Lower Gastrointestinal Bleeding in the Elderly Population

Author: Suzanne E. Johnson, DO, FACEP, Attending Physician, Alameda Hospital, Alameda, CA.

Peer Reviewer: Will B. Ignatoff, MD, Emergency Physician, Emergency Room Associates, Carondelet St. Joseph’s and Carondelet St. Mary’s Hospitals, Tucson, AZ.

As the population ages and more diseases of the elderly manifest themselves, colorectal diseases—and, in particular, lower gastrointestinal (GI) bleeding—present with increasing frequency to the emergency department (ED). The elderly often have co-existing illnesses that increase their morbidity and mortality. It is incumbent upon the emergency physician to be able to stratify these patients according to risk, recognize the presenting complaints of various diseases, and know the most common etiologies for GI bleeding in this population.

Although there are myriad potential causes for lower GI bleeding, the most common etiologies are diverticulosis, angiodysplasia, colorectal carcinoma, polyps, and radiation proctitis.1 These will be explained in detail, highlighting the pathophysiology, incidence, clinical presentation, and management. Additionally, some of the less frequent causes will be discussed to broaden the differential diagnosis. The cause of lower intestinal bleeding can be identified by routine investigation in 95% of cases.2

There are definite changes in the elderly bowel that predispose these patients to GI bleeding. These changes, as well as the most common locations for bleeding sites, will be elucidated.

Diagnostic studies have changed in the past 10 years, enabling the emergency physician and the internist to diagnose the dilemma more accurately. Because most of the diagnostic challenges will take place in an inpatient setting, the emergency physician needs to know which of these patients will require admission and where they should be admitted for appropriate observation.

Pearls and pitfalls regarding the management of rectal bleeding also will be discussed.

— The Editor

Introduction

Lower GI bleeding is an infrequent presenting complaint to the ED physician. For the patient, the occurrence of rectal bleeding or blood in the stool is alarming, and often will prompt immediate consultation with a physician.

Although rectal bleeding or lower GI bleeding is by no means exclusively a disease of the elderly, the preponderance of patients with this complaint will be older adults. Factors contributing to this include natural changes in the colonic mucosa that predispose the patient to diverticula, hemorrhoids, ischemic colitis, and angiodysplasia. There are certain diseases that present with rectal bleeding that almost exclusively are found in the elderly population, such as ischemic colitis, angiodysplasia, and mesenteric ischemia. As with many presenting complaints that in a younger population are usually of a benign origin, the physician must be vigilant regarding the presenting complaint of rectal bleeding in a geriatric patient. Often the etiology can cause considerable morbidity. Because the etiologies are more likely to be vascular, malignant, or ischemic, the incidence of mortality is considerably higher as well. The elderly often have pre-existing, co-morbid conditions that must be factored into the equation, as they will not tolerate blood loss and hemodynamic instability as well as their younger counterparts.

Often, the diagnosis will not be reached in the ED, as it will require invasive procedures to diagnose definitively the cause of rectal bleeding. But, with careful inquiry, prudent diagnostic testing, and a careful consideration of the differential diagnosis pertinent to the elderly population, the emergency physician often will be able to exclude maladies that need immediate surgical correction or thorough evaluation. This enables the physician to decide the disposition of the patient to home, to a medical ward bed, or to an intensive care unit (ICU) setting, and with confidence contact the appropriate consultant and jointly decide if the patient requires emergent or urgent diagnostic testing and further care.

Elderly patients often require hemodynamic stabilization, which can be tricky if there are other co-morbid illnesses that predispose the patient to fluid overload. Also, elderly patients often do not manifest volume loss as readily as their younger counterparts, so the physician must take extra caution when evaluating hemodynamics in these patients and err on the side of conservative care and admission. Almost all elderly patients with lower GI bleeding will require admission and evaluation of their disease.

There will be instances when the emergency physician will be able to make the definitive diagnosis of the cause of bleeding and will be able to send the patient home safely for follow-up care. Some pearls and pitfalls can assist the physician so that he or she is better able to make that decision. (See Table 1.)

Table 1. Pitfalls
• Don’t rely on the color of stool to determine the bleeding site. Colors change as transit times vary and blood products break down.
• All that bleeds bright red is not a hemorrhoid. Unless it’s bleeding before your eyes, look for another diagnosis.
• Elderly patients may not manifest orthostatic changes from blood loss as readily as their younger counterparts. 
• The initial hemoglobin may not be a reliable indicator of the volume of blood lost, as the volume may be contracted. 
• Look for other systemic causes if your investigation of the abdominal structures turns up negative and the patient still has abnormal vitals, especially if the rectal bleeding has ceased.
• Drop a nasogastric tube (NGT) in the presence of bright red rectal bleeding.
• Resuscitate the patient aggressively with fluids for abnormal vitals and hypovolemia.
• Order typed blood products.
• Peritoneal signs may take up to 20 hours to manifest.
• Perform a digital exam and anoscopy on a patient with anorectal bleeding.

As the population ages, we will continue to see an increase in the care of the elderly in the ED, and diagnoses that now are considered uncommon will be seen with increasing frequency. Therefore, it is incumbent upon emergency physicians to be as familiar with deadly, uncommon presentations as possible. The mortality in one series of patients with lower GI bleeding was 5%,3 although in a more recent study, the mortality of patients presenting with lower intestinal bleeding was 3.6%.1

Several pieces of historical information must be sought when questioning patients about their bleeding. These include whether there is a large or small amount of bleeding; whether the blood is bright red or the stools are darker (melanotic or maroon). There may be concomitant abdominal pain. Based on these factors, the emergency physician can narrow the differential diagnosis, appropriately work up these patients, and arrive at a disposition.

By definition, lower GI bleeding occurs distal to the ligament of Treitz. The patient may state that his or her stools are black and tarry (melanotic), or maroon and bloody, or they may report bright red blood in the toilet bowl or on the tissue paper. There is a fair amount of confusion regarding the factors that determine how much blood has been lost and where the loss is occurring to produce certain types of stool. Although eliciting the type of stool from the patient may yield important information to relay to the gastroenterologist, it rarely will assist the emergency medicine physician caring for a patient unless it is bright red blood, which usually indicates a stable anorectal source. Suffice it to say that melanotic stool usually comes from upper GI bleeding, because it takes eight hours for melena to be produced from as little as 60 mL of blood in the bowel. Stools may stay tarry for several days after the bleeding has stopped. Bloody or maroon stools indicate a more brisk and distal bleed, requiring more than 1000 mL of blood and fewer than four hours transit time.4 Bright red blood usually indicates an anorectal source, although if the bleeding is brisk from a distal site in the colon, the presentation also may be bright red.

Because of atherosclerosis, elderly patients may not manifest orthostatic changes like a younger adult with volume loss. Also, they may become dizzy for a variety of reasons, none of which may be related to their bleeding, so orthostatics may not be very helpful diagnostic tools.5 However, it will be important to monitor vital signs, which usually will indicate the severity of the bleed and dictate the disposition. Remember also that patients usually grossly exaggerate the amount of blood in the toilet because it is unnerving, and it only takes 10 mL of blood to turn toilet water bloody. Up to 20% of reported lower GI bleeding results from a non-GI source.4

Pathophysiology

There are slight changes in the anatomy and physiology of the epithelium of the digestive system due to aging. Connective tissue changes take place in midlife and increase as one ages. The tunica muscularis of the colon is protected by collagenous tissue, and as patients age, less of this fibrous tissue is available to prevent herniations of the intestinal mucosa, which results in pseudodiverticula.6 Because the elderly have more chronic concomitant diseases and often have sustained a lifetime of environmental insults (i.e., alcohol use, poor diet, smoking, and polypharmacy), it can be difficult to tease apart which factors are most responsible for the changes that take place. Angiodysplasia is more common among the elderly and is thought to be due partly to chronic, intermittent, low-grade obstruction of the submucosal veins, which results in mucosal ischemia. This causes the arteriovenous malformation, whether congenital or not, to bleed more easily from friable mucosa.

