Common Problems Diseases and Disorders in Infants

Common Problems,
Diseases, and Disorders

in Infants
03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 1

Congenital
Malformations
Musculoskeletal Disorders
Finger conditions
a. Polydactyly – presence
of one or more
additional fingers
b. Syndactyly – two fingers

which are fused due to
simple webbing
Surgery is the intervention

of choice.
03/25/20 07:28 AM 3
Polydactyly or poly
dactylism
• Polydactyly or polydactylism (from Greek
meaning 'many', and δάκτυλος (daktylos),
meaning 'finger'), also known
as hyperdactyly, is an anomaly
in humans and animals resulting
in supernumerary fingers and/or
toes. Polydactyly is the opposite
of oligodactyly (fewer fingers or toes).

What causes extra fingers
in humans?
• Polydactyly results if there's an irregularity in this
process: An extra finger forms when a
single finger splits in two. The vast majority of
occurrences of polydactyly are sporadic, meaning
that the condition occurs without an
apparent cause—while some may be due to a
genetic defect or underlying hereditary syndrome.

Can you remove extra
fingers?
• Treatment: Polydactyly is often treated with

surgery to remove the extra digit or digits. If
there is no bone involved, the extra digit may
be tied off. If surgery is needed, the surgeon
usually waits until the child is age 6 months
or older.

Syndactyly is defined as an
abnormal interconnection
between adjacent digits and
is described according to the
magnitude and extent of the
connection.

What causes syndactyly of
the toes?
It occurs when the toes or fingers do not
separate correctly during fetal
development. ... Syndactyly often
presents as webbing, so people often
refer to the condition as webbed toes or
fingers. The majority of cases of
webbed toes occur when the skin fails to
separate during fetal development.

Treatment
• Your child will probably receive general anesthesia,
so that they’re asleep during the surgery. A series of
zigzag incisions will be made to separate their
fused fingers or toes. It’s a procedure is called Z-
plasty.
• During Z-plasty, incisions will split the excess

webbing between your child’s fingers or toes. Their
surgeon will likely use pieces of healthy skin from
another part of your child’s body to cover the
separated area. This is called a skin graft.
Torticollis
(wry neck)

Torticollis (wry
•
neck)
Contraction of
sternocleidomastoid (neck
muscles) due to injury and
bleeding during birth
• Passive stretching exercises
• Surgery, then neck

immobilizer if it persists in
one year
12
Craniosyno
stosis

Craniosynostosis
• Premature closure of the
sutures of the skull
• Craniosynostosis is a birth
defect in which the bones in
a baby’s skull join together
too early. This happens
before the baby’s brain is
fully formed. As the baby’s
brain grows, the skull can
become more misshapen.
• Deformed face and orbits

• Increased ICP

Causes and Risk
Factors
• The causes of craniosynostosis in most infants are
unknown. Some babies have a craniosynostosis
because of changes in their genes.
• In some cases, craniosynostosis occurs because of
an abnormality in a single gene, which can cause a
genetic syndrome.
• However, in most cases, craniosynostosis is thought
to be caused by a combination of genes and other
factors, such as things the mother comes in contact
with in her environment, or what the mother eats
or drinks, or certain medications she uses during
pregnancy.
Treatments
• Many types of craniosynostosis require surgery.
• The surgical procedure is meant to relieve
pressure on the brain, correct the
craniosynostosis, and allow the brain to grow
properly.
• When needed, a surgical procedure is usually
performed during the first year of life. But, the
timing of surgery depends on which sutures are
closed and whether the baby has one of the
genetic syndromes that can cause
craniosynostosis.
Achondroplasia
Achondroplasia is a genetic disorder that results in
dwarfism. In those with the condition, the arms and
legs are short, while the torso is typically of normal
length.

