574 - 10sabiston Textbook of Surgery Acute Abdomen

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier
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Chapter 43 - Acute Abdomen

R. Scott Jones M.D. Jeffrey A. Claridge M.D.
The term acute abdomen designates symptoms and signs of intra-abdominal disease usually treated best by surgical operation. Many diseases, some of which do not require surgical treatment, produce abdominal pain, so the evaluation of patients with abdominal pain must be methodical and careful. The proper management of patients with acute abdominal pain requires a timely decision about the need for surgical operation. This decision requires evaluation of the patients history and physical findings, laboratory data, and imaging tests. The syndrome of acute abdominal pain generates a large number of hospital visits and may affect the very young, the very old, either sex, and all socioeconomic groups.[1] [2] [3] [4] All patients with abdominal pain should undergo evaluation to establish a diagnosis so that timely treatment can minimize morbidity and mortality. Abdominal pain accounts for 5% to 10% of all emergency department visits or 5 to 10 million patient encounters in the United States annually.[5] Another study demonstrated that 25% of patients presenting to the emergency department complained of abdominal pain.[6] Diagnoses vary according to age group: pediatric, geriatric, and everyone else. Chapter 70 deals with abdominal pain in children. Appendicitis is more common in children, whereas biliary disease, colonic diverticulitis, and intestinal infarction occur more commonly in the elderly. Hospitalized patients may develop abdominal pain during the course of their illness, making diagnosis and treatment more difficult.
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ANATOMY AND PHYSIOLOGY

