An 18 month old male is brought to the emergency department with a chief complaint of diarrhea and vomiting for 2 days. His mother describes stools as liquid and foul smelling, with no mucous, slime or blood. He reportedly is unable to keep anything down, vomiting after every feeding, even water. He has about 6 episodes of diarrhea and 4 episodes of vomiting per day. His mother reports that he is not feeding well and his activity level is decreased. He seems weak and tired. He has a decreased number of wet diapers. He attends daycare during the day when he is well. His last weight at his 15 month check up was 25 pounds (11.4 kg).
Exam: VS T 37.0, P 110, RR 25, BP 100/75, weight 11.3 kg (40th percentile). He is alert, in mother's arms, crying at times, and looks tired. HEENT: anterior fontanel closed, minimal tears, lips dry, mucous membranes tacky, no oral lesions or erythema, TMs normal. His neck is supple. Heart exam reveals mild tachycardia, no murmur. Lungs are clear. His abdomen is flat, soft, and non-tender with hyperactive bowel sounds. Testes are descended, non-swollen, non-tender. His diaper is dry. He moves all his extremities. No rashes are present. His capillary refill time is less than 3 seconds and his skin turgor is slightly diminished.
He is given 40 cc/kg of IV normal saline over two hours in the emergency department, but when given 30 cc of fluid to drink in the ED, he is unable to hold this down and he passes another large diarrheal stool. He is then hospitalized for further management.
Acute gastroenteritis is an ailment that is very common among children. During the first 3 years of life, a child will likely experience about 1 to 3 acute diarrheal illnesses. Diarrhea is defined as an increase in fluidity and volume of feces. Nearly all diarrheal infections are transmitted via the fecal-oral route. Many bacterial etiologies are also food borne.
When evaluating a child with diarrhea and/or vomiting, several important points and observations in the history and physical can help to assess severity and determine its etiology and pathogen involved. Information on the number, volume, and/or fluidity of stools and emesis should be obtained (1). However, this can be rather cumbersome if the number of episodes is large since recording the volume of each stool and emesis is unrealistic and not very helpful clinically, once the number of episodes exceeds 5 to 10. A history of fever, blood or mucus in the diarrhea, foul odor to the diarrhea, a large quantity of diarrhea or diarrhea for a prolonged duration are suggestive of a bacterial etiology. Diarrheal "mucus" is not something that is intuitive to most parents. The best question to ask is whether they have noticed any slimy, gooey, gelatinous, or mucous-like material in the diarrhea. The presence of mucus in the diarrhea is generally indicative of sheets of white blood cells in the diarrhea. The vomiting history should determine whether the vomitus is bilious or bloody (i.e., red or brown) and whether this is associated with abdominal pain. Parents will often convey that the vomitus contains mucus, but unlike the mucus in diarrhea, this is normal gastric mucus that is not helpful clinically. Other important historical items include: weight loss, dietary (intake) history, ill contacts and travel history. The physical exam should focus on signs of dehydration, conditions that may suggest an acute surgical condition and other systemic conditions which may cause these symptoms. The differential diagnosis of vomiting is extensive including systemic conditions such as meningitis, increased intracranial pressure, heart failure, pneumonia, urinary tract infection and many acute surgical conditions such as appendicitis, intussusception, midgut volvulus, etc. The differential diagnosis of diarrhea is more limited and is most often due to gastroenteritis.
Many organisms can cause acute infectious diarrhea and vomiting. These include bacteria, viruses, and parasites. Bacterial etiologies include: Campylobacter, E. coli, Staph aureus, Salmonella, Shigella, Vibrio, Yersinia and a few others. Viral gastroenteritis is by far more common. Amebic and parasitic etiologies are not very common in the United States, but such cases are treatable, making the identification of the pathogen essential.
Lab tests available include: CBC, stool Wright stain, stool culture, stool Rotazyme, serum electrolytes and glucose. In most instances, no laboratory studies are required. A CBC might raise the clinical suspicion of a bacterial etiology if a very high band count is present; however, this may also occur in viral etiologies, therefore it is not very helpful in most instances. A positive stool Wright stain identifies WBCs in the stool. This is suggestive of a bacterial etiology (similar to the history or observation of mucus in the stool), but since it is unable to determine the specific pathogen, it does not help clinicians in determining whether antibiotics are indicated. Thus, in most instances of gastroenteritis, a Wright stain is not helpful. A stool culture can be obtained by swabbing a diarrhea sample or by inserting a swab into the rectum, then rotating it to obtain organisms from the rectal mucosal surface. This latter method is called a rectal swab and it has a higher yield for identifying enteric pathogens, which are more likely to be found on the rectal mucosal surface than in the diarrhea itself. Thus, if a stool culture is to be obtained, it should be done via a rectal swab. A stool Rotazyme is a rapid test which identifies the presence of rotavirus in the diarrhea. A positive Rotazyme negates the need for a stool culture and antibiotic therapy. Serum electrolytes and glucose may be helpful in determining the degree of electrolyte imbalance, metabolic acidosis and hypoglycemia.
