J. Eduardo Calonje, MD, DipRCPath

• Director of Diagnostic Dermatopathology, Department of Dermato-Histopathology, St John's Institute of Dermatology, St Thomas' Hospital, London, UK

Patients with hepatic failure gastritis diet 6 weeks discount diarex uk, glycogen storage diseases gastritis quick relief purchase diarex 30 caps free shipping, mitochondrial diseases gastritis body aches discount diarex 30 caps fast delivery, fatty acid -oxidation defects gastritis pain diarex 30caps visa, pyruvate metabolism defects gastritis diet of worms discount diarex 30 caps with visa, Krebs cycle and gluconeogenesis defects chronic gastritis months order diarex 30 caps amex, organic acidurias, or hereditary fructose intolerance may be hypoglycemic. Blood glucose level determination is essential in the evaluation of hepatomegaly, particularly in patients with alterations in their mental status. In the majority of conditions, hypoglycemia is associated with ketosis and lactic acidosis. Hypoglycemia in the absence of or with low levels of ketones in the urine strongly suggests a fatty acid -oxidation defect or a mitochondrial disorder. The urea cycle is a series of enzymatic reactions converting highly toxic ammonia into less toxic urea. Alkaline phosphatase is found in several other tissues, including bone, small intestine, placenta, and kidney. Because children have a significant proportion of serum alkaline phosphatase activity originating from bone, this test may be of less value in the assessment of pediatric liver disease. Even minor bone trauma or vitamin D deficiency can lead to elevation of alkaline phosphatase. The tissue origin of alkaline phosphatase can be determined by fractionation of alkaline phosphatase isoenzymes. Shunting of portal blood in cirrhosis or in congenital portosystemic shunts permits large amounts of ammonia and other toxins to bypass the liver and reach the systemic circulation directly. Hepatomegaly with an acute change in mental status should raise the possibility of a serious metabolic condition. Since both hypoglycemia and hyperammonemia can lead to severe and irreversible brain damage, correction of these abnormalities should be considered an emergency. The liver is the main site of biosynthesis and processing of cholesterol, lipids, and lipoproteins. In cholestatic liver disease there may be extreme elevations of free cholesterol and phospholipids. These abnormalities are accompanied by the presence of an abnormal low-density lipoprotein fraction called lipoprotein X. Enzymatic analysis of cultured lymphocytes or hepatic tissue may aid in the diagnosis. Extrahepatic Involvement High levels of unconjugated bilirubin suggest the possibility of a concurrent hemolytic disorder or may reflect inborn errors of conjugation (see Chapter 15). Renal involvement can be reflected by elevated creatinine, inability to concentrate urine, or by Fanconi syndrome. This could raise suspicion for autosomal recessive polycystic kidney disease, tyrosinemia, glycogen storage disease type Ib, Wilson disease, hereditary fructose intolerance, or galactosemia. Air may be seen within the portal venous system, a late finding in bowel infarction and necrosis, intraabdominal sepsis, and associated inflammatory bowel disease. Air may also be present within the biliary tree, especially in patients who have undergone recent biliary tract surgery or who have an enterobiliary fistula. Coarse calcifications may be found in hepatoblastoma and laminated calcifications in hepatocellular carcinoma. It can assess gallbladder size, detect gallstones and sludge in the bile ducts and gallbladder, demonstrate ascites, and define cystic or obstructive dilatation of the biliary tree. Mass lesions in the liver, including tumors, cysts, abscesses, vascular malformations, and hematomas, can be defined. Abnormal echogenicity may suggest diffuse parenchymal liver disease including fatty infiltration or fibrosis. Doppler studies may be used to differentiate between vascular and nonvascular structures. The study may be particularly useful for assessing portal hypertension, in which portal venous flow may be decreased or reversed. Magnetic resonance cholangiography is commonly used to assess the biliary tract with visualization of details previously possible only with transhepatic or endoscopic retrograde cholangiography. Hepatic scintigraphy can be useful for assessing the liver parenchyma and biliary tree. Biliary imaging with this technique provides information about patency of the biliary tract and gallbladder. Most malignant tumors, hemangiomas, abscesses, and cysts lack Kupffer cells and appear as "cold" spots on these scans. In contrast, a nodule taking up the isotope suggests a benign lesion containing Kupffer cells, such as a regenerative nodule of cirrhosis, fatty change, or focal nodular hyperplasia. Liver biopsy is essential in establishing a diagnosis and possibly prognosis in patients with chronic viral hepatitis, drug-induced liver disease, autoimmune hepatitis, and various metabolic disorders. Abnormal storage of material in hepatocytes or Kupffer cells and viral inclusions may also be found. Electron microscopy and immunohistochemical methods may aid in identification and localization of these abnormalities. The first goal is to identify potentially life-threatening conditions, to focus on emergency measures to manage immediate threats to life, and to prevent irreversible end-organ damage. The second goal is to identify potentially treatable disorders requiring timely interventions. Ultimately, the clinician should focus on other chronic conditions in order to establish the diagnosis and prognosis. Some disorders may be corrected by liver transplantation; such patients should be promptly referred to a transplant center for evaluation. Hepatomegaly in the Infant Hepatomegaly in the neonate is commonly associated with liver dysfunction and jaundice (see Chapter 15). In infants, jaundice is a frequent presenting feature of liver disease rather than a later manifestation of advanced liver disease, as in the older child or adult. The majority of infants with cholestatic liver disease manifest the disease during the first month of life. Changes in mental status, such as irritability or lethargy, poor feeding, and vomiting, are frequent symptoms in metabolic disorders. Urea cycle defects lead to hyperammonemia and acute encephalopathy associated with astrocyte swelling without axonal damage. Symptomatology of galactosemia and tyrosinemia depends on the presence of nutritional substrates; thus irritability, lethargy, hepatomegaly, ascites, edema, and coagulopathy may manifest soon after feedings are initiated and evolve over the first weeks of life. A profound impairment of hepatic synthetic function, often in excess of that expected for the degree of cholestasis, may be an early indication of metabolic liver disease. Multiple organs (brain, heart, skeletal muscle) may be involved in addition to the liver. Affected patients often have lactic acidosis, hypoglycemia, hypertriglyceridemia, and