Developmental Anatomy
The developmental anatomy of the abdominal cavity and of its viscera determines normal structure and influences the pathogenesis and clinical manifestations of most abdominal diseases.[7] Peritoneal attachments and visceral sensory innervation are particularly important to the evaluation of acute abdominal disease. After the 3rd week of fetal development, the primitive gut divides into foregut, midgut, and hindgut. The superior mesenteric artery supplies the midgut (the fourth portion of the duodenum to the midtransverse colon). The foregut includes the pharynx, the esophagus, the stomach, and the proximal duodenum, whereas the hindgut comprises the distal colon and the rectum. The afferent fibers accompanying the vascular supply provide sensory innervation to the bowel and associated visceral peritoneum. Thus, disease in the proximal duodenum (foregut) stimulates celiac axis afferents to produce epigastric pain. Stimuli in the cecum or appendix (midgut) activate afferent nerves accompanying the superior mesenteric artery to cause periumbilical pain, and distal colon disease induces inferior mesenteric artery afferent fibers to cause suprapubic pain. The phrenic nerve and afferent fibers in C3, C4, and C5 dermatomes accompanying the phrenic arteries innervate the diaphragmatic musculature and the peritoneum on its undersurface. Stimuli to the diaphragm therefore cause referred shoulder pain. The parietal peritoneum, abdominal wall, and retroperitoneal soft tissue receive somatic innervation corresponding to the segmental nerve roots ( Fig. 43 1 ). The richly innervated parietal peritoneum is particularly sensitive. Parietal peritoneal surfaces sharply localize painful stimuli to the site of the stimulus. When visceral inflammation irritates the parietal peritoneal surface, localization of pain occurs. Maneuvers that exacerbate this irritation then intensify the pain. The many peritoneal signs useful in the clinical diagnosis of the acute abdomen originate in this fashion. Dual-sensory innervation of the abdominal cavity by both visceral
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Figure 43-1 Sensory innervation of the viscera. (From White JC, Sweet WH: Pain and the Neurosurgeon. Springfield, IL, Charles C Thomas, 1969, p 526.)
afferents and somatic nerves produces clinical pain patterns that aid in diagnosis. For example, the pain of acute appendicitis originates with poorly localized periumbilical pain progressing to sharply localized right lower quadrant pain when the inflammation involves the parietal peritoneal surface. Peripheral nerves mediate sharp, sudden, well-localized pain. Sensory afferents involved with intraperitoneal abdominal pain transmit dull, sickening, poorly localized pain of more gradual onset and protracted duration. The vagus nerve does not transmit pain from the gut. Small, unnamed sympathetic
afferent nerves transmit pain from the esophagus to the spinal cord. Afferent nerves from the liver capsule, the hepatic ligaments, the central portion of the diaphragm, the splenic capsule, and the pericardium enter the central nervous system from C3 to C5. The spinal cord from T6 to T9 receives pain fibers from the periphery of the diaphragm, the gallbladder and the stomach, the pancreas, and the small intestine. Pain fibers from the colon, appendix, and pelvis viscera enter the central nervous system at the 10th and 11th thoracic segments. The sigmoid colon, rectum, renal pelvis and capsule, ureter, and testes pain fibers enter the central nervous system at T11 and L1. The bladder and the rectosigmoid colon send afferent nerves to the spinal cord from S2 to S4.[8] [9] Cutting, tearing, crushing, or burning usually does not produce pain in the abdominal viscera. However, stretching or distention of the peritoneum produces pain. Bacterial or chemical peritoneal inflammation produces visceral pain, as does ischemia. Cancer can cause intra-abdominal pain by invading sensory nerves. Abdominal pain may be visceral, parietal, or referred. Visceral pain is dull and poorly localized, usually in the epigastrium,
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periumbilical region, or suprapubic region, and it usually does not lateralize well. Patients with visceral pain may also experience sweating, restlessness, and nausea. The parietal or somatic pain associated with intra-abdominal disorders may be more intense and precisely localized. Referred pain is perceived at a site distant from the source of stimulus. For example, irritation of the diaphragm may produce pain in the shoulder. Disease in the bile duct or gallbladder may produce shoulder pain. Distention of the small bowel can produce pain referred to the back. During the 5th week of fetal development, the bowel outgrows the peritoneal cavity, protrudes through the base of the umbilical cord, and undergoes a 180-degree counterclockwise rotation. During this process, the bowel remains outside the peritoneal cavity until approximately the 10th week, when it returns to the abdomen, and an additional 90-degree counterclockwise rotation occurs. This embryologic rotation places the viscera in their adult positions, and subsequent fusion of the portions of the colonic and duodenal mesenteries with the mesothelium of the posterior abdomen forms the normal ultimate peritoneal attachments. Knowledge of these attachments is clinically important during the evaluation of patients with the acute abdomen because of variation in the exact position of the viscera (e.g., pelvic or retrocecal appendix) and the compartmentalization of the abdomen by mesenteric attachments.[10] The latter, for example, may channel duodenal or gastric contents from the site of a perforated ulcer to the right lower quadrant.
Peritoneal Pathophysiology
Mesothelial cells cover the visceral and parietal peritoneal surfaces. Openings into radially arranged lymphatics penetrate the diaphragmatic peritoneal surface. Introduction of bacteria into the peritoneal cavity can cause an outpouring of fluid from the peritoneal membrane. This loss of fluid from the circulation may lead to dehydration and may produce the clinical signs of resting or orthostatic hypotension and tachycardia. Diaphragmatic lymphatics are the major route for the clearance of bacteria and cellular debris from the abdominal cavity. This process leads to an intraperitoneal circulation of fluid toward the subdiaphragmatic regions bilaterally. Fluid not cleared in this fashion tends to accumulate in the deep end of the pelvis. Thus, subdiaphragmatic, subhepatic, paracolic, or pelvic fluid collections can accompany visceral perforation. The peritoneal surfaces localize bacteria and the products of inflammation. The peritoneum responds to inflammation by increased blood flow, increased permeability, and the formation of a fibrinous exudate on its surface. The bowel also responds to inflammation with localized or generalized paralysis. The fibrinous surface thus created, aided by decreased intestinal movement, causes adherence between bowel and omentum and effectively walls off inflammation. An abscess may produce sharply localized pain with normal bowel sounds and gastrointestinal function, whereas a disseminated process, such as a perforated ulcer, produces generalized abdominal pain with a quiet abdomen. Peritonitis may affect the entire abdominal cavity or a portion of the visceral or parietal peritoneum. Transudation can produce an increase in the peritoneal fluid, which is rich in protein and leukocytes that facilitate the formation of fibrin on peritoneal surfaces. Peritonitis denotes peritoneal inflammation from any cause. Primary or spontaneous peritonitis can occur as a diffuse bacterial infection without an obvious intra-abdominal source of contamination. Primary peritonitis, most commonly caused by Pneumococcus or hemolytic Streptococcus, occurs more commonly in children than in adults. However, adults with ascites and cirrhosis are susceptible to spontaneous peritonitis resulting from Escherichia coli and Klebsiella. [11] The more common secondary peritonitis results from perforation, infection, or gangrene of an intra-abdominal organ, usually of the gastrointestinal tract. Gastrointestinal secretions, pancreatic secretions, bile, blood, urine, and meconium cause chemical peritonitis when in contact with the peritoneum. A common form of chemical peritonitis follows perforation of a peptic ulcer. Bile peritonitis may result from perforation of the gallbladder or leakage from the bile ducts. Ordinarily, slow bleeding into the abdominal cavity produces relatively few signs of inflammation; the addition of bacteria to blood produces suppuration ( Box 431 ). The sickest postoperative patients may have tertiary peritonitis that kills 30% to 64% of affected patients. The syndrome of poorly localized intra-abdominal infection, an altered microbial flora, progressive organ dysfunction, and high mortality define tertiary peritonitis.[12] [13] Peritonitis causes abdominal pain, either generalized or localized, depending on the disease. Appendicitis usually causes localized pain. Perforated peptic ulcer usually produces generalized abdominal pain. Acute cholecystitis causes right upper quadrant pain referred to the right scapula or shoulder. Physical findings of patients with peritonitis are abdominal tenderness, guarding, and rebound tenderness. Box 43-1. Causes of Hemoperitoneum Gastrointestinal Traumatic laceration of liver, spleen, pancreas, mesentery, bowel Gynecologic Ruptured ectopic pregnancy Ruptured graafian follicle Ruptured uterus Vascular Ruptured aneurysm: aortoiliac, hepatic, renal, and splenic artery
Urologic Ruptured bladder Hematologic Ruptured spleen
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Figure 43-2 Pain from intra-abdominal viscera.
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CLINICAL DIAGNOSIS
History and Present Illness
Pain is the focal issue in the evaluation of the patient suspected of having an acute abdomen.[8] [9] [14] The history should therefore characterize and document the pain as precisely as possible. The duration of the pain is important, but the location, mode of onset, and character of the pain help in making a diagnosis. Abdominal pain that persists for 6 hours or more with severe intensity increases the likelihood that surgical operation will be required. If the pain ebbs after a few hours, however, the probability of surgical disease decreases, but not to zero. Visceral pain caused by distention, inflammation, or ischemia usually feels dull and poorly localized in the midabdomen. Depending on the organ involved, the pain may be felt in the epigastrium, the periumbilical area, or the lower abdomen ( Fig. 432 ). Diseases of the kidneys or ureters produce pain in the flanks. Parietal pain, however, is sharper and better localized. Localized parietal peritonitis can produce pain confined to one of the four quadrants of the abdomen. In an evaluation of the location of the pain, the concept of referred pain becomes important. Subdiaphragmatic disorders can produce pain referred to the shoulder. Blood or pus beneath the left diaphragm can cause left shoulder pain. Biliary disease can cause referred pain in the right shoulder or the back. Diseases above the diaphragm such as basal pneumonia can cause pain referred to the neck or shoulder in the C4 distribution. Upper abdominal pain suggests peptic ulcer, acute cholecystitis, or pancreatitis. Conversely, ovarian cysts, diverticulitis, and ruptured tubo-ovarian abscesses produce lower abdominal pain. Small bowel obstruction usually causes midabdominal pain sometimes referred to the back ( Fig. 433 ). Migratory pain shifting from one place to another can give insight into the diagnosis. For example, pain that moves from the epigastrium to the periumbilical area to the right lower quadrant suggests acute appendicitis. Distention and inflammation of the appendix produce visceral pain perceived in the periumbilical area.[15] When the inflammation spreads and produces parietal peritonitis, the pain localizes in the right lower quadrant of the abdomen. Another example of moving or migratory pain occurs with perforated duodenal ulcer. The leakage of duodenal contents from a perforated ulcer causes intense and localized epigastric pain. However, if the leaked duodenal content gravitates down the right paracolic gutter into the right lower quadrant, the patient may also experience right lower quadrant pain. Although the location of abdominal pain may be helpful, particularly early in the course of the disease, it may not be typical in all patients. Late in many cases, the pain may become generalized because of diffuse peritonitis.
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Figure 43-3 Common causes of abdominal pain.
Box 43-2. Abdominal Pain Secondary to Inflammatory Lesions of the Gastrointestinal Subsystem Stomach Gastric ulcer Duodenal ulcer Biliary tract Acute cholecystitis with or without choledocholithiasis Pancreas Acute, recurrent, or chronic pancreatitis
Small intestine Crohns disease Meckels diverticulum Large intestine Appendicitis Diverticulitis
The initial manifestations of the acute abdomen and the evolution of the pain syndrome may give some insight into the cause of the pain. The pain can start suddenly or instantly with no prior symptoms. Sudden or explosive onset of severe abdominal pain suggests free perforation of a viscus such as the duodenum or acute intestinal ischemia from a visceral artery embolus. This type of pain onset can awaken patients from sleep or can incapacitate them during work or play. Sudden, generalized, excruciating pain suggests an intra-abdominal catastrophe that may produce shock requiring resuscitation and prompt operation. In other conditions, the pain comes on with progressively increasing intensity over 1 to 2 hours. This progressive pain represents the usual manifestation of the diseases that commonly produce the acute abdomen such as acute cholecystitis, acute pancreatitis, and proximal small bowel obstruction. Some illness begins with vague Box 43-3. Abdominal Pain Secondary to Obstructing Lesions of the Gastrointestinal Tract Jejunum Malignancy Volvulus Adhesions Intussusception Ileum Malignancy Volvulus Adhesions Intussusception Colon Malignancy Volvulus: cecal or sigmoid Diverticulitis
general abdominal discomfort that progresses to abdominal pain over a few hours. The pain becomes more intense and subsequently localizes. This group of illnesses generally includes acute appendicitis, incarcerated hernia, distal small bowel obstruction, colon obstruction, diverticulitis, and contained or walled-off visceral perforation ( Box 432 ). The quality, severity, and periodicity of the pain may provide clues to the diagnosis. Steady, sharp pain accompanies perforated duodenal ulcer or perforated appendix. The early pain of small bowel obstruction is vague and deep seated. This pain then assumes a crescendo-decrescendo character described as colicky pain ( Box 433 ). However, if obstruction produces intestinal infarction, then the pain becomes dull and constant. The pain of ureteral obstruction is extremely severe and intense.
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Patients with kidney stones appear restless, agitated, or hyperactive and tend to move about, in contrast to patients with peritoneal inflammation, who prefer to lie quietly and remain undisturbed. Sudden, excruciating pain in the upper abdomen or the lower chest or interscapular region suggests aortic dissection. Radiation of pain or referral of pain may help in diagnosis. Radiation of pain around the right costal margin to the right shoulder and scapula suggests acute cholecystitis. Pancreatitis usually produces epigastric pain that may radiate along the costal margins to the back or straight through to the back.
Kidney stones may cause pain radiating to the groin or the perineal area. Vomiting may occur from the severity of the pain or because of disease in the gastrointestinal tract. Generally, patients with abdominal pain requiring surgical treatment experience the pain before vomiting occurs. Vomiting frequently precedes the pain in patients with medical conditions. Patients with appendicitis usually have pain and anorexia for a while before vomiting, and patients with gastroenteritis experience vomiting before abdominal pain. Vomiting frequently occurs in patients with acute cholecystitis, acute gastritis, acute pancreatitis, and bowel obstruction. Proximal small bowel obstruction produces more vomiting than distal small bowel obstruction. Vomiting occurs uncommonly in patients with colon obstruction. Small bowel obstruction of longer duration can cause feculent vomiting. Obstruction distal to the ampulla of Vater causes bile-stained vomitus, whereas obstruction proximal to the ampulla causes clear vomitus. Most patients with acute abdominal pain have no desire to eat. Anorexia may precede the pain of acute appendicitis. Bowel function, including a history of constipation, diarrhea, or a recent change in bowel habits, can be important. Watery diarrhea associated with abdominal pain suggests gastroenteritis. Immunosuppressed patients can contract cytomegalovirus (CMV) infection, salmonellosis, or cryptosporidiosis, which may produce diarrhea. A past history of diarrhea raises the suspicion of inflammatory bowel disease, either Crohns disease or ulcerative colitis. Failure to pass gas or bowel movements suggests mechanical intestinal obstruction. A history of jaundice, hematemesis, hematochezia, or hematuria is important in the evaluation of acute abdominal pain. A careful menstrual history is important in women with abdominal pain. Ovulation can produce significant abdominal pain. Furthermore, abdominal pain in a woman with a missed menstrual period or irregular menstrual periods can be related to complications of an undiagnosed pregnancy or an ectopic pregnancy. The drug history is important in managing patients with acute abdominal pain. Corticosteroids predispose to gastroduodenal ulceration and the possibility of perforation. Corticosteroids also immunosuppress patients and obscure the manifestations of acute intra-abdominal disease. Furthermore, patients who have taken steroids for long periods require perioperative steroid supplementation. Patients who take diuretics need evaluation of their fluid and electrolyte status. Anticoagulants can cause intra-abdominal, intestinal, and mesenteric bleeding. The effects of anticoagulants must be reversed preoperatively. Cocaine can cause abdominal pain. Of course, many patients developing acute abdominal pain are taking cardiovascular drugs, hormones, tranquilizers, diuretics, and numerous other classes of agents that must be managed in the perioperative period. Past history becomes important, especially regarding prior surgery. For example, if a patient has had an appendectomy, cholecystectomy, and so forth, it has a significant impact on the differential diagnosis of acute abdominal pain. Past history can also give clues to the diagnosis of the present illness. In addition, past history may reveal significant comorbid conditions requiring careful management during the perioperative period. Systemic illnesses or cardiac or pulmonary disease must be excluded as possible causes of the abdominal pain syndrome.
Physical Examination
The physical examination usually provides important information that helps in the diagnosis and management of patients with acute abdominal pain.[8] [14] The patients overall appearance, ability to communicate, habitus, and signs of pain should be noted. Does the patient lie quietly in bed or actively move about? Does the patient lie on his or her side with knees and hips flexed? Does the patient appear dehydrated with dry mucous membranes? An apprehensive patient lying quietly in bed, avoiding motion, and complaining of abdominal pain probably has serious intra-abdominal disease. The physical examination continues with the evaluation of the vital signs. Low fever often accompanies diverticulitis, appendicitis, and acute cholecystitis. High fever more often occurs in pneumonia, urinary tract infection, septic cholangitis, or gynecologic infection. Rapid heart rate and hypotension may mean advanced complicated disease with peritonitis. Peritonitis causes hypovolemia as plasma volume leaves the intravascular space. The general appearance of the patient and the vital signs determine the urgency of the diagnostic work-up and implementation of therapy. Examination of the abdomen always begins with inspection, with particular attention to scars, hernias, masses, or abdominal wall defects. Hernias incarcerated in the groin, umbilicus, or incisions of obese patients can be difficult to detect. The examiner should observe whether the contour of the abdomen appears scaphoid, flat, or distended. Abdominal distention can mean intestinal obstruction, ileus, or fluid including ascites, blood, or bile. Palpation is a crucial step in evaluating the patient with acute abdominal pain. For this examination, the patient and the examiner should be positioned comfortably to conduct gentle palpation. The examiner should assess the patients facial expression for signs of pain or discomfort during the examination. Careful palpation for tenderness is important. This must be done gently to avoid hurting the patient and should begin in an area away from the pain site if possible. The finding and the description
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of tenderness are the most important steps in palpation of the abdomen of patients with acute abdominal pain. Localized tenderness over the McBurney point suggests appendicitis. Tenderness in the right upper quadrant suggests an inflamed gallbladder. Diverticulitis produces tenderness in the left lower quadrant. Tenderness throughout the abdomen may reflect diffuse peritonitis. The detection of increased abdominal muscle tone during palpation is called guarding. Guarding may be voluntary, involuntary, localized, or generalized. To detect guarding, the examiner should press gently but slowly and firmly on the patients abdomen. Using two hands works best. The detection of muscle spasm denotes guarding. If, after asking the patient to relax and breathe deeply, the patients muscles relax, it denotes voluntary guarding. If the muscles remain rigid or tense, it indicates involuntary guarding, which means underlying peritonitis. Guarding may be localized or generalized. Generalized intense guarding produces the boardlike abdomen characteristic of perforated duodenal ulcer. Careful deep palpation can detect abdominal masses. Acute cholecystitis, acute pancreatitis, abdominal aortic aneurysm, and diverticulitis can produce abdominal masses. Severe guarding can interfere with the detection of abdominal masses by palpation. Rebound tenderness is also a sign of peritonitis. To detect rebound tenderness, the examiner presses deep into the patients abdomen with flattened fingers. Sudden withdrawal of that hand may cause an increase in the abdominal pain, and this symptom indicates peritonitis. Rebound tenderness can be elicited directly over the site of the abdominal pain. Pressing and releasing the abdomen away from the site of pain can exacerbate the pain at the original site. Careful, deep palpation can detect abdominal masses. Severe guarding can interfere with the detection of abdominal masses by palpation. In acute cholecystitis, palpation in the right subcostal area during deep inspiration by the patient may elicit pain. This finding is called a positive Murphys sign. This sign can be detected either with the patient sitting or supine. The gallbladder may be palpated during this maneuver. Direct compression by the probe may cause pain during ultrasound examination. Auscultation of the abdomen should give information about the presence or absence of bowel sounds. A quiet abdomen indicates ileus. Hyperactive bowel sounds may occur in gastroenteritis. Periods of quiet interrupted by the onset of high-pitched hyperactive bowel sounds characterize the peristaltic rushes of mechanical small bowel obstruction. Evaluation of bowel sounds requires careful auscultation for several minutes. During auscultation of the abdomen, the examiner can effectively evaluate tenderness and guarding further by palpating gently with the stethoscope. The examiner should also note the presence or absence of bruits in the abdomen.
Percussion is an important part of the abdominal examination. When percussion elicits tenderness, it indicates inflammation and has the same implication as rebound tenderness. Hyper-resonance or tympany to percussion of the abdomen means gaseous distention of the intestine or Box 43-4. Abdominal Pain Secondary to Lesions of the Gynecologic Subsystem Ovary Ruptured graafian follicle Torsion of ovary Fallopian tube Ectopic pregnancy Acute salpingitis Pyosalpinx Uterus Uterine rupture Endometritis
stomach. Resonance to percussion over the liver suggests free intra-abdominal gas. Other tests or maneuvers can aid in the assessment of patients with abdominal pain. Pain during gentle tapping of a fist or deep palpation at the costovertebral angles may suggest pyelonephritis. An inflamed retrocecal appendix or a psoas abscess can produce pain or tenderness on motion of the psoas muscle. If passively extending the hip or actively flexing the hip against resistance causes pain, this is called a positive iliopsoas sign. If internal or external rotation of the flexed hip causes pain, it is referred to as a positive obturator sign. During the bimanual pelvic examination, the physician should seek evidence of uterine or adnexal masses or tenderness. Acute salpingitis, tubo-ovarian abscess, or torsion of an ovarian cyst can cause acute abdominal pain ( Box 434 ). The speculum examination allows inspection of the cervix for discharge. Rectal examination should include tests for occult blood, and the examiner should note the presence of masses or tenderness. An inflamed pelvic appendix or a pelvic abscess can cause tenderness detected by rectal examination.
Laboratory Testing
Laboratory investigation of most patients with acute abdominal pain usually includes a complete blood count. Intra-abdominal inflammation can produce elevation in the white blood cell count, although this is not always true. One study demonstrated a poor correlation between the white blood cell count and the degree of intra-abdominal inflammation in patients operated on because of acute abdominal pain.[16] If a patient with unequivocal and persistent abdominal pain has a normal or low white blood cell count, a differential count may disclose a marked left shift, which can be more significant than finding an elevation in the white blood cell count. If patients have obvious dehydration, a history of vomiting or diarrhea, or if they have been taking medications such as diuretics that may influence their serum electrolyte values, one should measure the concentrations of serum sodium, potassium,
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blood urea nitrogen, creatinine, glucose, chloride, and carbon dioxide. In addition, these laboratory tests enable one to detect diabetes, renal failure, or other systemic diseases. Measurements of serum amylase and lipase may help in the evaluation of upper abdominal pain by giving evidence of pancreatitis. Although elevated serum amylase accompanies pancreatitis, other diseases such as perforated duodenal ulcer and small bowel infarction can also cause increased serum amylase concentrations. Patients with right upper quadrant abdominal pain should have measurements of serum bilirubin, alkaline phosphatase, and serum transaminase because of the possibility of obstructive jaundice or acute hepatitis. Urinalysis can detect evidence of urinary tract infection, hematuria, proteinuria, or hemoconcentration. Women of childbearing age who have acute abdominal pain or hypotension should have measurement of the serum or urine -human chorionic gonadotropin concentration.
Diagnostic Imaging
History and physical examination are the most important and useful steps in the evaluation of patients with abdominal pain. However, advances in imaging of the abdomen have improved the diagnostic accuracy and the overall management of patients experiencing acute abdominal pain. Before the widespread availability of ultrasonography and computed tomography (CT), surgeons performed a careful history and physical examination, obtained laboratory tests, and reviewed plain films of the abdomen and chest. With that information, a decision to operate or not was made usually on the basis that the patient probably had some disease best treated surgically. The laparotomy was considered diagnostic as well as therapeutic. Historically, before modern imaging tests, as many as 20% of patients operated on for acute appendicitis did not have it. Plain films still have usefulness in several circumstances. A radiograph centered on the diaphragm detects pneumoperitoneum better than other radiographic techniques. An upright chest radiograph can detect under the diaphragm as little as 1 mL of air injected into the peritoneal cavity.[17] For the occasional patient who cannot stand up, a lateral decubitus radiograph of the abdomen can also detect pneumoperitoneum effectively. A cross-table lateral radiograph with the patient in the left lateral position can detect 5 to 10 mL of gas under the lateral abdominal wall. Free air in the peritoneal cavity indicates a perforation of the gastrointestinal tract. Perforated duodenal ulcers usually allow small amounts of air to escape into the peritoneal cavity. About 75% of patients with perforated duodenal ulcers have radiographically detectable pneumoperitoneum. Perforations of the stomach and the colon can cause extensive pneumoperitoneum. The amount of pneumoperitoneum can also depend on the duration of the leak from the perforation.
Plain films of the abdomen can show extensive pneumoperitoneum. If the film defines both the serosal and the related mucosal walls of the bowel, it means free air is at that serosal surface. In addition, free air can delineate the falciform ligament on plain abdominal films. An extensive hydropneumoperitoneum
Figure 43-4 Plain film findings in hydropneumoperitoneum. A, Upright view shows fluid level too long to be within a loop of bowel. B, In the supine position, the free air is well defined by the interface with the fluid in the peritoneal cavity (arrows).
appears as an extremely long air-fluid level on an upright film. A supine film can show a large air collection beneath the abdominal wall that does not conform to any bowel loop ( Fig. 434 ). Plain films show abnormal calcifications. About 10% of gallstones and 90% of kidney stones contain sufficient calcium to be radiopaque. Appendicoliths can calcify and appear radiographically in 5% of patients with appendicitis. Pancreatic calcifications characteristic of chronic pancreatitis show on plain films, and vascular calcifications can aid in the evaluation of abdominal aortic aneurysms, visceral artery aneurysms, and atherosclerosis of visceral vessels. Supine and erect plain films of the abdomen show gastric outlet obstruction; proximal, mid, and distal small bowel obstruction; and colon obstruction. The characteristics
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of small bowel obstruction include multiple air-fluid levels in dilated, centrally located loops of intestine with visible valvulae conniventes and an absence or paucity of colon gas. Obstructed colon usually appears as peripherally located distended bowel with haustral markings. If the ileocecal valve is incompetent, colon obstruction will cause distention of the distal small bowel. Some patients with an acute abdomen have plain abdominal films that show a bowel pattern suggesting mechanical obstruction when no obstruction exists. Paralytic ileus can produce distended bowel with multiple air-fluid levels. Plain radiographs show paralytic ileus resulting from intra-abdominal or retroperitoneal inflammation. The radiographic findings of paralytic ileus include excessive distention and fluid with gas distributed from stomach to rectum. Plain films of the abdomen may also detect gas in the portal or mesenteric venous system, intramural gas in the gastrointestinal tract, gas in the biliary ducts or gallbladder, and gas in the urinary tract or retroperitoneal areas. When plain films show gas in the portal or mesenteric veins, it usually means advanced and serious disease. CT can show small amounts of gas in veins and also may delineate the cause of the abnormality. If the patients history suggests renal colic, an intravenous pyelogram may confirm the diagnosis of a kidney stone. CT scanning has provided definite improvements in diagnostic accuracy in evaluating patients with abdominal pain and also reveals anatomic and pathologic detail not possible with plain radiographs ( Fig. 435 ).[18] Therefore, CT and ultrasonography now occupy the central imaging role in this situation. Although history and physical examination provide essential information in evaluating patients with the acute abdomen, modern imaging techniques, including ultrasound and CT, can lead to an anatomic diagnosis in most cases. One prospective study of 40 patients with acute abdominal
pain revealed that CT significantly improved the diagnostic accuracy of clinical evaluation plus plain radiographs.[19] Clinical examination and plain films were 50% correct, but CT scanning was 95% correct. CT scans accurately detected the specific anatomic lesion in 57.5% of cases compared with 17.5% with clinical examination and plain films. This study included no patients with appendicitis, the most common cause of the acute abdomen, because the surgeons did not refer any cases of suspected appendicitis for inclusion in the study. However, other investigators evaluated the role of CT in the diagnosis of acute appendicitis in 100 consecutive patients studied prospectively.[20] The CT interpretation had 98% sensitivity, 98% specificity, 98% positive predictive value, 98% negative predictive value, and 98% overall accuracy for diagnosing or ruling out appendicitis. According to the authors calculations, these 100 CT scans produced a net savings of $44,731 in the care of the study patients because of improved diagnostic accuracy. CT scans can add important value to the diagnosis of acute appendicitis. However, focused specialists using excellent equipment in an environment of inquiry conducted this study, and the results may not be reproducible in all hospitals.[20] Other workers questioned the value of CT scanning in the diagnosis of acute appendicitis.[21]
Figure 43-5 Unsuspected perforated duodenal ulcer. A, Small amount of extraluminal gas (arrow) lies lateral to duodenal bulb (d). g, gallbladder. B, At 3 cm caudad, gas (arrow) tracks behind the gallbladder (g) laterally. C, The air-fluid level (arrow) identifies the loculated extravasated duodenal contents. Inflammatory changes are present in the surrounding mesenteric fat.
Ultrasonography is useful for patients with acute abdominal pain because it provides rapid, safe, low-cost evaluation of the liver, gallbladder ( Fig. 43 6 ), bile ducts, spleen, pancreas, appendix, kidneys, ovaries, adnexa, and uterus. Transabdominal and intravaginal ultrasonography can aid in the evaluation of the ovaries, adnexa, and uterus. Ultrasonography also detects and characterizes the
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Figure 43-6 Acute cholecystitis. Ultrasound evaluation shows two small stones (curved arrow) present in the neck of the gallbladder. The wall of the gallbladder in the fundus (straight arrow) is thickened, and pericholecystic fluid is present.
Figure 43-7 Thrombus in portal vein evident on pulsed Doppler ultrasonography. An echogenic thrombus (arrow) is within the lumen of the portal vein. The Doppler tracing indicates flow within the portal vein.
distribution of intra-abdominal fluid. Color-Doppler ultrasonography allows evaluation of the intra-abdominal and retroperitoneal blood vessels. Aortic and visceral artery aneurysms, venous thrombosis, arteriovenous fistulas, and vascular anomalies can be evaluated with ultrasound ( Fig. 437 ). Unfortunately, patients with acute abdominal disease frequently have excessive abdominal gas that interferes with careful and detailed sonographic evaluation of the abdominal organs, but overlying gas, bone, and
Figure 43-8 Acute appendicitis. On ultrasonography, a radiographically nonopaque appendicolith (arrow) is evident within a thick-walled, distended appendix (longitudinal view).
fat do not impair imaging with CT. Therefore, CT has become important for evaluating causes of the acute abdomen. Appendicitis, the most common cause of the acute surgical abdomen in North America, can be difficult to diagnose.[1] [2] Plain films and barium enema studies generally add little to the diagnosis. However, in patients with uncomplicated appendicitis, ultrasonography can detect appendicoliths, demonstrate a distended or thick-walled appendix, or detect periappendiceal and pericecal inflammatory changes ( Fig. 438 ). Ultrasound is reliable and sensitive for the detection of appendicoliths and the demonstration of an abnormally distended or thick-walled appendix.[22] Conversely, CT detects acute appendicitis and defines the changes of complicated appendicitis ( Fig. 439 ). CT scans can enable the examiner to differentiate diffuse periappendiceal inflammation from an abscess. In addition, CT scans detect many of the diseases included in the differential diagnosis of acute appendicitis. CT detects blood and other fluids in the abdominal cavity. Intramural intestinal hemorrhage is readily detected by CT ( Fig. 4310 ). CT scans accurately reveal mesenteric venous thrombosis ( Fig. 4311 ). CT scans can delineate diverticulitis and its complications, such as abscess and even pyelophlebitis ( Fig. 4312 ). CT is especially helpful in evaluating pancreatitis by revealing minimal edema, extensive edema, fluid collections, hemorrhage, and necrosis; in addition, it effectively evaluates the complications of pancreatitis such as abscess or
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Figure 43-9 Appendicitis. A, CT scan of uncomplicated appendicitis. A thick-walled, distended, retrocecal appendix (arrow) is seen with inflammatory change in the surrounding fat. B, CT scan of complicated appendicitis. A retrocecal appendiceal abscess (A) with an associated phlegmon posteriorly was found in a 3-week-postpartum, obese woman. Inflammatory change extends through the flank musculature into the subcutaneous fat (arrow).
Figure 43-10 Intramural hematoma of small bowel. Uniform, concentric, high-density thickening of the wall of jejunal loops is characteristic.
Figure 43-11 Small bowel infarction associated with mesenteric venous thrombosis. A, Note the low-density thrombosed superior mesenteric vein (solid arrow) and incidental gallstones (open arrow). B, Thickening of proximal small bowel wall (arrow) coincided with several feet of infarcting small bowel at time of surgery.
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Figure 43-12 Acute pyelophlebitis resulting from diverticulitis with abscess. A, Minute quantities of gas (arrows) within peripheral branches of the portal venous system were not visible on a plain radiograph. B, A gas-containing thrombus (arrow) is visible in the inferior mesenteric vein at its junction with the splenic vein. C, A chain of abscesses (arrow) extended along the course of the thrombosed inferior mesenteric vein. D, The septic thrombus led directly to a pericolonic abscess (arrow) caused by diverticulitis of the sigmoid colon.
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Figure 43-13 Hemorrhage and false aneurysm complicating pancreatitis. A, Intraparenchymal hemorrhage enlarges the body and tail of the pancreas. The lumen of the false aneurysm (arrow) is shown as an area of increased density resulting from the enhancement of the flowing blood. B, Selective splenic arteriogram. A false aneurysm (arrow) arises from a branch of the splenic artery and was successfully treated with transcatheter embolization.
Figure 43-14 Peritonitis. CT scan shows inflammatory thickening of the parietal (large arrow) and visceral (small arrow) peritoneum. The ascitic fluid is of high density, characteristic of peritonitis.
pseudocyst ( Fig. 4313 ). CT scans show the signs of advanced peritonitis ( Fig. 4314 ). With this technique, one can also evaluate the complications of colon perforation ( Fig. 4315 ) and of small bowel disease such as intussusception ( Fig. 4316 ). Although history and physical examination provide essential information in evaluating patients with the acute abdomen, modern imaging techniques, including ultrasound and CT, can lead to an anatomic diagnosis in the majority of cases.
CLINICAL MANAGEMENT
Differential Diagnosis
Information from the patients history, physical examination, laboratory tests, and imaging studies usually permits a diagnosis, but uncertainty can still remain (see Fig. 433 ). Because appendicitis is a common disease, it must remain in the differential diagnosis of any patient with persistent abdominal pain, particularly right lower quadrant pain.[3] [4] The diagnosis of appendicitis is easy to miss, and perforation substantially increases morbidity and mortality from the disease.[1] [2] Delay in diagnosis is the principal reason for unfavorable outcomes in appendicitis. Appendicitis is the most common cause of the acute abdomen in childhood; however, in older patients, acute cholecystitis, bowel obstruction, cancer, and acute vascular conditions assume importance in addition to appendicitis. The differential diagnosis in young women can be difficult because they can have salpingitis, dysmenorrhea, ovarian lesions, and urinary tract infections as well as complications of pregnancy, which can confound the evaluation of abdominal pain. Of course, the medical causes of abdominal pain must be considered, but patients with medical disease generally lack specific localized tenderness and guarding. The other problem is that about one third of patients who present with acute abdominal pain have nonspecific abdominal pain, and no clear diagnosis is ever established.
Decision to Operate
These difficulties notwithstanding, the surgeon must make a decision to operate or not. Certain indications for surgical treatment exist. For example, definite signs of
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Figure 43-15 Pyopneumoperitoneum secondary to a perforated descending colon. A, Pyopneumoperitoneum interface (large arrow) and inflammatory thickening of visceral peritoneum (small arrows) are shown. Seven liters of grossly infected ascitic fluid (A) were drained percutaneously. B, A trail of small gas bubbles in the left flank led to a point of discrete perforation of the descending colon (arrow), which was confirmed by contrast material enema and was surgically repaired.
Figure 43-16 Acute small bowel intussusception. The patient had a sudden onset of severe mid-abdominal pain with nonspecific plain film findings. Cross-sectional (A) and longitudinal (B) CT scans showed a small bowel intussusception (arrows). Mesenteric fat (f) accompanies the intussusceptum. A benign spindle cell tumor was the cause.
Figure 43-17 Patients with unrelenting abdominal pain, tenderness, guarding, and rebound should undergo laparoscopy or laparotomy following suitable resuscitation and preparation.
peritonitis such as tenderness, guarding, and rebound tenderness support the decision to operate ( Fig. 4317 ). Likewise, severe or increasing localized abdominal tenderness should prompt an operation. Patients with abdominal pain and signs of sepsis that cannot be explained by any other finding
should undergo operation. Those patients suspected of having acute intestinal ischemia should be operated on after complete evaluation. Certain radiographic findings confidently predict the need for operation. These findings include pneumoperitoneum and radiologic evidence of gastrointestinal perforation. Patients presenting with abdominal pain and free intra-abdominal gas seen on radiograph warrant operation with limited exceptions ( Fig. 4318 ). Observation with serial examinations may be
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Figure 43-18 Most patients with free air in the peritoneal cavity should undergo laparoscopy or laparotomy following suitable resuscitation and preparation.
Figure 43-19 Patients with abdominal pain and doubtful findings for an acute abdomen should undergo imaging tests beginning with abdominal ultrasound.
appropriate for a patient with free gas after a colonoscopy.[23] Intra-abdominal gas can persist for a day or two following celiotomy. Imaging tests can reveal signs of vascular occlusion requiring operation. After careful examination and evaluation, diagnostic uncertainty can remain. Some patients may have equivocal physical findings ( Figs. 4319 and 43 20 ). When this occurs and the diagnosis is unclear and the patients wellness is unclear, it may be advisable to defer operation and to re-examine the patient carefully after several hours.[24] This is best done in a short-stay unit in the hospital, in a special unit in the emergency department, or if necessary, by regular hospital admission. In a period of hours, vague pain with minimal physical findings may proceed to definite
Figure 43-20 When obesity impairs physical examination, CT scan of the abdomen can aid in the evaluation of abdominal pain.
localized pain with tenderness, guarding, and rebound tenderness; if that occurs, operation should follow. After several hours, the patients symptoms and signs may also resolve. When that happens, the patient can be dismissed, although the patient should have a follow-up appointment scheduled within a day or so to permit re-examination to be certain that an important diagnosis was not missed. Certain patients are difficult to evaluate because of special characteristics. For example, patients who are neurologically impaired as a result of a stroke or a spinal cord injury may be difficult to evaluate. [25] Patients who are under the influence of drugs or alcohol may require special or subsequent examination. Patients who take steroids or are otherwise immunosuppressed deserve special mention because steroids and immunosuppression mask the intensity of abdominal pain and the physical findings of severe, life-threatening intra-abdominal disease. Patients in this category who have persistent, unequivocal abdominal pain and even minimal findings should be considered for surgical operation. Some patients with clear findings of the acute abdomen may be treated without surgical operation. For example, patients with perforated duodenal ulcer who seek attention late in the course of their disease after they have been sick for several days may be treated best by careful supportive care including nasogastric suction, intravenous fluids, and pain relief. Certain patients with empyema of the gallbladder, especially those with other serious concomitant illnesses, can be treated by percutaneous drainage of the infected gallbladder and careful supportive care rather than with cholecystectomy. Some patients who have acute appendicitis may not seek attention until several days into the course of the illness, at which time they may have walled off the perforation and may have an appendiceal abscess. These patients have right lower quadrant pain, tenderness, and perhaps guarding, but if they have an appendiceal abscess, this is usually best managed by percutaneous drainage of the abscess and
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Figure 43-21 Pancreatitis can produce the acute abdomen. Acute pancreatitis should be managed with supportive care. Complications of acute pancreatitis may require operation.
avoidance of appendectomy at that time. Acute diverticulitis is usually best managed nonsurgically. If a patient with diverticular disease has a diverticular abscess, percutaneous drainage and supportive care will suffice, and the diverticular disease may be removed electively later. Most patients with acute pancreatitis should be managed without operation unless they have a specific indication for operation ( Fig. 4321 ). Indications for operation include the development of an abscess.
Preoperative Preparation
In a stable, otherwise healthy patient, preoperative procedures should include insertion of a nasogastric tube, establishment of access for intravenous fluid administration, insertion of a Foley catheter in the urinary bladder to record urinary output, and pain relief. Once a decision has been made to perform an operation, the patient should be given a narcotic or other suitable analgesic unless he or she is being taken immediately to the operating room. Most patients with an acute abdomen requiring an operation have conditions in which infection is either present or likely. For that reason, antibiotics should be administered preoperatively. Unstable patients must have more careful evaluation and resuscitation before one proceeds to surgical intervention. These patients also require a nasogastric tube, a Foley catheter, intravenous fluids, and antibiotics, but if patients have hypotension, tachycardia, or oliguria and evidence of dehydration, they will need a period of supportive care and intravenous fluids before they undergo general anesthesia and operation. After evaluation of their fluid and electrolyte status and degree of dehydration, these patients should receive sufficient quantities of intravenous fluid to establish urinary output of 0.5 mL/kg per hour. Preoperative blood pressure should be greater than 100 mm Hg systolic, and the pulse should fall to less than 100 beats/min. Patients taking steroids should have supplemental doses administered before and after the operation, including their maintenance dose. Diabetic patients should have attention to control their hyperglycemia and acid-base balance. Cardiovascular function must be monitored in patients with a history of heart disease, and they should have preoperative and postoperative management of their current drugs. Patients with an acute abdomen should be operated on when they become hemodynamically stable and have satisfactory urinary output. Patients who are hypokalemic should have potassium infusion after the establishment of urine flow.
Operation
After concluding that a patient with abdominal pain needs an operation, the surgeon must plan the surgical approach. General inhalation anesthesia administered through an endotracheal tube should be used in most cases. Then the surgeon must choose whether to employ laparotomy or laparoscopy. That choice depends on the surgeons experience and the probable diagnosis. Some factors such as multiple prior laparotomies, hemodynamic instability, or advanced abdominal distention preclude laparoscopy. For open operation, the surgeon must choose an incision. In cases of probable appendicitis, a right lower quadrant muscle-splitting incision works well. If acute cholecystitis is nearly certain, a right subcostal incision should be used. An incarcerated groin hernia should be approached through a groin incision. When the diagnosis is uncertain, a midline incision works well. The use of laparoscopy has become more common and more effective in the management of acute abdominal pain. In 1975, Sugarbaker and associates [26] demonstrated the utility of laparoscopy in the management of patients with acute abdominal pain. In this study, 56 patients required hospitalization because of acute abdominal pain. Twenty-seven of these patients had a definite clinical diagnosis and underwent laparotomy. Six, or 22%, of these patients had a negative laparotomy, whereas 21 patients had diseases managed best by laparotomy. Twenty-nine patients without an exact diagnosis underwent laparoscopy. Eighteen of those patients had, at laparoscopy, a definitive diagnosis of a disease that did not require laparotomy, and 11 patients required laparotomy after laparoscopy. Laparoscopy required 20 minutes on average and incurred no complications. The patients in the
laparoscopy group had shorter hospital stays and lower hospital charges. Since 1975, of course, laparoscopic surgical skills and technology have improved dramatically, and the usefulness of laparoscopy in managing patients with acute abdominal pain is generally recognized and accepted. Laparoscopy has become an important technique in the management of patients with acute abdominal pain. In a study of 255 patients with acute abdomen, laparoscopy
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proved helpful.[27] In this set of patients, laparoscopy provided a definitive diagnosis in 93%, and the remaining 7% required laparotomy for diagnosis. The treatment of the acute abdominal pain was exclusively laparoscopic in 73% of the patients, whereas 23% were treated by conventional surgery. Four percent had a combined procedure of conventional surgery assisted by laparoscopy. Eight patients died from the natural course of their disease, five from nonresectable intestinal infarctions, and three from disseminated peritoneal malignant disease. Excluding these patients, the operative mortality was 2%, that is, 5 of 247 cases. One 80-year-old patient had a fatal stroke, an 89-year-old patient who was operated on for a large intestinal obstruction had multiple organ failure, an 82-year-old patient had an intraoperative complication resulting in massive blood loss and died on the 48th postoperative day, and an 89-year-old patient died of a thoracic empyema. More recently, several authors reported favorable experiences using laparoscopy in the diagnosis and treatment of patients with acute abdominal pain.[28] [29] [30] [31] [32] [33] The diagnostic accuracy of laparoscopy varied from 93% to 100%. Laparoscopic techniques accomplished definitive treatment of the underlying disease in 44% to 73% of cases. From 10% to 38% of patients required laparotomy for definitive treatment. In 20% to 38% of patients, laparoscopy revealed either no abnormality or discovered a disease requiring no surgery for proper treatment. The morbidity rates ranged from 0 to 20%, and the mortality rates ranged from 0 to 5%. Diagnostic and therapeutic laparoscopic techniques have an important place in the management of patients with acute abdominal pain. The diagnostic accuracy spares many patients an unnecessary laparotomy and also allows definitive laparoscopic therapy that prevents additional patients from undergoing unnecessary laparotomy. Evidence suggests that diagnostic laparoscopy reduces the cost of managing patients with acute abdominal pain. Whether diagnostic laparoscopy and therapeutic laparoscopy reduce the cost remains unclear. Most patients with acute abdominal pain should be suitable candidates for laparoscopy. Laparoscopy should be avoided in hemodynamically unstable patients and in patients with extensive gaseous distention of the abdomen. Whether pregnant women with the acute abdomen should undergo laparoscopy is a practical question. One study suggested that laparoscopy in this setting was safe and effective.[34]
Outcomes
It is difficult to know the mortality rate for patients with the acute abdomen. A study from the United Kingdom of patients hospitalized with abdominal pain revealed a mortality rate for all patients of 3.0% and an operative mortality of 7.7%.[35] Another study of 300 consecutive patients undergoing laparotomy within 6 hours of consultation for gastrointestinal perforation, intestinal infarction, or hemorrhage demonstrated a mortality rate of 20%.[36] This study included mostly critically ill patients. Other studies revealed a 16% to 40% mortality rate for emergency in older patients.[35]
ACUTE VISCERAL ISCHEMIA Although patients experiencing acute visceral ischemia account for a small percentage of the population seeking medical attention for acute abdominal pain, this topic deserves special attention because of extreme difficulty in establishing a correct and timely diagnosis and because the condition has a high mortality rate. Acute arterial disease may be either occlusive or nonocclusive, and venous disease can also produce the syndrome. Arterial occlusion may be either embolic or thrombotic. Generally, acute superior mesenteric artery embolism causes a sudden onset of extremely severe abdominal pain. This ischemic pain persists for a long time before the development of intestinal necrosis. Because the pain results from ischemia and not from peritonitis, these patients have no abdominal tenderness, guarding, or rebound. Therefore, abdominal pain out of proportion to the abdominal physical findings should raise a question about this diagnosis. Because ischemia stops bowel motility promptly, the abdomen may be quiet to auscultation, depending on the amount of ischemic bowel. The heart is the most likely source of a superior mesenteric artery embolus. Therefore, any patient with cardiac arrhythmias, particularly atrial fibrillation, a known mural thrombus, or a recent myocardial infarction who develops acute abdominal pain should have acute superior mesenteric artery embolism high in the differential diagnosis. Patients with atherosclerosis can develop thrombosis at a superior mesenteric artery stenosis. Patients with acute visceral ischemia usually have marked leukocytosis and acidosis. Because cardiovascular disease is important in the development of acute visceral ischemia, most patients with that condition are persons who are middle aged or older. Conversely, venous thrombosis can cause visceral ischemia, and those patients can be younger. Birth control pills have been implicated in venous thrombosis in young women. Patients suspected of having acute visceral ischemia should undergo arteriography. Although duplex scanning can provide information about the visceral circulation, arteriography provides better images for planning arterial reconstruction or embolectomy. However, arteriography may not help in venous disease. CT scans or magnetic resonance imaging studies can reveal and delineate clots in visceral veins. Most patients with acute visceral ischemia should undergo laparotomy. Some patients develop visceral ischemia because of poor perfusion resulting from decreased cardiac output. Patients usually develop nonocclusive visceral ischemia while they are in the hospital, particularly in an intensive care setting. Improving cardiac output to restore intestinal perfusion is an important step in managing this problem. Arteriography may be required for complete evaluation and allows direct infusion of vasodilators for therapy.
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ACUTE ABDOMINAL PAIN

