Table„68-2 is drawn from a combined series of over 10,000 cases of acute (<1 week duration) abdominal pain presenting to over 200 EDs in 17 countries during a 10-year period. The data were collected on a highly standardized instrument.
In virtually all large series of acute abdominal pain, the substantial majority of final diagnoses include nonspecific abdominal pain (NSAP), appendicitis, and biliary tract disease (usually cholecystitis), in that order, accounting for nearly 75 percent of all acute abdominal pain. However, as shown in Table„„68.-3, as patients age, the triad remains but the order changes to biliary tract disease (again, usually cholecystitis), followed by NSAP and appendicitis.
INTRAABDOMINAL DIAGNOSES (BY ORGAN SYSTEM) Gastrointestinal APPENDICITIS In spite of a large number of algorithms and decision rules incorporating many different clinical and laboratory features, an accurate preoperative diagnosis of appendicitis has remained elusive for more than a century. In at least 20 percent of patients with appendicitis, the diagnosis is missed; conversely, normal appendices are found in 15 to 40 percent of all operations performed for suspected appendicitis. Thus, the diagnosis of appendicitis turns out to either be a false positive or false negative just about as often as it turns out to be correct. 18
Among patients presenting to an ED with acute abdominal pain, the pretest probability, or prevalence, of appendicitis is roughly 10 to 25 percent. 19 Converting this to odds to facilitate multiplication by LRs, the pretest odds of appendicitis in acute abdominal pain is roughly between 0.1 and 0.3. Five clinical features appear to have sufficiently powerful LR(+) values that the presence of any one should drive up the clinical odds to the point that an imaging procedure is indicated. Of those radiographic procedures available, appendiceal CT appears to be the best, 20 although there are many imaging alternatives, as listed in Tab.le.„„6.8:.4. Those clinical features with some predictive value include pain location in the RLQ [LR(+)=8]; pain migration from the periumbilical area to the RLQ [LR(+)=3]; rigidity [LR(+)=4]; pain before vomiting [LR(+)=2 to 3]; and a positive psoas sign [LR(+)=2].19 The widely held belief that anorexia is an essential prerequisite of appendicitis is unsupported by evidence. In fact, about one patient in three with surgically documented appendicitis is not anorectic preoperatively.19
In excluding the diagnosis of appendicitis, the absence of several of the following features is moderately helpful: The absence of RLQ pain [LR(-)=0.2], presence of similar previous pain [LR(-)=0.3], and absence of typical pain migration to the RLQ [LR(-)=0.5]. 19 Therefore, clinical exclusion of the diagnosis of appendicitis depends upon a persuasive aggregate of absent features or a strong competing alternative diagnosis. Lacking either of these two conditions, a CT should be seriously considered in the interest of avoiding missed appendicitis. In support of this strategy, a recent report of the impact of targeted appendiceal CT on treatment in suspected appendicitis showed that CT altered management in the majority (59 percent) of cases and represented a substantial cost savings. 2 21
BILIARY TRACT DISEASE This is the most common diagnosis in ED patients above age 50.1 Among patients found to have pathologically confirmed acute cholecystitis, the majority lack fever and a significant minority lack a leukocytosis (about 40 percent). 2223 and 24 Pertinent diagnostic tests are shown in Table„68-5.
Recognition that the diagnoses of cholecystitis, "biliary colic," and symptomatic common duct obstruction may represent pathologically distinct entities that cannot be reliably distinguished from one another clinically has led some authors to redefine the clinical target disorder as simply "biliary tract disease." Although there is an association between symptomatic biliary tract disease and steady, postprandial upper abdominal pain radiating to the upper back, the likelihood ratios of individual signs, symptoms, and combinations of signs and symptoms are "relatively weak discriminators."25 Just over one-third of patients have pain isolated to the RUQ, although about two-thirds have tenderness in that location. Most of the remainder complain of diffuse pain in the upper half of the abdomen; among those with pain in the lower abdomen, it is almost invariably in the RLQ. Among the one-third who do not have RUQ tenderness, the distribution is about equally divided between the upper half, the right side, and generalized tenderness throughout the abdomen. 6
Looking specifically at the common bile duct (CBD), overall clinical accuracy for the identification of obstruction is about 60 percent [95%CI 49 to 70%]. Accuracy is defined here as the proportion of all clinical diagnoses that were correctly identified as obstructed or nonobstructed CBDs.