Campylobacter is a major cause of diarrhea in the world. Many species have been identified as enteropathogens, but C. jejuni and C. coli are the two predominant species causing acute diarrhea in humans. C. jejuni is the most commonly documented bacterial cause of diarrhea. Transmission occurs by the fecal-oral route, through contaminated food and water or by direct contact from infected animals and people. The main source of C. jejuni and C. coli infection in humans is poultry, although dogs, cats, and hamsters are also potential sources. Outbreaks of diarrhea caused by C. jejuni and C. coli have been associated with consumption of undercooked poultry, red meat, unpasteurized milk and contaminated water. In industrialized nations, C. jejuni mainly affects children younger than 5 years of age, and individuals 15-29 years old. In temperate climates, infections occur mostly during the warm months, and in tropical climates, the incidence is greater during the rainy season. Prodromal symptoms begin after an incubation period of 1-7 days. These include fever, headache, chills and myalgia. Diarrhea accompanied by nausea, vomiting, and crampy abdominal pain occurs within 24 hours. Stools vary from loose and watery, to grossly bloody. Abdominal pain affects more than 90% of patients older than 2 years, and if severe enough, may mimic appendicitis. The clinical presentation may also mimic inflammatory bowel disease. Gradual resolution is to be expected, but in 20% of cases, diarrhea can last longer than 2 weeks. The variation in clinical presentation of Campylobacter diarrhea makes clinical diagnosis difficult. In order to differentiate it from other causes of colitis such as Salmonella, Shigella, E. coli 0157:H7, one has to rely on microbial diagnosis (2).
Rehydration and correction of electrolyte abnormalities are the mainstay of treatment. The use of antimicrobial therapy remains a controversial issue since resolution without antibiotics usually occurs, but early initiation of antibiotic therapy can shorten the duration of infectivity (i.e., the excretion of the organisms), and the duration of symptoms. Erythromycin is the antibiotic of choice for the treatment of C. jejuni enteritis. Since it is not possible to reliably identify Campylobacter as the etiology prior to a positive culture, erythromycin is generally not prescribed until several days after a culture has been obtained. A notable exception might be when diarrhea develops in a contact of an individual who was known to have Campylobacter gastroenteritis.
C. jejuni has also been associated with septicemia, abortion and Guillain-Barre syndrome. C. pylori, now called Helicobacter pylori, does not cause diarrhea, but is associated with peptic ulcer disease. C. fetus rarely causes diarrhea, but is recognized as a cause of fever, bacteremia in immunocompromised hosts, and spontaneous abortion.
E. coli is one of the most common causes of bacterial diarrhea in humans worldwide. Normal bowel flora consists mostly of E. coli; however, some strains of E. coli are pathogenic. Several categories of E. coli cause diarrhea: EHEC (enterohemorrhagic), ETEC (enterotoxigenic), EIEC (enteroinvasive), EPEC (enteropathogenic), and EAEC (enteroaggregative).
EHEC causes a hemorrhagic colitis syndrome manifested by bloody diarrhea without fever. Illness is characterized by abdominal pain with diarrhea that is initially watery, but becomes blood streaked or grossly bloody. E. coli O157:H7 has most commonly been associated with this syndrome, which can also be caused by other strains of EHEC which produce large quantities of a potent cytotoxin. The cytotoxin produced by E. coli is called Verotoxin 1, and is virtually identical to the shigatoxin. Unlike shigellosis or EIEC disease, fever is uncommon in this diarrheal illness. The strains of E. coli producing this potent cytotoxin, are important because 5% to 8% of symptomatic patients go on to develop hemolytic uremic syndrome (HUS).
ETEC typically causes explosive diarrhea, accompanied by nausea, vomiting, abdominal pain, with little or no fever. Symptoms resolve in a matter of days, but these organisms can have a major effect on the hydration status of infants. ETEC is often responsible for the syndrome of "traveler's" diarrhea, since it is more common in non-industrialized countries (note the "T" in enteroToxigenic and Traveler's).
