Diarrhea is defined as an increase in the liquidity and/or frequency of the stools and can be a primary feature of both acute and chronic conditions


Diarrhea is defined as an increase in the liquidity and/or frequency of the stools

and can be a primary feature of both acute and chronic conditions. It reflects an

increase in stool water content due to impaired water absorption and/or active

water secretion by the intestine. Although the advent of oral rehydration therapy

(ORT) has dramatically reduced the mortality rates in the past 50 years, diarrhea

remains a major cause of morbidity and mortality in children, particularly among

those in developing countries.


Most episodes of diarrhea occur secondary to 1 of 5 types of mechanisms:

malabsorptive, secretory, osmotic, dysmotility, and inflammatory. Malabsorption

is due to a decrease in absorptive surface area, as occurs after intestinal resection

(short bowel syndrome) or with intestinal villous atrophy, as seen in celiac

disease. Secretory diarrhea is caused by secretagogues such as bacterial toxins

(eg, cholera), gut regulatory peptides (eg, vasoactive intestinal polypeptide),

short-chain fatty acids, and bile salts, which can induce intestinal water secretion

while inhibiting absorption. Secretory diarrhea characteristically persists even

when the patient is in a fasting state. Osmotic diarrhea results from the

intraluminal presence of malabsorbed solutes, such as lactose, which exert

significant osmotic pressure that results in secretion of water into the intestines.

In contrast to secretory diarrhea, osmotic diarrhea characteristically decreases or

stops completely during fasting. Dysmotility can lead to increased peristalsis,

causing diarrhea due to rapid transit, or to decreased peristalsis, causing diarrhea

due to bacterial overgrowth. Inflammatory disorders cause diarrhea by several

mechanisms including release of prosecretory eicosanoids and cytokines; altered

tight junction function, decreasing the mucosal absorptive capacity or the

capacity to reabsorb bile acids; and/or disturbances in motility. One or more of

these mechanisms may be operative in an individual during an episode of


Acute diarrhea (lasting < 1 week in duration) accounts for 2 to 3 million

deaths per year, with most deaths occurring in young children in developing

countries. In the United States, it is estimated that 220,000 children under 5

years of age are hospitalized each year for acute diarrheal illnesses, which

account for 9% of all hospitalizations in this age group. Enteric infections account for most

cases of acute diarrhea, with viruses being responsible for the majority (60–80%)

in children, especially in those under the age of 2 years. Of these, rotaviruses

were previously the most prevalent cause in the United States, but noroviruses

have supplanted rotavirus as the most common cause of medically attended

diarrhea in children in the era of rotaviral vaccination. Worldwide rotavirus

remains the most common cause of moderate to severe diarrhea. This is due to

incomplete penetration of the vaccine and diminished vaccine efficacy in

children in developing countries. In the Northern hemisphere, rotavirus occurs

with a peak incidence in the winter. Other winter-predominant viral agents, such

as astroviruses and caliciviruses, tend to infect older children and cause illness of

shorter duration. Norovirus, a calicivirus, is an important cause of foodborne

illness and causes outbreaks of gastroenteritis in the community, including

schools, daycare centers, hospitals, cruise ships. In contrast to rotavirus,

enteroviruses tend to peak during the summer months and cause diarrhea that is

more prolonged. Viral gastroenteritis is typically transmitted by the fecal-oral



Manifestations of acute diarrhea will depend on the causative agent and severity

of involvement. Viral-induced diarrhea typically begins with vomiting followed

by loose to watery stools. The diarrhea may be accompanied by low-grade fever

and abdominal cramping. Most cases are mild and self-limiting with complete

resolution within 5 to 7 days. In moderate to severe cases, excessive fluid and

electrolyte losses can result in dehydration and, in some cases, hypovolemic

shock. Bacterial pathogens often cause diarrhea via toxins that bind to

enterocytes and are eliminated with villous cell turnover. For this reason, the

diarrhea induced by these agents is usually of shorter duration. Common

bacterial pathogens associated with diarrhea include Campylobacter, Shigella,

Salmonella, Yersinia enterocolitica, and various types of Escherichia coli.

