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Gastrointestinal disorders

This document provides information on gastrointestinal disorders in children. It begins with an introduction to common GI problems in children such as diarrhea, gastroesophageal reflux, hepatitis, and malnutrition. It then discusses specific conditions in more detail, including the definition, causes, symptoms, and treatment of diarrhea. Nursing management of diarrhea is also outlined, focusing on restoring fluid balance, preventing spread of infection, and health education. The document concludes with a discussion of prognosis and references a research study on risk factors for dehydrating diarrhea in infants.

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BY, MR. ABHIJIT P. BHOYAR M SC NURSING CHILD HEALTH SEMINAR ON
Gastrointestinal Disorder  Gastrointestinal problems are very common in childhood .  Number of medical & surgical problems are found among children.  GI disturbances are influenced by problems of liver & pancreas. Digestion , absorption and metabolism are the combined actions of gastrointestinal and hepato- pancreative system. INTRODUCTION
List Of Disease Condition:- Diarrhea Gastroesophagial reflux Hepatitis Childhood cirrhosis Liver transplantation Malabsorption syndrome Malnutrition
Review Of Anatomy & Physiolog y
Overall Digestive System Function  - Breaks up food physically and chemically.  - Stores food for a short period of time.  - Absorbs the digested foods and passes them into the circulatory system.  - Stores and eliminates undigested food from the body.
DIARRHEA DEFINATION:- Diarrhea is defined as the passage of loose , liquid or watery stool ,more than three times per day
 Acute diarrhea is an attack of loose motion with sudden onset which usually lasts 3-7 days but may last upto 10-14 days. It is associated with gastric mucosa & small intestines.  Chronic diarrhea is termed when the loose motion is occurring for 3 weeks or more .It is usually related to underlying organic diseases with or without mal-absorptions types
AGENT FACTORS- The infectious agent causing diarrheas with enteric infection include the following:  VIRUSES: rotavirus, adenovirus, enterovirus, measles virus etc.  BACTERIA: E.coli, shigella, salmonella, vibrio etc.  PARASITES: E.histolytica, malaria.  FUNGI: candida albicans  . Etiology of diarrhea
ENVIRONMENTAL FACTORS - Bacterial diarrhea is a more frequently occur in summer and rainy season, whereas viral diarrhea (especially rotavirus) found in winter. Diarrheal diseases are commonly seen in unhygienic environment. MODE OF TRANSMISSION- is mainly feco-oral route. it is water-born disease or may transmit via fingers, fomites , flies or dirt. Conti..
SECRETORY DIARRHEA- It has tendency to be watery, voluminous and persistent, even if no oral feeding is allowed. This is decrease absorption and increased secretion. OSMOTIC DIARRHEA- It is due to ingestion of poorly absorbed solute or maldigestion or a small bowel defect. It tends to be watery and acidic with reducing substances. MOTILITY DIARRHEA- It is associated with the increased or delayed motility of the bowel. There is decreased transmit time of bacteria leading to overgrowth Other types of DIARRHEA
PATHOPHYSIOLOGY Bacterial toxins stimulating active transport of electrolytes into the small intestine: cells in the mucosal lining of the intestine are irritated and secrete increased amounts of water and electrolytes. Organisms invading and destroying intestinal mucosal cells, decreasing intestinal surface areas, and impairing the intestine’s capacity to absorb fluids and electrolytes Inflammation, which decreases the intestine’s ability to absorb fluid, electrolyte and nutrients. Increased intestinal motility, resulting in impaired intestinal absorption.
CLINICAL MANIFESTATION Symptoms vary with severity, specific cause, and type of onset (insidious versus acute). 1) Low-grade fever to 100° F (37.8° C) 2) Anorexia 3) Vomiting (can precede diarrhea by several days); mild and intermittent to severe 4) Stools appearance of diarrhea from a few hours to 3 days  Loose and fluid consistency  Greenish or yellow-green  May contain mucus, pus, or blood  Frequency varies from 2 to 20 per day  Expelled with force; may be preceded by pain
Conti… 5) Behavioral changes  Irritability and restlessness  Weakness  Extreme prostration  Stupor and convulsions  Flaccidity 6) Physical changes  Little to extreme loss of subcutaneous fat  Up to 50% total body weight loss  Poor skin turgor; capillary refill longer than 2 seconds  Dry mucous membranes and dry, cracked lips Normal capillary refill time is usually less than 2 seconds.
Contii…  Pallor  Sunken fontanelles and eyes  Petechiae seen with bacterial infections  Excoriated buttocks and perineum.  Urine with blood 7) Vital sign and urine output changes (signal imminent cardiovascular collapse)  Low BP  High pulse  Respirations rapid and hyperapneic  Decreased or absent urine output
ASSESSMENT OF DEHYDRATION  Diarrhea Less than 4 liquid stools per day 4 to 10 liquid stools per day More than 10 liquids stools per day  Vomiting None or small amount Some Very frequent  Thirst Normal Greater than normal Unable to drink  Urine Normal A small amount and dark No urine for 6 hours 2. LOOK AT  Condition Well, alert Restless, irritable or sleepy, unwell Lethargic or unconscious, floppy  Eyes Normal Sunken Very sunken and dry  Tears Present Absent Absent  Mouth and tongue Moist Dry Very dry  Breathing Normal Faster than normal Very fast and deep 3. FEEL  Skin pinch Goes back quickly Goes back slowly Goes back very slowly  Pulse normal Faster than normal Very fast, weak or cannot feel 4. DECIDE DEGREE OF DEHYDRATION The patient has NO SIGNS OF DEHYDRATION If the patient has two or more signs including at least one sign there is SOME DEHYDRATION If the patient has two or more signs including at least one sign there is SEVERE DEHYDRATION
DIAGNOSTIC EVALUATION - STOOL: Cultures (for bacteria, ova, parasites, rotavirus), ph, red blood cells, leukocytes, glucose, blood . - BREATH HYDROGEN TEST: Check for carbohydrate malabsorption. - BLOOD TEST: Especially blood cells counts, electrolytes, blood urea nitrogen, glucose, and blood cultures. - X-RAYS: Check for possible bowel abnormalities.
MANAGEMENT  Treatment is based on the degree of dehydration; mild (less than 5%), moderate (5% to 10%), and severe (greater than 10% weight loss)  Goal is to prevent spread of disease; communicable disease is suspected until proved otherwise; enteric precautions are followed.  Bowel rest may be required based on degree of diarrhea and vomiting, if blood present, or electrolyte abnormalities.
Conti…  For mild to moderate dehydration (5%), oral rehydration solution is given to maintain fluid and electrolyte balance (WHO solution, Pedialyte, Infalyte) and BRATS (Bananas, Rice cereal, Apple & sauce, dry Toast, and Saltine crackers) diet is followed to provide rest for the inflamed intestines.  For oral rehydration, 100 mL/kg over 4 hours, with additional fluids after each liquid bowel movement.  Candidates for oral rehydration include mild to moderate (greater than 10%) dehydration, older than age 4 months, no persistent vomiting, and probable gastroenteritis.
 For moderate to severe dehydration (10% or greater): I.V. fluid and electrolyte replacement is given slowly as ordered (usually 20 mL/kg); usually over 2 days to prevent hypotonic hypervolemia (water intoxication).  Supportive care is given: monitoring oral and I.V. fluid intake, output from all sources, and patient's response to treatment.
Conti.. Specific antimicrobial therapy may be given in some cases such as immunosuppression, bacteremia, documented C. difficile.  Metronidazole 20 mg/kg/day in divided doses orally or I.V. may be used.  Vancomycin I.V. for resistant C. difficile
Conti… REHYDRATION THERAPY- INGREDIENTS OF ORAL REHYDRATION SALTS: COMPONENT CONTENT PER LITER WATER Sodium chloride 3.5gm Potassium chloride 1.5 gm Sodium citrate 2.9gm Glucose anhydrous 20.0gm
ASSESSMENT FOR DEHYDRATION IN CHILDREN CLINICAL SIGNS DEGREE OF DEHYDRATION MILD MODERATE SEVERE General Infant's behavior Thirsty, alert, restless Restless or lethargic; irritable to touch Limp, drowsy; cyanotic extremities Child's behavior Thirsty, alert, restless Thirsty, alert; postural hypotension Usually conscious; cyanotic extremities Respirations Slightly increased Increased Deep and rapid
CONTI.. CLINICAL SIGNS DEGREE OF DEHYDRATION MILD MODERATE SEVERE Pulse Slightly increased Increased Rapid Blood pressure Normal Decreased May be unrecordable Capillary refill <2 seconds 2 TO 3 seconds >3 seconds
CLINICAL SIGNS DEGREE OF DEHYDRATION MILD MODERATE SEVERE Skin turgor Normal Slightly reduced Reduced Skin color Pale Gray Mottled Weight loss Up to 5% Up to 10% Up to 15%
CONTI… CLINICAL SIGNS DEGREE OF DEHYDRATION MILD MODERATE SEVERE Mucous membrane Tacky Tacky/dry Parched Specific gravity <1.020 >1.030 >1.035 Anterior fontanelle Flat Slightly depressed Sunken Urine volume Small Oliguria Oliguria/anuria
Complications Severe dehydration and acid-base derangements with acidosis Shock
NURSING MANAGEMENT  Fluid volume deficit related to diarrhea.  Risk for cross infection related to infective loose motions.  Potential to altered skin integrity related to frequent passage of stools.  Altered nutritional status, less than body requirement related to malabsorption and poor oral intake.  Fear and anxiety related to illness and hospital procedures.  Knowledge deficit related to causes of diarrhea and its prevention.
Nursing Interventions GOAL- Restoring Fluid Balance  Monitor amount and rate of I.V. fluid therapy, which have been calculated by the health care provider. Fluid needs are based on fluid deficit, ongoing losses, and body weight.  Prevent overload of circulatory system.  Check flow rate and amount absorbed hourly and totally
CONTI..  Adhere to prescribed volume carefully when oral feedings are given in conjunction with I.V. fluid.  Never administer I.V. fluids to pediatric patient without safeguard of a volume-control infusion device or pump.  Observe for signs of fluid overload: edema, increased BP, bounding pulse, labored respirations, and crackles in lung fields.