The blood supply of the colon is from both the inferior and superior mesenteric arteries. There is contributing vasculature and blood supply from the iliac arteries as well. Because the rectum has a redundant blood supply, it is not as susceptible to ischemic events. Elderly patients have a greater predisposition to tortuosity among their blood vessels, as well as to thrombus and plaque formation. This reduces colonic blood supply. If the main blood supply is reduced by a thrombus, then a low-flow state, such as congestive heart failure (CHF), can result in ischemia. This sets into motion autonomic regulation and the renin-angiotensin system, which causes vasospasm of the arterioles, resulting in arteriovenous shunting in the vascular plexus supplying the mucosal villi. End arterioles that supply the vascular plexus in the submucosal layer are very sensitive to vasospasm. High colonic intraluminal pressures exacerbate this shunting. Ischemia and injury of the villi and mucosa of the intestine will cause sloughing and produce bloody diarrhea or bloody mucus.

The pathophysiology of individual entities will be discussed in more detail.

ED Evaluation

Obviously, careful attention to the patient’s vital signs will dictate how aggressively to manage the patient and institute volume replacement. Do not withhold volume resuscitation just because the patient has concomitant diseases that may result in fluid overload. Because the colon can hold a large amount of blood, these patients often have been bleeding for some time before they present, and are more hypovolemic than is evidenced by their vital signs. Excess fluid always can be removed. Replenish bleeding patients with at least a liter of normal saline or lactated Ringer’s solution and monitor vital signs for improvement. All patients need a complete blood count, chemistry panel, and coagulation studies. Remember that initial hemoglobin studies may not reflect the degree of blood loss due to volume contraction, and may fall significantly after hydration. The blood urea nitrogen (BUN) level may be elevated, without a concomitant rise in creatinine, due to the absorption of proteins from blood in the GI tract and dehydration.7 Blood type and screen also should be ordered. If the patient is hemodynamically unstable even after attempts at fluid resuscitation, order four units of cross-matched blood in anticipation of transfusion. If the patient demonstrates resultant chest pain because of anemia or has a strong cardiac history, an electrocardiogram (ECG) should be obtained, as well. A rigid abdomen, inactive bowel sounds, rebound, or guarding indicate the possibility of perforation, so an upright chest x-ray (CXR) is in order, as this is the most sensitive test for elucidating a perforated viscus.8

The pertinent history should include such details as how much bleeding has occurred, the color of the stool, preceding weight loss, decreased appetite, fever, abdominal pain, vomiting, hematemesis, syncope or chest pain, prior GI bleeding episodes, prior episodes of diverticulitis or other GI disorders, prior abdominal surgeries, alcohol intake, previous GI tests, and medication use. The patient should be asked about the presence of peripheral vascular disease, atherosclerosis, and aneurysms, which are diseases more commonly found in the elderly.

In many instances, the physical examination of the elderly patient with lower GI bleeding will be relatively benign. Except for the obvious finding of blood on rectal exam, the abdominal exam could well be nondescript. This does not exclude serious illness, as several entities are hallmarked by a benign physical examination. Examine the patient for signs of peripheral vascular disease, such as decreased pulses, loss of hair on lower extremities, or the presence of bruits either on the abdomen or upon carotid exam. Abdominal tenderness to palpation will lead to specific diagnoses, which will be discussed later. Look for signs of liver disease, which could indicate colonic varices. Absence of bowel sounds or rigidity prompt evaluation for a perforation or obstruction. In the elderly population, it is well documented that signs of hypovolemia can be masked by arteriosclerotic disease, rendering the patient less able to exhibit tachycardia and hypotension. So, if these signs are present, the emergency physician should be even more vigilant to the presence of a large bleed or chronic bleed. Remember also that, due to changes in peripheral pain fibers that occur with age, elderly patients may not experience the same amount of tenderness to abdominal palpation as their younger counterparts. In fact, belly exams can be deceptively benign. Peritoneal signs in the elderly population can be delayed for up to 20 hours.4

Contrast-enhanced computed tomography (CT) scans of the abdomen have claimed a large role in the evaluation of GI bleeding. Sensitivity for detecting acute ischemic events in the mesenteric vasculature is upwards of 64-82%. Contrast infusion allows delineation of the bowel wall and highlights pneumatosis in the bowel wall and bowel wall thickening. Most thromboemboli in the superior mesenteric artery and superior mesenteric vein are detected easily on CT. CT also can help distinguish the presence of vasculitis. It has a 75% sensitivity for detecting portions of bowel with ischemic colitis secondary to an obstructing neoplasm.8 Additionally, CT allows for the delineation of other disease processes that may be responsible for the bleeding. In one study, CT identified the pathology of 9% of lesions existing outside the colon. The sensitivity of unenhanced CT following oral contrast was found to be equal to or better than that of a barium enema. Six percent of the barium studies had to be abandoned because the patients were too frail to continue the study. The overall sensitivity was 75% for identifying the pathology associated with colonic complaints. The specificity was 96%, and the negative predictive value was 96%.8

Remember that the cause of acute lower GI bleeding may be upper GI bleeding. (See Tables 2 and 3.) Although a negative aspirate from a nasogastric tube (NGT) is not definitive for ruling out an upper GI bleed, it is 98% sensitive. In one clinical series, 11% of patients presenting with hematochezia had an upper GI source. Unless the bleeding is minor and self-limited, an NGT should be placed to rule out an upper GI source. Also, the visualization of a potential source of bleeding (with anoscopy for instance) does not exclude the possibility of a more proximal site for bleeding.7

Table 2. Most Common Causes of
Major Lower GI Bleeding3
Diagnosis %
Diverticulosis 23
Angiodysplasia 11
Undetermined 6
Radiation proctitis 3
Cancer 3
Polyps 2
Ischemic colitis 1
Anticoagulants 1

Table 3. Most Common Causes
of Minor Lower GI Bleeding3
Diagnosis %
Diverticulosis 16
Undetermined 5
Polyps 5
Cancer 4
Hemorrhoids 3
Fecal impaction 2
Anal stricture 2
Stercoral ulcer 2
Ischemic colitis 2
Fistula-in-ano 1
Inflammatory bowel disease 1
Radiation colitis 1

Disposition

The American College of Gastroenterology guidelines state that patients with the acute presentation of hematochezia coupled with anemia and unstable vital signs and/or the need for blood transfusion should be admitted. The gray area occurs in patients with a history of rectal bleeding that on exam have brown stool with a positive gastroccult card, chronic bleeding of obscure origin, or obvious self-limited bleeding where the likelihood of a change in vital signs or anemia is low.7

One study stratified patients with acute upper or lower GI bleeding into low risk and high risk for adverse outcomes during hospitalization. Patients with comorbid illnesses, a higher BUN, a lower albumin, and a higher prothrombin time fared worse than their cohorts. ICU admission is indicated for this group, as the in-hospital mortality rate was 15%7.