EIEC causes a dysentery-like illness or watery diarrhea caused by an enterotoxin called the EIEC enterotoxin. This illness is clinically indistinguishable from shigella dysentery, and is characterized by fever, abdominal pain, tenesmus, watery or bloody diarrhea.
EPEC rarely causes diarrhea in older children and adults, but has been incriminated in sporadic and epidemic diarrhea in infants and children in the first 2 years of life. This can be remembered as pediatric diarrhea (note the "P" in enteroPathogenic and Pediatric). The diarrhea is non-bloody, and contains mucus. These organisms can cause prolonged diarrhea, especially in the first year of life, a feature that in not shared by the ETEC, EIEC, or EHEC.
EAEC have been associated with acute and chronic diarrhea in developing countries. They can cause significant fluid losses. Like EPEC, these organisms can cause a prolonged diarrhea, and severe abdominal pain, lasting 2-4 weeks.
Management of fluid and electrolyte losses should be the focus of treatment. Early refeeding (within 8-12 hours or initiation of rehydration) should be encouraged, because a prolonged delay in feeding can lead to chronic diarrhea and dehydration. The decision to treat with antibiotics is difficult, because of the lack of a rapid diagnostic test. EPEC and ETEC respond well to treatment with trimethoprim-sulfamethoxazole, but antimicrobial treatment of EHEC organisms may increase the risk of hemolytic uremic syndrome (1). Thus, it is preferable to withhold antibiotics until a culture proven etiologic indication for antibiotics is determined.
S. aureus is a major cause of food poisoning. Symptoms begin within 1-6 hours after ingestion contaminated with preformed S. aureus heat-stable enterotoxins. Symptoms include nausea, vomiting, abdominal pain, diarrhea without fever, and last less than 12 hours (1).
The term "food poisoning" describes a phenomenon in which bacterial contamination of food results in toxin production by the bacteria. This toxin ingestion is what causes the acute symptoms. Typically, the onset after exposure is rapid (i.e., no incubation period is required) and resolution is relatively rapid. Food poisoning should be distinguished from food borne infection, in which the latter is due to contamination of food which is ingested and symptoms develop several days later after a period of incubation.
Salmonella is one of the most frequently reported causes of food borne outbreaks in the United States. Three main species are identified: S. cholerae-suis, S. typhi (known as typhoid), and S. enteritidis. Salmonella gastroenteritis occurs throughout life, but is most common in the first year of life. Many outbreaks of S. enteritidis have been associated with ingestion of contaminated eggs. For clinical disease to occur, 10,000 to 100,000 viable organisms must be ingested. The incubation period for salmonella gastroenteritis is 6 to 72 hours. The major virulence trait of salmonella species, especially S. typhi, is their ability to invade the intestinal epithelium. Nontyphoidal salmonella can also display this trait, but most are associated with watery diarrhea. Salmonella causes several clinical syndromes: 1) acute gastroenteritis, 2) a subacute or prolonged carrier state, 3) enteric fever, bacteremia or both, and 4) dissemination with localized suppuration (i.e., abscesses), osteomyelitis, or meningitis (3).
The most common manifestation of disease caused by salmonella is gastroenteritis. The most prominent symptom is diarrhea, which is usually self-limited, lasting 3-7 days. However, the diarrhea can range from a few stools, to profuse bloody diarrhea to a cholera-like syndrome. Abdominal cramps and fever are usually present (3).
The diagnosis is made by stool culture. Antimicrobial agents such as ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole and some third generation cephalosporins can be used in patients with severe and progressing disease. Initiation of empiric antibiotic treatment is not indicated unless: 1) the infant is very young, 2) the patient is immunocompromised, or 3) sepsis or disseminated infection is suspected.
Infection by shigella is rare in the first 6 months of life, but is common between 6 months and 10 years, and is most common in the 2nd and 3rd year of life. There are 4 major serogroups of Shigella: S. sonnei, S. flexneri, S. boydii, and S. dysenteriae. S. sonnei and S. flexneri are more common causes of diarrhea in the U.S. and Europe. Infection occurs mostly during the warm months in temperate climates, and during the rainy season in tropical climates. Transmission is mainly via person-to-person contact and by contamination of food and water. Only a small inoculum of shigella is required to cause illness (as few as 10 organisms). After ingestion, an incubation period of 12 hours to several days follows, before the development of symptoms. Shigella organisms invade the epithelial cells of the colon, causing colitis. Infected individuals may present with: 1) asymptomatic excretion, 2) enterotoxin-like diarrhea, 3) bacillary dysentery (bloody diarrhea), 4) arthritis similar to Reiter's, 5) HUS after infection with S. dysenteriae (1).