CONTII..  Check I.V. site for infiltration or improper flow so site can be changed as necessary.  Use appropriate protective devices to prevent the child from injuring involved extremity or causing I.V. to malfunction.  Weigh the patient daily as a guide for fluid needs and patient status.  Monitor urine output and keep accurate intake and output record, including vomitus and liquid stools.
Preventing Spread of Infection  Ensure adherence to good hand-washing and gown technique protocols for all people having contact with infant or child.  Follow your facility's policy on care of diapers.  Handle specimens collected using universal precautions, and transport to laboratories in appropriate containers per policy.  Collect stool sample for culture before instituting antibiotic therapy.  Teach good hygiene measures to older children
•The important preventive measures are improvement of food hygiene, personal hygiene and environmental hygiene. These include safe water , adequate sewage disposal, hand washing practices, clean utensil, avoidance of exposure of food to dust and dirt, fly control, washing of fruits and vegetables •Avoidance of bottle feeding is most significant practice needed for prevention of diarrhea. •Boiling or filtering to be practiced for safe drinking water. Prevention of LBW and prematurity, exclusive breastfeeding, appropriate weaning practices, balanced diet, immunization are significant aspects of child care which prevents malnutrition and diarrheal episodes PREVENTIVE MEASURES-
PROGNOSIS-  Mortality is higher in neonates and infants than the older children  Malnourished children are having poor prognosis and greater mortality.  Antibiotic resistant type E. coli and Shigella cause very severe illness and poor prognosis.  Presence of severe dehydration, electrolyte imbalance  Early diagnosis with prompt and appropriate management helps in good prognosis.
RESEARCH- Case-control study of risk of dehydrating diarrhoea in infants in vulnerable period after full weaning  BMJ 1996; 313 doi: http://dx.doi.org/10.1136/bmj.313.7054.391 (Published 17 August 1996)  Cite this as: BMJ 1996;313:391  Objectives: To investigate risk factors for dehydrating diarrhoea in infants, with special interest in the weaning period.
 Results: In infants aged <12 months the risk of dehydrating diarrhoea was significantly higher in the first 9 months of life (P<0.001), and in those aged 12-23 months the risk was again greater in younger children (12-17 months) (P = 0.03). The type of milk consumed before start of diarrhoea episode was strongly associated with dehydration independent of socioeconomic, environmental, maternal reproductive, demographic, and health services factors. Compared with infants exclusively breast fed, bottle fed infants were at higher risk (odds ratio (95% confidence interval) for cow's milk 6.0 (1.8 to 19.8), for formula milk 6.9 (1.4 to 33.3)). Compared with those still breast feeding, children who stopped in the previous two months were more likely to develop dehydrating diarrhoea (odds ratio 8.4 (2.4 to 29.6)). This risk decreased with time since breast feeding stopped.
Conclusion: These results confirm the protective effect of breast feeding and suggest there is a vulnerable period soon after breast feeding is stopped, which may be of relevance for developing preventive strategies.
Gastroesophageal Reflux Disease (GERD)
Introduction:- Gastroesophageal Reflux Disease (GERD) is a digestive disorder that occurs when acidic stomach juices, or food and fluids back up from the stomach into the esophagus. GERD affects people of all ages—from infants to older adults.
 Delayed neuromuscular development  Physiological immaturity  Cerebral defects  Increased abdominal pressure  Obesity  Coughing &wheezing in case of cystic fibrosis  Bronchopulmonary dysplasia  Asthma  Indwelling orogastric or nasogastric tube Causes-
 Primary barrier to gastro esophageal reflux is the lower esophageal sphincter  LES normally works in conjunction with the diaphragm  If barrier disrupted, acid goes from stomach to esophagus PATHOPHYSIOLOGY.
Symptoms  In Infants-  The feature are unexplained vomiting immediate after feeding Regurgitation Refusal to eat & features of dehydration Irritability Excessive crying Sleep disturbances Arching and stiffening Respiratory symptoms like cough, strider, and pneumonia may found. Loss of weight or failure to gain weight
cont.  In Older Children-  Non cardiac chest discomfort  Upper abdominal discomfort  Chronic cough  StridOr  Nocturnal asthma  Dysphasia  Anemia
Other symptoms Difficulty or pain when swallowing Sudden excess of saliva Chronic sore throat Laryngitis or hoarseness Inflammation of the gums Cavities  Bad breath Chest pain
Diagnosis  X-ray of the upper digestive system  Endoscopy (examines the inside of the esophagus)  Ambulatory acid (pH) test (monitors the amount of acid in the esophagus)  Esophageal impedance test (measures the movement of substances in the esophagus)
Treatment & Management  Medical Management:-  1.Positioning-  It helps to reduce the amount of reflux.  Infants younger than 6 months should be placed on right lateral position during sleep, head of the crib should be raised at least 6 inches. The infant may also be held upright.  Older children should be placed in head raised to 30-45 degree angle position. Avoid recumbent position after meal for at least 3 hours .Upright of semi upright position during awaking is helpful.
Conti-  2. Feeding-  Special precautions to be taken during feeding of infants and older children.  Infants to be given thickened feed in small amount frequently followed by appropriate positioning, to prevent the reflux.  Older children should be allowed nothing per mouth 2hours before bed time. Low fat diet , spicy and acidic foods (onion, citrus products , apple juice , tomato) , esophageal irritants ( chocolate , peppermint , passive smoke) and carbonated beverages should be avoided .Chewing gum can be allowed to stimulate parotid secretions which increases esophageal clearance.
Conti- 3. Medications-  Antacids H2 –receptor antagonists (cimetidine) , prokinetic drugs (metaclopromide) and proton pump inhibitors(omeprazole) can be given alone or in combination
Surgical Management-  Fudoplication (Nissen’s operation) is most popular method. A gastric wrap procedure is done. Wrapping of the fundus around the lower oesophageal sphincter (a 360 degree wrap) completely prevent reflux episodes. Fundoplication is a surgical procedure that helps treat some gastroesophageal conditions. During a fundoplication for gastroesophageal reflux disease (GERD), for example, a surgeon will attach part of the stomach to the lower esophageal sphincter, which helps reduce acid reflux
 Antroplasty or pyloroplasty may be performed in some cases. Gastrotomy may be needed for feeding purposes or temporarily to decompress the stomach. Pyloroplasty is surgery to widen the opening in the lower part of the stomach (pylorus) so that stomach contents can empty into the small intestine (duodenum). The pylorus is a thick, muscular area. When it thickens, food cannot pass through
Nursing Management :  Preventing aspiration by positioning and appropriate feeding technique.  Maintaining fluid & electrolyte balance by I/V fluid therapy , (whenever needed) ,intake and output recording and estimation of electrolyte level.  Providing adequate nutritional intake  Continuous monitoring of vital signs , Assessment of features of complication and necessary investigations.
Conti-  Reducing fear of eating and modifying feeding schedule  Providing preoperative and postoperative care as for abdominal surgery of children.  Providing emotional support  Giving health education regarding , positioning , feeding, home based care and follow up.
Complication-  Aspiration pneumonia  Chronic esophagitis  Failure to thrive  Anemia  Asthma  Sudden infant death syndrome  ESophageal stricture An esophageal stricture is an abnormal tightening or narrowing of the esophagus.
HEAPATITIS
Function Of Liver-  Bile production that is essential to digestion  Filtering of toxins from the body  Excretion of bilirubin, cholesterol, hormones, and drugs  Metabolism of carbohydrates, fats, and proteins  Activation of enzymes (specialized proteins essential to metabolic functions)  Storage of glycogen, vitamins (a, d and k), and minerals  Synthesis of plasma proteins, such as albumin  Synthesis of clotting factors HEPATITIS means inflammation of liver
Causes of Hepatitis  ACUTE:  Viral hepatitis  Non-viral infection  Alcohol  Toxins  Drugs  Ischemic hepatits  Autoimmune  Metabolic diseases  CHRONIC:  Viral hepatitis  Alcohol  Drugs  Non-alcoholic steatohepatitis  Autoimmune  Heredity
Classification of Hepatitis Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Pathophysiology Targets of the Hep viruses are hepatocytes: Hepatocyte uptake involves a receptor on the plasma membrane of the cell After entry into the cell, viral RNA is uncoated, and host ribosomes bind to form polysomes. Viral proteins are synthesized, and the viral genome is copied by a viral RNA polymerase Minimal cellular morphologic changes result from hepatocyte infection Lymphocytic infiltrate; varying degree of necrosis.
Diagnosis Of Hepatitis  Physical Exam  Liver Biopsy  Liver Function Tests  Ultrasound  Blood Tests  Viral Antibody Testing
Diagnosis: HAV  Serum Serology: presence of serum antigens and immunoglobins  HAV: IgM anti-HAV: positive at the time of onset of symptoms; results remain positive for 3-6 months after the primary infection  Anti-HAV IgG appears soon after IgM and generally persists for many years.  Treatment: supportive
Hepatitis B  Epidemiology  HBV is a DNA virus that belongs to the hepatovirus family.  2 billion people worldwide have past or present infections  400 million people are chronic HBV carriers.  Eight genotypes of HBV identified and re-labeled A through H.  HBV is the cause of 60% to 80% of worldwide Hepatocellular Carcinoma(HCC).  500,000 to 1 million deaths worldwide are attributed to it.  5% to 10% of all liver transplants are attributed to HBV.
AT Risk Groups  IV drug users  People receiving multiple blood transfusions  Sexual promiscuity  People in contact with HBV carriers  Travelers to endemic areas of South America, Southern Asia, and Africa  Resident and employees of residential care facilities Promiscuity is the practice of engaging in sexual activity frequently with different partners or being indiscriminate in the choice of sexual partners. The term can carry a moral judgment if the social ideal for sexual activity is monogamous relationships.