During Pregnancy
The development of acute abdominal pain during pregnancy presents a diagnostic challenge because of the enlarged uterus and the difficulty in evaluating the abdomen.[34] Appendicitis occurs once in 1500 pregnancies, evenly distributed in the trimesters. The diagnosis may be particularly difficult because the pregnant uterus can push the cecum and appendix into the right upper quadrant. Cholecystitis also occurs during pregnancy. Cholecystectomy has been performed in 3% to 8% of 10,000 pregnancies. Other conditions, such as acute pancreatitis and perforated ulcer, occur less frequently. Preeclamptic patients may experience spontaneous rupture of the liver. This is a serious and difficult complication to manage. Other causes of abdominal pain during pregnancy include placental abruption, ruptured uterus, torsion of the ovary, urinary tract infection, and pulmonary embolus. The pregnant patient with right-sided abdominal pain, tenderness, and guarding should be strongly suspected of having appendicitis. Ultrasound examination may help to detect evidence of appendicitis. In this setting, the patient should undergo operation, probably laparoscopy. The patient and the fetus are likely to face more risk from a ruptured appendix than from the procedure. If possible, surgical treatment of symptomatic cholelithiasis should be avoided during pregnancy. Patients with infrequent, mild, self-limited attacks of right upper quadrant pain should delay the operation until after delivery. If biliary colic becomes disabling but not an emergency, operation should be delayed and performed in the second trimester. Procedures are safer during the second trimester of pregnancy. Procedures during the first trimester pose a risk to the fetus, whereas procedures during the third trimester carry the risk of premature labor. If a pregnant patient with cholelithiasis develops unrelenting right upper quadrant abdominal pain, tenderness, guarding, and fever, she should undergo operation, probably laparoscopic cholecystectomy. Hemodynamic monitoring, perhaps including an arterial line, should be used. When laparoscopy is used, intra-abdominal pressures up to 15 mm Hg should be safe. Carbon dioxide values should be monitored. Fetal heart tones should be monitored, and exsufflation should follow any sign of fetal distress.
The Patient in the Medical Intensive Care Unit
Patients in the medical intensive care unit (MICU) who develop abdominal pain while undergoing treatment for another primary condition pose a common and difficult management challenge. Gajic and associates[37] studied a cohort of 77 abdominal catastrophe patients from 6000 MICU admissions (1.3%). The conditions producing the acute abdomen in that cohort included peptic ulcer, ischemic bowel, cholecystitis, bowel obstruction, and bowel inflammation. The APACHE III score on admission to the MICU predicted a mortality rate of 31% in this group of patients who experienced an actual mortality rate of 63%. The development of an acute abdomen in this setting doubled the mortality risk. All of the 26 patients not undergoing operation died, while 23 of the 51 patients undergoing operation died postoperatively. In the unoperated group some patients were judged too ill for surgery, 2 died during resuscitation, and 3 cases were only diagnosed at autopsy. For the patients undergoing operation significant predictors of mortality included delay in surgical evaluation, delay in surgical intervention, admission APACHE III scores, renal insufficiency, and ischemic bowel. Surgical delay occurred in patients with altered mental state, absence of peritoneal signs, opioid analgesia, antibiotics, and mechanical ventilation. It is noteworthy that in this cohort 84% of patients had abdominal pain, 95% had abdominal tenderness, 73% had abdominal distention, and 33% had free intra-abdominal air on radiograph or CT. MICU intensivists should maintain a low threshold for obtaining surgical consultation for patients with abdominal pain. The surgeon will approach such patients with high clinical suspicion. Repeated abdominal examinations, radiologic and sonographic investigations, and abdominal paracentesis must be evaluated carefully. Laparoscopy may help in this setting. Gagne and colleagues[38] reported using bedside minilaparoscopy to evaluate abdominal pain in ICU patients. Minilaparoscopy can be performed with a 3.3-mm laparoscope and instruments using local anesthesia and intravenous sedation. In any case, early surgical intervention remains crucial to survival of patients developing the acute abdomen in the MICU.
AIDS, IMMUNOSUPPRESSION, AND THE ACUTE ABDOMEN The diagnosis and treatment of acute abdominal pain in patients with immunodeficiency pose special problems.[39] [40] One must recognize the immunosuppressed patient and determine the degree of immunosuppression.[41] Mild to moderate immunodeficiency occurs in the elderly, the malnourished, the diabetic, the uremic, and patients with malignancy. In addition transplant patients on maintenance immunosuppression therapy and acquired immunodeficiency syndrome (AIDS) patients with CD4+ counts greater than 200/mm3 fall in this category. Patients in this mild to moderate immunodeficient category have the same kinds of diagnoses and surgical problems as other patients except they present in later or more advanced stages of the acute abdominal disease. Severe immunodeficiency includes AIDS patients with CD4+ counts less than 200/mm3 , transplant patients taking high doses or potent immunosuppressants, and cancer patients taking chemotherapy especially if neutropenic. Severe immunodeficient patients with the acute abdomen have unusual diseases and seek medical attention late in the course of their disease. Their symptoms are vague, and they are unlikely to have fever, abdominal tenderness, or guarding. Immunodeficient patients have particular susceptibility to unusual infections caused by fungi, mycobacteria, viruses, and infestations
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by parasites. They are also prone to develop unusual malignant tumors. Parente and coworkers[42] studied 458 AIDS patients hospitalized 752 times over 4 years. Seventy-one of the patients had an episode of abdominal pain severe enough to require surgical consultation. Forty-two of those patients had a premortem diagnosis of the condition causing the pain. Twenty-three patients had the cause of the abdominal pain explained by postmortem examination. The most common causative disorders in decreasing order included gastrointestinal non-Hodgkins lymphoma, acute pancreatitis, CMV colitis/enteritis, Mycobacterium avium-intracellulare colitis/enteritis, sclerosing cholangitis, CMV gastritis, cryptosporidial infection, acute cholecystitis, and gastrointestinal Kaposis sarcoma. Ten patients underwent emergency laparotomy: six for perforated viscus or peritonitis, two for intestinal obstruction, one for toxic megacolon, and one for hemoperitoneum. The postoperative survival was 40% at 1 month, 30% at 3 months, and 10% at 6 months. The median survival of the abdominal pain patients was 180 days from the diagnosis of AIDS, significantly lower than the median survival rate of the patients without abdominal pain, which was 540 days. Patients with advanced AIDS are debilitated, malnourished, and catabolic. In addition to being particularly susceptible to unusual bacterial, viral, and fungal agents, these patients are also at risk for the common causes of the acute abdomen. Patients with AIDS are particularly prone to CMV infections, and these infections commonly invade the gastrointestinal tract and produce mucosal ulceration, bleeding, and even perforation. One should avoid surgery in patients with CMV infection unless perforation occurs. If the diagnostic work-up indicates that a patient with AIDS has an acute abdomen from a common AIDS-unrelated disease, he or she should have conventional treatment without delay. Patients who have received organ transplants, particularly patients taking high doses of steroids, are at risk of developing the same diseases as those that occur in AIDS patients.[8] [43] Because immunosuppression obscures the signs and symptoms of intra-abdominal infections and perforation, physicians caring for organ transplant recipients must have a heightened awareness of the serious significance of acute abdominal pain in their patients. Transplant recipients with intestinal perforation, appendicitis, and so forth should be operated on as soon as possible. Any new complaint of abdominal pain expressed by an immunocompromised patient requires professional attention. Internists and family physicians should consult surgeons promptly in this situation. The surgeon should obtain a careful description of the nature of the pain and its onset. Immunocompromised patients may harbor advanced intra-abdominal disease yet exhibit minimal physical findings including fever, abdominal tenderness, guarding, and rebound. Imaging tests may help with the decision to operate. Although establishing strict criteria or guidelines for operating remains difficult, severely immunocompromised patients with unrelenting abdominal pain should undergo laparoscopy or laparotomy. In such cases the risks of intervention remain far less than the risks of untreated potentially catastrophic disease. Box 43-5. Nonsurgical Causes of Abdominal Pain Cardiac Myocardial infarction Acute pericarditis Pulmonary Pneumonia Pulmonary infarction Gastrointestinal Acute pancreatitis Gastroenteritis Acute hepatitis Endocrine Diabetic ketoacidosis
Acute adrenal insufficiency Metabolic Acute porphyria Familial Mediterranean fever Hyperlipidemia Musculoskeletal Rectus muscle hematoma Central and peripheral nervous system Tabes dorsalis Nerve root compression Genitourinary Pyelonephritis Acute salpingitis Hematologic Sickle cell crisis
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NONSURGICAL CAUSES OF ACUTE ABDOMINAL PAIN Many diseases produce acute abdominal pain and may be treated best by means other than surgery.[44] Certain nonsurgical conditions can cause acute abdominal pain, such as spontaneous bacterial peritonitis, as mentioned earlier ( Box 435 ). Sickle cell anemia may produce an attack of severe abdominal pain, referred to as sickle cell crisis, and this condition may result from a splenic infarction. These patients also may have attacks of bone and joint pain. Gastroenteritis may produce severe abdominal pain. Patients who develop abdominal pain and who have had a recent exposure to antibiotic therapy may have Clostridium difficile colitis or pseudomembranous colitis, which can mimic the acute abdomen. This diagnosis can usually be clarified by a careful history, and sigmoidoscopy reveals the pseudomembrane, which is virtually pathognomonic for the condition. Other diseases, such as lead poisoning, acute porphyria, and familial Mediterranean fever, may also cause abdominal pain. Pneumonia can produce abdominal pain, and of course, acute myocardial infarction may produce epigastric pain and can mimic acute pancreatitis or perforated ulcer. Hepatitis may produce abdominal pain. Acute adrenal insufficiency may cause abdominal pain, and patients with hyperlipidemia may have acute abdominal pain with or without acute pancreatitis.
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To manage patients with abdominal pain effectively, the surgeon must always remember that many nonsurgical diseases cause abdominal pain and may mimic the acute abdomen. Surgical and nonsurgical causes of abdominal pain are not mutually exclusive. Patients with sickle cell disease can develop acute cholecystitis or appendicitis. After performing a careful history, physical examination, and imaging tests, the surgeon must evaluate the strength of the evidence that the patient actually has a nonsurgical disease versus the strength of the evidence for an acute surgical abdomen. Diagnostic laparoscopy should find liberal application in this situation.
Selected References
Jeffrey RB Jr: CT and Sonography of the Acute Abdomen. New York, Raven, 1989. This textbook provides complete discussion and illustration of the use of CT and sonography in the evaluation of patients with acute abdominal pain. Lee JKT, Sagel SS, Stanley RJ: Computed Body Tomography with MRI Correlation, 2nd ed. New York, Raven, 1989. This textbook is an important source of information on the use of CT and MRI in the diagnosis of abdominal pain. Rao PM, Rhea JT, Novelline RA, et al: Effect of computed tomography of the appendix on treatment of patients and use of hospital resources. N Engl J Med 338:141146, 1998. This careful prospective study determined the sensitivity and specificity of CT imaging in the diagnosis of acute appendicitis. The authors also evaluated the role of CT in patient outcome. Salky BA, Edye MB: The role of laparoscopy in the diagnosis and treatment of abdominal pain syndromes. Surg Endosc 12:911914, 1998. The authors reviewed their experiences with 121 patients with acute abdominal pain who underwent laparoscopy for diagnosis and treatment. They discussed the role of laparoscopy for acute abdominal pain. Silen W: Copes Early Diagnosis of the Acute Abdomen, 19th ed. New York, Oxford University Press, 1995. All surgical residents and all surgeons who treat patients for acute abdominal pain should review this classic book.
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32. Sanna A, Adani GL, Anania G, et al: The role of laparoscopy in patients with suspected peritonitis: Experience of a single institution. J Laparoendosc Adv Surg Tech A 13:1719, 2003.
33. Vander 34. Gurbuz
Velpen GC, Shimi SM, Cuschieri A: Diagnostic yield and management benefit of laparoscopy: A prospective audit. Gut 35:16171621, 1994. AT, Peetz ME: The acute abdomen in the pregnant patient: Is there a role for laparoscopy? Surg Endosc 11:98102, 1997. IE: Abdominal pain as a cause of acute admission to hospital. J R Coll Surg Edinb 37:389393, 1992.
35. Hawthorn
36. Rozycki GS, Tremblay L, Feliciano DV, et al: Three hundred consecutive emergent celiotomies in general surgery patients: Influence of advanced diagnostic imaging techniques and procedures on diagnosis. Ann Surg 235:681689, 2002. 37. Gajic
O, Urrutia LE, Sewani H, et al: Acute abdomen in the medical intensive care unit. Crit Care Med 30:11871190, 2002. DJ, Malay MB, Hogle NJ, et al: Bedside diagnostic minilaparoscopy in the intensive care patient. Surgery 131:491496, 2002.
38. Gagne 39. Bizer
LS, Pettorino R, Ashikari A: Emergency abdominal operations in the patient with acquired immunodeficiency syndrome. J Am Coll Surg 180:205209, 1995. RB Jr: Abdominal imaging in the immunocompromised patient. Radiol Clin North Am 30:579596, 1992. CE, Fabrega AJ: Gastrointestinal problems in the immunocompromised host: A review for surgeons. Surg Endosc 10:959964, 1996.
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41. Scott-Conner 42. Parente
F, Cernuschi M, Antinori S, et al: Severe abdominal pain in patients with AIDS: Frequency, clinical aspects, causes, and outcome. Scand J Gastroenterol 29:511515, 1994.
43. Meyers
WC, Harris N, Stein S, et al: Alimentary tract complications after renal transplantation. Ann Surg 190:535542, 1979. FU: Medical conditions mimicking the acute surgical abdomen. Med Clin North Am 57:15591567, 1973.
44. Steinheber
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Chapter 44 - Acute Gastrointestinal Hemorrhage