Diarrhea is initially watery and of large volume, and develops into frequent small volume, bloody and mucoid stools. Other clinical features include, vomiting, severe abdominal pain, high fever, and painful defecation. As many as 40% of children with bacillary dysentery will develop neurologic findings. Seizures, headache, confusion, lethargy, and/or nuchal rigidity may be present before or after the onset of diarrhea. In very young and malnourished patients, sepsis and disseminated intravascular coagulation can develop as complications. When sepsis occurs, the mortality rate is high. In those infected with S. dysenteriae serotype 1, hemolytic anemia and hemolytic uremic syndrome are common complications caused by shigatoxin. Post infectious arthritis occurs 2 to 5 weeks after dysenteric illness, and is seen characteristically in patients with HLA-B27 (1).
Stool culture (rectal swab) is the gold standard for diagnosis. The presence of fecal leukocytes, fecal blood, and a CBC leukocytosis with left shift can help support a presumptive diagnosis of bacterial gastroenteritis. Fluid and electrolyte correction and maintenance should be the initial focus of treatment. Drugs that delay intestinal motility (Lomotil, loperamide) should be avoided. Empiric antibiotic treatment of all children strongly suspected of having shigellosis is highly encouraged, and should be initiated as soon as possible. However, other bacterial etiologies may be worsened by antibiotic treatment, so it may be preferable to await culture results.
Vibrio cholera and parahaemolyticus
Vibrio species are common causes of diarrhea worldwide. V. cholera serogroups O1 and O139 have been responsible for cholera epidemics in many developing countries. These serogroups produce profuse watery diarrhea (known as rice water stools) after adhering to and multiplying on small intestinal mucosa. They cause diarrhea by producing several toxins. The most important toxin is the cholera toxin which is a heat stable enterotoxin. V. parahaemolyticus is a common marine organism found in water, shellfish, fish, and plankton. It is generally an uncommon cause of diarrhea, but people who consume raw shellfish and seafood are at higher risk. Infected individuals experience diarrhea, abdominal cramps, nausea, and less frequently, vomiting, headache, low grade fever and chills (1).
Y. enterolitica is a gram negative bacillus that appears to be a common cause of gastroenteritis among children in Europe and Canada, but is uncommon in the United States. Outbreaks have been associated with ingestion of contaminated milk or food. The clinical manifestations vary depending on the age of the involved person. It usually causes acute gastroenteritis in younger children, and mesenteric adenitis in older children. Most infections occur in children 5 to 15 years of age, and incidence is greater during the winter months. Children younger than 5 years old usually have self-limited gastroenteritis, lasting from 2 to 3 weeks. Symptoms include diarrhea accompanied by fever, vomiting, and abdominal pain. The abdominal pain is colicky, diffuse, or localized to the right lower abdomen. Stools may be watery, containing blood or mucus, and fecal leukocytes are commonly present. Children older than 6 years often present with abdominal pain associated with mesenteric adenitis that mimics acute appendicitis. Intussusception secondary to Y. enterolitica has also been described in children.
While isolation of Y. enterolitica from stool specimens is difficult, it is readily isolated from blood or lymph nodes. Serologic diagnosis can be obtained with enzyme-linked immunosorbent assays. Antibodies are detectable from 8-10 days after the onset of clinical symptoms, which persist for several months.
Y. enterolitica gastroenteritis is usually self-limited, therefore antibiotic therapy is only indicated for complicated infections, and compromised patients. It is usually susceptible to trimethoprim-sulfamethoxazole, aminoglycosides, tetracycline, chloramphenicol, and third generation cephalosporins. It is resistant to penicillin, ampicillin, carbenicillin, erythromycin, and clindamycin (4).
Other bacteria that cause an acute diarrheal illness include Bacillus cereus, Aeromonas hydrophila and Plesiomonas shigelloides. Clostridium difficile is associated with pseudomembranous colitis, and Clostridium perfringens can cause a short duration food poisoning syndrome.
