Ppt

1. MANAGEMENT OF COMMON CHILDHOOD
DISEASE

2. Learning Objectives
• Identify and use simple clinical signs to classify and treat a child with acute
respiratory infection
• Distinguish the clinical manifestations and manage the gastrointestinal
infections and infestations among under 5 child
• Describe and manage febrile illness (malaria, meningitis, measles) among
under 5 child
• Assess, identify clinical manifestation and treat nutritional deficiencies in
under 5 children.

3. Acute Air Obstruction
• Obstruction of the air way (larynx and trachea) is potentially life
threatening
Cardinal features
• stridor, hoarseness, barking cough
• severity assessed by degree of sternal and sub costal recession, respiratory
and heart rate increase, agitation or drowsiness or central cyanosis

4. Croup
• Defined as an acute clinical syndrome with inspiratory stridor, barking
cough, hoarseness and variable degree of respiratory distress.

5. Acute Laryngo-tracheo-bronchitis
• Viral croup
• Is the commonest > 95%
• Peak incidence is the second year ( 6 month – 5 year)
• Stridor is usually preceded by fever, coryza
• Symptoms tend to worse at night
• Narrowing is mild stridor present when child is hyperventilates or upset
• As the narrowing progress the stridor becomes both inspiratory and
expiratory and present with the child as rest

6. Recurrent or spasmodic croup
• Same children have repeated episodes of croup without preceding fever
and coryza
• Symptoms sudden onset at night often present for only few hrs associated
with atopic disease ( asthma, eczema, hay fever)
• The episode can be severe, but are more commonly self limiting

7. Bacterial tracheitis or pseudomembranous croup
• Is dangerous
• Complication of croup
• Etiology streptococcus pneumoniae, staphylococcus aureus, H-influenza B,
• Results in copious, purulent secretion and mucosal necrosis.
• High fever, marked respiratory obstruction
• Croupy cough and absence of drooling help distinguish this condition
from epiglottitis

8. Emergency treatment of croup
• Do not frighten them more by sticking things in their throat or painful injection.
• Ensure adequate oral fluid intake.
• Humidified oxygen should be given through nasal cannula or face mask.
• Paracetamol
• Steroid 0.6 mg/kg dexametasone once or twice /day
• Severe obstruction should be given nebulised epinephrene (5ml of 1 in 1000)
with oxygen through face mask.

9. Conti
• If needed intubation should be under anesthesia
• Tracheostomy
• If toxic and with measles should receive antibiotic effective against Str.
Pneumonia, H. influenza and staph. Aureus.
• If available, cefuraxime 150mg/kg/day in 4 doses IV or cephalexin
25mg/kg 6 hrly po

10. Acut epiglotitis
• Severe infection caused by H- influenza
• Incidence 2 – 3 years.
• Less common cause of croup
• Cough is not a prominent feature
• Stridor has a soft quality.
• Child tends to drool and assume an upright position

11. Do not Do
• Do not Examine the throat
• Do not Lie the child down
• Do not X-ray of the neck
• Do not Perform massive
procedure
• Do not Use a nasopharynx tube
oxygen
• Use to reassure to calm the child
• Attach pulse oxymeter
• Give worm humidified oxygen if
SaO2< 95%
• Call anesthetist for examination

12. Management
• Effective intubation under general anesthesia
• Dx confirmed by laryngoscope (cherry-red epiglottis)
• Rx chloramphenicol 50 mg/kg immediately then 25mg/kg 6hrly
• Cefotaxim 50mg/kg 6hrly
• Ceftriaxone 50mg/ once daily

13. Contrasting features of croup and epiglottitis
Features croup epiglottis
• Onset over days
• Coryza yes
• Cough severe barking
• Able to drink yes
• Drooling saliva no
• Appearance unwell
• Fever < 38.5c
• Stridor harsh, rasping
• Voice muffled hoarse
• Need for intubation 1%
• Over hours
• No
• Absent or slight
• No
• Yes
• Toxic very ill
• > 38.5c
• soft
• Reluctant to speak
• 80%

14. Providing care for the child with tonsillitis:
• Is an inflammation and formation of edema of the tonsils.
Cause
– Viral (rare), or Bacterial (most common)
– Group A β-hemolytic streptococcus is the most common cause .
• Both the tonsils and adenoid are a major cause of upper airway
obstruction in children.
– Manifested by obstructive sleep apnea, and upper airway resistance
syndrome

15. A= The diffuse tonsillar and pharyngeal erythema seen here is a nonspecific finding
B= This intense erythema, seen in association with acute tonsillar enlargement and
palatal petechiae,
is highly suggestive of group A β-streptococcal though other pathogens also possible
C= This picture of exudative tonsillitis
is most commonly seen with either group A streptococcal or Epstein-Barr virus infection.

