Theme Shigellae infections. Salmonellae infections. Escherichia infections. Yersiniosis. Rotaviral infection Theme Viral hepatitis A, B, С, d et al. Gastrointestinal infections: guidance, data and analysis
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Hepatitis C in the newborn Criteria of Hepatitis Severity (in icteric period)
Mild Moderate Severe Degree of intoxication in preicteric period Mild, short
Severe Body temperature subfebrile t 38-39 ℃ (in preicteric period)
t 39 ℃ and more Jaundice Mild
Mild-to moderate Severe
Liver size increases Up to 2 сm On 2-5 cm More than 5 cm Bilirubin increases Indirect bilirubin increases Up to 85 μmol/l Up to 25 85-200
25-50 > 200
> 50 Aminotranspherases level 5-10 times more than normal 10-15 times more than normal 15-30 times more than normal
70-80 %
60-70 % < 60% Tymol test Mildely increased Moderately increased Severely increased
On 25-35
th day from the beginning On 40-50 th day On 50-60 th day When the jaundice appears the toxic sign Decreases Continues for 2-3 days
Continues, sometimes increases
––
In 1.5 % Is typical Diuresis Normal
Decreased Markedly decreased
Normal
Normal Decreased Icteric phase course 7-10 days 1-2 wks 2-3 wks
Posticteric period • Urine becomes lighter • Stools becomes darker • Jaundice decrease • Decreasement of the liver sizes • Normalization of bilirubin, ALT and AST, other indexes. • Anti-HAV Ig G, (Hepatitis A). The presence of anti-HAV IgG in the absence of IgM indicates past infection or vaccination. • Anti-НВс IgM, anti-Нве IgM, later- anti-НВс (total) IgM and anti-НВс IgG (Hepatitis B). • Anti-НВс IgM, anti-Нве IgM, later- anti-НВс (total) IgM and anti-НВс IgG and anti- HDV IgG (Hepatitis D). • Anti-HCVcore IgG (past Hepatitis C). • Anti-HCVcore IgG, anti-HCV NS in Hepatitis C latent phase. • Anti-HCVcore IgM and IgG (with IgM predominance), anti-HCV NS and HCV- RNA in Hepatitis C reactivation phase. • Anti-HEV Ig G (Hepatitis E). • anti-E2 is usually detected only after the loss of HGV RNA in the serum. Anti-E2 can persist for years after clearance of the virus and is therefore a marker of recovery from HGV infection (Hepatitis G). Liver biopsy is the most accurate method of evaluating the extent of Hepatitis C virus– related liver disease. Liver biopsy is recommended for all patients before they start antiviral therapy. Fulminant Hepatitis criteria: - Acute hepatic failure - Confusion and drowsiness, somnolence, disturbances in sleep pattern - Delirium (mental confusion) and convulsions - Coma I-II - Hepatic smell form the mouth - Hemorrhagic syndrome (Gastrointestinal bleeding) - Decreasing of diuresis - Liver decreases in size - Total bilirubin increases - Coagulopathy (Prothrombin time is prolonged) - Decreased ALT, AST - Decreased protein (albumen) Atypical (unicteric, effaced, subclinical) forms criteria: - Contact with patient who had hepatitis - Hepatomegaly - Increasing of ALT, AST, GGTP The clinical picture of GBV-C infection is commonly similar to that of the subclinical and anicteric types of hepatitis with normal or low aminotransferase activities. GBV-C-associated hepatitis runs with normal biochemical parameters in 75% of patients. There are reports on the occurrence of acute, fulminant and chronic (mild and moderate) Hepatitis And hepatic fibrosis. Coinfection of HGV with Hepatitis B, C, and D viruses is significantly more frequently detected than monoinfection. Hepatitis G infections may persist indefinitely in immunocompromised persons, but frequently resolves in immunocompetent persons.
