Etiology and Pathophysiology

Common viral etiologies of acute infectious diarrhea in immunocompetent children include rotavirus, enteric adenoviruses, noroviruses, and astroviruses. Common bacterial pathogens include Salmonella spp., Escherichia coli, Shigella spp., and Campylobacter jejuni (Figure 96-2). Clostridium difficile is the most common cause of antibiotic-associated diarrhea, although its role in infants younger than 1 year of age is unclear. Additional causes are discussed in Table 96-1 with further discussion of treatment. These pathogens cause diarrhea by a variety of pathogenic means: (1) osmotic or malabsorptive, (3) inflammatory, and (3) toxigenic. In immunocompromised hosts, cytomegalovirus and herpes simplex virus should also be considered as causes of infectious diarrhea.

Figure 96-2 Bacillary dysentery.

Clinical Presentation

Patients with gastroenteritis often present with symptoms that include emesis, diarrhea, and abdominal pain, which may be associated with fever. Clinical examination findings are usually nonspecific and do not point toward the etiologic organism.

Electrolyte losses and dehydration account for the high morbidity of acute gastroenteritis. In a systematic meta-analysis conducted by Steiner et al., useful individual clinical signs to predict 5% dehydration in children are an abnormal capillary refill time, abnormal skin turgor, and abnormal respiratory pattern for clinical signs of dehydration. Other studies have found that a combination of clinical signs and symptoms is more reliable in the demonstration of at least 5% dehydration: capillary refill time longer than 2 seconds, absent tears, dry mucous membranes, and ill general appearance.

Certain infectious agents are associated with extraintestinal manifestations. Shigella spp. organisms produce a toxin that has been associated with seizure. Yersinia enterocolitica infection has been associated with reactive arthritis. Additional extraintestinal manifestations can be seen in Table 96-1.

Differential Diagnosis

A broad differential diagnosis must be entertained with acute gastroenteritis. Diarrhea can be the presenting symptom of other infections, anatomic, or malabsorptive issues such as bowel obstruction or inflammatory bowel disease. In addition, vomiting may indicate other infections such as meningitis, lower lobe pneumonia, sepsis, or urinary tract infection, as well as metabolic disorders, toxin ingestion, heart failure, and trauma.

Evaluation and Management

The laboratory evaluation of children with gastroenteritis is often guided by history and clinical presentation, particularly the degree of dehydration. Assessment and treatment of dehydration is at the forefront of management of gastroenteritis in children. Serum electrolyte testing helps in the management of patients who appear severely dehydrated and in the detection of hyponatremic or hypernatremic dehydration. Hemoccult testing of stool can aid in identifying pathogens that cause bloody diarrhea. Stool culture should be performed in patients in whom a bacterial etiology is suspected, especially in cases lasting longer than 3 days and with bloody diarrhea. Identifying diarrhea-associated E. coli can be difficult because most clinical laboratories cannot differentiate diarrhea-associated E. coli strains from normal intestinal flora. Bacterial toxin testing is used to identify A and B toxins from C. difficile, as well as Shiga-type toxins. Viral antigen detection or molecular polymerase chain reaction–based tests can be used to identify rotavirus, adenovirus, and caliciviruses (norovirus).

Treatment of patients with gastroenteritis includes supportive care and fluid management. In some cases of bacterial gastroenteritis, antimicrobial therapy may be helpful, although it is not routinely recommended.

A brief discussion of rehydration is provided here, but more detailed discussions can be found in the Suggested Readings section at the end of the chapter. Current recommendations from the American Academy of Pediatrics encourage use of ORT in managing acute gastroenteritis in children. Oral rehydration occurs in two phases of treatment: a rehydration phase in which water and electrolytes are given in the form of an oral rehydration solution (ORS) for existing losses and a maintenance phase. ORS introduces glucose as well as sodium at the same time to allow for coupled transport. The World Health Organization’s components for rehydration solution consist of at least a complex carbohydrate or 2% glucose and 50 to 90 m Eq/L of sodium. Early refeeding is now encouraged after previous losses are corrected. Antimicrobial therapies for certain bacterial etiologies are discussed in Table 96-1.

Future Directions

New research into prevention and treatment continues. The use of vaccination for rotavirus may reduce the morbidity and mortality of gastroenteritis in young children. Use of probiotics is an ongoing controversial issue with future research still necessary to see if it aids recovery from gastroenteritis.