Barbara Lee Bass M.D. Douglas J. Turner M.D.
Hemorrhage from the gastrointestinal tract is a common and serious clinical problem. In the United States, 1% to 2% of acute hospital admissions are for patients requiring evaluation and treatment of gastrointestinal hemorrhage. With an incidence of 170 per 100,000 adults per year, gastrointestinal hemorrhage is a leading diagnosis in patients admitted to intensive care units (ICUs).[1] Although the overall mortality rate for these patients ranges from 5% to 12%, the mortality rate in patients with persistent or recurring hemorrhage approaches 40%. Mortality is linked not only to the degree of hemorrhage but also, more importantly, to the coexisting medical conditions in the patient with hemorrhage.[2] Up to 85% of bleeding episodes cease spontaneously, allowing a less urgent approach to identify the source of bleeding and to provide definitive therapy; however, 15% of patients present with major, ongoing bleeding that requires aggressive emergency diagnosis and management to allow successful clinical outcomes. These high-risk patients are most likely to require surgical intervention and to have poor outcomes.[3] Hemorrhage can arise in any area of the gastrointestinal tract: the esophagus, stomach and duodenum, small bowel, and colon as well as organs that empty secretions into the gastrointestinal tract, such as the liver through the biliary system and the pancreas through the pancreatic duct. Although the spectrum of conditions giving rise to acute hemorrhage are legion, more than 85% of major bleeding episodes can be linked to one of four diagnoses: peptic ulcer disease, variceal hemorrhage, colonic diverticulosis, or angiodysplasia. Other sources of hemorrhage are distinctly less common. Gastrointestinal hemorrhage spans the socioeconomic strata and is equally common in urban and rural environments. Only advancing age appears to be a risk factor for hemorrhage that applies across the full spectrum of bleeding conditions of the intestinal tract. Up to half of patients with acute gastrointestinal hemorrhage are older than 60 years of age. Numerous advances in medical technology during the 1990s, particularly the improved availability and application of diagnostic and therapeutic endoscopy, have been instrumental in the evaluation and successful treatment of patients with major bleeding. Although surgery is required for control of hemorrhage in only 5% to 10% of patients hospitalized with gastrointestinal hemorrhage, it remains an essential emergency intervention for those patients with severe or recurrent hemorrhage from both the upper and lower gastrointestinal tract. Successful collaboration between the surgeon and the gastroenterologist is essential for optimal management of these complicated patients. In all patients, regardless of bleeding source, successful initial management requires that the treating physician be mindful of the potential severity of gastrointestinal hemorrhage. Appropriate resuscitation to restore volume and red blood cell deficits is critical in patients with major hemorrhage. This resuscitation phase must be followed by rapid diagnosis of the source of bleeding. Thereafter, institution of appropriate specific therapies may be offered to effect successful management. This chapter focuses on diagnosis and treatment of the two major categories of gastrointestinal hemorrhage: upper gastrointestinal hemorrhage, bleeding originating in the gastrointestinal tract proximal to the ligament of Treitz; and lower gastrointestinal hemorrhage, bleeding
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arising in the bowel distal to the ligament. Upper gastrointestinal hemorrhage is present in 85% of patients with acute gastrointestinal bleeding; lower gastrointestinal bleeding occurs in 10% to 15% of patients, with the small bowel as the source in only 1% to 5% of patients. Hemorrhage from small bowel sources may be difficult to diagnose and is frequently referred to as hemorrhage of obscure origin. The introduction of video capsule endoscopy 3 years ago has enhanced the diagnosis and treatment of the uncommon small bowel lesion.
INITIAL EVALUATION AND TREATMENT OF PATIENTS WITH ACUTE GASTROINTESTINAL HEMORRHAGE Initial management of a patient with acute gastrointestinal hemorrhage has four primary goals: (1) comprehensive patient assessment, with attention to hemodynamic status and identification of significant medical comorbidities; (2) institution of appropriate resuscitation and monitoring; (3) identification of the major source of gastrointestinal bleeding; and (4) institution of specific therapeutic interventions to stop or control the bleeding. When the level of severity of the bleeding is clarified and initial assessment and resuscitation are complete, the patient may be triaged to the appropriate level unit of care.
Goal 1: Initial Patient Assessment
Most patients with acute gastrointestinal hemorrhage present for initial assessment in the emergency department. One quarter of patients develop gastrointestinal hemorrhage during hospitalization for a concurrent illness; this group is particularly high risk for subsequent mortality.[4] Initial assessment in either case calls for a focused history and physical examination, with attention to risk factors for gastrointestinal hemorrhage and laboratory evaluation.
History
Except for patients in hemorrhagic shock, revealing information can be obtained from the patients history. The essential elements to be ascertained are the characteristics of the bleeding; the onset and duration of bleeding (hours or days antecedent); the associated symptoms; the use of concurrent medications; and previous significant medical conditions, particularly liver disease.
Characteristics of Bleeding
Acute gastrointestinal hemorrhage can present with hematemesis (vomiting of blood or bloody gastric contents), melena (passage of dark tarry or maroon stool), or hematochezia (passage of bright red blood from the rectum). On initial evaluation of a patient with acute gastrointestinal hemorrhage, it is important to determine whether the patient has experienced hematemesis, melena, or hematochezia. Gastrointestinal bleeding that is slow or intermittent is usually not evident to the patient; hence, the term occult is associated with this pattern of blood loss. Such patients present to primary care venues with secondary signs of slow blood loss, such as anemia or fatigue. Hematemesis is diagnostic of upper gastrointestinal bleeding, that is, bleeding from the esophagus, stomach, or duodenum. Rarely, hematemesis may result from brisk hemorrhage from the nasal passages or pharynx when the patient swallows large volumes of blood. Melena can be indicative of either upper or lower gastrointestinal hemorrhage. Dark, tarry stools are most commonly a sign of an upper gastrointestinal source in which the blood has traversed the small bowel and colon. Gastric acid degrades hemoglobin to hematin, and the actions of digestive enzymes and luminal bacteria further contribute to the appearance of melena. Melena may also represent bleeding from lesions in the small bowel or right colon. Hematochezia is the characteristic sign of colonic hemorrhage and reflects rapid elimination of blood from the bowel. Ten percent of patients with very rapid upper gastrointestinal hemorrhage may also have a history of hematochezia and syncope. It is essential to determine the onset of bleeding and the frequency of episodes of hematemesis, melena, or hematochezia and to make a rough estimate of volume.
Associated Symptoms
Inquiry regarding associated symptoms is also of value. A history of orthostatic dizziness or syncope indicates rapid and profound blood loss. Antecedent dyspepsia is suggestive of peptic ulcer disease; crampy abdominal pain is more consistent with upper gastrointestinal bleeding, whereas hematochezia is usually painless. Antecedent vomiting may suggest Mallory-Weiss tears; weight loss raises the possibility of malignancy.
Medications
The risk for gastrointestinal ulceration and hemorrhage is elevated in patients taking salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs). Use of these medications is linked not only to gastritis and gastric and duodenal ulcers but also to much less commonly seen ulcerated lesions of the colon and small bowel. Further, salicylates and NSAIDs impair platelet function and may contribute to poor coagulation in patients who develop the complication of hemorrhage. These agents are widely used by middle-aged and elderly patients; up to half of patients older than 50 years of age may use NSAIDs over the course of a given 30-day period. Use of other medications that predispose to hemorrhage, such as warfarin and low-molecular-weight heparin, should be elicited. All medications should be reviewed, particularly those for cardiovascular disorders, including blockers, calcium-channel blockers, and antihypertensives, because these agents alter the normal physiologic signs of hypovolemia.
Past Medical History
The past medical history should identify previous episodes of gastrointestinal bleeding or past history of
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conditions associated with acute hemorrhage. A history of dysphagia or reflux esophagitis, recent gastrointestinal distress with vomiting, peptic ulceration, Helicobacter pylori infection, liver disease, alcohol abuse, inflammatory bowel disease, intestinal polyps, diverticulosis, or malignancy may point to the source of bleeding. Equally important is identification of comorbid medical conditions that alter the patients ability to respond to hemorrhage. Complications and mortality are much more likely to occur in patients with a history of renal insufficiency, atherosclerotic cardiovascular disease, congestive heart failure, chronic respiratory conditions, preexisting liver disease, or central nervous system disability.[5]
Physical Examination
The major initial objective of the physical examination is to determine the degree of blood loss and volume depletion. Patients in shock with hypotension (systolic blood pressure <90 mm Hg in the supine position), tachycardia, and cold extremities can be assumed to have a deficit of at least 40% of blood volume. Patients with less severe but substantial blood loss of 20% to 40% show hypotension in the upright position. Orthostatic vital signs should be checked in all patients not in shock by allowing the patient to sit up with the legs dangling for a period of 5 minutes. An elevation in pulse of more than 20 beats/min or a fall in blood pressure of more than 10 mm Hg is a positive sign, indicative of at least a 20% blood volume loss. Signs of peripheral hypoperfusion, such as clammy, cool, pale extremities, also reflect a volume loss of at least 20%. These signs are less reliable in elderly patients, who may show exaggerated postural changes or blunted changes in heart rate, or are more likely to be using -blocker medication. All patients showing a volume deficit of greater than 20% of blood volume require prompt and aggressive resuscitation. The physical examination generally offers few specific signs relative to the source of gastrointestinal hemorrhage. The oropharynx and nose should be
examined to exclude the rare unrecognized nasopharyngeal source of bleeding. Although epigastric tenderness may be elicited in patients with peptic ulcer conditions, this is not a reliable sign. Patients with hematemesis and cirrhosis may show jaundice, abdominal distention with ascites, palmar erythema, and caput medusae, suggesting bleeding related to portal hypertension; even these signs, however, are not sufficient to forego complete diagnostic evaluation for the actual bleeding source. A rectal examination, noting the quality of the stool (i.e., brown, melena, or hematochezia) should also be completed. Peutz-Jeghers syndrome, a rare heritable condition, is characterized by small intestinal polyposis and may be identified by melanin spots on the lips, oral mucosa, and digits; patients with Osler-Weber-Rendu syndrome may have cutaneous telangiectasias.
Initial Laboratory Assessment
All patients with gastrointestinal hemorrhage should have basic laboratory testing, including hemoglobin and hematocrit, coagulation profile, liver function tests, serum electrolytes, and renal function. The initial hematocrit may not reflect the actual degree of hemorrhage because intravascular volume repletion from extracellular fluids may not have occurred.[6] The finding of initial hemoglobin of less than 10 g/100 mL is associated with an increased risk for morbidity and mortality. A specimen should also be sent to the blood bank for type and crossmatching.
Goal 2: Resuscitation
Based on the estimated volume deficit, rapid restoration of intravascular volume is indicated. All patients with gastrointestinal hemorrhage should have two large-bore intravenous lines for administration of lactated Ringers solution. Patients in shock should receive prompt transfusion of packed red blood cells if immediate response to electrolyte solutions is not evident. Patients with major hemorrhage, elderly patients, and patients with significant comorbidities (including cardiac, pulmonary, hepatic, or renal insufficiency) should be monitored with central venous or pulmonary artery catheters. Urine output should be monitored with a Foley catheter. Ongoing hemorrhage requires continuous resuscitation with saline and red blood cell transfusion. Coagulation defects should be corrected with component therapy or fresh frozen plasma and platelets. These measures should be instituted in the hospital environment that can best support these rapid maneuvers. In some hospitals, this is the emergency department; in others, this resuscitation is best accomplished in an ICU. Patients with massive hematemesis and mental obtundation are at high risk for pulmonary aspiration. These and hemodynamically unstable patients should have endotracheal intubation performed to protect the airway. Despite general improvements in management of critically ill patients, the mortality rate for patients with major gastrointestinal hemorrhage, particularly upper gastrointestinal hemorrhage related to peptic ulceration, has remained unchanged at 5% to 12%. In fact, elderly patients with defined comorbid risk factors, including impaired cardiac, renal, and pulmonary function, may have mortality rates for major upper gastrointestinal hemorrhage in excess of 60%. These patients rarely die of hemorrhage, however. Rather, they die of multisystem organ failure precipitated by episodes of shock due to initial or recurrent episodes of hemorrhage or as a consequence of pneumonia or cardiac events. Hence, appropriate management on initial presentation is essential to salvage these patients.
Goal 3: Identification of Source of Bleeding
Successful management of a patient with acute gastrointestinal hemorrhage requires knowledge of the site of bleeding. The specific aspects of diagnostic testing are considered in the detailed sections that follow. The general considerations are reviewed here. Patients with hematemesis, melena, or hematochezia require emergency upper endoscopy by an endoscopist capable of therapeutic intervention. Preparatory to this
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examination, a large-caliber orogastric tube should be placed to lavage the gastric lumen to enhance visual examination. Airway protection may require endotracheal intubation. Active volume resuscitation must continue during the examination. If patients are hemodynamically stable and show no signs of ongoing hemorrhage, endoscopic examination may be deferred to an urgent status (within 12 hours) provided the patient can be carefully observed in the interim. Patients presenting with melena and hematochezia without a history of hematemesis should have a nasogastric tube inserted to examine the gastric contents. Findings of blood-tinged secretions, coffee grounds, or guaiac-positive fluid should prompt upper endoscopy. Patients with melena and hematochezia with hemodynamic instability should have initial emergency upper endoscopy. Bleeding peptic lesions in the duodenum can elicit pyloric spasm precluding reflux of sufficient amounts of blood into the gastric lake to cause hematemesis. Endoscopy is essential to examine the duodenum in these patients. Even in stable patients, this examination should be performed within 24 hours of the bleeding episode to optimize outcome.[7] Hemodynamically stable patients with hematochezia and patients with melena with a negative upper gastrointestinal examination may be presumed to have acute lower gastrointestinal hemorrhage. For these patients, the choice of initial diagnostic test remains controversial. Mesenteric arteriography, colonoscopy, and labeled red blood cell scintigraphy are potentially valuable based on the clinical presentation. Diagnostic approaches are considered later in the section on lower gastrointestinal hemorrhage.
Goal 4: Institution of Specific Therapy
After resuscitation and identification of the source of bleeding, specific therapy can be instituted. For the 15% of patients with ongoing gastrointestinal hemorrhage and hemodynamic instability, the time interval until this intervention should be less than 2 hours, and all measures to provide ongoing support to avoid shock should be employed during the interval. Fortunately, bleeding stops spontaneously in most patients, allowing a more deliberate evaluation. After the source of bleeding has been identified, specific intervention can be provided. An algorithm for diagnosis of acute upper gastrointestinal bleeding is shown in Figure 441 . Interventions for specific conditions are reviewed in the following sections.
ACUTE UPPER GASTROINTESTINAL HEMORRHAGE

Definition and Incidence
Upper gastrointestinal bleeding is defined as bleeding from a source proximal to the ligament of Treitz. Acute upper gastrointestinal hemorrhage is a common and potentially deadly condition accounting for approximately 85% of hospital admissions for gastrointestinal bleeding. Despite the availability of effective antiulcer medications and an improved understanding of the pathogenesis of ulcer disease, gastroduodenal ulcer disease remains the most common cause, responsible for half of bleeding episodes. In urban environments, hemorrhage from esophageal and gastric varices secondary to portal hypertension of alcoholic cirrhosis constitutes the next most frequent source, identified in 10% to 20% of patients.[8] Acute mucosal lesions, broadly characterized as gastritis or duodenitis, are observed in 15% to 30% of patients with hemorrhage in both urban and nonurban settings. Other causes have remained relatively stable in frequency since the early 1970s, including Mallory-Weiss mucosal tears at the gastroesophageal junction (8% to 10%), esophagitis (3% to 5%), malignancy (3%), Dieulafoys lesion (1% to 3%), and more recently, watermelon stomach (1% to 2%). A differential diagnosis for acute upper gastrointestinal hemorrhage is shown in Box 441 .
Clinical Presentations
Hematemesis and melena are the most frequent clinical findings in significant upper gastrointestinal bleeding. However, massive bleeding from an upper source may be associated with hematochezia. Even in instances where a lower gastrointestinal bleeding source is suspected, the passage of a nasogastric tube is required to interrogate for the presence of blood in the stomach. Although all sources of gastrointestinal bleeding have high associated morbidities, upper gastrointestinal bleeding has the highest risk for life-threatening hemorrhage.
Etiology
Although the conditions described earlier (see Box 441 ) share similar clinical presentations and initial assessment and resuscitation protocols are similar, definitive endoscopic evaluation is essential to correctly determine the cause of bleeding. Each condition has unique features of management that can be appropriately applied only with timely definitive diagnosis. Diagnostic endoscopy is the mandatory initial diagnostic test. However, endoscopy in the setting of acute hemorrhage carries specific risks compared with elective endoscopy. Complication rates of 0.9%, most of which are cardiopulmonary in nature, are reported for patients undergoing emergency endoscopy for hemorrhage, as compared with rates of 0.1% to 0.3% in the elective setting. Arterial desaturation during the procedure occurs four times as frequently in patients undergoing emergency compared with elective upper endoscopy. Patients with hypotension have a decreased level of consciousness and are at increased risk for pulmonary aspiration. The gastric lumen may contain large amounts of blood or clot; thorough evacuation of the lumen with a large-bore orogastric tube may not only facilitate visualization but also help prevent aspiration. Elderly patients with these and other comorbid conditions are most likely to have these risks. Careful airway protection is mandatory, and elective orotracheal intubation is often
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Figure 44-1 Algorithm for the management of upper gastrointestinal bleeding. NSAID, nonsteroidal anti-inflammatory drug; PPI, proton-pump inhibitor; LGIB, lower gastrointestinal
bleeding; AGML, acute gastric mucosal lesions; OR, operating room.
appropriate for these patients. Despite the risks, endoscopy is essential.