For HAV, HEV - Recovering - Residual fibrosis of liver (posthepatitis hepatomegaly) - Biliary dyskinesia - Chronic cholecystitis and cholecystocholangitis - Chronic HEV infection in immunocompromised persons For HBV, HCV, HDV - Recovery - presence of RNA (GBV-C) without biochemical or histological signs of liver disease - Fulminant hepatitis (rare) - Residual fibrosis of liver (posthepatitis hepatomegaly) - Biliary dyskinesia - Chronic cholecystitis and cholecystocholangitis - Development of chronic hepatitis (Patients with chronic Hepatitis B infection can be immune tolerant or have an inactive chronic infection without any evidence of active disease, and they are also asymptomatic. Patients with chronic active hepatitis, especially during the replicative state, may have symptoms similar to those of acute hepatitis); - Cirrhosis which may result in portal hypertension and liver failure - Hepatocellular carcinoma - Autoimmune manifestations, often including antinuclear antibodies and smooth muscle antibodies - Death Signs of chronic hepatitis: - Hepatomegaly - Splenomegaly - Muscle wasting - Palmar erythema - Spider angiomas - Vasculitis (rarely) Signs of liver cirrhosis: - Ascites - Jaundice - History of variceal bleeding - Peripheral edema - Gynecomastia - Testicular atrophy - Abdominal collateral veins (caput medusa) Diagnosis example: Hepatitis A, typical form, icteric period, mild severity, acute course. Differential diagnosis Prejaundice period: - viral upper respiratory tract infections - intestinal infection - acute appendicitis - diseases caused by parasites - acute pancreatitis Jaundice period: - suprahepatic icterus (Hemolytic anemia), - hepatic icterus (Gilbert, Krigler-Nadjar syndrome, Infectious mononucleosis, Leptospirosis, Pseudotuberculosis, Congenital liver diseases, Drug-induced hepatitis, Mushroom toxicity, Autoimmune Hepatitis, Liver Abscess), - subhepatic icterus (Biliary obstruction, Cholangitis, Cholecystitis). Differential diagnosis of Viral hepatitis Signs HB HA HC HE HD Patients age All age
groups Elder than 1 yr. All age
groups Elder than 1 yr. All age
groups Incubation period 2-6 mo.
14-45 days 2 wks. - 3 mo. 15-45 days 2 wks. - 6 mo.
Beginning Subacute Acute Subacute Acute Acute
Intoxication in preicteric period
Mild Moderate
Mild
Moderate Often moderate Intoxication in icteric period Severe
Mild Absent or mild Absent or mild Severe
Allergic rashes May be
present Absent
May be present
Absent May be
present Severity Often
moderate and severe
Mild and moderate Mild and moderate Mild Severe and fulminant Duration of the icteric period
3-5 wks 1-1.5 wks
2 wks
1-2 wks
2-8 wks
Transformation in chronic hepatitis Often -
primary chronic
–
In 50 % Possible in immunocomp romised
person
Often Tymol test Often normal Elevated High High
Moderately elevated Specific markers HBsAg HBeAg
anti НВс IgМ Anti HAV IgМ Anti HCV Ig RNA HCV Anti HEV HBsAg, anti НВс, anti HDV IgМ
Basic treatment of an acute hepatitis: - bed regime up to toxic signs disappear, - semi-bed regime (up to icterus disappear, normalization of ALT, AST), - special diet: • Exclude heavy fats (like pork), spices, fried food, and “fast food”; avoid stimulators of gastrointestinal secretion; the diet should be rich with metionine, lecithin, and choline to stimulate synthesis of proteins and enzymes in the liver. Diet with normal value of proteins and vitamins, with restriction of fats, carbohydrates and salt.