Another study reviewed 219 admitted patients with acute lower GI hemorrhage, and found a very low mortality rate of 3.6% overall. Only one death was directly related to bleeding. The recurrence of hemorrhage was 9% at one year.1

The vast majority of elderly patients presenting with hematochezia will require admission and prompt evaluation. Only if the ED physician is able to concretely establish an anorectal source as a cause, or the bleeding is occult and self-limited in nature, will it be safe to send the patient home. Although mortality overall is low, these patients can mask hypovolemia and, because of comorbid illnesses, are more likely to require monitoring, stabilization, and further immediate care. They also are more prone to morbid complications. (See Figure 1.)

Figure 1. Stratification of Patients Presenting with 
Acute Upper or Lower GI Bleeding7,14


Etiologies of Lower GI Bleeding

Colonic Diverticulosis. Classified in the category of painless large bleeding, colonic diverticulosis is a disease of Western culture and our refined, low-fiber diet. Diverticula are rare in patients younger than age 30 and are present in two-thirds of patients 85 years or older.9

First described by Koch in 1903, diverticulosis originally was thought to be a rare cause of lower GI bleeding.10 Fifteen percent of diverticula cause bleeding problems, with most bleeding diverticula originating from the right colon and most asymptomatic diverticula located in the sigmoid portion.11 Significant hemorrhage occurs in 3-5% of those with diverticula. Diverticular disease in one study accounted for 9% of acute surgical admissions.3 One study reported it to be the most common cause of bleeding in the elderly population, at a rate of 41.6%.1 (See Table 4.) Another study found that out of 112 patients admitted for acute lower GI hemorrhage, two died following massive bleeding; none who underwent surgery died. The median age of those who died was 80 years. One-third of patients admitted with a complication of diverticular disease will be admitted again within five years.12

Table 4. Final Diagnosis in Patients 
Hospitalized for Acute Lower GI Bleed1
Diagnosis %
Colonic diverticulosis 42%
Colorectal malignancy 9%
Ischemic colitis 9%
Acute colitis 5%
Hemorrhoids 5%
Angiodysplasia 3%
Crohn’s disease 2%
Stercoral ulcer 3 patients
Vasculitis 2 patients
Infectious colitis 2 patients
Radiation proctitis 2 patients
Polyp 1 patient
Diverticulitis 1 patient
Meckels' diverticulum 1 patient
Unknown 1 patient

Diverticula are saccular outpockets of the colon, containing all layers of the bowel wall. Bleeding usually is caused by a fecalith within a diverticulum that erodes a branch of the colonic artery. Intimal thickening and medial thinning of the vasa recta as it courses over the dome of the diverticula predisposes a segmentally weakened artery to rupture.9

Because diverticula are arteriolar bleeds, they can be quite massive, requiring multiple units of blood for transfusion. Up to one-third of patients have severe hemorrhage with diverticular bleeding. In one study, 42% of 144 patients had massive bleeding, requiring more than 1500 mL of blood transfusion.13

Diverticular bleeding is characterized by the passage of voluminous red or maroon blood clots. Patients can present with perforation, obstruction, or fistula formation, in addition to hematochezia.9 One group reported 42% of patients had only black, tarry stools. Most patients had experienced some GI symptoms prior to their bleeding episode, including constipation, diarrhea, or vague abdominal pain. Many have experienced prior colonic bleeding or prior diverticulitis.13 The signs of hypovolemia may be very mild in these patients. If perforation (which is present in 11% of patients with diverticulitis) is suspected, a CXR will confirm pneumoperitoneum.9

In one review, 76% of lower GI bleeding due to diverticular disease stopped spontaneously.7 Diverticula rarely rebleed after the episode is finished completely, though a patient may experience rebleeding during the episode in a stuttering fashion. This may require emergent colonoscopy for definitive care in the form of cauterization. If the bleeding is massive or continuous and does not appear to be abating, call the gastroenterologist for an emergent consultation and probable colonoscopy.14 Up to one-third of all patients with bleeding from diverticula were massive bleeders, defined as needing more than 1500 mL of transfused blood. Patients who needed fewer than four units of blood almost always stopped bleeding spontaneously. Patients who needed more than four units went to surgery.13,15

Primary resection was the former treatment for all diverticula bleeding.10 The advancement of endoscopy and interventional radiology has enabled the physician to use less invasive means of controlling bleeding diverticula. Surgical consultation and resultant hemicolectomy remains the procedure of choice for patients who continue to bleed despite conservative therapy, or who are evidencing significant hemodynamic complications as a result of their massive bleeding.8 Diverticulitis rarely bleeds.7 (See Table 5.)

Table 5. Bleeding and Pain Associated with Sources of GI Bleeding
Presentation Large amounts of bleeding/Pain  Minimal bleeding/No pain Minimal bleeding/Pain Large amounts of bleeding/No pain
Diverticulitis 
Angiodysplasia
Radiation proctitis
Colorectal carcinoma
Colonic polyps
Ischemic colitis
Inflammatory bowel disease
Acute mesenteric ischemia
Hemorrhoids 
Infectious diarrhea
Vasculitis

Angiodysplasia. One of the most common causes of bleeding in the elderly population, angiodysplasia falls into the category of painless, voluminous bleeding. One-quarter of the elderly population have mucosal vascular ectasias without any evidence of bleeding. They usually are right-sided, colonic lesions, and occur in multiples. A study of 183 patients attempted to differentiate between bleeding diverticula and vascular ectasias. Of the 20 patients angiographically proven to have arteriovenous malformations (AVMs), only two had demonstrable bleeding at the time of the event. More than 80% of the subjects had three or more recurrent episodes of bleeding. They received a mean of five units of blood during hospitalization. The author favored angiography as both a diagnostic tool and, with vasopressor agents infused into the mesenteric circulation at the site of bleeding, a curative tool. Proof of the cause of bleeding was established when the patients received hemicolectomies and no further bleeding was found. For example, if a vascular ectasia was identified angiographically on the right side of the colon but was not actively bleeding, as was usually the case, the information gathered from angiography was used to dictate which portion of the colon should be removed. The patients then were followed prospectively, and if there was no rebleeding episode, the author concluded that the diagnosis and location had been accurate.3,16

More recent studies have concluded that angiodysplasia was not nearly as prevalent a cause of GI bleeding as previously was thought, with reports of actual cause closer to 3%.1 In 15% of patients with angiodysplasia, massive lower GI bleeding is the presenting feature. Because the bleeding is venous and capillary in origin, it usually is less dramatic than diverticular bleeding, which is arterial in origin. Most bleeding stops spontaneously, and mortality is unusual.