16. Signs and Symptoms
– Fever
– Reddened, swollen tonsils, sore throat
– Exudates may be seen on inspection
– Difficulty swallowing
Diagnosis
– Physical examination, History, and throat culture
Management:
– Antibiotics usually Penicillin group.
– Tonsillectomy- In severe and recurrent case
Nursing Management:
– Supportive treatments- includes encourage fluid intake, treat fever and avoid
hot drinks, but soothing

17. Common Cold (Acute Viral Rhinitis or Coryza)
– Is an acute catarrhal/runny nose infection of the upper
respiratory tract.
– It is often includes self-limited involvement of the sinus mucosa
and is more correctly termed rhino-sinusitis.
Etiology
– Rhino viruses (100 serotypes) are the major causes.
– Para influenza viruses, respiratory syncytial viruses (RSV),
influenza and adeno viruses cause common cold in children.

18. Epidemiology and occurrence:
– Worldwide, both endemic and epidemic.
– Each individual can expect one or more colds every year.
– Incidence is highest in < 5 children, gradually declining
with increasing age.
Transmission
- Viruses that cause the common cold are spread by aerosols,
and direct contact.

19. Clinical manifestations
– Nasal discharge: first watery, then mucoid and purulent
– Sneezing
– Some fever may be present
– Headache
– Dry or painful throat
– Nasal obstruction are prominent;
– Systemic symptoms and signs such as myalgia and fever are absent or
mild.

20. Treatment
• Is primarily of symptomatic treatment
• Specific antiviral therapy is not currently available for rhinovirus
infections.
• Pleconaril for rhinovirus being developed, although the role, if any,
remains to be determined???.
• Oseltamivir reduces the frequency of influenza-associated
infection???.

21. Supportive measures
• Zinc has been evaluated as a treatment for common cold symptoms.
• Bed rest, Steam inhalation, High fluid intake and Anti –pain.
• Antipyretic treatment is generally not indicated
• Topical adrenergic agents xylometazoline, is available as either intranasal
drops or nasal sprays in children >2 yr old.
• It has side effect of rhinitis
• Vitamin C and inhalation of warm, humidified air are no more effective than
placebo for the treatment of colds.

22. Pertusis (Whooping Cough):
Pertusis is an acute bacterial infection of the respiratory tract.
Etiology
• Bordetella Pertussis and Bordetella Parapertussis
• Only B. Pertusis expresses Pertusis toxin (PT), the major virulence protein
the toxin has activities e.g. histamine sensitivity, insulin secretion,
leukocyte dysfunction- causes inflammation.

23. Clinical Manifestations:
• The disease has insidious onset and 3 phases.
1. Catarrhal phase (runny nose)
– Lasts 1-2 wks
– Cough, congestion and rhinorrhea.
– Variably accompanied by low-grade fever, sneezing, lacrimation, and conjunctival suffusion.
– As initial symptoms wane, coughing marks the onset of the paroxysmal stage.

24. 2. Paroxysmal phase (outburst)
– Lasts for 2–6 wk.
– Characterized by repeated violent coughs without intervening
inhalation.
– Cyanosis and sub conjunctival hemorrhage occurs due to violent cough.

25. 3. Convalescent phase (recovering)
– ≥2 wk, during this phase the cough may diminish slowly.
– Paradoxically, in infants, cough and whooping may become louder and
more classic in convalescence
– Immunized children have foreshortening of all stages of Pertusis
– Highly communicable in the early catarrhal stage before the paroxysmal
cough stage.
– Infants >3 mo of age do not display classical stages
– Dx: Clinical findings especially in paroxysmal phase

26. Treatment
• Antibiotics for super infections like pneumonia.
• Erythromycin
• Azithromycin is the preferred agent for neonates
Nursing Care
• Proper feeding of the child, rest
• Proper ventilation
• Reassurance the mother (care giver)
Prevention and Control: Immunization of children.