• Boiled, steamed and baked food is recommended; meals 5 times daily. Treatment of mild hepatitis – only basic therapy Treatment of moderate hepatitis - basic therapy - peroral detoxication 40-50 ml/kg with water balance control - enterosorption 1-2 wks (in case of cholestatic variant) - choleretics in the recovery period: • cholagon, • allocholum, • cholenzym, • galstena, • hepabene. Treatment of severe hepatitis • basic therapy, • intravenous detoxication (totally – 50-100 ml/kg/day): - 0.9 % NaCl, Ringer’s solution, - Ringer’s lactate solution, - 5 % glucose, - albumen 5 ml/kg; • enterosorption 2-3 wks, • lactulose for 10-14 days in age appropriate doses, • deoxycholic acid (ursofalk) in case of cholestasis 10 mg/kg, • prednisolone (in possibility of fulminant form development) and for infants under 1 year with unfavorable premorbidity): in daily dose 1-3 mg/kg 4 times daily divided in equal doses , in a course of 7-10 days, Treatment of fulminant form • straight bed regimen, • diet with protein restriction up to 40 % of an age requirements, • intravenously: - prednisolone 10-15 mg/kg/day in 4 equally divided doses, - detoxication therapy (totally – 50-100 ml/kg/day) with diuresis control: - 0.9 % NaCl, Ringer’s solution, - Ringer’s lactate solution, - 5 % glucose, - albumen 5 ml/kg; • extracorporeal detoxication in case of ineffective previous therapy (plasmapheresis), • hyperbaric oxygenation, • in case of edema, ascytis – water-electrolyte balance correction, • K-serving diuretics (verospiron, triampur), • Fresh frozen plasma 10 ml/kg as donator of coagulation factors, • Heparin 100-300 IU/kg in possibility of DIC-syndrome development, • Protease-inhibitors (trasilol, contrical, gordox) in the age appropriate doses in case of DIC-syndrome development, • Antibacterial therapy for bacterial complication prophylaxis (less hepatotoxic medicine), • Enema and gastric lavage, • Lactulose for 10-14 days. Liver transplantation is indicated in patients with fulminant liver failure. Patients with evidence of decompensated liver disease or fulminant liver failure should be immediately transferred to a center capable of performing a liver transplantation.
From the time of initial diagnosis, optimal management of Hepatitis B virus (HBV) infection requires a lifetime of routine monitoring, even when patients are asymptomatic. The aims of treatment of chronic Hepatitis B are to achieve sustained suppression of HBV replication and remission of liver disease. The ultimate goal is to prevent cirrhosis, hepatic failure, and hepatocellular carcinoma (HCC). Children with HBV infection may not need treatment until well into their adolescent years or adulthood. Either interferons (IFN-a2b and peginterferon-a2a) or nucleoside or nucleotide analogues (lamivudine, adefovir, entecavir, tenofovir), may be used as monotherapy or in combination.
times/wk SC for 16-24 wk; not to exceed 10 million Units/dose 3 times/wk ) use has a defined, self-limited course; in contrast, therapy with nucleoside or nucleotide analogues can be long- term, often indefinite treatment. PEG-INF-alfa-2a is indicated for the treatment of adults with HBeAg-positive and HBeAg- negative chronic Hepatitis B infection Lamivudine (≥2 years: 3 mg/kg PO qDay; not to exceed 100 mg/day) is now considered first-line therapy. Adefiovir (≥12 years old: Administer as in adults, 10 mg PO qDay). Entecavir is indicated for treatment of CHB with evidence of active viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease in children ≥2 years and weigh at least 10 kg Administer PO once daily
– 10-11 kg: 0.15 mg (3 mL) – >11-14 kg: 0.2 mg (4 mL) – >14-17 kg: 0.25 mg (5 mL) – >17-20 kg: 0.3 mg (6 mL) – >20-23 kg: 0.35 mg (7 mL) – >23-26 kg: 0.4 mg (8 mL) – >26-30 kg: 0.45 mg (9 mL) – >30 kg: 0.5 mg (10 mL oral solution or one 0.5-mg tab) Tenofovir (8 mg/kg PO qDay; not to exceed 300 mg/day) is indicated for chronic Hepatitis B in children aged 2 years or older. Hepatitis C antiviral treatment For acute Hepatitis C virus (HCV) infection, supportive care is the mainstay of treatment. Early initiation of antiviral therapy is not defined.
Treatment of chronic HCV infection has two goals. The first is to achieve sustained eradication of HCV (ie, SVR), which is defined as the persistent absence of HCV RNA in serum 12 weeks after completing antiviral treatment. The second goal is to prevent progression to cirrhosis, hepatocellular carcinoma (HCC), and decompensated liver disease requiring liver transplantation. In chronic HCV infection, the goal is to identify complications and suitable candidates for antiviral therapy. Priority should be given to: - Patients with advanced fibrosis, those with compensated cirrhosis, liver transplant recipients, and those with severe extraheptic complications. - patients at high risk for liver-related complications and severe extrahepatic Hepatitis C complications. - patients whose risk of HCV transmission is high and in whom HCV treatment may result in a reduction in transmission (eg, men who have high-risk sex with men, active injection drug users, incarcerated persons, and those on hemodialysis). The World Health Organization recommends treatment to all individuals aged 12 years or older diagnosed with HCV, regardless of their disease stage. Long-term monitoring is essential because the risk of liver cancer is high. The first direct-acting antiviral drugs were approved for adolescents in 2017. Sofosbuvir (Sovaldi, 400 mg PO qDay with weight-based ribavirin dose in 2 divided doses with food as - 35-47 kg: 15 mg/kg/day - 47-49 kg: 600 mg/day - 50-65 kg: 800 mg/day - 66-80 kg: 1000 mg/day - >80 kg: 1200 mg/day). And the combination product, ledipasvir/sofosbuvir (Harvoni), 1 tablet (90mg/400mg) PO qDay for 12-24 wks, depending on previous treatment and presence of cirrhosis), is approved for chronic HCV infection in pediatric patients aged ≥12 years or who weigh at least 35 kg. Sofosbuvir is indicated for HCV genotypes 2 or 3 and is used in combination with ribavirin. Ledipasvir/sofosbuvir is indicated for HCV
genotypes 1,
4, 5,
or 6.