Transmission 3 main ways: Parenterally/percutaneous route----IV Drug Users, needle sticks, Hemodialysis patients Sexually Vertical/ Perinatal route
Clinical Manifestation- Acute Hepatitis B – Less than 6 months; based on significant aminotransferase activity due to necro inflammatory injury  Symptoms are often non-specific symptoms such as myalgia, malaise , nausea, fatigue , pruritus, abdominal pain, jaundice  Fulminant hepatitis--acute HBV results in liver failure
Chronic Hepatitis B – Greater than 6 months; based on grade, stage, and etiology. Fibrosis and necroinflammatory processes; can last for decades  Immune tolerant--high viral replication, low inflammation and fibrosis. Seen in children or those affected early in life.  Immune active--high liver enzymes and high hbv dna and hbeag, active replication  Carrier state with low replication  Seroconversion from hbeag to hbeab  Low HBV levels, reduced liver inflammation
•Diagnosis-  Serology-  Liver Chemistry tests  Histology--Immunoperoxidase staining  HBV Viral DNA--Most accurate marker of viral DNA and detected by PCR  Liver Biopsy--to determine grade(Inflammation) and stage(Fibrosis) in chronic Hepatitis
Progress-  Incubation Period: 30-180 days Acute HBV Infection: 90% resolve by themselves; less than 1% develop fulminant hepatitic failure  Chronic HBV Infection: 2-10% progress to chronic state  90% in children less than five progress to chronic state  Risk of Liver Cirrhosis: 5 year accumulation risk of 8% to 20%
Treatment- 1) Interferon therapy – First Line Method of action is the inhibition of viral replication of cells thus assisting the immune system Side effects: "Flulike Symptoms", alopecia, rash, diarrhea
2) Nucleoside Analogues -- Lamivudine, Entecavir, Telbivudine Method of action is the inhibition of viral reverse transcriptase  Lamivudine  Dose : 100 mg PO q daily  Problem: High rates of resistant mutations  Side effect: lactic acidosis  Entecavir – 1st line  0.5 to 1mg PO  very effective;  more effective than lamivudine  Side effect: lactic acidosis  Telbivudine  Dose: 600mg daily  Side effect: lactic acidosis
3) Nucleotide analogues Method of action is the inhibition of viral reverse transcriptase  Tenovir  Dose: 300mg od  Highly effective with low resistance  Well tolerated  Adefovir – 1st line  Dose: 10mg daily  Resistance less than Tenovir  Side effect: nephrotoxicity
Hepatitis C  Spherical, enveloped, single-stranded RNA virus Incubation period: 7-8 wks  170 million infected worldwide  Parenteral Transmission: IV drug users  Most common indication for liver transplantation
Diagnosis: HCV  HCV: Anti-HCV; cannot distinguish acute from chronic infection  EIA: antibodies against core protein and nonstructural proteins; may appear 3 – 5 months after infection 80% of cases: patients are asymptomatic and do not develop icterus. Treatment: Interferon alpha, Ribavirin; (better sustained absorption, a slower rate of clearance, )
Hepatitis D This is also called “delta hepatitis.” Hepatitis D is a serious liver disease caused by the Hepatitis D virus (HDV), which is contracted through puncture wounds or contact with infected blood. This is a rare form of hepatitis that occurs in conjunction with hepatitis B infection.
Hepatitis E  Hepatitis E virus (HEV) RNA virus of the genus Hepevirus  Enterically transmitted infection; fecal-oral route, typically self-limited  Most outbreaks occur in developing countries.  Symptoms of acute hepatitis  Incubation period of hepatitis E virus is 2-9 weeks  Case fatality rate is 4%
Diagnosis- Serum, liver, and stool samples can be tested for HEV RNA Anti-HEV antibodies: - IgM (acute) - IgG (chronic) Treatment: supportive
Hepatitis F  It is well documented that even after a detailed serological study, 10 percent of children will not have marked to the known viruses A to E.  These could be HBV variants with mutation, or a budding RNA virus French workers have identified an enteric virus in this non A-E group and call it the hepatitis French virus(HFV).
HEPATITIS G Hepatitis G (HGV) virus is a single stranded RNA flavi virus which shares limited identity with HCV. It is distributed widely among the population and spreads by parenteral route.
Surgical Management: Liver Transplantatiion
Preventive Management Of Hepatitis Hygiene Practicing good hygiene is the main way to avoid catching hepatitis.  If you are travelling to a country with low sanitary standards, avoid: Drinking local water Ice Sea food Raw fruit and vegetables
Conti-  Hepatitis controlled through contaminated blood can be prevented by:  Not sharing drug needles  Not sharing razors  Not using someone else’s toothbrush  Not touching spilled blood
Nursing Management:-  Imbalanced Nutrition Less Than Body Requirements  Acute pain related to swelling of the liver is inflamed liver and portal vein dam.  3. Hyperthermia related to invasion agents in the blood circulation secondary to liver inflammation.  4. Fatigue related to chronic inflammatory process secondary to hepatitis.  5. Risk for impaired tissue integrity related to pruritus secondary to accumulation of bilirubin pigments in bile salts.
Complications of Hepatitis Chronic liver disease Cirrhosis (scarring of the liver) Cancer of the liver (in rare cases)
HAV HBV HCV HDV HEV HGV[*] Virology RNA DNA RNA RNA RNA RNA Incubation (days) 15–19 60–180 14–160 21–42 21–63 ? Transmission Parenteral Rare Yes Yes Yes No Yes Fecal-oral Yes No No No Yes Possible Sexual No Yes Yes Yes No Yes Perinatal No Yes Rare Yes No Yes Chronic infection No Yes Yes Yes No Yes Fulminant disease Rare Yes Rare Yes Yes No
INDIAN CHILDHOOD CIRRHOSIS
Childhood Cirrhosis  Indian childhood cirrhosis is a disease peculiar to the Indian infants and children, usually occurs between 6 months & 4 years of age. It may also found in Indian subcontinent and west Indies
Etiology-  Hepatotoxic agents- Hepatotoxic harmful agents like guttis or aspergillus flavus that grow on ground nuts, maize and rice may cause ICC .  Metabolic Defects- They may cause ICC specially disturbed lactose ,zinc, copper and magnesium metabolism.  Immunologic Disturbances- These are found in high levels of circulating immune complexes which can cause immune mediated injury of the liver.
Conti-  Genetic factors- Familiar occurrence of ICC points the possibility of underlying genetic factor along with environmental factors.  Nutritional Factors- previously it was believed that malnutrition was an important cause of cirrhosis.  Viral Infection- ICC has been thought to be a consequence of neonatal hepatitis or infective hepatitis.
Pathophysiology- Due to the disease process. The basic pathologic change is the diffuse liver damage by way of degeneration going on to necrosis and replacement fibrosis . The capsule shows patchy thickening and the surface is finely nodular . THE microscopic study shows marked hepatocyte damage as degenerative changes in the cytoplasm. Kupffers cell shows mild degree of proliferation. Gross pericellular fibrosis in the hepatic lobules are found.
Clinical Manifestation-  Onset is acute  Irritability  Disturbed appetite  Chalky & pasty stools with constipation or diarrhe  Mild fever  Progressive growth failure usually present in spite of adequate diet.
Conti-  Within few months to a years, there is hepatomegaly , jaundice and features of portal hypertension including splenomegaly , ascities, hematemasis , anemia, prominent superficial abdominal veins and thrombocytopenia  There may be high incidence of intravascular hemolysis.  Liver is usually gross enlarged with proturbent abdomen  The child generally have hepatic failure and intercurrent infections which may be fatal  Duration of illness may be 6 month to 3 years
Diagnosis- Liver Biopsy Cupriuresis test –it may be performed by oral administration of D- penicillamine, using urinary copper / creatinine ratio as the index parameters, sensitivity and specificity with positive and negative values are obtained.
Management-  Medical Management:-  Few cases of ICC improve spontaneously and survive without specific treatment.  Penicilline therapy is used as copper- chelating agent from the liver, which improves the survivals.  Immunomodulating agents like levamisole , corticosteroids, gammaglobulins may also be used.  Symptomatic treatment should be done especially for infections and vitamins and minerals deficiency
Conti-  Supportive care should be provided as rest , diet with good quality proteins , I/V glucose drip , oxygen therapy, antibiotic s therapy and good nursing care  Nursing intervention – improving nutritional status, promoting of activity tolerance , protecting skin integrity , preventing injury & bleeding.  Exchange transfusion may be effective to remove circulating toxins  In case of portal hypertension causing hematemesis, sengastaken tube may be of help to control esophageal bleeding
sengastaken tube
Nursing Mangement- Nursing intervention should provide special attention on improving nutritional status  promoting of activity tolerance protecting skin integrity preventing injury and bleeding and expert care for unconscious patients if needed.
Preventive Management- Continue breastfeeding upto six months and avoiding boiling of milk in copper or copper alloy pots Increasing public awareness about the preventive measures is important regarding lowering of copper intake through copper- rich food , water and utensils.
Liver Transplantation
Indications for Pediatric Liver Transplantation INDICATIONS PER CENT OF TRANSPLANTS (%) Biliary atresia 39 Metabolic liver disease 13 α1-Antitrypsin deficiency 5 Tyrosinemia 1 Wilson disease 1 Other 6 Acute hepatic necrosis 12 Biliary hypoplasia including Alagille syndrome 5 TPN-associated liver disease 5 Idiopathic cirrhosis 4 Autoimmune hepatitis 3 Tumors including hepatoblastoma 3 Neonatal hepatitis 2 Cystic fibrosis 2 Primary sclerosing cholangitis 2 Congenital hepatic fibrosis 1 Other 9
Benefits  Transplant can be done on an elective basis because the donor is readily available  There are fewer possibilities for complications and death while waiting for a cadaveric organ donor .
Screening for donors All donors are assessed medically to ensure that they can undergo the surgery Confidentiality The transplant team provides both the donor and family thorough counseling and support which continues until full recovery is made.
Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. MALABSORPTION SYNDROME
Classification Selective, as seen in lactose malabsorption. Partial, as observed in a-beta-lipoproteinaemia.  Total as in coeliac disease.