Etiology and Pathogenesis

The pathogenesis of appendicitis begins with obstruction of the appendiceal lumen, often by lymphoid hyperplasia of the Peyer’s patches on the walls of the appendix. These lymphoid tissues increase in size likely because of exposure to infection. With the hyperplasia of the lymphoid tissue, foreign material such as fecal material, food, or parasites are more likely to get caught in the appendix, creating an obstruction. The obstruction leads to thickening of the appendiceal wall, bacterial overgrowth, invasion, inflammation, and ischemia of the appendix. Polymicrobial infection with fecal flora is often reported, with E. coli, Peptostreptococcus spp., Bacteroides fragilis, and Pseudomonas aeruginosa.

Perforation with peritonitis is a common complication in children. The appendix is longer and thinner, which makes obstruction and perforation more likely with an omentum that is thinner and less likely to sequester inflammation. Therefore, peritonitis is more likely to be a complication of appendicitis in children than in adults.

Clinical Presentation

Appendicitis is often difficult to diagnose clinically in children because the typical signs and symptoms are often absent. The classical presentation of acute appendicitis is abdominal pain that migrates from the periumbilical area to the right lower quadrant of the abdomen (McBurney’s point), fever, anorexia, nausea, vomiting, and diarrhea. However, obtaining this history, especially in a preverbal child, is difficult. A recent systematic review tried to identify which historical and clinical examination findings are useful in determining which children warrant further diagnostic and surgical evaluation. Dysuria can also be a presenting symptom.

Clinical evaluation should include a full head-to-toe examination, including a pelvic examination for sexually active young women. Signs that have been associated with appendicitis in adults (with few pediatric studies) are Rovsing’s sign, the psoas sign, and the obturator sign. Rovsing’s sign involves palpation of the left lower quadrant, which leads to pain in the right lower quadrant. The psoas sign involves flexing the right hip against resistance. The obturator sign is raising the patient’s right leg with knee flexed and then internally rotating. Rectal examination is especially important in infants for whom a rectal mass can be palpated about 30% of the time in the setting of appendicitis.

Differential Diagnosis

The differential diagnosis for appendicitis is quite broad. Gastroenteritis with abdominal pain can often mimic appendicitis, with Yersinia infection known as the great imitator of appendicitis. Other abdominal processes such as mesenteric adenitis, intussusception, and Meckel’s diverticulitis are included as well. Urinary tract infection can also cause abdominal pain and vomiting, and urine should be evaluated. In girls, ovarian and pelvic processes, including tubo-ovarian abscess with torsion and pelvic inflammatory disease, can also mimic appendicitis. Nonabdominal processes, particularly right lower lobe pneumonia, can also cause right-sided abdominal pain.

Evaluation and Management

In the discussion above about history and physical evaluation, abdominal pain and concerning abdominal examination findings appear to be the most common history and physical findings. Rebound and guarding are concerning for appendiceal rupture or perforation.

Although appendicitis can often be identified by history and physical examination alone, reliance solely on clinical presentation may miss atypical presentations and then can result in delays in treatment and unnecessary hospital admissions. Adjunctive laboratory and radiologic testing can be helpful in the diagnosis of appendicitis.

Although no laboratory test is sensitive and specific for appendicitis, evaluation for signs of inflammation can give adjunctive data to the diagnosis. A complete blood cell count with white blood cell (WBC) count with increased bands or leukocytosis and C-reactive protein (CRP) can help evaluate for inflammation. Urinalysis should be performed because an inflamed appendix overlying the bladder wall may cause pyuria.

Controversy remains as to which radiologic study should serve as an adjunct in the diagnosis of appendicitis. One-view abdominal radiography has limited utility; it can show a calcified fecalith, localized ileus, or free air if perforation is suspected. Ultrasound is often used as the first imaging modality because it can be diagnostic and does not expose the child to X-rays. Findings seen on abdominal ultrasound concerning for appendicitis are dilatation of the appendix, a thickened wall, or free fluid. Abdominal computed tomography (CT) has significantly higher sensitivity for diagnosing appendicitis than ultrasound, with sensitivity of about 94% and specificity of 95%. Recent studies have also shown that intravenous (IV) contrast is equivalent to IV and rectal contrast in the evaluation for acute appendicitis.