an abnormal acylcarnitine profile. Patients with neonatal hemochromatosis may benefit from treatment with plasmapheresis and may require liver transplantation. Hemochromatosis will develop in up to 80% of infants of mothers with a child diagnosed with hemochromatosis. A number of clinical features may provide clues about the cause of neonatal cholestasis. An enlarged liver with a firm or hard consistency is more commonly found in infants with extrahepatic bile duct obstruction or neonatal hemochromatosis. Congenital infection may be associated with low birthweight, hepatomegaly, microcephaly, purpura, and chorioretinitis. Dysmorphic facial features may be seen in association with chromosomal abnormalities and with Alagille syndrome. Congenital malformations, including cardiac anomalies, polysplenia, intestinal malrotation, and situs inversus, may be found in the syndromic form of biliary atresia. The spleen may also be enlarged with infection or as a result of portal hypertension. Hepatomegaly, as well as a mass in the right upper quadrant, may be felt in infants with a choledochal cyst. Infants may present with hepatomegaly, cholestasis, and sometimes hepatic failure related to infection. Cytomegalovirus, herpes simplex virus, enteroviruses, echovirus, coxsackievirus and parvovirus B19 are sometimes isolated from infants with cholestasis and hepatomegaly. Hepatomegaly and cholestasis can also be associated with bacterial sepsis, syphilis, tuberculosis, and toxoplasmosis. Infants with storage diseases can present with isolated hepatomegaly or hepatosplenomegaly and few other symptoms in the early stages. Hepatomegaly is a feature of these disorders because of a pathologic accumulation of undegraded or partially degraded macromolecules. The mucopolysaccharidoses, the lipid storage diseases, the mucolipidoses, and glycoprotein storage disease are examples of these disorders. The clinical features of lysosomal storage diseases are determined by where the deficient enzyme is expressed and the rate of accumulation of the abnormal material. Hepatomegaly in the neonate can occur in Gaucher disease, Niemann-Pick disease type A, and Wolman disease. Neonatal hepatosplenomegaly and jaundice may occur in Niemann-Pick disease type C. Significant liver disease may occur in some of these disorders, leading to chronic liver failure and cirrhosis. On the basis of clinical features and manifestations, specific enzymatic activities may be determined in peripheral white blood cell culture or in cultured skin fibroblasts to establish a precise diagnosis. Although of limited efficacy, bone marrow transplantation has been used in patients with several of these disorders, including the mucopolysaccharidoses and Gaucher disease. Since brain energy metabolism heavily depends on the availability of glucose, severe hypoglycemia can lead to metabolic strokes, irreversible brain damage, and death. Hepatomegaly in the Child and Adolescent Hepatomegaly in the child or adolescent may be an isolated finding on a routine physical examination or may be associated with many other clinical features related to systemic disease or impaired liver function. Steatohepatitis Fatty liver disease in the child and adolescent is associated with childhood obesity. Nonalcoholic steatohepatitis should be suspected in any obese child with hepatomegaly and/or abnormal liver test results. Many of these children have features of metabolic syndrome, such as insulin resistance, arterial hypertension, and elevated serum cholesterol and triglyceride levels. In overweight children presenting with hepatomegaly and liver dysfunction, nonalcoholic steatohepatitis should be the primary diagnostic consideration, but other disorders, such as autoimmune hepatitis and chronic viral hepatitis, must be ruled out. Liver biopsy is the definitive diagnostic test and should be considered in patients with persistently abnormal aminotransferases. The purpose of the biopsy is to establish the diagnosis of nonalcoholic steatohepatitis, rule out other conditions and evaluate the degree of steatosis, inflammation, and fibrosis. Steatohepatitis is associated with increased mortality from cardiovascular disease and liver cancer. Obese patients with steatohepatitis should be enrolled in a weight-management program. Viral Hepatitis Acute viral hepatitis should be considered in the child with hepatomegaly and liver dysfunction. The patient may be acutely ill with sudden onset of fever, anorexia, nausea, and vomiting. Initial manifestations of Wilson disease may include portal hypertension, ascites, edema, and esophageal hemorrhage. Wilson disease can also present with extrahepatic symptoms, such as hemolytic anemia, movement disorders, or mood disorders. Wilson disease is due to mutations in a copper-transporting P-type adenosine triphosphatase, which leads to a failure of biliary copper excretion and a progressive accumulation of copper in the liver and other organs. Lipid peroxidation, particularly of mitochondrial membranes, results from copper overload leading to the functional alterations in the liver and the brain. The diagnosis is confirmed with a quantitative determination of copper in a liver-biopsy specimen. Treatment of Wilson disease involves chelation and urinary excretion of the excess copper. In response to chelation therapy, urinary copper excretion increases markedly, and this is associated with a gradual clinical improvement. Liver transplantation may be required for treatment of fulminant Wilson disease or in patients with decompensated cirrhosis. Hepatitis C is an indolent infection with the potential to evolve to cirrhosis over several decades. However, some children, particularly when co-infected with human immunodeficiency virus, may have more rapidly progressive liver disease. As new antiviral agents are becoming available, eradication of hepatitis C is possible in the majority of adult patients though there are no clinically tested pediatric protocols currently. Autoimmune Liver Disease Several forms of autoimmune liver disease may also manifest with hepatomegaly during childhood and adolescence. Autoimmune hepatitis is defined as a continuing inflammatory process manifested by elevated aminotransferase concentrations and a number of circulating autoantibodies. The severity at presentation is highly variable; affected children may have only biochemical evidence of liver disease, may have stigmata of chronic liver disease, or may present in hepatic failure. In 25-30% of patients with autoimmune hepatitis, particularly children, the illness may mimic acute viral hepatitis; however, in most patients, the onset is insidious. The patient may be asymptomatic or have fatigue, malaise, behavioral changes, anorexia, and amenorrhea. Months or even years may pass before a liver problem is recognized with onset of jaundice or bleeding. There is a high association with extrahepatic disorders, including arthritis, vasculitis, nephritis, thyroiditis, celiac disease, inflammatory bowel disease and Coombs-positive anemia.