Diarrhea and vomiting caused by viruses are usually self-limited. It usually manifests as watery diarrhea, without blood or mucus. The most common accompanying symptom is vomiting. Other symptoms include abdominal cramps, nausea, headaches, myalgias and fever. Four viral groups are regarded as medically important causes of acute gastroenteritis (rotaviruses, astroviruses, enteric adenoviruses, and calciviruses). They are all spread largely via the fecal-oral route.
Rotavirus accounts for 82,000 hospitalizations and 150 deaths per year in the United States. It is a very common cause of acute gastroenteritis in infants and children, responsible for over 50% of cases of acute diarrhea in children. Rotavirus causes severe illness in children 6-24 months. Most children (more than 90%) have been exposed to rotavirus by their 3rd birthday. It is the most common cause of diarrhea in infants and children in the winter months in colder climates, and is responsible for 35-50% of hospitalization for infants and children with acute diarrhea. Clinical features range from asymptomatic infection, to diarrhea preceded by severe vomiting. The incubation period is 2-4 days, and viral shedding occurs from a few days before, to 10 days after the onset of illness. Newborns tend to have asymptomatic infections in the first few months of life, because transplacental antibodies and breastfeeding are protective. Clinical symptoms in infants and children usually consist of fever, abrupt onset of vomiting and watery diarrhea. One third of children will also have a concurrent respiratory infection. The diagnosis can be made by a number of enzyme immunoassays (Rotazyme) and latex agglutination tests with good specificity and sensitivity. Stools collected early in the course of the illness are more likely to contain virus, than those collected 8 or more days after the onset of illness. Treatment is directed toward correction of dehydration with oral fluid replacement. Breastfeeding is the most important and available preventive strategy, because human colostrum contains rotavirus antibodies (5).
Adenovirus commonly causes a wide range of human diseases, including conjunctivitis, pneumonia, and upper respiratory infections. A subgroup of adenovirus (enteric adenovirus) has been found to cause acute gastroenteritis, lasting 4 to 20 days. After rotavirus, enteric adenovirus is the next most common cause of viral gastroenteritis in infants and children, accounting for 5% to10% of hospitalizations for acute gastroenteritis in children. They have been linked to outbreaks in child care centers, and asymptomatic excretion can occur. Most episodes occur in children less than 2 years. Infection increases in the summer months. Symptoms are indistinguishable from those associated with rotavirus but are less severe. The diagnosis is a presumptive one. Research laboratory confirmation can be made by solid phase immunoassays, electron microscopy, and viral culture but these studies are not routinely available. As with rotavirus, treatment is aimed at replacing fluid losses, and at correcting electrolyte abnormalities (5).
Caliciviridae primarily infect infants and young children. Human caliciviruses (HuCVs) have been associated with outbreaks from contaminated food or water in restaurants, schools, hospitals, summer camps and cruise ships. They are divided into 4 genera: Norwalk-like calciviruses (which causes illness mostly in adults), Sapporo-like calcivirus (which primarily cause pediatric gastroenteritis), rabbit-like calcivirus, and swine-like calicivirus. Hepatitis E, which was previously classified as a calcivirus, is no longer classified in this family. The gastroenteritis is indistinguishable from that of rotavirus. The incubation period is 12 hours to 4 days. Excretion lasts 5-7 after the onset of symptoms, and can continue for 4 days after the resolution of symptoms (5). The diagnosis is presumptive, but epidemiologic and research confirmation of these etiologic agents can be made by electron microscopy.
Astrovirus infection is believed to occur very commonly, since 80% or more adults have antibodies against the virus. They cause watery diarrhea, especially in children younger than 4 years. Symptoms are mild, consisting of fever and malaise, followed by watery diarrhea. Vomiting is uncommon. The incubation period is 3 to 4 days, and excretion typically lasts for 5 days after onset of symptoms (5).
Protozoan and parasitic gastroenteritis
Several protozoans cause diarrhea: Giardia lamblia, Entamoeba histolytica, Cryptosporidium parvum, Isospora belli, Microsporidium species, and Cyclospora cayetanensis. Within the intestinal tract, 3 organisms, namely Giardia lamblia, Entamoeba histolytica, and Cryptosporidium parvum are the most important.