Pathophysiology  The main purpose of the gastrointestinal tract is to digest and absorb nutrients, micronutrients , water, and electrolytes.  Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.
Causes • HIV related malabsorption • Intestinal tuberculosis Due to infective agents • Blind loops • Inflammatory bowel diseases, as in Crohn's Disease • Fistulae, diverticulae and strictures Due to structural defects • Coeliac disease • Cows' milk intolerance • Soya milk intolerance • Fructose malabsorption Due to mucosal abnormality • Lactase deficiency inducing lactose intolerance • Sucrose intolerance • Intestinal disaccharidase deficiency  Due to enzyme deficiencie •Cystic fibrosis •Chronic pancreatitis •Carcinoma of pancreas  Pancreatic insufficiencies
Clinical features-  Diarrhoea, often steatorrhoea, is the most common feature.  Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption.  Weight loss can be significant despite increased oral intake of nutrients.  Growth retardation, failure to thrive, delayed puberty in children
Conti-  Swelling or oedema from loss of protein  Anaemias, commonly from vitamin B12, folic acid and iron deficiency presenting as fatigue and weakness.  Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis  Bleeding tendencies from vitamin K and other coagulation factor deficiencies.
Diagnosis  Blood tests  Stool studies  Radiological studies - Barium enema may be undertaken to see colonic or ileal lesions -CT abdomen is useful in ruling out structural abnormality, -Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP.  Interventional studies -Colonoscopy -Biopsy of small bowel showing coeliac disease
Other investigations  Glucose hydrogen breath test for bacterial overgrowth  Lactose hydrogen breath test for lactose intolerance  Sugar probes or 51Cr-EDTA to determine intestinal permeability.
Management Medical Management-  Replacement of nutrients, electrolytes and fluid may be necessary.  In severe deficiency, hospital admission may be required for nutritional support Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy.  Pancreatic enzymes are supplemented orally in pancreatic insufficiency.
Conti-  Dietary modification is important in some conditions:  Gluten-free diet in coeliac disease.  Lactose avoidance in lactose intolerance.  Antibiotic therapy to treat Small Bowel Bacterial overgrowth.  Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.
Nursing Management-  Improvement of nutritional status by appropriate diet planning and supplemention of deficient nutrients or substituting them.  Restoration of fluid and electrolyte balance by oral and parentral therapy.  Continuous monitoring and recording of patient’s condition.  Relief of pain by medications , Fower’s position and comfort. Analgesics ,antiflatulents and antidiarrheal agents are administered as prescribed.
Conti-  Maintenance of skin integrity specially of perineal area .  Health education to the parent about general cleanliness , nutrition , hydration, danger signs, home care and follow up for necessary medical help  Relief of fear and anxiety about long –term illness and hospitalization by appropriate explanation , reassurance and necessary support.
MALNUTRITION
Definitions  MALNUTRITION WHO defines Malnutrition as "the cellular imbalance between the supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions.  “ Malnutrition is the condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function.
Causes Of PEM-  Inadequate intake of food both in quality and quantity  Infection especially ARI ,diarrhea, measles & worm infestations lead to the condition which increases in requirement for calories, proteins and other nutrients, while decreasing important cause of PEM.
Classification Of PEM- Syndromal Classification- Kwashiorkor Nutritional Marasmus Prekwashiorkor Nutritional dwarfing
 Classification by Indian Academy Of Pediatrics-  When the child is having weight more than 80% of expected weight for age , considered as normal. The grade of malnutrition is described as follows;  Grade I- between 71-80% of expected weight for the age  Grade II- between 61-70% of expected weight for the age  Grade III- between 51-60% of expected weight for the age  Grade IV- between 50% or less of expected weight for the age
Pathophysiology- Inadequate dietary intake protein/ calories Malabsorption and altered metabolism Nutrient less so appetite loss Weight loss, growth flattering Immunity lowered Incidence of infection, increased Prolonged duration of condition Malnutrition
Kwashiorkor- Kwashiorkor was first described by Dr.Cicely Williams in 1933 , but the particular term “kwashiorkor” was introduced in 1935, according to local name for the disease in Ghana. The term was said to mean “red boy” due to characteristics pigmentary changes.
Essential features of Kwashiorkor-  Marked growth retardation with low weight and low height gain.  Muscle wasting with retention of some subcutaneous fat  Psychomotor changes characterized by mental apathy with listless , inertness , lack of interest about the surrounding , Lethargy , Dullness  loss of appetite.
Pitting edema ,especially over the pretibial region , due to hypoalbunenia, and increased capillary permeability with damage cell membrane. To determine the extent of the pitting edema, your doctor will push on your skin, measure the depth of the indention, and record how long it takes for your skin to rebound back to its original position. They will then grade it on a scale from 1-4.
Non –Essential features of Kwashiorkor-  Skin changes- It is found initially with erythema and hyperpigmented skin patches but later found as desquamated and hypopigmented patch with the appearance like old paint flaking off the surface of the wood (flaky –paint dermatosis).
Hair changes-hair • Light colored hair or reddish brown color hair which becomes thin , dry, coarse, silky with easy pluckability. •The affected child may have alopecia with alternate band of light and dark color hair as ‘flag sign’ which indicates period of inadequate , adequate and inadequate nutrition over a prolonged period.
Conti-  Superadded Infections- These children usually suffer from repeated infections of GI tract with diarrhea ,vomiting, anorexia, and dehydration. Respiratory infections (ARI, tuberculosis) , skin infection, & septicemia , are common & difficult to manage in these patients.
Marasmus- Essential features of nutritional marasmus-  Marked growth retardation with less than 60% of expected weight for age & subnormal height/ length.  Gross wasting of muscle & subcutaneous tissue.  Marked stunting & absence of edema.
Non Essential features of nutritional marasmus-  Hair changes usually not present or may be hypopigmented.  Skin looks dry , scaly with prominent loose folds and having reduced mid-upperarm circumference.  Superadded infection are common .Skin infections and diarrhea with vomiting & abdominal distention usually occur.
Conti-  Liver usually shrunk and the child is having craving for food & hunger.  Psychomotor changes usually present with irritability , apathy & miserable appearance  Features of mineral deficiencies (anemia) & vitamin deficiencies are usually found.
Preventive Management  Health Promotion-  Improvement of health of pre-pregnant state , pregnant mother and lactating women towards healthy mother for healthy child.  Promotion of exclusive breastfeeding upto 4-6 months of age to prepare firm base of child health and promotes nutritional status.  Appropriate weaning practices and nutritional supplementations.  Improvement of family dietary habit with locally available , low cast food items for balanced diets.
Conti-  Nutrition education and nutrition counseling to promote correct feeding practices , food habits ,food hygiene , safe water , environmental sanitation and to eliminate misconceptions regarding food & feedings.  Improvement of home economics , earnings income generating activities , adequate dietary budget & diet planning for family members.  Birth spacing & regulating family size
Conti-  Promotion of educational status especially women literacy to improve the family health  Provision of nutritional supplementations from ICDS centers & schools  Maintenance of healthy family environment , congenital for physical , social and psychological development of children.
Specific Protection-  Provision of balance diet with adequate proteins & energy for all children according to the age.  Immunization against vaccine preventable diseases  Promotion & maintenance of hygienic measures  Food fortification to enrich the food items.
Early Diagnosis & Treatment  Periodic health check –up of all children for health supervision & maintenance of growth chart.  Detection of growth lag or growth failure as early as possible  Early diagnosis and management of infections , worm infections & common childhood illnesses.
 Promotion of early rehydration therapy in the child having diarrhea, without restriction of feeding.  Implementation of supplementary feeding programs & services.
Rehabilitation- Nutritional rehabilitation services Hospital management of advanced PEM cases Follow up care
Nursing Responsibilities-  Assessment of nutritional status of the children with collection of appropriate dietary history ,history of breastfeeding, weaning, food habits, balanced diet , socioeconomic status, presence of illness etc. physical examination and anthropometric assessment also important to detect the nutritional deficiency states.
Conti-  Implementing nutritional rehabilitation activities  Encouraging the parents for home care & follow up at regular interval.  Nutrition education , demonstration & counseling according to identified problems of particular child informing about breast feeding, weaning , balanced diet , food hygiene , personal hygiene, appropriate feeding practices and food habits, cultural taboos , irrational beliefs , quality of common foods , food values , food preservations.etc.  Promoting preventive measures for individuals , family & community to overcome the problem of PEM
Conti-  Assisting in diagnostic investigations whenever necessary  Maintenance of growth chart by regular health check-up at home , clinic or health centre for early detection of growth failure  Participating in the hospital management in complications & life threatening situations related to PEM & other related illnesses.
NURSING ASSESSMENT  Imbalance nutrition less than body rquirement related to unhealthy dietary practices  Altered growth and development related to deficit of protein  Risk for infection related to lowered resistence to disease  Activity intolerance related to weakness  Fear and anxiety related to hospitalization
BIBLIOGRAPHY:-  Assuma Beevi. T.M, Textbook of pediatric nursing,,1ST edition, published by Elseiver pvt, ltd. Noida,  2) Parul dutta, pediatric nursing,3RD edition, jaypee publication, page no.288-315.  3) Marlow R.D. “Textbook of pediatric Nursing” 6TH edition ,W.B. Saunders company,  4) Wong L.D. Hockenberry J.M. “Nursing care of infants & children” 7TH edition.,Philadelphia,  5)Piyush gupta , “Essential Pediatrics Nursing”, 3rd edition, CBS Publcation & distributers pvt.ltd.  6)Swarna Rekha Bhat, Achars, Textbook of pediatrics , 4th edition, published by universities press ( india) pvt. Ltd.  7)Rimple Sharma, Essentials of pediatric Nursing, 1st edition, jaypee publication , page no- 456-458.  8) WWW.GOOLE search
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Gastrointestinal disorders

  • 1.
