Giardiasis in Children

Giardia lamblia is a flagellated protozoan that infects the duodenum and small intestine. Infection results in clinical manifestations that range from asymptomatic colonization to acute or chronic diarrhea and malabsorption. Infection is more prevalent in children than in adults.

Life Cycle:
The life cycle of G. lamblia (also known as Giardia intestinalis or Giardia duodenalis) is composed of 2 stages: trophozoites and cysts.

Giardia infects humans after ingestion of as few as 10–100 cysts. Ingested cysts, which measure 8–10 mm in diameter, each produce 2 trophozoites in the duodenum. After excystation, trophozoites colonize the lumen of the duodenum and proximal jejunum, where they attach to the brush border of the intestinal epithelial cells and multiply by binary fission. The body of the trophozoite is teardrop shaped, measuring 10–20 mm in length and 5–15 mm in width. Giardia trophozoites contain 2 oval nuclei anteriorly, a large ventral disk, a curved median body posteriorly, and 4 pairs of flagella. As detached trophozoites pass down the intestinal tract, they encyst to form oval cysts that contain 4 nuclei.

Cysts are passed in stools of infected individuals and may remain viable in water for as long as 2 months. Their viability often is not affected by the usual concentrations of chlorine used to purify water for drinking.

Clinical Manifestations:
The incubation period of Giardia infection usually is 1–2 wk but may be longer. A broad spectrum of clinical manifestations occurs, depending on the interaction between G. lamblia and the host. Children who are exposed to G. lamblia may experience asymptomatic excretion of the organism, acute infectious diarrhea, or chronic diarrhea with persistent gastrointestinal tract signs and symptoms, including failure to thrive and abdominal pain or cramping. Most infections in both children and adults are asymptomatic.

Introduction to Esophageal Varices in Children

Portal hypertension is defined as an elevation of portal venous pressure to levels 10–12 mm Hg higher than pressures present in the inferior vena cava. Decompression of this hypertension through portosystemic collateral circulation via the coronary vein, in conjunction with the left gastric veins, gives rise to esophageal varices. Most esophageal varices are “uphill varices”; less commonly, those that arise in the absence of portal hypertension and with superior vena cava (SVC) obstruction are termed “downhill varices.” Their treatment is directed at the underlying cause of the SVC abnormality.

Clinical Presentation:
Hemorrhage from esophageal varices is the major cause of morbidity and mortality due to portal hypertension. Presentation is with significant hematemesis and melena; whereas most patients have liver disease, some children with entities such as extrahepatic portal venous thrombosis may have been previously asymptomatic. Any child with hematemesis and splenomegaly should be presumed to have esophageal variceal bleeding until proven otherwise.

Diagnosis:
Varices are occasionally seen on fluoroscopic barium contrast studies, but upper endoscopy is preferred because it provides definitive diagnosis as well as therapy for acute bleeding episodes via either sclerotherapy or band ligation.

Treatment of Pancreatic Insufficiency

Treatment of exocrine pancreatic insufficiency by oral enzyme replacement usually corrects steatorrhea, but steatorrhea is difficult to correct completely. This is due to variability of lipase activity in different commercial preparations, inadequate dosage, incorrect timing of doses, lipase inactivation by gastric acid, and the observation that chymotrypsin in the enzyme preparation digests and thus inactivates lipase. In enzyme supplements, the true lipase activity has been shown to be as much as twice the labeled amount. Pancrease, Creon, Ultrase, and Panceacarb are the preparations most widely used. These products are enteric-coated preparations that resist gastric acid inactivation. Generic enzyme preparations are less effective and should be avoided.

The dosage of pancreatic replacement for children depends on the amount of food eaten and is established by trial and error. Because these products contain excess protease compared with lipase, the dosage is estimated from the lipase requirement of 500–1,500 IU/kg/meal. An adequate dose is one that is followed by the return of the stools to normal fat content, size, color, and odor. Enzyme replacement should be given at the beginning of and with the meal. Tablets should be chewed; powder and granules can be mixed with a small quantity of food. Enzymes must also be given with snacks. Increasing enzyme supplements beyond the recommended dose does not improve absorption, may retard growth, and may cause fibrosing colonopathy.