Infection with E. histolytica occurs more frequently in tropical countries, especially in areas with poor sanitation. The life cycle of E. histolytica has 2 stages: the trophozoite which is found in diarrheal stools, and the cyst, which is more predominant in formed stools. The cysts are transmitted primarily by the fecal-oral route in contaminated food and water. The minimum incubation period is 8 days, but ranges up to 95 days. The clinical symptoms that occur in patients with amebiasis consist of: 1) Intestinal amebiasis, with the gradual onset of colicky abdominal pain and frequent bowel movements, tenesmus, and flatulence. 2) Amebic dysentery, characterized by profuse diarrhea containing blood, mucus, and constitutional signs such as fever and dehydration. 3) Hepatic amebiasis, presenting with an amebic abscess within the liver often without diarrhea. 4) Asymptomatic infection. E. histolytica can usually be identified in stool samples, or acute infection can be confirmed by serology. Metronidazole is the treatment of choice.
Giardia lamblia is a flagellated protozoan that is a major cause of diarrhea, especially in patients who travel to endemic areas. It is the most common intestinal protozoan found in the United States. Children seem to be more susceptible to Giardia than adults. Like E. histolytica, the life cycle consists of 2 stages: the trophozoite (motile form), and the cyst. IgA deficiency and hypogammaglobulinemia predispose patients to symptomatic infection. The clinical manifestations are foul-smelling diarrhea, with nausea, anorexia, abdominal cramps, bloating, belching, flatulence, and weight loss. Abdominal distention and cramps can last for weeks to months. The illness is usually self-limited, lasting 2 to 6 weeks, but may become chronic. Chronic symptoms can include fatigue, nervousness, weight loss, steatorrhea, lactose intolerance, and growth retardation. The easiest way to diagnose Giardia is by identifying cysts in a stool specimen. However, these specimens are frequently falsely negative. The diagnosis can also be made by antigen detection tests, endoscopic examination of the upper small intestine, by mucosal biopsy or by collection of jejunal contents. The treatment of choice for both symptomatic and asymptomatic patients is furazolidone or metronidazole. An alternative drug is quinacrine (6).
Cryptosporidium organisms are small protozoans that are a common cause of enteric infection worldwide. The oocyst form of cryptosporidium is found in feces, and is the infective form. Cryptosporidium parvum is thought to be the cause of infection in humans. Cryptosporidium causes cryptosporidiosis mainly in immunocompromised patients, infecting approximately 3% to 4% of patients with AIDS in the United States. Another high risk group for acquiring infection with this organism, are children 6 to 24 months old. It is acquired by fecal-oral transmission, and has an incubation period of 2 to 14 days. Because the oocyst is highly stable in the environment, contaminated drinking water, swimming pools and apple cider are major sources of outbreaks. Several outbreaks of diarrhea in day care centers have been attributed to cryptosporidium. In the United States, 13% of children less than 5 years old, 38% of those 5 to 13 years of age, and 58% of adolescents 14 to 21 years old are seropositive for C. parvum. Symptoms are self-limited in immunocompetent patients, consisting of watery nonbloody diarrhea, accompanied by vomiting, flatulence, abdominal pain, myalgias, anorexia, weight loss, and low-grade fever. Symptoms last an average of 9 days in immunocompetent patients, but can last months in immunocompromised hosts, causing large fluid losses, profound malabsorption and weight loss. The diagnosis of cryptosporidiosis is made by demonstrating the presence of cryptosporidium oocysts in stool specimens. Patients with diarrhea who attend day care centers, those with AIDS or other immunodeficiencies are at higher risk. There is no specific antimicrobial therapy for cryptosporidiosis (7).
Fluid losses resulting from acute vomiting and diarrhea can lead to dehydration. Diarrhea is the most common cause of dehydration in infants and children, and is a leading cause of death worldwide in children less than 4 years of age. Quantifying the degree of fluid loss by history and the amount and type of fluid intake can help to determine dehydration severity and the risk of electrolyte imbalance. The amount of urine output and the presence or absence of tears as well as the presence of documented weight loss, can help determine the severity of dehydration present. Other important aspects of the history include the presence of fever, sweating and hyperventilation, which may cause insensible losses, contributing to the degree of dehydration.
