An accurate history is essential. Description of the onset and character of the pain as well as exacerbating or relieving factors is helpful in diagnosis. All conscious patients should be asked to localize the pain to a discreet site with one finger. Acute abdominal pain awakening patients from sleep or
persisting more than 6 h frequently represents a surgical problem. Acute abdominal pain generally arises from one of three mechanisms: (a) visceral ischemia, (b) serosal inflammation, or (c) distention of a hollow viscus. Pain of sudden onset suggests a vascular catastrophe or perforation of a hollow viscus. Pain of gradual onset that builds to a crescendo is more typical of hollow viscus overdistention, as is intermittent pain in a “colicky” pattern. Steady pain suggests serosal inflammation, especially when it is markedly exacerbated by changes in position or local pressure (e.g., rebound tenderness). A pleuritic component raises the possibility that an “intra-abdominal process” either abuts the inferior surface of the diaphragm or actually extends into the chest. (This is why lower-lobe pneumonia, empyema, and pericarditis may be mistakenly diagnosed as an acute abdominal process.) Pain associated with hip flexion and that radiating to the back suggests a retroperitoneal process.

New symptoms associated with the pain, such as nausea or vomiting, or change in bowel or urinary habits are extremely helpful. For obvious reasons, a history of hematemesis or hematochezia is informative. A detailed gynecologic history is essential in all female patients with special attention to previous gynecologic problems or change in menstrual habits.

The patient’s resting position can be a clue to the cause of abdominal pain: patients with peritonitis often lie motionless because any movement exacerbates pain; those with pancreatitis get relief by sitting up and leaning forward and are often found in this position. Patients with biliary colic or nephrolithiasis often are unable to remain still, writhing in pain. The abdomen should first be examined visually, then auscultated, percussed, and finally palpated. Inspection may reveal the distention of ileus, ascites, or mass; or the discoloration of Grey-Turner’s or Cullen’s signs of pancreatitis. Auscultation may reveal a silent abdomen in established peritonitis, high-pitched bowel sounds of partial bowel obstruction, or perhaps even a friction rub associated with splenic infarct or pneumonia. Percussion can distinguish distention from gas (tympany) and ascites, blood, or tumor (dullness), and in a patient with peritonitis, the reaction to percussion may obviate the need for deep palpation. Palpating the abdomen as the first part of the examination is likely to produce voluntary guarding or induce bowel sounds, even in patients with severe ileus. The most painful area of the abdomen should be examined last. Rectal and pelvic examinations must be performed. Rectal examination may detect colonic impaction, tumor, GI bleeding, and the localized tenderness of retrocecal appendicitis. Pelvic examination should search for evidence of pregnancy, fallopian tube infection, and ovarian masses. When completed, the abdominal examination should answer the following questions: (a) Is there rebound tenderness? (b) Are the bowel sounds absent? (c) Are there palpable masses? (d) Is there evidence of free air or fluid in the abdomen? An affirmative answer to any of these questions strongly indicates that surgical intervention will be necessary. Peritoneal signs are the most reliable in predicting the need for urgent laparotomy. The development of shock in a patient with an acute abdomen is also highly indicative of a need for surgery.

Routine laboratory tests are rarely diagnostic. Although nonspecifically elevated leukocyte counts and white cell differentials may be normal even with severe intra-abdominal disease, a reduced packed cell volume (PCV) is indicative of either slow chronic blood loss or acute severe hemorrhage with volume replacement. The serum amylase and lipase can be helpful if pancreatitis is suspected, but both false-negative and false-positive results occur. Similarly, elevations in hepatic transaminase, bilirubin, or alkaline phosphatase levels suggest liver disease but are nonspecific. Although commonly done, separate determinations of conjugated and unconjugated bilirubin are of little value. The combination of an acutely elevated bilirubin and alkaline phosphatase is probably most helpful, suggesting obstructive biliary tract disease. A triad of hyperkalemia, hyperphosphatemia, and metabolic (lactic) acidosis (in the absence of renal failure) suggests well-advanced bowel infarction. Bladder pressure measurements should also be considered if abdominal compartment syndrome (ACS) is a possibility. Because ectopic pregnancy represents a potentially fatal cause of abdominal and pelvic pain, and an intrauterine pregnancy dictates some diagnostic and management choices, a rapid, sensitive pregnancy test should be obtained in the evaluation of any potentially fertile woman.