Diagnosing Inflammatory Bowel Disease In Children

The laboratory evaluation of a patient with possible IBD is crucial to making the diagnosis, yet there is not one specific laboratory result that is pathognomonic of IBD.

Acute-phase reactants, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are sensitive markers of acute inflammation, but are nonspecific, and may also be less accurate in patients with chronic nutritional deficiencies, including hypoproteinemia.

Liver assessment is important but also nonspecific. It can uncover mild abnormalities in the transaminase levels in CD, or help identify the 10% to 15% of patient with UC who also have sclerosing cholangitis, an autoimmune disease of the biliary tract that may be even more devastating to the patient than UC itself.

A complete blood count and peripheral smear often uncover the microcytic anemia of iron deficiency, resulting from either chronic GI blood loss, poor intake of iron in the diet, or malabsorption of enteral iron. Macrocytic anemia can be seen in IBD patients with a history of terminal ileal resection or chronic disease, due to poor absorption of vitamin B12, or rarely in patients with proximal small bowel disease who malabsorb folic acid.

Lipase may be useful to check, because a small percentage of CD patients may manifest pancreatitis due to CD, or possibly due to medications commonly used for the treatment of IBD.

Approach to Chronic Abdominal Pain in Children

Children with chronic abdominal pain account for 5% of all outpatient visits in the pediatric age group. Up to one-third of all children have this complaint, yet less than 10% of these children will have an identifiable organic etiology for their pain. These issues can have great impact on the functioning of the entire family, often causing work absence for the parents, excessive school absence for the child, and feelings of helplessness for the entire family unit.

Definition
Chronic abdominal pain is defined as at least 3 episodes occurring within a 3-month time-span that interferes with normal activity.

Incidence
It is slightly more common in girls than in boys, and usually occurs between the ages of 5 and 12 years. There is an increased incidence of recurrent abdominal pain in the families of these children.

History
The evaluation of a child with chronic abdominal complaints—or for that matter, any problem at all—starts with a comprehensive history. This should start with an interview of the child, as long as he is of the developmental stage in which he can respond to questions with verbal answers. Once exhausting the information available from the child, the parent or caretaker is interviewed. This allows the child to become part of the process, rather than feeling like an excluded object, and generally ensures that you will be able to interview the parent without as much interruption when the child has been asked to speak first.

Two major questions that help separate functional gastrointestinal complaints from disease-based problems are:

1. Does the pain wake you up out of sleep in the middle of the night?
2. Can you point with one finger to the spot that hurts?

Hookworms Infection in Children

Two major genera of hookworms, which are nematodes or roundworms, infect humans. Necator americanus, the only representative of its genus, is a major anthropophilic hookworm and is the most common cause of human hookworm infection. Hookworms of the genus Ancylostoma includes the major anthropophilic hookworm Ancylostoma duodenale that also causes classic hookworm infection and the less common zoonotic species.

Life Cycle:
The infective larval stages of the anthropophilic hookworms live in a developmentally arrested state in warm, moist soil. Larvae infect humans either by penetrating through the skin (N. americanus and A. duodenale) or when they are ingested (A. duodenale). Larvae entering the human host by skin penetration undergo extraintestinal migration through the venous circulation and lungs before they are swallowed, whereas orally ingested larvae may undergo extraintestinal migration or remain in the gastrointestinal tract. Larvae returning to the small intestine undergo 2 molts to become adult sexually mature male and female worms ranging in length from 5 to 13 mm.

Epidemiology:
Hookworm infection is 1 of the most prevalent infectious diseases of humans, affecting an estimated 576 million individuals worldwide. Because of the requirement for adequate soil moisture, shade, and warmth, hookworm infection is usually confined to rural areas, especially where human feces are used for fertilizer or where sanitation is inadequate. Hookworm is an infection associated with economic underdevelopment and poverty throughout the tropics and subtropics. Sub-Saharan Africa, East Asia, and tropical regions of the Americas have the highest prevalence of hookworm infection.