SMALL BOWEL OBSTRUCTION The central issues in small bowel obstruction (SBO) are diagnosis of the primary disorder and early detection of secondary strangulation or ischemia when present. Only two historical and two physical findings appear to have predictive value: previous abdominal surgery and intermittent/colicky pain plus abdominal distention and abnormal bowel sounds. Although about two-thirds of patients with SBO present with generalized or central abdominal pain and about half have generalized tenderness, the LRs of these findings alone or in combination are such that SBO is another diagnosis that requires imaging confirmation. The general limitations of bowel sounds has been noted previously. As shown in Iable„„6..8..-6, and also discussed above, the abdominal flat plate is hampered by the large number of indeterminate readings, leaving it with LRs that are of limited usefulness. The CT, however, has an excellent LR(-), indicating that a negative result makes SBO highly unlikely. The LR(+) of CT is not as powerful as the LR(-), but probable SBO on CT increases pretest odds of this diagnosis by about sixfold (which is slightly better than the abdominal plain film).
Those patients with ischemic bowel secondary to strangulation are extremely difficult to detect clinically or by using plain radiographs. Here again the CT may be of substantial assistance in exclusion of the diagnosis of SBO with ischemia. Unfortunately, there is as yet no radiographic means to confirm the early diagnosis of ischemia due to SBO.26
ACUTE PANCREATITIS About 80 percent of acute pancreatitis in the United States is caused by alcohol or gallstones, with one etiology predominating over the other depending upon the population studied.27 The pain and tenderness of acute pancreatitis are limited to the anatomic area of the pancreas in the upper half of the abdomen in only a minority of instances.6 Most patients' pain and tenderness includes this area; in about half, however, it extends well beyond the upper abdomen to cause generalized tenderness. This may be related to the absence of a capsule that might otherwise contain the inflammation and to the difficulty of localizing pathology that—much like the pathology of an abdominal aortic aneurysm—resides deep in the belly and includes the retroperitoneum. Other features of the history and physical examination—such as the quality of the pain, which is steady and graded as severe in the majority of patients, or vomiting—have not been shown to have sufficient discriminatory power to make them clinically useful. Thus, most patients with upper, central, or generalized abdominal pain and tenderness who lack an alternative explanation for their presentation will require further testing.
As lipase assays have improved in accuracy and speed over the last several years, serum lipase has largely replaced amylase as the best "everyday" screening test for suspected acute pancreatitis. By setting the threshold for a positive test at twice the upper limit of normal serum lipase, the likelihood ratios for lipase are better than twice as powerful as those of serum amylase in making or excluding the diagnosis of acute pancreatitis. 28 As shown in Iable„68:7, there are other biochemical markers for acute pancreatitis that have superior test properties, but these are not yet widely available. Early evidence that ratios of urine to serum amylase or of lipase to amylase improve diagnostic accuracy has not been validated.
Depending upon institutional custom, a diagnosis of acute pancreatitis may be sufficient to determine the appropriate admitting service. However, in settings where not all pancreatitis is admitted to the department of surgery or where it is expected that the ED will make a decision regarding admission to a monitored versus an unmonitored floor bed, it may be necessary for the ED to assess the patient for biliary pancreatitis and, perhaps, for the likelihood of complications. While ultrasound is nearly as good as CT for assessment of common bile duct obstruction (see Tab.le.„„6.8.-.7.), CT with contrast enhancement by intravenous bolus is far superior for identifying peripancreatic fluid collections and the extent of glandular necrosis. Both of these findings are associated with increased need for surgery and increased mortality (Table„„68.-7.).
