” emesis signifying chronic bleeding. Hematemesis is the result of bleeding from the oropharynx to the ligament of Treitz.Melena- Passage of black and tarry stool caused by digested blood.
37Gastrointestinal Bleeding Melena is usually the result of severe upper GI bleeding. Melena without hematemesis is caused by severe bleeding distal to the ligament of Treitz.Hematochezia- Passage of maroon to red blood and blood clots.
38Gastrointestinal Bleeding As little as mL of blood in the GI tract produces melena. Melena can persist from 5-7 days after a 2 unit bleed and stools can remain occult positive up to 3 weeks.With upper GI blood loss blood urea nitrogen levels may be elevated to mg/dL. A BUN: Creatinine ratio greater than 36:1 likely represents blood loss from an upper GI source.
39Upper Gastrointestinal Bleeding Some dependency on socioeconomic factors. Peptic ulcers are more common in suburban hospitals, while gastritis and varices are more common in urban centers. Patients 60 years old and older represent ~ 60% of patients presenting with upper GI bleeding with a mortality rate of 20-25%. For younger patients the mortality rate drops to 4%.
40Upper Gastrointestinal Bleeding Although elective surgeries for duodenal ulcers have dropped off significantly due to H2 blockers and proton pump inhibitors, the number of surgeries for bleeding duodenal ulcers has remained stable.Sudden cessation of H2 blockers or proton pump inhibitors may result in a rebound increase in acid secretion resulting in GI bleeding.
41Upper Gastrointestinal Bleeding Nose bleeds- Rarely the cause of major bleeding. It must be ruled out by a careful examination of the posterior pharynx to insure blood is not running down the esophagus, causing hematemesis .
42Upper Gastrointestinal Bleeding Esophagitis- Hiatus hernia and reflux esophagitis are not common causes of upper GI bleeding. Reflux esophagitis is more likely to result in chronic occult bleeding usually associated with grade II-III esophagitis with friable mucosa. Significant bleeding in this area is more commonly associated with para- esophageal hernias.
43Upper Gastrointestinal Bleeding Varices- Bleeding esophageal and gastric varices in the presence of liver disease account for about 10% of upper GI bleeds and are life threatening situations associated with a high mortality rate. Alcoholism is the most common cause of portal hypertension but hepatitis B and C are becoming common causes.
44Upper Gastrointestinal Bleeding Varices- In pediatric patients 95% of all upper GI bleeds are caused by variceal hemorrhage, usually as a consequence of extra hepatic portal venous obstruction. In patients with cirrhosis and portal hypertension variceal hemorrhage accounts for 50-75% of all upper GI bleeds. Variceal hemorrhage is usually precipitated by ulceration of the varix secondary to reflux esophagitis or increased pressure within the varix.
45Upper Gastrointestinal Bleeding Varices- In patients with liver disease bleeding is precipitated by the inability of the liver to synthesize clotting factors. Initial therapy includes sclerotherapy, ligation and vasopressin. Ligation is as effective as sclerotherapy with fewer complications. If unsuccessful shunting or transplant may be necessary.
46Upper Gastrointestinal Bleeding Mucosal tear (Mallory-Weiss)Esophagogastric mucosal tear or Mallory-Weiss tear account for 5-10% of all upper GI bleeds. Mallory-Weiss tears present in a classic pattern. Initially the patient has vomiting without blood. Continued emesis leads to pain from the tear and eventually the patient develops hematemesis. 90% of Mallory-Weiss bleeding resolves spontaneously and require no further therapy.If bleeding persists, endoscopic therapy with injection of vasoconstrictive agents, IV vasopressin or balloon tamponade with Sengstaken-Blakemoore tube may be necessary.
47Upper Gastrointestinal Bleeding GastritisUp to 1/3 of upper GI bleeds are caused by diffuse gastritis. Erosions are usually multiple and found primarily in the fundus and body of the stomach. Chronic slow bleeds are most commonly associated with H. pylori, while more brisk bleeding is usually a result of ingested substances harmful to the gastric mucosa such as NSAIDs, alcohol, steroids, or other drugs.Treatment is with vasopressin, iced saline lavage, sucralfate, H2 blockers, and proton pump inhibitors. Bleeds refractory to these treatments may require electrocautery, vagotomy and antrectomy or even total gastrectomy.