Dysentery is characterized by the presence of blood, pus, and mucus in the

stools, and usually occurs with bacterial causes of diarrhea. Shigella is a

common cause of dysentery and is highly contagious, and even a very small

number of organisms can cause infection. In contrast, Salmonella species

generally require high inoculums. Y enterocolitica can cause colitis, appendicitis,

and peritonitis. Enterohemorrhagic E coli, including the prototypical strain

O157:H7, elaborate Shiga-like toxins that predispose to hemolytic uremic

syndrome, typically developing 2 to 14 days after onset of diarrhea.

Enteroinvasive E coli is similar in presentation to Shigella but requires a higher

inoculum. Clostridium difficile causes a disease spectrum ranging from mild

diarrhea to fulminant pseudomembranous colitis. Most cases of C difficile

infection are associated with antibiotic use, but this is not an absolute

requirement for disease. Owing to its formation of persistent spores, C difficile

has become a major source of nosocomial morbidity. Common causes of non–

dysentery bacterial diarrheas include Aeromonas, Plesiomonas, and Vibrio

cholerae. Cholera is the most rapidly fatal diarrheal disease worldwide,

presenting in severe cases with profuse watery (“rice water”) stools leading to

acute dehydration and intravascular volume depletion.

Protozoal enteric infections can manifest either as acute or chronic diarrhea.

Giardia lamblia is a common food and waterborne protozoan that infects the

duodenum. Acute giardiasis is marked by sudden onset of profuse watery

diarrhea, abdominal cramps, bloating, and at times vomiting. Cryptosporidium

parvum typically causes large-volume watery diarrhea, nausea, vomiting, and

fever. It has been associated with communitywide outbreaks and is a relatively

common cause of diarrhea in immunocompromised individuals such as those

with AIDS.


In children presenting with acute diarrhea, the history should focus on duration

of symptoms, frequency and volume of stool output, and stool characteristics.

Watery diarrhea suggests more proximal small intestinal disease, while diarrhea

containing blood and mucus more commonly implies colonic inflammation.

Vomiting in addition to diarrhea suggests the presence of an organism impacting

the upper intestine, such as enteric viruses, enterotoxin-producing bacteria, or

giardia. Pain in the lower abdomen and rectum or pain with defecation

(tenesmus) indicates distal colonic involvement and inflammation, as seen with

bacterial infections. A history of childcare center attendance, sick contact

exposures, travel to a diarrhea-endemic area, recent use of antimicrobial drugs,

and ingestion of seafood, unwashed vegetables, unpasteurized milk,

contaminated water, or uncooked meats provide valuable clues as to the possible

cause of the diarrhea. Institutionalized children and those recently returning from

developing countries are more likely to have bacterial or parasitic pathogens.

Additional information obtained on history should be aimed at determining

the severity of the stool fluid losses and identifying other conditions that could

place the child at added risk for an adverse outcome. Thirst is an early symptom

of impending dehydration. The amount of oral intake of fluids and voiding

frequency should be determined as part of the history. Increased respiratory rate

or work of breathing may indicate acidosis, while lethargy and a decrease in

sensorium are features of shock. Past histories of underlying chronic disease,

immunodeficiency state, or history of prior intestinal surgery are all important

features to be determined in the history.

In children with acute diarrhea, the physical examination should be focused

on identifying clinical signs of dehydration with careful evaluation of vital signs

and mental status. Loss of skin tissue turgor and a decrease in mucous membrane

moisture are clinical indicators of dehydration. With mild dehydration (0–5%),

the mucus membranes are slightly dry and skin tissue turgor is slightly

decreased. As dehydration progresses to a moderate degree (5–10%), the mucus

membranes will be obviously dry and the decrease in tissue turgor is easily

elicited. Dehydration that progresses beyond this stage (≥ 10%) is accompanied

by additional features of sunken eyes and a sunken fontanelle in the young

infant. Further inadequate replacement of fluid losses will result in hypovolemic

shock, which can lead to death if left untreated. Clinical features of shock

include tachycardia, cool extremities, and delayed capillary refill in the early

stages (state of compensated shock). Children with hypotension and altered level

of consciousness suggest later stages of hemodynamic changes (state of

uncompensated shock).