28. Pneumonia
• Is an inflammation of the parenchymal structure of the lungs, such as the
alveoli, interstitial tissue and bronchioles.
Etiology
• Bacteria-the most common cause, and viruses-rare
Epidemiology
• Pneumonia is responsible for 70-80% deaths that occur due to ARIs
worldwide.
• In Ethiopia, pneumonia is the cause of 1/3 infant mortality and 1/5 of under 5
mortality.

29. • Pneumonia is more severe in developing countries due to the
high prevalence of risk factors such as
– Malnutrition
– Overcrowding and in-door air pollution
– Recurrent infections such as measles, whooping cough, malaria and
diarrhea
– Immune-deficiency status

30. Clinical Manifestations
• Cough, Sudden onset of fever,
• Respiratory distress (rapid and difficult breathing, nasal flaring,
intercostals retraction, chest indrawing and cyanosis).
• Fast breathing and chest in drawing are important clinical findings in the
assessment of severity of pneumonia.
• Assess cough or difficult breathing: A child should assessed for: How
long the child has had cough or difficult breathing, Fast breathing, chest in-
drawing, and stridor in a calm child.

31. Steps for assessing cough or difficult breathing
• Ask:
– Does the child have cough or difficult breathing?
• If Yes, Ask: ------- Look, Listen, and Feel:
– For how long? Count the breaths in one minute.
– Look for chest indrawing and listen for stridor child must be calm
• “Difficult breathing” is any unusual pattern of breathing. Mothers may describe:
that their child’s breathing is “fast” or “noisy” or “interrupted.”
• If the mother answers NO, look to see if you think the child has cough or
difficult breathing.

32. If the mother answers YES, ask the next question.
• ASK: For how long? A child who has cough or difficult breathing for more
than 21 days has a chronic cough.
• This may be a sign of tuberculosis, asthma, whooping cough or another
problem.
• Count the breaths in one minute: Count the breathing rate as you would in a
young infants.
• The cut-off for fast breathing depends on the child's age. Normal breathing
rates are higher in children up to 12 months than in children age up to 5
years.

33. If the child is: The fast breathing:
2 up to 12 months: 50 BPM or more
12 months up to 5 years: 40 BPM or more.
Note: Those exactly 12 months old has fast breathing if you count 40
BPM or more.
Look for Chest In drawing: As you would look for chest indrawing in a
young infant; However, unlike in the young infant, mild chest indrawing is
not normal in older infants and children.

34. Look and Listen For Stridor
• A harsh noise made when the child breathes in, occurs when swelling of the
larynx, trachea or epiglottis that interferes with air entering the lungs.
• It is life-threatening when causes airway blocked.
• A child who has stridor when calm has danger sign.
• Look to see when the child breathes in, put your ear near the child's mouth
because stridor can be difficult to hear.

35. Classification table for cough or difficult breathing.
Sign Classify As Treatment
Any general danger
sign(stridor in calm child)
Severe pneumonia or very
severe disease
Give first dose of
antibiotics refer urgently
to hospital
Fast breathing or
chest indrawing
Pneumonia
Give antibiotics for 5 days,
Soothe throat, relieve
cough, Advice mother
when to return
immediately.
Follow-up in 2 days
No signs of pneumonia or
very severe disease.
No pneumonia cough or
cold
If coughing more than 21
days, refer for assessment,
Soothe throat, relieve the
cough .

36. A general danger sign is present if
• Not able to drink or breastfeed
• Vomits everything
• Has had convulsions
• Convulsing now
• Lethargic or unconscious

37. Gastrointestinal infections and infestations
Diarrhea
• defined as increased total daily stool output, is usually associated with
increased stool water content.
• It is common in children between 6 months to 2yrs, and more common in
babies under 6 months who are drinking cow’s milk or infant feeding
formulas.
• The number of stools normally passed in a day varies with the diet and age of
the child. Babies who are exclusively breast fed often have stools that are
soft, this is not diarrhea.

38. Types of Diarrhea
– Acute watery diarrhea
– Persistent diarrhea
– Dysentery

39. Acute watery diarrhea
• is an abrupt onset of watery diarrhea occurred due to poisoning and
infection of virus and bacteria. Most common bacteria are cholera,
shigella, and those causes food poisoning.
• The disease remains a burden in many underdeveloped countries that
cannot afford to establish essential infrastructure for safe water supply
and sanitation.

40. • Seasonal disease occurs in resource-poor endemic settings;
epidemics arise during natural disasters and complex emergencies
resulting in significant mortality and economic damage.