Achondroplas
ia
• A form of dwarfism related
to deficient cartilage in
utero
• <140 cm height
• Stunted legs and arms
• Prominent forehead
• Flattened bridge of the
nose
• X-ray: abnormal flaring of

epiphysis

Is achondroplasia
inherited?
• In more than 80 percent of cases, achondroplasia isn’t inherited, according
to the National Human Genome Research Institute (NHGRI). These cases are
caused by spontaneous mutations in the FGFR3 gene.
• About 20 percent of cases are inherited. The mutation follows an autosomal
dominant inheritance pattern. This means that only one parent needs to
pass down a defective FGFR3 gene for a child to have achondroplasia.
• If one parent has the condition, the child has a 50 percent chance of getting
it.
• If both parents have the condition, the child has:
 a 25 percent chance of normal stature
 a 50 percent chance of having one defective gene that causes
achondroplasia
a 25 percent chance of inheriting two defective genes, which would result in
a fatal form of achondroplasia called homozygous achondroplasia

How is achondroplasia
treated?
• There’s no cure or specific treatment for
achondroplasia. If any complications arise, then
your doctor will address those issues. For instance,
antibiotics are given for ear infections and surgery
may be performed in severe cases of spinal
stenosis.
• Some doctors use growth hormones to increase the
growth rate of a child’s bones. However, their long-
term effects on height haven’t been determined
and are thought to be modest at best.

Talipes
Deformities

Talipes
Deformities
Congenital club foot
(Talipes equinovarus)

clubfoot
• The exact cause is usually not identified.
• Both genetic and environmental factors are
believed to be involved.
• If one identical twin is affected, there is a
33% chance the other one will be as well.
• The underlying mechanism involves
disruption of the muscles or connective
tissue of the lower leg, leading to
joint contracture.

four components of the
clubfoot deformity:
Cavus: the foot has a high

arch, or a caved Adductus: the forefoot curves
appearance. inwards toward the big toe

four components of the
clubfoot deformity:
Equinus: the foot is pointed

Varus: the heel is inverted, or downward, forcing one to walk
turned in, forcing one to walk on tiptoe. This motion occurs
on the outside of the foot. naturally, but in clubfoot the foot
This is a natural motion but in is fixed in this position. This is
clubfoot the foot is fixed in because the Achilles tendon is
this position.. tight and pulls the foot
downwards.
treatment
• Initial treatment is most often with the Ponseti
method. This involves moving the foot into an
improved position followed by casting, which is
repeated at weekly intervals.
• Once the inward bending is improved, the Achilles
tendon is often cut, and braces are worn until the
age of four.
• Initially, the brace is worn nearly continuously and
then just at night.[

• The Ponseti method is a manipulative
technique that corrects
congenital clubfoot without invasive surgery.
It was developed by Ignacio V. Ponseti of
the University of Iowa Hospitals and Clinics,
USA in the 1950s, and was repopularized in
2000 by John Herzenberg in the USA and
Europe and in Africa by NHS surgeon Steve
Mannion.
• It is a standard treatment for club foot.

Talipes
Deformities
• Nursing interventions:
• Change diapers frequently
• Teach on:
• Checking for perfusion
• Cyanosis
• Blanching
• Performing passive for exercises

Hip dysplasia

Hip dysplasia
• Flattening of the acetabulum of the pelvis
• Sublaxation
• Dislocation of the hip joint
• Six times more common in females

• Flaring of hips
• Relaxin
• Traction or surgery
32
Hip dysplasia:
Nursing care
Multiple diapers/splints Pavlik harness Spica cast
Good diaper care Worn continuously Teach on neurovascular

assessment
•Change frequently Teach on: •Temperature
•Removing during •Circulation
•Wash thoroughly with bathing and reducing hip
water before using the harness
•Apply ointment: A & D, •Skin assessment

Vaseline or Desitin

Overview: Nursing
Process
1. Concept of illness to a child
Younger children (2-7)

Cause of illness is magical or a consequence of breaking a rule
Getting well is conditional
Fourth graders (7-10)

Aware of the role of germs
Passive role in getting well
Eighth graders (13 above)

Several causes of illness
Active role in getting well

35
Overview: Nursing
Process
2. Nursing process for an ill child
Anxiety r/t separation from parents
Fear r/t diagnostic and therapeutic

procedures
Parental health-seeking behavior

Musculo-
Skeletal
Disorders
Children
Nursing process:
Assessment
•History & physical examinations
•X-ray, bone scan, arthroscopy,

electromyography, biopsy

Nursing process:
Diagnoses
• Pain r/t chronic inflammation of joints.
• Impaired physical mobility r/t cast on leg.
• Self-esteem disturbance r/t continued use of body

brace.
• Diversional activity deficit r/t the need for imposed

activity restriction for weeks

Medical/Surgical
Management
Elevate leg
CASTING
Assess perfusion status
POP (Plaster of Paris or q 15 min x 1st hour
open-woven bandage) q 1H x 24 H
q 4H subsequent VSM
Protects broken bone and
prevent movement
Allow independence: pacing
After removal: check pedal pulses;