As stated above, the elderly are at a higher risk for GI bleeding. Chronic intestinal mucosal changes from intracolonic pressure and low-grade obstruction of the submucosal veins, and consequently, the venous capillary system, cause a loss of patency of the arteriolar-capillary-venular valves, resulting in an arteriovenous malformation.3 The bleeding site usually is located in the cecum or ascending colon. Patients with cardiovascular disease have an increased predisposition to angiodysplasia, so this historical information should alert the emergency physician to the possibility of angiodysplasia.17

One study of 131 patients with obscure GI bleeding for which a cause previously had not been found used visceral angiography and found that many of the patients had both diverticula and vascular ectasias. The culprit was chosen by an educated guess as to which was responsible for the presenting bleed. The author found that patients with colonic angiodysplasia presented more often with rectal bleeding, whereas those with vascular anomalies of the small bowel presented more often as melena. The study showed an overall 84% success rate for identifying all causes of lower intestinal bleeding. The author concluded from his methods that angiodysplasia was the most common cause, accounting for 40% of all patients. Eight percent of his patients had a second possible cause for hemorrhage associated with angiodysplasia. He also suspected angiodysplasias to be the cause of bleeding in 50% of patients presenting with chronic anemia.2

Colorectal Carcinoma. In the category of minimally pain-ful, minor bleeding, colorectal carcinoma is more insidious. Colon cancer is the third most common cancer found, disproportionately affecting geriatric patients. One group evaluated 822 patients with colorectal carcinoma and found that 90% of colorectal cancers develop in patients older than 65.18 Of patients with known tumors, two-thirds will bleed at some point in time from the tumor, and 5% of lower GI bleeding is due to colorectal cancer, according to most studies.

Patients complain of intermittent bright red bleeding, anemia, weight loss, and changes in stools or constipation over a prolonged period of time. There may be a report of vague abdominal discomfort and bloating. Complications include obstruction, intussusception, massive bleeding from an eroded arterial supply within the tumor, perforation, and fistula formation.19

An upright abdominal x-ray will help rule out an obstruction or perforation, both of which are not uncommon with colorectal cancer. Provided there are no acute complications present, these patients can be worked up as outpatients, although it must be stressed to the patient the importance of prompt follow-up.18 If the diagnosis is not definitive, consider admitting these patients for further observation and care.

Although colonoscopy is the modality of choice for discovering these lesions, CT scan of the abdomen is very sensitive for delineating a tumor, particularly if the lesion is complicated by proximal ischemic changes or obstruction.20

Ischemic Colitis. Almost exclusively a disease of the elderly, more than 90% of the patients with ischemic colitis are older than 70 years. It is the most common form of GI ischemia and often mimics other inflammatory diseases of the colon, such as inflammatory bowel disease (IBD), infectious diarrhea, and neoplasms.

Classified into occlusive and nonocclusive types, the most common occlusive cause is iatrogenic interruption of the inferior mesenteric artery during aortic surgery. Thromboembolism is another occlusive cause of ischemic colitis. Low-flow states, such as CHF, renal disease and shock, and atherosclerosis, account for the nonocclusive causes. Colonic ischemia is the end result when blood flow is restricted to the colon for any reason. Therefore, the number of inciting agents producing colonic ischemia is quite extensive.21 It encompasses a spectrum of severity. Reversible, transient, self-limited disease confined to the mucosa and submucosa is the most common ailment; fulminant ischemia, which is transmural and progresses to necrosis, is the most rare and confers the most dismal prognosis. Chronic ischemia, producing ulcerating colitis, strictures, and gangrene, is rare.22 As opposed to mesenteric ischemia, which requires immediate surgical or aggressive intervention and affects the superior mesenteric artery, ischemic colitis usually affects the inferior mesenteric artery (IMA). Areas of the colon supplied by the IMA have a better collateral and redundant blood supplies, rendering them less sensitive to ischemic insult. Ischemic damage to the tissue is caused by hypoxia during the ischemic period and by reperfusion, which releases free radicals.23

Presentation falls into the category of pain with minimal bleeding, usually maroon or bloody stools.10 Patients usually present with colicky abdominal pain, abdominal distension, and bloody diarrhea. Blood loss usually is minimal, and on physical exam, the patients are only mildly tender. If the bleed is massive enough to cause hemodynamic changes, look for another cause.

Thumbprinting, suggesting ulcerations of the mucosal wall, may be seen on abdominal x-ray, but this is rare.23 A more common finding would be dilated colon, or a gasless abdomen. Late radiographic findings indicative of colic perforation and full mucosal thickness involvement would include free peritoneal air, air within the bowel wall, and air within the portal venous system.24 A CT scan would be much more helpful in delineating the ulcerative regions and mucosal thickenings, although usually the diagnosis is made by endoscopy. CT allows distinction of an ischemic segment in 20% of cases. Barium enemas, with a sensitivity of 85%,22 and colonoscopy are much more sensitive for this diagnosis, revealing the clear demarcation of ulceration and normal bowel wall.25 A high WBC count may help establish the diagnosis of ischemic colitis, although this is nonspecific.

The treatment is conservative, with bowel rest, optimal hemodynamic status, and broad-spectrum antibiotics. Patients usually recover in 24-48 hours. If acute, irreversible ischemic changes have occurred, these can result in gangrene and necrosis of the bowel wall and will require immediate surgical intervention. These patients present with signs and symptoms consistent with perforation and peritonitis.14 Few patients develop severe cases of ischemic colitis and progress to gangrene, necrotizing colitis, clostridial colitis, and colonic infarction.21,24 Even fewer require immediate surgical resection, although some require blood transfusions. Mortality attributed to sequelae of peritonitis is high in this small group of sick patients with complications.

The differential diagnosis of colonic ischemia includes infectious diarrhea, IBD, pseudomembranous colitis, colon carcinoma, and acute mesenteric ischemia. All patients most likely will need admission for a complete GI work-up, since it will be difficult to differentiate ischemic colitis from mesenteric ischemia.25 A stool culture also should be obtained for infectious causes.

Mesenteric Vascular Insufficiency. Ischemia and necrosis of the bowel wall can result from an acute loss of intestinal blood supply secondary to arterial embolus, venous or arterial thrombosis, or nonocclusive or low-flow states. Mesenteric ischemia causes minor bleeding with major pain. The average age of patients affected is 65 years; most patients have comorbid illnesses, such as arteriosclerotic heart disease, peripheral vascular disease, diabetes, and hypertension.15 The mortality is as high as 90% in these patients, due to the combination of delayed diagnosis, co-existing illnesses, frail health, and resultant bowel necrosis.26

The highest risk population are those patients with CHF, cardiac arrhythmias, valvular disease, arteriosclerotic heart disease, hypovolemia or hypotension, recent myocardial infarction, or history of emboli in the extremities. Sixty-six percent have evidence of peripheral vascular disease.22,27 The chronic mesenteric venous occlusion usually presents as weight loss, and post-prandial angina, and the pain resembles the squeezing pain of claudication. The pain is much more insidious at onset and more moderate in nature. The classic historical presentation of acute embolism or thrombosis is a patient in severe abdominal pain who looks sick, with a relatively benign physical exam.28

Acute embolic occlusion may present with bloody diarrhea and vomiting, and will include rapid onset of severe abdominal pain and a history of either prior embolic events or a cause such as atrial fibrillation, valvular prosthesis, or arrhythmia.26 Because the pathology is one of sudden restriction of blood flow without collateral circulation, intense intestinal spasm results, manifesting as acute onset of violent unremitting abdominal pain with forceful vomiting and diarrhea without significant physical findings. In a patient with a high WBC count and a prior embolic event, this diagnosis should jump to the top of the physician’s differential list. Arterial embolic events account for 75% of acute mesenteric ischemia.25,28

The physical exam on most of these patients is non-diagnostic with the complaint of pain far out of proportion to their abdominal physical findings. Occlusions usually don’t present with rectal bleeding, although in one report, one-third of patients presented with grossly bloody stools.25

The mortality of mesenteric venous thrombosis hovers around 20%. The percentage of cases attributable to mesenteric venous occlusion is 5-15%. It is more likely to be reversible than arterial occlusion, accounting for its lower mortality.29 The mortality of superior mesenteric arterial occlusion surpasses 50-80%.28

Acute thrombotic occlusions tend to occur in older patients with peripheral vascular disease. These patients usually present with severe cramping, abdominal pain, and often, bloody diarrhea. They generally have fewer physical findings, a higher WBC count, and more peripheral arterial occlusions than other patients with acute abdominal pain.26

Non-organic causes or low-flow states would be an abnormal blood flow from another vascular source that limits the blood flow to the mesentery. Examples of this would be CHF, renal failure, sepsis, and hypovolemia. This is the most lethal cause of mesenteric ischemia, with a mortality of 90%.27 These patients often present with acute onset of pain without defecation or with no urge to defecate.

