20
Gastrointestinal Bleeding
Siobhan A. Corbett
Objectives
1. To outline the initial management of a patient with an acute GI hemorrhage.
2. To differentiate upper versus lower GI hemor- rhage.
3. To discuss the differences in evaluation and man- agement of the patient presenting with hemateme- sis, melena, hematochezia, and guaiac positive stool.
4. To discuss medical versus surgical management of the common causes of GI hemorrhage.
Case
History
A 65-year-old man presents complaining of the passage of bright red blood and clots per rectum earlier that evening. This episode was pre- ceded by mild lower abdominal cramping. The patient denies any nausea, vomiting, or abdominal pain at this time, but he states that he feels “light-headed.” He reports one episode of rectal bleeding 2 months prior that was limited, and he did not seek medical advice at that time. His past medical history is significant for hypertension.
The patient denies any past surgical history. He takes one baby aspirin per day and denies any allergies. He is a nonsmoker and uses only occasional alcohol.
Review of Systems
The patient denies change in bowel habits, has no history of divertic- ulosis, and reports no recent weight loss.
355
Physical Exam
Temperature 99.0°F; blood pressure 90/45; heart rate 122; respiratory rate 25. The patient appears pale and anxious. Head, ears, eyes, nose, and throat exam is normal; his neck veins are flat.
Lungs: Clear to ausculatation with equal breath sounds bilaterally.
Heart: RR, sinus tachycardia, no murmurs.
Abdomen: Active bowel sounds, soft, nontender; no masses or organomegaly.
Rectal: Gross blood on digital exam, prostate is normal.
Extremities: Skin is cool and clammy. His radial pulses are equal, but they are weak and thready.
Initial Management
Assess the Severity of Bleeding
The first step in managing a patient with a gastrointestinal (GI) hem- orrhage is to assess the rate of bleeding and to estimate the blood loss (Table 20.1; Algorithm 20.1). Patients may present in a variety of ways.
For example, they may have anemia from occult bleeding, but they otherwise may be asymptomatic. Alternatively, patients may exhibit gradual bleeding with black or tarry stools that commonly is referred to as melena. Black stools occur as the result of oxidation of heme by bacterial and digestive enzymes. A major bleeding episode is likely to have occurred if there is profuse vomiting of blood (hematemesis) or bright red blood per rectum (BRBPR or hematochezia), accompanied by supine hypotension or a postural blood pressure or pulse change.
Other findings indicative of hypovolemia include a weak, thready pulse, moist, clammy skin, decreased skin temperature of the distal extremities, tachypnea, and mental status changes (confusion, agita-
Table 20.1. Physical findings in hemorrhagic shock.
aClass I Class II Class III Class IV Blood loss (mL) <750 750–1500 1500–2000 >2000 Blood loss UP to 15% 15%–30% 30%–40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased Pulse pressure (mm Hg) Normal Decreased Decreased Decreased
Respiratory rate 14–20 20–30 30–40 >35
Urine output (mL/h) >30 20–30 5–15 Negligible CNS/mental status Slightly Mildly Anxious, Confused, anxious anxious confused lethargic
a
Alcohol or drugs (e.g., beta-blockers) may alter physical signs.
Source: Adapted from American College of Surgeons. Shock. In: Advanced Trauma Life
Support Manual. Chicago: American College of Surgeons, 1997:87–107. Reprinted from
Nathens AB, Maier RV. Shock and resuscitation. In: Norton JA, Bollinger RR, Chang AE,
et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001,
with permission.
tion, or obtundation). The overall approach to managing the patient is determined by the rate of bleeding, since this reflects the likeli- hood that the hemorrhage will stop spontaneously. Patients with a rapid rate of bleeding may require a laparotomy, so it is important to involve a surgeon early.
Case Presentation: Assessment
The history of BRBPR accompanied by clots indicates that this patient may have a significant GI bleed. The patient’s vital signs are indicative of hypovolemic shock. This diagnosis is supported by his physical findings. He appears pale and anxious. He has a weak, thready pulse, and cool, clammy skin. Taken together, this would indicate a class III/IV hemorrhage.