It is important to differentiate acute infectious diarrhea from acute surgical

conditions and more chronic diarrhea disorders to minimize the potential for

serious morbidity and mortality. Young children with intestinal intussusception

may present with bloody mucoid diarrhea associated with severe cramping,

abdominal pain, inconsolable crying, and, in some cases, lethargy. Acute

appendicitis can present initially with diarrhea prior to onset of the classic

symptoms of abdominal pain. The inflamed appendix can irritate the colon and

produce frequent small-volume mucous-containing stools. This same process

can occur in the case of an intra-abdominal or pelvic abscess. C difficile–induced

pseudomembranous colitis and shigellosis can progress to toxic megacolon, with

potential complications that include perforation, peritonitis, systemic sepsis

syndrome, and shock. Infections with Shiga-like toxin–producing organisms

such as enterohemorrhagic E coli often present with bloody diarrhea and can

progress to the hemolytic uremic syndrome characterized by the triad of

hemolytic anemia, thrombocytopenia, and acute renal insufficiency.

Laboratory tests are seldom required in children with acute diarrhea in the

absence of clinical features of dehydration or other worrisome findings, such as

blood in the stools. The decision to perform any investigations and the choice of

test will depend on the clinical concern. Analysis of a urine sample for specific

gravity, blood, leukocytes, and culture provides information on the child’s

hydration status and may identify a urinary tract infection as the cause of the

diarrhea. Blood samples for determining electrolytes, carbon dioxide, and urea

nitrogen are sometimes needed to evaluate for electrolyte imbalances, acidosis,

and acute renal insufficiency. A complete blood count with differential and

platelet count may help in evaluating for sepsis or the hemolytic uremic

syndrome (anemia and thrombocytopenia). In cases of dysentery or suspected

bacterial causes of diarrhea, stool samples should be sent for microscopy and

culture. Fecal leukocytes indicate the presence of inflammation in response to

invasive or cytotoxin-secreting pathogens but are not a sensitive screening

method. A stool culture should be performed in every child with bloody diarrhea

because bacterial pathogens have been implicated in up to 20% of such cases.

Microbiological investigations should also be considered in the following

circumstances: children with underlying chronic conditions (eg, cancer, sickle

cell disease, inflammatory bowel disease), severe clinical conditions (eg, sepsis),

prolonged symptoms (> 7 days), during outbreaks (eg, childcare, school,

hospital), and a history of travel to at-risk areas. Stool rotavirus assays using

immunologic or polymerase chain reaction (PCR) techniques are widely

available for the diagnosis of this common cause of acute gastroenteritis. Testing

for rotavirus is generally not necessary in cases of suspected viral diarrheas

because it is unlikely to have any impact on the management of the child. More

recently, some centers have begun to use rapid gastrointestinal PCR arrays (eg,

FilmArray) to assess for common viral, bacterial, and protozoal infections.

Diarrhea in the child with a chronic illness, immunocompromised state, or

primary immunodeficiency requires more extensive evaluation for opportunistic

infections. Very young infants are at increased risk for complications of diarrheal

illnesses with dehydration occurring more rapidly in this age group. Infants

under 2 months of age with bacterial diarrhea infections are at increased risk for

an associated bacterial septicemia.