The abdominal radiograph may provide clues to the etiology and urgency of acute abdominal pain and is discussed in detail in Chapter 11; however, a few salient points will be reviewed here. In patients with acute abdominal pain, supine and upright films of the abdomen may be helpful but are rarely diagnostic. For example, even when the film reveals “free air,” such a finding does not guarantee gut perforation and furthermore does not localize the site of perforation. (Free air may be the result of pulmonary barotrauma with intra-abdominal dissection of air.) Similarly, finding multiple air fluid levels in small bowel does not precisely identify the site of nonpathologic cause of bowel obstruction. Radiographic signs that should be sought include (a) calcification, (b) mass effect, (c) extraluminal gas, (d) obliteration of normal soft tissue planes, (e) localized ileus, (f) thumbprinting of bowel, and (g) evidence of gas in the biliary tree. Because it is difficult, if not impossible, to obtain upright films in the critically ill, lateral decubitus views usually must be substituted. An upright chest radiograph should also be reviewed in all patients with acute abdominal pain to look for subdiaphragmatic air or a lower-lobe pneumonia.

Ultrasound (US) examination utilizes highfrequency sound energy to define anatomic structure and, when combined with Doppler technology, characterizes blood flow. Because wound dressings, adipose tissue, and air-tissue interfaces deflect ultrasonic energy, US is a poor imaging mode for the obese or in patients with prominent bowel distention or abdominal surgical dressings. US also suffers from the problem that the views it generates are difficult to interpret by the nonradiologist (unlike computed tomographic [CT] images). US has the desirable features of being portable, rapidly accomplished, relatively inexpensive, and devoid of ionizing radiation and contrast media.

US is an excellent method for detecting pelvic processes in women (e.g., ectopic or intrauterine pregnancy, ovarian cysts, or pelvic tumors) and staging normal pregnancy. Likewise, because a bowel gas interface does not usually need to be crossed by the beam in the right upper quadrant, US is outstanding for viewing the liver and gallbladder. Thus, US is an excellent method to detect cholelithiasis, biliary tract dilation, and pericholecystic fluid or edema. Clear images of the kidneys and ureters can also be routinely obtained because they can be imaged from the rear, avoiding overlying bowel gas. The presence or absence of bowel gas makes visualization of the pancreas inconsistent. With the exceptions of imaging the right upper quadrant, pelvis, and kidneys, CT is superior to US for imaging the abdomen.

Because the abdominal CT now provides amazing image quality with high sensitivity, it has supplanted most other imaging modalities and, in many situations, is more useful than the physical examination in the ICU population. The CT scan requires transport of the patient to the radiology suite, but in contrast to magnetic resonance scanning, it offers dramatically more rapid imaging and is not precluded by the presence of metallic devices. CT images are easier to interpret than sonograms, especially for the nonradiologist, and they offer high-resolution views of essentially every intraabdominal and retroperitoneal structure. Enteral contrast material is required to distinguish bowel from other gas or fluid-filled structures like abscesses, but in many cases, nephrotoxic intravenous (IV) contrast can be avoided. The CT scan does have some disadvantages, however; it requires ionizing radiation and iodinated contrast material to evaluate vasculature. If searching for gallstones, or pelvic processes in a woman, US is as good an imaging modality.

The magnetic resonance imaging (MRI) has significant limitations in the ICU patient population because of the requirement for transport to the scanner, the relatively long scanning times, the need for a motionless patient, and the prohibition of metallic support devices. Brain and soft tissue detail, however, is superb. A major problem recognized with MRI since the last edition of this text is the syndrome of fibrosing nephrogenic dermopathy following gadolinium contrast administration to patients with renal insufficiency.

The performance of biliary tract scans relies on the use of a radioactive analog of iminodiacetic acid (HIDA) that, after administration, is taken up by
the liver and secreted into the bile, where it outlines the major intrahepatic ducts, gallbladder, and common bile duct. Radionuclide scans (“IDA” scans) are sensitive but lack specificity for biliary tract inflammation, particularly in the absence of gallstones. The high sensitivity of these tests renders them useful for excluding the diagnosis of cholecystitis, provided an adequate study is obtained. Failure to visualize the gallbladder may result from obstructive biliary tract disease, starvation, total parenteral nutrition (TPN) use, or severe parenchymal liver failure—often the very problems necessitating ICU admission.

The question of abdominal abscess arises frequently and is difficult to resolve noninvasively. In the past, gallium and indium scans may have been useful in the search for inflammation. Unfortunately, there are many problems in using these studies. Indiumlabeled white blood cells (WBCs) are difficult to produce because the isotope is very expensive, short lived, and cyclotron generated. Indium scanning is not likely to work if WBCs are dysfunctional, as in patients with acquired immune deficiency syndrome, with malnutrition, or receiving dialysis. False-positive abdominal scans may result in the presence of pneumonia, sinusitis, GI bleeding, or tumors of the bowel. Indium may be used to localize acute infections, but chronic infections may not have sufficiently numerous or active WBCs to enable visualization. Gallium-67 concentrates in any site of inflammation (not just areas of infection) and may visualize tumors, hematomas, fractures, infections, sarcoidosis, or acute respiratory distress syndrome (ARDS). Gallium is normally excreted into the colon and kidney, producing “physiological hot spots.” Resolution is characteristically poor, and precise localization is difficult. Simply stated, current quality of CT scan and US images has made gallium and indium scans all but obsolete. The specific advantages and limitations of the various imaging modalities are outlined in Tables 36-1 and 36-2.