color; warmth; numbness/tingling

Medical/Surgical
Management
CRUTCHES Proper fitted crutches
Weight on the grip

Prescribed :
Rubber should be intact
Keep weight off
Support
Maintain balance

Medical/Surgical
Management
TRACTION VS: BP
Assess perfusion status

Used to: q 15 min x 1st hour
reduce dislocations q 1H x 24 H
q 4H subsequent VSMonitoring
immobilize fractures edema, pallor, pain
Skin care
Involves: pull and back, elbows, heels
counter-pull
Trapeze
Do not move weights
03/25/20 07:28 AM 42
Medical/Surgical
Management
DISTRACTION
Separates opposing bones to encourage new growth
Lengthens the bone
Immobilize fractures or correct defects

Medical/Surgical
Management
OPEN REDUCTION
Surgery to align and repair bone
Internal fixation (rods, screws) is rarely used in

children unless with scoliosis

Skeletal disorders:
Genetics a. Achondroplasia
b. Osteogenesis
imperfecta (fragilitas
ossium/brittle bones)
Uncommon hereditary
generalized
connective tissue
disorder; with
multiple fractures

Skeletal disorders:
Metabolic
a. Avitaminoses/hypervitaminoses
1. Chronic hypervitaminosis A
Excess Vitamin A
Elevated periosteum
Subperiosteal calcification
Appears 1-3 years old

Skeletal disorders:
Metabolic
2. Vitamin C
(ascorbic acid )
deficiency Scurvy
Interferes in bone
formation
Hemorrhage:
defective capillary
walls

Skeletal disorders:
Metabolic
3. Vitamin D
deficiency
Rickets in
children
Osteomalacia in
adults

Skeletal disorders:
Endocrine
a. Hypopituitary dwarfism b. Hyperpituitarism
Due congenital anomaly Gigantism – excessive

growth hormone r/t
Destruction of the APG adenoma; acidophil
tumor, histiocyosis, adenoma
chronic infection
Acromegaly – gradual
bone thickening;
acidophil adenoma

Skeletal disorders:
Endocrine

Skeletal disorders:
endocrine
c. Cretinism (hypothyroidism)
 Hypofunction of the thyroid gland at the

second 6 months of life
 May be caused by congenital lack of thyroid
tissue
 Inability of the gland to synthesize hormone
 Impairment of mental development
Irregular and delayed ossification of epiphysis

Skeletal disorders:
Hip condition
CONGENITAL HIP DISLOCATION
Types:
1. Teratologic (intra-utero)
2. Typical (unstable, dislocated, sublaxated)
>50% unilateral: left hip involvement; in females than males

(8:1)
Ortolani’s or Barlow’s test
Age-appropriate management
Skeletal disorders: Hip
Condition
Age Clinical manifestations MS management
(+) Ortolani’s test – to detect
instability dislocated hip
(+) Barlow’s test – dislocated Reduction of the hip with
Birth – three months but not dislocatable (unstable); maintenance in flexion and
limitation of passive abduction abduction for four months.
of the flexed hip, extra skin
creases on the surface of the
thighs
More marked adduction Continuous traction to

contracture lengthen tight adductors
Leg length discrepancy Closed reduction of the hip
Three months – 18 months follows
Prominence hip
Hip spica casts between 6-18
Galeazzi’s sign
months to marked flexion and
Telescoping sign moderate abduction
Limping gait
18 months – five years T-berg sign Open reduction
Waddling gait

Skeletal disorders:
Knee Condition
a. Chondromalacia patella
Softening of the articular
cartilage of the patella
Progressive with
conservative
management
3 categories:
Primary idiopathic
Secondary adolescent
type
Adult type

Skeletal disorders:
Knee Condition
b. Genu varum (bow c. Genu valgum (knock-
legs) knee)
Lateral bowing of the tibia Medial surface of the
with the medial
malleoli of the ankles knees touch and the
touching and the malleoli are separated
medial surfaces of the by more than three
knees are over two inches.
inches apart
• Seen in 2 years old • Seen in 3-4 years old
• Corrected @ 3; latest • Gradually corrects
@ school age itself; latest at school
age
• If beyond school age:
orthopedist