41. Persistent diarrhea
• is diarrhea lasts 14 days or more.
• Persistent diarrhea often causes nutritional problems.
• There are two classifications for persistent diarrhea:
– Severe persistent diarrhea
– Persistent diarrhea

42. Severe persistent diarrhea
• If a child has had diarrhea for 14 days and has some or severe
dehydration.
• Stool exam is mandatory.
• Treatment: Treat the child's dehydration and give vitamin A. drugs are
respective to the diagnosis

43. Persistent diarrhea
• A child who has had diarrhea for 14 days or more and has no signs of
dehydration.
• Treatment: Special feeding is the most important. Vitamin A is given as
recommended in the treat chart. In addition, give zinc supplementation for
10 days. Advise mother when to return immediately. Follow-up in 5 days.

44. Dysentery
• is child with diarrhea and blood in the stool with or without mucus.
• The most common causes of dysentery are shigella bacteria (60%).
• Amoebic dysentery is not common in young children.
• A child may have both watery diarrhea and dysentery. Finding the actual cause
of the dysentery requires a stool culture, (can take at least 2 days).
• Treatment: Treat dehydration. Treat for 5 days with Cotrimoxazole. In addition,
give zinc supplementation for 10 days. Advice mother when to return
immediately. Follow-up in 2 days.

45. Assess Diarrhea: is assessed for:
• Duration of diarrhea?
• Blood in the stool?
• Signs of dehydration?
• Look at the following steps
Ask: Does the child have diarrhea?
– If No, no need to assess for signs related to diarrhea.
– ask about the next symptom.
– If Yes, or said earlier diarrhea was the reason, record the answer.
Then assess the child for signs of dehydration, persistent diarrhea
and dysentery.

46. • ASK: for how long? Give the mother time to answer.
• ASK: Is there blood in the stool? ask the mother if she has blood in the stools
• Check for signs of dehydration?
– When dehydrated- at first restless and irritable.
– If dehydration continues-lethargic or unconscious.
• Look and Feel for the following signs:
• Lethargic or unconscious?
• Restless and irritable?
• Dehydration?

47. Check dehydration
– Look for sunken eyes: ask the mother if thinks eyes look unusual.
– Check thirsty: Offer fluid, not able to drink, drinking poorly, eagerly?
– Check turg0r: Pinch the skin (abdomen), see if go back: Very slowly (>2
sec), or Slowly (< 2 sec).

48. • Classifying of Dehydration: There are three possible classifications of
dehydration in a child with diarrhea:
– Severe DHN
– Some DHN
– No DHN
•Sign Classify as Treatment
Two of the following signs:
Lethargic unconscious,
Sunken eyes, Not able to
drink or drinking poorly,
Skin pinch goes back
very slowly
Severe
dehydration
→ Admission is required
Give IV fluid (Plan C). or
Refer URGENTLY to hospital
with mother giving frequent sips
of ORS on the way. Advise the
mother to continue breastfeeding.

49. Two of the following
signs : Restless,
irritable
Sunken eyes
Drinks eagerly,
thirsty
Skin pinch goes
back slowly.
Some
dehydration
Give Rx at the OPD: ORS solution or
Zinc (Plan B)
After 4 hours of treatment of ORS,
usual milk or nutritious food.
continue breastfeeding.
Advise mother when to return
immediately.
Follow-up in 5 days if not improving.
Not enough signs to
classify as some or
severe dehydration
No dehydration Give fluid at home (Plan A):
4 rules of home treatment
Follow-up in 5 days if not improving.

50. MANAGEMENT OF DIARRHEA
• There are three classifications of treatment plans:
– A. Plan A-Treat Diarrhea at Home
– B. Plan B -Treat Some Dehydration with ORS
– C. Plan C -Treat Severe Dehydration Quickly

51. Plan- A- treat diarrhea at home
• Antibiotics are not effective in treating diarrhea.
• Never give anti diarrheal drugs and anti-emetics to children and infants.
• Plan A treatment of a child who has diarrhea with No dehydration, has four
Rules of Home Treatment are:
1. Give extra fluid (as much as the child will take)
2. Give zinc supplementation
3. Continue feeding
4. When to return

52. • Plan A involves counseling the child's mother about the 4 Rules of Home
Treatment. Therefore, your teaching and advising skills are very important for
Plan A.
• Counsel the mother on 4 Rules of Home Treatment:
– give extra fluids (as much as the child will take)
– Advice breast fed frequently and for longer at each feed.
• If the child is EBF, give ORS.
– Up to 2 yrs 50 to 100ml a/r each loose stool.
– 2 yrs or more 100 to 200ml a/r each loose stool.