The vital signs can offer clues on the degree of dehydration present. Tachycardia can indicate moderate dehydration, whereas hypotension is a late sign of severe dehydration. The absence of tachycardia cannot be used to rule out dehydration. An increase in the respiratory rate is associated with a higher degree of dehydration, whereas in mild dehydration, the respiratory rate is normal. Attention should be paid to the child's overall appearance and mental status (alert, irritable, tired-appearing, poorly responsive, unresponsive). Other pertinent exam findings include the fontanelle (sunken or not), the eyes (presence or absence of tears, sunken or not), the mouth (dry lips, tacky or sticky mucous membranes), the skin (cool or warm, skin turgor). Measurement of the capillary refill time is a variable and unreliable indicator of dehydration. It should be performed in a warm room. Light pressure is applied to the finger nailbed. And the time from blanching to restoration of color to the nailbed is measured. It may be preferable to assess capillary refill centrally (over the chest or forehead) and peripherally (fingers), so that the two can be compared. A delay of less than 2 seconds is normal. Delays of 2 to 3 seconds may indicate moderate dehydration, and more than 3 seconds in delay may indicate severe dehydration. Most children with clinically significant dehydration, will have 2 of the following 4 clinical findings: 1) capillary refill greater than 2 seconds, 2) tacky mucous membranes, 3) no tears, and 4) ill appearance (8).
The decision to hospitalize or to attempt outpatient management will be based on the clinical findings, combined with a history of fluid intake, the frequency of urination, assessment of concurrent stool losses and the response to therapy.
Once a child is presumed to be dehydrated, the degree of dehydration needs to be determined. Acute weight loss can be used to determine the degree of dehydration, but accurate baseline weights in growing children are almost never known. Clinical criteria can be used to estimate degrees of dehydration. Mild dehydration is 5% or less, moderate is about 10%, and severe dehydration is about 15% or greater. This classification is relative and not well standardized. If severe dehydration or uncompensated shock is present, the patient should be immediately treated with an IV fluid infusion (20 cc/kg of normal saline or lactated Ringer's) to restore the intravascular volume. It is likely that more than one fluid bolus may be necessary to restore the patient's intravascular volume, since 20 cc/kg only corrects 2% of the body weight. Therefore, the patient should be reassessed after each fluid bolus (8).
Children with mild to moderate dehydration can be initially treated with oral rehydration. Contraindications to oral rehydration therapy (ORT) include severe dehydration, intractable vomiting, and severe gastric distention. Children who had initially received IV fluid infusions for severe dehydration who now feel well enough to take oral fluids should also be considered for oral rehydration. Oral rehydration therapy (ORT) can be as effective as IV therapy. It is noninvasive and inexpensive. The AAP recommends that rehydration solutions contain 70-90 mEq/L of sodium, 20 mEq/L of potassium, and 2.0-2.5 grams/dL glucose. Examples of rehydration solutions (ORS) are: Rehydralyte (70mEq/L Na, 20 mEq/L K, 2.5% glucose, and the WHO solution (90m Eq/L Na, 20 mEq/L K, 2% glucose). ORT should initially be given in small, frequent volumes, 5 to 20 cc every 5-10 minutes, and advanced slowly to approach 5 cc/min. The degree of dehydration and the presence of ongoing losses dictate the volume of fluids to be administered. If the degree of dehydration is mild (3-5%), the volume of ORS administered should be 50 cc/kg (i.e., 5% of the body weight) over 4 hrs. Those with significant dehydration (5-10%) should received 100 cc/kg (i.e., 10% of the body weight) of ORS over 4 hours. In either case, an additional 10 cc/kg should be given for each diarrheal stool seen. Once rehydration is complete, maintenance fluid is given. Examples of maintenance oral solutions are: Pedialyte and Infalyte, containing 45-50 mEq/L Na, 2-2.5 mEq/L K, 1.5-2.5% glucose (9).
Patients with mild dehydration can potentially be managed without laboratory analysis. However, in moderate or severe dehydration, laboratory studies should be obtained to look for electrolyte abnormalities of to measure the degree of metabolic acidosis.
Children who are severely dehydrated and those who cannot retain oral fluids because of intractable vomiting should be hospitalized and treated with IV fluid. Once the initial resuscitation phase is completed, replacement IV therapy should be instituted, taking into account fluid and electrolyte deficits as well as ongoing losses. Usually, half of the replacement therapy in addition to the maintenance fluid requirement is given over the first 8 hours, and the second half is given over the next 16 hours. However, patients with hypernatremic dehydration (serum sodium >150mEq/L) require special intervention. After initial management with normal saline or lactated Ringer's, the replacement fluid is given more slowly, over 48 hours or more. This is done because rapid correction of hypernatremia can result in acute brain swelling, brain herniation, and death. Therefore, care should be taken to avoid dropping the serum sodium by more than 15mEq/L per 24 hours.