This asynchronous activity between detrusor muscle and sphincter contraction leads to higher intravesical pressures gastritis diet ������ buy discount diarex on-line. Complications may include thickening gastritis caused by stress buy diarex uk, trabeculations gastritis and bloating purchase diarex 30caps free shipping, or diverticula of the bladder gastritis diet questions purchase diarex discount. This is often referred to as the "nonneurogenic neurogenic bladder gastritis x ray purchase diarex amex," a syndrome representing the extreme end of the spectrum of dysfunctional voiding gastritis diet ���� buy generic diarex pills. Inappropriate voluntary contraction of the external sphincter during voiding produces high intravesical pressure and a functional outlet obstruction, leading to abnormal bladder function, hydronephrosis, and possibly renal failure. With time, the voiding pattern becomes habitual, and the anatomic changes in the bladder impede the ability to void normally. Biofeedback and clean intermittent straight catheterization may restore bladder emptying and function and prevent renal failure. This is the most common form of urinary obstruction leading to kidney failure in male infants and children. It is a result of persistence of fetal folds in the posterior urethra, which act as a valve to create urinary obstruction. Poor urinary stream and bladder distention are the most common urinary complaints, but dribbling and incontinence are also observed. Early obstruction during embryogenesis leads to hydronephrosis, hydroureter, abdominal distention, abdominal musculature deficiency, and excessive skin folds, thus giving the wrinkly "prune" appearance of the abdomen in severe cases. This is a result of duplication of the ureteric bud during embryogenesis, causing a double collecting system, or 2 ureters. Duplicated ureters can open separately inside the bladder, but in rare cases, an ectopic ureter can end in the vagina, urethra, or vestibule, leading to dribbling and incontinence. Normal insertion of the ureter into the bladder submucosal wall forms a flap-valve mechanism that prevents urine backup during filling and contraction. Urine flow mechanics are disrupted by the constant filling of the bladder with urine that has flowed backward and then returns to the emptied bladder. This is an uncommon electrolyte disorder in children but can be observed in primary hyperparathyroidism, vitamin D intoxication, immobilization, Williams syndrome, malignancy, and idiopathic hypercalcemia of infancy. This leads to renal sodium and water losses and thus to polyuria and volume contraction. In chronic hypercalcemia, increased calcium excretion over time can lead to nephrocalcinosis, tubular damage, and poor urinary concentrating ability, thus enhancing polyuria. In children, it occurs clinically as a result of diuretic use, aldosterone excess states, Cushing syndrome, and intrinsic renal disorders that affect potassium handling. This results in distortion of normal neural tissues in the spinal cord or nerve roots. The range of anomalies includes meningocele, lipomeningocele, primary tethered cord, dermoid cyst, syrinx, and sacral agenesis. Hypokalemia interferes with water reabsorption in the collecting duct of the kidneys. Polyuria and urinary incontinence can be the 1st symptoms of diabetes mellitus and are secondary to hyperglycemia and the osmotic diuresis resulting from chronic glycosuria. The renal threshold for reabsorption of glucose is exceeded when the blood glucose level is higher than approximately 180 mg/dL. If oral intake of fluid decreases, as occurs when diabetic ketoacidosis causes anorexia and emesis, significant dehydration and shock frequently develop. The defect can be complete or partial, and thus the degree of polyuria is variable. In the idiopathic form, infiltrative diseases such as Langerhans cell histiocytosis (Letterer-Siwe syndrome) should be sought. The resultant decreased ability to concentrate leads to a higher incidence of nocturnal enuresis in affected patients. Juvenile nephronophthisis is an autosomal recessive disorder that leads to end-stage renal failure between preadolescence and early adulthood. Patients have high urine output because of poor renal concentrating ability and renal salt wasting. The salt wasting causes salt craving, and patients have a preference for salty foods or even eat salt directly from the saltshaker. A small percentage of these patients have retinitis pigmentosa, which may cause blindness at birth or later in life. Infants may present with poor growth, severe dehydration, seizures, and central nervous system injury or death. In families in which the diagnosis has already been made, early intervention in infants can prevent these symptoms and lead to an excellent outcome. In children, the presentation includes failure to thrive, polyuria, and polydipsia. Hypercalciuria and low urine citrate excretion combine to produce nephrocalcinosis. The autosomal recessive form of the disease is frequently associated with hearing loss. When associated with other proximal tubular defects, such as salt wasting, phosphate wasting, glycosuria, and aminoaciduria, it is referred to as Fanconi syndrome. This autosomal recessive disorder results from a defect in cystine transport and results in the lysosomal accumulation of cystine throughout the body. Acidosis, rickets, polyuria, and severe failure to thrive are hallmarks of the disease. Early intervention with oral cysteamine to bind cysteine has dramatically improved the outcome in affected patients. Hemoglobin S is a genetic defect in hemoglobin A that results in red blood cells that deform under low oxygen tension (see Chapter 37). The renal medulla is a site with high osmolality, low oxygen tension, and relative acidosis, all conditions that promote sickling. This results in occlusion of blood vessels and damage Primary Nocturnal Enuresis Establishing whether the primary nocturnal enuresis is the only symptom or whether there are associated symptoms such as diurnal incontinence, constipation, sleep disorders, or behavioral issues, such as attention-deficit/hyperactivity disorder, is necessary before a treatment strategy is developed. It is also helpful to let the family and child know that almost all patients "outgrow" primary nocturnal enuresis. If treatment is sought, the enuresis alarm has a high success rate, but patient selection is important. These devices are designed to awaken patients when micturition begins and result in the development of