DIVERTICULITIS In one large study, the clinical accuracy of a diagnosis of colonic diverticulitis among patients with abdominal complaints was only 34 percent [95%CI 26 to 42%]. When the "possible/equivocal" clinical diagnoses were removed from analysis and only those patients with a pretest diagnosis of either "highly suspected" or "very unlikely" were included as clinical positives and negatives, respectively, the LR(+) was 2 to 3, and the LR(-) was 0.4, neither of which offers much help in the revision of disease probability. Of those patients with diverticular abscesses, diagnostic performance was somewhat better, with 70 percent categorized as "highly suspected" and the remainder as "possible/equivocal." No documented abscesses were categorized clinically as "very unlikely." 29
Pain in diverticulitis was confined to the LLQ in less than one-quarter of the documented cases and to the lower half of the abdomen in only an additional one-third of patients. With respect to tenderness, it was as likely to be generalized as it was to be limited to the lower half of the abdomen or to the LLQ. About 10 percent of patients with operatively confirmed diverticulitis did not complain of abdominal pain and 20 percent had no abdominal tenderness whatsoever. 6 Elderly patients are at risk for a severe and often fatal complication of diverticulitis that is only rarely seen in younger age groups: perforation of the colon. 16 Diagnostic imaging tests for acute diverticulitis are shown in TableSS-B.
Genitourinary RENAL COLIC As in appendicitis, a number of clinical decision rules have been developed in an effort to identify patients with the preimaging diagnosis of ureterolithiasis. Most algorithms include features of the pain—e.g., location (unilateral flank), onset (abrupt), quality (colicky), radiation (groin/testicle/labia). Hematuria appears as the only laboratory test in most algorithms. The utility of plain abdominal radiographs, as in other causes of abdominal pain, is highly questionable, as shown in Ta.bie.l6.8.-9..
A critical examination of ureteral stones documented on intravenous pyelography (IVP) reveals that, in one series, just over half reported colicky pain and groin radiation, with microscopic hematuria seen in about two-thirds.30 An examination of Tabjei68-9 shows that the IVP has a specificity comparable to that of helical noncontrast CT; however, because of the IVP's poor sensitivity, CT shows far better LRs, thus making noncontrast helical CT the current criterion standard in the diagnosis of ureteral stones. In older patients, any presentation that resembles renal colic, with or without hematuria, mandates the exclusion of an abdominal aortic aneurysm (AAA) [reported in 18 percent (95% CI 11 to 24%) of suspected AAAs in one series]. This is yet another reason to obtain a noncontrast helical CT, since it performs extremely well in the detection of both ureteral stones and AAAs.
Because the GU tract is mostly retroperitoneal, it uncommonly causes significant anterior abdominal tenderness. One notable exception to this is an impacted stone at the ureterovesical (UV) junction, where the ureter enters the bladder, producing ipsilateral lower-quadrant pain and tenderness. Because stones at the UV junction [like those at the ureteropelvic (UP) junction] are less likely to produce the typical pain of renal colic than are stones located between the top and bottom of the ureter, impaction of a stone at the UV junction on the right may easily mimic appendicitis and will require a noncontrast CT to identify stone disease ( Tab!e68.-l9l). If this shows neither a stone nor evidence of other intraabdominal pathology, an appendiceal CT should be considered to confirm or exclude the diagnosis of appendicitis. 20
ACUTE URINARY RETENTION Another situation in which GU disease may cause abdominal tenderness is in the setting of acute urethral obstruction, producing a distended bladder. When the obstruction is truly acute, the bladder often feels like a solid mass rather than a fluid-filled hollow viscus. However, if one always considers this common entity when confronted with a midline mass of variable tenderness arising from the lower half of the abdomen, insertion of a urethral catheter easily makes the diagnosis and treats the acute problem.
ACUTE SCROTUM Testicular torsion is the only cause of acute scrotal pain that must either be confidently excluded from the differential or treated within hours of onset. Consequently, the single target of all diagnostic strategies developed to determine the cause of acute scrotal pain is aimed at identification or exclusion of testicular ischemia. Although the etiology of acute scrotal pain in adults is usually either torsion or epididymitis, there are other causes—including inguinal hernia, acute hydrocele, and torsion of the appendiceal epididymis—none of which threatens testicular survival. Although the pain may radiate upward into the ipsilateral groin and lower quadrant, physical examination in adults leaves little doubt that the primary problem resides in the scrotum and not in the abdominal cavity itself (with the notable exception of torsion in an undescended testis).
