Direct Mechanical Injury

Blunt and penetrating trauma can initiate bleeding from any part of the GI tract. Ingestion of certain foreign bodies (e.g., coin batteries) may result in mucosal injury and even bowel perforation. Repeated vomiting or retching may create esophageal mucosal defects called Mallory-Weiss tears that can bleed. Surgical interventions, such as dental procedures and tonsillectomy, may result in blood loss that is swallowed and subsequently vomited.

Mucosal Erosion

The GI tract has a robust and sophisticated mucosal defense mechanism designed to prevent erosion. These protective elements include (1) the superficial “unmixed” layer of mucus, bicarbonate, and other factors that form a neutralizing barrier against acid, enzymatic, and abrasive injury; (2) the epithelial cells that generate this superficial layer; (3) continuous cell renewal coupled with (4) uninterrupted nutrient blood flow to the mucosa and (5) sensory innervation that optimizes this blood flow; and (6) endothelial production of prostaglandins and nitric oxide, which synergize to promote all of the aforementioned mechanisms. Disruption of any of these factors may predispose a given region of mucosa to erosion, local loss of vascular integrity, and resultant bleeding.

Infection

Infections disrupt mucosal integrity by direct cytotoxicity and/or by promoting inflammation. For example, herpes simplex virus is known to cause florid esophagitis, particularly in immunocompromised individuals, with nearly one-third of these patients experiencing an acute upper GI bleed. Additionally, infections may elicit specific peculiar responses. For example, cytomegalovirus is occasionally associated with massive gastric epithelial proliferation leading to a hypertrophic gastropathy called Menetrier’s disease. This causes protein wasting (including coagulation factors) from the leaky mucosa, as well as a higher risk of mucosal erosion and bleeding. Helicobacter pylori is perhaps the most infamous of the infectious causes of gastritis and duodenitis because of its chronicity, high prevalence (especially in certain populations of children, such as immigrants, the poor, and those attending daycare centers), its associations with peptic ulcers and adenocarcinoma of the stomach and duodenum, and its resistance to eradication (Figure 108-2).

Figure 108-2 Etiology and pathogenesis of Helicobacter pylori infection.

Polyps

Polyps are mucosal projections into the intestinal lumen caused by disordered epithelial growth. Various spontaneous and familial polyposis entities exist. Regardless of the specific underlying process, they are a source of bleeding (generally painless) secondary to mechanical irritation or wholesale shearing by passing fecal material. In contrast to adults, the vast majority of polyps in children are juvenile polyps. These non-neoplastic polyps are typically composed of many cystic, dilated glands; copious inflammation; and surface erosions, the last of which is the cause of bleeding. Juvenile polyps have a peak incidence from 2 to 6 years of age, represent more than 90% of all pediatric polyp diagnoses, and are found in about 1% of school-age children.

Vascular Abnormalities

Congenital vascular defects may result in fragile vascular arrangements vulnerable to erosive and mechanical insults. Whereas hemangiomas represent proliferative vessel abnormalities that may regress, true malformations (including disorders such as arteriovenous malformations, blue rubber bleb nevus syndrome, and Osler-Rendu-Weber syndrome) are nonproliferative and do not regress. Processes that compromise the full thickness of bowel, such as Crohn’s disease and bowel surgery, may result in vessel-to-bowel fistulas associated with significant bleeding. Vasculitides, such as Henoch-Schönlein purpura, may result in occlusion of mesenteric vessels and intestinal ischemia (see Chapter 28).

Portal Hypertension

The final common pathway for many chronic liver diseases is cirrhosis, in which the underlying disease causes excessive production of extracellular matrix; destruction of normal liver architecture; and, ultimately, severe organ dysfunction. Cirrhosis is the most common cause of portal hypertension. Other potential causes include portal venous thrombosis, veno-occlusive disease in patients receiving chemotherapy, and hepatic vein thrombosis (Budd-Chiari syndrome). Backpressure from the high-resistance liver increases the intravascular pressure experienced by the portal vein and its collaterals, resulting in esophageal varices (abnormally dilated venous system in the distal esophagus) and portal gastropathy (increased venous pressure throughout the gastric wall). Varices are a known cause of catastrophic GI bleeds. The bleeding from these engorged vessels is only exacerbated by inadequate hepatic synthesis of coagulation factors.

Blood from Extrinsic Sources

In neonates, swallowed maternal blood from delivery or breastfeeding is a potential cause of bloody emesis or stool. Blood swallowed from the airway in patients with frequent, severe coughing (e.g., pneumonia, cystic fibrosis, tuberculosis) may be mistaken for hematemesis. Rarely, hepatic injury from trauma or an abscess may cause hemobilia, with blood draining from the biliary system into the duodenum.