Diagnosis rests largely on maintaining a high level of suspicion, since definitive diagnostic studies are intensive and can be difficult to obtain, and physical exam and ordinary studies usually are non-specific and not helpful. Because of its non-specific complaints and rarity, it is a difficult diagnosis to make before the patient becomes moribund. The first 24 hours are critical, with a survival rate of 60% if discovered in this time period.27 Once abdominal signs, such as peritoneal findings, become apparent, bowel necrosis already has taken place. The late occurrence of ileus, abdominal distension, shock, and sepsis is a bad prognostic indicator.

One researcher advocated highly aggressive management with early angiography to identify the pathology and use of local vasodilators to interrupt persistent splanchnic vasoconstriction. It is the persistent vasoconstriction of the splanchnic vasculature that is responsible for the majority of bowel necrosis. With this approach, he increased the survival rate to 54% vs. the usual 20-30% reported in other literature.27 Although angiography is the gold standard for definitive testing and therapy, it often is not performed, either because the diagnosis is not suspected clinically or because the patient requires emergent surgical intervention. CT has appeared in the literature as a viable option for diagnosing thrombotic and occlusive events with good accuracy and sensitivity. In one series, CT had a 93% sensitivity for detecting superior mesenteric venous thrombosis.22 CT with contrast often is much easier to obtain in the ED.29 Unfortunately, often the bowel will be dying while studies are taking place and the physician is trying to figure out the etiology of the pain. Remember: Time is bowel. A normal, plain abdominal film in a high-risk patient is compatible with the diagnosis of ischemia, although 80% of plain films in one study revealed ileus or free abdominal fluid.26,27 Unfortunately, by the time a plain film is diagnostic, with thumb-printing or dilated segments of colon or small bowel indicative of fluid collection, there already is bowel infarction and necrosis.27 Contrast-enhanced CT scans, useful in the diagnosis of mesenteric venous thrombosis, reveal a high density mesenteric vein wall with a central mesenteric clot. In several studies, the use of CT scans and magnetic resonance imaging (MRI) enabled the early detection of clots, obviating the need for surgical resection.25 The sensitivity of the CT scan for diagnosing a mesenteric arterial occlusion ranges from 37-80%. Conversely, almost all mesenteric venous thrombosis can be detected by CT.30

Once diagnosed, the patient requires emergent laparotomy, unless the cause is a low-flow state, which needs to be reversed systemically or locally with a vasodilator. If this diagnosis is suspected and there are risk factors present, and as diagnostic studies are done to corroborate the diagnosis, contact the gastroenterologist immediately for consultation, as well as the general surgeon.

Anorectal Causes. Anorectal causes of GI bleeding include: hemorrhoids, fissures, fistula, abscess, prolapse, proctitis, and impaction. These usually cause minor bleeding. Hemorrhoids are found in 70% of the geriatric population, and are the most painless common cause of minor GI bleeding.

Internal hemorrhoids occur above the pectinate line in the rectum and appear as varicosities of the hemorrhoidal venous capillary plexuses covered with mucosa. They usually present with painless, bright red bleeding from the rectum. Hemorrhage is possible, though rare, and usually can be treated with endoscopic intervention and cauterization.31

External hemorrhoids originate below the pectinate line. Covered in skin, they usually present with painful bleeding and often are visible on anoscopy. Although hemorrhoids can bleed profusely, usually the bleeding is self-limited and minor in nature, obviating the need for an extensive work-up beyond an anoscopy. The patient usually will complain of bright red, painful bleeding.

Anal fissures are a common cause of anorectal pain and bleeding. They can be caused by hard stools, diarrhea, infection, and idiopathic causes. Most fissures or ulcerations of the anal squamous epithelium occur in the posterior midline from the anal verge to the dentate line. Diagnosis usually is accomplished by careful inspection of the anal canal, which may require sedation because of concomitant pain. Medical management includes a high-fiber diet, bulk laxatives, and warm sitz baths. Follow-up care is provided by the primary care physician.

Anal tumors are rare, accounting only for 1-6% of all anorectal tumors. The mean age of patients with these cancers is 60-70 years. Presenting symptoms include painless rectal bleeding, painful defecation, anal pruritis, discharge, and a sensation of a rectal mass. Easily overlooked, the diagnosis often is missed initially, delaying appropriate treatment. In the elderly population, the examining clinician must perform a digital exam and anoscopy, looking for any suspicious lesions. A high index of suspicion must prevail in this population. If any anorectal masses or ulcerations are detected, these patients should be referred to a surgeon for further evaluation. Local surgical excision has an excellent survival rate.32

Rectal prolapse usually is mild and easily reducible or self-reducing, and treatment is on an outpatient basis with referral to a general surgeon. Rectal prolapse is more common in elderly women, as their pelvic musculature has been weakened by child-bearing. When a patient strains to defecate, the force pushes the rectal mucosa outside the anus, producing pain with defecation and mucoid, bloody discharge with stools.33

If the prolapse is not easily reduced by the emergency physician manually, or the tissue appears necrotic or blanched, consider an incarcerated prolapse, which requires surgical intervention to prevent mucosal necrosis.

Radiation proctitis, caused by radiation therapy weakening the mucosa and its supplying vasculature, can be the etiology of bloody rectal discharge. Commonly found in those who have received radiation therapy, the bleeding can occur during radiation therapy and for up to six months after therapy has concluded.

Upper Gastrointestinal Sites. In one clinical series, 11% of patients who presented with a lower GI bleed had an upper GI source. Therefore, placement of an NGT should be done in all patients with significant lower GI bleeds. Because blood from a duodenal source may not reflux into the stomach, an aspirate negative for blood doesn’t positively exclude an upper bleed, although the test is 98% sensitive. The GI consultant most likely will perform upper endoscopy on patients with hematochezia.7

Idiopathic Inflammatory Bowel Disease. In the category of painful, minor rectal bleeding, 5-10% of all cases of inflammatory bowel disease in patients age 65 and older are caused by Crohn’s disease or ulcerative colitis, both of which are long-standing conditions. The hallmark of presentation is bloody diarrhea and weight loss, with abdominal cramps and, sometimes, fever. Occasionally, patients may present with constipation and rectal bleeding. Usually, the onset is insidious, with vague abdominal cramps and discomfort and gradual changes in the frequency and character of stools. Gross blood in the stool is a universal finding.