Some of the features that favor epididymitis over torsion include the presence of fever, chills, dysuria, pyuria, and, most important, localization of the painful area to a swollen, tender epididymis, located posterior to and palpably separate from the testicle itself. The time course over which the pain began—its onset is characteristically more gradual in epididymitis than in torsion—may be helpful. However, it can also be misleading in patients who torse, detorse, and retorse.
The two diagnostic tests for torsion in common use are radionuclide scrotal scanning (RSI) and color Doppler imaging (CDI) (see TiablnenM618.-10.). Although CDI appears slightly superior to RSI, particularly in younger patients, these findings are not consistent across studies. Both tests have incorrectly identified normal blood flow to testes later found to be ischemic or necrotic at operation. It is difficult to determine to what extent these errors reflect technologic limitations versus operator skill and experience with CDI. With RSI, the problem appears to be one of image resolution in children whose prepubescent testicles represent smaller targets. Because of these limiting features, most authors suggest that imaging be used adjunctively and not as the criterion standard for deciding which patients require exploration. The most conservative indication for surgery, which is likely to result in the fewest missed torsions and the largest number of negative explorations, is inability to distinguish a normal testis and normal epididymis on physical examination. In many institutions, the time required to obtain a nuclear scan is prohibitive, and unless the urology consultant is rapidly available and proficient at Doppler imaging, torsion will, for the present, remain among the steadily dwindling causes of "abdominal" pain in which the diagnosis is made at surgery.
Gynecologic Pain ACUTE PELVIC INFLAMMATORY DISEASE Absence of a criterion standard has further confounded the already clinically difficult diagnosis of acute pelvic inflammatory disease (PID). Laparoscopic and histopathologic findings, both of which have been proposed as the criterion diagnostic standard, are discordant. Because gross laparoscopic findings have historically been used as the standard in most well-designed studies, 31 the LRs of clinical features, laboratory results, and sonographic findings that follow, unless otherwise noted, have been measured against direct macroscopic inspection of the adnexa.
Symptoms such as lower abdominal pain, which would be expected to have a high LR(-) for PID, have not been studied because they typically represent inclusion criteria for study enrollment. To date, there have been no historical features associated with laparoscopic PID that demonstrate clinically useful LRs in more than one study population.31 Signs—such as adnexal tenderness (unilateral on laparoscopy in only 5 to 10 percent of cases) and cervical motion tenderness—like lower abdominal pain, have not been well studied because they have been used as inclusion criteria in most investigations. The only physical finding associated with laparoscopic PID across more than one study population is an abnormal vaginal discharge. 31 In spite of this statistical association, the LRs of vaginal discharge range from 0.5 to 2.5, representing very limited power to alter disease probability. Elevated temperature and a palpable mass have been inconsistently associated with PID. The WBC count has not been found to be helpful in any of the studies that examined it. For the performance characteristics of other laboratory tests that have been associated with PID—e.g., the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), see Iab!el68:11.,.. As in the evaluation of ectopic pregnancy (see below), the role of culdocentesis in the diagnosis of PID is not supported by evidence.
ECTOPIC PREGNANCY In ruptured ectopic pregnancy, abdominal pain is almost universally present. However, as emphasis in ectopic pregnancy has shifted to identification of patients prior to rupture—with the goal of preserving fertility—pain may be absent at this earlier stage, with vaginal bleeding as the only sentinel complaint. Therefore, any woman of childbearing age who presents to the ED with abdominal pain or abnormal vaginal bleeding generally receives a qualitative pregnancy test as a screening measure.
The poor predictive performance of historical features, such as "risk factors," and of the physical examination [sensitivity 19 percent, LR(-)=0.8 among women with a positive hCG], argue strongly that ectopic pregnancy is not a diagnosis that can easily be excluded on clinical grounds.
For this reason, the results of the pregnancy test, independent of most other data, will determine if further testing is indicated to exclude an ectopic pregnancy. If the qualitative hCG is positive, the preferred test is a bedside transvaginal sonogram (TVS). See TiabMlnenM618.-1.2..
Vascular ABDOMINAL AORTIC ANEURYSM Although abdominal aortic aneurysms (AAAs) have little in common with aortic dissections, these two major forms of catastrophic disease of the aorta are often lumped together. Dissections are uncommon causes of abdominal pain and, because they almost invariably originate in the thoracic aorta, usually produce chest or upper back pain before migrating into the abdomen as the dissection moves distally.