increased bladder capacity. Its effect may not be seen for up to 12 weeks, and therefore the family and patient must be highly motivated. Older patients who are ready to take charge of the problem and who do not have difficulty waking are the best candidates. Its safety profile has been excellent, but patients should be given careful instruction on restricting fluid intake after the bedtime dose. Imipramine, a tricyclic antidepressant, has been shown to be effective, but its side effects and toxicity have limited its use for this benign condition. Red Flags Dysfunctional Voiding Treatment of mild voiding dysfunction should begin with nonpharmacologic management. Children should be instructed to void on a regular schedule, typically every 1-2 hours, even if they do not feel the urge to void. This encourages voiding when the patient is relaxed and will lead to fewer contractions of the external sphincter during micturition. Keeping a diary of the voiding schedule involves the child in management and makes him or her more aware of bladder habits. Aggressive management of constipation (see Chapter 16) improves good bladder emptying and decreases bladder instability. When incontinence continues despite nonpharmacologic methods, anticholinergic therapy should be added in the treatment of a child with an overactive or unstable bladder. Oxybutynin should be started at a low dosage and titrated to its maximum dosage if necessary. This may keep the child free of infection and may prevent the painful urination that reinforces exaggerated external sphincter contraction and urine holding. Biofeedback is reserved for patients with moderate to severe dysfunctional voiding. Patients can learn to increase bladder capacity and inhibit detrusor contractions through this method. Polyuria Polydipsia Failure to thrive Poor urinary stream Encopresis Secondary enuresis Abnormal gait, including toe walking Recurrent urinary tract infections Cutaneous lesions over lumbosacral spine Diminished lower extremity reflexes Abnormal genitalia Palpable bladder Hypertension Headache Visual disturbances Obstructive sleep apneas Neuropathic Bladder and Anatomic Disorders the treatment of these disorders depends on the specific defect. In patients with neuropathic bladders resulting from spina bifida, chronic intermittent catheterization of the bladder may be the only way to achieve continence. Uninhibited bladder contractions may necessitate anticholinergic therapy as an adjunct. Urodynamic testing can be very helpful in this population to define the problem leading to incontinence. In certain disorders, such as diabetes mellitus, hypokalemia, or hypercalcemia, the underlying disorder can be corrected. In contrast, there is no effective therapy for reducing urine output in patients with disorders such as juvenile nephronophthisis or obstructive uropathy. A combination of sodium restriction and a thiazide diuretic can decrease this high urine output by producing a subtle volume depletion that results in less water being delivered to the collecting duct. Relationship between age at initiation of toilet training and duration of training: a prospective study. Dysfunctional elimination syndromes-how closely linked are constipation and encopresis with specific lower urinary tract conditions A review of bowel and bladder control development in children: how gastrointestinal and urologic conditions relate to problems in toilet training. Sequential acquisition of toilettraining skills: a descriptive study of gender and age differences in normal children. Bladder dysfunction and neurological disability at presentation in closed spina bifida. Treatment of occult tethered cord for neuropathic bladder: results of sectioning the filum terminale. Toilet training of healthy young toddlers: a randomized trial between a daytime wetting alarm and timed potty training. Urodynamic testing in children: indications, technique, interpretation and significance. Nocturnal enuresis is associated with moderate-to-severe obstructive sleep apnea in children with snoring. Sources of hydrogen ions include protein metabolism and incomplete metabolism of carbohydrates and fat; urine or stool losses of bicarbonate may contribute to acidemia. The hydrogen ions formed from endogenous acid production are neutralized by bicarbonate from the bicarbonate buffer system. These compensatory mechanisms never return the pH back to normal until the underlying disease process has subsided or has been effectively treated. The latter should be suspected if the compensation in a given patient differs from the predicted values (see Table 46. Metabolic acidosis results in increased minute ventilation (manifesting as increased respiratory rate and/or effort) because of respiratory compensation. A patient may have tachypnea present with a metabolic acidosis from a diarrheal illness, metabolic disorder, ingestion, or infection. Severe acidosis may also lead to hypotension, pulmonary edema, and asystole; its harmful effects are accentuated in the presence of hypoxia. Chronic metabolic acidosis leads to growth retardation and hypercalciuria with subsequent bone disease because bone buffering of acid produces marked mineral losses. One should consider metabolic alkalosis in a child who has been vomiting or in a child who has had chronic diuretic use. Some of these signs and symptoms are related to decreased concentration of serum ionized calcium as a result of its increased binding to protein in the presence of alkalosis. In metabolic disorders, extracellular buffers (bicarbonate) rapidly titrate the presence of strong acids or bases. In contrast, secondary metabolic compensation for respiratory disorders occurs more slowly, beginning within hours but requiring 2-5 days for completion. Urinary sodium is <10 mEq/L in acute renal failure secondary to glomerular disease. The 2nd role of the kidneys is to excrete H+ that is produced from protein and phospholipid catabolism. This active secretion can generate an H+ ion gradient of 1000: 1 between tubular fluid and cells, permitting the urine pH to fall to as low as 4. The active H+ secretion is significantly influenced by the luminal electronegativity caused by active Na+ reabsorption in the cortical collecting duct. Thus, in the cortical collecting duct, H+ excretion is influenced by distal Na+ delivery and reabsorption. The ability to excrete large amount of H+ ions is dependent on the presence of buffers. The H+ ions are buffered by phosphates and, to a lesser extent, by other nonreabsorbable anions.