53. Plan B: Treat Some Dehydration with ORS
• includes an initial treatment period of 4 hours in the clinic. During the 4 hours,
the mother slowly gives a recommended amount of ORS solution. The mother
gives it by spoon or a cup.
• After 4 hours, reassess and classify the child for dehydration using the
ASSESS AND CLASSIFY chart.
• If there is still some dehydration, the child repeats Plan B.

54. Amount of ORS to give during the first 4 hrs
AGE Up to 4
Months
4 up to 12
Months
1 up to 2
years
2 up to 5
years
Wt in KG <6 kg 6-10 kg 10-12 kg 12-19 kg
ORS in ml 200-400 400-700 700-900 900-1400
*Use the child’s age only when you do not know the weight.
The approximate amount of ORS required (in ml) can also be calculated by
multiplying the child’s weight (In kg) times 75. Also counsel the mother on the 4
Rules of Home Treatment.

55. Plan C: Treat Severe Dehydration Quickly
• Children need to have IV water and salts replaced.
• Rehydration therapy using IV fluids or using a nasogastric (NG) tube is
recommended only for children who have Severe Dehydration.
• The treatment of severely dehydrated child depends on:
– The type of equipment available at the clinic
– The training you have received, and
– Whether the child can drink or not
• Start IV fluid immediately. Give 100ml/kg Ringer’s Lactate Solution
(or, if not available, Normal Saline), divided as follows:

56. • If the child can drink, give ORS by mouth while the drip is set up.
• Solutions for Intravenous Infusion:
• A number of IV solutions lack some of the electrolytes in the
concentration needed by severely dehydrated. To ensure adequate
electrolyte, some ORS solution should be given as patient able to drink,
even while IV is being given.
AGE First give 30mg/kg
in:
Then give 70mg/kg
in:
Infants (under 12
Months)
1 hour 5 hours
Children (12 Months
up to 5 years)
30 minutes 2 ½ hours

57. Preferred Solution
• Ringer's Lactate Solution: also called Hartmann's Solution for
Injection, is the best commercially available.
• Has adequate concentration of sodium and sufficient lactate, which is
metabolized to bicarbonate, for the correction of acidosis.
• Ringer's Lactate Solution can be used in all age groups for dehydration
due to acute diarrhea of all causes. Early provision of ORS solution and
early resumption of feeding will provide the required amounts of
potassium and glucose.
• Acceptable Solutions: The following acceptable solutions may not
provide adequate sodium and bicarbonate to the patient.

58. Normal Saline: also called Isotonic or Physiological Saline, is often
readily available.
• It will not correct the acidosis nor replace potassium losses.
Half-Normal Saline in 5% Dextrose: contains less sodium chloride than
is needed for efficient correction of dehydration. Like Normal Saline,
this will not correct acidosis nor replace potassium losses.
Unsuitable Solution
• Plain Glucose and Dextrose Solutions: should not be used. They
provide only water and sugar; they do not contain electrolytes. Thus,
they do not correct the electrolyte losses or the acidosis.

59. Febrile illness (malaria, measles)
MALARIA
• Definition: It is an acute infection of the blood caused by protozoa.
• Etiology: a protozoa of genus plasmodium.
• There are four different malaria species:
• Falciparum
• Vivax
• Ovale
• Malaria

60. Epidemiology & Occurrence
• Endemic in tropical and sub-tropical countries.
• Malaria affects 40% of the world’s population.
• In Ethiopia, areas below 2000 m altitude are said to be malarias.
• People who are especially at risk of getting malaria are: Under
five, pregnant women, travelers and new comers to endemic areas.
• Plasmodium Falciparum 60% and Vivax 40% are common in
Ethiopia.

61. Clinical Manifestations:
fever, general malaise, joint pains, nausea, vomiting, chills, head ache
and may anemia.
A typical fever attack is divided in three stages:
• Cold: Temperature is rising and the Pt shivers. It lasts 1-2 hrs. In this
stage the RBCs are brusting and many ring forms are seen in the blood
smear.
• Hot: temperature is high (40ºC), skin is dry and hot, there is severe
head ache. It lasts 3-4 hrs.
• Sweating: temperature falls rapidly. The Pt sweats profusely, his closes
are soaked. The Pt is relieved but exhausted. It lasts 2-4 hrs.