AAAs, on the other hand, tend to enlarge, become aneurysmal over years, and—rather than dissect—leak and rupture. Fewer than half of AAAs present with the triad of hypotension, abdominal/back pain, and a pulsatile abdominal mass. Over three-quarters appear normotensive. Spontaneous containment of bleeding is the principal determinant of prehospital survival. Extent of containment further determines the degree of hypotension, if any, on presentation. The absence of abdominal pain or tenderness is entirely compatible with a contained leak extending into the retroperitoneum. Because the aorta is deep in the abdomen, it is extremely difficult to confirm by palpation that it is too small to represent an AAA, even in thin patients. Neither absence of femoral pulses nor an abdominal bruit have LRs that deviate very far from 1 and therefore lack the power to alter disease probability. Thus, a patient in the retirement-age group presenting with recent onset of abdominal, flank, or low back pain is likely to require either a normal aortic sonogram (performed by an experienced operator) or, preferably, a noncontrast helical CT (criterion standard test) before a AAA can be removed from the working differential diagnosis. Because the direction and extent of leakage or rupture—which can occur anywhere in the abdomen or retroperitoneum—determines the location of pain and tenderness, knowledge of aortic anatomy is not of much help in the diagnosis of AAA. The technology of magnetic resonance angiography (MRA) has not yet reached the stage where MRA can serve as an emergency procedure and conventional angiography has been supplanted by the superior, faster, noninvasive images of the helical CT. As noted earlier, the appearance of renal colic in this age group should be regarded as representing an AAA until the helical CT proves otherwise. See lTab!e.68:13.
MESENTERIC ISCHEMIA Mesenteric ischemia can be divided into arterial and venous disease [mesenteric venous thrombosis (MVT)]. Arterial disease can be subdivided into occlusive and non-occlusive (NOMI or low-flow state). Finally, occlusive arterial disease (generally understood to mean superior mesenteric artery occlusion) may be further categorized into thrombotic or embolic. Several features combine to produce a very high mortality associated with mesenteric ischemia:
1. Unless relatively young patients have an arrhythmia (usually atrial fibrillation causing embolization) or a hypercoagulable state (causing MVT), patients with mesenteric ischemia tend to have a substantial degree of age-related comorbidity.
2. The small bowel, which is supplied by the superior mesenteric artery, has a warm ischemia time of only 2 to 3 h.
3. The clinical picture is characterized initially by poorly localized visceral abdominal pain, without tenderness.
4. Patients may become transiently better after a few hours of ischemia, at the time of onset of mucosal infarction, only to later develop peritoneal findings as full-thickness necrosis of the bowel wall becomes apparent.
5. Timely diagnosis requires that an angiogram be obtained very early in the evolution of the pathologic process—so early, in fact, that it may seem clinically premature to order such an invasive test on an elderly patient who may not appear ill.
Elevation of serum phosphate was initially thought to be a sensitive marker for mesenteric ischemia, but this was not confirmed by later work showing a preoperative sensitivity for the diagnosis of acute mesenteric ischemia in the range of only 25 to 33 percent. In contrast, as shown in Ta.b.!§...6.8.-14., serial serum lactates that remain persistently normal reduce the clinician's pretest likelihood of diagnosing mesenteric ischemia by more than tenfold. Unfortunately, lactate is elevated in many abdominal and extraabdominal conditions and therefore lacks specificity in the diagnosis of mesenteric ischemia.
There are some distinctions that can be made among the four major forms of mesenteric ischemia: (1) embolic disease is the most abrupt in onset, MVT the most indolent, with the temporal profile of arterial thrombosis somewhere in between; (2) NOMI is usually accompanied by clinical evidence of a low-flow state, typically due to cardiac disease and responding to improvement in cardiac output;32 (3) MVT may be more amenable to noninvasive diagnosis with CT,33 occurs in younger patients, has a lower mortality, and can be treated with immediate anticoagulation; (4) following diagnosis, arteriography with papaverine infusion may be an important component of treatment in patients with splanchnic vasoconstriction.