Chronic infection is to be differentiated from postinfectious malabsorption seen in some immunocompetent children gastritis nutrition diet discount 30 caps diarex, in whom the small intestinal mucosa may require 3-8 weeks to recover its absorptive ability gastritis wiki diarex 30 caps with amex. The etiology of acute diarrhea is suggested by both the history and characteristics of the stool gastritis je purchase diarex us. Watery diarrhea is typical of viral gastroenteritis gastritis attack discount diarex online mastercard, as well as some bacterial and parasitic infections gastritis diet ���������� best diarex 30caps. Dysentery gastritis diet ������ diarex 30 caps on-line, characterized by severe diarrhea and the presence of blood and mucus in the stool, suggests bacterial colitis. Most Shigella infections in the United States occur in young children 1-4 years of age, with a peak seasonal incidence in late summer and early autumn. It may also be the most common bacterial cause of diarrhea outbreaks in daycare settings. During a 12- to 72-hour incubation period, patients may develop a nonspecific prodrome characterized by fever, chills, nausea, and vomiting. A predominantly rectosigmoid colitis develops and results in abdominal cramps and watery diarrhea. In more severe infections (bacillary dysentery), blood and mucus are passed in small, very frequent stools. High fever in young infants may induce febrile seizures, and some patients may develop hemolytic uremic syndrome. Many animal species, including poultry, farm animals, and household pets, serve as reservoirs for Campylobacter jejuni. Transmission occurs through ingestion of contaminated food, especially undercooked food, and through person-to-person spread via the fecal-oral route. The disease is common in infants and adolescents, and both daycare and college outbreaks have been reported. Campylobacter infection causes disease that may range from mild diarrhea to frank dysentery. The organism causes diffuse, invasive enteritis that involves the ileum and colon. Fever, cramping, abdominal pain, and bloody diarrhea are characteristic and may mimic symptoms of acute appendicitis or inflammatory bowel disease. Fever and diarrhea usually resolve after 5-7 days; prolonged illness or relapse occasionally occurs. Campylobacter infection is also known to cause meningitis, abscesses, pancreatitis, and pneumonia. The organism is present in animals and may be spread to humans by consumption of undercooked meat (especially pork), unpasteurized milk, and other contaminated foods. Young children are particularly susceptible to disease, and the frequency of infections increases during the summer months. Systemic manifestations, including myalgia, fatigue, and headache may accompany gastrointestinal symptoms. Bacterial Diarrhea Most bacterial diarrheal illnesses are foodborne and affect infants and young children more frequently than adults. Bacterial infections of the intestine cause diarrhea via direct invasion of the intestinal mucosa, followed by intraepithelial cell multiplication or invasion of the lamina propria. Cellular invasion may be followed by the production of cytotoxin, which disrupts cell function, and/or the production of enterotoxin, which alters cellular electrolyte and water balance. Bacterial adherence to the mucosal surface may result in flattening of the microvilli and disruption of normal cell functioning. Symptomatic differentiation from viral causes of diarrhea may be difficult, and sequelae of infections are varied (Table 11. Nontyphoidal Salmonella organisms are estimated to cause 1 million annual gastrointestinal infections in the United States. The attack rate is highest in infancy; the incidence of symptomatic infections is lower in patients older than 6 years. Salmonella infection may cause an asymptomatic intestinal carrier state (rare in children), enterocolitis with diarrhea, or bacteremia without gastrointestinal manifestations but with subsequent local infections, such as meningitis or osteomyelitis. Salmonella infection is usually spread through contaminated water supplies or food. Although an infected food handler may contaminate food sources, farm animals or pets are often the vector. Outbreaks may occur among institutionalized children; outbreaks in daycare centers are rare. After a 12- to 72-hour incubation period, gastroenteritis develops and is characterized by the sudden onset of diarrhea, abdominal cramps and tenderness, and fever. The diarrhea is watery, with stools containing polymorphonuclear leukocytes and, on occasion, blood. Antibiotics are not effective in alleviating symptoms of Yersinia enteritis or in shortening the period of bacterial excretion. At least 2 separate mechanisms are responsible for diarrhea: adherence to intestinal epithelial cells leading to villous injury and mucosal inflammation, and production of a toxin similar to that of Shigella organisms. Definitive diagnosis requires enterotoxin identification, and this method is not widely available. Other manifestations include asymptomatic infection and watery diarrhea without progression to hemorrhagic colitis. Clostridium difficile causes acute and chronic diarrhea in children when the normal colonic flora is disrupted. Pseudomembranous colitis is the most severe form of this infection, occurring as a result of a severe inflammatory response to the C. Transmission occurs through person-to-person contact and through environmental contamination via the spores formed by C. Infection is highly associated with recent antibiotic exposure, particularly to broad-spectrum antibiotics, which disrupt the endogenous colonic flora that inhibits the growth of C. Illness associated with this organism varies from a mild, self-limited, nonbloody diarrhea to severe hemorrhagic colitis, protein-losing enteropathy, toxic megacolon, colonic or cecal perforation, peritonitis, sepsis, shock, and death. The colitis is caused by potent toxins produced by the organism: toxin A, a lethal enterotoxin that causes hemorrhage and fluid secretion in the intestines; and toxin B, a cytotoxin detectable by its cytopathic effects in tissue culture. Both toxins play a role in disease production, although toxin A may be more important. Sigmoidoscopy or colonoscopy reveals pseudomembranes in 30-50% of cases, typically in association with more severe disease. Aeromonas species are gram-negative bacilli that are found in a variety of freshwater sources and that are capable of causing a wide array of disease, including a mild, self-limited diarrheal illness in children. The most common manifestation is a watery, nonbloody, nonmucoid diarrhea seen during the late spring, summer, and early fall. More severe infections may resemble ulcerative colitis, with chronic bloody diarrhea and abdominal pain. Plesiomonas shigelloides is a Vibrio-like organism found in soil and water that is sometimes implicated in childhood diarrhea. It has been linked to consumption of raw shellfish or contaminated water, exposure to reptiles and tropical fish, and travel to Mexico and Asia. After an incubation period of 1-2 days, patients typically develop watery diarrhea and vomiting, although some may develop dysentery. Symptoms may last up to 2 weeks, although the disease is typically self-limited in immunocompetent individuals. Giardia intestinalis is a flagellated protozoan that can cause diarrhea, malabsorption, abdominal pain, and weight loss. It spreads through contaminated food and water, as well as through person-to-person contact