    BY, MR. ABHIJIT P.BHOYAR M SC NURSING CHILD HEALTH SEMINAR ON
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    Gastrointestinal Disorder  Gastrointestinalproblems are very common in childhood .  Number of medical & surgical problems are found among children.  GI disturbances are influenced by problems of liver & pancreas. Digestion , absorption and metabolism are the combined actions of gastrointestinal and hepato- pancreative system. INTRODUCTION
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    List Of DiseaseCondition:- Diarrhea Gastroesophagial reflux Hepatitis Childhood cirrhosis Liver transplantation Malabsorption syndrome Malnutrition
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    Overall Digestive SystemFunction  - Breaks up food physically and chemically.  - Stores food for a short period of time.  - Absorbs the digested foods and passes them into the circulatory system.  - Stores and eliminates undigested food from the body.
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    DIARRHEA DEFINATION:- Diarrhea is definedas the passage of loose , liquid or watery stool ,more than three times per day
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     Acute diarrheais an attack of loose motion with sudden onset which usually lasts 3-7 days but may last upto 10-14 days. It is associated with gastric mucosa & small intestines.  Chronic diarrhea is termed when the loose motion is occurring for 3 weeks or more .It is usually related to underlying organic diseases with or without mal-absorptions types
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    AGENT FACTORS- The infectiousagent causing diarrheas with enteric infection include the following:  VIRUSES: rotavirus, adenovirus, enterovirus, measles virus etc.  BACTERIA: E.coli, shigella, salmonella, vibrio etc.  PARASITES: E.histolytica, malaria.  FUNGI: candida albicans  . Etiology of diarrhea
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    ENVIRONMENTAL FACTORS -Bacterial diarrhea is a more frequently occur in summer and rainy season, whereas viral diarrhea (especially rotavirus) found in winter. Diarrheal diseases are commonly seen in unhygienic environment. MODE OF TRANSMISSION- is mainly feco-oral route. it is water-born disease or may transmit via fingers, fomites , flies or dirt. Conti..
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    SECRETORY DIARRHEA- Ithas tendency to be watery, voluminous and persistent, even if no oral feeding is allowed. This is decrease absorption and increased secretion. OSMOTIC DIARRHEA- It is due to ingestion of poorly absorbed solute or maldigestion or a small bowel defect. It tends to be watery and acidic with reducing substances. MOTILITY DIARRHEA- It is associated with the increased or delayed motility of the bowel. There is decreased transmit time of bacteria leading to overgrowth Other types of DIARRHEA
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    PATHOPHYSIOLOGY Bacterial toxins stimulatingactive transport of electrolytes into the small intestine: cells in the mucosal lining of the intestine are irritated and secrete increased amounts of water and electrolytes. Organisms invading and destroying intestinal mucosal cells, decreasing intestinal surface areas, and impairing the intestine’s capacity to absorb fluids and electrolytes Inflammation, which decreases the intestine’s ability to absorb fluid, electrolyte and nutrients. Increased intestinal motility, resulting in impaired intestinal absorption.
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    CLINICAL MANIFESTATION Symptoms varywith severity, specific cause, and type of onset (insidious versus acute). 1) Low-grade fever to 100° F (37.8° C) 2) Anorexia 3) Vomiting (can precede diarrhea by several days); mild and intermittent to severe 4) Stools appearance of diarrhea from a few hours to 3 days  Loose and fluid consistency  Greenish or yellow-green  May contain mucus, pus, or blood  Frequency varies from 2 to 20 per day  Expelled with force; may be preceded by pain
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    Conti… 5) Behavioral changes Irritability and restlessness  Weakness  Extreme prostration  Stupor and convulsions  Flaccidity 6) Physical changes  Little to extreme loss of subcutaneous fat  Up to 50% total body weight loss  Poor skin turgor; capillary refill longer than 2 seconds  Dry mucous membranes and dry, cracked lips Normal capillary refill time is usually less than 2 seconds.
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    Contii…  Pallor  Sunkenfontanelles and eyes  Petechiae seen with bacterial infections  Excoriated buttocks and perineum.  Urine with blood 7) Vital sign and urine output changes (signal imminent cardiovascular collapse)  Low BP  High pulse  Respirations rapid and hyperapneic  Decreased or absent urine output
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    ASSESSMENT OF DEHYDRATION Diarrhea Less than 4 liquid stools per day 4 to 10 liquid stools per day More than 10 liquids stools per day  Vomiting None or small amount Some Very frequent  Thirst Normal Greater than normal Unable to drink  Urine Normal A small amount and dark No urine for 6 hours 2. LOOK AT  Condition Well, alert Restless, irritable or sleepy, unwell Lethargic or unconscious, floppy  Eyes Normal Sunken Very sunken and dry  Tears Present Absent Absent  Mouth and tongue Moist Dry Very dry  Breathing Normal Faster than normal Very fast and deep 3. FEEL  Skin pinch Goes back quickly Goes back slowly Goes back very slowly  Pulse normal Faster than normal Very fast, weak or cannot feel 4. DECIDE DEGREE OF DEHYDRATION The patient has NO SIGNS OF DEHYDRATION If the patient has two or more signs including at least one sign there is SOME DEHYDRATION If the patient has two or more signs including at least one sign there is SEVERE DEHYDRATION
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    DIAGNOSTIC EVALUATION - STOOL:Cultures (for bacteria, ova, parasites, rotavirus), ph, red blood cells, leukocytes, glucose, blood . - BREATH HYDROGEN TEST: Check for carbohydrate malabsorption. - BLOOD TEST: Especially blood cells counts, electrolytes, blood urea nitrogen, glucose, and blood cultures. - X-RAYS: Check for possible bowel abnormalities.
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    MANAGEMENT  Treatment isbased on the degree of dehydration; mild (less than 5%), moderate (5% to 10%), and severe (greater than 10% weight loss)  Goal is to prevent spread of disease; communicable disease is suspected until proved otherwise; enteric precautions are followed.  Bowel rest may be required based on degree of diarrhea and vomiting, if blood present, or electrolyte abnormalities.
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    Conti…  For mildto moderate dehydration (5%), oral rehydration solution is given to maintain fluid and electrolyte balance (WHO solution, Pedialyte, Infalyte) and BRATS (Bananas, Rice cereal, Apple & sauce, dry Toast, and Saltine crackers) diet is followed to provide rest for the inflamed intestines.  For oral rehydration, 100 mL/kg over 4 hours, with additional fluids after each liquid bowel movement.  Candidates for oral rehydration include mild to moderate (greater than 10%) dehydration, older than age 4 months, no persistent vomiting, and probable gastroenteritis.
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     For moderateto severe dehydration (10% or greater): I.V. fluid and electrolyte replacement is given slowly as ordered (usually 20 mL/kg); usually over 2 days to prevent hypotonic hypervolemia (water intoxication).  Supportive care is given: monitoring oral and I.V. fluid intake, output from all sources, and patient's response to treatment.
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    Conti.. Specific antimicrobial therapymay be given in some cases such as immunosuppression, bacteremia, documented C. difficile.  Metronidazole 20 mg/kg/day in divided doses orally or I.V. may be used.  Vancomycin I.V. for resistant C. difficile
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    Conti… REHYDRATION THERAPY- INGREDIENTS OFORAL REHYDRATION SALTS: COMPONENT CONTENT PER LITER WATER Sodium chloride 3.5gm Potassium chloride 1.5 gm Sodium citrate 2.9gm Glucose anhydrous 20.0gm
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    ASSESSMENT FOR DEHYDRATIONIN CHILDREN CLINICAL SIGNS DEGREE OF DEHYDRATION MILD MODERATE SEVERE General Infant's behavior Thirsty, alert, restless Restless or lethargic; irritable to touch Limp, drowsy; cyanotic extremities Child's behavior Thirsty, alert, restless Thirsty, alert; postural hypotension Usually conscious; cyanotic extremities Respirations Slightly increased Increased Deep and rapid
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    CONTI.. CLINICAL SIGNS DEGREE OF DEHYDRATION MILDMODERATE SEVERE Pulse Slightly increased Increased Rapid Blood pressure Normal Decreased May be unrecordable Capillary refill <2 seconds 2 TO 3 seconds >3 seconds
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    CLINICAL SIGNS DEGREE OF DEHYDRATION MILDMODERATE SEVERE Skin turgor Normal Slightly reduced Reduced Skin color Pale Gray Mottled Weight loss Up to 5% Up to 10% Up to 15%
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    CONTI… CLINICAL SIGNS DEGREE OF DEHYDRATION MILDMODERATE SEVERE Mucous membrane Tacky Tacky/dry Parched Specific gravity <1.020 >1.030 >1.035 Anterior fontanelle Flat Slightly depressed Sunken Urine volume Small Oliguria Oliguria/anuria
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    Complications Severe dehydration andacid-base derangements with acidosis Shock
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    NURSING MANAGEMENT  Fluidvolume deficit related to diarrhea.  Risk for cross infection related to infective loose motions.  Potential to altered skin integrity related to frequent passage of stools.  Altered nutritional status, less than body requirement related to malabsorption and poor oral intake.  Fear and anxiety related to illness and hospital procedures.  Knowledge deficit related to causes of diarrhea and its prevention.
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    Nursing Interventions GOAL- RestoringFluid Balance  Monitor amount and rate of I.V. fluid therapy, which have been calculated by the health care provider. Fluid needs are based on fluid deficit, ongoing losses, and body weight.  Prevent overload of circulatory system.  Check flow rate and amount absorbed hourly and totally
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    CONTI..  Adhere toprescribed volume carefully when oral feedings are given in conjunction with I.V. fluid.  Never administer I.V. fluids to pediatric patient without safeguard of a volume-control infusion device or pump.  Observe for signs of fluid overload: edema, increased BP, bounding pulse, labored respirations, and crackles in lung fields.
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    CONTII..  Check I.V.site for infiltration or improper flow so site can be changed as necessary.  Use appropriate protective devices to prevent the child from injuring involved extremity or causing I.V. to malfunction.  Weigh the patient daily as a guide for fluid needs and patient status.  Monitor urine output and keep accurate intake and output record, including vomitus and liquid stools.