Resuscitate and Stabilize the Patient
Patients who have evidence of massive blood loss should be resusci- tated immediately. The airway is assessed to ensure that there is no obstruction, and oxygen administration is required for all patients.
Obtunded patients, those who cannot protect their airway, and those with massive vomiting that presents an aspiration risk should be endo- tracheally intubated, and ventilator support should be provided for adequate respiration. Large-bore intravenous access (¥2) with 18-gauge or larger catheters should be placed. Central venous access with a Swan-Ganz introducer (8.5 Fr) may be helpful for rapid infusion if peripheral access is inadequate, but it is hazardous to place it in a hypo- volemic patient with empty, flat neck veins. If a central line is required, Hematemesis, Melena
or Hematochezia
Assess the severity of Bleeding
Resuscitate and Stabilize the Patient
Evaluate the Patient:
History and Physical
Determine the Bleeding Site
Manage Specific Bleeding Problem Algorithm 20.1. Algorithm for initially manag-
ing a patient presenting with GI bleeding.
a femoral line is a reasonable alternative that can be replaced by upper extremity access once the patient is stabilized.
At the time of the insertion of the intravenous catheters, blood should be sent for type and crossmatch, and six units of packed red blood cells should be made available. Additional laboratory evalua- tion should be performed to determine the complete blood count (CBC), chemistries [including electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests], and a coagulation profile. It is important to note that, in the early stages of hemorrhage, the hemat- ocrit level may not reflect the extent of the blood loss.
Normal saline and Ringer’s lactate are the fluids of choice used to resuscitate a patient suffering from class I or class II shock. The crys- talloid replacement should be in a quantity sufficient to replace plasma losses plus the interstitial loss and should be on the order of 3 mL of crystalloid for each 1 mL of estimated blood loss. In a young person, up to 3 L of crystalloid may be given at the rate of 1 L every 15 to 30 minutes until the clinical signs of shock have been corrected. Adequate resuscitation can be monitored by a slowing of the heart rate and a return of urine output. However, it is important to be cautious about overloading the intravascular compartment in those patients with cardiac or renal impairment. If the bleeding has ceased, crystalloid volume replacement usually will be adequate therapy for class I or class II hemorrhage, although patients with preexisting medical con- ditions may require earlier transfusion at this level. Patients present- ing with class III or class IV shock who are estimated to have lost more than 35% of their circulating blood volume are given type- specific blood in addition to crystalloid until crossmatched blood is available. (In the true emergency, O negative blood may be required.) Foley catheter placement to monitor urine output is essential in this instance.
Patients with persistent hemodynamic instability or evidence of ongoing blood loss should be monitored closely and should be pre- pared for possible laparotomy.
Remember: anticipate that unstable patients who have required multiple blood transfusions may become cold and develop dilutional coagulopathy that will increase the morbidity and mortality of an operative procedure. Under these circumstances, replacement of clot- ting factors with fresh frozen plasma is important, and it takes time for the transfusion services to make this component necessary. Therefore, think ahead. Cryoprecipitate may be required, but it should not be given unless factor VIII deficiency is demonstrated. Platelets should be administered if the platelet count is less than 50,000.
Case Discussion: Resuscitation
Immediate action is required to treat class III/IV hemorrhage. Make
sure that the patient’s airway is secure and provide supplemental
oxygen. Start 2 large-intravenous bore (IV) lines and begin resuscita-
tion with a 500-mL to 1-L bolus of crystalloid solution. Send blood for
type and crossmatch and additional laboratory values including CBC,
chemistries, and coagulation profile. Six units of packed red blood cells
(pRBCs) should be available. Place a Foley catheter to monitor urine output. Reassess vital signs frequently.
Evaluating the Patient
History
A brief, pertinent history from the patient regarding the degree of hematemesis, melena, or hematochezia contributes to an assessment of the degree of blood loss and the severity of the bleed. Inquiring about the duration of the symptoms also may help determine the rate of blood loss. As a rule, melanotic stools typically originate from the upper GI tract and maroon stools from the distal ileum or right colon, and bright red blood is indicative of bleeding from the left colon. The differential diagnoses for GI bleeding in the adult are listed in Table 20.2.