via the fecal-oral route. The latter mode of transmission is responsible for outbreaks of diarrhea in daycare centers and residential facilities. Symptomatic illness usually develops 1-3 weeks after exposure and may mimic acute gastroenteritis with low grade or no fever, nausea, vomiting, and watery diarrhea. In some patients, a chronic illness develops, characterized by intermittent, foul-smelling diarrhea, abdominal bloating, nausea, abdominal pain, and weight loss. Up to 40% of patients may develop secondary lactase deficiency following infection. If microscopy is performed, three separate samples of fresh stool should be examined for cysts or trophozoites, because excretion of the organism is only intermittent. Treatment is typically indicated in the presence of symptoms, to prevent institutional outbreaks, or to prevent spread to immunocompromised individuals. Entamoeba histolytica is acquired in warm climates via the ingestion of cysts in fecally contaminated food or water. Amebic dysentery may occur, but hepatic abscess and other remote infections are uncommon. Because cysts are shed in the stool on an intermittent basis, examination of several fecal specimens may be required for identification. Treatment is indicated to prevent the development of extraintestinal manifestations or spread to other individuals. This intracellular protozoan causes watery diarrhea in both immunocompetent and immunocompromised hosts and is an important cause of severe diarrhea in individuals infected with the human immunodeficiency virus. Cryptosporidium has also been recognized as an occasional cause of self-limited diarrhea in travelers, as well as in children in daycare centers and persons in residential institutions. Identification via microscopy requires specialized staining techniques that should be requested if Cryptosporidium infestation is suspected. Bacillus cereus, a gram-positive sporulating organism found in soil, is usually associated with contamination of refried rice or vegetables. A short incubation period disease (1-6 hours) results from ingestion of preformed toxin and is characterized by nausea, vomiting, and diarrhea, similar to staphylococcal food poisoning. A long incubation period disease (8-16 hours) is caused by in vivo production of an enterotoxin and is characterized by abdominal pain, tenesmus, and profuse watery diarrhea. Both syndromes resolve spontaneously within 24 hours and are managed with supportive care. Clostridium perfringens food poisoning has been associated with ingestion of contaminated beef and poultry. The disease results from the production and release of an enterotoxin into the lower bowel 8-24 hours after ingestion of the vegetative form of the organism. Acute diarrhea that accompanies infections outside of the gastrointestinal tract is termed parenteral diarrhea. Upper respiratory tract and urinary tract infections may be associated with increased bowel movement frequency or stool water. The mechanism is unclear but may involve alterations in bowel motility, changes in diet, or the effects of antibiotic treatment. Various nonlaxative prescription and over-thecounter medications may cause acute diarrhea (Table 11. The most commonly implicated agents are antibiotics, acting through mechanisms other than C. Staphylococcal food poisoning results from ingestion of preformed enterotoxin, produced in contaminated food that has incubated at or above room temperature for a suitable period. Staphylococcal food poisoning is suggested by the sudden onset of vomiting that is followed by explosive diarrhea, usually within 4-6 hours after ingestion of the contaminated food. In developing countries, chronic diarrhea is frequently caused by acute infections, as malnutrition tends to prolong the course of infectious enterocolitis. The most common etiologies of chronic diarrhea in developed countries are functional intestinal disorders, nutrient malabsorption (cystic fibrosis), celiac disease, and inflammatory bowel diseases, but persistent infections of the intestinal tract may also occur. History the history should establish the age of onset, as well as the frequency and nature of the stools, including the presence of blood, nighttime stooling, urgency, weight loss, and any associated systemic symptoms. History should also ascertain any recent travel, other sick contacts, or swimming in freshwater sources. The toxin is produced by symbiotic or infecting bacteria in the fish species Barracuda, red snapper, grouper, amberjack Minutes to 2 hr Minutes to 2 hr Ciguatoxin poisoning 2-24 hr Itching, arthralgias, metallic taste, Paresthesias, cramps, visual disturbances, "Loose" painful teeth Epidemic watery diarrhea Prominent vomiting, no fever, duration less than 24 hr Norovirus Staphylococcal enterotoxins Bacillus cereus Emetic form: short incubation 24-48 hr 2-8 hr Contaminated ice machines, shellfish, ready-to-eat foods Ham, poultry, pastries (cream-filled), mixed salads, egg salad Nucleic acid amplification assays Identification of preformed toxin or isolation of 105 colony-formingunits of organism from food Identification of preformed toxin or isolation of 105 colony-formingunits of organism from food 2-8 hr Prominent vomiting, no fever, duration less than 48 hr Diarrheal form: longer incubation 8-14 hr Abdominal cramps, severe diarrhea, no fever, duration less than 48 hr Abdominal cramps, severe diarrhea, no fever, duration less than 48 hr Abdominal cramps, watery diarrhea may be prolonged up to 7 days Prolonged febrile diarrhea and/or dysentery Abdominal cramps, watery diarrhea (rice-water stools). May be prolonged up to 1 wk Prolonged febrile diarrhea and/or dysentery Fried rice, macaroni-and-cheese, vegetables, other ready-to-eat foods left at room temperature. Symptoms and rapidity of onset are due to presence of preformed toxin Fried rice, macaroni-and-cheese, vegetables, other ready-to-eat foods left at room temperature. Family history should be probed for the presence of gastrointestinal disorders or immunodeficiency. Growth parameters should be obtained and charted on appropriate age-matched growth charts. The physical examination should assess for signs of malnutrition, vitamin and micronutrient deficiency, and dermatologic manifestations of systemic diseases. Signs of fat-soluble vitamin deficiency include bone deformities in vitamin D deficiency, dry scaly skin and Bitot spots in vitamin A deficiency, hyporeflexia or gait abnormalities in vitamin E deficiency, and bruises or bleeding in vitamin K deficiency. Joint examination may reveal arthritis associated with inflammatory bowel disease. Abdominal examination may reveal evidence suggestive of neuroendocrine tumors, and perianal examination may reveal evidence of inflammatory bowel disease (fistula, skin tags). Presence of blood in stools Persistent right upper or right lower quadrant abdominal pain Involuntary weight loss or growth failure Delayed puberty Presence of associated symptoms, such as unexplained fever, suggesting inflammatory arthritides or other systemic diseases Nocturnal fecal urgency or diarrhea Perirectal/perianal disease Persistent dysphagia Diagnostic Evaluation the clinician should attempt to focus the diagnostic evaluation on only those conditions suggested by the history and physical examination. Invasive diagnostic procedures should be limited to those patients whose presentation contains red flags for serious disease (Table 11. Laboratory investigation should begin with microbiologic studies for bacteria and parasites in the stool.