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    Preventing Spread ofInfection  Ensure adherence to good hand-washing and gown technique protocols for all people having contact with infant or child.  Follow your facility's policy on care of diapers.  Handle specimens collected using universal precautions, and transport to laboratories in appropriate containers per policy.  Collect stool sample for culture before instituting antibiotic therapy.  Teach good hygiene measures to older children
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    •The important preventivemeasures are improvement of food hygiene, personal hygiene and environmental hygiene. These include safe water , adequate sewage disposal, hand washing practices, clean utensil, avoidance of exposure of food to dust and dirt, fly control, washing of fruits and vegetables •Avoidance of bottle feeding is most significant practice needed for prevention of diarrhea. •Boiling or filtering to be practiced for safe drinking water. Prevention of LBW and prematurity, exclusive breastfeeding, appropriate weaning practices, balanced diet, immunization are significant aspects of child care which prevents malnutrition and diarrheal episodes PREVENTIVE MEASURES-
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    PROGNOSIS-  Mortality ishigher in neonates and infants than the older children  Malnourished children are having poor prognosis and greater mortality.  Antibiotic resistant type E. coli and Shigella cause very severe illness and poor prognosis.  Presence of severe dehydration, electrolyte imbalance  Early diagnosis with prompt and appropriate management helps in good prognosis.
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    RESEARCH- Case-control study ofrisk of dehydrating diarrhoea in infants in vulnerable period after full weaning  BMJ 1996; 313 doi: http://dx.doi.org/10.1136/bmj.313.7054.391 (Published 17 August 1996)  Cite this as: BMJ 1996;313:391  Objectives: To investigate risk factors for dehydrating diarrhoea in infants, with special interest in the weaning period.
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     Results: Ininfants aged <12 months the risk of dehydrating diarrhoea was significantly higher in the first 9 months of life (P<0.001), and in those aged 12-23 months the risk was again greater in younger children (12-17 months) (P = 0.03). The type of milk consumed before start of diarrhoea episode was strongly associated with dehydration independent of socioeconomic, environmental, maternal reproductive, demographic, and health services factors. Compared with infants exclusively breast fed, bottle fed infants were at higher risk (odds ratio (95% confidence interval) for cow's milk 6.0 (1.8 to 19.8), for formula milk 6.9 (1.4 to 33.3)). Compared with those still breast feeding, children who stopped in the previous two months were more likely to develop dehydrating diarrhoea (odds ratio 8.4 (2.4 to 29.6)). This risk decreased with time since breast feeding stopped.
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    Conclusion: These resultsconfirm the protective effect of breast feeding and suggest there is a vulnerable period soon after breast feeding is stopped, which may be of relevance for developing preventive strategies.
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    Introduction:- Gastroesophageal Reflux Disease (GERD)is a digestive disorder that occurs when acidic stomach juices, or food and fluids back up from the stomach into the esophagus. GERD affects people of all ages—from infants to older adults.
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     Delayed neuromusculardevelopment  Physiological immaturity  Cerebral defects  Increased abdominal pressure  Obesity  Coughing &wheezing in case of cystic fibrosis  Bronchopulmonary dysplasia  Asthma  Indwelling orogastric or nasogastric tube Causes-
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     Primary barrierto gastro esophageal reflux is the lower esophageal sphincter  LES normally works in conjunction with the diaphragm  If barrier disrupted, acid goes from stomach to esophagus PATHOPHYSIOLOGY.
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    Symptoms  In Infants- The feature are unexplained vomiting immediate after feeding Regurgitation Refusal to eat & features of dehydration Irritability Excessive crying Sleep disturbances Arching and stiffening Respiratory symptoms like cough, strider, and pneumonia may found. Loss of weight or failure to gain weight
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    cont.  In OlderChildren-  Non cardiac chest discomfort  Upper abdominal discomfort  Chronic cough  StridOr  Nocturnal asthma  Dysphasia  Anemia
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    Other symptoms Difficulty orpain when swallowing Sudden excess of saliva Chronic sore throat Laryngitis or hoarseness Inflammation of the gums Cavities  Bad breath Chest pain
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    Diagnosis  X-ray ofthe upper digestive system  Endoscopy (examines the inside of the esophagus)  Ambulatory acid (pH) test (monitors the amount of acid in the esophagus)  Esophageal impedance test (measures the movement of substances in the esophagus)
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    Treatment & Management Medical Management:-  1.Positioning-  It helps to reduce the amount of reflux.  Infants younger than 6 months should be placed on right lateral position during sleep, head of the crib should be raised at least 6 inches. The infant may also be held upright.  Older children should be placed in head raised to 30-45 degree angle position. Avoid recumbent position after meal for at least 3 hours .Upright of semi upright position during awaking is helpful.
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    Conti-  2. Feeding- Special precautions to be taken during feeding of infants and older children.  Infants to be given thickened feed in small amount frequently followed by appropriate positioning, to prevent the reflux.  Older children should be allowed nothing per mouth 2hours before bed time. Low fat diet , spicy and acidic foods (onion, citrus products , apple juice , tomato) , esophageal irritants ( chocolate , peppermint , passive smoke) and carbonated beverages should be avoided .Chewing gum can be allowed to stimulate parotid secretions which increases esophageal clearance.
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    Conti- 3. Medications-  AntacidsH2 –receptor antagonists (cimetidine) , prokinetic drugs (metaclopromide) and proton pump inhibitors(omeprazole) can be given alone or in combination
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    Surgical Management-  Fudoplication(Nissen’s operation) is most popular method. A gastric wrap procedure is done. Wrapping of the fundus around the lower oesophageal sphincter (a 360 degree wrap) completely prevent reflux episodes. Fundoplication is a surgical procedure that helps treat some gastroesophageal conditions. During a fundoplication for gastroesophageal reflux disease (GERD), for example, a surgeon will attach part of the stomach to the lower esophageal sphincter, which helps reduce acid reflux
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     Antroplasty or pyloroplastymay be performed in some cases. Gastrotomy may be needed for feeding purposes or temporarily to decompress the stomach. Pyloroplasty is surgery to widen the opening in the lower part of the stomach (pylorus) so that stomach contents can empty into the small intestine (duodenum). The pylorus is a thick, muscular area. When it thickens, food cannot pass through
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    Nursing Management : Preventing aspiration by positioning and appropriate feeding technique.  Maintaining fluid & electrolyte balance by I/V fluid therapy , (whenever needed) ,intake and output recording and estimation of electrolyte level.  Providing adequate nutritional intake  Continuous monitoring of vital signs , Assessment of features of complication and necessary investigations.
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    Conti-  Reducing fearof eating and modifying feeding schedule  Providing preoperative and postoperative care as for abdominal surgery of children.  Providing emotional support  Giving health education regarding , positioning , feeding, home based care and follow up.
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    Complication-  Aspiration pneumonia Chronic esophagitis  Failure to thrive  Anemia  Asthma  Sudden infant death syndrome  ESophageal stricture An esophageal stricture is an abnormal tightening or narrowing of the esophagus.
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    Function Of Liver- Bile production that is essential to digestion  Filtering of toxins from the body  Excretion of bilirubin, cholesterol, hormones, and drugs  Metabolism of carbohydrates, fats, and proteins  Activation of enzymes (specialized proteins essential to metabolic functions)  Storage of glycogen, vitamins (a, d and k), and minerals  Synthesis of plasma proteins, such as albumin  Synthesis of clotting factors HEPATITIS means inflammation of liver
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    Causes of Hepatitis ACUTE:  Viral hepatitis  Non-viral infection  Alcohol  Toxins  Drugs  Ischemic hepatits  Autoimmune  Metabolic diseases  CHRONIC:  Viral hepatitis  Alcohol  Drugs  Non-alcoholic steatohepatitis  Autoimmune  Heredity
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    Pathophysiology Targets of theHep viruses are hepatocytes: Hepatocyte uptake involves a receptor on the plasma membrane of the cell After entry into the cell, viral RNA is uncoated, and host ribosomes bind to form polysomes. Viral proteins are synthesized, and the viral genome is copied by a viral RNA polymerase Minimal cellular morphologic changes result from hepatocyte infection Lymphocytic infiltrate; varying degree of necrosis.
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    Diagnosis Of Hepatitis Physical Exam  Liver Biopsy  Liver Function Tests  Ultrasound  Blood Tests  Viral Antibody Testing
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    Diagnosis: HAV  SerumSerology: presence of serum antigens and immunoglobins  HAV: IgM anti-HAV: positive at the time of onset of symptoms; results remain positive for 3-6 months after the primary infection  Anti-HAV IgG appears soon after IgM and generally persists for many years.  Treatment: supportive
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    Hepatitis B  Epidemiology HBV is a DNA virus that belongs to the hepatovirus family.  2 billion people worldwide have past or present infections  400 million people are chronic HBV carriers.  Eight genotypes of HBV identified and re-labeled A through H.  HBV is the cause of 60% to 80% of worldwide Hepatocellular Carcinoma(HCC).  500,000 to 1 million deaths worldwide are attributed to it.  5% to 10% of all liver transplants are attributed to HBV.
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    AT Risk Groups IV drug users  People receiving multiple blood transfusions  Sexual promiscuity  People in contact with HBV carriers  Travelers to endemic areas of South America, Southern Asia, and Africa  Resident and employees of residential care facilities Promiscuity is the practice of engaging in sexual activity frequently with different partners or being indiscriminate in the choice of sexual partners. The term can carry a moral judgment if the social ideal for sexual activity is monogamous relationships.