Once a child is adequately rehydrated, the question of when to start feedings arises. It was previously perceived that a period of "gut rest" should follow rehydration of patients with acute gastroenteritis. However, numerous trials have shown no advantage to this strategy. The concept of early refeeding is replacing the old concept of "gut rest". Numerous trials have shown that early feeding of age-appropriate foods results in faster recovery. Breast fed infants should continue nursing despite diarrhea. Following rehydration, children with mild diarrhea who drink milk or formula can tolerate full strength feedings. The traditional BRAT diet (bananas, rice, applesauce, toast), although acceptable, should be considered to be a concept representative of a bland diet rather than a specific diet. Controlled clinical trials have shown that starches, complex carbohydrates (rice, wheat, bread, potatoes, cereals), soups, fresh fruits and vegetables, yogurt, and lean meats are better choices, and well tolerated (9). Fatty foods, juices, teas, sweetened cereals, soft drinks, are poor choices, and should be avoided. Some patients may benefit from lactose-free or low-lactose formulas.
Most pediatricians and experts recommend against using anti-diarrheal agents such as Imodium (loperamide), Pepto-Bismol (bismuth subsalicylate), and Kaopectate. This is more of a precaution since many studies do show some beneficial effects from these medications in patients with mild diarrhea. However, patients with mild diarrhea will get better on their own so these medications are usually not necessary. For young children with severe gastroenteritis, there is insufficient data to confirm the benefit and safety of these medications, which is why they cannot be recommended routinely at this time.
1. Which diarrhea causing organism may be also cause neurologic symptoms?
2. What is the most common viral cause of acute gastroenteritis, and what are its associated symptoms?
3. How is Giardia lamblia most easily diagnosed and how is it treated?
4. List 4 physical signs of dehydration in children?
5. How are children with mild dehydration initially treated?
6. How are children with severe dehydration initially treated?
1. Pickering LK, Cleary TG. Chapter 52-Approach to patients with gastrointestinal tract infections and food poisoning. Feigin RD, Cherry JD (eds). Textbook of Pediatric Infectious Diseases, 4th edition. 1998, Philadelphia: W.B. Saunders, pp. 567-589.
2. Ruiz-Palacios GM, Pickering LK. Chapter 163- Campylobacter and Helicobacter. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 953-956.
3. Chacon-Cruz E, Pickering LK. Chapter 179- Salmonella infections. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 1002-1006.
4. Cleary TG, Gomez HF. Chapter 187- Yersenia Enterolitica. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 1042-1044.
5. Matson DO, Pickering LK, Douglas K. Mitchell DK. Chapter 212-Viral Gastroenteritis. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 1147-1150.
6. Klish WJ. Chapter 224- Giardia Lamblia. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 1176-1177.
7. Hughes WT. Chapter 223- Cryptosporidiosis. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 1174-1176.
8. Shaw KN. Chapter 18- Dehydration. In: Fleisher GR, Ludwig S, Henretig FM (eds). Textbook of Pediatric Emergency Medicine, 4th edition. 2000, Philadelphia, Lippincott Williams & Wilkins, pp. 197-201.
9. American Academy of Pediatrics. Practice parameter: the management of Acute Gastroenteritis in Young Children. Pediatrics 1996;97:424-435.
10. Sharifi J. Ghavami F. Oral rehydration therapy if severe diarrhea dehydration. Clin Pediatr 1984;23:87-90.
11. Bezerra JA, Stathos TH, Duncan B, et al. Treatment of infants with acute diarrhea: What's recommended and what's practiced. Pediatrics 1991:90:1-4.
12. Reis EC. Goepp JG, Katz S, et. al. Barriers to the use of oral rehydration therapy. Pediatrics 1994:93:708-711.
13. Feigin RD, Kaplan JB. Chapter 156-Aeromonas. In: McMillan JA, DeAngelis CD, Feigin RD, et al (eds). Oski's Pediatrics, 3rd edition. 1999, Philadelphia: Lippincott Williams & Wilkins, pp. 932-933.
Answers to questions
2. Rotavirus. It causes fever, vomiting, and watery diarrhea
3. The diagnosis can be made by antigen detection, identifying cysts in the stool, endoscopy or examination of jejunal contents. It is treated with metronidazole or furazolidone.
4. Sunken fontanelle, absence of tears, sunken eyes, sticky/tacky oral mucosa, delayed capillary refill, reduced skin turgor, inactivity/lethargy, tachycardia, hypotension.
5. With oral rehydration, small frequent volumes 5-20cc every 5-10 minutes, advanced slowly.
6. With IV fluid infusion of normal saline or lactated Ringer's at 20cc/kg. Oral rehydration with ORS is commonly employed in other countries.