Often gastritis in english language order 30caps diarex fast delivery, a pulmonary ejection click may be present because of the dilated pulmonary root gastritis fever buy 30caps diarex overnight delivery. The S2 is narrowly split or single because the high pulmonary artery diastolic pressure closes the valve early gastritis symptoms bad breath buy diarex with visa. A diastolic decrescendo murmur then begins with pulmonary valve closure and is high in frequency because the pulmonary artery pressure is high chronic gastritis meaning purchase diarex with visa. There is usually an aortic ejection click that is well separated from S1 gastritis diet mayo clinic generic diarex 30 caps overnight delivery, does not vary with respiration gastritis test buy generic diarex 30 caps line, and is usually best heard at the apex. The S2 split is normal, although the A2 may be loud and may have a "tambour" quality. They occur in synchrony with cardiac movement and can be heard during the early period after myocardial infarction and most frequently after cardiac surgery (see Chapter 7). Many diseases have profound effects on the pulmonary circulation and can elevate pressures within the pulmonary arteries. These include diseases of lung, pulmonary vasculature, heart, or liver; collagen vascular diseases; and obstruction of the upper airways. One consistent physical finding detected in pulmonary hypertension is an active right ventricular parasternal tap with a distinctive, sharp palpable P2. There may be no audible murmur; a high-pitched murmur of pulmonary valve insufficiency or a high-pitched systolic murmur of tricuspid valve insufficiency may be present. Recognition of pulmonary hypertension warrants a diligent search for the underlying cause. If the reason for the elevated pulmonary artery pressure remains unclear, the disorder is referred to as primary pulmonary hypertension. If an etiology can be found, the disorder is termed secondary pulmonary hypertension. In contrast to the low-pressure murmur of pulmonary valve insufficiency (in the absence of pulmonary hypertension), the murmur of aortic valve insufficiency is high pitched and audible from the aortic area extending to the apex. The peripheral pulses and the intensity and length of the murmur provide clinical quantification of the magnitude of regurgitant flow. Malformations associated with profound and fixed cyanosis without heart failure are usually associated with right-sided obstructive lesions and a right-to-left shunt. Transposition of the great arteries with intact ventricular septum also manifests with profound and fixed hypoxia, with mild tachypnea, and with no heart failure. In addition, obstructed total anomalous pulmonary veins may produce severe cyanosis, pulmonary venous engorgement, and pulmonary hypertension. Lesions associated with left-sided obstruction (critical aortic stenosis, interrupted aortic arch, hypoplastic left heart syndrome) produce significant cardiogenic shock, poor perfusion, and profound lactic acidosis. The chest radiograph may provide helpful clues to the cause of the lesion, depending on the paucity (pulmonary atresia) or plethora (obstructed total anomalous pulmonary venous return) of the pulmonary vascular markings; the left- or right-sided (tetralogy of Fallot, truncus arteriosus) position of the aorta; the configuration of the heart (boot-shaped, as in tetralogy of Fallot; egg-shaped, as in transposition of the great arteries; or massive enlargement, as in Ebstein anomaly); or the side of the chest (risk of heart disease is higher with dextrocardia, especially if the stomach bubble is on the left side of the abdomen or if the liver is midline). The chest radiograph is of some help in distinguishing heart disease from congenital pneumonia, respiratory distress syndrome, pneumothorax, and congenital diaphragmatic hernia. After closure of the aortic valve (A2), regurgitation of leakage at this site creates the high-pitched, early diastolic decrescendo murmur of aortic insufficiency. This murmur is heard best at the third left or right intercostal space while the patient is sitting. The most common form of aortic insufficiency is acquired, most often as a consequence of severe rheumatic carditis, and can be present in both acute rheumatic fever and chronic rheumatic heart disease. The left ventricular impulse is abnormal and hyperdynamic, and a wide pulse pressure is present. A long, low-frequency musical diastolic rumble beginning onethird of the time into diastole may occur, especially in the left lateral decubitus position in patients with significant valve insufficiency. It is believed to be related to regurgitant aortic flow passing across the anterior mitral valve and fluttering of the leaflet in conjunction with mitral valve inflow. The electrocardiogram in infancy is of help in discriminating atrial and ventricular enlargement or hypertrophy and very helpful when there is an abnormal superior vector (complete atrioventricular canal, tricuspid atresia). Two-dimensional real-time color Doppler echocardiography is most useful in identifying the anatomy of congenital heart lesions. The echocardiogram enables assessment of the 4 chambers, the interconnecting valves, the great arteries, the pulmonary venous return, and the anatomic relationships between these structures. Furthermore, color Doppler flow studies can determine the presence, direction, and magnitude of right-to-left or left-to-right shunts. Echocardiography has replaced cardiac catheterization for all but the most complex congenital heart lesions. Valvulitis, as manifested by specific and new heart murmurs, is often part of the initial clinical picture. The specific heart murmurs are 3: mitral regurgitation, aortic regurgitation, and the rare Carey-Coombs murmur, a mid-diastolic rumble at the apex. After the acute rheumatic fever has run its course, any remaining murmurs become part of chronic rheumatic heart disease. If the patient has continued permanent reliable penicillin prophylaxis, the severity of the mitral regurgitation often disappears; this happens less commonly with aortic regurgitation. The development of mitral valve stenosis is part of the natural history of severe repeated episodes of acute rheumatic fever. Pure aortic stenosis does not develop, although in the presence of long-standing rheumatic heart disease with severe aortic regurgitation, some aortic stenosis may be present. In some very severe cases, tricuspid valve regurgitation has been documented, but it is rare. The diagnosis of acute rheumatic fever is suggested (although not definitively confirmed) by application of the revised Jones criteria, last edited in 2015 (Table 8. In addition, evidence of a group A streptococcal pharyngitis must be present, which may include a positive throat culture, positive streptococcal antigen or antistreptococcal antibody, or a history of prior episodes of rheumatic fever. In cases where carditis may be subclinical (no audible murmur), the diagnosis is supported by echocardiographic evidence of subclinical carditis (no audible murmur) by demonstrating significant mitral regurgitation with a regurgitant jet seen in 2 planes with chaotic flow and being holosystolic and extending 1 cm into the left atrium. Criteria for subclinical significant echocardiographic aortic regurgitation include its being seen in 2 imaging planes, being holodiastolic, and extending 1 cm into the