Viral Gastroenteritis in Children

Introduction

Infectious diarrhea is a leading cause of disease and death worldwide. During a 1-year period in Asia, Africa, and Latin America, it was estimated that 3 to 5 billion episodes of infectious diarrhea accounted for 5 to 10 million deaths. Rotaviruses; adenoviruses; small, round viruses (eg, Norwalk agent); caliciviruses; coronaviruses; and astroviruses are responsible for acute viral gastroenteritis. Rotaviruses, adenoviruses, and small, round viruses account for the majority of viral gastroenteritis in childhood.

Epidemiology
Since their initial identification as a cause of human disease in 1973, rotaviruses have been found to be the most important cause of acute gastroenteritis in infants and young children in all countries. Studies in the United States, England, Australia, Japan, and Bangladesh found that 34 to 63% of children hospitalized with acute diarrhea were infected with rotaviruses. Rotavirus causes 3 to 4 million cases of diarrhea, 500,000 outpatient visits, 50,000 hospitalizations, and approximately 40 deaths per year in the United States. Rotavirus-induced gastroenteritis primarily affects children 6 to 24 months of age, and most initial infections are symptomatic. The peak prevalence of the disease occurs between November and April in temperate climates, and year-round in tropical climates; infections are usually sporadic and occasionally epidemic. Rotaviruses are transmitted from person-to-person by the fecal-oral route, with an incubation period of 1 to 3 days.

Adenoviruses are probably the second most important cause of acute gastroenteritis in childhood. Disease is associated primarily with adenovirus types 40 and 41. . Similar to rotaviruses, enteric adenoviruses primarily infect children younger than 2 years of age, but unlike rotaviruses, adenovirus infections occur year-round. Although outbreaks in hospital nurseries have occurred, these viruses appear to be endemic rather than epidemic. Enteric adenoviruses have an incubation period of 3 to 10 days, which is longer than that for infection with either rotaviruses or small, round viruses.
In 1968, an outbreak of illness characterized by vomiting and fever occurred in a group of elementary school children in Norwalk, Ohio. Virus particles, 27 nm in diameter, were subsequently isolated from this outbreak by electron microscopy. Norwalk agent was the forerunner of a group of morphologically similar noncultivable agents named for the geographic location where they were found to cause disease (eg, Montgomery County agent, Hawaii agent). The morphologic similarity of a number of smaller viruses associated with gastroenteritis (including parvoviruses) led to the description of these agents as small, round viruses. Unlike rotaviruses and adenoviruses, infections with small, round viruses are usually epidemic and responsible for family and community-wide outbreaks of gastroenteritis in school-aged children, family contacts, and adults. Small, round viruses are transmitted by the fecal-oral route, with an incubation period of 1 to 2 days.

Bacterial Colonization and Function in the Bowel

Bacteria colonize the colon because it contains elements that are critical for their growth: a warm, moist, stable environment with an abundant supply of nutrients both of exogenous (ie, dietary) and endogenous (ie, sloughed cells, mucus, secretions) origin. The resulting flora is among the most diverse in nature, incorporating over 400 different species of bacteria. It is replenished at a rate of 150 to 400 g daily, with each gram containing more than 1011 organisms.

Development of this complex ecosystem begins at birth. Initially, the colon is sterile and has a pH of 6.5 to 7.0. Within hours after birth, aerobes and facultative anaerobes (eg, Escherichia coli and Streptococcus) colonize to levels of 106 to 108 organisms per gram of feces. This results in an environment that is increasingly reduced in oxygen and thus favors the growth of strict anaerobes.
In breast-fed infants, Bifidobacterium appears by day 4 to 7, reaching levels of 108 to 1011 organisms per gram. Clostridium, Lactobacillus, and even Bacteroides also may colonize at this time. The presence of these organisms is associated with an acidic luminal pH of 5.1.
It has been noted that Bifidobacterium produces primarily lactate and acetate via lactose fermentation. The resulting milieu has been suggested to retard the growth of pathogenic bacteria such as E. coli and Salmonella and to promote the growth of Bifidobacterium.