Glecaprevir/pibrentasvir (Maviret) was approved for adolescents in April 2019. Treatment- naïve adolescents aged 12-17 yr, or weighing at least 45 kg (99 lb) with chronic Hepatitis C virus (HCV) genotypes 1-6 without cirrhosis or with compensated cirrhosis 3 tablets (ie, 300 mg/120 mg total dose) PO once daily with food for 8-16 wks, depending on previous treatment and presence of cirrhosis.
adverse effects are often problematic. The response rate is lower for individuals infected with genotype 1, the most common genotype that causes infection, and the less common genotype 4.
higher rates of response, especially with non–genotype 1 Hepatitis C virus (HCV) infections. Peginterferon alfa-2b (PEG Intron) plus ribavirin (Rebetol) is approved for children aged 3 years or older, whereas peginterferon alfa-2a (Pegasys) plus ribavirin (Copegus) is approved for children aged 5 years or older.
No pharmacologic treatment for HDV has been approved. Peginterferon alfa-2a (PEG-IFNa2a) and nuceloside analogues have been used to manage chronic HBV infection, but only PEG-IFN has shown anti-HDV activity. The efficacy rate of interferon-based therapy does not exceed 30%, with frequent termination of therapy owing to serious side effects, and the relapse rate is very high.
option for transplant recipients with chronic Hepatitis E. Also sofosbuvir, a nucleotide analogue, inhibits RNA replication of HEV genotype 3 in vitro.
In patients co-infected with HCV and HGV, interferon has similar efficacy with regard to both, but the responses of the two viruses are independent.
* patients with mild and moderate forms can be treated at home; • discharge on 15-20 th day of illness is possible with the remained hepatomegaly, slightely increased ALT, AST, dysproteinemia); • Supervision of the patient should be continued in an outpatient department: first examination – in 7 days after discharge, then – in 1, 3, 6 months. Supervision should be stopped in case of complete recovery of the patient after 6 mo of dispensaryzation; • physical education should be restriced on 3-6 months, sports on 12 months.
All persons with chronic Hepatitis B who are not immune to Hepatitis A should receive 2 doses of Hepatitis A vaccine 6-18 months apart. Infants of HBsAg-positive women should receive Hepatitis B immunoglobulin and Hepatitis B vaccination within 12 hours of birth, a complete set of 3 vaccinations, and long-term follow-up.
Reserve routine screening using ultrasonography and alpha-fetoprotein determination for patients with severe chronic active hepatitis, cirrhosis, or both. Hepatitis C Long-term monitoring is essential in patients with chronic HCV infection because the risk of liver cancer is high, even in sustained virologic responders.
The prothrombin time is useful for assessing liver function. The serum alpha-fetoprotein assay is a potential screening test for HCC. Ultrasonography is potentially useful to monitor for Hepatitis C virus–related complications such as portal hypertension and HCC.