Additional history should include associated symptoms that may indicate the source of the bleeding:
1. A history of nasopharyngeal lesions, trauma, or surgery should be obtained to exclude an oral or nasopharyngeal source for hematemesis.
2. A history of known ulcer disease, gastroesophageal reflux, prior epigastric pain relieved by antacids, or excessive use of aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), or steroids may implicate the esophagus, stomach, or duodenum as the source.
Alternatively, a known history of diverticular disease or angiodys- plasia may implicate a lower GI source.
Table 20.2. Differential diagnosis for gastrointestinal (GI) bleeding in the adult upper GI bleed: common causes.
Esophagus Esophagitis Esophageal tumor Esophageal varices Mallory-Weiss tear Stomach
Gastric ulcer Gastritis
Gastric neoplasm Duodenum
Duodenal ulcer Duodenitis
Upper GI bleed: rare causes Angiodysplasia
Aortoenteric fistula Hematobilia Crohn’s disease Pancreatitis Marginal ulcer
Lower GI bleed: common causes Adult
Most common cause Upper GI bleed Small bowel
Vascular malformation Meckel’s diverticulum Neoplasm
Inflammatory bowel disease Ischemic bowel
Neoplasm
Large bowel/rectum/anus Angiodysplasia Diverticulosis Hemorrhoids Rectal fissures Polyps Neoplasms Ischemic colitis
Ulcerative or infectious colitis
3. A documented history of cirrhosis may suggest the possibility of esophageal varices.
4. A history of recent vomiting could indicate a Mallory-Weiss tear.
5. A history of crampy abdominal pain and diarrhea, accompanied by urgency, tenesmus, diarrhea, and excessive amounts of mucus, may point to inflammatory bowel disease in an adult.
6. A history of the character of rectal bleeding should be obtained along with a report of a change in bowel habits or recent weight loss.
Bright red blood found only on the toilet paper or blood that drips into the toilet bowl most commonly is associated with an anorectal source of bleeding, while blood that is streaked on the stool or mixed in with the stool suggests a proximal source. Try to get an accurate assessment of the amount of bleeding that has occurred.
7. It is important also to uncover previous episodes of bleeding and whether there have been any previous studies, such as a barium enema or colonoscopy.
The physician taking the past medical history also should inquire about associated major medical problems, such as cardiac, renal, and pulmonary diseases that will influence resuscitation and determine how well the patient can tolerate anemia. For the past surgical history, the physician should inquire about previous ulcer surgery. A history of previous gastric resection may suggest a marginal ulcer as the source of bleeding. Previous abdominal aortic aneurysm repair or aortobifemoral bypass could indicate an aortoenteric fistula.
The patient’s current medication list should be obtained, with at- tention to the possible use of medications that could interfere with coagulation (e.g., aspirin, NSAIDs, and dypiridamole) or alter the assessment of the hemodynamic status (e.g., beta-blockers and anti- hypertensive agents).
The social history should include relevant risk factors, including alcohol, intravenous drug, or tobacco abuse.
Physical Examination
The physical exam seldom provides accurate determination of the source of the bleeding. However, the severity of the blood loss and identification of comorbid illnesses can be assessed, and the physical exam should be performed carefully, although the results often are normal.
The physical exam should consist of the following:
1. Complete vital signs should be obtained to assess the severity of bleeding.
2. Postural changes in the pulse and/or blood pressure should be assessed.
3. Sclera should be examined for evidence of icterus.
4. The mouth and the oropharynx should be examined to exclude
nasopharyngeal causes of hematemesis.
5. Pertinent physical findings should be sought that are indicative of comorbid disease, including signs of chronic hepatic disease, including ascites or spider angiomata.
6. An abdominal examination should be done, as it will reveal the pres- ence of a mass caused by a colonic neoplasm or the presence of an aortic aneurysm.
7. A rectal exam should be performed for evidence of frank blood or possibly a tumor mass.
8. Hemocult exam of any melenic-appearing stool should be done, since the ingestion of several substances, such as iron or spinach, can impart a dark color to the stool.