Bleeding Peptic Ulcer
Peptic gastric and duodenal ulcers are the most common cause of acute hemorrhage in the upper gastrointestinal tract, each accounting for about 25% of cases. Despite improved understanding of the pathogenesis of ulcer disease and improved therapies to manage bleeding with nonsurgical endoscopic therapies, only a few recent studies have indicated that surgical and mortality rates for this condition may have declined slightly since about 1995. About 5% of patients with peptic ulcer disease have hemorrhage as the initial manifestation of the condition, and up to 20% of patients with peptic ulcers develop bleeding at least once. Hemorrhage remains the most lethal form of complicated ulcer disease; 80% of ulcer deaths in the elderly occur as a consequence of an episode of acute hemorrhage.
Pathogenesis
Bleeding ulcer is caused by acid-peptic erosion into the submucosal or extraluminal vessels. In the stomach, the vessel is typically a small submucosal artery with a mean
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Box 44-1. Differential Diagnosis of Acute Upper Gastrointestinal Hemorrhage Peptic disorders Duodenal ulcer Gastric ulcer Reflux esophagitis Gastritis Duodenitis Nonsteroidal anti-inflammatory drugassociated disorders Acute gastric mucosal lesions Portal hypertensionrelated causes Esophageal varices Gastric varices Portal hypertensive gastropathy Watermelon stomach Mallory-Weiss tear Neoplasms of the esophagus, stomach, or duodenum Esophagitis due to infection Dieulafoys lesion Aortoduodenal fistula Angiodysplasias Crohns disease Hemobilia Hemorrhage from a pancreatic source
diameter of 0.7 mm (range, 0.1 to 1.8 mm).[9] Larger arteries are associated with increased bleeding and higher morbidity and mortality rates and may be refractory to effective endoscopic therapy. Although bleeding may occur from any duodenal ulcer, posterior duodenal ulcers are at greatest risk for hemorrhage because of erosion of the ulcer into the retroperitoneal, extraluminal vasculature supplying the duodenum and pancreas. In the duodenum, major bleeding most frequently arises from branches of the gastroduodenal and superior pancreaticoduodenal arteries. Our understanding of the pathogenesis of peptic ulcer disease changed dramatically during the 1990s. It is widely recognized that H. pylori infection is the causative agent of duodenal and gastric ulcers and gastritis in up to 80% of patients not taking NSAIDs. H. pyloriassociated ulcers represent 40% to 50% of cases of peptic disease. NSAIDs are responsible for the remaining cases, and up to 30% of these patients may also have H. pylori infection. H. pylori is not uniformly identifiable in non-NSAIDusing patients with bleeding peptic ulcer. In some series, only 40% to 60% of patients with
bleeding ulcer were found to have H. pylori infection. Hence, the role of physiologic acid hypersecretion in patients with complicated ulcer disease is being reappraised. Patients using NSAIDs have a 15% to 20% greater risk for bleeding ulcer than patients with H. pylori infection, and NSAID use may be an independent indicator of adverse outcome. Only 1% to 2% of patients with ulcer disease develop the condition as a result of acid hypersecretion caused by gastrin-secreting endocrine tumors of the gastrointestinal tract (Zollinger-Ellison syndrome). The gastrointestinal toxicity of NSAIDs has been extensively investigated.[10] It is estimated that 13 million people use NSAIDs on a regular basis for some form of arthritis. About 10% to 20% of patients taking NSAIDs develop dyspepsia, and 100,000 hospitalizations per year are related to some form of NSAID toxicity, with gastrointestinal bleeding the most common. Elderly patients are at greatest risk for NSAID toxicity. NSAIDs damage the gastrointestinal mucosa by multiple mechanisms. Topical injury occurs because NSAIDs are weak acids that remain in a nonionized lipophilic form in the acidic gastric lumen. In this nonionized state, they migrate through the gastric mucus into the surface epithelial cells, where they dissociate into the ionized form, causing epithelial acidification and injury. NSAIDs also decrease hydrophobicity of the gastric mucus. The greater toxicity from NSAIDs, however, is likely a result of inhibition of mucosal prostaglandin synthesis caused by systemic absorption of the agent resulting in suppression of gastric mucosal cyclooxygenase-1 (COX-1) activity. Prostaglandins are essential for mucosal bicarbonate and mucus secretion and are important agents of mucosal protection. Finally, NSAIDs have an inherent antiplatelet effect through inhibition of both thromboxane synthesis and platelet aggregation, both COX-1 activities.[11] Until 1999, all NSAIDs inhibited both COX-1 and COX-2 activities. The anti-inflammatory, antiarthritic, and analgesic therapeutic benefits of NSAIDs are related to the inhibition of COX-2 activity, which is induced by inflammatory stimuli in many different tissues, including macrophages and synovial cells; the equal inhibition of COX-1 in the gastric mucosa leading to gastroduodenal injury is an unfortunate byproduct. COX-2selective NSAIDs were introduced in 1999.[12] Prospective trials comparing nonselective NSAIDs versus agents with COX-2 selectivity have shown a reduction in lower gastrointestinal blood loss and clinical events in the COX-2selective group.[6] [11] COX-2selective inhibitors are the agents of choice for elderly patients requiring long-term use for chronic arthritic conditions. Numerous studies have indicated that NSAIDs increase the risk for upper gastrointestinal bleeding from a variety of sources, including superficial minor gastritis, diffuse gastritis, and gastric and duodenal ulcer. Bleeding may be related not only to gastrointestinal toxicity but also to platelet dysfunction as a result of NSAID use. In 160 consecutive patients with upper gastrointestinal hemorrhage, 19% of the patients had a prolonged skin bleeding time on initial presentation. Excluding those patients with chronic liver disease, the bleeding time was significantly higher in patients using NSAIDs than in patients not taking NSAIDs. Although acid suppression is recommended for patients who must continue to use NSAIDs after an episode of bleeding, there is no prospective trial that has proved the ability of proton-pump inhibitors, type 2 histamine (H2 ) receptor antagonists, or misoprostol to prevent rebleeding. Rather, NSAIDs should be discontinued and alternative therapy provided for the original condition whenever possible.
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TABLE 44-1 -- Mortality Associated With Underlying Medical Illnesses and Gastrointestinal Bleeding Condition Renal disease Acute renal failure Liver disease Jaundice Pulmonary disease Respiratory failure Cardiac disease Congestive heart failure Mortality Rate (%) 29 63 25 42 23 57 13 28
From Lieberman D: Gastrointestinal bleeding: Initial management in gastrointestinal bleeding. Gastroenterol Clin North Am 22:723, 1993.
Clinical Prognostic Features
Many reviews have identified clinical features associated with poor clinical outcomes ( Table 441 ). Organ-specific complications, need for emergency surgery, and death are the primary factors cited as adverse outcomes after acute upper gastroduodenal hemorrhage. The primary factors associated with poor outcome are severe magnitude (rate and volume) of the initial hemorrhage; persistence or recurrence of major hemorrhage during the hospitalization for the acute hemorrhage; advanced age, generally older than 60 years of age; and presence of medical comorbid conditions. Several risk assessment measures have been developed. The BLEED risk classification schema predicts risk on initial presentation based on five criteria: ongoing bleeding; low systolic blood pressure (i.e., <100 mm Hg, excluding orthostatic measures); elevated prothrombin time (i.e., >1.2 times the control value); altered mental status; and presence of an unstable comorbid disease (defined as any ongoing organ system abnormality that ordinarily would require ICU admission, e.g., myocardial ischemia, hepatic dysfunction).[13] The presence of any one of these factors places a patient at a roughly threefold increased risk for in-hospital complications of recurrent gastrointestinal hemorrhage, need for surgical intervention, or death. This risk tool can be applied independently of findings at endoscopy and may allow appropriate triage to the ICU or other levels of care. Similar estimates of mortality can be made based on age, systolic blood pressure on presentation, appearance of initial nasogastric aspirate, and transfusion requirement, as shown in Table 442 .
Prognostic Findings at Endoscopy
The actual appearance of the ulcer at endoscopy is the most important predictor of rebleeding. Ulcers generally have one of five appearances: a clean ulcer base; a flat, pigmented spot, which may be purple, brown, or black, on the ulcer surface; an adherent clot; a visible vessel, which appears as a smooth surfaced or tubular protuberance on the smooth ulcer surface; or active bleeding with either spurting blood, continuous oozing, or oozing around an adherent clot. The latter four appearances are TABLE 44-2 -- Prognostic Indicators for Mortality From Peptic Ulcer Hemorrhage Clinical Parameter Overall Age Mortality Rate (%) 58
60 years 80 years Systolic blood pressure on presentation 8090 mm Hg <80 mm Hg Nasogastric aspirate on presentation Coffee-ground appearance Red blood Transfusion requirement 10 units From Dudnick R, Martin P, Friedman LS: Management of bleeding ulcers. Med Clin North Am 75:948, 1991.
1015 2530 1215 3035 610 1820 2834
considered to be stigmata of hemorrhage.[14] The probability of rebleeding can be estimated based on this endoscopic appearance: a clean ulcer base rarely bleeds; a flat, pigmented spot ulcer bleeds again in about 10% of patients; an adherent, nonbleeding clot carries a rebleeding risk of about 20%; and a visible vessel carries a rebleeding risk of 40% to 80%. Descriptive identification of the ulcer characteristics has also been reported as the Forrest classification system, wherein FI ulcers show active bleeding, FIIa represents an ulcer with a visible vessel or pigmented protuberance, FIIb represents an ulcer with an adherent clot, FIIc represents an ulcer with a pigmented spot, and FIII shows a clean ulcer base without stigmata of bleeding. Rebleeding rates increase with ulcer size; ulcers greater than 2 cm in diameter are high risk. As discussed later, endoscopic therapy is appropriate for ulcers with stigmata of bleeding. In contrast, active bleeding not controlled with endoscopic measures mandates immediate surgical intervention. The transendoscopic Doppler device has been evaluated to assess blood flow beneath the ulcer surface.[14] A positive Doppler study indicating a blood vessel beneath the ulcer was a strong predictor of rebleeding, although the value of this method of evaluation to predict rebleeding is yet to be demonstrated in a large cohort.
Therapeutic Interventions Medical Management.
Therapy is based on clinical presentation and endoscopic findings. A patient with minimal bleeding and a clean ulcer base on endoscopy is at very low risk for recurrent hemorrhage. Young patients may be discharged with specific antiulcer therapy: an antisecretory agent (either an H2 -receptor antagonist or proton-pump inhibitor), cessation of NSAIDs if applicable, and H. pylori eradication with antibiotics if H. pylori positive.[15] Older patients with this clinical presentation should be
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admitted for a brief period of in-hospital observation before discharge on a similar regimen. Follow-up endoscopy is indicated at 6 weeks for patients with gastric ulcer to ensure healing and exclude malignancy but not for patients with duodenal ulcer. Patients with more significant hemorrhage and findings on endoscopy with stigmata for lesions at increased risk for rebleeding should be admitted to the hospital. Patients with clinical risk factors for adverse outcome should be admitted to the ICU. Recent evidence has focused on the ability of antisecretory therapy to decrease the incidence of rebleeding following endoscopic therapy. Several recent large clinical trials have been reported demonstrating reduced rates of recurrent bleeding with the use of intravenous proton-pump inhibitors.[16] [17] An additional recent study also showed favorable rebleeding results with oral proton-pump inhibitor therapy versus placebo.[18] All the trials demonstrating benefit for proton-pump inhibitor therapy have been completed in patients with significant hemorrhage who have also had a therapeutic endoscopy and were not treated solely with medication. Hence, the proton-pump inhibitors were used as adjuncts to endoscopic therapy.
Endoscopic Therapy.
Endoscopic therapy can be used to arrest active ulcer bleeding and to prevent rebleeding in patients with ulcers at high risk for rebleeding (FI, FIIa, and FIIb ulcers). Several endoscopic devices can deliver the thermal energy required to achieve coagulation. Transendoscopic bipolar electrocoagulation and heater probe therapy can decrease rebleeding rates and the need for surgical intervention by up to 50%. In skilled hands, light amplification by stimulated emission of radiation (LASER) coagulation offers similar results, although the risk for perforation is higher; LASER is generally not used as the initial therapeutic modality in most institutions. Each of these modalities can result in activation of bleeding or transmural bowel injury with consequent perforation, although these are rare, with reported incidence rates of less than 0.5%. Injection therapy is an equally effective nonthermal method to secure hemostasis. Available sclerosing or vasoconstricting agents include absolute alcohol, epinephrine, fibrin glue, and polidocanol. The choice of method and agent is the preference of the endoscopist and equipment availability. Sclerosants are injected around the ulcer perimeter or visible vessel. Rebleeding rates are reduced by half, relative to those ulcers with similar characteristics not subjected to endoscopic therapy. Irrespective of the method of endoscopic hemostasis, endoscopy is highly successful in stopping initial active bleeding, with initial success rates in more than 95% of cases in ulcers that are actively bleeding or with nonbleeding visible vessels.[19] Nevertheless, bleeding recurs in about 20% of patients, and 97% of this rebleeding occurs within 96 hours of the initial endoscopy.[20] Individual studies have not shown a significant decrease in mortality in patients subjected to endoscopic therapies for hemorrhage; however, two metaanalyses have suggested this benefit. Overall reduction in mortality rate is roughly 40% in patients subjected to endoscopic interventions relative to those patients not subjected to endoscopic treatments.[21] Endoscopic therapy fails in about 20% of patients, manifest as either failure to control hemorrhage on initial presentation or as early recurrent hemorrhage. In the recent past, rebleeding patients were treated surgically, but more recent experience suggests that repeat endoscopy may be a safe and effective alternative for these patients. Repeat endoscopy may be able to salvage half of these patients; however, morbidity and mortality are high in this subset of patients,[22] with high risk of perforation and overall worse outcomes when surgery was required. Optimal management strategies for this high-
risk group remain controversial. Before embarking on repeat endoscopy to control recurrent hemorrhage, surgical options should be considered, particularly in patients who are at high risk for rebleeding and in elderly patients who are at high risk for multisystem organ dysfunction and death from recurrent episodes of hypotension and stress.
Surgical Therapy.
Surgery is ultimately required in roughly 10% of patients with bleeding ulcer. Surgery is indicated for patients with active hemorrhage not responsive to endoscopic measures, significant recurrent hemorrhage after endoscopic treatment, an ongoing transfusion requirement, or transfusion requirements exceeding 6 units of packed red blood cells in a 24-hour interval. Given the now extensive successful experience with endoscopic therapy, surgery is generally reserved for those patients in whom endoscopic measures have failed as the primary intervention, assuming expert endoscopy is readily available. There are surgical reports to support early elective operation after initial endoscopic hemostasis in elderly patients with lesions at high risk for rebleeding (FI and FIIa ulcers); however, this practice has not been uniformly embraced by gastrointestinal surgeons.[23] Before improved success with endoscopic methods, the presence of a visible vessel was considered an absolute indication for surgery. Now, the decision for surgery is balanced by endoscopic expertise, patient characteristics, and transfusion requirements. In contrast, expertise in interventional endoscopy may not be available in some communities; thus, surgery becomes an important treatment modality earlier in the course of disease in patients in these locations. A number of studies have attempted to clarify the group of patients that can benefit from early definitive surgical therapy.[24] Unfortunately, no study series with a sizable cohort has been collected since the advent of effective endoscopic therapy. Earlier, pre-endoscopy series support a role for early surgery for patients with clear evidence of ongoing hemorrhage (>4 units of packed red blood cells), presence of shock, history of previous hemorrhage, endoscopic evidence of high risk for rebleeding (FI or FIIa lesions), and age older than 65 years. A retrospective review of 66 patients managed with early definitive surgery accrued from an urban hospital between 1986 and 1990 showed that these patients were successfully managed without a death. Unlike more recent surgical series, however, the average age of the patients in this study was 53 years, in contrast to the current average age of 63 years in patients with acute upper gastrointestinal
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hemorrhage. Moreover, it is likely that many patients were treated surgically who by todays standards would not have required surgical therapy. Clinical judgment is essential in deciding who will benefit from surgical intervention at what time. Early definitive surgical intervention is clearly indicated for patients in whom primary endoscopic therapies fail. It is also clear that elderly patients with lesions at highest risk for rebleeding fair better with early definitive operation than with episodes of recurrent hemorrhage as a result of failed repeated efforts at hemostasis. Whether early elective operation should be provided to elderly patients after initial successful endoscopic therapy for a high-risk FI or FII lesion has not been definitively settled. Such a decision needs to take into consideration local technical expertise, critical care support, and ongoing advances in endoscopic intervention.
Choice of Operation.
The goal of surgical intervention in bleeding peptic ulcer is to control hemorrhage. This may be achieved by either direct suture ligation of the bleeding vessel or, in the case of gastric ulcer, with gastric resection or ulcer excision. The role for a definitive acid-reducing procedure is a secondary, but important, objective of the surgical procedure.
Bleeding Duodenal Ulcer.
Operative intervention for bleeding duodenal ulcer requires direct exposure of the ulcer in the duodenum by way of duodenotomy or duodenopyloromyotomy. Because these ulcers are typically located on the posterior duodenal wall, direct suture ligation with a nonabsorbable suture suffices in most patients to arrest bleeding. Occasionally, direct suture ligation fails to stop bleeding, so that four-quadrant suture ligation around the perimeter of the bleeding ulcer may be necessary to control bleeding. Rarely, these two measures fail, and ligation of the gastroduodenal artery cephalad and inferior to the duodenum may be necessary. Provided the patient is stable and free of lifethreatening, preoperative comorbid conditions, a definitive antisecretory procedure is indicated ( Fig. 44 2 ). Truncal vagotomy is the least time-consuming and a highly effective procedure to decrease acid secretion. Alternatively, the parietal cell vagotomy has been advocated by some surgeons. In this procedure, a limited duodenotomy is performed for ulcer ligation, preserving normal gastric emptying in conjunction with the parietal cell vagotomy. Because the typical patient undergoing emergency or urgent surgery for bleeding ulcer is at high risk for adverse outcome, careful consideration should be used before proceeding with this more time-consuming operation. The patient should be well resuscitated and hemodynamically stable. In actual practice, parietal cell vagotomy with limited duodenotomy is rarely applied in this setting today, given the typical clinical features of patients with refractory bleeding ulcer. Although technically feasible, similar concerns have limited the use of the laparoscopic approach to patients with actively bleeding ulcer. Gastric resection is generally not indicated in the management of duodenal ulcer hemorrhage. Suture ligation of bleeding duodenal ulcer with pyloroplasty and truncal vagotomy is successful in acutely controlling hemorrhage in 90% of patients. Up to 10% of patients may develop early rebleeding. Repeat surgical intervention is rarely required for these patients, however, because bleeding frequently ceases with supportive measures. Reported operative mortality rates range from less than 1% to 50% based on the patients comorbid conditions.
Bleeding Gastric Ulcer.
Again, the primary goal of surgical intervention for bleeding gastric ulcer disease is to stop
Figure 44-2 Truncal vagotomy and parietal cell vagotomy. A, During truncal vagotomy, both vagal trunks are divided at the esophageal hiatus. The vagal branches to the gastric cardia, fundus, antrum, and pylorus are divided, as are the hepatic and celiac branches. A gastric-emptying procedure, either pyloroplasty or gastrojejunostomy, is required because pyloric opening is impaired. B, Parietal cell vagotomy denervates only the parietal cell mass. Innervation of the antropyloric region and the hepatic and celiac branches is preserved. Parietal cell vagotomy preserves normal gastric emptying, but the procedure requires considerably longer operative time and should be used only in stable patients who do not have significant risk factors for poor outcome. (A and B, From Mulholland MW: Duodenal ulcer. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice, 2nd ed. Philadelphia, Lippincott-Raven, 1997, p 766.)
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hemorrhage. Unlike duodenal ulcer, there is a chance that a gastric ulcer may be malignant; up to 10% of gastric ulcers prove to be a gastric adenocarcinoma or lymphoma. Additionally, rebleeding rates for gastric ulcer treated with simple ligation approach 30%. Ideally, therefore, the surgical procedure should include ulcer excision. Ulcers of the incisura, antrum, and distal body of the stomach should be managed with distal gastrectomy and Billroth I or II reconstruction ( Fig. 44 3 ). Truncal vagotomy is indicated in the setting of hemorrhage in stable patients and those free of life-threatening comorbid conditions. Fortunately, most bleeding gastric ulcers arise in these regions of the stomach, reflecting the distribution of gastric ulcers. Fewer than 10% of gastric ulcers are located high on the lesser curvature. Ulcers in this position can be managed with either subtotal or near-total gastrectomy or with local ulcer excision and distal gastrectomy without vagotomy. Aggressive proximal gastric resections carry high morbidity and mortality rates, however, particularly in the setting of hemorrhage, and the need for such resections is infrequent.
Ulcer Surgery in Patients with H. pylori Infection.
A role for definitive antisecretory ulcer surgery is clear in the setting of hemorrhage from peptic ulcer in patients taking NSAIDs who must continue this therapy. Some gastroenterologists and surgeons have questioned the need for definitive antiulcer surgery in patients with H. pylori associated ulcer disease. A definitive judgment cannot be made at this time. A role for excluding a definite antisecretory procedure in perforated duodenal ulcer is supported by a recent study showing that in H. pyloriinfected patients with perforated duodenal ulcers, those treated with H. pylori therapy after closure alone had significantly less ulcer recurrence than those treated with closure and omeprazole alone.[15] Eradication of H. pylori can decrease the incidence of rebleeding in patients with H. pylorirelated ulcer disease with bleeding, as shown in another recent study. However, this may be true only of patients with relatively minor bleeding, not those with significant hemorrhage of a magnitude to warrant transfer or surgery.[25] Gastrointestinal surgeons who have cared for many of these critically ill patients with severe bleeding will note that only 10% of patients with H. pylori infection develop ulcer disease related to their infection, and of those 10%, only 1 in 5 develops hemorrhage as a complication. Of that 2%, only 1 in 10 ultimately requires surgery to control bleeding; that is, 0.2% of all H. pyloriinfected patients eventually face surgery for bleeding peptic ulcer disease. Moreover, recent evidence also suggests that patients requiring surgical intervention for bleeding peptic ulcer had an H. pylori infection rate that was far lower than that commonly seen in other populations with ulcer disease.[25] Extrapolation of the data from uncomplicated patients has led to the postulation that simple oversewing of the bleeding ulcer and H. pylori treatment would be sufficient surgical therapy; however, recent evidence demonstrates that more than 50% of these patients would be at high risk for recurrent hemorrhage. Hence, using the long-standing effective modality of acid-reducing surgery as definitive management of ulcer diathesis in these patients seems prudent at this time.
Figure 44-3 A, Lines mark limits of gastric resection for antrectomy. For patients with more proximal gastric ulcers, the proximal line of resection can be extended or tailored to include the ulcer in the resection. B, Billroth I reconstruction with gastroduodenostomy. Note that truncal vagotomy is included in the procedure. (A and B, From Sabiston DC Jr: Atlas of General Surgery. Philadelphia, WB Saunders, 1994, pp 271272.)
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Bleeding Caused by Portal Hypertension
For completeness we briefly discuss bleeding related to portal hypertension, a frequent cause of upper gastrointestinal bleeding. This is more extensively covered in Chapter 51 . Bleeding from esophagogastric varices is responsible for one third of all deaths in patients with cirrhosis and portal hypertension. As many as 90% of cirrhotic patients develop esophageal varices, and 25% to 30% of these develop hemorrhage. The mortality risk from each episode of hemorrhage approaches 25%. After bleeding has occurred, repeated hemorrhage develops in 70% of patients. Esophageal varices are dilated submucosal veins that communicate with the portocollateral circulation and the systemic venous system. Varices range in size from small (1- to 2-mm) irregular protuberances to large (1- to 2-cm) serpentine structures that abut into the esophageal lumen. Most varices are initially restricted to the distal esophagus, although with time gastric varices along the cardia and high greater curvature of the stomach are evident in most patients.
Treatment of Acute Variceal Hemorrhage
Hemorrhage from varices in cirrhotic patients is a potentially highly lethal event. The clinical presentation includes massive hematemesis, melena, and occasionally hematochezia. Hemodynamic instability is common. Initial management calls for prompt resuscitation with particular attention to correction of volume deficit, coagulopathy, and airway management. Patients with poor liver function as reflected by Childs classification system are at high risk for mortality. Treatment in an ICU is imperative. Emergency endoscopy is required to evaluate the source of bleeding. Although varices may be suspected based on clinical stigmata of cirrhosis, bleeding is equally likely to be caused by gastritis, ulcer disease, or portal hypertensive gastropathy in patients without a prior history of bleeding varices. About 70% of patients with prior episodes of variceal hemorrhage are bleeding from varices. An algorithm for the management of bleeding resulting from portal hypertension is shown in Figure 444 . Endoscopy is necessary both to confirm the source of bleeding and to allow endoscopic therapy. Both variceal sclerotherapy and rubber band ligation are effective endoscopic measures. Sclerotherapy can be completed with a variety of sclerosants, and both intravariceal and paravariceal injections are equally effective. Complications of sclerotherapy include esophageal ulceration, bleeding perforation, mediastinitis, pleural effusion, and pulmonary edema. Late stricture has also been observed. Esophageal variceal rubber band ligation is comparable to sclerotherapy, although complications may be less common than with sclerotherapy, particularly those related to mediastinal and pulmonary inflammation. Gastric varices are not effectively treated by sclerotherapy. In good-risk patients with bleeding gastric varices, prompt surgical decompression should be considered. Concomitant treatment with vasoactive drugs is indicated. The somatostatin analogue octreotide, given by continuous intravenous infusion, offers the best efficacy and safety profile. Somatostatin decreases splanchnic blood flow, thereby decreasing portal and variceal pressure without eliciting coronary vasoconstriction. Vasopressin alone and vasopressin plus nitroglycerin by continuous systemic intravenous infusion are also of benefit in decreasing splanchnic blood flow and decreasing variceal bleeding. One of these agents should be started as soon as the diagnosis of variceal hemorrhage is established. In patients with a known history of variceal hemorrhage, the infusions should begin empirically in the emergency department on presentation with hematemesis. Endoscopic therapy and somatostatin infusions are effective in arresting hemorrhage in 80% to 90% of cases. Sclerotherapy may be repeated up to two times in the initial 48 hours if initial efforts fail. If sclerotherapy is successful, attention must be directed toward future prevention of rebleeding, which occurs in more than 70% of patients with portal hypertension who have bled from esophageal varices. If sclerotherapy is ineffective, a SengstakenBlakemore tube should be inserted. This device has a large gastric balloon and an esophageal balloon that can be passed through the mouth into the stomach. Careful positioning is required to avoid esophageal perforation. When in position, the gastric balloon is inflated, and traction is applied to the tube, placing pressure on the esophagogastric junction venous plexus. This results in cessation of bleeding in most patients. In the few that continue to bleed, the esophageal balloon should be inflated. With this intraluminal control, resuscitation, correction of coagulopathy, and definitive management plans can be pursued. Failure to control bleeding with these measures carries a mortality rate in excess of 70% in patients with Childs class C liver dysfunction. The patient with acute variceal hemorrhage who continues to bleed after endoscopic and medical therapies have been applied can be considered for transjugular intrahepatic shunt (TIPS) or emergency surgical decompression of the portal circulation. The TIPS procedure involves placement of a transvenous intrahepatic portosystemic stent to decompress the portal circulation. Results have varied widely in different institutions. Clinical expertise and aggressive medical management are required for a successful outcome, particularly in high-risk candidates, those with ongoing bleeding and poor liver function. Childs class A and B patients have a 30-day mortality rate of 10%, whereas Childs class C patients have a reported 30-day mortality rate in excess of 50%. Rebleeding is also likely and occurs in 22% of patients within the first month, usually a result of TIPS thrombosis. In most reported series, emergency decompressive surgery for patients (procedures discussed in Chapter 51 ) with uncontrolled hemorrhage carries an operative mortality rate in excess of 50%. This reflects the fact that ongoing hemorrhage is more likely to occur in patients with poor liver function (Childs class C). The risks for early and late mortality after variceal hemorrhage are largely determined by the patients liver
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Figure 44-4 Algorithm for the management of acute hemorrhage due to portal hypertension. TIPS, transjugular intrahepatic portosystemic shunt. (From Rikkers LF: Portal hypertension. In Levine BA, Copeland E, Howard R, et al [eds]: Current Practice of Surgery, Vol. 3. New York, Churchill Livingstone, 1995.)
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TABLE 44-3 -- Childs Criteria for Hepatic Functional Reserve Measure Serum bilirubin (mg/100 mL) Serum albumin (g/100 mL) Ascites Encephalopathy Nutrition A: Minimal <2.0 >3.5 None None Excellent 23 33.5 Easily controlled Minimal Good B: Moderate >3 <3 Poorly controlled Advanced, coma Poor, wasting C: Advanced
From Boyer TD: Portal hypertension and its complications: Bleeding esophageal varices, ascites, and spontaneous bacterial peritonitis. In Zakim D, Boyer TD (eds): Hepatology: A Textbook of Liver Disease. Philadelphia, WB Saunders, 1982, pp 464499. function at the time of hemorrhage. Several classification schemes have been developed to predict the degree of liver dysfunction, but the most durable has been based on the original assessment presented by Child. Simply stated, assessment of the degree of encephalopathy, hyperbilirubinemia, ascites, albumin, and prolongation of the prothrombin time can provide a good estimate of 30-day mortality. Table 443 shows Childs classification parameters. Predicted 30-day mortality rates after an episode of variceal hemorrhage are as follows: Childs class A, less than 10%; Childs class B, 30%; and Childs class C, 50%. Mortality rates increase at the 1-year interval to Childs class A, 24%; Childs class B, 45%; and Childs class C, 85%, overall.
Acute Gastric Mucosal Lesions
Acute gastric mucosal lesions (AGMLs) include a broad category of acute erosive mucosal conditions that develop in critically ill patients. Also known as stress gastritis, acute mucosal ischemia, erosive gastritis, or stress ulceration, these conditions share a common epidemiology and clinical presentation. They are characterized by stigmata of mucosal injury evidenced by mucosal pallor, petechiae, and erosions. The lesions can be distributed throughout the gastric mucosa but are predominantly identified in the body of the stomach. Bleeding is the clinical presenting sign in critically ill patients. The bleeding may be massive and life threatening. Prompt correction of the factors leading to the critical illness is the most important priority in management. Lesions resembling AGMLs are also observed in patients on chronic NSAID therapy. Up to 40% of patients using NSAIDs for a
chronic condition may have endoscopic evidence of gastritis, but evolution of the lesions to AGMLs with stigmata of bleeding is unusual. Significant bleeding from AGMLs is seen in fewer than 1% of all NSAID users. Hence, the NSAID-associated mucosal erosions are clinicopathologically distinct from the AGMLs of critical illness. Patients at risk for non-NSAIDassociated AGML include virtually all critically ill patients in medical and surgical ICUs. Particular risk factors include sepsis, respiratory failure, hemodynamic instability, coma following head injury or intracranial operation, burns covering more than 35% of body surface area, multiple trauma, cardiopulmonary bypass, and coagulopathy. The condition is particularly lethal in postoperative cardiovascular patients and in patients with sepsis and multiorgan failure. The pathogenesis of AGML is related to a combination of both gastric acid and activated pepsin injuring the gastric mucosa and is exacerbated by mucosal ischemia secondary to hypoperfusion. Activated pepsin is a proteolytic enzyme that directly digests the mucosal lining and is inactivated at a pH of approximately 4.5. This understanding has led to broad application of prophylaxis against stress ulceration in critical care practice. In fact, such prophylaxis has greatly diminished the incidence of major bleeding from this condition; thus, surgical intervention for control of bleeding is now a rare procedure.
Prophylaxis
AGML can be prevented by any of several strategies. The most widely applied methods involve neutralization of the contents in the gastric lake. Administration of antacids to maintain the intragastric pH above 4.0 is effective provided that dosing is at a frequency and volume sufficient to maintain the desired pH range. Antisecretory therapy with either H2 -receptor antagonists (multiple trials) and proton-pump inhibitor therapy (limited trials) is also efficacious, administered by either a continuous intravenous infusion or bolus dosing.[26] Again, pH monitoring is required to ensure efficacy because acid hypersecretion may be present in these patients, rendering conventional dosing inadequate. Despite the proven efficacy of gastric pH neutralization at reducing clinically significant bleeding, many intensivists have questioned whether this normalization contributes to nosocomial pneumonia by allowing bacterial colonization of the gastric lake. Although early trials appeared to confirm this fear, a more recent large comparative trial showed no increased incidence in pneumonia in patients receiving H2 -receptor therapy rather than sucralfate (while clinically important bleeding episodes were significantly decreased).[27] With these observations, the current recommendation regarding stress ulceration calls for gastric neutralization with either H2 -receptor antagonists or proton-pump inhibitors.
1254 DIAGNOSIS AND TREATMENT
AGMLs in hospitalized patients are heralded by gastrointestinal bleeding evidenced by hematemesis, nasogastric aspiration of blood or coffee ground like material, or an unexplainable drop in hematocrit. The magnitude of bleeding may be slight or massive; both forms tend to cease spontaneously with appropriate management, which includes resuscitation, transfusion, and correction of coagulopathy. Emergency evaluation with upper endoscopy, a procedure that should be completed in the ICU, is indicated. Careful attention to prevent aspiration and hypovolemia during the procedure is mandatory. Findings at endoscopy are characterized by diffuse petechiae, superficial erosions, and mucosal pallor. If a solitary site of bleeding is identified, endoscopic therapy, such as thermal or bipolar electrocoagulation, fibrin glue application, or injection therapy, is appropriate. Frequently, however, bleeding is too diffuse to allow endoscopic therapy. In this case, aggressive medical management with transfusion and component therapy to correct coagulation defects and anemia is indicated. Measures to correct hypoperfusion, hypovolemia, and gastric acid neutralization are also important elements of management. The role of angiography in stress ulceration is limited to diffuse, unremitting hemorrhage. Selective celiac catheterization may allow identification of the bleeding arteries of origin. Embolization with coils or collagen gel or selective intra-arterial infusion of vasopressin may arrest bleeding in up to 80% of patients provided that selective bleeding vessels can be identified.[28] Recurrent bleeding is common, however, and the mortality of patients with this degree of hemorrhage is in excess of 50%. Death ensues from multisystem failure precipitated by ongoing hemorrhage and recurrent shock. Surgery is rarely used to treat AGML. Only those patients who have failed aggressive medical management and endoscopic therapy and who have treatable critical illness are candidates for surgery. These are particularly challenging patients because they are critically ill with preexisting multisystem failure, sepsis, or other highly lethal conditions. Frequently, noncorrectable coagulopathy secondary to sepsis or hepatic failure is present. In the few patients that do come to surgery, the goal of surgery is hemostasis. At laparotomy, a generous gastrotomy is made to evaluate the sites of hemorrhage. In the unlikely finding of a single bleeding site or bleeding from only a few small sites, oversewing of these sites and truncal vagotomy and drainage are appropriate. Unfortunately, multiple sites are usually found, leaving only subtotal or near-total gastrectomy, with Roux-en-Y gastrojejunostomy as the only viable option. Regardless of surgical procedure, the postoperative mortality rate is high, in excess of 50%. Death is usually from multisystem organ failure.
Mallory-Weiss Tears
About 10% of cases of upper gastrointestinal hemorrhage are caused by Mallory-Weiss tears. The lesion is characterized by a tear in the proximal gastric mucosa near the esophagogastric junction. The clinical presentation is typified by an antecedent history of vomiting, retching, or coughing followed by hematemesis. The mean age for patients with this condition is older than 60 years; 80% are men. Alcoholism, disease-related bleeding diatheses, hiatal hernia, and NSAID use are frequently observed. Up to 10% of patients may have bleeding of sufficient magnitude to have hematochezia and hypotension as presenting signs. Up to 90% of these lesions stop bleeding spontaneously without specific intervention. Patients with cirrhosis and portal hypertension with coagulopathy are at greatest risk for morality, which overall averages 3%.[29] Initial assessment and treatment should include prompt history and physical examination, resuscitation, and endoscopic evaluation. The tear is typically located on the lesser curvature and measures 15 to 20 mm in length and 2 to 3 mm in width. Findings at initial endoscopy may reveal active bleeding or oozing, stigmata of recent bleeding, or a clean-based tear. Endoscopic therapy by either injection or thermal energy is efficacious in patients with active bleeding. Transfusion of packed red blood cells is required in 40% to 70% of patients. Patients with active bleeding at initial endoscopy and those with coagulation disorders are at greatest risk for rebleeding; roughly 30% bleed again within the first 24 hours. Rebleeding is rare in patients without coagulation disorders. Medical therapy includes acid reduction with antisecretory agents. Although this is not an acid-peptic condition, findings of associated gastritis are common in these patients. Surgery is rarely required for control of hemorrhage. If bleeding fails to stop after endoscopic therapy, laparotomy for oversewing of the mucosal tear through a high gastrotomy is appropriate. An acid-reducing procedure is not required. Rebleeding is most likely related to ongoing, or uncorrectable, coagulopathy; thus, aggressive, ongoing efforts to maintain a normal coagulation profile are needed.
Unusual Causes of Acute Upper Gastrointestinal Hemorrhage Esophageal Sources
The esophagus is the source of major hemorrhage in fewer than 3% of patients admitted for evaluation of acute upper gastrointestinal hemorrhage. The most common causes are infectious esophagitis, gastroesophageal reflux disease, Barretts epithelium, malignancy (including adenocarcinomas and squamous carcinomas), medication-induced erosions, Crohns disease, and radiation. Patients with human immunodeficiency virus (HIV) infection and other immunocompromised patients are at particular risk for infectious esophagitis, including erosive esophagitis caused by Candida albicans, other fungi, herpes simplex virus, cytomegalovirus, and mycobacterial infection. Bleeding may be massive, although episodes of less severe hemorrhage are typical. Therapy is targeted to the cause of bleeding. If active hemorrhage is identified, endoscopic electrocoagulation or heater probe therapy is usually effective in stopping hemorrhage, at least temporarily while definitive management
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is planned. Specific therapy is targeted to the etiology and includes appropriate antibiotics for infectious causes, proton-pump inhibitors for refluxassociated conditions, and definitive multimodality cancer therapies for malignant tumors. Sucralfate is a useful adjunct to specific therapies in patients with acute inflammatory conditions of the esophagus. Emergency surgery to control hemorrhage is rarely required. Treatment with definitive surgical management, resection for tumors, or antireflux therapy for patients with reflux-induced esophagitis is dictated by the specific cause of the hemorrhage.
Dieulafoys Lesion
Dieulafoys vascular malformations are rare causes of acute upper gastrointestinal hemorrhage. The lesions are unusually large submucosal or mucosal vessels found in the gastric mucosa, most commonly along the lesser curvature in the mid-stomach. The lesion is most frequently diagnosed in middle life and is not associated with identifiable factors for mucosal injury, vascular disease, or medical conditions. Bleeding occurs when superficial erosion into the vessel occurs, resulting in brisk, voluminous hemorrhage that ceases spontaneously. Endoscopic diagnosis is difficult because the lesion is rarely associated with an obvious ulcerated lesion. Rather, reliable diagnosis depends on fortuitous timely endoscopy during hemorrhage to allow visualization of bleeding from a pinpoint mucosal defect. Occasionally, the endoscopist may appreciate a vessel wall at the site of bleeding. If a lesion is definitively identified, the site should be marked endoscopically with India ink injection to allow precise surgical resection. Recurrent hemorrhage is common; often, several episodes occur before accurate diagnosis. Efforts at endoscopic ablation with sclerotherapy and electrocoagulation have not proved effective in the few reported series. Rather, appropriate definitive management calls for wedge resection of the gastric wall. Precise endoscopic localization of the lesion allows this limited resection in lieu of more extended blind gastric resection. Because the condition is not associated with peptic mucosal injury, vagotomy is not indicated.
Aortoenteric Fistula
Aortoenteric fistula is an uncommon condition in which an inflammatory tract develops between the aorta and the gastrointestinal tract. The fistula may develop as a primary process resulting from infectious aortitis, or inflammatory aortic aneurysm, or as a secondary process following aortic replacement with a synthetic graft for treatment of abdominal aortic aneurysm. The secondary aortoenteric fistulas are by far the more common cause, and this complication may develop in up to 1% of patients after aortic aneurysm repair. The fistulas characteristically develop between the proximal anastomosis and the overlying small bowel (duodenum or jejunum), although communication to the colon has also been noted. It is thought that a low-grade infection at the site of contact between the anastomosis and the bowel leads to the fistula formation. This diagnosis must be considered in any patient with acute gastrointestinal hemorrhage and a history of aortic surgery. The herald bleed, an episode of acute hemorrhage that ceases spontaneously, occurs hours to days prior to the inevitable exsanguinating hemorrhage that will ensue if the condition is not recognized and treated. Emergency upper endoscopy is mandatory for all patients with suspected aortoenteric fistula. If endoscopy is negative, computed tomography (CT) to look for evidence of inflammation at the aortic anastomosis is indicated. Others advocate emergency angiography, including lateral views, to identify the small mycotic aneurysm that is frequently present. Angiography should be pursued in all patients with negative CT scans. In patients with exsanguinating hemorrhage, emergency laparotomy with control of the proximal aorta is indicated. Effective surgical management calls for removal of the aortic graft and extra-anatomic vascular bypass to restore distal aortic flow.
ACUTE LOWER GASTROINTESTINAL HEMORRHAGE