In bottle-fed infants, the initial metabolic events differ. Strains of enterobacteria such as E. coli and Klebsiella pneumoniae predominate in a relatively neutral pH environment. By the end of the second week, in both breast- and bottle-fed infants, the rapid fluctuations both in bacterial numbers and in bacterial metabolic end products stabilize, and Bifidobacterium, Eubacterium, Clostridium, and Lactobacillus become the predominant species. This balance is maintained throughout adult life.

Pediatric Crohn’s Disease

Crohn disease (CD), or Crohn’s disease, is a chronic inflammatory bowel disease. Once considered rare in the pediatric population, Crohn disease is recognized with increasing frequency among children of all ages. Approximately 20-30% of all patients with Crohn disease present when they are younger than 20 years.

Pathophysiology
The pathogenesis of Crohn disease is multifactorial. After a triggering event occurs in a genetically susceptible individual, an altered immune response leads to chronic inflammation of the intestine. Although the etiology of the precipitating event is unknown, luminal bacteria or specific antigens are thought to be involved.

The macroscopic findings at the time of endoscopy and colonoscopy or surgery include various degrees of edema, erythema, ulceration, friability, thickening of the bowel wall and mesentery, and extension of fat over the serosal surface of the intestine.

Skipped areas of inflammation anywhere in the upper or lower GI tract are characteristic of Crohn disease, in contrast to the continuous diffuse colonic inflammation found with ulcerative colitis(UC). Microscopic findings on intestinal mucosal biopsy consist of chronic inflammation with architectural distortion. Granulomas are sometimes noted on biopsy findings in Crohn disease.

Clinical PresentationPatients with suspected Crohn disease (CD), or Crohn’s disease, should initially be evaluated by their primary care team. The patients’ symptoms should be elicited in detail. A medical history, detailed review of systems, and family history should be obtained, and growth parameters should be documented.

Introduction to Colic

Colic is commonly described as a behavioral syndrome characterized by excessive, paroxysmal crying. Colic is most likely to occur in the evenings, and it occurs without any identifiable cause. During episodes of colic, an otherwise healthy neonate or infant aged 2 weeks to 4 months is difficult to console. They stiffen, draw up their legs, and pass flatus. Colic is one of the common reasons parents seek the advice of a pediatrician or family practitioner during their child’s first 3 months of life.

Definition
The most widely used definition of colic is based on the amount of crying (i.e, paroxysms of crying lasting >3 hours, occurring >3 days in any week for 3 weeks).

Causes
Colic is a poorly understood phenomenon. It is equally likely to occur in both breastfed and formula-fed infants. Although potential adverse sequelae have been described, the disorder is generally believed to be self-limited and benign. Different feeding practices and crying may result in large amounts of air entering the gastric lumen, which suggests that excessive aerophagia may be associated with colic. Colonic fermentation is the second proposed source of excessive intestinal gas in infants. However, no experimental evidence supports either theory.

Epidemiology

• Colic affects 10-30% of infants worldwide.
• This condition is encountered in male and female infants with equal frequency.
• The colic syndrome is commonly observed in neonates and infants aged 2 weeks to 4 months.

Managing Acute Abdominal Pain in Children

Abdominal pain is one of the most common reasons for a parent to bring his or her child to medical attention. Evaluation of a “stomach ache” can challenge both parents and the physician.

Possible causes for a child’s abdominal pain range from trivial to life-threatening, with little difference in the child’s complaints. Fortunately, abdominal pain in a child usually improves quickly. Each parent or caregiver faces the difficulty deciding whether a complaint needs emergency care or not.

Abdominal pain is a common problem in children. Although most children with acute abdominal pain have self-limited conditions, the pain may herald a surgical or medical emergency.