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    Transmission 3 mainways: Parenterally/percutaneous route----IV Drug Users, needle sticks, Hemodialysis patients Sexually Vertical/ Perinatal route
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    Clinical Manifestation- Acute HepatitisB – Less than 6 months; based on significant aminotransferase activity due to necro inflammatory injury  Symptoms are often non-specific symptoms such as myalgia, malaise , nausea, fatigue , pruritus, abdominal pain, jaundice  Fulminant hepatitis--acute HBV results in liver failure
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    Chronic Hepatitis B– Greater than 6 months; based on grade, stage, and etiology. Fibrosis and necroinflammatory processes; can last for decades  Immune tolerant--high viral replication, low inflammation and fibrosis. Seen in children or those affected early in life.  Immune active--high liver enzymes and high hbv dna and hbeag, active replication  Carrier state with low replication  Seroconversion from hbeag to hbeab  Low HBV levels, reduced liver inflammation
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    •Diagnosis-  Serology-  LiverChemistry tests  Histology--Immunoperoxidase staining  HBV Viral DNA--Most accurate marker of viral DNA and detected by PCR  Liver Biopsy--to determine grade(Inflammation) and stage(Fibrosis) in chronic Hepatitis
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    Progress-  Incubation Period:30-180 days Acute HBV Infection: 90% resolve by themselves; less than 1% develop fulminant hepatitic failure  Chronic HBV Infection: 2-10% progress to chronic state  90% in children less than five progress to chronic state  Risk of Liver Cirrhosis: 5 year accumulation risk of 8% to 20%
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    Treatment- 1) Interferon therapy– First Line Method of action is the inhibition of viral replication of cells thus assisting the immune system Side effects: "Flulike Symptoms", alopecia, rash, diarrhea
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    2) Nucleoside Analogues-- Lamivudine, Entecavir, Telbivudine Method of action is the inhibition of viral reverse transcriptase  Lamivudine  Dose : 100 mg PO q daily  Problem: High rates of resistant mutations  Side effect: lactic acidosis  Entecavir – 1st line  0.5 to 1mg PO  very effective;  more effective than lamivudine  Side effect: lactic acidosis  Telbivudine  Dose: 600mg daily  Side effect: lactic acidosis
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    3) Nucleotide analogues Methodof action is the inhibition of viral reverse transcriptase  Tenovir  Dose: 300mg od  Highly effective with low resistance  Well tolerated  Adefovir – 1st line  Dose: 10mg daily  Resistance less than Tenovir  Side effect: nephrotoxicity
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    Hepatitis C  Spherical,enveloped, single-stranded RNA virus Incubation period: 7-8 wks  170 million infected worldwide  Parenteral Transmission: IV drug users  Most common indication for liver transplantation
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    Diagnosis: HCV  HCV:Anti-HCV; cannot distinguish acute from chronic infection  EIA: antibodies against core protein and nonstructural proteins; may appear 3 – 5 months after infection 80% of cases: patients are asymptomatic and do not develop icterus. Treatment: Interferon alpha, Ribavirin; (better sustained absorption, a slower rate of clearance, )
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    Hepatitis D This isalso called “delta hepatitis.” Hepatitis D is a serious liver disease caused by the Hepatitis D virus (HDV), which is contracted through puncture wounds or contact with infected blood. This is a rare form of hepatitis that occurs in conjunction with hepatitis B infection.
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    Hepatitis E  HepatitisE virus (HEV) RNA virus of the genus Hepevirus  Enterically transmitted infection; fecal-oral route, typically self-limited  Most outbreaks occur in developing countries.  Symptoms of acute hepatitis  Incubation period of hepatitis E virus is 2-9 weeks  Case fatality rate is 4%
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    Diagnosis- Serum, liver, andstool samples can be tested for HEV RNA Anti-HEV antibodies: - IgM (acute) - IgG (chronic) Treatment: supportive
  • 75.
    Hepatitis F  Itis well documented that even after a detailed serological study, 10 percent of children will not have marked to the known viruses A to E.  These could be HBV variants with mutation, or a budding RNA virus French workers have identified an enteric virus in this non A-E group and call it the hepatitis French virus(HFV).
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    HEPATITIS G Hepatitis G(HGV) virus is a single stranded RNA flavi virus which shares limited identity with HCV. It is distributed widely among the population and spreads by parenteral route.
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    Preventive Management OfHepatitis Hygiene Practicing good hygiene is the main way to avoid catching hepatitis.  If you are travelling to a country with low sanitary standards, avoid: Drinking local water Ice Sea food Raw fruit and vegetables
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    Conti-  Hepatitis controlledthrough contaminated blood can be prevented by:  Not sharing drug needles  Not sharing razors  Not using someone else’s toothbrush  Not touching spilled blood
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    Nursing Management:-  ImbalancedNutrition Less Than Body Requirements  Acute pain related to swelling of the liver is inflamed liver and portal vein dam.  3. Hyperthermia related to invasion agents in the blood circulation secondary to liver inflammation.  4. Fatigue related to chronic inflammatory process secondary to hepatitis.  5. Risk for impaired tissue integrity related to pruritus secondary to accumulation of bilirubin pigments in bile salts.
  • 81.
    Complications of Hepatitis Chronicliver disease Cirrhosis (scarring of the liver) Cancer of the liver (in rare cases)
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    HAV HBV HCVHDV HEV HGV[*] Virology RNA DNA RNA RNA RNA RNA Incubation (days) 15–19 60–180 14–160 21–42 21–63 ? Transmission Parenteral Rare Yes Yes Yes No Yes Fecal-oral Yes No No No Yes Possible Sexual No Yes Yes Yes No Yes Perinatal No Yes Rare Yes No Yes Chronic infection No Yes Yes Yes No Yes Fulminant disease Rare Yes Rare Yes Yes No
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    Childhood Cirrhosis  Indianchildhood cirrhosis is a disease peculiar to the Indian infants and children, usually occurs between 6 months & 4 years of age. It may also found in Indian subcontinent and west Indies
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    Etiology-  Hepatotoxic agents-Hepatotoxic harmful agents like guttis or aspergillus flavus that grow on ground nuts, maize and rice may cause ICC .  Metabolic Defects- They may cause ICC specially disturbed lactose ,zinc, copper and magnesium metabolism.  Immunologic Disturbances- These are found in high levels of circulating immune complexes which can cause immune mediated injury of the liver.
  • 86.
    Conti-  Genetic factors-Familiar occurrence of ICC points the possibility of underlying genetic factor along with environmental factors.  Nutritional Factors- previously it was believed that malnutrition was an important cause of cirrhosis.  Viral Infection- ICC has been thought to be a consequence of neonatal hepatitis or infective hepatitis.
  • 87.
    Pathophysiology- Due to thedisease process. The basic pathologic change is the diffuse liver damage by way of degeneration going on to necrosis and replacement fibrosis . The capsule shows patchy thickening and the surface is finely nodular . THE microscopic study shows marked hepatocyte damage as degenerative changes in the cytoplasm. Kupffers cell shows mild degree of proliferation. Gross pericellular fibrosis in the hepatic lobules are found.
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    Clinical Manifestation-  Onsetis acute  Irritability  Disturbed appetite  Chalky & pasty stools with constipation or diarrhe  Mild fever  Progressive growth failure usually present in spite of adequate diet.
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    Conti-  Within fewmonths to a years, there is hepatomegaly , jaundice and features of portal hypertension including splenomegaly , ascities, hematemasis , anemia, prominent superficial abdominal veins and thrombocytopenia  There may be high incidence of intravascular hemolysis.  Liver is usually gross enlarged with proturbent abdomen  The child generally have hepatic failure and intercurrent infections which may be fatal  Duration of illness may be 6 month to 3 years
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    Diagnosis- Liver Biopsy Cupriuresis test–it may be performed by oral administration of D- penicillamine, using urinary copper / creatinine ratio as the index parameters, sensitivity and specificity with positive and negative values are obtained.
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    Management-  Medical Management:- Few cases of ICC improve spontaneously and survive without specific treatment.  Penicilline therapy is used as copper- chelating agent from the liver, which improves the survivals.  Immunomodulating agents like levamisole , corticosteroids, gammaglobulins may also be used.  Symptomatic treatment should be done especially for infections and vitamins and minerals deficiency
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    Conti-  Supportive careshould be provided as rest , diet with good quality proteins , I/V glucose drip , oxygen therapy, antibiotic s therapy and good nursing care  Nursing intervention – improving nutritional status, promoting of activity tolerance , protecting skin integrity , preventing injury & bleeding.  Exchange transfusion may be effective to remove circulating toxins  In case of portal hypertension causing hematemesis, sengastaken tube may be of help to control esophageal bleeding
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    Nursing Mangement- Nursing interventionshould provide special attention on improving nutritional status  promoting of activity tolerance protecting skin integrity preventing injury and bleeding and expert care for unconscious patients if needed.
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    Preventive Management- Continue breastfeedingupto six months and avoiding boiling of milk in copper or copper alloy pots Increasing public awareness about the preventive measures is important regarding lowering of copper intake through copper- rich food , water and utensils.
  • 96.
  • 97.
    Indications for PediatricLiver Transplantation INDICATIONS PER CENT OF TRANSPLANTS (%) Biliary atresia 39 Metabolic liver disease 13 α1-Antitrypsin deficiency 5 Tyrosinemia 1 Wilson disease 1 Other 6 Acute hepatic necrosis 12 Biliary hypoplasia including Alagille syndrome 5 TPN-associated liver disease 5 Idiopathic cirrhosis 4 Autoimmune hepatitis 3 Tumors including hepatoblastoma 3 Neonatal hepatitis 2 Cystic fibrosis 2 Primary sclerosing cholangitis 2 Congenital hepatic fibrosis 1 Other 9
  • 98.
    Benefits  Transplant canbe done on an elective basis because the donor is readily available  There are fewer possibilities for complications and death while waiting for a cadaveric organ donor .
  • 99.
    Screening for donors Alldonors are assessed medically to ensure that they can undergo the surgery Confidentiality The transplant team provides both the donor and family thorough counseling and support which continues until full recovery is made.
  • 100.
    Malabsorption is astate arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. MALABSORPTION SYNDROME
  • 101.
    Classification Selective, as seenin lactose malabsorption. Partial, as observed in a-beta-lipoproteinaemia.  Total as in coeliac disease.
  • 102.
    Pathophysiology  The mainpurpose of the gastrointestinal tract is to digest and absorb nutrients, micronutrients , water, and electrolytes.  Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.
  • 103.