Case Evaluation
The patient responds well to a 2-L infusion of lactated Ringer’s. His vital signs stabilize. His blood pressure improves to 120/70, and his heart rate decreases to 90. Relevant information from this patient’s history and physical include the following: There is no history of hematemesis, but the patient reports a similar episode of rectal bleed- ing 2 months prior for which he did not seek medical advice. This episode of bright red blood per rectum had no antecedent symptoms.
He has no history of diverticulosis. He reports no change in bowel habits or recent weight loss. His review of systems was negative for cardiac, pulmonary, or renal symptomatology, and he denies any sur- gical history. He takes no medications and has no allergies. It seems likely that this patient is experiencing a lower GI bleed. However, his history and physical exam do not exclude an upper GI source of hemorrhage.
Determine the Bleeding Site
If hematemesis, melena, or hematochezia have not been documented, it is important to establish the site of bleeding. This can be accomplished by placing a nasogastric tube (NGT) (at least 18 Fr).
Remember: an upper GI source can be a common cause of a lower
GI bleed. Even if the patient has massive rectal bleeding, 10% of the
time the source is proximal to the ligament of Treitz. Therefore, an
NGT should be placed. If bile is aspirated from the NGT without blood,
it is unlikely that a major upper GI bleed has occurred. However, about
25% of the patients with duodenal bleeding do not reflux blood into
the stomach even with gagging. This group usually can be identified
by lavaging the stomach with saline if blood or bile is not obtained on
initial NGT placement. An attempt should be made to irrigate old
blood or new bleeding from the stomach, and the NGT should be
lavaged until clear. There is no advantage between iced-saline and
room temperature lavage. Over 90% of patients with bloody gastric
aspirate will be found to have a lesion proximal to the ligament of
Treitz.
Case Discussion
Although an upper GI source is unlikely in this case, the NGT would help to detect one. An NGT is inserted. It returns bilious contents that are guaiac negative. The absence of blood in the NGT aspirate in the presence of bile makes upper GI bleeding very unlikely.
Management of Specific Bleeding Problems
Upper GI Bleeding Making the Diagnosis
If the patient is stabilized in the emergency room and hematemesis or bloody nasogastric aspirate has been documented, the first step in management is an upper endoscopy or esophagogastroduo- denoscopy (EGD) (see Algorithm 20.2). An EGD is essential for man- aging patients with upper GI hemorrhage. Only 10% to 20% of patients presenting with upper GI bleeding have peptic ulcers as the cause for the bleed. However, 50% of all cases of severe upper GI bleeds are caused by bleeding peptic ulcer disease. Because of the diagnostic and therapeutic potential for endoscopy, it should be included early in the management of these patients, since its utility and accuracy in iden- tifying the bleeding source have been well documented in the litera- ture. A patient with a history of hematemesis in whom the rate of bleeding is high should undergo an emergent EGD that should be performed within 1 hour. The stable patient with melanotic stools dictates an urgent EGD.
The EGD is an excellent diagnostic tool, and it also is valuable ther- apeutically. In skilled hands, endoscopic maneuvers, such as injection sclerotherapy, banding of varices, electrocoagulation, the use of a heater probe, the injection of ethanol or epinephrine, and laser coagu- lation, effectively can manage the bleeding source. Which patients require therapeutic EGD? Patients presenting with clinical scenarios listed in Table 20.3 should be considered for therapeutic EGD. Addi- tionally, patients at high risk for complications secondary to bleeding should be considered as candidates for therapeutic endoscopy; these would include patients over 60 years of age or those who rebleed fol- lowing an initial bleeding episode.
The National Institutes of Health convened a consensus conference examining the role of EGD for upper GI hemorrhage. The panel eval- uated a variety of devices used for endoscopic intervention (Table 20.4). Of these, the heater probe and bipolar electrocoagulation device were determined to be the most useful. The panel concluded that endoscopic intervention was safe and effective when performed by appropriately trained practitioners. Surgical backup was considered essential. At the time that the panel convened, long-term follow-up was not available, leaving many questions regarding the long-term efficacy for endoscopic control of bleeding.