62. Treatment
• For uncomplicated malaria:
– For Chloroquin non-resistance species:
• Chloroquin 25mg/kg over a 3 day period.
– For Chloroquin resistance species:
• Fansidar 3 tabs stat, or (not currently)
• Quinine po 8mg/kg TID for 07 days.
• For complicated malaria:
– Pts should be admitted and given parentral quinine.
– Add dextrose in to the quinine fluid

63. MEASLES
• Measles is highly contagious viral febrile illness during childhood In some
areas of the world, measles remains a serious threat to children.
Etiology
• Measles virus is a single-stranded lipid enveloped RNA virus. (humans are the
only host of measles virus)
Transmission
• The portal of entry is through the respiratory tract or conjunctival contact with
droplet aerosols.
• Patients are infectious from 3 days before the rash up to 4–6 days after its onset.

64. Pathology
• Measles infection causes necrosis of the respiratory tract epithelium and
lymphocytic infiltrate.
Measles consists of 4 phases
• Incubation period: virus migrates to regional lymph nodes. primary viremia
• Prodromal illness: associated with epithelial necrosis and giant cell formation in
body tissues. Cells are killed by cell-to-cell plasma membrane fusion and Virus
shedding begins.
• Exanthematous phase: With onset of the rash, antibody production begins and
viral replication and symptoms begin to subside.
• Recovery: subsides the sign and symptom.

65. Clinical Manifestations:
• high fever, cough, an enanthem, coryza, conjunctivitis with photophobia, and
a prominent exanthem/rash.
• The enanthem or Koplik spots is discrete red lesions with bluish white spots in
the center on the inner aspects of the cheeks. it is the pathognomonic sign of
measles (1 to 4 days prior to the onset of the rash).
• The rash begins around the forehead behind the ears, and on the upper neck as a
red maculopapular eruption, then spreads downward.
Complications.
• Lowers serum retinol, immune suppression, Pneumonitis (58%), encephalitis
(20%).

66. Diagnosis
• Clinical and epidemiologic findings
• Reduction in the total WBC count.
• ESR are normal, if no bacterial infection.
• Serologic - identification of Ig-M antibody. (appears 1–2 days after the onset
of the rash)
• Viral isolation from blood, urine, or respiratory secretions (by culture at the
CDC)
• Molecular detection by polymerase chain reaction is possible

67. Treatment: Management is supportive.
– Antipyretics-
– Airway humidification and supplemental oxygen
– Oral rehydration and may require intravenous therapy.
– Ribavirin is active in vitro against measles virus.
– Vitamin A several controlled trials of vitamin A therapy reduced
morbidity and mortality from measles.
Prevention:
• Isolation at shedding period. (standard and airborne precautions)
• Vaccination

68. Nutritional deficiencies
Protein Energy Malnutrition
• Deficiency of a single nutrient is an example of malnutrition, but usually is
accompanied by a deficiency of several other nutrients.
• Protein-energy malnutrition (PEM) is manifested primarily by inadequate
dietary intakes of protein and energy, either because less dietary intakes of
these nutrients than required or because the needs for growth are greater than
can be supplied by what otherwise would be adequate intakes.
• However, it is almost always accompanied by deficiencies of other nutrients.

69. • For this reason, the term severe childhood under nutrition, which more accurately
describes the condition, is preferred.
• The terms primary malnutrition and secondary malnutrition refer, respectively,
to malnutrition resulting from inadequate food intake and malnutrition resulting
from increased nutrient needs, decreased nutrient absorption, and/or increased
nutrient losses.
• Malnourished children often present with gastroenteritis or pneumonia.

70. • Severe childhood under nutrition (SCU)- is ranging from mild under
nutrition (some decrease in length-for-age or wt-for-age) through severe
under nutrition (marked deficits in weight-for-age and length-for-age and
wasting (a low weight-for-length measure).
• Historically, the most severe forms of SCU are Marasmus (non-edematous
SCU with severe wasting) and kwashiorkor (edematous SCU), were
considered distinct disorders.
• MARASMUS was believed to result from inadequate intakes of both
energy (primarily ) and protein, whereas

71. • Kwashiorkor was believed to result primarily from inadequate protein
intake.
• Marasmic-kwashiorkor
• A third disorder, has features of both disorders (wasting and edema).
• The 3 conditions have distinct clinical and metabolic features, but they also have a number
of overlapping features.
• A low plasma albumin concentration, often believed to be a manifestation of edematous, is
common in both .
• In addition, the underlying causes of this spectrum of conditions are quite similar.