What Are the Route and Appearance of the Bleeding?

Visible GI bleeding presents in different forms depending on the location of origin. Traditionally, authors have grouped causes of GI bleeding into upper and lower sources divided by the ligament of Treitz. In 2007, the American Gastroenterological Association promoted the refinement of this classification into upper, middle, and lower GI tract bleeding, with the dividing point between the upper and middle tract being the ampulla of Vater (pancreatic outlet into the duodenum) and the dividing point between the middle and lower tract being the ileocecal valve.

Hematemesis, which is vomiting of either fresh blood or coagulated, denatured blood (“coffee grounds”), indicates upper GI bleeding. Coffee-ground hematemesis generally represents old blood or bleeding that is occurring at a slow rate, as opposed to red blood, which raises concern for active bleeding. Melena (black, tarry, foul-smelling stool containing oxidized blood) usually comes from the upper GI tract, but it can emanate from a middle GI source if the transit rate is not rapid. Hematochezia (red blood per rectum) generally suggests middle or lower GI bleeding, although it may also represent a massive upper GI bleed. Indeed, hematemesis combined with melena or hematochezia is an ominous combination that must be investigated promptly. Therefore, in any patient with bloody stool, the clinician must be convinced that there is no evidence of upper GI bleeding. It is important to remember that many cases of GI bleeding are occult (i.e., microscopic), which are not visible to the eye and can occur anywhere along the GI tract. It is also essential to determine whether the blood could be emanating from a non-GI source, epistaxis and menstruation being two common examples.

What Is the Age of the Patient?

Most causes can present in a variety of ages. However, some disorders tend to present more commonly in specific age groups. For example, juvenile polyps have a peak incidence in young school-age children. Inflammatory bowel disease, although it can present at almost any age, is generally rare in very young children, and when it does occur in that group, its presence prompts concerns of a possible immunodeficiency.

Several disorders appear almost exclusively in neonates and infants. In newborns, particularly premature infants, necrotizing enterocolitis is a life-threatening emergency in which segments of bowel become inflamed and necrotic, leading to hematochezia, melena, or both; abdominal distension; and fever. Neonates at delivery or breastfeeding infants may also swallow blood (the latter from cracked maternal nipples), which can then appear in reflux or emesis. The Apt test can help distinguish maternal blood from that of the patient. Milk protein allergy most often presents in the first few months of life as fussiness and mild hematochezia in an otherwise well-appearing infant who has been exposed to cow’s milk proteins, either through formula or indirect transmission via the mother’s breast milk.

Is the Bleeding Acute or Chronic?

A history of repeated bleeding episodes over a period of time suggests causes that have the potential for chronicity. For example, inflammatory bowel disease does not typically present with sudden, catastrophic bleeds but tends to have a more insidious course marked initially with other symptoms such as weight loss or diarrhea. Peptic ulcers are another example in which bleeding may begin as occult but worsen over time if left untreated or exacerbated by other factors such as NSAID use. In such cases, a patient may exhibit pallor and fatigue but can remain functional, at least for a time, because of the body’s adaptation to the progressive anemia. On the other hand, rapid onset of significant bleeds should sway the clinician toward other causes. For example, two significant causes of sudden melena or hematochezia are Meckel’s diverticulum and vascular malformations. In patients with known liver disease, esophageal varices are a critical consideration.

Is the Bleeding Associated with Pain?

Abdominal pain associated with GI bleeding may suggest structural compromise. Bleeding coincident with pain in the epigastric region may be caused by peptic disease or necrotizing pancreatitis. If the pain is associated with distension or vomiting, the clinician should be concerned for causes of intestinal obstruction potentially associated with bleeding, such as intussusception, although upper GI blood itself can stimulate vomiting. If significant bleeding of rapid onset occurs with generalized abdominal pain disproportionate to the rest of the physical examination, ischemia may be the contributing cause. Bowel inflammation, as occurs with ulcerative colitis, can cause cramping pain. An ill-appearing patient with peritoneal signs (involuntary guarding, rebound tenderness, exquisite pain with movement) may be experiencing bowel perforation and requires urgent medical and surgical evaluation.

What Is the Relationship Between the Blood and Stool?