The definitive treatment of patients with appendicitis is surgical intervention. In preparation for surgical intervention, broad-spectrum antimicrobials to cover fecal flora can be used and are part of the mainstay of therapy particularly in ruptured appendicitis. A review of pediatric hospital practice of the use of aminoglycoside-based triple therapy versus monotherapy for ruptured appendicitis yielded findings that single-agent antibiotic therapy may be used and may result in decreased lengths of stay and hospital charges.

Etiology and Pathogenesis

Primary peritonitis also known as spontaneous bacterial peritonitis (SBP) denotes pathogenic bacteria in the peritoneal fluid without a clear intraabdominal source. Hematogenous or lymphoid seeding of bacteria into ascites is often how SBP is initiated.

Secondary peritonitis, which is more common, is inflammation from a source such as a perforated viscus or interrupted abdominal wall (as with foreign material catheters). Appendiceal rupture or perforation from appendicitis can occur after gangrene of appendiceal wall and can lead to peritonitis. Foreign materials in the abdomen, particularly chronic peritoneal dialysis catheters and ventriculoperitoneal (VP) shunts, are associated with secondary peritonitis. Peritoneal dialysis catheters provide a track for microorganisms to enter from the environment into the peritoneum. VP shunts can transmit descending intraventricular infections to the abdomen. Risk factors include appendicitis, chronic renal failure, liver failure, peritoneal dialysis, and VP shunts.

Peritonitis may lead to formation of a phlegmon and may then proceed to abscess formation. Additional abscesses in the abdomen may occur within organ structures, especially the liver and spleen, through bacteremia. Amebic abscesses in the liver are discussed in Chapter 99. The microbes involved in peritonitis and abscesses are listed in Table 96-2. The most common targets of therapy are E. coli and Bacteroides spp.

Clinical Presentation

The clinical presentation is nonspecific. As many as 10% of patients with peritonitis and abscesses do not have any symptoms at presentation. Fever, abdominal pain, distension, and lethargy are symptoms commonly associated with peritonitis. The presentation in children with medical devices is often even more elusive. In particular, children who are on immunosuppressive regimens for renal disease may have blunted signs of inflammation and pain. With all patients, complete physical examination is warranted, with particular attention to examination for shifting dullness or fluid in abdominal examination.

Patients with abscesses often present with fever and localization to the viscus that is infected. For example, patients with hepatic pyogenic abscesses present with fever, jaundice, and right upper quadrant pain.

Differential Diagnosis

As with other GI infections, a broad differential diagnosis must be entertained when concerned for peritonitis. This includes sepsis, gastroenteritis, appendicitis, pyelonephritis, and lower lobe pneumonia.

Evaluation and Management

Laboratory and radiologic evaluation are helpful adjuncts in the diagnosis of peritonitis and abdominal abscesses. General evaluation for inflammation through WBC count and CRP may be helpful, but negative test results do not rule out the diagnoses. Blood culture can be positive in about 75% of primary spontaneous peritonitis. Paracentesis can aid in supporting the diagnosis: WBC greater than 250/mm³, total protein greater than 1 g/L, lactate greater than 25 mg/dL, and glucose less than 50 mg/dL. Fluid should be sent for bacterial, mycobacterial, and fungal cultures, especially in patients undergoing peritoneal dialysis. Radiologic studies are recommended to localize infection and to guide future surgical management. Plain films can reveal free peritoneal air from ruptured viscus. Ultrasound can aid in visualizing free fluid and can be used to guide paracentesis, but it is limited in visualizing all aspects of the abdomen. CT scans with oral and IV contrast provide the most detailed information about the abdominal cavity.

Management of patients with peritonitis targets the microbes believed to be involved. In primary peritonitis, therapy should be directed against Streptococcus pneumoniae; usually a third-generation cephalosporin; and in more life-threatening or VP shunt–associated infections, vancomycin can be added to cover S. aureus and penicillin-resistant S. pneumoniae. The duration of therapy is often 14 days. Aminoglycoside therapy should be added for secondary peritonitis in order to cover P. aeruginosa. Alternate regimens include ampicillin–sulbactam, ticarcillin–clavulanate, piperacillin–tazobactam, or carbapenems, which can be used especially if there is concern for drug-resistant nosocomial flora.

Surgical intervention in drainage of abscess formation is recommended to aid in narrowing antimicrobial coverage and more rapid resolution of abscesses.