Immediate diagnosis and surgical correction are needed to salvage patients with a ruptured abdominal aortic aneurysm. A ruptured or leaking
aneurysm typically presents with back and abdominal pain and shock occurring in a middle-aged or elderly patient with known arteriovascular disease and/or hypertension. An expanding abdomen or pulsatile abdominal mass with the loss of one or both femoral pulses completes the classic presentation. The retroperitoneal irritation produced by a leaking abdominal aneurysm can mimic nerve compression or a ureteral stone by causing “sciatica” or testicular pain. Rarely, rupture of an aortic aneurysm into the duodenum causes the massive hemoptysis of an aortoenteric fistula. (This dramatic clinical situation almost always occurs in patients with aortic grafts in place.) Unfortunately, hypotension often impedes comparison of pulse volumes, and examination of the abdomen and pulses may be difficult in obese patients. Because such patients are losing “whole blood,” the hematocrit often remains stable until volume replacement is substantial or the patient nears exsanguination.

In the past when clear signs and symptoms of a ruptured abdominal aneurysm were present, patients were taken directly to the operating room for surgical repair while initiating fluid and blood resuscitation. In the last 5 years, dramatic advances in endovascular stenting now allow many aneurysms to be repaired without an open procedure. If the patient is hemodynamically stable, multiple large-bore IV lines should be inserted and blood ordered before diagnostic testing. Regardless, early consultation by a vascular surgeon is indicated. A contrasted CT scan and aortogram are the best tests to confirm and delineate the aneurysm in the stable patient. Ultrasonography is a quick noninvasive bedside test to confirm the presence of an aneurysm, but clear visualization is likely to be obscured by bowel gas.

Ruptured ectopic pregnancy typically presents as acute abdominal pain, hypotension, vaginal bleeding, and a mass in the cul-de-sac. (Acute pain
occurs in almost all patients; about three quarters have vaginal bleeding and about half have a pelvic mass; fever is rare.) A reported history of a recent menstrual period is sufficiently unreliable that it cannot be used to exclude pregnancy. Hence, a serum β-human chorionic gonadotropin (HCG) should be performed on every fertile female with acute abdominal pain. Urinary HCG testing, although possibly more readily available, is less sensitive. Hematocrit determinations are usually not helpful because of the acute nature of the bleeding. Ectopic pregnancy is especially likely in patients with a history of salpingitis, tubal ligation, or prior ectopic pregnancy and in patients using intrauterine devices for birth control. Young women with unexplained acute abdominal pain and shock should probably undergo immediate laparotomy for a presumed ruptured ectopic pregnancy. (The rapid availability of US in many emergency departments and ICUs now permits confirmation of the diagnosis in less time than it takes to ready the operating room.) In patients with acute abdominal pain, stable blood pressure, and no evidence of peritoneal signs, serum pregnancy testing and ultrasonographic evaluation should be performed before surgery.

The transabdominal and transvaginal US examinations are complementary in evaluation of painful pelvic disease: Lesions located “high” in pelvis (e.g., ovarian masses) are often best seen by transabdominal screening (provided bowel gas does not obscure the view). Conversely, transvaginal scanning is often better at detecting early intrauterine pregnancy and ectopic pregnancies. Use of transabdominal scanning can allow detection of pregnancy as early as 4 weeks of gestation—transvaginal scanning can detect the same gestational sac 1 week earlier. The only certain US sign of ectopic pregnancy is visualizing a gestational sac outside the uterus, while finding a viable intrauterine pregnancy is strong evidence against a concurrent ectopic pregnancy. Ovarian tumors or cysts may also produce pelvic pain if they undergo torsion or ischemia. Rupture of a normal ovarian follicle into the peritoneum may produce worrisome but otherwise benign peritoneal signs.