Skeletal disorders:
foot/ankle
a. Pes planus (flatfoot)
Complete loss of the medial
longitudinal arch
Congenital or acquired
Exercises/shoe modification
b. Pes cavus
Unusually high-arch;
clawfoot, pes arcuatos, hollow
foot
Primary or secondary
03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN

Skeletal disorders:
foot/ankle
• Primary deformities
• Inversion and adduction of the forefoot
• Varus of the calcaneous (heel inversion)
• Equinus (plantar flexion)
• Internal tibial torsion
• Secondary deformities
• Contractures of the tissues on the medial side of the foot
• Underdeveloped evertor muscles on the lateral side of the leg
• Underdeveloped and contracted muscles
• More common in males
• Management : osteotomy, arthrodesis, and tendon transfer

Infectious and inflammatory
disorders of the bones and
joints
OSTEOMYELITIS
An infection caused by of the bone which typically begins at
the metaphysis
S. aureus in older children
H. influenzae in younger children
Septicemia
Sickle cell anemia (Salmonella invasio)
Outside invasion: penetrating wound, open fracture,
surgical contamination
Altered bone growth

disorders of the bones and
joints
SYNOVITIS
An acute, non-purulent inflammation of the
synovial membrane of a joint, which occurs most
commonly in the hip joint of children
Peak: between 2 and 10 years

disorders of the Bones and
Joints
JUVENILE RHEUMATOID ARTHRITIS
Unknown cause in childhood
Chronic inflammation of the synovium with

joint effusion and eventual erosion
Management:
Steroids, NSAIDS, slow-acting anti-inflammatory
medications or cytotoxic drugs; surgery, bracing or shoe
correction

Infectious and
inflammatory disorders of
the bones and joints
Nursing care: Juvenile rheumatoid arthritis
Interventions Rationale
Exercise:
•institute a set of exercise To preserve and strengthen muscle
and joint functions
•avoid running, jumping, prolonged To prevent strains of the joint

walking and kicking
Heat application:
•use warm water; 20-30 minutes To reduce pain and inflammation
soaking
•hot baths To eliminate stiffness
•paraffin soaks To reduce inflammation in wrist and
fingers

Disorders of the spine:
Scoliosis
The lateral deformity of
the spine with vertebral
rotation
Incidence: thoracic >

lumbar curve

Scoliosis NON-STRUCTURED SCOLIOSIS
Lateral curvature of vertebral
column not associated with nay
true structural deformity at the
vertebra
Associated with abnormal

posture, by length discrepancy,
muscle spasm (disc herniation),
tumors, inflammation
Non-progressive; develop through

structural scoliosis and
progressive if prolonged

Scoliosis
STRUCTURAL SCOLIOSIS
Lateral spine curve that cannot be fully
corrected by lateral flexion
Associated with bony changes and fixed

rotatory deformity of the vertebral
bodies toward the convexity of the
curve
• Involves bony deformity

• 65% idiopathic or acquired
• Surgery or braces

scoliosis
PREOP POSTOP
Deep breathing; incentive Do not BEND
spirometry
Child lie flat
Set expectations
Postop complications Position on sides q 2H
NGT
Show equipment NVS q 2H and record VS
NPO until (+) BM

Disorders of the skeletal
muscle: Myasthenia gravis
Acetylcholine
receptor reduction in
the post junctional
membrane

Characteristics:
More in young adult Slurred speech with nasal twang
Males > females Difficulty in mastication and

swallowing
1/50,000 of population
Fluctuating bulbar palsy
DX: Endophorium chloride test
TX: anticholisnesterase, Chronic fatigability and muscle

immunosuppressants, weakness
Prostigmin

Myasthenia gravis

Nursing Management:
Soft diet with SAP
WOF signs of respiratory arrest

Severe muscle weakness

Duchenne muscular
dystrophy
Progressive symmetric
wasting of the leg and
pelvic muscles
Muscles weakness
produces waddling gait
and pronounced lordosis

Duchenne muscular
dystrophy
If mother’s a carrier, 50% of male
children and 50% of females are
carriers (9:1)
Boys are asymptomatic until 3-6

years old
Macroglossia, (+) Gower’s sign, tip-

toeing, IQ 30% reduction,
wheelchair dependency by 9-10
years, lumbar lordosis with
protruberant abdomen, (+)
waddling gait, T-berg’s sign and
gait