Treatment of children with acute diarrhea should first be directed toward

preventing dehydration and maintaining nutrition. Maintenance of hydration is

best achieved by replacing stool fluid and electrolyte losses with oral rehydration

solutions at the onset of symptoms. Use of ORT provides rapid, safe, effective,

and inexpensive therapy for diarrheal disease. Oral rehydration solutions are

effective for treating children regardless of the cause of diarrhea or the child’s

serum sodium level at the onset of therapy. Most replacement solutions contain

50 to 90 mmol/L of sodium and 20 to 30 mmol/L of potassium. The addition of

glucose (optimally 110–140 mmol/L or 20–25 g/L) enhances the rate of water

uptake by promoting transport of sodium across the enterocyte via the brush

border membrane glucose-sodium cotransporter. Glucose-sodium–coupled

uptake is an energy-dependent, active process and, as such, occurs rapidly. In

contrast, water uptake is a passive process dependent on the movement of

solutes from the intestinal lumen across the mucosa. Liquids such as fruit juices

and sodas have high levels of sugars but contain insufficient electrolytes to

replace fecal losses and are therefore less effective options. In addition, because

of the high sugar content, they are hypertonic, which can lead to increased stool

water losses. For these reasons, they should not be used in place of appropriate

ORT solutions. In infants, the glucose- and electrolyte-containing ORT solutions

should be offered in addition to the regular breast milk, formula, or solid feeds.

Vomiting is frequently present during the early stages of an acute viral diarrhea

illness but is not a contraindication to the attempted use of oral fluid therapy.

Oral fluids in small volumes at frequent intervals are generally well tolerated and

minimize the potential for vomiting. Children with acute diarrhea who maintain

their hydration status have less anorexia and hence tend to maintain their nutrient

intake. Continued feeding is recommended because amino acids and short-chain

fatty acids promote enterocyte growth and mucosal repair. Although absorption

of nutrients is compromised during an episode of infectious diarrhea, dietary

carbohydrate, protein, and fat can still be absorbed. Children who remain wellnourished

generally recover from the diarrheal illness faster than those in whom

nutritional status is compromised.

For children presenting with clinical signs of dehydration, therapy should be

aimed at first correcting the fluid deficit and then maintaining hydration by

replacing ongoing losses while maintaining nutrition. Correction of fluid deficits

can usually be accomplished via oral administration of appropriate glucose

electrolyte solutions. Intravenous fluid therapy is required in only a small

number of cases in which there is an accompanying ileus or the vomiting is of

such magnitude that oral therapy fails. The fluid deficit is calculated on the basis

of the clinical degree of dehydration and should provide 50 mL/kg body weight

for mild dehydration (5%) and 100 mL/kg body weight for moderate

dehydration (10%). The calculated deficit volume should be replaced over a

period of 4 to 6 hours by offering frequent small volumes from a bottle, cup, or

spoon, or it can be delivered as a continuous slow-rate infusion via a nasogastric

tube. Enteral administration of fluid replacement therapy through a nasogastric

tube is effective and it is associated with fewer side effects than intravenous (IV)

rehydration. However, this practice may be limited by low acceptance by

families and/or healthcare workers. This process can be repeated if the

dehydration is not fully corrected at the end of the 6-hour period. Once the child

is fully rehydrated, the process of providing fluids to maintain hydration should

begin, and the child should be encouraged to resume regular feedings.

Children with moderate to severe dehydration who also have clinical findings

of shock require urgent therapy to reestablish an adequate circulating blood

volume. Fluid resuscitation in these cases requires intravenous administration of

an isotonic crystalline solution such as normal saline. An initial rapid infusion of

20 mL/kg body weight of normal saline will correct the shock in most children

with dehydration due to diarrhea. In those with persistent clinical signs of shock,

a second infusion of 20 mL/kg body weight can be administered. After the

child’s circulatory compromise has been corrected, the process of rehydration

with maintenance therapy and early reintroduction of feeds as outlined

previously should follow.

Antibiotics generally are not recommended for children presenting with acute

bloody diarrhea unless a specific pathogen has been isolated. Antibiotics are

indicated in immunocompromised children or those with septicemia due to

Salmonella, Campylobacter, or Yersinia. In patients with diarrhea due to

enterohemorrhagic E coli, antibiotic therapy has been implicated as a risk factor

for the subsequent development of hemolytic uremic syndrome. Confirmed

shigellosis and cholera should be treated with an antibacterial drug. Depending

on local sensitivities, trimethoprim/sulfamethoxazole or ampicillin may be used

for shigella and azithromycin is most effective in children with cholera. Some

probiotic supplements have been shown to decrease the duration of the acute

diarrheal illnesses. Probiotics may exert an immunomodulatory effect on the host

and static effect on some enteropathogens, thereby altering the intestinal

microflora. Saccharomyces boulardii, a nonpathogenic yeast, has been used to

treat and decrease the recurrence rate of C difficile enterocolitis, and

Lactobacillus rhamnosus GG may lessen the severity of rotaviral dehydration.