    Causes • HIV relatedmalabsorption • Intestinal tuberculosis Due to infective agents • Blind loops • Inflammatory bowel diseases, as in Crohn's Disease • Fistulae, diverticulae and strictures Due to structural defects • Coeliac disease • Cows' milk intolerance • Soya milk intolerance • Fructose malabsorption Due to mucosal abnormality • Lactase deficiency inducing lactose intolerance • Sucrose intolerance • Intestinal disaccharidase deficiency  Due to enzyme deficiencie •Cystic fibrosis •Chronic pancreatitis •Carcinoma of pancreas  Pancreatic insufficiencies
  • 104.
    Clinical features-  Diarrhoea,often steatorrhoea, is the most common feature.  Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption.  Weight loss can be significant despite increased oral intake of nutrients.  Growth retardation, failure to thrive, delayed puberty in children
  • 105.
    Conti-  Swelling oroedema from loss of protein  Anaemias, commonly from vitamin B12, folic acid and iron deficiency presenting as fatigue and weakness.  Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis  Bleeding tendencies from vitamin K and other coagulation factor deficiencies.
  • 106.
    Diagnosis  Blood tests Stool studies  Radiological studies - Barium enema may be undertaken to see colonic or ileal lesions -CT abdomen is useful in ruling out structural abnormality, -Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP.  Interventional studies -Colonoscopy -Biopsy of small bowel showing coeliac disease
  • 107.
    Other investigations  Glucosehydrogen breath test for bacterial overgrowth  Lactose hydrogen breath test for lactose intolerance  Sugar probes or 51Cr-EDTA to determine intestinal permeability.
  • 108.
    Management Medical Management-  Replacementof nutrients, electrolytes and fluid may be necessary.  In severe deficiency, hospital admission may be required for nutritional support Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy.  Pancreatic enzymes are supplemented orally in pancreatic insufficiency.
  • 109.
    Conti-  Dietary modificationis important in some conditions:  Gluten-free diet in coeliac disease.  Lactose avoidance in lactose intolerance.  Antibiotic therapy to treat Small Bowel Bacterial overgrowth.  Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.
  • 110.
    Nursing Management-  Improvementof nutritional status by appropriate diet planning and supplemention of deficient nutrients or substituting them.  Restoration of fluid and electrolyte balance by oral and parentral therapy.  Continuous monitoring and recording of patient’s condition.  Relief of pain by medications , Fower’s position and comfort. Analgesics ,antiflatulents and antidiarrheal agents are administered as prescribed.
  • 111.
    Conti-  Maintenance ofskin integrity specially of perineal area .  Health education to the parent about general cleanliness , nutrition , hydration, danger signs, home care and follow up for necessary medical help  Relief of fear and anxiety about long –term illness and hospitalization by appropriate explanation , reassurance and necessary support.
  • 112.
  • 113.
    Definitions  MALNUTRITION WHOdefines Malnutrition as "the cellular imbalance between the supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions.  “ Malnutrition is the condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function.
  • 114.
    Causes Of PEM- Inadequate intake of food both in quality and quantity  Infection especially ARI ,diarrhea, measles & worm infestations lead to the condition which increases in requirement for calories, proteins and other nutrients, while decreasing important cause of PEM.
  • 115.
    Classification Of PEM- SyndromalClassification- Kwashiorkor Nutritional Marasmus Prekwashiorkor Nutritional dwarfing
  • 116.
     Classification byIndian Academy Of Pediatrics-  When the child is having weight more than 80% of expected weight for age , considered as normal. The grade of malnutrition is described as follows;  Grade I- between 71-80% of expected weight for the age  Grade II- between 61-70% of expected weight for the age  Grade III- between 51-60% of expected weight for the age  Grade IV- between 50% or less of expected weight for the age
  • 117.
    Pathophysiology- Inadequate dietary intakeprotein/ calories Malabsorption and altered metabolism Nutrient less so appetite loss Weight loss, growth flattering Immunity lowered Incidence of infection, increased Prolonged duration of condition Malnutrition
  • 118.
    Kwashiorkor- Kwashiorkor was firstdescribed by Dr.Cicely Williams in 1933 , but the particular term “kwashiorkor” was introduced in 1935, according to local name for the disease in Ghana. The term was said to mean “red boy” due to characteristics pigmentary changes.
  • 119.
    Essential features ofKwashiorkor-  Marked growth retardation with low weight and low height gain.  Muscle wasting with retention of some subcutaneous fat  Psychomotor changes characterized by mental apathy with listless , inertness , lack of interest about the surrounding , Lethargy , Dullness  loss of appetite.
  • 120.
    Pitting edema ,especially overthe pretibial region , due to hypoalbunenia, and increased capillary permeability with damage cell membrane. To determine the extent of the pitting edema, your doctor will push on your skin, measure the depth of the indention, and record how long it takes for your skin to rebound back to its original position. They will then grade it on a scale from 1-4.
  • 121.
    Non –Essential featuresof Kwashiorkor-  Skin changes- It is found initially with erythema and hyperpigmented skin patches but later found as desquamated and hypopigmented patch with the appearance like old paint flaking off the surface of the wood (flaky –paint dermatosis).
  • 122.
    Hair changes-hair • Lightcolored hair or reddish brown color hair which becomes thin , dry, coarse, silky with easy pluckability. •The affected child may have alopecia with alternate band of light and dark color hair as ‘flag sign’ which indicates period of inadequate , adequate and inadequate nutrition over a prolonged period.
  • 123.
    Conti-  Superadded Infections-These children usually suffer from repeated infections of GI tract with diarrhea ,vomiting, anorexia, and dehydration. Respiratory infections (ARI, tuberculosis) , skin infection, & septicemia , are common & difficult to manage in these patients.
  • 125.
    Marasmus- Essential features ofnutritional marasmus-  Marked growth retardation with less than 60% of expected weight for age & subnormal height/ length.  Gross wasting of muscle & subcutaneous tissue.  Marked stunting & absence of edema.
  • 126.
    Non Essential featuresof nutritional marasmus-  Hair changes usually not present or may be hypopigmented.  Skin looks dry , scaly with prominent loose folds and having reduced mid-upperarm circumference.  Superadded infection are common .Skin infections and diarrhea with vomiting & abdominal distention usually occur.
  • 127.
    Conti-  Liver usuallyshrunk and the child is having craving for food & hunger.  Psychomotor changes usually present with irritability , apathy & miserable appearance  Features of mineral deficiencies (anemia) & vitamin deficiencies are usually found.
  • 129.
    Preventive Management  HealthPromotion-  Improvement of health of pre-pregnant state , pregnant mother and lactating women towards healthy mother for healthy child.  Promotion of exclusive breastfeeding upto 4-6 months of age to prepare firm base of child health and promotes nutritional status.  Appropriate weaning practices and nutritional supplementations.  Improvement of family dietary habit with locally available , low cast food items for balanced diets.
  • 130.
    Conti-  Nutrition educationand nutrition counseling to promote correct feeding practices , food habits ,food hygiene , safe water , environmental sanitation and to eliminate misconceptions regarding food & feedings.  Improvement of home economics , earnings income generating activities , adequate dietary budget & diet planning for family members.  Birth spacing & regulating family size
  • 131.
    Conti-  Promotion ofeducational status especially women literacy to improve the family health  Provision of nutritional supplementations from ICDS centers & schools  Maintenance of healthy family environment , congenital for physical , social and psychological development of children.
  • 132.
    Specific Protection-  Provisionof balance diet with adequate proteins & energy for all children according to the age.  Immunization against vaccine preventable diseases  Promotion & maintenance of hygienic measures  Food fortification to enrich the food items.
  • 133.
    Early Diagnosis &Treatment  Periodic health check –up of all children for health supervision & maintenance of growth chart.  Detection of growth lag or growth failure as early as possible  Early diagnosis and management of infections , worm infections & common childhood illnesses.
  • 134.
     Promotion ofearly rehydration therapy in the child having diarrhea, without restriction of feeding.  Implementation of supplementary feeding programs & services.
  • 135.
    Rehabilitation- Nutritional rehabilitation services Hospitalmanagement of advanced PEM cases Follow up care
  • 136.
    Nursing Responsibilities-  Assessmentof nutritional status of the children with collection of appropriate dietary history ,history of breastfeeding, weaning, food habits, balanced diet , socioeconomic status, presence of illness etc. physical examination and anthropometric assessment also important to detect the nutritional deficiency states.
  • 137.
    Conti-  Implementing nutritionalrehabilitation activities  Encouraging the parents for home care & follow up at regular interval.  Nutrition education , demonstration & counseling according to identified problems of particular child informing about breast feeding, weaning , balanced diet , food hygiene , personal hygiene, appropriate feeding practices and food habits, cultural taboos , irrational beliefs , quality of common foods , food values , food preservations.etc.  Promoting preventive measures for individuals , family & community to overcome the problem of PEM
  • 138.
    Conti-  Assisting indiagnostic investigations whenever necessary  Maintenance of growth chart by regular health check-up at home , clinic or health centre for early detection of growth failure  Participating in the hospital management in complications & life threatening situations related to PEM & other related illnesses.
  • 139.
    NURSING ASSESSMENT  Imbalancenutrition less than body rquirement related to unhealthy dietary practices  Altered growth and development related to deficit of protein  Risk for infection related to lowered resistence to disease  Activity intolerance related to weakness  Fear and anxiety related to hospitalization
  • 140.
    BIBLIOGRAPHY:-  Assuma Beevi.T.M, Textbook of pediatric nursing,,1ST edition, published by Elseiver pvt, ltd. Noida,  2) Parul dutta, pediatric nursing,3RD edition, jaypee publication, page no.288-315.  3) Marlow R.D. “Textbook of pediatric Nursing” 6TH edition ,W.B. Saunders company,  4) Wong L.D. Hockenberry J.M. “Nursing care of infants & children” 7TH edition.,Philadelphia,  5)Piyush gupta , “Essential Pediatrics Nursing”, 3rd edition, CBS Publcation & distributers pvt.ltd.  6)Swarna Rekha Bhat, Achars, Textbook of pediatrics , 4th edition, published by universities press ( india) pvt. Ltd.  7)Rimple Sharma, Essentials of pediatric Nursing, 1st edition, jaypee publication , page no- 456-458.  8) WWW.GOOLE search