Pelvic inflammatory disease (PID), the most common cause of pelvic pain in young women, is often difficult to differentiate from appendicitis or a ruptured ectopic pregnancy. PID usually starts within 7 days of the menstrual period, a helpful point in the differential with ectopic pregnancy, if the history is reliable. (The serum HCG should also be negative.) The pain of PID is gradual in onset and usually bilateral, whereas the pain of appendicitis tends to be of more rapid onset and unilateral when fully developed. Diffuse bilateral tenderness elicited by moving the cervix during pelvic examination is key to detecting PID. The ultrasonographic and CT features of PID are subtle and nonspecific unless a frank abscess forms. Untreated, PID can progress to the formation of a pus-filled fallopian tube, a tubo-ovarian abscess (TOA). TOA is an especially common problem among women with repeated or prolonged episodes of PID. Surprisingly, TOA can have such a sufficiently long timecourse that it can be confused radiographically with ovarian or even adjacent colon carcinoma. TOA is most frequently characterized by pelvic pain, fever and chills, and a vaginal discharge. Examination reveals lower abdominal and adnexal tenderness (usually asymmetric). Leukocytosis occurs in about two thirds of patients. Both US and pelvic CT scanning are excellent for imaging the lesion. Most tubal abscesses are polymicrobial infections that include enteric aerobic Gram-negative rods, Haemophilus, anaerobes, and Streptococcus. Pelvic US or CT demonstrates an adnexal mass in more than 90% of patients. Initial therapy should include appropriate cultures, hemodynamic stabilization, and administration of antibiotics. (A fluoroquinolone plus metronidazole, a third-generation cephalosporin plus doxycycline, a second-generation cephalosporin plus doxycycline, and clindamycin plus gentamicin and metronidazole are acceptable alternative antibiotic regimens.)

Mesenteric ischemia afflicts the elderly, particularly those with underlying heart (e.g., congestive heart failure and atrial fibrillation) and vascular disease who develop shock. (There are now many instances of mesenteric ischemia in young people resulting from cocaine-induced vasoconstriction.) The mortality of bowel infarction approaches 70%, primarily because of delayed diagnosis but also because victims tend to be older and have other underlying diseases. The differential diagnosis includes bowel obstruction, diverticulitis, and inflammatory bowel disease.

Bowel ischemia may result from arterial or venous occlusion of the superior or inferior mesenteric vessels. Most is arterial. About 50% of
patients with acute bowel ischemia have superior mesenteric artery (SMA) disease. (Half of these cases are embolic, a quarter are thrombotic, with the remainder resulting from nonocclusive ischemia.) SMA occlusion usually presents as the sudden onset of acute abdominal pain and a striking leukocytosis. Conversely, inferior mesenteric artery occlusion (accounting for about 25% of cases of bowel ischemia) usually has a more subtle, chronic pattern. The remaining 25% of cases stem from mesenteric venous thrombosis resulting from portal hypertension, pelvic infection, trauma, pancreatitis, intra-abdominal neoplasm, and thrombophilic disorders.

Arterial embolism is the single most common cause of bowel infarction and is most likely among patients with atrial fibrillation or recent myocardial infarction complicated by mural thrombus. The possibility of cholesterol embolism should also be considered in patients who develop symptoms after aortic instrumentation (e.g., cardiac catheterization, aortic balloon pump). Thrombotic occlusion occurring near the aortic origin of mesenteric vessels in patients with extensive atherosclerotic disease is the second most common cause of infarction. In patients with slowly progressive occlusion, a history of “intestinal angina” may be elicited. Vasculitis from lupus, radiation, or polyarteritis is rarely responsible. Many critically ill patients have nonocclusive bowel infarction due to the combination of hypotension and vasopressor drugs. By virtue of advanced age and atherosclerosis, many victims also have some degree of chronic vascular narrowing. (Concern over nonocclusive bowel infarction has increased recently with the resurgence of the powerful splanchnic vasoconstrictor, vasopressin, to treat septic shock.) Initially, ischemia produces mucosal and submucosal injury and edema. Later, mucosal sloughing occurs. Unless corrected within hours, bowel necrosis and perforation result, producing generalized peritonitis and death.

The signs and symptoms of mesenteric ischemia are often minimal or poorly localized, although a benign abdominal exam in a patient complaining of severe abdominal pain should be a tip-off. Unfortunately, severe illness and sedation often obscure the timely detection in the ICU patient. In addition, severe forms of Clostridium difficile colitis can be confused with mesenteric ischemia since they can present with abdominal pain, bloody stool, fever, and leukocytosis. The most common symptom of mesenteric ischemia is constant, nondiscrete back and abdominal pain. (The onset is sudden if embolic, more gradual if thrombotic or nonocclusive.) More than half of all patients have either occult blood in the stool or bloody diarrhea. Bowel sounds increase early in this process but decrease later. Shock may be the presenting symptom if perforation or infarction has already occurred. Atrial fibrillation or congestive heart failure is present in as many as half of all patients with bowel infarction.