If EGD reveals no lesions in the stomach or duodenum, there are
alternative diagnostic tests that may identify the bleeding site. Entero-
clysis, which is the direct introduction of barium sulfate into the small
Assess severity of bleeding
? VS
?Amount of bleeding
Volume resuscitation Transfusion PRN
Active upper GI bleed
Bleeding continues after saline lavage?
No Urgent EGD
Source located in stomach or
duodenum?
No
Enteroclysis Yes
Indication for therapeutic EGD?
No Continue observation
and supportive
care
Yes Continue symptomatic
and supportive
treatment
Surgery required No No D(x) allow pharmacologic
or radiologic intervention?
Bleeding stops?
Yes Yes
Emergent EGD
NG aspirate positive
Acute colonic bleeding
Assess severity of bleeding
? VS
? Amount of bleeding
Volume resuscitation Transfusion PRN
NG aspirate negative
Go to Algorithm 20.3 Hematemesis
Algorithm 20.2. Algorithm for management and treatment of upper GI bleeding. EGD, esophagogas-
troduodenoscopy; NG, nasogastric; VS, vital signs.
bowel, followed by an x-ray examination of the duodenum and jejunum, should be done next. However, the absence of a lesion on this test does not rule out a bleeding source in this area. Tagged red cell scans may confirm the presence of active bleeding, but these are not helpful in determining the exact anatomic location of the bleeding site.
This important information is extremely helpful if the bleeding episode necessitates surgical intervention. If the tagged red cell scan is positive, arteriography then may be considered. For arteriography to be suc- cessful in identifying the location of the hemorrhage, the bleeding must be brisk (>1 mL/min). If a lesion such as an arteriovenous malforma- tion is identified, however, arteriography does offer the potential of therapeutic intervention through embolization.
What are the options for a patient who has persistent or recurrent bleeding that is believed to originate in the small bowel? In this instance, intraoperative endoscopic exploration may be warranted. A pediatric colonoscope may be introduced either orally or through a Table 20.3. Predictors of peptic ulcer rebleeding.
Magnitude of bleeding Hemodynamic instability
Bloody emesis or nasogastric lavage that fails to clear Blood-red stools
Host factors
Anticoagulated patient
Patient hospitalized for a related or unrelated condition Endoscopic features
Visible vessel
Arterial spurting or oozing
Raised pigmented discoloration on ulcer base Adherent clot on ulcer base
Source: Reprinted from Consensus conference: therapeutic endoscopy and bleeding ulcers. JAMA 1989;262:1369–1372.
Table 20.4. Comparison of endoscopic devices for the control of GI bleeding.
Requires en
Device face application? Advantages/disadvantages Use?
Bipolar electrocoagulation No Portable; depth easily controlled Yes
Heater probe No Portable; depth easily controlled Yes
Nd : YAG laser Yes Not portable Maybe
Injection therapy No Inexpensive; simple technique Maybe
Topical therapy Yes Not effective No
Argon laser Yes Not effective long term; better No
techniques are now available
Monopolar electrocoagulation Yes Depth of tissue damage difficult No to control; multiple cleanings of probe required
Nd : YAG, neodymium : yttrium-aluminum-garnet.
Source: Reprinted from Livingston EH. Stomach and duodenum. In: Norton JA, Bollinger RR, Chang AE, et al, eds.
Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
distal jejunal enterotomy, and the small bowel mucosae then may be examined.
Peptic ulcers, acute gastritis, esophageal varices, and Mallory- Weiss tears account for >90% of all upper GI bleeds. The manage- ment options for these problems are reviewed briefly below.
Peptic Ulcer Disease: Bleeding from peptic ulcer disease frequently occurs and generally is a self-limited process. Advances in endoscopic therapy have made surgery for this problem uncommon. Patients usually present with melena, or, if the bleeding is severe enough, hematemesis or hematochezia are present. Bleeding is unpredictable, mandating careful observation of patients suspected of having GI hemorrhage. The treatment team must be prepared to manage severe life-threatening hemorrhage that may occur with little notice. The routine medical treatment for documented gastroduodenal ulcer disease includes the withdrawal of any exacerbating factors (aspirin or NSAIDs), acid reduction/suppression, and eradication of Heliobacter pylori, if present.