Acute lower gastrointestinal bleeding is hemorrhage arising distal to the ligament of Treitz. The colon is the source of hemorrhage in more than 95% to 97% of cases, with the remaining 3% to 5% arising in small bowel sites. Lower gastrointestinal bleeding accounts for about 15% of major episodes of gastrointestinal hemorrhage and hence is much less common than upper gastrointestinal bleeding. The incidence of lower gastrointestinal bleeding increases with age, reflecting the parallel increase in acquired lesions responsible for colonic bleeding: diverticulosis and angiodysplasias. The differential diagnosis of acute lower gastrointestinal hemorrhage is shown in Box 442 .
Clinical Presentation
The hallmark of acute lower gastrointestinal hemorrhage is hematochezia; passage of bloody stool, blood, or blood clots per rectum. If bleeding is slower and of lesser volume, melena may also be a presenting sign, although this is more characteristic of an upper gastrointestinal source. Similarly, up to 15% of patients with massive hemorrhage from an upper gastrointestinal source may present with hematochezia, which is indicative of at least 1000 mL of hemorrhage over a short interval from an upper gastrointestinal source. Roughly half of patients present with both a decrease in hemoglobin and hematocrit and hemodynamic instability; 30% have orthostatic changes, 10% syncope, and 19% shock. Although lower gastrointestinal hemorrhage represents a genuine emergency, it is generally less life-threatening than upper gastrointestinal hemorrhage. Patients are less likely to present in shock, more likely to cease bleeding spontaneously, and usually have a lower transfusion requirement.
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Box 44-2. Differential Diagnosis of Lower Gastrointestinal Hemorrhage Diverticulosis Angiodysplasia Neoplasm Polyps Meckels diverticulum Inflammatory disorders Ulcerative colitis Crohns disease Infectious colitis Radiation-induced disorders Nonsteroidal anti-inflammatory drugassociated disorder Hemorrhoids Varices Dieulafoys lesions Osler-Weber-Rendu syndrome Aortoenteric fistula Vasculitis Mesenteric ischemia
Etiology
Unlike upper gastrointestinal hemorrhage, in which endoscopic findings can accurately identify mucosal lesions responsible for acute hemorrhage, validating the source of an episode of hemorrhage from the colon is more problematic. First, lower gastrointestinal hemorrhage is characterized by episodes of intermittent hemorrhage; bleeding may well have ceased by the time the diagnostic procedure is obtained. Second, up to 42% of patients are found to have multiple potential bleeding sources at the time of diagnostic evaluation. It is therefore important to have a clear understanding of the significance of findings on diagnostic evaluation and to keep in mind the limited certainty that may accompany some of these findings. The direct observation of a bleeding lesion or findings of stigmata of recent hemorrhage at endoscopy are required to establish a definitive diagnosis.[30]
Understanding the degree of certainty of a bleeding source is of great importance when contemplating surgical resection to treat hemorrhage.
Diverticulosis
Colonic diverticulosis represents the most common source of lower gastrointestinal hemorrhage, responsible for 40% to 55% of cases of hemorrhage in most series. Colonic diverticula are common acquired lesions of the abdominal colon. Although 40% of patients in the 5th decade of life have diverticula, this incidence rises to 80% by the 9th decade. Hemorrhage complicates 3% to 5% of patients with diverticulosis. The anatomic basis for bleeding is thought to be asymmetrical rupture of intramural branches (the vasa recta) of the marginal artery at the dome of the diverticulum or at its antimesenteric margin. It appears likely that luminal traumatic factors, including impacted fecaliths with abrasion of the vessels, lead to hemorrhage. Hemorrhage is rarely associated with the inflammation of clinical diverticulitis. Diverticular hemorrhage ceases spontaneously in up to 90% of patients. Transfusion of greater than 4 units of packed red blood cells is rare. Although left colon diverticula are more common, bleeding tends to be more common from right colon diverticular sources. Hemorrhage from right colon lesions may also be of greater rate and volume than that from left-sided diverticula. After an initial episode of hemorrhage, rebleeding is likely to occur in 10% of patients in the first year; thereafter, the risk for rebleeding increases to 25% at 4 years. Given the prevalence of colonic diverticulosis, and the fact that most episodes of hemorrhage tend to cease spontaneously, many episodes of lower intestinal hemorrhage are attributed to colonic diverticulosis as a presumptive rather than a definitive diagnosis.
Angiodysplasia
Angiodysplasias are responsible for 3% to 20% of cases of acute lower intestinal bleeding. Angiodysplasias, also referred to as arteriovenous malformations, are small ectatic blood vessels in the submucosa of the gastrointestinal tract. The overlying mucosa is often thin, and superficial erosion at the site of an angiodysplasia has been observed on histologic examination of surgical or autopsy specimens. Angiodysplasias are identified in 1% to 2% of autopsy evaluations and increase in frequency with the age of the patient. Angiodysplasias may occur throughout the gastrointestinal tract and represent the most common cause of hemorrhage from the small bowel in patients older than 50 years of age. Angiodysplasias are evident on colonoscopy as red, flat lesions about 2 to 10 mm in diameter. Lesions may appear stellate, oval, sharp, or indistinct. Colonoscopy is the most sensitive method to identify angiodysplasias, although angiography is also able to identify these lesions. The use of meperidine during colonoscopy may decrease the ability to identify angiodysplasias because of a reduction in mucosal blood flow. Another study has identified that the use of a narcotic antagonist may increase the size of angiodysplasias and enhance the detection rate. On angiography, angiodysplasias appear as ectatic, slowly emptying veins or as arteriovenous malformations with brisk, early venous filling. More than half of angiodysplasias are localized to the right colon, and bleeding from angiodysplasia correlates with this distribution. Angiodysplasias may be associated with many medical conditions, including end-stage renal disease, aortic stenosis, von Willebrands disease, and others. It is not clear whether this association reflects the greater tendency of angiodysplasias to bleed in these conditions or whether, in fact, angiodysplasias are more common structural findings in them.
Neoplasia
Colonic neoplasms, including adenomatous polyps, juvenile polyps, and carcinomas, present in a variety
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of manners. Typically, bleeding from these lesions is slow, characterized by occult bleeding and secondary anemia. These neoplasms can bleed briskly, however, and in some series, up to 20% of cases of acute hemorrhage are ultimately found to arise from colonic polyps or cancers. Juvenile polyps are the second most common cause of hemorrhage in patients younger than the age of 20 years.
Inflammatory Conditions
A wide variety of inflammatory conditions can cause acute lower gastrointestinal hemorrhage. Hemorrhage is rarely the presenting sign; rather, it develops in the course of the disease, and the cause is suspected based on the patients history. Up to 20% of cases of acute lower gastrointestinal hemorrhage may be due to one of these inflammatory conditions. Most episodes of bleeding cease spontaneously or with specific therapy directed at the cause. Hemorrhage complicates the course of ulcerative colitis in up to 15% of cases. Emergency colectomy for persistent hemorrhage accounts for 6% to 10% of emergency surgical colectomies in patients with this disease. Crohns disease is less likely to cause massive colonic hemorrhage and occurs in roughly 1% of patients with this condition. Infectious causes include Escherichia coli, typhoid, cytomegalovirus, and Clostridium difficile. Radiation injury is most common in the rectum after pelvic radiotherapy for prostate or gynecologic malignancies. Bleeding is most common 1 year after radiation treatments but may occur up to 4 years later. Patients with immunosuppression or acquired immunodeficiency syndrome (AIDS) are at risk for acute lower intestinal hemorrhage from a unique set of causes. Cytomegalovirus is the most common cause; Kaposis sarcoma, histoplasmosis, and perianal fistulas and fissures are also problematic and are more likely to hemorrhage in patients with AIDS-induced thrombocytopenia.
Vascular Causes
Vascular causes of acute lower intestinal hemorrhage include the vasculitides (polyarteritis nodosa, Wegeners granulomatosis, rheumatoid arthritis, and others), which are associated with punctate ulceration of the colon and small bowel. Colonic ischemia with mucosal ulceration and friability may also result in acute hemorrhage, often in the setting of acute abdominal pain and sepsis. Acute mesenteric ischemia may be heralded by an episode of hematochezia in the context of severe abdominal pain, preexisting vascular disease, arterial embolism risk, or hypercoagulability. Although hemorrhage is an element in the clinical management of these patients, only rarely does the control of hemorrhage become the major focus of therapy. Rather, restoration of visceral perfusion is the primary therapeutic objective.
Hemorrhoids
Hemorrhoids are usually noted on physical examination in more than half of patients with lower gastrointestinal hemorrhage. In fewer than 2% can the hemorrhage be attributed to these lesions, however. Unless unequivocal signs of bleeding are evident on anoscopy, investigation of the patient for another source of lower intestinal bleeding should be pursued. Patients with portal hypertension may develop massive hemorrhage from hemorrhoids, as can patients with HIV-associated thrombocytopenia with hemorrhoids.
Uncommon Causes
Rare causes of lower gastrointestinal hemorrhage include solitary rectal ulcer, Dieulafoys lesion of the colon, portal colopathy, NSAIDs,
intussusception, or bleeding following colonoscopic biopsy or polypectomy.