ISCHEMIC COLITIS Ischemic disease of the large intestine has as little in common with mesenteric ischemia as aortic dissection does with AAA. As is the case with all vascular diseases, ischemic colitis is predominantly a disease of older patients. About 80 percent of individuals have diffuse or lower abdominal visceral pain, accompanied by diarrhea in about 60 percent, often mixed with blood. In contrast to mesenteric ischemia, ischemic colitis is not generally due to large-vessel occlusive disease, angiography is not usually indicated, and, if performed, is typically normal. Not surprisingly, the severity of the presentation appears to be related to the extent of ischemia. In the majority of cases, only segmental portions of the mucosa and submucosa slough. These then go on to heal uneventfully with conservative management. At the opposite end of the spectrum is full-thickness infarction of the colon, occurring in about 10 percent of cases. Bowel necrosis, whether segmental or pancolitic, causes peritonitis, requiring partial or complete colectomy. The mortality in this latter group approaches that of mesenteric ischemia.
In between mucosal/submucosal involvement and full-thickness infarction is an intermediate form of ischemic colitis involving portions of the muscular layer of the large bowel. These areas of deep but incomplete ischemia may later heal with stricture formation, placing the patient at risk for subsequent obstruction of the large bowel. In many instances, the attack of ischemic colitis that lead to the stricture may have been so mild that medical care was not sought at the time and the episode forgotten entirely by the patient. See Iable.68-14.
EXTRAABDOMINAL Cardiopulmonary If the patient is complaining of pain in the upper half of the abdomen, particularly if the pain is confined to the RUQ or LUQ (with or without tenderness), the chest should be examined for basilar involvement of lung parenchyma or pleura. Because the stethoscope is neither sensitive nor specific for the diagnosis of pneumonia, pulmonary infarction, small pleural effusions, or small pneumothoraces, a chest film should be obtained. Whether a decubitus or expiratory film is requested depends upon clinical suspicion of effusion or pneumothorax, respectively. A negative film, especially if the pain is pleuritic in quality, introduces the differential diagnosis of pulmonary embolism.
If the pain is epigastric and the patient is in an age/gender group where coronary artery disease is prevalent, a further cardiac history and electrocardiogram (ECG) should be obtained. Ischemic cardiac pain referring to the epigastrium is not associated with significant tenderness, although cutaneous dysesthesia may be present, like that found in the upper extremity in other patterns of ischemic cardiac pain.
Abdominal Wall Pain originating from the abdominal wall may be confused with visceral pain because superficial innervation from the lower thoracic roots enters the spinal cord via the same dorsal horn as the deeper visceral afferents. A useful and underutilized test is the sit-up test, also known as Carnett's sign. Following identification of the site of maximum abdominal tenderness, the patient is asked to fold his or her arms across the chest and sit up halfway. The examiner maintains a finger on the tender area, and if palpation in the semi-sitting position produces the same or increased tenderness, the test is said to be positive for an abdominal wall syndrome. The logic of this is that tensing of the abdominal muscles would be likely to protect the underlying organs, thus reducing tenderness if the cause of pain were deep. In patients unable to perform the maneuver, just raising the head and shoulders off the bed may be sufficient.
Abdominal wall syndromes overlap with hernias, neuropathic causes of abdominal pain, and NSAP.
HERNIAS Hernias represent a special type of abdominal wall syndrome characterized by a defect through which intraabdominal contents protrude, often only intermittently during transient increases in intraabdominal pressure. Hernias are ordinarily asymptomatic or, at worst, moderately uncomfortable, but they do not generally cause significant pain unless they have become incarcerated or strangulated. Although the vast majority of hernias are inguinal, there are many other types that must be considered, including incisional, periumbilical, and—especially in women—femoral hernias. In a series of 120 cases, sonography of the abdominal wall was shown to be very helpful in identifying hernias and other causes of abdominal wall pain.
OTHER ABDOMINAL WALL SYNDROMES Other causes of abdominal wall pain include rectus sheath hematomas and trauma to other portions of the abdominal wall. In older patients or in those on anticoagulants, the trauma may be very minor and forgotten. In circumstances where the injury is due to stretching causing tearing of muscle fibers, the overlying skin will not show any evidence of bruising that might provide a clue to the presence of bleeding into the abdominal wall.
Toxic-Metabolic TOXIC infectious A large number of infectious agents irritate the GI tract, producing pain that is usually crampy. Concomitant vomiting or diarrhea suggests a gastroenteritis or enterocolitis, respectively. Many agents cause both upper and lower tract symptoms; in adults, however, one symptom complex usually predominates over the other. The hallmark of these infections, because most are confined to the lumen (mucosa) of the GI tract, is an absence of significant tenderness. This is because the parietal peritoneum is not irritated by luminal disease. If infarction, penetration, or perforation of the bowel wall occurs, as may happen with some of the invasive dysenteries—e.g., salmonellosis—peritoneal tenderness follows. This is why abdominal tenderness of any significance should never be attributed to uncomplicated "gastroenteritis." Furthermore, because the overall incidence of symptomatic GI infections declines markedly with age, the prior probability of "gastroenteritis" as the basis for abdominal complaints, particularly pain, in the elderly is very low indeed.
Other infections are associated with abdominal pain, although the pathophysiology is less clear. These include group A beta-hemolytic streptococcal pharyngitis (with or without associated scarlet fever), Rocky Mountain spotted fever, and early toxic shock syndrome.
poisonings The toxicologic causes of abdominal pain are also legion; they tend to be nonspecific and nondiagnostic in most instances. Some exceptions to this include envenomation by the female black widow spider, which is said to mimic peritonitis. This might represent a diagnostic dilemma if no history was taken and only the abdomen was examined. However, because the rigid abdomen following envenomation is due to muscular spasm, which begins at the site of the bite and gradually spreads to involve other large muscle groups of the back and proximal extremities, the prominence of extraabdominal signs and symptoms, as well as their historical evolution, should point the clinician away from a primary intraabdominal process. Isopropanol-induced hemorrhagic gastritis may be associated with cramping pain from this ingestion. Cocaine-induced intestinal ischemia, progressing to infarction and perforation, has been reported. The first stage of iron poisoning produces abdominal pain and may cause hematemesis due to the direct corrosive effects of iron on the GI tract. Large amounts of iron left in the stomach may also cause perforation. Mercury salts cause severe corrosion of the GI tract, associated with shock. Acute inorganic lead toxicity is typically associated with severe, crampy abdominal pain. This is in contrast to chronic lead toxicity, in which abdominal pain is minimal or absent. The development of abdominal pain following electrical injury suggests a potentially serious complication and the need for admission. Opiate withdrawal produces abdominal pain, usually crampy in character, associated with diaphoresis and piloerection. In some individuals, the abdominal skin appears dysesthetic to light touch, but significant tenderness should not be present. Mushroom toxicity, though rarely fatal, is commonly accompanied by a chemical gastroenteritis and severe abdominal pain out of proportion to tenderness.
METABOLIC acidosis These causes of abdominal pain include acute anion-gap metabolic acidoses, commonly seen in diabetic ketoacidosis (DKA) and alcoholic ketoacidosis (AKA) and less frequently in lactic acidosis. Although the pain associated with DKA and AKA has been attributed to gastric distention and paralytic ileus, this has not been clearly substantiated. In DKA or AKA, it is critical to consider the possibility that an underlying abdominal problem may have triggered the DKA or AKA, rather than the reverse. This is a particularly challenging clinical problem when amylase or lipase levels are elevated, since both AKA and DKA can be a consequence or a cause of acute pancreatitis. If the acidosis is difficult to "break" or the pain persists after normalization of the pH, intraabdominal disease should be sought.
endocrinologic Of the endocrinopathies associated with abdominal pain, adrenal crisis is the most striking. Patients are often shocky and may exhibit peritoneal signs. The syndrome appears to be principally related to hypocortisolism rather than hypoaldosteronism. Without a history of similar prior episodes following reduced intake or absorption of adrenal steroids, these patients may be indistinguishable from those with an intraabdominal catastrophe in need of urgent exploration. Other endocrinopathies and electrolyte abnormalities associated with abdominal pain include thyroid storm, hypo- and hypercalcemia. This pain is generally crampy, and tenderness is absent unless the hyperthyroid state has caused acute hepatomegaly and distention of the liver capsule. Hypoglycemia has been reportedly associated with abdominal pain, but the evidence supporting this is unconvincing.