Causes to be kept in MindAlthough many cases of acute abdominal pain are benign, some require rapid diagnosis and treatment to minimize morbidity. Numerous disorders can cause abdominal pain. The most common medical cause is gastroenteritis, and the most common surgical cause is appendicitis.

In the acute surgical abdomen, pain generally precedes vomiting, while the reverse is true in medical conditions. Diarrhea often is associated with gastroenteritis or food poisoning. Appendicitis should be suspected in any child with pain in the right lower quadrant. Signs that suggest an acute surgical abdomen include involuntary guarding or rigidity, marked abdominal distention, marked abdominal tenderness, and rebound abdominal tenderness.

The list that should be in mind while evaluating a child with abdominal is is as follows:

Medical causes

• Diabetic ketoacidosis
• Inflammatory bowel disease
• Acute adrenal failure
• Gastroenteritis
• Food Poisioning
• Urinary tract infection
• Hepatitis
• Sickle cell crisis
• Henoch-Schönlein purpura

Surgical Causes

• Acute appendicitis
• Bowel obstruction
• Intussusception/ volvulus
• Testicular torsion
• Meckel’s diverticulum

Others

• Infantile colic
• Functional pain

History and Physical Examination
In a child presenting with acute abdominal pain a complete history and detailed physical examination is important to reach a proper diagnosis and then appropriate management

Approach to a Child with Cyclic Vomiting Syndrome

Cyclic vomiting syndrome (CVS) is a rare disorder characterized by recurrent episodes of severe nausea and vomiting. An episode may last for a few hours to several days and then is followed by a period of time during which affected individuals are free of severe nausea and vomiting. This alternating pattern of disease and disease-free periods distinguishes cyclic vomiting syndrome from other similar disorders.

Etiology

Cyclic vomiting syndrome (CVS) is a chronic functional disorder of unknown etiology that is characterized by paroxysmal, recurrent episodes of vomiting. The pathophysiology is unknown, but data suggest a strong genetic component.

Cyclic vomiting usually develops during childhood usually ages 3–7; although it often remits during adolescence, it can persist into adult life.

Epidemiology
Cyclic vomiting syndrome occurs in all races but seems to disproportionately affect whites.
Females show a slight predominance over males.

Causes and Risk Factors
The cause of cyclic vomiting syndrome is unknown, but the bouts of vomiting that characterize the condition can be triggered by:

• Colds, allergies or sinus problems
• Emotional stress or excitement
• Foods such as chocolate or cheese
• Overeating or eating right before going to bed
• Hot weather
• Physical exhaustion

Many children who have cyclic vomiting syndrome have a family history of migraines or begin having migraines themselves when they get older. 

Abdominal migraine — a type of migraine more common in children — causes abdominal pain but not the severe vomiting associated with cyclic vomiting syndrome.

Differential Diagnosis of Diarrhea in Children

Children may present with diarrhea which is defined as the passage of loose stools. It is a very common complaint and a list of differential diagnosis should be kept in mind while dealing with a child presenting with this problem.

1. Infection

Viral: Usually resolves in a few days and can be treated symptomatically. Rotavirus, adenovirus and Norwalk virus are more common.

Bacterial: Shigella, salmonella, Campylobacter, E coli , Vibrio, Clostridium species are commonly involved. Spectrum of illness may range from asymptomatic to life threatening. Staph aureus and C perfringens are often associated with food poisoning. Enterohemorrhagic E coli causes bloody diarrhea and may be associated with hemolytic uremic syndrome.

Parasitic: Giardia is often contracted by drinking contaminated water and can cause abdominal distension, diarrhea and at times failure to thrive. Giardia is easily passed through fecal oral route and is common in day care centers. Entamoeba histolytica produces severe coilitis.

2.Postinfectious State
Several viruses can cause severe enteritis resulting in prolonged intestinal mucosal damage, acquired carbohydrate intolerance and malabsorption in infants.