Initial Assessment
The initial history and physical examination are directed to determining the potential source of the hemorrhage and the severity of initial hemorrhage. Most cases eventually are determined to result from angiodysplasia or diverticulosis, both of which are usually asymptomatic before initial hemorrhage. Nonetheless, the initial history should exclude other, less common causes of the bleeding. Specific inquiry should be made regarding use of NSAIDs or anticoagulants. Abdominal pain or recent diarrhea and fever may point to colitis, either infectious or ischemic. Patients with prior aortic surgery should be considered to have an aortoenteric fistula until proved to the contrary. Prior radiation therapy for pelvic malignancy may indicate radiation proctitis. Recent colonoscopy may suggest bleeding from a biopsy or polypectomy site. The cause of previous episodes of bleeding should be elicited, as should the possibility of a history of inflammatory bowel disease. Family history of polyposis syndromes or colonic malignancy may also be pertinent. Young patientsthose less than 30 years of ageare at greatest risk for bleeding from Meckels diverticula or intestinal polyps. Physical examination should include measurement of orthostatic vital signs in patients without overt shock. All patients should be resuscitated, as outlined in the previous section. Pertinent findings on physical examination may include scars from previous abdominal incisions, the presence of abdominal masses, or skin and oral lesions suggestive of polyposis syndromes. Stigmata of cirrhosis suggestive of bleeding from hemorrhoids or varices secondary to portal hypertension should be considered. The rectal examination is important to identify any anorectal pathology, including tumors, ulcers, or polyps. The color of the rectal contents and the presence of formed stool or blood clot should also be noted. Anoscopic examination to exclude hemorrhage from hemorrhoids should be completed. A nasogastric tube should be inserted to look for blood or coffee groundlike material to exclude an upper gastrointestinal source. In patients with hematochezia and hemodynamic instability, emergency upper endoscopy is required.
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Diagnosis
Emergency surgical intervention for ongoing massive hemorrhage is rarely necessary before attempts are made to localize the precise source of bleeding. This allows an orderly approach to identification of the bleeding site, which is essential for appropriate therapy. After the patient has been resuscitated and stabilized, diagnostic testing should begin. The choice of initial investigation remains controversial and is dependent to some degree on local availability of procedures and expertise. The three options for primary diagnostic testing are colonoscopy, selective visceral angiography, and technetium 99m (99m Tc)-labeled red blood cell scintigraphy. An algorithm for diagnosis of acute lower gastrointestinal bleeding is shown in Figure 44 5.
Colonoscopy
Recognition that most episodes of hemorrhage cease spontaneously and that stigmata of bleeding are subtle has led to efforts to perform colonoscopy as early as possible in the course of evaluation. Urgent colonoscopy, completed within 12 hours of admission, is indicated in patients who have ceased to have ongoing significant hemorrhage and in whom resuscitation and hemodynamic stability have been achieved. In this setting, colonoscopy can be completed after colonic purging.[31] Positive findings on colonoscopy include identification of an active bleeding site, identification of a nonbleeding visible vessel, clot adherent to a diverticular ulcerated orifice, clot adherent to a discrete focus of mucosa, or fresh blood localized to a colonic segment. Similarly, the finding of fresh blood
Figure 44-5 Diagnostic steps in the evaluation of acute lower gastrointestinal hemorrhage. RBC, red blood cell; UGI, upper gastrointestinal. (Modified from Turnage RH: Acute gastrointestinal hemorrhage. In Greenfield LJ, Mulholland MW, Oldham KT [eds]: Surgery: Scientific Principles and Practice. Philadelphia, Lippincott-Raven, 1997, p 1158.)
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only in the terminal ileum after a negative upper endoscopy strongly suggests the small bowel as a bleeding source. It is important that incidental lesions, such as blood clots in multiple diverticular orifices, nonbleeding arteriovenous malformation, nonbleeding polyps, and nonbleeding diverticula, are not concluded to be the site of recent hemorrhage. Hemorrhage can be attributed only to lesions with clear stigmata of bleeding. Patients presenting with massive lower gastrointestinal hemorrhage are poor candidates for emergency colonoscopy. The procedure is technically difficult because of the inability to clear the mucosal surfaces of old or new hemorrhage. Finding a discrete, actively bleeding vessel in the unprepared bowel is difficult even for the most experienced endoscopist. Second, patients with massive hemorrhage have hemodynamic instability, precluding the use of sedation and increasing the risk for hypoxemia and complication. Further, resuscitation may be compromised during the procedure. Hence, colonoscopy is most appropriately used as the initial diagnostic procedure in patients presenting with acute hemorrhage that has ceased or in patients with a more moderate degree of bleeding. Colonoscopy is the procedure of choice in patients who develop hemorrhage after colonoscopic polypectomy.
Selective Visceral Angiography
Mesenteric arteriography has been widely used in the evaluation and treatment of patients with lower gastrointestinal hemorrhage. Selective injection of radiographic contrast into the superior mesenteric or inferior mesenteric arteries identifies hemorrhage in patients bleeding at a rate of 0.5 mL/min or greater. The study can accurately identify arterial hemorrhage in 45% to 75% of patients if they are actively bleeding at the time of contrast injection. Given the characteristic intermittent bleeding seen in lower gastrointestinal hemorrhage associated with diverticulosis, arteriovenous malformations, and other causes, bleeding may have ceased by the time of the study. Some radiologists have advocated evocative testing, including intra-arterial vasodilators, heparin, and fibrinolytic agents, in an effort to identify a bleeding source accurately. This approach does not appear to be warranted except in patients with refractory intermittent episodes of hemorrhage in a fully staffed suite. Because 90% of cases of hemorrhage cease spontaneously, and only 10% rebleed, such evocative testing is inappropriate for most patients. About 10% of patients develop a complication of angiography. Major complications include stroke, renal failure, femoral artery thrombosis, lower extremity immobilization, and hematoma formation. Given that most patients with lower gastrointestinal hemorrhage are older than 60 years of age, medical comorbidities, including vascular disease and renal insufficiency, may place these patients at high risk for the procedure. Hence, angiography is reserved for patients with evidence of significant ongoing hemorrhage.
Technetium 99m-Red Blood Cell Scintigraphy
Tc-red blood cell scintigraphy has met with mixed success in the diagnosis of lower gastrointestinal hemorrhage. In this noninvasive nuclear medicine imaging procedure, the patients red blood cells are labeled with a technetium isotope and reintroduced into the circulation. With each
99m
bleeding episode, labeled blood is shed into the colonic lumen, creating an isotopic focus that can be imaged with whole abdominal scintigraphy. Rates of bleeding as low as 0.1 mL/min can be detected. Images are obtained at distinct intervals after injection, within the first 2 hours, and thereafter at 4- to 6-hour intervals, or at the time of clinical evidence of rebleeding.[29] After extravasation into the lumen, the blood moves through the colonic lumen, generally from the right colon to the left, but occasionally in retrograde fashion because of colonic contractions. If bleeding is present at the time of injection and initial imaging, 99m Tc-red blood cell scans can accurately identify a source of bleeding in up to 85% of cases.[32] If bleeding is not active at the time of the initial study, or if delayed bleeding occurs, subsequent imaging to detect the luminal isotope can be inaccurate because of the sporadic movement of the tracer in the gut lumen.[33] The study is accurate in only 40% to 60% of patients, little better than a 50:50 ratio, to isolate bleeding to the left or right colon. Hence, patients in whom a surgical resection is anticipated to control recurrent or persistent hemorrhage should have the bleeding confirmed with either a positive angiogram or a positive colonoscopy. The red blood cell scans serve primarily to target the subsequent confirmatory study.
Treatment
Endoscopic Treatment
Endoscopic therapy includes the use of the same modalities available for upper gastrointestinal hemorrhage. Thermal heater probes, electrocoagulation, and sclerotherapy have been used. Reports suggest that electrocoagulation can be successfully applied for bleeding colonic diverticula, although this approach has not been widely embraced. Efforts at endoscopic control of diverticular hemorrhage may precipitate more significant bleeding. In contrast, angiodysplasias are readily treated with endoscopic measures. Acute bleeding can be controlled in up to 80% of patients with bleeding angiodysplasias, although rebleeding may develop in up to 15%. Care must be taken to avoid precipitating massive hemorrhage when treating angiodysplasias. Many endoscopists recommend approaching the lesion from the perimeter, obliterating feeder vessels before cauterization of the central vessel. Endoscopic therapy is also appropriate for patients with bleeding from a recent snare polypectomy site. Bleeding develops in 1% to 2% of patients after polypectomy and may occur up to 2 weeks after polypectomy. An endoscopic approach is recommended for these lesions.
1260 Angiographic Treatment
In patients whose bleeding source is identified by angiography, a trial of angiographic therapy may be appropriate as a perioperative temporizing measure or as a definitive measure for high-risk surgical candidates.[34] Provided selective catheterization of a mesenteric vessel leading directly to the bleeding site can be completed, intra-arterial vasoconstrictor therapy with vasopressin can temporarily achieve control of bleeding in up to 80% of patients. Rebleeding is common, however, after discontinuing the therapy. Complications are frequent and serious and include myocardial ischemia, pulmonary edema, mesenteric thrombosis, and hyponatremia. Transarterial vasopressin should not be used in patients with coronary artery disease or other vascular disease. The primary role of this therapy is to achieve temporary control of bleeding before emergency definitive surgical resection. Transcatheter embolization of massive bleeding may also be used for patients who are poor candidates for surgical resection. Embolization of gelatin sponges or microcoils can achieve temporary control of bleeding from angiodysplasias and diverticula. Given the lack of collateral blood supply to the colonic wall, these procedures may be complicated by colonic infarction heralded by abdominal pain, fever, and sepsis. Hence, like vasoconstrictive therapy, this procedure should be restricted to patients who cannot tolerate surgery or as a temporizing measure in massive hemorrhage in patients for whom a definitive surgical resection is imminent.
Surgery
Surgery is indicated for patients with ongoing or recurrent hemorrhage. Transfusion of more than 6 units of packed red blood cells, ongoing transfusion requirement, or persistent hemodynamic instability is an indication for colectomy in acute hemorrhage. Patients who develop recurrent lower gastrointestinal hemorrhage are also appropriately treated with colectomy because the risk for subsequent hemorrhage increases with time. Segmental colectomy is indicated in patients with persistent or recurrent colonic hemorrhage. Every effort should be made to localize the source of bleeding so that a hemicolectomy can be performed rather than a blind subtotal abdominal colectomy. Certainty of the site of bleeding is important; operation based on a positive 99m Tc-red blood cell scan alone can result in recurrent hemorrhage in up to 35% of patients. Blind total abdominal colectomy carries significantly higher perioperative morbidity, and associated mortality rates approach 25% in some series. Diarrhea and rapid transit after total abdominal colectomy can also be debilitating conditions for elderly patients. There is no indication for a blind segmental colectomy, for which rebleeding rates as high as 75% are seen. Mortality after colectomy for acute lower gastrointestinal hemorrhage overall is less than 5%. As in upper gastrointestinal hemorrhage, bleeding is not the cause of death; rather, pneumonia, cardiovascular events, and renal failure lead to poor outcomes, primarily in elderly patients with recurrent hemorrhage. Thoughtful timely management can lead to a successful outcome in most patients.
ACUTE GASTROINTESTINAL HEMORRHAGE FROM AN OBSCURE SOURCE