72. Causes
– Economic- poverty and ignorance,
– Social- food taboos
– Biologic- maternal malnutrition and inadequate intakes of breast milk
and other foods,
– Environmental- overcrowded and unsanitary living conditions.
MARASMUS
• Failure to gain weight and irritability, followed by weight loss and listlessness until
emaciation results. The skin loses turgor and becomes wrinkled and loose as subcutaneous
fat disappears

73. • Loss of fat from the sucking pads of the cheeks often occurs late in the course
of the disease
• Infants are often constipated, but may have starvation diarrhea, with
frequent, small stools containing mucus. The abdomen may be distended
or flat, with the intestinal pattern readily visible.
• There is muscle atrophy and resultant hypotonia.
• As the condition progresses, the temperature usually becomes subnormal and
the pulse slows.

74. Kwashiorkor
• May initially present as vague manifestations that include lethargy, apathy,
and/or irritability.
• When advanced, there is lack of growth, lack of stamina/energy, loss of
muscle tissue, increased susceptibility to infections, vomiting, diarrhea,
anorexia, flabby subcutaneous tissues, and edema.
• The edema usually develops early and may mask the failure to gain weight. It
is often present in internal organs before it is recognized in the face and limbs.

75. • Liver enlargement may occur early or late in the course of disease.
• Dermatitis is common, with darkening of the skin in irritated areas, but in
contrast to pellagra, not in areas exposed to sunlight.
• De-pigmentation may occur after desquamation in these areas.
• The hair is sparse and thin, and in dark-haired children, it may become streaky
red or gray.
• Eventually, there is stupor, coma, and death.

76. PATHOPHYSIOLOGY OF SCU.
• The manifestations of SCU are adaptive responses to inadequate energy and
protein intakes: activity and energy expenditure decrease.
• Despite this response, fat stores are mobilized to meet the ongoing (albeit
lower), energy requirement.
• Once these stores are depleted, protein catabolism must provide the ongoing
substrates for maintaining basal metabolism.

77. • Why edematous or non-edematous SCU develops is unknown. Factor have
been suggested for variability among infants:
– Nutrient requirements
– Body composition
– Giving excess carbohydrate to a child with non-edematous SCU:
reverses the adaptive responses to low protein intake,
• Eventually, albumin synthesis decreases, resulting in hypo- albuminemia
with edema.
• Fatty liver also develops secondary lipo-genesis from the excess carbohydrate
intake and reduced a lipopoprotein synthesis.

78. Treatment Of SCU.
• The usual approach includes 3 phases
Initial phase (1–7 days): Is a stabilization phase.
• Dehydration, if present, is corrected (oral-preferred)
• Antibiotic to control bacterial or parasitic infection. If IV is necessary, estimates of dehydration
should be reconsidered frequently, during the first 24 hr
• The initial oral treatment is F75 diet (75 kcal or 315 kg/100 mL).
• NB Vitamin A and Iron is not given b/c liver has damaged and may aggravate
bacterial infection in small intestine.
The rehabilitation: diet is F100 diet (100 kcal or 420 kg/100 mL).

79. • Feedings are initiated with higher frequency and smaller volumes; over time, the
frequency is reduced from 12 to 8 to 6 feedings/24 hr.
• The initial caloric intake is estimated at 80–100 kcal/kg/day.
• If diarrhea starts or fails to resolve and lactose intolerance is suspected, a non–lactose-
containing formula should be substituted.
• If milk protein intolerance is suspected, a soy protein hydrolysate formula can be used.
• Follow up: discharged client may require follow up

81. DEFICIENCY OF MICRO- NUTRIENT ( VIT A, D, IODIN)
• A substance that an organism requires for normal growth and
development but only in very small quantities, e.g. a vitamin or
mineral.
• Vitamins are essential organic compounds that are required in very small
amounts and are involved in fundamental functions in the body, such as
growth, maintenance of health, and metabolism.
• Because our bodies has low store vitamins, they must be supplied by the diet
or as supplements.

82. • Based on their chemical properties, they are classified as either water-soluble
or fat-soluble
• The water-soluble vitamins (except vitamin C) are members of the B-
complex.
• Vit A, vit D, Iron, Iodin are some of the most Common among children.