The proportion of elderly patients who develop Crohn’s disease after age 60 is 16%. Seventy percent of patients with Crohn’s disease ultimately will require surgical resection of the diseased bowel.34

Ulcerative colitis. Ulcerative colitis appears for the first time in elderly patients in 12% of cases.35 In the case of ulcerative colitis in the elderly, the predilection for disease is proctitis and proctosigmoiditis.35 Therefore, on anoscopy aphthous ulcers and rectal and anal inflammatory mucosal changes may be seen with ulcerative colitis.10

Crohn’s Disease. A characteristic physical finding in Crohn’s disease is right lower-quadrant abdominal pain, representing inflamed bowel and mesentery, and sometimes an abscess, although it has been found in elderly patients to have a predilection for the left lower quadrant.35 If the presentation is one consistent with inflammatory changes, fever, marked tenderness, and leukocytosis, CT scan of the abdomen is an excellent tool to differentiate the etiology of the pain. The differential diagnosis would include radiation proctitis, infectious diarrhea, lymphocytic colitis, ischemic colitis, diverticulitis, and colon cancer.

In mild cases, outpatient therapy is warranted, and topical steroids, sulfasalazine, and broad spectrum antibiotics that include anaerobic coverage are acceptable forms of treatment. If the patient is otherwise stable and not evidencing marked lab abnormalities, marked tenderness, or toxicity, he or she may follow up as an outpatient with the gastroenterologist.34 Consultation with a gastroenterologist is advisable before beginning empiric treatment on these patients. This also will ensure prompt outpatient referral.

Zebras. Unusual etiologies ("zebras") represent 5% of all causes of lower GI bleeding. They include the following conditions:

Rectal ulcer—A chronic and benign condition that causes rectal bleeding, stool with mucus, and tenesmus, patients with a rectal ulcer usually will complain of difficulty with defecation and straining, often utilizing digital disimpaction to assist defecation. Most bleeding is minor and probably will be mistaken for an internal hemorrhoid, which is fine in this instance, since the diagnosis is made by sigmoidoscopy and the patient in either case will be worked up as an outpatient.

Infectious diarrhea—Commonly found in the elderly, infectious diarrhea may be due to viruses, bacteria, or parasites. If the diarrhea is bloody or mucoid, obtain a stool culture and blood culture before empiric treatment begins. Patients usually present with crampy abdominal pain, fever, bloody diarrhea, and hematochezia.14 Infection caused by Clostridium difficile can cause pseudomembranous colitis, and must be kept in mind if a patient has been on broad-spectrum antibiotics. It is of particular concern in nursing homes, as it spreads rapidly through sequestered populations. It is thought by some to be the most common cause of diarrhea in the geriatric population.35,36

Radiation proctitis—Under the category of minor painful bleeding, radiation proctitis can occur shortly after radiation therapy or months later. It is due to the vascular changes associated with radiation, as well as ischemia of the delicate mucosal tissue. Proctitis (characterized by rectal bleeding, crampy abdominal pain, and bowel disturbances) is the most common presentation. A careful history probably will deduce this entity. Patients may be worked up on an outpatient basis, provided they are stable.25

Colonic polyps—A common finding in the elderly population, colonic polyps may be asymptomatic in many cases. These will be discovered by colonoscopy and biopsied. From an ED standpoint, the bleeding usually is not severe, presents as hematochezia, generally requires admission and a work-up, but will not render the patient hemodynamically unstable or require transfusions.

Constipation—Common in the elderly population for a variety of reasons, chronic constipation can cause excessive pressure on the mucosal walls as well as mucosal irritation that causes GI bleeding.37 Severe constipation can cause abdominal pain, fecal incontinence, infection, and toxic megacolon. Stercoral ulcer, which is a colonic ulcer secondary to inspissated fecal material eroding the colonic wall, is a secondary complication of constipation and accounts for a small number of bleeding episodes in various studies.

A careful history and an abdominal film revealing large amounts of stool will lead to the diagnosis. These patients need disimpaction, whole-gut irrigation with non-absorbable plyethylene glycol (GoLytely), and enemas (mineral oil is preferred) until the fecal impaction has been dissolved and evacuated.38 Obviously, if the patient is unstable, has a volvulus from toxicity, or has a high fever, he or she will require admission and whole bowel evacuation, as well as antibiotic therapy.39

Colonic varices—Colonic varices are found in 0.07% of GI bleeds. The most common cause is portal hypertension due to liver disease.25 In almost all cases, the bright red bleeding is intermittent, but often is massive. Obviously, seeing massive amounts of bright red blood pouring from the patient will prompt the emergency physician to admit, type and cross, and call the gastroenterologist. The giveaway to diagnosing this entity will be the history of liver disease.

Diversion colitis—Seen with colostomies and stomas 3-36 months after surgery, in diversion colitis the bowel wall distal to the anastamosis becomes inflamed and produces purulent and sometimes bloody discharge into the anus. The patient complains of abdominal pain, pelvic pain, low-grade fever, tenesmus, and bloody or mucoid discharge. It is seen in up to 50% of patients with a diverting colostomy. The pathogenesis is thought to be related to the diversion of the fecal stream, causing an imbalance in the colonic flora and starvation of the colorectal epithelial cells, which then necrose and bleed. The cure is reanastamosis: Call the surgeon. These patients almost always are clinically stable, making admission optional.40

Vasculitis—Found in the category of minor bleeding with pain, vasculitides are characterized by inflammation and necrosis of blood vessels and are classified by the size of the affected vessels. The GI tract is involved in 20% of patients with vasculitis.25 Polyarteritis nodosa affects small vessels. GI symptoms are due to visceral ischemia and are marked by abdominal pain, nausea, anorexia, diarrhea, and, if ischemia ensues, GI hemorrhage. Churg-Strauss syndrome affects larger vessels, but the presenting symptomatology is the same. Henoch-Schonlein purpura affects small vessels, causing abdominal pain in 20-69% of patients, 50% of whom present with melena. Systemic lupus erythematosus can cause inflammation in any organ system, the intestinal tract being no exception. Patients can develop ulcerations, hemorrhages, and infarctions. High morbidity and mortality are associated with bowel vasculitis.

Small intestinal ulceration—Small intestinal ulceration is uncommon, but causes considerable morbidity and mortality. A whole litany of etiologies is included, but anything that can cause an ulceration and subsequent abdominal pain, perforation, intestinal obstruction, and hemorrhage is fair game. The causes vary from celiac sprue to Crohn’s disease to syphilis and typhoid fever. Although most of these lesions can be worked up on an outpatient basis, the patient obviously will require admission in the presence of obstruction, bleeding, or perforation. Most of these patients will present to their primary clinicians with insidious symptomatology and will not present to the ED unless they have a complication.25

Small bowel vascular anomalies—Thirty-eight percent of patients in one series had a lesion in the distal duodenum or jejunum, presenting as obscure bleeding. Vascular ectasias were the most common.7

Meckels’ diverticulum—In the category of painless bleeding, Meckels’ diverticulum is a diverticulum of the ileum located within 100 cm of the ileocecal valve and is the most common congenital intestinal abnormality, affecting 1-3% of the population. Most Meckels' diverticula remain asymptomatic throughout life, with the majority of complications and bleeding occurring in childhood. Bleeding and obstruction are extremely rare in the adult population. It presents with hematochezia and would be treated like other diverticula from an ED perspective, since it would be impossible, from our perspective, to differentiate one diverticular bleeding source from another.25

Gastric vascular anomalies—Painless, brisk bleeding characterizes gastric vascular anomalies. More than likely, these also would cause upper GI bleeding. Patients may present with hematochezia if the bleeding is brisk, which is another reason to insert an NGT with lower GI bleeding. GI vascular anomalies are responsible for 2-8% of all cases of bleeding.41

Diagnostics in the ED and Beyond

Colonoscopy. Endoscopy is the test of choice for the evaluation of lower GI bleeding, and the yield for positive results is more than of 80%.7 One researcher evaluated 304 patients with rectal bleeding, and found that 45% of patients with normal barium studies had significant lesions found on colonoscopy. Cancer, telangiectasias, inflammatory bowel disease, and polyps were the most common findings. The overall incidence of finding significant lesions by colonoscopy is 41.5%.42

Barium Enema. Barium enemas are only 50% sensitive in identifying the source of bleeding, and no longer are advocated as really useful diagnostic tools. They will miss 20% of all cancers and up to 30% of polyps larger than 5 mm. They also are poorly tolerated by the elderly population, and often must be aborted before the tests are complete.42

Angiography. Although older literature stated that angiography was the procedure of choice both for identification of the lesion and therapeutic value, it clearly has fallen by the wayside in the GI literature, replaced by colonoscopy as a more definitive test. It now is advocated for patients with such massive bleeding that nothing can be seen with an endoscope, or when colono-scopy has not identified the source. The diagnostic yield is 40-70% and the complication rate is higher than with colonoscopy.