Therapeutic intervention with endoscopic treatment may be indi- cated in patients with active arterial bleeding at the time of endoscopy or with a visible nonhemorrhaging vessel. The success of endoscopic therapy in controlling peptic ulcer bleeding greatly has reduced the need for surgical intervention. However, surgery must be considered when endoscopic treatment has failed or is impractical. In general, when patients have required more than six units of blood to be trans- fused in a 24-hour period, they should be considered for surgery. An additional indication for surgery exists if a patient stops bleeding clin- ically and then massively rebleeds. When surgery is performed, the procedure of choice is oversewing of the bleeding ulcer plus truncal vagotomy and pyloroplasty, truncal vagotomy and antrectomy, or highly selective vagotomy.
Stress Ulcers: Stress ulcers are small, numerous lesions occurring in the superficial mucosa of the gastric fundus. NSAID ulcers may appear similar to stress ulcers, but they are distributed primarily in the gastric body and antrum. Their major clinical consequence is the tendency to bleed (but not to perforate). The pathogenesis of these lesions remains unclear. Like most gastric ulcers, the major defect appears to be in the mucosal defense system. However, acid may play a role, the extent of which remains unknown. Because these lesions are a manifestation of other underlying disease processes, the mortality associated with a total gastrectomy for stress gastritis is 50% to 80%. If at all possible, explorations should be avoided in these patients.
Gastric Ulcers: Bleeding gastric ulcers that are discrete should be
resected, which easily can be accomplished for greater curvature
lesions by performing a wedge resection. Lesser curvature or very large
lesions may require a total gastrectomy. Frozen section should be
obtained to identify gastric carcinoma. Because gastric ulcers cannot
be distinguished from gastric carcinoma by gross examination, histo-
logic evaluation is mandated. If carcinoma is found, a formal gastrec-
tomy should be performed: total gastrectomy for proximal lesions and subtotal for antral lesions.
Mallory-Weiss Tear: Mallory-Weiss tears of the esophagus and proxi- mal stomach can occur following emesis. Classically associated with alcoholics, the syndrome is manifested by hematemesis that follows episodes of intense vomiting. More recently, the syndrome has been observed following endoscopy, childbirth, coughing, and CPR. The diagnosis is suggested by a history of vomiting before the onset of hematemesis. Endoscopy reveals linear tears below the gastro- esophageal junction, occasionally extending proximally into the esoph- agus. Initial management includes resuscitation and correction of any coagulopathy. Bleeding usually is self-limited. Endoscopic scle- rotherapy of a bleeding vessel is effective. Rarely is surgical inter- vention required.
Acute Variceal Bleeding: Initial mangement of the patient with acute variceal bleeding includes resuscitation as outlined above. However, intravascular volume replacement should be performed largely with blood products because the crystalloid solutions in patients with cir- rhosis results in the rapid development of ascites and edema. Patients with active bleeding should be managed in an intensive care unit setting with appropriate hemodynamic monitoring and airway pro- tection. Blood in the GI tract is not well tolerated by cirrhotics, with increased risk of bacterial translocation and sepsis as well as inducing encephalopathy. Lactulose should be given orally or via an NGT or enemas in the comatose patient.
It should be remembered that up to 60% of GI bleeding in alcoholic cirrhotics is of nonvariceal origin. Therefore, EGD plays a significant role in both the diagnosis and treatment of acute variceal bleeding.
The goal of EGD is to identify active bleeding, detect signs of recent bleeding, and exclude other sources of GI bleeding. Identification of varices as the bleeding site should be accompanied by initial scle- rotherapy or banding. Acute bleeding can be stopped in 90% of the patients with an endoscopic approach. The use of octreotide has sup- planted vasopressin as pharmacologic intervention to prevent bleed- ing. Somatostatin and its synthetic analogue octreotide are potent vasoconstrictors at supraphysiologic doses. Octreotide is given initially as a 50-mg bolus followed by an infusion of 50-mg per hour; this is con- tinued through endoscopic intervention and usually for the subsequent 24 hours.
