Lower Gastrointestinal Hemorrhage


Introduction

Lower gastrointestinal hemorrhage refers to blood loss originating distal to the ligament of Treitz that is symptomatic and necessitates hospital admission. It is a serious and potentially life-threatening situation. Although rectal hemorrhage can be seen in any age group, most patients requiring admission to the hospital are elderly and have coexistent medical problems. Because of these comorbidities, management is complex. Many patients stop bleeding spontaneously, but up to 30% experience bleeding again during or after their hospitalization. In the adult population, diverticulosis and vascular ectasias cause more than 90% of cases of lower gastrointestinal hemorrhage. Other less common causes are listed in Box 50-1 . Although the focus of this chapter will be on general evaluation and management of lower gastrointestinal hemorrhage, it is worthwhile to briefly examine and contrast the two most common causes.

BOX 50-1
Cause of Colonic Hemorrhage

  • Diverticular disease

  • Vascular ectasias

  • Colonic neoplasms

  • Ischemic colitis

  • Radiation colitis

  • Infectious colitis

  • Inflammatory bowel disease

  • Trauma

  • Hematologic disorders

  • Rectal varices

  • Hemorrhoids

  • Anal disease

  • Endometriosis

  • Solitary rectal ulcer

  • Postpolypectomy bleeding

Etiology

In Western society, up to 65% of the population will have diverticulosis by age 85 years. Twenty percent of patients with diverticulosis coli will present with bleeding during their lifetime, and 5% will experience a severe hemorrhage. Although almost all of these patients stop bleeding spontaneously, bleeding will recur in 25%. Most diverticula are located in the sigmoid and descending colon, likely as a result of the sigmoid colon’s high intraluminal pressure. Despite this left-sided predilection, diverticular bleeding is distributed fairly equally between the right and left sides of the colon. The pathogenesis is believed to be injury to the submucosal arterial branches of the vasa recta that become stretched over the diverticulum and are then subject to trauma by the passage of stool. It has been speculated that the wider necks of the right-sided diverticula permit a greater length of the artery to be exposed to injury, thus increasing the percentage of bleeding from proximal diverticulosis. Diverticulitis is not usually associated with bleeding vasa recta.

Vascular ectasias of the colon are also believed to be acquired lesions because they are rarely observed in patients younger than 40 years. Also known as angiodysplasia or arteriovenous malformations, these lesions are predominantly located on the right side of the colon. It is likely that the increased wall tension of the cecum accounts for the presence of these lesions. As described by Boley, repeated low-grade obstruction of the submucosal veins over many years leads to the characteristic tortuous, dilated, thin-walled vessels, which can be identified both grossly and histologically. Arteriovenous connections occur relatively late in this process and result from increased pressure, leading to disruption of the precapillary sphincters. A high incidence of cardiac disease, especially aortic stenosis, has been observed in patients with vascular ectasias, and as many as 25% of patients who present with bleeding arteriovenous malformations are noted to have aortic stenosis. First described in 1958, Heyde syndrome describes a triad of aortic stenosis, an acquired coagulopathy, and anemia occurring as a result of intestinal angiodysplasia. Although bleeding has been reported to cease with aortic valve replacement, gastrointestinal hemorrhage is not an indication for open heart surgery. Rather, the decision to perform aortic valve replacement should be made on the basis of traditional indications, with surgery for lower gastrointestinal bleeding proceeding first if critical aortic stenosis is not present. Bleeding from vascular ectasias tends to be venous and, therefore, is not usually as brisk as that seen with diverticulosis. In more than 90% of patients, bleeding will stop spontaneously, but repeated episodes of bleeding are common, with an incidence that approached 85% in one study.

Initial Evaluation and Resuscitation

Because many patients who present with lower gastrointestinal hemorrhage lose a large amount of blood, resuscitation must accompany the initial evaluation. Despite the varied causes for lower gastrointestinal hemorrhage, the initial approach is standard.

In trying to quantify the degree and characteristics of a patient’s bleeding, it is important to realize that even small amounts of blood in the toilet can appear massive to the patient. Because blood is a cathartic, more importance can be attached to the frequency of bloody bowel movements prior to presentation than in trying to quantify the exact amount of blood loss. Significant lower gastrointestinal bleeding often causes hemodynamic instability, and it is essential to treat this condition while evaluating underlying causes. A lack of hemodynamic instability does not necessarily imply a minor bleed, however. A study from our institution revealed that, at presentation, 90% of patients with positive findings of an arteriogram were normotensive or hypotensive, and only 30% were tachycardic.

As the initial evaluation progresses, the basics of cardiopulmonary resuscitation must be followed. Large-bore intravenous catheters should be placed with infusion of a balanced salt solution. Blood samples are drawn for laboratory studies, including hemoglobin, hematocrit, coagulation studies, blood typing, and crossmatching. Attempts should be made to keep the patient normothermic. Placement of a Foley catheter permits accurate assessment of urinary output and assists in fluid replacement. Patients with massive hemorrhage, severe cardiac disease, or multiple comorbidities require intensive monitoring, which may include systemic arterial, pulmonary arterial, electrocardiographic, and oximetric monitors.

Early in the evaluation, a nasogastric tube should be placed. In many studies of lower gastrointestinal bleeding, as many as 10% of patients initially believed to be bleeding from a colonic source were ultimately determined to be bleeding from an upper gastrointestinal lesion. If clear bile is not returned upon nasogastric aspiration, an upper endoscopy should be performed as part of the evaluation. Even if clear bile is noted upon lavage, upper gastrointestinal bleeding can be seen in up to 16% of patients. The nasogastric tube can be left in place to use as access for a rapid mechanical bowel preparation to expedite a colonoscopy.

While resuscitation is proceeding, important information should be obtained from the patient’s history in relation to the risk for continued or recurrent bleeding. Asking about alcohol or aspirin ingestion, a prior history of gastrointestinal bleeding, the presence of any bleeding diathesis, coagulopathy from anticoagulation therapy, and comorbid diseases is extremely important.

Upon physical examination, particular attention should be directed to identifying stigmata of advanced liver disease. In addition, the presence of an abdominal mass may indicate an unsuspected colon carcinoma. Although diverticulitis is not commonly seen with bleeding diverticulosis, a finding of abdominal tenderness may suggest that possibility. More likely, however, would be a diagnosis of ischemic colitis or inflammatory bowel disease when a patient presents with abdominal pain, tenderness, and lower gastrointestinal hemorrhage.

Finally, rigid sigmoidoscopy is essential early in the evaluation of patients with lower gastrointestinal bleeding. It is generally performed in the emergency department to rule out an anorectal source of bleeding. Hemorrhoids associated with portal hypertension can bleed massively, and other low rectal or anal sources of bleeding may be treatable in the acute setting. Additionally, observation of the rectal mucosa may suggest a possible source of bleeding, such as infectious, inflammatory, or ischemic proctocolitis.

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