83. Vit A deficiency
• Vitamin A is an essential micronutrient and must be obtained from plants.
• At birth, the vitamin A content in the liver is low, but normally, it increases
60-fold during the first 6 mo of life.
• However, even subclinical vitamin A deficiency may have serious
consequences.
• Vit A helps in vision, epithelium (mucus secretion) in intestine (barrier
against a pathogenic)and respiratory (disposal of inhaled pathogens)

84. Clinical manifestations
• Defective epithelial barriers to infection; diarrhea, ARI, increased infections
in pancreatic and salivary ducts, kidney- infection pyuria and hematuria
• Skin manifestations: Skin- dry, scaly, hyperkeratotic patches, commonly on
the arms, legs, shoulders, and buttocks.
• Low immune response, anemia, apathy/lack of energy
• Mental retardation
• Lowered response to inflammatory stress

85. Specific signs of vitamin A deficiency:
• Eye lesions: is delayed adaptation to the dark; later it leads to night blindness.
• Photophobia: is a common symptom. As vitamin A deficiency progresses, the
epithelial tissues of the eye become severely altered.
• xerophthalmia: In early vitamin A deficiency, the cornea keratinizes, becomes
opaque, is susceptible to infection, and forms dry, scaly layers of cells called
xerophthalmia.

86. Keratomalacia
• In later stages, infection occurs, lymphocytes infiltrate, and the cornea becomes
wrinkled; it degenerates irreversibly called keratomalacia, resulting in
blindness.
• The conjunctiva keratinizes and develops plaques (Bitot spots), it becomes dry
(conjunctival xerosis), and the lacrimal glands keratinize.
• When it degenerates, the rods and cones have no support, so they break down
and blindness results.

87. Diagnosis
• Dark adaptation tests- for early-stage
• Xerophthalmia is a very characteristic lesion of vitamin A deficiency.
• Exclude other similar eye abnormalities
• Plasma retinol level (in severe deficiency); the normal range vitamin A
levels is 20–60 ug/dL; a level <20 μg/dL occurs in deficiency.

88. Treatment
• A daily supplement of 1,500 μg of vitamin A is sufficient for treating latent
vitamin A deficiency.
• In overt vitamin A deficiency, mortality rates from viral infections such as
measles can be lowered by daily administration of 1,500–3,000 μg of vitamin A,
under careful monitoring to avoid toxicity
• Xerophthalmia is treated by giving 1,500 μg /kg body weight orally for 5 days
followed by intramuscular injection of 7,500 μg of vitamin A in oil, until
recovery.

89. Vitamin D deficiency
• Vitamin D deficiency remains the most common cause of rickets globally, even
in industrialized countries.
• Vitamin D can be obtained from dietary sources or from cutaneous synthesis.
• Vitamin D deficiency most commonly occurs in infancy due to a combination of
poor intake and inadequate cutaneous synthesis.
• Trans-placental transport provides enough vitamin D for the 1st 2 mo of life
unless severe maternal deficiency.

90. • Breast-fed infants rely on cutaneous synthesis or vitamin supplements
because of the low vitamin D content of breast milk.
• Cutaneous synthesis can be limited due to
– The ineffectiveness of the winter sun
– Avoidance of sunlight due to concerns about cancer,
– Neighborhood safety, or cultural practices;
– Decreased cutaneous synthesis because of increased skin pigmentation.

91. Clinical Manifestations.
• Failure to thrive, Protruding abdomen
• Muscle weakness
• Fractures
• Craniotabes (softening of the cranial bones)
• Frontal bossing, Delayed fontanel closure Delayed dentition;
Craniosynostosis
• Scoliosis, Kyphosis, Lordosis

92. Diagnosis
• History taking
• Typical laboratory findings

93. Treatment
Children should receive vitamin D, calcium and phosphorus.
• Two strategies for administration of vitamin D.
• With therapy, 300,000–600,000 IU of vitamin D orally or intramuscularly as
2–4 doses over 1 day.
• The alternative is daily, high-dose vitamin D, with doses ranging from 2,000–
5,000 IU/day over 4–6 wk.
• dietary calcium and phosphorus; will provided by milk, formula.
• may need IV calcium acutely, followed by oral calcium supplements- tapered
over 2–6 wk (20 mg/kg of calcium chloride or 100 mg/kg of calcium
gluconate).

94. Prevention.
• Most cases of nutritional rickets can be prevented by universal administration of
a daily multivitamin containing 200–400 IU of vitamin D to children who are
breast-fed. For other children, the diet should be reviewed to ensure that there is
a source of vitamin D.