Sigmoidoscopy. Sigmoidoscopy can be used as the initial diagnostic tool for evaluation of hematochezia, which has a greater likelihood of an anorectal disorder as the etiology. Although some EDs have rigid sigmoidoscopy, the ability to utilize such a device is not the standard among ED physicians—leave it up to the GI consultant.

CT Scan. CT is an excellent test for the evaluation of abdominal complaints in the elderly. Some authors recommend CT as the diagnostic tool of choice for diverticulitis and diverticulosis. It is quite sensitive for detecting ischemic colitis; the most common finding is bowel wall thickening, although this is non-specific. It also can detect mesenteric vein thrombosis, mesenteric or portal venous gas, and other abnormalities.30 The sensitivity of CT scans for this purpose is 64-82%. The sensitivity of detecting a strangulated obstruction ranged from 83-100%.8 It reportedly also is useful for differentiating tumoral vs. ischemic segments of bowel in 75% of cases. When contrast is given overnight and CT is performed the next day, the sensitivity for detecting the etiology of colonic complaints was 75%. The negative predictive value was 96%. Although this may be more optimal than giving patients oral contrast in the ED and scanning them within two hours, immediate CT scanning still is relatively sensitive.20 In addition, perhaps one of the greatest values of CT scanning is that it provides information on other possible etiologies for an abdominal complaint.

MRI. MRI is excellent for detection of bowel wall infarction and thickening, intramural pneumatosis, mesenteric or portal venous gas, or mesenteric occlusion.

Labeled RBCs. Usually, technetium scans are utilized. Scans in lower GI bleeds are positive 26-72% of the time. The literature is quite diverse on the opinion of whether a positive scan is the site of true anatomic bleeding. Therefore, the usefulness of the test, particularly in an acute setting, is questioned.

Anoscopy. Anoscopy is useful in the ED for identifying distal lesions, such as hemorrhoids and fissures. Never attribute the bleeding to a hemorrhoid unless it is bleeding during the procedure.

NGT. Drop an NGT with lower GI bleeding; 11% of lower GI bleeding will be caused by upper GI bleeding. NGT is 98% sensitive for detecting an upper GI source. If no blood or bile is aspirated, you cannot determine if the test is negative or positive. If the patient is passing bright red blood in front of you and the aspirate is bilious and the gastrocult is negative, it’s not an upper GI bleed.

Plain Abdominal Films. Plain films do not offer much bang for the buck. They are best for detecting ileus, megacolon, small bowel obstruction, or constipation and fecal impaction, and are too insensitive to detect ischemia, edema of the bowel wall, source of bleeding, etc.

Conclusion

Acute lower GI bleeding in the elderly population may be associated with significant morbidity and mortality. Pay close attention to the patients’ vital signs, comorbid illnesses, availability of follow-up care, toxicity, and duration of bleeding. These factors will guide admissions, as well as how intensively patients should be monitored if admitted.

Give volume generously to patients who appear hypovolemic, unless otherwise contraindicated. Once rehydrated, recheck the hemoglobin, as it may have been falsely elevated from volume contraction. A chemistry panel will alert you to chronic or large amounts of blood in the GI tract, as evidenced by an elevated BUN. Coagulation panels will direct anticoagulant therapy or reversing anticoagulant therapy. An elevated WBC count will alert you to the possibility of an infection, although there can be demargination.

Involve your consultants early, as they may want to plan for a colonoscopy sooner rather than later. They also may have a specific diagnostic tool in mind, such as angiography or contrast CT. Depending on the probable lesion, the first consultant most likely is going to be the gastroenterologist, who will want to endoscope the patient emergently or urgently, depending on the severity of the bleed. If you suspect diverticulosis with massive bleeding, these patients need stabilization and emergent surgical intervention. Likewise, if presented with peritoneal signs and symptoms, elevated WBC counts, or perforation, call for immediate surgical intervention. Severe abdominal pain in a patient with risk factors for an embolic event and an otherwise nonspecific exam and lab studies merits consultation with a surgeon and probable CT scanning to look for a mesenteric occlusion or ischemia.

Use anoscopy as an adjunct. If the hemorrhoidal bleeding is not apparent, don’t attribute the GI bleed to a hemorrhoid. Remember that in the elderly, postural vital signs are pretty useless, and these patients can be delayed in how long it takes them to evidence volume loss with compensatory mechanisms.

In these days of managed care and decreasing admission rates, you may be asked to send some of the minimally symptomatic patients home. Most of the literature suggests that patients with lower GI bleeding with stable vital signs, who are non-toxic in appearance, and who have a normal hemoglobin not requiring transfusion, have a low risk of morbidity and mortality. An upper GI cause must be ruled out first. Additionally, it is imperative that the patient have close follow-up and a GI work-up. Conservative treatment would dictate admission for the acute onset of hematochezia, as this is the most common presenting symptom for lower GI bleed. This is not the disposition for patients with chronic bleeding of obscure origin, self-limited rectal bleeding, or occult positive stool. Most of these patients can be sent home safely for an outpatient evaluation.

References

1. Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: A population-based study. Am J Gastroenterol 1997;92:419-424.

2. Thompson JN, Salem RR, Hemingway AP. Specialist investigation of obscure gastrointestinal bleeding. Gut 1987;28:47-51.

3. Boley SJ, et al. Lower intestinal bleeding in the elderly. Am J Surg 1979;137:57-64.

4. Schelble DT. Lower Gastrointestinal Bleeding. In: Harwood-Nuss et al, eds. The Clinical Practice of Emergency Medicine. Philadelphia, PA: Lippincott Williams & Wilkins;1996:713-715.

5. Ruckenstein,MJ. The dizzy patient: How you can help. Consultant 2001;1:29-34.

6. Khodadadi J, Rozencwajg J, Nacasch N, et al. Mesenteric vein thrombosis. Arch Surg 1980;115:315-317.

7. Zuccaro G. Management of the adult patient with acute lower gastrointestinal bleeding. Am J Gastroenterol 1998;93:1202-1208.

8. Ha HK, Rha SE, Kim AY, et al. CT and MR diagnoses of intestinal ischemia. Semin Ultrasound CT MR 2000;21:40-55.

9. Stollman NH, Raskin JB. Diverticular disease of the colon. J Clin Gastroenterol 1999;29:241-252.

10. Roberts PL, Veidenheimer MC. Current management of diverticulitis. Adv Surg 1994;27:189-208.

11. Parks TG. Natural history of diverticular disease of the colon. BMJ 1969;13:639-642.

12. Elliot TB, Yego S, Irvin TT. Five-year audit of the acute complications of diverticular disease. Br J Surg 1997;84:535-539.

