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.

1. BY,
MR. ABHIJIT P. BHOYAR
M SC NURSING
CHILD HEALTH
SEMINAR ON

2. 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

3. List Of Disease Condition:-
Diarrhea
Gastroesophagial reflux
Hepatitis
Childhood cirrhosis
Liver transplantation
Malabsorption syndrome
Malnutrition

4. Review
Of
Anatomy
&
Physiolog
y

5. 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.

6. DIARRHEA
DEFINATION:-
Diarrhea is defined as the passage of loose , liquid
or watery stool ,more than three times per day

7.  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

8. 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

9. 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..

10. 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

11. 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.

12. 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

13. 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.

14. 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

15. 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

16. 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.

17. 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.

18. 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.

19.  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.

20. 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

21. 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

22. 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

23. 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

24. 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%

25. 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

26. Complications
Severe dehydration and acid-base
derangements with acidosis
Shock

27. 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.

28. 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

29. 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.

30. 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.

31. 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

32. •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-

33. 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.

34. 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.

35.  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.

36. 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.

37. Gastroesophageal Reflux
Disease (GERD)

38. 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.

39.  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-

40.  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.

41. 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

42. cont.
 In Older Children-
 Non cardiac chest discomfort
 Upper abdominal discomfort
 Chronic cough
 StridOr
 Nocturnal asthma
 Dysphasia
 Anemia

43. 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

44. 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)

45. 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.

46. 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.

47. Conti-
3. Medications-
 Antacids H2 –receptor antagonists (cimetidine) ,
prokinetic drugs (metaclopromide) and proton pump
inhibitors(omeprazole) can be given alone or in
combination

48. 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

49.  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

50. 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.

51. 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.

52. 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.

53. HEAPATITIS

54. 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

55. 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

56. Classification of Hepatitis
Hepatitis
A
Hepatitis
B
Hepatitis
C
Hepatitis
D
Hepatitis
E

57. 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.

58. Diagnosis Of Hepatitis
 Physical Exam
 Liver Biopsy
 Liver Function Tests
 Ultrasound
 Blood Tests
 Viral Antibody Testing

59. 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

60. 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.

61. 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.

62. Transmission 3 main ways:
Parenterally/percutaneous route----IV Drug
Users, needle sticks, Hemodialysis patients
Sexually
Vertical/ Perinatal route

63. 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

64. 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

65. •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

66. 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%

67. 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

68. 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

69. 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

70. 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

71. 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, )

72. 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.

73. 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%

74. Diagnosis-
Serum, liver, and stool samples can be tested for
HEV RNA
Anti-HEV antibodies:
- IgM (acute)
- IgG (chronic)
Treatment: supportive

75. 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).

76. 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.

77. Surgical Management:
Liver Transplantatiion

78. 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

79. 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

80. 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.

81. Complications of Hepatitis
Chronic liver disease
Cirrhosis (scarring of the liver)
Cancer of the liver (in rare cases)

82. 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

83. INDIAN CHILDHOOD
CIRRHOSIS

84. 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

85. 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 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.

88. 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.

89. 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

90. 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.

91. 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

92. 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

93. sengastaken tube

94. 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.

95. 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.

96. Liver Transplantation

97. 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

98. 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
.

99. 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.

100. Malabsorption is a state arising from abnormality in
absorption of food nutrients across the gastrointestinal
(GI) tract.
MALABSORPTION
SYNDROME

101. Classification
Selective, as seen in lactose malabsorption.
Partial, as observed in a-beta-lipoproteinaemia.
 Total as in coeliac disease.

102. 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.

103. 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

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 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.

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
 Glucose hydrogen 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-
 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.

109. 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.

110. 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.

111. 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.

112. MALNUTRITION

113. 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.

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-
Syndromal Classification-
Kwashiorkor
Nutritional Marasmus
Prekwashiorkor
Nutritional dwarfing

116.  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

117. 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

118. 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.

119. 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.

120. 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.

121. 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).

122. 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.

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 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.

126. 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.

127. 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.

129. 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.

130. 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

131. 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.

132. 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.

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 of early rehydration therapy in the child
having diarrhea, without restriction of feeding.
 Implementation of supplementary feeding programs &
services.

135. Rehabilitation-
Nutritional rehabilitation services
Hospital management of advanced PEM cases
Follow up care

136. 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.

137. 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

138. 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.

139. 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

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