48Upper Gastrointestinal Bleeding Peptic ulcerMost common cause of upper GI bleed, encompassing 1/2- 2/3 of patients. Bleeding is presenting symptom in up to 10% of these patients. Duodenal bleed is four times more common than gastric ulcer bleed. Duodenal ulcers are usually posterior and involve branches of the gastroduodenal artery.Benign gastric ulcers bleed more than malignant ulcers. There will be significant bleeding in 10-15% of peptic ulcers and surgical intervention is needed in 20% of these patients
49Upper Gastrointestinal Bleeding Stress ulcersStress ulcers refer to acute gastroduodenal lesions that arise after episodes of shock, sepsis, surgery, trauma, burns (Curling’s ulcer), or intracrainial pathology or surgery (Cushing’s ulcer). Specific risk factors associated with these ulcers are, multi system trauma, hypotension, respiratory failure, sepsis, jaundice, recent surgery and burns.It is believed that stress ulceration is the result of bile reflux damage to the gastric protective barrier combined with decreased gastric blood flow secondary to splanchnic vasoconstriction. Sepsis, coagulopathy, and activation of cytokines may also play a role in the formation of stress ulcers.
50Upper Gastrointestinal Bleeding Other causesMiscellaneous causes may contribute up to 18% of upper GI bleeds. Gastric neoplasms both malignant and benign can cause bleeding which is usually mild and chronic. Dieulafoy’s vascular malformations are dilated arterial lesions usually amendable to endoscopic injection.Aorto-enteric fistulas can present as a herald bleed followed by a massive bleed in patients with prior aortic reconstructions. Hematobilia can be found in patients following hepatic injuries or manipulations.
51Upper Gastrointestinal Bleeding Management- Complete history with inquiries of peptic ulcer disease, alcohol use, cirrhosis, heart burn, reflux, and medications. Exam looking for signs of cirrhosis including spider angiomata, palmer erythema, prominent abdominal veins, caput medusa, and ascites. Examine mucous membranes for melanin spots associated with Puetz-Jeghers syndrome. Perform rectal exam and check for occult blood in the stool.
52Upper Gastrointestinal Bleeding Management- Fluid resuscitation, foley, naso-gastric tube, gastric lavage and arterial line.Labs- Complete blood count with platelets, comprehensive metabolic panel with liver functions, and coagulation studies. Cross match for blood transfusion.
53Upper Gastrointestinal Bleeding Studies/Treatment :EGD with sclerotherapy or electrocautery, tagged red blood cell scan, arteriography with embolization.If esophageal bleeding does not respond to sclerotherapy, ligation, or intravenous vasopressin, Sengstaken-Blakemoore tube should be used.
54Upper Gastrointestinal Bleeding TIPS- for portal hypertensionTrans jugular intrahepatic porto-systemic shunt. Used for bleeding secondary to portal hypertension. Associated with in hospital mortality rate of 35-56%. Encephalopathy rate is the same as for patients who undergo porto-caval shunts. Stenosis or occlusion of TIPS is up to 50% at one year.
55Lower Gastrointestinal Bleeding Small Bowel- Small bowel accounts for 10-15% of all lower GI bleeds. Usually a diagnosis of exclusion. Seeing blood exiting the ileo-cecal valve accounts for 10% of diagnoses. Causes include, Meckel’s diverticulum, Crohn’s disease, intussusception, neoplasm, vascular malformations, intestinal varices, blood dyscrasias, non-Meckel’s diverticulum, mesenteric thrombosis, drug reactions, enteric infections, and polyps.
56Lower Gastrointestinal Bleeding Colon- Most often related to polyps or neoplastic disease (occult). Right sided lesions usually present through anemia and guaiac positive stools. Larger bleeds can arise from diverticuli or angiodysplastic lesions on either the right or left side.
57Lower Gastrointestinal Bleeding Angiodysplastic lesions have the following characteristics. They are not congenital or neoplastic but degenerative. They are not associated with other vascular lesions. They increase with age. They are usually small < 5mm. They can be diagnosed by colonoscopy. 80% of angiodysplastic bleeds will stop spontaneously and 50% will re- bleed within 3 years.Ulcerative colitis- Usually cause chronic bloody diarrhea, but massive bleeds can occur
58Lower Gastrointestinal Bleeding Management- Complete H&P. Fluid resuscitation, foley, naso-gastric tube, gastric lavage and arterial line.Labs- Complete blood count with platelets, comprehensive metabolic panel with liver functions, and coagulation studies. Cross match for blood transfusion.
59Lower Gastrointestinal Bleeding Studies/Treatment:Normalize coagulation. Colonoscopy, tagged red blood cell scan 91% sensitive and 100% specific. Angiography with or without coil embolization.Local resection of defined bleeds, otherwise if bleeding continues and no source can be identified within the colon, total colectomy is indicated.
60Rectal and Anal Bleeding Fresh red blood on the exterior of stool usually represents hemorrhoids, fissures, or proctitis. Bleeding that drops into the toilet water is most likely the result of fissures or hemorrhoids. All rectal bleeding should be fully investigated with full H&P, anoscopy / proctoscopy and if necessary exam under anesthesia.
62AcknowledgmentThe preceding educational materials were made available through the ASSOCIATION FOR SURGICAL EDUCATIONIn order to improve our educational materials we welcome your comments/ suggestions at: