Understanding the Varied Presentation and Management of Children with Acute Abdominal Disorders
Authors: David McLario MD, Clinical Assistant Professor, Pediatric Emergency Medicine, Emory University, Atlanta, GA; Steven G. Rothrock MD, FACEP, Department of Emergency Medicine, Orlando Regional Medical Center, Orlando, Florida.
Peer Reviewer: David Rogers, MD, Associate Professor of Surgery and Pediatrics, Medical College of Georgia, Augusta, GA.
Abdominal pain and vomiting are often present in children with nonsurgical disorders (e.g., gastroenteritis, constipation) and non-abdominal disorders (e.g., respiratory infections and streptococcal pharyngitis) that bring children to the ED. Emergency physicians must be able to differentiate these common disorders from rarer surgical emergencies. Unfortunately, the history and physical exam are often unhelpful in making this discrimination. Moreover, laboratory adjuncts and basic radiologic tests are often unhelpful or even confounding in children with surgical disorders. Studies have shown that plain films are usually normal or misleading in children with acute surgical abdominal emergencies.1,2 While the white blood cell count is elevated in 70-90% of children with appendicitis and more than 24 hours of pain, this marker is only elevated in 20% within the first 24 hours.3 Furthermore, the fact that a leukocytosis can be seen in many other nonsurgical disorders (e.g., gastroenteritis, pelvic inflammatory disease, respiratory infection) limits this tests ability to assist in differentiating between appendicitis and other disorders.3 These facts may, in part, explain why 28-50% of children with acute appendicitis and intussusception are initially misdiagnosed.4,5 Fortunately, newer tests (e.g., ultrasound, computerized tomography, scintography) have improved our ability to make accurate diagnoses in children who present to the ED with acute surgical disorders.51 However, even these tests have limitations.
Evaluation of children with GI-related illness requires an awareness of the typical and atypical clinical features as well as an understanding of the manner in which symptoms develop over time. Clinicians must have an understanding of the utility as well as limitation of diagnostic adjuncts. To better understand difficulties encountered in diagnosing serious abdominal disorders in children, the authors of this review use a case based approach to describing varied serious abdominal disorders in the young.
The Editor
Gastrointestinal complaints are common in children presenting to the ED. Together, abdominal pain, vomiting, and diarrhea, comprise nearly 20% of general and pediatric ED cases.1 They are exceeded by only injury, fever-related complaints, and various forms of upper respiratory illness as the reason for ED evaluation of children.6
While abdominal pain and vomiting are common in children presenting to the ED, less than 10% with these symptoms will have surgical abdominal disorders. (See Table 1.) Correspondingly, clinicians must be able to discern which children require acute surgical intervention. With this in mind, four cases are presented that underscore the difficulties often encountered in children who present with surgical abdominal emergencies: abdominal pain, bilious vomiting, altered mental status, and abdominal distention.
Case #1. A 10-year-old female was in her usual state of good health until six hours prior to ED arrival, when she began to complain of periumbilical abdominal pain. A few hours following the onset of pain, she experienced one episode of non-bilious emesis followed by a few "loose stools." Because of worsening abdominal pain, she was brought to the ED for evaluation. As her unremarkable medical history was reviewed, her parents mentioned somewhat hopefully that the "stomach flu" had been "going around" at school.
Initial physical examination revealed an alert, generally well-appearing child who was able to ambulate normally. Vital signs included a temperature of 37.8°C; heart rate, 108; respiratory rate 20; and blood pressure, 100/66. Mild periumbilical tenderness was noted. No rebound tenderness or right-lower-quadrant tenderness was appreciated.
A urinalysis, CBC with differential, and C-reactive protein level were obtained. Repeat physical examination in one hour demonstrated a somewhat less active child, lying on the stretcher with her knees slightly flexed. At this time, her temperature was 38.4°C. This subsequent abdominal examination was suggestive of migration of abdominal pain to the right lower quadrant. Rectal examination, performed initially during the second evaluation, revealed focal right-sided tenderness. All lab tests were normal. Ultrasound examination of the abdomen demonstrated a non-compressible appendix with increased wall thickness. Laparotomy demonstrated a distinctly inflamed but unperforated pelvic appendix that was subsequently removed.
Epidemiology. Abdominal pain is a common reason for the ED evaluation of children, involving as many as 5% of pediatric patient visits.7 Appendicitis, however, is comparatively uncommon, occurring in as few as 4.3% of pediatric patients presenting with abdominal pain.7 Therefore, the emergency physician is challenged to identify the small minority of patients with appendicitis within the much larger group presenting with abdominal pain.
In children older than 2 years, appendicitis is the most frequently occurring pediatric abdominal surgical disorder, with approximately 60,000 cases diagnosed annually in children in the United States.8 Unfortunately, accurate diagnosis of pediatric appendicitis is often difficult. Of these 60,000 children, 27-42% experience appendiceal perforation.9-17
When appendicitis is misdiagnosed, there is a significant risk of associated litigation. In one study, misdiagnosed appendicitis was the most frequent successful malpractice claim and the fifth most expensive cause of claims against emergency physicians.4
Considerable effort has been devoted to the study of factors that may affect the rate of appendiceal perforation.4,18,19 (See Table 1.) Numerous studies suggest that the rate of perforation varies inversely with the age of the child.4,11-26 Savrin and Clatworthy17 assessed perforation rates at various patient ages: In patients 2 years of age or younger, the incidence of appendiceal perforation was 93%; in those 3-5 years of age, 71%; between 6 and 10 years of age, 40%; and in those over 10 years of age, 33%. Other factors associated with appendiceal perforation are listed in Table 2.
Clinical features considered atypical for appendicitis, as noted in the represented case, are also commonly associated with delayed diagnosis and increased risk of subsequent appendiceal perforation. One study found that 50 of 181 (28%) pediatric appendicitis cases were initially misdiagnosed.13 Dysuria, constipation, diarrhea, signs or symptoms of respiratory illness, and the absence of right-lower-quadrant tenderness were more common in patients incorrectly diagnosed.4 The most frequent misdiagnoses given to children eventually shown to have appendicitis is gastroenteritis.13 (See Figure 1.) Other misdiagnoses in children later proven to have appendicitis include urinary tract infection (UTI), respiratory infection, constipation, sepsis, abdominal trauma, septic arthritis, testicular torsion, bowel obstruction, inflammatory bowel disease, nephrolithiasis, and cholecystitis.4
The risk of appendiceal perforation increases as a function of time elapsed following the onset of symptoms with most cases perforated beyond 48 hours of pain.18 In patients with possible appendicitis, the likelihood of appendiceal perforation may influence the interpretation of the patient’s physical examination and other diagnostic tests. Clinicians are, therefore, well-advised to attempt to pinpoint the time of pain onset, since the sequence and timing of the progression of symptoms provide important diagnostic clues.27
The potential for delay in the definitive diagnosis of appendicitis is well illustrated using the concept of the various "recognition phases" that must occur for an affected child to make it to surgery. First, his or her parents must recognize that their child needs to be evaluated by a physician. Second, the physician initially evaluating the child must recognize the possibility of appendicitis and appropriately refer to a surgeon. Finally, the surgeon must make the decision to perform laparotomy for suspected appendicitis. Various studies have linked the frequency of perforation to prolongation of the second phase, implicating the interval from "first physician evaluation" to "surgical evaluation."28,29 Marcuse et al pointed out that professional delay of more than 36 hours increased the risk of perforation in their study to 65%, almost double the incidence of perforation in a group of patients with symptoms of shorter duration.28 Linz et al suggest that trends toward higher perforation rates in recent years are associated with prolongation of the time spent in "presurgical" evaluation, specifically resulting from changes in health care delivery that prevent direct patient access to surgical subspecialists.29
Pathophysiology of appendicitis. Appendicitis occurs as a result of obstruction of the appendiceal lumen due to fecal matter (e.g., fecalith), hypertrophied lymphoid tissue (following viral illness), parasites, or other foreign bodies. Distention distal to the obstruction produces an increase in intraluminal pressure. Interstitial pressure within the appendix is elevated and causes venous stasis and engorgement. As the process continues, arterial blood flow is eventually impaired and ischemia occurs. Enteric bacteria subsequently invade the vulnerable appendix, causing infection. The combination of bacterial infection and arterial insufficiency produces inflammationgangrene and rupture follow if the process is allowed to continue.
Unfortunately, appendicitis in children is often easily confused with gastroenteritis and viral respiratory infections. Younger children are less able to verbalize their complaints and classic features often found in adults such as migration of pain to the right lower quadrant and abdominal pain that precedes vomiting which are easily missed by parents and physicians. A study of children with nonrecurrent, nontraumatic abdominal pain found that only fever and vomiting correlated with the presence of appendicitis while pain duration and rates of anorexia, lethargy, and diarrhea did not differ between children with and without appendicitis.30
Vital signs. Temperature is the vital sign that generates the greatest attention in patients with possible appendicitis. Temperature higher than 39.0°C at the onset of illness is not characteristic of unperforated appendicitis, where a normal temperature or low grade fever is more likely.31,37 Conversely, the majority of patients with appendicitis who have signs and symptoms for more than 48 hours have higher temperatures, usually higher than 39°C, and appendiceal perforation.33,34 Varying degrees of tachypnea and tachycardia are occasionally present in patients with appendicitis but neither are specific or sensitive signs for this illness.
Observation. Examination of the child with abdominal pain should begin with simple observation. In regard to movement, does he or she lie very still or is he or she continuously active, unable to achieve a comfortable position? Children experiencing somatic pain due to peritoneal inflammation are characteristically very still, with knees flexed slightly in an attempt to avoid stretch of the parietal peritoneum. In contrast, patients with colicky visceral pain provide the impression of being more ill than their abdominal examination would suggest, often writhing about in apparent agony. Strategically, all attempts to palpate the site of suspected maximal tenderness (the right lower quadrant), should be undertaken only after the remainder of the abdominal exam has been completed.
Auscultation. Although reduced bowel sounds are more common in patients with appendicitis than those without, this finding is neither sufficiently sensitive or specific to be used as a primary factor in any decision regarding diagnosis.
Pain characteristics. An understanding of factors influencing the patient’s perception of pain location is also essential to the understanding of appendicitis. In addition to initiating autonomic responses, visceral afferent nerve fiber activation may also trigger somatic afferent impulses in the same spinal cord segment causing referral of pain to a site distant from the affected organ. In the early stages of appendicitis, visceral afferent stretch receptors within the appendix transmit sensory impulses to mesenteric nerve fibers and eventually to the 10th thoracic nerve.35 For reasons that are not well understood, the visceral pain of appendicitis is often referred to the somatic dermatome at the level of the umbilicus (T10), explaining the initial complaint of periumbilical discomfort that characterizes the early stages of appendicitis.
Somatic pain due to peritoneal inflammation is usually of more insidious onset and progression and characterized by avoidance of movement. As the distended appendix becomes inflamed, irritation of the surrounding serosa occurs. Palpation during this phase provides greater opportunity for localization of the site of discomfort. Children with somatic pain are usually able to identify the area of maximal abdominal discomfort, and focal right-lower-quadrant tenderness continues to be considered the single most sensitive feature for appendicitis, occurring in 75-83% of cases.4,36 In cases where signs of anterior abdominal wall irritation are not present, clinicians are well advised to conceptualize the abdomen as a six-sided cavity, with irritation of any of the specific sides manifesting characteristic unique physical signs. For example, retroperitoneal irritation resulting from a posteriorly pointing appendix may be associated with a psoas sign or an obturator sign caused by irritation of these posteriorly located muscles.
It should be mentioned that certain authors suggest that clinicians are well-advised to place more emphasis on the migration of pain than on its precise anatomic location.37 Migration of pain to a specific and persisting site of focal discomfort is not characteristic for uncomplicated gastroenteritis.
The digital rectal examination has traditionally been a component of the evaluation of patients with abdominal pain and suspected appendicitis. The majority (51-73%) of children with appendicitis experience localized tenderness during digital rectal examination.13,38,39 However, in view of the frequency of positive digital rectal examinations in patients who do not have appendicitis (42.7-63%), the usefulness of this time-honored tradition has been challenged.13,38,39 Many emergency physicians dutifully perform this examination only because they think it is expected of them and may be heartened to learn that many studies suggest that it seldom assists clinicians in the majority of cases of suspected appendicitis.37,39,43 Certainly, multiple digital rectal examinations performed by different physicians during the course of evaluation are unnecessary.32
Digital rectal examination may be useful in detection of the mass effect present with a pelvic appendiceal abscess. For digital rectal examination to be useful, explanation to the patient of the need for cooperation and communication is essential. It is helpful to direct the supine child to bear down as if attempting a bowel movement; this succeeds in dilating the rectum, facilitating the examination. Some authors recommend that the pediatric rectal examination be performed with the patient lying supine, allowing a simultaneous bimanual examination of the abdomen.44 The examiner should observe carefully for signs of focal tenderness, attending to subtleties such as changes in facial expression. It should be mentioned that many clinicians maintain that performing a rectal examination prior to discarding the diagnosis of appendicitis in patients with abdominal pain fulfills the "standard of care."
Plain radiography. A calcified fecalith visible on a plain abdominal film is the most useful plain radiographic finding and is considered virtually pathognomonic of appendicitis when noted during the evaluation of abdominal pain. Unfortunately, a fecalith is so seldom present (visualized in as few as 2-13% of plain abdominal radiographs in patients with appendicitis) as to seldom be useful in making a diagnosis.45
As with other diagnostic tests, plain radiographs seldom definitively confirm or exclude appendicitis. Plain abdominal radiographs are interpreted as diagnostic or suggestive of appendicitis in only a minority of cases, with reported sensitivity ranging from 20% to 48%.3,37,45,46 Moreover, the vast majority of plain radiographic abnormalities are also non-specific (e.g., rightward scoliosis, a gasless abdomen, and sentinel loops), being present in a wide variety of self-limited, non-surgical conditions. In fact, while plain radiographs are usually normal in cases of appendicitis, the predictive value of "positive" abdominal radiographs is sufficiently poor that they are just as likely to be misleading as they are to lead the clinician to the correct diagnosis of appendicitis.1,2
Laboratory testing. It must be emphasized that no single laboratory test has the ability to definitively include or exclude appendicitis and that considerable effort has been devoted to the task of developing panels of tests to predict the presence or absence of appendicitis.
The white blood cell count is below 10,000/mm3 during the first 24 hours of symptoms in up to 82% of children with acute appendicitis.34 With time, the white blood cell count will be elevated above 10,000 cells/mm3 in 70-90% of patients with appendicitis.47 Unfortunately, leukocytosis is so frequently present in a variety of other disorders that must be differentiated from appendicitis as to be of very limited value in determining the presence of appendicitis, limiting its diagnostic value.48 Nearly half of all children with gastroenteritis, and a large number of adolescent females with pelvic inflammatory disease, experience an elevated white blood cell count, making differentiation between these disorders and appendicitis on the basis of this test alone nearly impossible.3 Moreover, a small but significant proportion of patients with appendicitis maintain normal white blood cell counts over time.
Studies conflict as the utility of the white blood cell count in discriminating between perforated and non-perforated appendicitis.31,36,49 Traditional teaching suggests that white blood cell counts, following appendiceal perforation, are significantly higher than in patients with unperforated appendices.50 However, one study demonstrated that patients with perforated appendices actually had slightly lower total white blood cell counts than patients with non-perforated appendicitis. Other studies suggest that the white blood cell count differs only modestly between perforated and nonperforated appendicitis.31,49
Another clinical strategy has employed the use of serial white blood cell counts. Increasing white blood cell counts occurring in patients considered to be at risk for appendicitis have been advocated as suggestive of the diagnosis. Unfortunately, Lyons et al found this strategy to be useless at differentiating appendicitis from non-appendiceal disease.51 The investigators noted considerable variability in white blood cell counts during a typical period of observation in patients ultimately diagnosed with appendicitis; approximately equal numbers of patients experienced an increase, decrease, and no change in white blood cell count.
In contrast to the frequent presence of normal total white blood cell counts during appendicitis, the presence of a moderate left shift is to be expected during the early stages of appendicitis.34 In one study, investigators noted an elevation in the percentage of neutrophils in more than 95% of children with appendicitis during the first 24 hours of symptoms.34 Unfortunately, a left shift is not specific for appendicitis, occurring in other illnesses causing abdominal pain, and therefore does not definitively "rule in" the diagnosis.
The urinalysis has been labeled one of the most useful lab test in patients with suspected appendicitis. Certainly, UTI should be included in the differential diagnosis when evaluating patients with abdominal pain. The presence of nitrite in the urine, although not sensitive, is very specific for UTI. A gram-stain examination of an appropriately collected catheter or supra-pubic specimen may reveal large numbers of bacteria. However, appendicitis may mimic the lab characteristics of UTI. Inflammation of the distal ureter or bladder by an inflamed adjacent appendix may result in mucosal inflammation with dysuria, urinary frequency, and the presence of up to 20-30 white blood cells or red blood cells/high power field in 16.5-30% of cases.37,39,51 Therefore, moderate pyuria does not exclude the diagnosis of appendicitis in favor of UTI.
The C-reactive protein level has gained popularity in the evaluation of suspected appendicitis due to its impressive specificity and sensitivity in selected studies.52,53 A study by Mikalesson and Arnbjornsson54 noted 100% sensitivity for perforated appendices and appendiceal abscess, while Albu55 noted greater than 85% sensitivity for patients with appendicitis with symptoms of more than 12 hours duration. However, the CRP is also elevated in up to 90% of patients with mesenteric adenitis, a common mimicker of pediatric appendicitis.54 Moreover, the CRP is frequently not elevated during the early stages of appendicitis and, therefore, may be most sensitive if used to study patients with symptoms of longer duration, specifically those with abdominal pain greater than 12-24 hours duration.55
Considerable effort has been devoted to the ability of lab testing to safely exclude ("rule out") the possibility of appendicitis. Combining tests known to have high sensitivity for appendicitis is a strategy studied by Dueholm et al,52 who noted that 100% of children with appendicitis had at least one of the following abnormal lab test results: A white blood cell count of greater than 9,000; a neutrophil differential of more than 75%; and a C-reactive protein of greater than 0.6 mg/dL. If all three lab tests were below these parameters, no patient had appendicitis. Repetition of these findings with larger numbers of patients with varying durations of pain may hold promise in reducing the number of negative laparotomies in patients of intermediate risk.
Additional diagnostic tests. Because it is simple, noninvasive, and likely to yield valuable information, ultrasonography is frequently used when the diagnosis of abdominal pain is uncertain. Ultrasound evaluation is reported to be a highly sensitive and specific diagnostic tool in patients with a non-perforated appendix.56 In appendicitis, a dilated appendiceal lumen, a thickened appendiceal wall and/or noncompressible appendix, as well as periappendiceal fluid, may be noted. Criteria for a positive test include total outer wall to outer wall diameter of greater than 6 mm and single wall diameter greater than 2 mm. Positive-predictive values of 73-84% and negative-predictive values of 88-97% have been noted in studies including pediatric patients suspected of having appendicitis.57,58
Ultrasound may be most useful during the early stages of illness when the diagnosis is in doubt. Janik and Firor,29 studying a group of patients categorized as being of intermediate risk for appendicitis, noted sensitivity and specificity of 96% and 94%, respectively. Interestingly, Larson noted sensitivity and specificity of only 76% and 71%, respectively, in cases where appendicitis was considered definite on pre-ultrasound examination.59 This reduced accuracy may be a result of larger numbers of patients with perforated appendices being studied in the population where appendicitis was considered certain. In one study assessing patients known to have perforated appendicies, sensitivity of ultrasound was only 28.5%.56 Data provided by ultrasound are operator-dependent, and communication between clinician and ultrasonographer is important. The noninvasive nature of ultrasonography is particularly useful in female patients in whom adnexal pathology may be a diagnostic consideration.
Malone et al found unenhanced abdominal CT scan to be a useful test in the diagnosis of appendicitis in adults.69 Sensitivity was reported to be 87%, with specificity of 97%. Balthazar et al61 used IV and PO contrast and found CT to be 96% sensitive for appendicitis while Rao et al62 used IV plus rectal contrast with spiral imaging and found CT to be 100% sensitive for appendicitis. However, the majority of patients in these studies were adults and no studies have prospectively evaluated the role of CT in children with suspected appendicitis. Moreover, CT is expensive and time-consuming, involves radiation exposure, and may not be readily available in certain institutions. Therefore, its role in the ED evaluation of suspected appendicitis in children is, at present, yet to be defined.3
Differentiation of appendicitis from other abdominal disorders
Several important features can help differentiate abdominal pain due to appendicitis from a non-surgical cause of pain.
Differential Point #1. Which appeared firstpain or vomiting? Vomiting occurs in 49-83% of patients with appendicitis and can contribute to misdiagnosis.4,3,63 Although infectious gastroenteritis is a very common cause of acute abdominal pain of visceral origin in the pediatric population, there are associated features that may distinguish this illness from appendicitis. Viral gastroenteritis characteristically presents with nausea and vomiting. A viral-induced ileus produces intestinal distention and emesis, which may be exacerbated by increased intraluminal fluid extravasation. In gastroenteritis, abdominal pain characteristically follows or occurs concomitantly with the initial nausea and vomiting. The abdominal pain of gastroenteritis is also frequently intermittent, crampy, and poorly-localized or evanescent. When vomiting does occur in patients with appendicitis, it almost universally follows the onset of abdominal pain, usually by several hours.
Unfortunately, young children often are unable to verbalize their complaints accurately, and parents may not recognize the presence of abdominal pain until a tangible event such as vomiting occurs. One study found that 33% of misdiagnosed cases of pediatric appendicitis had vomiting documented as beginning before pain onset.4 In cases of appendicitis diagnosed accurately, only 8% recorded the onset of vomiting as occurring before the onset of pain. Therefore, it is important to inquire regarding irritability and other behaviors that may serve as markers for the presence of "pain" occurring early in the course of illness in young pediatric patients suspected to have appendicitis. Other historical features characteristic for appendicitis are noted in Table 3.
Differential point #2: Does a history of diarrhea suggest infectious gastroenteritis? Usually, but not always! In viral gastroenteritis, diarrhea usually appears subsequent to vomiting and is frequently watery and copious. In contrast, the "diarrhea" of appendicitis, when it occurs, is often a result of irritation of a relatively small segment of the terminal colon by the inflamed appendix.27 Tenesmus and frequent mucoid small-volume stools may occur. It is important to remember that a history of frequent stooling in the context of abdominal pain should not necessarily cause one to embrace the diagnosis of gastroenteritis; practitioners should inquire specifically regarding the volume and nature of stool evacuated.
Although constipation is frequently considered in the differential diagnosis of abdominal pain, it has been noted in up to 8% of patients with appendicitis. Moreover, when constipation is present, the possibility of appendicitis should not be discarded. In one study, children with appendicitis who were considered to be constipated were more than three times more likely to be initially misdiagnosed.4
Differential point #3: Is the discomfort of appendicitis always localized to the right lower quadrant? The concept of McBurney’s point continues to be etched in the minds of clinicians, continuing to the present time. However, barium enema studies have demonstrated that the usual location of the appendix is inferior and medial to McBurney’s point.64 Only 35% of appendiceal bases lie within 5 cm of McBurney’s point, whereas 15% of appendiceal bases are positioned 10 cm or more from McBurney’s point.64 It is important to realize that an atypical location of the somatic pain of appendicitis increases the risk of misdiagnosis, perforation, and peritonitis. In fact, various positions of the appendix have been described. An appendix may be subcecal, preileal, or postileal in location.3 Clinicians should understand that the somatic pain of appendicitis is not always maximal at McBurney’s point and may present elsewhere. Conversely, despite the belief that a retrocecal appendix will lead to atypical features, this location characterizes the majority of the population. It is important to remember that children with gastroenteritis usually do not describe "point" tenderness, but frequently complain of variable, diffuse, and/or crampy pain, often coinciding with episodes of vomiting and/or diarrhea.
Management considerations. The optimal treatment for appendicitis is, of course, early appendectomy. As a general rule, appendectomy should be performed in doubtful cases to avoid gangrene and rupture and, historically, an aggressive approach has been considered necessary due to the imperfect sensitivity of clinical examination, lab, and diagnostic testing.32 This tenet of clinical practice is particularly true in younger pediatric patients. The limited pediatric omentum, shorter and thinner than that of an adult, may not "wall off" and contain a perforated appendix, contributing to the increased prevalence of diffuse peritonitis and sepsis, in children.33
Once a patient with suspected appendicitis has been examined, fluid deficits should be aggressively replaced and hydration status maintained until it is decided that the patient does not have a surgical abdominal disorder. Nothing should be given by mouth.
A number of recent studies have demonstrated a significant improvement in the accuracy of diagnosis of appendicitis resulting from the admission of selected, questionable cases and repeat serial assessment.65-67 Graff and Radford,65 in a study of 252 patients, noted a temporal increase in a clinical appendicitis score in patients admitted for observation who were ultimately determined to have appendicitis, while the group of patients who did not have appendicitis demonstrated a significant decline in the appendicitis score. Importantly, the decline in the number of negative laparotomies in this study was not associated with an increased rate of appendiceal perforation. It should be stressed that the in-hospital observation should be intensive whenever the strategy to observe is employed.
Case # 4. A 2-year-old female appeared to be in her usual state of good health until two days prior to presentation when she began to experience the first of approximately six episodes of emesis. No other signs of illness were present. The mother believed the emesis may have been green in color from the onset. On examination, the child appeared extremely well; she was active, happy, alert, and showed no signs of dehydration. The abdominal examination was unremarkable. Rectal examination was non-focal; stool was negative for occult blood.
The mother was advised to administer small amounts of clear fluid, advance the diet carefully as tolerated, and to observe for the development of signs of dehydration. In approximately 36 hours, the child returned for re-evaluation. Physical examination revealed moderate dehydration. Abdominal and rectal examinations were unchanged. She had not developed diarrhea or other sign of illness. She was admitted for intravenous rehydration and assessment of persistent vomiting. Plain abdominal radiography was unremarkable, but an upper GI contrast examination revealed marked narrowing in the third portion of the duodenum, consistent with an intramural duodenal hematoma. This case was referred to child social services for investigation regarding possible child abuse.
Case Discussion. Bilious emesis should evoke strong suspicion of mechanical obstruction distal to the ligament of Treitz, and should be considered a potential surgical emergency. In addition, the absence of other signs or symptoms normally associated with a self-limited systemic viral illness, such as rhinitis, sneezing, fever, myalgia, and diarrhea supports a mechanical cause of vomiting.68 Additional risk factors for mechanical bowel obstruction in patients with bilious emesis include young age and an early bilious appearance to the emesis. For example, bilious emesis in the youngest of patients, the newborn, should be presumed to be due to mechanical obstruction until proven otherwise and should be treated as a surgical emergency. Intestinal gangrene resulting from intestinal malrotation with volvulus may be avoided only with expeditious surgical repair.
This case vignette describing a duodenal hematoma deals with a relatively rare cause of bilious emesis and contrasts with the vast majority of such disorders in that non-operative management may be employed. Mechanical bowel obstruction in this patient is suggested by the generally well initial appearance, the absence of signs of systemic illness, and the initial bilious appearance of the emesis. Conversely, bilious emesis in a 12 year old with fever, sneezing, headache, and voluminous diarrhea, and who has had multiple prior episodes of non-bilious emesis within the current illness, is more likely a result of a gastroenteritis. Common causes of bilious emesis are listed in Table 4.69
Duodenal hematomas are uncommon, and usually result from a forceful, focused, and direct blow to the epigastrium. When faced with a duodenal hematoma in the absence of a plausible mechanism of injury such as a motor vehicle accident or a bicycle handlebar injury, the clinician should consider the possibility of non-accidental trauma (i.e., child abuse). Bleeding into the duodenal wall causes compression of the intestinal lumen, and hence, symptoms of obstruction distal to the ligament of Treitz; gastric distention and bilious vomiting. Upper gastrointestinal contrast study may show duodenal obstruction or the classical diagnostic "coil spring" sign.70 Ultrasonography may also be used for diagnosis. Concomitant pancreatic injury should be suspected as well. As mentioned, treatment for this particular type of mechanical obstruction is unusual insomuch as emergent surgery is not usually required. Conservative therapy with careful observation, gastric tube decompression, and total parenteral nutrition may be used successfully in most cases. Occasionally, spontaneous resolution of the obstruction does not occur and surgical evacuation is necessary.
Intramural hematomas of the more distal small intestine causing mechanical obstruction and bilious emesis may also occur as a result of motor-vehicle accidents. These injuries are frequently associated with lap belt use in the absence of a shoulder harness. Young children are more vulnerable to this type of injury pattern due to their poorly developed abdominal musculature and small stature. The lap belt will often slide above the hips in younger patients and act as a fulcrum against the child’s more protuberant abdomen, causing focused and forceful compression of the intestine against the lumbar vertebrae during rapid deceleration. A transverse fracture of a lumbar vertebrae, termed a Chance fracture, may also result from forceful flexion forces following motor vehicle accidents where only lap belt restraint is employed. It is important that clinicians attend to signs such as abdominal wall ecchymosis (lap belt sign), suggestive of considerable force applied to the pediatric abdomen, following motor vehicle accidents where only a lap belt was used.
Altered Mentation and Vomiting
Case # 5. A 7-month-old male was in his usual state of good health until one hour prior to ED presentation. His parents described a fairly abrupt onset of vomiting, with pallor as well as alternating irritability and somnolence. He had not stooled for at least 12 hours. Past medical history included a recent upper respiratory infection. The most recent episodes of vomiting were described as being yellow-green in color.
Intravenous access was established. Routine laboratory tests were ordered and sent. Left lateral decubitus, prone cross-table lateral, and supine abdominal radiographs, in addition to a chest x-ray, were obtained. The left lateral decubitus abdominal radiograph did not demonstrate an entirely air-filled ascending colon. Moreover, air was not noted in the rectum on the prone cross-table lateral film. The supine abdominal radiograph demonstrated an apparent mass effect in the right upper quadrant, with what appeared to be a thin rim of surrounding air, suggestive of an intussusceptiens surrounding an intussusceptum. Surgical consultation agreed to proceed with an air enema, which was successful in reducing an ileocolic intussusception. Following the hydrostatic reduction, the infant passed a stool containing blood and mucus.
Discussion. This case illustrates the importance of not waiting for the appearance of all components of the classic triad of intussusception (currant jelly stool, colicky abdominal pain, and vomiting) prior to initiating diagnostic and therapeutic efforts specific for this illness.
Intussusception occurs when one segment of bowel invaginates into a more distal segment. The central invaginated bowel is termed the intussusceptum, while the surrounding bowel is termed the intussuscepiens. As the proximal bowel is pulled along by peristaltic waves, telescoping into the more distal bowel, its mesentery is compressed and angled, resulting in lymphatic and vascular compromise. The intussuscepted mass also causes obstruction of the intestinal lumen, with resulting distention and waves of peristalsis that may cause colicky pain. One model used to illustrate the mechanism of intussusception uses the turning of a stocking partially "inside-out." Location characteristically occurs at, or proximal to, the ileocecal valve. Intussusception is the leading cause of acute intestinal obstruction beyond the neonatal period and occurs most frequently in infants during the second six months of life, with approximately 75-80% of affected patients between the ages of 3 months and 2 years of age.71,72
Intussusception is more common in boys, and most are well-nourished, otherwise healthy infants.71 The exception is the child with cystic fibrosis and concomitant failure to thrive.
Rarely, intussusception may occur in much older patients, with occasional cases reported in adults.73 When intussusception occurs in patients older than 4 years of age, clinicians should harbor an increased suspicion regarding an associated "lead point," (i.e., a mass that carries the proximal bowel segment downstream into the distal segment). Although a Meckel’s diverticulum is frequently mentioned as the most common "pathologic" lead point71 other masses should be suspected. Intestinal polyp, lymphoma, parasitic infection, intramural fecalith, and hemangioma may be associated with intussusception.71-73 Submucosal hemorrhage may serve as the apex for an intussusception and explains the association with abdominal trauma, hemophilia, hematologic disease, and Henoch-Schoenlein purpura.71-73 In cystic fibrosis patients, inspissated feces in the terminal ileum may serve as a lead point.71-73
It should be emphasized that most cases of intussusception in infants are not associated with identifiable lead points. The vast majority of cases (75-95%) of intussusception are idiopathic, meaning no lead point is identified. Most cases of idiopathic intussusception are ileocolic in location, involving prolapse of the terminal ileum through the ileocecal valve. Peaks of idiopathic intussusception occurring in the spring and fall parallel viral gastrointestinal and upper respiratory illnesses where hypertrophy of intestinal lymphoid tissues occurs. In well-nourished children, this lymphoid tissue is particularly prominent in the terminal ileum, providing a possible explanation of why most cases of idiopathic intussusception are ileocolic.71,74 These hypertrophied peyer’s patches may serve as "innocent" lead points in such cases of "idiopathic" intussusception. Rotavirus, reovirus, and echovirus have been associated with intussusception and are capable of causing hypertrophy of peyer’s patches in the terminal ileum.
Pathophysiology of intussusception. Initial occlusion of venous and lymphatic flow from the intussuscepted segment occurs due to compression and kinking within the trapped mesentery. Obstructed venous drainage produces edema of the affected bowel wall, and, ultimately, increased intramural bowel wall pressure compromises arterial blood flow. Bowel necrosis results if the process continues. Increased intraluminal venous blood and mucus produce the characteristic currant jelly stool.74
Presentation. The prototypical case involves a well-nourished male between 6 and 12 months of age with the sudden appearance of colicky abdominal pain and vomiting. The vomiting may become bilious as bowel obstruction progresses. The appearance of blood in the stool varies from the classic description of currant jelly to only microscopic hemoccult positive material. Between bouts of crying, children may appear listless and lay quiet and prostrate. Unfortunately, as was the case in our patient, the classic sign and symptom triad is noted at presentation in as few as 10-40% of patients. In fact, while 85% of patients manifest pain and 75% of patients experience vomiting, heme-positive stools occur in only 60% of cases,74,75 and the characteristic currant jelly stool often does not present until relief of the obstruction has been accomplished.76 In the majority of patients, early symptoms consist of vague abdominal complaints that are often difficult to distinguish from more benign conditions such as gastroenteritis.
Occasionally, infants ultimately diagnosed with intussusception present with profound apathy and listlessness without signs or symptoms referable to the GI system. Speculation regarding head injury, sepsis/meningitis, ingestion, or other acute illness effecting the central nervous system usually results. The observation of miosis in combination with decreased level of consciousness has given rise to speculation regarding intussusception-induced endogenous opioid secretion.77 A trial of naloxone has been advocated and has been speculated as being successful in reversing both miosis and coma. Other authors speculate the absorption of a toxic substance from ischemic bowel as the cause of increasing patient unresponsiveness.78
Although altered consciousness has been considered a late and ominous sign that correlates with the degree of bowel non-viability, other studies suggest this presentation may occur early during the course of illness.78 In describing patients with apparently painless intussusception, Ein et al pointed out that affected patients were often markedly pale, listless, and generally quite ill-appearing during the initial evaluation.71 When compared with those patients manifesting pain, children with painless intussusception presented later, had a greater incidence of failed hydrostatic reduction, were taken directly to the operating suite more often, and were more likely to require bowel resection.79 In two studies, normal consciousness returned following hydrostatic reduction.80,81 In summary, the absence of apparent pain is likely to delay diagnosis of intussusception. Moreover, it is important that clinicians include intussusception in the differential diagnosis of infants with a depressed level of consciousness.
Physical Examination. The child with intussusception is often pale, and may appear quite uncomfortable and/or listless. Palpation of the abdomen reveals a right upper quadrant or mid-abdominal mass in up to two-thirds of cases.74 The mass is frequently described as "sausage shaped." Unfortunately, an abdominal mass is often noted only late in the course of illness, and its absence does not rule out intussusception. Dance’s sign is described as a paucity of abdominal contents in the right lower quadrant, with the abdomen being described as concave or scaphoid. This sign is appreciated in as few as 5% of patients.74 Stool guiac testing is recommended and may reveal the first evidence of blood and/or mucus. However, the absence of occult blood does not rule out intussusception, particularly during the early stages of illness. Rarely, prolapse of the intussuscepted segment from the rectum may be noted or is palpable on digital rectal examination.
Radiography. Patients with intussusception have abnormal abdominal radiographs in up to 89% of cases.74 Unfortunately, most positive reports are non-specific and include findings such as "sparse intestinal gas," "air fluid levels," and "dilated bowel loops." Clinicians attempting radiographic analysis of young patients with suspected idiopathic intussusception may be well-advised to include a left lateral decubitus view. Since most cases of idiopathic intussusception involve prolapse of the intussusceptum into the ascending colon, visualization of an entirely air-filled cecum and ascending colon provides some reassurance that an ileocolic intussusception is not present. Occasionally, as was the case in the case vignette, a rim of air surrounding a soft tissue mass is noted on plain film, and has been described as an "adipose rose."82 Ultrasonography has been reported as 98% sensitive and 100% specific in the diagnosis of intussusception.82a
Clinicians frequently use barium contrast evaluation for the definitive diagnosis as well as treatment of intussusception. A lubricated straight catheter or foley catheter is inserted into the rectum to facilitate instillation of contrast material. The classic appearance of the intussuscepted segment demonstrates breaking of the air column, where contrast material abruptly terminates at the point of obstruction. A coiled-spring appearance is also frequently noted, created by a thin surrounding layer of contrast between the valvulae convenientes of the intussusceptum’s intestinal loops.
Treatment. Initial treatment for patients with suspected intussusception should begin with a few very basic interventions. Intestinal decompression with a gastric tube and intravenous access should be accomplished in a timely fashion. Aggressive volume replacement should occur. If symptoms have persisted for longer than 24 hours, and particularly if the child has fever or signs of peritonitis, antibiotic administration is indicated. Surgical participation should be secured in advance of contrast enema study in view of the unpredictable possibility of perforation or non-reduction during this evaluation.
For more than 20 years, the preferred management of intussusception has been nonoperative, with barium enema supplanting surgical reduction as the treatment of choice. Sedation is helpful during attempts at non-operative reduction. A column of barium is instilled from a short height above the patient, exerting hydrostatic pressure in an attempt to mechanically reduce the intussuscepted segment. The filling of the bowel with contrast is observed fluoroscopically. Successful hydrostatic reduction occurs in 50-90% of cases.74 Reduction is deemed satisfactory when the intussusceptum is reduced back through the ileocecal valve. Contrast material may also be visualized as it refluxes into proximal adjacent small bowel loops.74
Air can be used as a substitute for barium in both the diagnosis and reduction of an intussusception. Pneumatic reduction has been employed extensively in China, with a reported success rate of more than 90%.83 In recent years, the technique has gained popularity in the West as an alternative to hydrostatic reduction, with its proponents claiming it is faster, safer, less expensive, and more effective than barium enema. The procedure is fluoroscopically monitored, as air is insufflated into the rectum. Perforation with massive pneumoperitoneum causing respiratory comprise has been reported. Emergent treatment of this complication may be accomplished by needle decompression.
Older patients experience a much lower success rate for non-operative reduction; this is likely due to the much higher likelihood of lead points in this subset of patients. Those with symptoms for more than 24 hours are also less likely to experience successful hydrostatic reduction and are more likely to require surgical exploration and reduction. In addition to unsuccessful reduction, other complications of barium and air enema include intestinal perforation, the reduction of necrotic bowel, and the non-diagnosis of a pathologic lead point. Additional absolute and relative contraindications to hydrostatic reduction are included in Table 5.
Recurrent intussusception occurs in 7-12% of patients following successful hydrostatic reduction, usually within 24 hours of the procedure.71 Therefore, customary practice is to admit and observe patients for up to 24 hours following successful reduction. The management of children with recurrent intussusception must be individualized. An attempt at repeat nonoperative reduction may be justified since pathologic lead points are infrequently identified. Conversely, in older patients, operative intervention may be justified following a solitary unsuccessful attempt at nonoperative reduction due to the higher incidence of small-bowel tumor acting as a lead point. Surgical reduction of intussusception results in a lower recurrence rate of 2-5%.71
Abdominal Distention with Constipation
Case # 6. A 4-month-old male presented with vomiting, abdominal discomfort, and distention. He had no bowel movement for three or four days. The parents in attendance commented that their child always seemed constipated and had experienced periodic difficulty with similar episodes of abdominal distention relieved by their administration of suppositories at home.
Physical examination revealed an irritable infant with apparent abdominal discomfort. Vital signs included a heart rate of 140 beats/minute, blood pressure of 88/60, respiratory rate of 26/minute, and temperature of 37.0°C. Examination of the abdomen revealed distention, a hyperresonant percussion note, and hyperactive bowel sounds. Digital rectal examination resulted in the expulsion of a large amount of liquid stool which was guiac positive. Pediatric surgery was consulted for evaluation of intestinal obstruction presumed secondary to Hirschsprung’s disease. Hirschsprung’s disease was subsequently confirmed with anorectal manometry. A leveling colostomy was subsequently performed prior to definitive surgical repair of this child’s disease when he reached one year of age.
Case discussion. Hirschsprung’s disease results from the absence of intestinal intramural parasympathetic ganglion cells and is the most common cause of lower intestinal obstruction in neonates. Arrest of caudal migration of neural crest cells during the first trimester of gestation causes agangliosis beginning in the distal rectosigmoid region and extending proximally a variable distance. Aganglionosis confined to the rectosigmoid portion of the colon predominates, but in a minority of patients total colonic aganglionosis occurs. Rarely, "short segment" disease affecting as little as 1 cm of the distal rectum occurs.82
Hirschsprung’s is characterized by impaired relaxation and motility of the smooth muscle of the affected segment; this results in chronic constipation and the potential for obstruction. An acquired form of aganglionosis can be caused by trypanosomiasis where destruction of ganglion cells in the rectum as well as the heart (manifested by various forms of heart block) may occur.74
Hirschsprung’s disease is four times more common in males vs. females and is frequently noted in association with Down syndrome.84 Eighty percent of Hirschsprung patients present to health care providers within the first two months of life, and most infants demonstrate evidence of disease during the first seven days of life. Failure to pass meconium during the first 48 hours of life occurs in the vast majority of affected patients, as does delayed transition of meconium to non-meconium stools. If not detected during the immediate post-partum period, a subsequent history of constipation as well as laxative or suppository use, as was the case in our patient, will often be present. Other features of Hirschsprung’s disease are listed in Table 6.
Physical examination findings may include abdominal distention and a palpable stool mass. A digital rectal examination may be very helpful in distinguishing Hirschsprung’s disease from chronic, severe constipation. In Hirschsprung disease, the rectum is usually empty, in contrast to patients with functional constipation, where stool is usually noted within the rectal ampulla. Plain abdominal radiography may demonstrate air distention of bowel loops proximal to the obstruction.
Evaluation with radio-opaque contrast enema is useful, but is not 100% sensitive for the presence of Hirschsprung’s disease. The characteristic feature is a funnel or cone-shaped "transition zone," with the narrow portion starting just above the rectal ampulla.74 The transition zone can be suspected using plain radiography as well. This transition zone is often absent in infants under 2 months of age. It is important that clinicians be aware that digital rectal examination or other mechanical stimulation within two or three days of the contrast enema may dilate the aganglionic segment and obscure visualization of the transition zone. Presence of retained contrast material above the transition zone for more than 24 hours following the study also suggests Hirschsprung’s disease. Mucosal ulceration, due to stasis of intestinal contents, may be noted during the contrast enema. A surgeon should be consulted early in the course of evaluation of possible Hirschsprung’s disease.
Anorectal manometry using an inflatable balloon catheter is an excellent diagnostic test but is often reserved for situations where the history and radiographic studies are inconclusive.74 The balloon is inserted above the internal anal sphincter and inflated. This simulates the mass effect of stool in this area and normally induces relaxation of the internal anal sphincter. In Hirschsprung’s, paradoxic contraction of the internal anal sphincter occurs and establishes the presence of neurogenic dysfunction of the bowel. Manometry is particularly useful in cases of short segment disease not well visualized during contrast radiography.74,85
Suction biopsy of the rectal mucosa is very reliable in the diagnosis of Hirschsprung’s.85 Biopsy specimens should be taken approximately 2-4 cm from the anal verge. The presence of ganglion cells excludes Hirschsprung’s disease. The absence of ganglion cells is diagnostic for the disease, but must be interpreted cautiously, as the biopsy specimen must be adequate and the pathologist’s search diligent. If the diagnosis continues to be in doubt following suction biopsy, full-thickness biopsy is necessary. Customary surgical management will often involve an initial decompressing colostomy followed by definitive repair at about one year of age, with concomitant colostomy closure.85 Many pediatric surgeons are attempting to omit the colostomy and perform rectal irrigations to keep the bowel decompressed. This allows the child to undergo a single procedure. There is also a trend toward performing a pull through on neonates without a colostomy.
The most ominous complication of unrecognized Hirsch-sprung’s disease is toxic megacolon, an acute enterocolitis complicating 9-12% of cases.85 Toxic megacolon is caused by the dramatically increased intraluminal pressure proximal to the obstruction. Decreased intramural capillary blood flow results in ischemic damage to the protective intestinal mucosal barrier. Affected patients present with marked abdominal distention and tenderness, fever, bloody diarrhea, and bilious emesis.
Emergency management of these patients begins with vigorous administration of intravenous fluids. Additional interventions that may be necessary include rectal and/or gastric tube decompression, and broad spectrum antibiotics for possible intestinal perforation, peritonitis, and sepsis.85
Evaluation of infants and children with GI-related complaints can be a daunting task. GI-related disorders are capable of vastly varied presentations as illustrated in the cases presented. While most infants and children do not have serious pathology, it is the task of the emergency physician to decide which patients are at risk for serious intra and extra-abdominal illness. Only through an understanding of the varied presentations of these disorders, appropriate diagnostic evaluation, and management will clinicians be able to improve the outcome of these patients.
References
1. Rothrock SG, Green SM, et al. Plain abdominal radiography in the detection of acute medical and surgical disease in children: A retrospective analysis. Ped Emerg Care 1991;7:280-285.
2. Rothrock SG, Greem SM, Hummel CB. Plain abdominal radiography in the detection of major diseases in children: A prospective analysis. Ann Emerg Med 1992;21:1423-1429.
3. Molpus B, Rothrock SG. Acute appendicitis: A practical approach to improving patient outcome. Res Staff Phys 1995:11-18.
4. Rothrock SG, Skeoch G, Rush JJ, et al. Clinical features of misdiagnosed appendicitis in children. Ann Emerg Med 1991;20:45-50.
5. Budwig K, Rothrock SG, Sudhipong V, et al. Misdiagnosis of pediatric intussusception. Ann Emerg Med 1994;23:635-636.
6. Nelson DS, Walsh K, Fleisher GR. Spectrum and frequency of pediatric illness presenting to a general community hospital emergency department. Pediatrics 1992;90:5-10.
7. Brewer RJ, Golden GT, Hitch DC, et al. Abdominal pain: An analysis of 1000 consecutive cases in a university hospital emergency room. Am J Surg 1976;131:219-223.
8. Daum RS. Appendicitis and pelvic abscess. In: Textbook of Pediatric Infectious Diseases. (3rd ed.) eds. Feigin RD, Cherry JD. Philadelphia, PA: WB Saunders; 1992:709-716.
9. Sadrieh M, Farpour A. Acute appendicitis. Review of 970 cases. Am J Proct 1975;26:51.
10. White JJ, Santillana M, Haller JA. Intensive in-hospital observation: A safe way to decrease unnecessary appendectomy. Am Surg 1975;41:739.
11. Marchildon MB, Dudgeon DL. Perforated appendicitis: Current experience in a children’s hospital. Ann Surg 1977;185:84.
12. Law D, Law R, Eisemen B. The continuing challenge of acute and perforated appendicitis. Am J Surg 1976;131:533.
13. Samuels GA. Appendicitis in children. West Indian Med J 1971;20:105.
14. Brickman ID, Leon W. Acute appendicitis in childhood. Surgery 1966;60:1083.
15. Foster JH, Edwards WH. Acute appendicitis in infancy and childhood: A twenty year study in a general hospital. Ann Surg 1957;146:70.
16. Boles ET, Ireton RJ, Clatworthy HW. Acute appendicitis in children. Arch Surg 1959;79:447.
17. Savrin RA, Clatworthy HW. Appendiceal rupture: A continuing diagnostic problem. Pediatrics 1979;63:37-43.
18. Braveman P, Schaff VM, Egerter S, et al. Insurance-related differences in the risk of ruptured appendix. N Engl J Med 1994;331:444-449.
19. Scher KS, Coil JA. Appendicitis: Factors that influence the frequency of perforation. South Med J 1980;73:1561-1563.
20. Rappaport W, Peterson M, Stanton C. Factors responsible for the high perforation rate seen in early childhood appendicitis. Am Surg 1989;55:602-605.
21. Barrlett RH, Eraklis AL, Wilkson RH. Appendicitis in infancy. Surg Gynecol Obstet 1970;130:99-105.
22. Brender ID, Marcuse EK, Koepsell TD, et al. Childhood appendicitis: Factors associated with perforation. Pediatr 1985;76:301-306.
23. Daehlin L. Acute appendicitis during the first three years of life. Acta Chir Scand 1982;148:291-294.
24. Ferguson E, Pirrung D. Acute appendicitis clinical vs. pathologic diagnosis. Am J Proctol 1969;20:269-278.
25. Golladay ES, Sarrett JR. Delayed diagnosis in pediatric appendicitis. South Med J 1988;81:38-41.
26. Graham IM, Pokorny WI, Harberg FI. Acute appendicitis in preschool age children. Am J Surg 1980;139:247-250.
27. Hatch EI. The acute abdomen in children. Ped Clin N Amer 1985;32:1151-1164.
28. Linz DN, Hrabovsky EE, Frnaceschi D, et al. Does the current health care environment contribute to increased morbidity and mortality of acute appendicitis in children? J Ped Surg 1993;28:321-328.
29. Janik JS, Firor HV. Pediatric appendicitis. Arch Surg 1979;114:717-719.
30. O’Shea JS, Bishop ME, Alario AJ, et al. Diagnosing appendicitis in children with acute abdominal pain. Pediatr Emerg Care 1988; 4:172-176.
31. Young DV. Results of urgent appendectomy for right lower quadrant tenderness. Am J Surg 1989;157:428-430.
32. Silen ML, Tracy TF. The right lower quadrant "revisited." Ped Clin N Amer 1993;40:1201-1211.
33. Rowe MI, O’Neill JA, Grosfeld JL, et al. In: Esssentials of Pediatric Surgery. St. Louis: Mosby-Year book; 1995.
34. Doriswamy NV. The neutrophil count in childhood acute appendicitis. Br J Surg 1977;64:342.
35. Wangensteen OH, Dennis C. Experimental proof of the obstruction origin of appendicitis in man. Ann Surg 1939;110:629.
36. Lewis FR, Holcroft JW, Boey J, et al. Appendicitis: A critcal review of diagnosis and treatment in 1000 cases. Arch Surg 1975;110:677.
37. Magee RB, Stowell JM, MacDuffee RC. Appendicitis: An analysis of 2,117 cases treated surgically in a community hospital during a period of twenty years. Penn Med 1967;70:47-49.
38. Bartlett RH, Eraklis AI, Wilkinson RH. Appendicitis in infancy. Surg Gynecol Obstet 1970;130:99-105.
39. Nase HW, Kovalcik PJ, Cross GH. The diagnosis of appendicitis. Am Surg 1980;46:504-507.
40. Bonello JC, Abrams JS. The significance of a "positive" rectal examination in acute appendicitis. Dis Colon Rectum 1979;22:97.
41. Dixon JM, Elton RA, Rainey JB, et al. Rectal examination in patients with pain in the right lower quadrant of the abdomen. Br Med J 1991;302:368.
42. Dunning PG, Goldman MD. The incidence and value of rectal examination in children with suspected appendicitis. Ann R Coll Surg Engl 1991;73:233.
43. Dickson JAS, Jones A, Telfer S, et al. Acute abdominal pain in children. Scan J Gastroenterol 1988;23:1988.
44. Mellick LB, Lau K. Pearls and pitfalls of pediatric assessment: Secrets of approaching children in the emergency department. Emer Med Rep 1994;15:19-30.
45. Graham AD, Johnson HF. The incidence of radiographic findings in acute appendicitis compared to200 normal abdomens. Milit Med 1996;131:273-276.
46. Bakhda RK, McNair MM. Useful radiologic signs in acute appendicitis in children. Clin Radiol 1977;28:193-196.
47. Hoffman J, Rassmussen OO. Aids in the diagnosis of acute appendicitis. Br J Surg 1989;76:775-779.
48. English, CD, Allen W, Cuppola Ed, et al. Excessive dependence on the leukocytosis cue in diagnosing appendicitis. Am Surg 1977; 43:339.
49. Graham JM, Pokorny WJ, Harberg FJ. Acute appendicitis in preschool age children. Am J Surg 1980;139:247-150.
50. Stone HH, Sanders SL, Martin ID. Perforated appendicitis in children. Surgery 1971;69:673-679.
51. Scott JH III, Amin M, Harty JL. Abnormal urinalysis in appendicitis. J Urol 1983;129:1015.
52. Dueholm S, Bagi P, Bud M. Laboratory aid in the diagnosis of acute appendicitis: A blinded, prospective trial concerning diagnostic value of leukocyte count, neutrophil differential count, and C-reactive protein. Dis Colon Rectum 1989;32:855.
53. Peltola H, Ahlqvost K, Rapola J, et al. C-reactive protein compared with white blood cell count and erythrocyte sedimentation rate in the diagnosis of acute appendicitis in children. Acta Chir Scand 1986;152:55.
54. Mikaelsson C, Ambjornsson E. The value of C-reactive protein (CRP) determinations in patients with suspected acute appendicitis. Ann Chir Gynaecol 1984;73:281-284.
55. Albu E. Diagnostic value of C-reactive protein in acute appendicitis. Dis Colon Rectum 1994;37:29-51.
56. Puylaert JBCM, Rutgers PH, Lalisang RI, et al. A prospective study of ultrasonography in the diagnosis of appendicitis. N Engl J Med 1987;317:6666.
57. Skaane P, Amland PF, Nordshus T, et al. Ultrasonography in patients with suspected acute appendicitis: A prospective study. Br J Radiol 1990;63:787-793.
58. Fa EM, Cronan JJ. Compression ultrasonography as an aid in the differential diagnosis of appendicitis. Surg Gynecol Obstet 1989; 169:290-298.
59. Larson IM, Peirce IC, Ellinger DM. The validity and utility of sonography in the diagnosis of appendicitis in the community setting. Am J Roent 1989;153:687-689.
60. Malone AJ, Wolf CR, Malmed AS, et al. Diagnosis of acute appendicitis: Value of unenhanced CT. Am J Radiol 1993;160:763-766.
61. Balthazar EJ, Birnbaum BA, Yee J, et al. Acute appendicitis: CT and US correlation in 100 patients. Radiology 1994;190:31-35
62. Rao PM, Rhea JT, Novelline RA, et al. Helical CT technique for the diagnosis of appendicitis: Prospective evaluation of a focused appendix CT examination. Radiology 1997;202:139-144.
63. Rothrock SG, Schneider RE. Overcoming limitations and pitfalls in the diagnosis of appendicitis. In: Updates in Gastroenterology II. Rothrock SG (Ed), Atlanta: American Health Consultants; 1992:19-31.
64. Ramsden WH, Mannion RA, et al. Is the appendix where you think it is, and if not, does it matter? Clin Radiol 1993;47:100-103.
65. Graff L, Radford MJ, Werne C. Probability of appendicitis before and after observation. Ann Emerg Med 1991;20:503-507.
66. White JJ, Santillana M, Haller JA. Intensive in-hospital observation: a safe way to decrease unnecessary appendectomy. Am Surg 1975;41:793-798.
67. Ricci MA, Trevisani MF, Beck WC. Acute appendicitis: A 5 year review. The American Surgeon 1991;51:301-305.
68. Seashore JH, Toulooukian RJ. Midgut volvulus: An ever-present threat. Arch Pediatr Adolesc Med 1994;148:43-46.
69. Cowan MR, Abramo TJ, Wiebe RA. A 7 month old with bilious emesis. Ann Emerg Med 1995;25:551-553.
70. Felston B, Levin EJ. Intramural hematoma of the duodenum: A diagnostic roentgenologic sign. Radiology 1954;63:823.
71. Ein SH, Stephens CA. Intussusception: 354 cases in 10 years. J Ped Surg 1971;6:16-27.
72. West KW, Stephens B, Vane DW, et al. Intussusception: Current management in infants and children. Surgery 1987;102:704-710.
73. Luks FI, Yazbeck S, Perreault G, et al. Changes in the presentation of intussusception. Am J Emerg Med 1992;10:574-576.
74, Clark MC. Gastrointestinal obstruction. In: Emergency Medicine. Howel J (ed). Philadelphia, PA: WB Saunders; 1997:323-337.
75. Stevenson, RJ. In: Rudolph AM, Hoffman JIE, Rudolph CD (eds) Pediatrics 20th ed. Stamford, CT: Appleton and Lange; 1996:1071-1072.
76. Losek JD. Intussusception: Don’t miss the diagnosis. Pediatr Emerg Care 1993;9:46-51.
77. Tenebein M, Wiseman NE. Early coma in intussusception: Endogenous opioid induced? Pediatr Emerg Care 19873:22-23.
78. Rachmel A, Rosenbach Y, Amir J, et al. Apathy as an early manifestation of intussusception. AJDC 1983;137:701-702.
79. Ein SH, Stephens CA, Minor A. The painless intussusception. J Pediatr Surg 1976;11:563-564.
80. Singer J. Altered consciousness as an early manifestation of intussusception. Pediatrics 1979;64:93-95.
81. Braun P, Germann-Nicod I. Altered consciousness as a precocious manifestation of intussusception in infants. Z Kinderchir Grenzgeb 1981;33:307-309.
82. Levine M, Schwartz S, Katz I, et al. Plain film findings in intussusception. Br J Radiol 1964;37:678-681.
82a. Shanbhogue RL, Hussain SM, Meradji M, et al. Ultrasonography is accurate enough for the diagnosis of intussusception. J Pediatr Surg 1994;29:324-327.
83. Guo J, Ma X, Zhou Q. Results of air pressure enema reduction of intuss. J Pediatr Surg 1986;21:1201-1203.
84. Swenson O, Raffensperger JG. Hirschsprung’s Disease. In: Raffensperger JG. Pediatric Surgery. Norwalk, CT: Appleton-Lang; 1990:555-577.
85. Orenstein JB. Hirschprung disease. In: Barkin RM. Pediatric Emergency Medicine. 2nd ed. St. Louis: Mosby Year Book; 1997;850.
Recommended Reading
Grosfeld IL, Weinberger M, Claworthy HW. Acute appendicitis in the first two years of life. J Pediatr Surg 1973;8:285-292.
Harrison MW, Lindner DI, Campbell IR, et al. Acute appendicitis in children: Factors affecting morbidity. Am J Surg 1984;147:605-610.
Lay YW, Fan St, Yip CW, et al. Acute appendicitis in children. NZ J Surg 1987;57:927-931.
Purr P, O’Donnell RB. Appendicitis in infancy. J Pediatr Surg 1978;13:173-174.
Stanley-Brown EG. Acute appendicitis during the first five years of life. Am J Dis Child 1964;108:134-138.
Williams H. Appendicitis in the young. Br Med J 1947;2:730-732.
Larson JM, Peirce JC, Ellinger DM, et al. The validity and utility of sonography in the diagnosis of appendicitis in the community setting. Am J Roent 1989;153:687-691.
Snell RS, Smith MS. In: Clinical Anatomy for Emergency Medicine. St. Louis: Mosby-Year book Inc; 1993.
Brickman ID, Leon W. Acute appendicitis in childhood. Pediatr Surg 1960;5:1083-1089.
Folkman J, Lund, DP. Appendicitis. In: Wyllie, R, Hyams JS. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis and Management. Philadelphia, WB Saunders Co.; 1993:691-697.
Reynolds SL, Jaffe DM. Diagnosing abdominal pain in a pediatric emergency department. Ped Emerg Care 1992;8:126-128.
McBurney C. Experiences with early operative interferences in cases of disease of the vermiform appendix. NY Med J 1989;5:676.
Arant, BS Jr. Renal and Genitourinary Diseases. In: Principles and Practice of Pediatrics. Oski FA, DeAngelis CD, Feigin RD, et al. Philadelphia, PA: JB Lipincott Co.; 1990:408-418.
Todd I. Adult Hirschsprung’s disease. Br J Surg 1977;64:311.
Physician CME Questions
26. Which of the following are true concerning appendicitis in children.
A. The presence of diarrhea effectively excludes the diagnosis of appendicitis.
B. Plain films will usually reveal a calcified fecalith.
C. The United States has a more than 85-90% sensitivity for diagnosing appendicitis.
D. It is much easier to diagnose in children due to less omentum and overlying fatty tissue.
27. The white blood cell count in appendicitis:
A. is usually elevated in the first 24 hours.
B. can be followed sequentially to reliably exclude appendicitis.
C. is more accurate than the neutrophil count in the first 24 hours.
D. is eventually elevated in 70-90% of children with appendicitis.
28. Bilious emesis in neonates:
A. can be caused by midgut volvulus.
B. should be considered a surgical emergency until proven otherwise.
C. can be caused by duodenal or ileal atresia.
D. all of the above
29. Intussusception in children:
A. can reliably be excluded if plain films are normal.
B. can reliably be excluded if stool is heme negative.
C. can usually be reduced using barium enema or air contrast enema.
D. usually has mass as the lead point under the age of 4 years.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content