Patients who have active bleeding that cannot be controlled by pharmacologic and endoscopic management require the placement of a Sengstaken-Blakemore tube. The goal is to use the tube to tampon- ade the bleeding as a temporizing maneuver only, while definitive management is being arranged. Key points of tube insertion include airway protection and correct positioning of the tube under radiologic guidance before the inflation of the balloon.
Definitive management for patients who fail endoscopic manage-
ment and require balloon placement include transjugular portasys-
temic shunts (TIPS) and emergency portocaval shunting. Since
emergency portocaval shunts are associated with a mortality of 50%, there currently is greater enthusiasm for the use of TIPS, an interven- tional radiologic procedure that creates a communication through the hepatic parenchyma between the hepatic and portal veins. Because the 30-day mortality is significantly better in patients with uncontrolled variceal hemorrhage who receive TIPS, surgical decompression of the portal system in the emergency setting is reserved for those patients in whom TIPS cannot be performed.
Meckel’s Diverticulum: Meckel’s diverticulum represents a true diver- ticulum composed of a remnant of the duct between the intestinal tract and the yolk sac. Based on autopsy series, Meckel’s diverticulum is present in 0.3% to 2.5% of the population. The size and shape can vary, but it usually is between 3 and 5 cm long and is found 10 to 150 cm from the ileocecal valve. Meckel’s diverticula contain a mesentery with an independent blood supply from the ileal vessels. Although usually lined by mucosa similar to that seen in the adjacent ileum, approxi- mately 16% to 34% of them can contain heterotopic mucosa, including that of a gastric or duodenal nature.
Meckel’s diverticula that contain heterotopic gastric mucosa can produce acid, resulting in ulceration in the adjacent ileal mucosa and subsequent hemorrhage. In fact, hemorrhage is the most common complication associated with Meckel’s diverticulum (31%). The passage of blood per rectum in an otherwise healthy child should raise the suspicion of a Meckel’s diverticulum. The diagnosis can be made utilizing a technetium 99 m (Tc-99 m) pertechnetate Meckel’s scan that detects the gastric mucosa within the Meckel’s diverticulum and that has been reported to be 90% accurate. Meckel’s diverticulum also can be detected angiographically in most cases, based primarily on the demonstration of a persistant vitellointestinal artery. When a Meckel’s diverticulum causes symptoms or complications, resection is indicated.
Lower GI Bleeding
Many pathologic lesions of the colon and rectum can cause lower GI hemorrhage that can be classified as either major (defined as greater than 100 mL) or minor (less than 20 mL). The most common causes of major lower GI hemorrhage are diverticular disease and arteriove- nous malformations (AVM). Other causes can include inflammatory bowel disease, neoplasms, ischemic colitis, and a variety of other lesions. Minor bleeding may be related to anal conditions, such as hemorrhoids and anal fissures, or to colonic or rectal lesions, such as neoplasms or mucosal inflammation. We focus on the management of patients who present with obvious rather than occult blood loss.
Any patient with significant lower GI bleeding should be admit- ted to the hospital. Appropriate resuscitation should be initiated as discussed above and as indicated in Algorithms 20.2 and 20.3. The patient should be assessed carefully to determine the rate of bleeding.
If the patient is stable, every attempt should be made to identify the
location of the hemorrhage site, including the placement of an NGT
because, as mentioned previously, a significant percentage of lower GI bleeding originates from an upper GI source. Finally, it should be recognized that about 85% of bleeding from lower GI sources stops spontaneously.
Making the Diagnosis
As indicated in Algorithm 20.3, the first step in management of patients who present with rectal bleeding, stable or unstable, is a rigid sigmoi-
Acute colonic bleeding
Volume resuscitation plus blood transfusion
NG aspirate negative
Proctoscopy Rule out anorectal bleeding Bleeding stopped or slowed down
Elective colonoscopy
Positive Negative Endoscopic
treatment Observe
Rebleeding Segmental
resection
Rebleeding See moderate bleeding or massive bleeding
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