The answer to this question can help guide the physician toward a region of pathology as long as one keeps in mind the limitations of these generalizations. Melena indicates bleeding from an upper or middle GI source. If the patient is having frequent, watery stool containing melena, this suggests small bowel pathology, as in Crohn’s disease. Pure melena without watery diarrhea suggests other causes, such as peptic ulcers or esophageal varices. If the patient has profuse diarrhea with cramping and hematochezia (dysentery), this is more suggestive of colitis, as can occur with ulcerative colitis and many infectious causes, such as Clostridium difficile, Yersinia spp., Shigella spp., and Campylobacter spp. If the patient has pure hematochezia, infectious and inflammatory causes are still possible, but one also needs to consider other causes such as Meckel’s diverticulum, polyps, or vascular malformations, particularly if the bleeding is painless. If the patient has formed stool coated with blood (rather than permeating it), this suggests a distal cause such as solitary rectal ulcer (caused by mucosal erosion in the rectum from hard stool) or an anal fissure.

Does the Patient Have Other Prominent Abnormalities by History or Examination?

Any associated findings may provide clues to the etiology. Cutaneous hemangiomas raise the possibility of internal hemangiomas affecting the GI tract. A history of failure to thrive or weight loss raises concern for small bowel dysfunction, such as occurs with Crohn’s disease, or, less commonly, malignancy. Inflammatory bowel disease can also be associated with a host of other extraintestinal findings, such as erythema nodosum and episcleritis. Polyps may often be a part of syndromes with other findings, a classic example being Peutz-Jeghers syndrome, in which hamartomatous polyps occur with mucocutaneous macules. Stigmata of liver disease, including jaundice, icterus, spider angiomas, and hepatosplenomegaly, may raise concerns for esophageal varices.

Determine Hemodynamic Status

Rapid comprehensive assessment of the patient, starting with the ABCs (airway, breathing, circulation) and including general appearance, vital signs, signs of injury, and mental status, should be performed first to determine the patient’s stability and the next step in management.

Determine High-Risk Historical Factors

The clinician must determine whether there are exogenous factors that have contributed to the patient’s clinical picture, including a history of trauma, ingestion, drug use, and other illnesses.

Laboratory Evaluations

Initial laboratory studies assess the patient’s hematologic status, screen for underlying contributory factors, and prepare for potential procedures. They should include a complete blood count (including platelet count), reticulocyte count, prothrombin and partial thromboplastin times, liver function tests (including aspartate aminotransferase, alanine aminotransferase, total and unconjugated bilirubin, and serum albumin), serum chemistries, and type and screen. The blood urea nitrogen may be elevated relative to the serum creatinine because of the absorption of amino acids produced by the enzymatic degradation of hemoglobin. As discussed earlier, the presence of blood should be confirmed by Hemoccult (stool) or Gastroccult (gastric aspirate), and the Apt test may be indicated in the neonatal setting if there is suspicion of swallowed maternal blood.

Additional Evaluations

Radiologic, endoscopic, and surgical evaluations are summarized in Table 108-1. The approach depends on the bleeding acuity and the setting in which the patient is seen. In general, when the source of bleeding is unclear, the goal is to get the patient to endoscopy, in which a fiberoptic camera is inserted into the mouth (upper endoscopy) or anus (lower endoscopy) to directly visualize the intestinal lumen. Endoscopy is the gold standard given its relative safety and its ability to directly visualize the mucosa, obtain tissue for pathologic diagnosis, and potentially administer therapy. However, other diagnostic methods offer particular advantages and may be indispensable to the patient’s assessment before endoscopy. Indeed, certain diagnoses, such as Meckel’s diverticulum or intussusception, may permit bypassing the need for endoscopy, and when bleeding is heavy, the ability to visualize the lumen is severely hampered.

Table 108-1 Diagnostic Modalities for Gastrointestinal Bleeding*

CT, computed tomography; GI, gastrointestinal; Hgb, hemoglobin; MRI, magnetic resonance imaging. RBC, red blood cell; SBFT, small bowel follow-through; Tc-99m, technetium-99m.

* Studies not suitable for the acute-care setting.

Therapeutic Interventions

Patients with significant anemia (hemoglobin <8 gm/dL), active bleeding, or symptomatic anemia should receive blood replacement with packed red blood cells at a dose of 10 to 15 mL/kg per transfusion. If coagulation abnormalities are found, they should be corrected with vitamin K, fresh-frozen plasma, or both depending on the clinical context. All patients with GI bleeding should presumptively be started on acid-suppression therapy, preferably with a proton pump inhibitor, until the patient is stable and an upper GI cause has been excluded. Additional interventions depend on the underlying cause. Endoscopy is capable of administering internal therapies, depending on the context (e.g., sclerotherapy or banding of varices, electrocautery or argon plasma coagulation for ulcers, clipping or injection for vessels). In severe bleeding, more drastic interventions such as continuous octreotide infusion or surgery may be required.