Follow-up is recommended for at least 6 months to determine if chronic Hepatitis B virus (HBV) and Hepatitis D virus (HDV) infection develop. Perform a liver biopsy to stage liver disease prior to beginning interferon alfa therapy. Treatment with interferon can be continued after the 1-year period if well tolerated and efficacy is demonstrated. Monitoring HDV RNA and Hepatitis B surface antigen (HBsAg) levels may help in guiding therapy. Prophylaxis of enteral hepatitis • Early isolation of ill person. • Supervising contacted, laboratory test every 10-15 days. • Personal hygiene. • Disinfection in the epidemic focus. • Passive prophylaxis by human immune globulin. • Immunization for the Hepatitis A virus (HAV) infection for patients at risk of the disease. Hepatitis E is preventable by vaccination (a recombinant genotype 1 HEV vaccine, genotype 4 HEV was also prevented with the vaccination, indicating cross-protection against different HEV genotypes).
who are traveling to countries where HAV infection is endemic. If the trip is shorter than 2 weeks, or if the patient is younger than 1 year, IG should be given. If the trip is longer than 3 months, a larger dose of IG (0.06 mL/kg) is needed for those who cannot receive the vaccine. Repeat dosing is recommended if the trip lasts longer than 5 months. HAV vaccine is currently licensed for use in children aged 12 months or older. When followed with a second dose 6 months later, the vaccine leads to 100% seroconversion.
Vaccination in areas of extremely high incidence of infection may only be cost-effective if prevaccination serology is obtained to target nonimmune individuals. Prophylaxis of parenteral hepatitis • Early isolation of ill person. • Sterilization of medical equipment. • Passive prophylaxis with human immune globulin. • For Hepatitis B active prophylaxis: universal vaccination refers to the administration of recombinant Hepatitis B vaccine to all newborn infants with a birth weight of greater than or equal to 2000 g
as a part of the routine childhood immunization schedule and to all children younger than 11 or 12 years who have not previously received a vaccine. Rapid (0-, 1-, and 2-mo) and standard (0-, 1- to 2-, 6-mo) schedules have identical efficacy. Some combination vaccines used in the routine vaccination schedule result in infants receiving 4 doses of HBV vaccine (eg, at 0, 2, 4, and 6 mo). This is considered acceptable. Ukrainian schedule: within the first 24 hours after birth, in 1, 6 months. For preterm infants who weigh less than 2000 g and are born to mothers with unknown HBsAg status, 0.5 mL HBIG should be given within 12 hours. When mother is HBs Ag positive – administer HBIG 0.5 mL intramuscularly with the first dose of recombinant HBV vaccine within 12 hours of birth. • No vaccine is available for HDV, but the HBV vaccination is effective against HDV.
Key words and phrases: Viral hepatitis, Hepatitis A virus, Hepatitis B virus, Hepatitis C virus, Hepatitis D virus, Hepatitis E virus, Hepatitis G virus, viral antigens, alanine aminotranspherase, aspartate aminotranspherase, Carole’s triad, “flu like syndrome”, clay-colored stools, special hepatitis markers, prodromal period, jaundice period, conjugate bilirubin, bile pigments. References: 1. USMLE Step 2 CK Lecture Notes 2018: Pediatrics. - Kaplan Medical, 2018. – P. 133-135. 2. USMLE Step 2 CK Lecture Notes 2018: Internal Medicine. - Kaplan Medical, 2018. – P. 248-251. 3. Manual of children's infectious diseases / O. Ye. Fedortsiv, I. L. Horishna, H.A. Pavlyshyn, I. M. Horishniy. - Vinnytsya: NOVA KNYHA, 2020. - 440 p. - ISBN 978-966-382-814-5. 4. Feigin and Cherry`s Textbook of Pediatric Infectious Diseases, 8 th Edition, Elsevier, Inc., 2019.- 3992 p. ISBN: 978-0-323-37692-1. 5. Manual of Childhood Infections: The Blue Book, 4 th Edition (Oxford Specialist Handbooks in Paediatrics) by Mike Sharland, Andrew Cant and al. Published by Oxford University Press Inc., New York, 2017 , 1035 p. ISBN: 978-019-872-92-27. 6. Illustrated Textbook of Paediatrics, 5th Edition. Published by Lissauer & Clayden, Elsevier, 2018, 559 p. ISBN: 9780723438724. 7. Nelson Textbook of Pediatrics, 2-Volume Set, 21st Edition. Kliegman, Geme. Published by Jenson & Stanton, Elsevier, 2019, 4264 p. ISBN: 9780323568890. 8. Oxford Textbook of Medicine: Infection by David Warrell, Timothy M. Cox, John Firth and Mili Estee Torok, Published by Wiley-Blackwell, 2012, 900 p. ISBN: 978-0199652136.
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