The small bowel is a rare source of acute hemorrhage. Only 2% to 5% of patients with acute gastrointestinal hemorrhage are ultimately determined to have bled from a small intestinal source. This low frequency is fortunate because the small bowel is a difficult organ to visualize and precise detection of the bleeding lesion is characteristically delayed.
Clinical Presentation
The clinical presentation of patients with acute small bowel hemorrhage is similar to that of acute lower gastrointestinal hemorrhage from a colonic source. Small bowel hemorrhage is frequently episodic, characterized by recurrent brisk hemorrhage, which ceases spontaneously only to recur weeks or months later. Most patients are evaluated on multiple occasions after multiple bouts of hemorrhage before a correct diagnosis is made and effective definitive therapy completed.[35] Szold and associates[36] reported that the typical patient referred with acute gastrointestinal hemorrhage of obscure origin had intermittent episodes of hemorrhage during a 26-month period, had undergone 1 to 20 diagnostic tests, and had received an average of 20 units of packed red blood cells before diagnosis.
Etiology
The causes of hemorrhage identified in the 71 patients as studied by Szold and associates are shown in Table 444 . In adults the most common source of bleeding from the small bowel is angiodysplasia, responsible for 50% to 75% of cases in older patients, and 30% to 40% of those in younger patients. These acquired lesions are most common in the right colon but can be found throughout the gastrointestinal tract.[37] The telangiectasias of Osler-WeberRendu syndrome are distinct from angiodysplasias. Most patients with this hereditary disorder present with skin and oral lesions in youth and acquire gastrointestinal lesions with bleeding in the 4th decade of life, or later. These telangiectasias are diffuse, and surgical intervention is not appropriate. Small bowel tumors are the second most common source of bleeding (25%) and include collectively gastrointestinal stromal tumors, lymphomas, adenocarcinomas, carcinoids, and metastatic melanomas. Less common possibilities include Meckels diverticulum (more common in children), small bowel diverticula, Crohns disease, radiation enteritis, ulcers due to NSAIDs, celiac sprue, and other rare findings.
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TABLE 44-4 -- Sources of Obscure Gastrointestinal Bleeding: Findings in 71 Patients Treated with Surgery Diagnosis Arteriovenous malformation Small bowel leiomyoma Small bowel adenocarcinoma Small bowel lymphoma Crohns disease Watermelon stomach Meckels diverticulum Small bowel leiomyosarcoma Metastatic colon carcinoma to small bowel Small bowel varices Small bowel melanoma Others Total From Szold A, Katz L, Lewis B: Surgical approach to occult gastrointestinal bleeding. Am J Surg 163:9093, 1992.
Initial Assessment
Patients (%) 40 11 7 6 6 4 4 3 3 3 3 10 100
Initial priorities in management are resuscitation followed by prompt diagnostic testing as described for patients with lower gastrointestinal bleeding. Emergency upper endoscopy is indicated in hemodynamically unstable patients with hematochezia; patients with melena should have nasogastric aspiration to check for blood in the gastric contents. If negative, selective visceral angiography or emergency colonoscopy should be completed based on the clinical assessment of the rate and degree of bleeding. The role of 99m Tc-red blood cell scintigraphy remains controversial, as in lower gastrointestinal hemorrhage. In the rare patient with significant, ongoing small bowel bleeding at the time of these initial evaluations, a positive small intestinal source may be identified. Colonoscopy may reveal hemorrhage coming through the ileocecal valve or pooling in the terminal ileum, whereas selective mesenteric angiography may reveal the bleeding source from any of many possible small bowel sources. Obviously, it is critical not only to identify the small bowel as the source of hemorrhage but also to identify the precise site within the small bowel, so that a limited bowel resection can be completed. In most patients, however, bleeding has ceased before the time these studies are completed, and only aggressive subsequent evaluation allows definitive diagnosis and treatment. Primary surgical exploration without investigation is to be condemned because the surgeon is rarely able to identify the actual source of small intestinal bleeding by visual inspection or palpation. Undirected exploration has a high risk of failure and should not be pursued except in patients with acute exsanguinating hemorrhage.
Diagnosis
The diagnostic evaluation of a patient with suspected bleeding from a small bowel source can be laborious and frustrating. Most of these patients have
already undergone many of the more common and previously described modalities without success. The choice of diagnostic test varies depending on the particular presentation of the patient.
Spiral Computed Tomography
CT scanning with intravenous and oral contrast medium is a noninvasive diagnostic tool that is particularly useful if there is concomitant abdominal pain or symptoms of obstruction. CT images can identify areas of bowel thickening, mass lesions, or extraintestinal lesions that may be contributing to the patients overall symptoms. These structural changes may be diagnostic of tumor, inflammatory conditions, or diverticula.
Enteroclysis
Enteroclysis is a small bowel contrast imaging study that can correctly identify mass lesions and structural mucosal processes, such as inflammatory or ulcerated lesions, in up to 80% of cases. It is unable, however, to identify angiodysplasias, the most common source of bleeding in these patients. Though still popular at some institutions, enteroclysis is poorly tolerated by patients and many centers have abandoned its use. When used strictly to evaluate the source of occult small intestinal bleeding, enteroclysis has a reported yield of only 10% to 21%. The ordinary small bowel follow-through contrast study is not adequate to evaluate these patients and should not be used, with a reported diagnostic yield of only 0 to 5.6%.[38]
Meckels Scans
Meckels diverticula may contain ectopic acid-secreting gastric mucosa that can lead to ulceration of the adjacent small bowel mucosa. The parietal cells in the gastric mucosa take up 99m Tc pertechnetate, allowing imaging by a gamma camera. Congenital duplications of the intestinal tract may also contain ectopic gastric mucosa and be imaged with this test. This procedure should be the initial evaluation in young patients (those <30 years of age), in whom Meckels diverticulum is the most common cause of small intestinal bleeding.
Small Bowel Endoscopy
Small bowel endoscopy, enteroscopy, has historically been completed by two methods. However, the recent introduction of video capsule endoscopy has greatly diminished the use of these technically challenging procedures. Push small bowel endoscopy uses a pediatric colonoscope to visualize the proximal small bowel directly.[39] The procedure is of limited value because only the proximal jejunum and duodenum can be visualized, even by skilled endoscopists. The Sonde (pull) enteroscopy has been abandoned in the United States. In
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this interesting historical method, a small fiberoptic imaging scope was pulled through the small bowel lumen by peristalsis to the ileocecal valve. Several hours later, the enteroscope was slowly pulled back through the intestine, and a careful inspection of the mucosa was completed through the 120-degree vision angle lens.[35] Although fine mucosal lesions and angiodysplasias could be identified with this technique, localization and therapy could not be accomplished.
Video Capsule Endoscopy
The Given wireless video capsule endoscope is an 11 26-mm capsule containing a miniature video camera, light source, battery, and transmitter.[40] It transmits video images to a torso-mounted recorder system at a rate of two images per second, up to 50,000 images overall, after being swallowed by the patient. The lens yields an 8-to-1 magnification, and the capsular coating prevents intestinal contents from interfering with the images. Relative contraindications include obstructive symptoms, motility disorders, and pacemakers. The major complication is capsule retention, which can occur at a stricture and has been reported in 5% of cases, although less than 1% of all mandated surgical retrieval.[41] Although it has not been available for long, in preliminary reports it has proven far superior to push endoscopy in diagnosis, and is tolerated much better as well. It does not have the capacity for therapeutic interventions as yet, nor can precise localizations within the bowel be achieved. It is, however, valuable in identifying diffuse disease that would not be amenable to surgical exploration and for identifying lesions for surgical or medical treatment. It is also an appropriate test to identify potential small bowel lesions prior to intraoperative endoscopy.
Intraoperative Endoscopy
A combined surgical and endoscopic procedure to evaluate and treat the small bowel sources of bleeding offers the best strategy for success. During exploratory laparotomy, small bowel enteroscopy is completed by an endoscopist. The operating surgeon carefully plicates the small bowel over the enteroscope while the lumen is visualized. The operating room lights are dimmed to image angiodysplasia better by transillumination. Identification of a mucosal ulcerated lesion or a single or multiple angiodysplasia allows definitive surgical treatment with small bowel resection. This combined approach may identify a bleeding source in up to 70% of patients; in patients with prior findings noted on video capsule endoscopy or angiography, the precise site of the abnormality can be identified to allow limited small bowel resection.
Treatment
The most common cause of small bowel bleeding, angiodysplasia, should be treated with endoscopic sclerotherapy or coagulation, if the lesion is within reach of the endoscope. For those in whom endoscopic measures fail, surgical segmental resection of the small bowel is indicated. Because angiodysplasias are acquired with age, up to 25% of patients develop new hemorrhage from other angiodysplasias in subsequent years; thus, long-term follow-up is required. With both these and with telangiectasias some success with conjugated estrogen therapy to decrease the frequency and degree of hemorrhage has been reported. Neoplasms are the second most common cause of small intestinal hemorrhage. Most are benign, although malignant tumors may also bleed. Therapy is surgical resection. Bleeding Meckels diverticulum and small bowel diverticula are also appropriately treated with resection as well.
RARE CAUSES OF GASTROINTESTINAL HEMORRHAGE FROM AN OBSCURE SOURCE Acute gastrointestinal hemorrhage from an obscure source has been reported to occur from a variety of conditions. These include radiation enteritis, small intestinal varices, Crohns disease, tuberculosis, syphilis, typhoid, histoplasmosis, vasculitis, small bowel ulcerated lesions in patients with gastrin-secreting tumors, and Dieulafoys lesions. Medical treatment is appropriate for most infectious causes and in patients with Zollinger-Ellison syndrome. Enterectomy is required in the other conditions. Disorders of the pancreas can cause acute gastrointestinal hemorrhage as blood is delivered into the duodenum through the pancreatic duct. Such bleeding has been reported in the setting of acute pseudoaneurysms after pancreatectomy and in pancreatic tumors. Bleeding is a rare complication of these disorders. Angiography may confirm the presence of a pseudoaneurysm and allow angiographic embolization for acute hemorrhage control. Pancreatic resection may be appropriate, depending on the clinical condition. The liver may also be the source of presumed acute gastrointestinal hemorrhage. Bleeding into the hepatic duct presents as gastrointestinal hemorrhage as blood enters the duodenum from the common bile duct, a condition known as hemobilia. Hemobilia has been reported to occur secondary to hepatic trauma with intrahepatic hematoma, hepatic aneurysms or other vascular malformations, hepatic tumors, hepatic abscess, or after hepatic resection or percutaneous liver biopsy. This diagnosis is usually considered when endoscopic visualization during acute hemorrhage shows blood entering the duodenum at the ampulla of Vater, depending on the clinical scenario. Selective visceral angiography is usually required to define the source and often allows definitive management by intra-arterial embolization.
Selected References
Church NI, Palmer KR: Ulcers and nonvariceal bleeding. Endoscopy 35:2226, 2003. This review article details the current strategies for managing patients with bleeding peptic ulcer based on a detailed analysis of the reported clinical experience. The cited references are excellent.
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Kollef MH, Canfield DA, Zuckerman G: Triage considerations for patients with acute gastrointestinal hemorrhage admitted to a medical intensive care unit. Crit Care Med 23:1048 1054, 1995. This important paper identifies clinical parameters, independent of endoscopic findings, to predict adverse outcome for patients with acute gastrointestinal hemorrhage and provides an algorithm for triage considerations. Rikkers LF: The changing spectrum of treatment for variceal bleeding. Ann Surg 228:536546, 1998. This paper, which will become a classic, details a single surgeons experience in managing patients with acute gastrointestinal hemorrhage secondary to portal hypertension. The authors contributions have defined the approach to the management of these patients during the past 4 decades, and the evolution of his current treatment strategy is presented. Vernava AM, Moore BA, Longo WE, et al: Lower gastrointestinal bleeding. Dis Colon Rectum 40:846858, 1997. This paper offers a complete summary of evaluation and work-up for lower gastrointestinal bleeding. Wara P: Endoscopic prediction of major rebleeding: A prospective study of stigmata of hemorrhage in bleeding ulcer. Gastroenterology 88:12091214, 1985. This classic paper describes the now widely embraced classification system for endoscopic stigmata that predict the risk for recurrent hemorrhage in patients with bleeding peptic ulcer. Wolfe MM, Lichtenstein DR, Singh G: Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. N Engl J Med 340:18881899, 1999. This review summarizes the pathogenesis on nonsteroidal anti-inflammatory druginduced gastrointestinal complications. Zuckerman GR, Prakash C, Askin MP, et al: AGA technical review on the evaluation and management of occult and obscure gastrointestinal bleeding. Gastroenterology 118:201 221, 2000. This paper provides a great summary of evaluation protocols in these patients.
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N, Amoateng-Adjepong Y, Qamar A, et al: Myocardial infarction in critically ill patients presenting with gastrointestinal hemorrhage: Retrospective analysis of risks and outcomes. Chest 114:11371142, 1998. RJ, Hagino RT, Jackson MR, et al: Gastrointestinal complications after aortic surgery. J Vasc Surg 28:404412, 1998.
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L, Peterson WL: Bleeding peptic ulcer. N Engl J Med 331:717727, 1994. MM, Lichtenstein DR, Singh G: Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. N Engl J Med 340:18881899, 1999. L, Connors LG, Reicin A, et al: Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use. Gastroenterology 124:288292, 2003. E: Building a better aspirin. Science 280:11911192, 1998.
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22. Lau JY, Sung JJ, Lam YH, et al: Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med 340:751756, 1999. 23. Rockall TA: Management and outcome of patients undergoing surgery after acute upper gastrointestinal haemorrhage. Steering Group for the National Audit of Acute Upper Gastrointestinal Haemorrhage. J R Soc Med 91:518523, 1998. 24. Imhof
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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

Chapter 43 - Acute Abdomen

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

ANATOMY AND PHYSIOLOGY

Urologic Ruptured bladder Hematologic Ruptured spleen

Figure 43-2 Pain from intra-abdominal viscera.

Copyright 2004 Elsevier Inc. All rights reserved.

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

Figure 43-3 Common causes of abdominal pain.

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

ACUTE ABDOMINAL PAIN

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

Copyright 2004 Elsevier Inc. All rights reserved.

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

Copyright 2004 Elsevier Inc. All rights reserved.

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

3. Owens 4. Yusuf 5. Graff

10. Buschard 11. Gilbert

12. Nathens 13. Rotstein 14. Boey 15. Van

16. Blennerhassett 17. Miller

19. Taourel 20. Rao

21. Morris 22. Jeffrey

23. Araghizadeh 24. White

26. Sugarbaker 27. Navez 28. Chung

30. Paterson-Brown 31. Salky

33. Vander 34. Gurbuz

38. Gagne 39. Bizer

41. Scott-Conner 42. Parente

Copyright 2004 Elsevier Inc. All rights reserved.

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

Chapter 44 - Acute Gastrointestinal Hemorrhage

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

ACUTE UPPER GASTROINTESTINAL HEMORRHAGE

bleeding; AGML, acute gastric mucosal lesions; OR, operating room.

appropriate for these patients. Despite the risks, endoscopy is essential.

1015 2530 1215 3035 610 1820 2834

Bleeding Caused by Portal Hypertension

1254 DIAGNOSIS AND TREATMENT

Unusual Causes of Acute Upper Gastrointestinal Hemorrhage Esophageal Sources

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Townsend: Sabiston Textbook of Surgery, 17th ed., Copyright 2004 Elsevier

ACUTE LOWER GASTROINTESTINAL HEMORRHAGE

intussusception, or bleeding following colonoscopic biopsy or polypectomy.

1260 Angiographic Treatment

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