ventricle (Table 8. The differential diagnosis is limited in the presence of carditis and arthritis (see Chapter 33) but includes systemic lupus erythematosus. Carditis is now defined as clinical and/or subclinical (echocardiographic valvulitis). Arthritis (major) refers only to polyarthritis in Low-Risk populations, but also to monoarthritis or polyarthralgia in Moderate/High-Risk populations. Revision of the Jones criteria for the diagnosis of acute rheumatic fever in the era of Doppler echocardiography: a scientific statement from the American Heart Association. Pan-diastolic jet in at least 1 envelope Pathologic Mitral Regurgitation (All 4 Met) 1. Endocarditis may develop in congenital heart anomalies in the unoperated and the postoperative state. Furthermore, up to 30% of cases of infective endocarditis occur on previously normal native valves. Endocarditis is the result of a bacteremia, which in a normal host is usually transient, asymptomatic, and without sequelae. Transient and predisposing bacteremias occur during dental procedures that induce bleeding (even dental cleaning); tonsillectomy or adenoidectomy; intestinal. The definitive diagnosis of infective endocarditis includes recovery of a microorganism from culture or histologic study of a heart, an embolized vegetation, or an intracardiac abscess. Vegetations may be demonstrated by the sensitive technique of transesophageal echocardiography but are usually seen on transthoracic echocardiography. In the absence of direct definitive evidence, the following are important diagnostic factors: persistently positive blood cultures with a pathogen compatible with the diagnosis (see Table 8. Candida species, Aspergillus species, Pseudallescheria boydii, Histoplasma capsulatum. Blood cultures are helpful if 2 or more drawn 12 hours apart are positive or if a majority. More than 85% of first blood cultures are positive; the yield approaches 95% with the second blood culture. Sufficient blood must be inoculated into the media to detect the low-grade bacteremia of infective endocarditis; excessive blood inoculation may inhibit bacterial growth by continued activity of leukocytes unless the technique involves centrifugation lysis. The cultures should be incubated for more than the routine 72 hours (often 1-2 weeks), and the laboratory should be notified of the possible diagnosis so that laboratory personnel can enrich the media to encourage the growth of fastidious nutrient-dependent organisms. To prevent infective endocarditis, high-risk patients, procedures, and factors that predispose to bacteremia need to be identified (Table 8. Patients needing infective endocarditis prophylaxis include those with intracardiac foreign bodies (prosthetic valve, grafts), prior episodes of infective endocarditis, a heart transplant with abnormal valve function, and certain congenital heart abnormalities including the following: (1) cyanotic congenital heart disease that has not been fully repaired, including children who have had surgical shunts and conduits; (2) a congenital heart defect that has been repaired with prosthetic material or a device for the first 6 months after the repair procedure; and (3) repaired congenital heart disease with residual defects, such as persisting leaks or abnormal flow at or adjacent to a prosthetic patch or prosthetic device. Prophylaxis is reasonable because endothelialization of prosthetic material occurs within 6 mo after the procedure. Most murmurs at all ages are not caused by cardiac disease and are not associated with symptoms or increased risk for disease. Red flags in the neonatal period include cyanosis or heart failure with or without the presence of other congenital anomalies or syndromes, such as trisomy 21. Such syndromes often manifest with multiple congenital anomalies, including those involving the cardiovascular, gastrointestinal, and central nervous systems. Sudden deterioration, cyanosis, or heart failure with increasing metabolic acidosis and a reduction in the murmur suggests closure of the ductus arteriosus. Another thing not to miss is the murmur associated with an arteriovenous malformation, such as the cerebral vein of Galen malformation, which manifests with heart failure and a cranial bruit. Finally, obstructed total anomalous venous return may be confused with persistent fetal circulation, and it may be difficult to establish the diagnosis. Total anomalous venous return is associated with fixed, profound cyanosis (PaO2 <35 mm Hg), severe pulmonary venous congestion, and a small heart. Acquired murmurs or symptomatic murmurs that change in quality should suggest acute or recurrent rheumatic fever, or infective endocarditis. Systemic symptoms and peripheral signs associated with these disorders are suggestive of the diagnosis. Arthritis (associated with rheumatic fever or endocarditis-induced immune complexes), fever, anemia, leukocytosis, cutaneous manifestations (erythema marginatum and subcutaneous nodules in rheumatic fever; Osler nodes, Janeway lesions, petechiae, and splinter hemorrhages in infective endocarditis), and evidence of prior infection (streptococcal antibodies) or current infection (positive blood cultures) help identify the nature of the acquired heart disease. Finally, heart murmurs in a normal heart may be caused by hemodynamic factors, such as severe anemia or thyrotoxicosis. Mortality associated with congenital heart defects in the United States: Trends and racial disparities, 19791997. The innocent supraclavicular arterial bruit-utility of shoulder maneuvers in its recognition. The second heart sound: Newer concepts, part I: Normal and wide physiological splitting. Balloon angioplasty of native coarctation: Clinical outcomes and predictors of success. Pulse oximetry screening for critical congenital heart defects in asymptomatic newborn babies: a systematic review and meta-analysis. Cyanotic congenital heart disease with decreased pulmonary blood flow in children. Value and limitations of auscultation in the management of congenital heart disease. Assessment and management of congenital heart disease in the newborn by the district paediatrician. Prospective comparison of clinical and echocardiographic diagnosis of rheumatic carditis: Long term follow up of patients with subclinical disease. Correlations among clinical presentation, surgical pathologic findings, and hemodynamic sequelae. Variation in group A streptococci and the prevalence of rheumatic fever: A half-century vigil. Morphology, prevalence and clinical significance of left ventricular false tendons in adults. Left ventricular false tendons in children: Prevalence as detected by 2-dimensional echocardiography and clinical significance. Musical murmurs: Clinical implications, long term prognosis, and echo-phonocardiographic features. Physiologic pressure differences between the main and branch pulmonary arteries in infants. Bacterial endocarditis in children: Trends in its diagnosis, course, and prognosis. Operative intervention in active endocarditis in children: Report of a series of cases and review. Prevention of infective endocarditis: guidelines from the American Heart Association. A guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. It is important to have a systematic, stepwise approach to the diagnosis and management of poor growth in young children and to follow growth over time.

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