Zinc is recommended as an adjunct to ORT in low-income countries. However,

its efficacy in nonmalnourished children is not supported by solid evidence.

Antidiarrheal agents are not recommended in the management of acute

diarrhea in infants and children. Adsorbents such as magnesium aluminum

silicate and psyllium fiber may alter stool consistency but do not reduce absolute

fecal water and electrolyte loss. Smectite has been shown to be effective in

reducing the duration and severity of diarrhea in selected settings including

Europe, South America, Malaysia, and China. Racecadotril, which is not

approved for use in the United States, is effective in reducing the duration and

severity of diarrhea; evidence is stronger in hospitalized children and in selected

settings including Europe, South America, Malaysia, and China. Ondansetron,

administered orally or intravenously, is effective in reducing vomiting and

avoiding hospital admission. A single dose may be considered in young children

presenting to the emergency department with vomiting to ensure oral rehydration

and reduce hospital admissions. However, ondansetron has a warning label from

the US Food and Drug Administration and the European Medicines Agency and

its use therefore is indicated with caution.

Opiate antimotility agents such as loperamide and diphenoxylate-atropine can

cause ileus, nausea, and sedation are generally discouraged. Furthermore, opiateinduced

ileus can cause pooling of secreted fluid in the intestine and may

promote intestinal bacterial overgrowth.


Enteric pathogens are largely acquired via the fecal oral route and therefore

prevention is accomplished best by public health educational efforts promoting

good hand hygiene, having access to clean water and ensuring safe food

preparation. Use of hand sanitizers containing at least 60% alcohol are beneficial

but are less effective than handwashing with soap and water for infections due to

C difficile. Children with acute diarrhea should be considered contagious until

the diarrhea has completely resolved and should be isolated from groups such as

those attending daycare centers while they are still symptomatic. The rotavirus

vaccine is recommended in all national immunization programs by the World

Health Organization. Its global efficacy has been demonstrated in preventing

against poor outcomes related to acute diarrhea in children younger than 5 years

of age.

Episodes of diarrhea lasting 7 to 13 days are usually defined as prolonged

diarrhea. Duration of 14 days or more is defined as chronic or persistent

diarrhea. Many, but not all, cases of prolonged diarrhea do not resolve and

become chronic or persistent. Most cases of chronic diarrhea occur as a result of

an initial acute infection with an enteric viral or bacterial pathogen. The ensuing

mucosal damage fails to resolve for reasons that are not entirely clear, leading to

a postinfectious enteropathy. Damage to the mucosal brush border can cause

malabsorption due to both loss of intestinal disaccharidases and decrease in the

absorptive surface area. Disaccharidase deficiency results in maldigestion of

carbohydrates with subsequent carbohydrate malabsorption producing an

osmotically induced chronic diarrhea . The prevalence of chronic

diarrhea is geographically dependent and is more common in resource poor

countries. Worldwide estimates vary from 3% to 20% with an incidence of about

3 episodes per child-year. Estimates in the United States are lower at 0.18

episodes per child-year in children ages 6 months to 3 years. The risk for acute

diarrhea becoming chronic depends on many factors, including the initial

pathogenic agent; nutritional status; dietary deficiency of micronutrients such as

zinc, folate, and vitamin A; underlying immunodeficiency; and socioeconomic

conditions. There is some evidence to suggest the incidence of chronic diarrhea

is decreasing worldwide and this may be a result of the introduction of rotavirus

vaccine, which has decreased the incidence of acute diarrhea in young children.

Source : Rudolph’s Pediatrics 23rd ed 2018 Page 5401