13. Ramanath HK, Hinshaw JR. Management and mismanagement of bleeding colonic diverticula. Arch Surg 1971;103:311-314.

14. Shoji BT, Becker JM. Colorectal disease in the elderly. Surg Clin North Am 1994;74:293-316.

15. Ambrosetti P, Robert JH, Witzig JA. Acute left colonic diverticulitis: A prospective analysis of 226 consecutive cases. Surgery 1993; 115:546-550.

16. Boley SJ, et al. Vascular Lesions of the Colon. St. Louis: Mosby Year Book Medical Publishers, Inc.; 1984.

17. Sharma R, Gorbien M. Angiodysplasia and lower gastrointestinal tract bleeding in elderly patients. Arch Intern Med 1995;155:807-812.

18. Paksoy M, Ipek T, Colak T, et al. Influence of age on prognosis and management of patients with colorectal carcinoma. Eur J Surg 1999;165:55-59.

19. Lorigan JG, DuBrow RA. The computed tomographic appearances and clinical significance of intussesception in adults with malignant neoplasms. Br J Radiol 1990;63:257-262.

20. Blaquiere R, Domjan J, Odurny A. Is minimal preparation computed tomography comparable with barium enema in elderly patients with colonic symptoms? Clin Radiol 1998;53:894-898.

21. Williams LF, Wittenberg J. Ischemic colitis: A useful clinical diagnosis, but is it ischemia? Ann Surg 1975;182:439-447.

22. Cappell MS. Intestinal (mesenteric) vasculopathy II. Gastroenterol Clin North Am 1998;27:827-861.

23. Greenwald DA, Brandt LJ. Colonic ischemia. J Clin Gastroenterol 1998;27:122-128.

24. Alapati SV, Mihas AA. When to suspect ischemic colitis. Postgrad Med 1999;105:177-187.

25. Miller LS, Barbarevech C, Friedman LS. Less frequent causes of lower gastrointestinal bleeding. Gastroenterol Clin North Am 1994; 23:21-52.

26. Bergan JJ, Dry L, Conn J, et al. Intestinal ischemic syndromes. Ann Surg 1969;169:120-126.

27. Boley SJ. Early diagnosis of acute mesenteric ischemia. Hosp Pract 1981;16:63-71.

28. Bergan JJ, Dry L, et al. Intestinal ischemic syndromes. Ann Surg 1969;169:120-126.

29. Rosen A, Korobkin M, Silverman PM, et al. Mesenteric vein thrombosis: CT identification. AJR Am J Roentgenol 1984;143:83-86.

30. Rha S, Ha H, Lee S. CT and MR imaging findings of bowel ischemia from various primary causes. Radiographics 2000;20:29-42.

31. Dobson CC, Nicholson AA. Treatment of rectal hemorrhage by coil embolization. Cardiovasc Intervent Radiol 1999;22:143-146.

32. Munson KD, Hensien MA, Jacob LN, et al. Diverticulitis. Dis Colon Rectum 1996;39:318-322.

33. Smith L. Hemorrhoids. Gastroenterol Clin North Am 1987;16:79-91.

34. Geoghegan JG, Carton E, O’Shea AM. Crohn’s colitis: The fate of the rectum. Int J Colorectal Dis 1998;13:256-259.

35. Lidner AE. Inflammatory bowel disease in the elderly. Clin Geriatr Med 1999;15:487-497.

36. Jones EM, MacGowan AP. Back to basics in management of Clostridium difficile infections. Lancet 1998;352:505.

37. Read NW, Abouzekry L, Read MDG, et al. Anorectal function in elderly patients with fecal impaction. Gastroenterology 1985;89: 959-966.

38. Puxty JA, Fox RA. Golytely: A new approach to faecal impaction in old age. Age Aging 1986;15:182-184.

39. Castle SC. Constipation: Endemic in the elderly? Clin Geriatr Med 1989;73:1497-1509.

40. Giardello FM, Lazenby AJ. The new colitides. Gastroenterol Clin North Am 1995;24:717-729.

41. Nardone G, Rocco A, Balzano T, et al. The efficacy of octreotide therapy in chronic bleeding due to vascular abnormalities of the gastrointestinal tract. Aliment Pharmacol Ther 1991;131:1429-1436.

42. Tedesco FJ, Waye JD, Raskin JB, et al. Colonoscopic evaluation of rectal bleeding. Ann Int Med 1978;89:907-909.


CME Objectives

Upon completing this program, participants will be able to:

• Quickly recognize or increase index of suspicion for specific conditions in the elderly patient;
• Understand the difference in treatment methods between the older adult and elderly patient and a younger adult patient;
• Understand the epidemiology, etiology, pathophysiology, and clinical features of the entity discussed;
• Perform necessary diagnostic tests correctly and take a meaningful patient history that will reveal the most important details  about the particular medical problem discussed; 
• Apply state-of-the-art therapeutic techniques (including the implications of the pharmaceutical therapy discussed) to patients with the particular medical problem  discussed;
• Understand the differential diagnosis of the entity discussed, and likely and rare complications that may occur; and
• Provide patients with any necessary discharge instructions.

 


Physician CME Questions

To earn CME credit for this issue of Geriatric Emergency Medicine Reports, please refer to the enclosed Scantron form for directions on taking the test and submitting your answers.

1. Bright red bleeding usually is due to:

A. diverticulitis.

B. diverticulosis.

C. ischemic colitis.

D. hemorrhoids.

2. Severe pain with a benign physical exam raises suspicion for:

A. acute mesenteric ischemia.

B. diverticulosis.

C. ischemic colitis.

D. Crohn’s disease.

3. Crampy abdominal pain and bloody diarrhea is consistent with:

A. ischemic colitis.

B. idiopathic inflammatory bowel disease.

C. infectious diarrhea.

D. diverticulitis.

E. All of the above

4. Painless rectal bleeding is consistent with:

A. internal hemorrhoids.

B. angiodysplasia.

C. colon cancer.

D. diverticulosis.

E. All of the above

5. Which of the following is mainly a disease of the elderly?

A. Acute mesenteric ischemia

B. Diverticulosis

C. Ischemic colitis

D. All of the above

6. Which of the following is correct in initially assessing the elderly patient?

A. The color of the stool does not always indicate where the bleed started.

B. The initial hemoglobin may be elevated falsely due to volume contraction.

C. An NGT should be dropped unless the bright red bleeding is self-limited and minor.

D. All of the above

7. Common pitfalls in evaluating the elderly patient include:

A. not resuscitating with fluids for fear of fluid overload.

B. not performing a type and cross of blood products.

C. attributing bright red bleeding to a hemorrhoid without visualizing the bleed.

D. using orthostatic vital signs as an indicator of volume loss and status.

E. All the above.

8. Massive painless bleeding is consistent with:

A. ischemic colitis.

B. diverticulosis.

C. inflammatory bowel disease.

D. stercoral ulcer.

9. The modality of choice for discovering cancerous lesions of the colon is:

A. CT scan.

B. colonoscopy.

C. upright abdominal x-ray.

D. barium enema.

10. An excellent initial diagnostic tool for evaluation of lower GI disorders is:

A. MRI of the abdomen.

B. CT scan of the abdomen.

C. labeled RBCs technetium scan.

D. angiography.