sickle cell crisis A painful sickle cell crisis is a common cause of abdominal pain, second only to musculoskeletal pain as the most common manifestation of a vasoocclusive crisis in homozygous (SS) sickle cell disease. Occasionally, patients with sickle cell disease and other symptomatic heterozygous forms may present with abdominal pain due to splenomegaly or splenic infarct. Those with heterozygous sickle trait (SA) are almost invariably asymptomatic. The most reliable means of determining whether the abdominal pain is part of a crisis or secondary to an underlying intraabdominal problem is to ask the patient whether or not this is the pain of a "typical crisis" or whether it represents a pattern break. If the latter, the problem is usually localized to the RUQ, either secondary to biliary tract disease (about 75 percent of those with SS have bilirubin stones due to chronic hemolysis) or hepatomegaly due to sinusoidal sludging of sickled cells. Additional considerations for SS patients include pancreatitis, salmonellosis, and mesenteric venous thrombosis.
Less common "metabolic" entities associated with abdominal pain include virtually all forms of vasculitis, especially systemic lupus and Henoch-Schonlein purpura, porphyria, and familial Mediterranean fever. Each of these may produce peritonitis.
Neurogenic The hallmark of neurogenic abdominal pain is a dysesthetic sensation, particularly in response to light touch in the area of discomfort. This has been characterized by one author as the "hover" sign, in which the patient shows signs of discomfort when the examining hand is passed very lightly across the area of dysesthesia. A positive hover sign may be mistakenly interpreted as indicating a generally hyperreactive patient rather than a normal physiologic response to a dysesthetic stimulus.
Because deep and superficial nerve fibers from the same area of the abdomen may enter the cord together, dysesthesias have also been reported with other, more serious intraabdominal disease, such as appendicitis. In the latter, however, the problem is usually more acute, and either upon presentation or subsequently is accompanied by tenderness (in contrast to dysesthesia alone, defined here as an abnormal sensation in response to light touch). This category includes nerve entrapment syndromes, such as rectus nerve entrapment, and iliohypogastric entrapment following a Pfannenstiel incision. A number of other incisional entrapment syndromes have been described. Many of these patients will have a positive Carnett test, but the hover sign is probably more indicative of neurogenic abdominal pain.
Radicular problems causing abdominal pain include diabetic or zosteriform radiculopathy, the latter being characterized by dysesthesias outlining a dermatome, usually with some "spillover" into contiguous dermatomes on either side of the involved root. The dysesthesias may present as lancinating, ticlike bouts of shooting pain or continuous burning. Accompanying vesicles confirm the diagnosis, although the pain may precede the cutaneous eruption by several days. Diabetic neuropathic involvement of a root, plexus, or nerve can be confirmed by electromyography.
There is some evidence that greater attention to the examination of the abdominal wall might reduce the frequency with which the diagnosis of nonspecific abdominal pain (NSAP) is made. In one report, about 25 percent of patients with the diagnosis of NSAp were found to have significant tenderness confined to the abdominal wall.
NONSPECIFIC ABDOMINAL PAIN Despite a thorough evaluation, the largest single group of patients seen in the ED will have no definite diagnosis and will receive the designation of NSAP. As Lukens et al. point out, the term undifferentiated abdominal pain (UAP) would be preferable to nonspecific, since the cause of the patient's pain may turn out to be very specific.11 Unfortunately, the term NSAP is relatively entrenched in the English literature. It is essential that diagnostic terms with specific meanings, such as gastroenteritis or gastritis, not be used as catch-all phrases to describe patients with NSAP.
Although NSAP is a diagnosis of exclusion, there are some clinical features characteristically associated with it. Nausea, present in nearly half the patients, is the most common symptom after abdominal pain. Pain location is often midepigastric or in the lower half of the abdomen. Tenderness is not usually severe, is absent in about one-third of the patients, and localized to the RLQ or midepigastrium in another third. Laboratory tests are usually normal, although a mild leukocytosis is entirely compatible with NSAP. Abdominal radiographs are virtually always normal or nonspecific. 11
The key to confirming NSAP is reexamination within 24 h (see below).
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