NURSING CARE: Duchenne Muscular Dystrophy
STAGE I: STAGE II: STAGE III:
Ambulatory Wheelchair Totally dependent
Confirm diagnosis Select appropriate Maintain activities that

wheelchair patient can do
Routine nursing care Maintain maximum
self-care Perform general
Maximize self-care Plastic body jacket nursing care and
assist in ventilation
Encourage activities Pulmophyisotherapy
Ambulation (exercise) Teach client and

family

Injuries of
extremities
FRACTURE Nursing Management:
Traumatic injury in the continuity Encourage weight bearing on lower
of the bone tissue extremity fracture and active
movement
Fat embolism: a common
complication Reassure and calm the child’s
parents
Management:
Traction, casting, closed
reduction and plaster
immobilization

FRACTURE

Injuries of
extremities
SPRAIN R est
I ce
Over stretching/tearing of C ompression
ligaments or tendons or both to
joint trauma
E levation
STRAIN I ce
C ompression
An injury to the muscle E levation
S support

A T IC
A U M
TR U RY
IN J
Head injury
Scalp injury
May result in abrasion, contusion, lacerations, or hematoma
beneath the layers of the tissue of the scalp (subglial
hematoma)
Skull fracture
Break in the continuity of the skull caused by forceful
trauma (with/without brain damage)
Classified as: linear, comminuted, depressed and basilar

Head injury
Brain injury Nursing interventions:
An irreversible damage and Elevate head of bed
cell death which occurs when
the blood supply is
interrupted for a few Monitor ICP
minutes Mannitol
ALOCRS Monitor RR
Pco2 <25 mmHg
Dexamethasone

Head injury
Concussion Manifestations:
Irrational behavior (frontal lobe)
Temporary injury from a
hard, jarring shock
Complete loss of consciousness
Types:
Temporary amnesia (temporal
Coup injury (anterior lobe)
brain)
Countercoup (posterior Temporary loss of neurologic
brain) function without apparent
structural damage

Head injury
Contusion
A more severe injury; bruising of the brain
Abnormal motor function, abnormal eye

movements, increased ICP
RICE

Head injury
Subdural hematoma Epidural hematoma
Venous bleeding between the Bleeding between the dura and the
dura and the arachnoid skull due to rupture of the meningeal
membrane (bilateral) artery
Infants > older children Decortication, unequal pupils,

convulsions, hemiparesis, and loss of
consciousness
SX: amnesia, seizures, vomiting,
increased ICP (3 days after to 20
days) Surgery/cautery
TX: subdural function in infants

and surgery in older children

Head injury
Intracerebral hemorrhage and hematoma
Bleeding in the brain due t injury or trauma
Insidiuos onset, beginning with the development of

neurologic deficits followed by headache
TX: control ICP, HTN, F & E

Abdominal trauma
Non-penetrating; direct blow to the abdomen
damaging liver and spleen
Monitor IV line
CBC
Vaccination
Pain management
Emesis
Monitor for infection

Near drowning
DROWNING
Death due to suffocation from submersion of liquid
NEAR DROWNING
Submersion injury requiring emergency treatment; recovery
24H post-injury
TX: CPR, mechanical ventilation, 100% O2, plasma

administration and NGT for compression

Poisoning
Accidental intake of substance
e.g., soap, cleaner, plants
Between 3-12 years old children
What to do?
Call poison control center
Induce vomiting

Poisoning
Nursing management: Remove poison and prevent
Terminate exposure absorption
• Induce vomiting
Empty mouth; flush eyes with NSS
(15-20 mins.); flush skin and wash • Ipecac:
with soap, use soft cloth; remove • 6-12 mos. – 10 mL; DNR
contaminated clothes; allow to • 1-12 years – 15 mL;
breathe fresh air • >12 years – 30 mL
Identify the poison • repeat after20 min if no vomiting

• Position with head below
• Activated charcoal with catharctic

Frostbite
Exposure to extreme cold
leading to peripheral
vasoconstriction
Erythemtous – necrotic (1st –

4th)
Assess for T
Give analgesics and
antibiotics; wound care

Bites
Injury caused by an animal/insect
TX: use rubber suction to remove venom; lie quietly to slow

circulation; cold compress to slow the spread and reduce edema

Burn trauma
THERMAL
Heat > 104oF (40oC)
Infection leads to death

ELECTRICAL
Superficial: 2-3 days Most devastating
Superficial partial thickness: 7-21
days Sx of CNS injury (1 mo-3 years)
Deep partial thickness: 3- 5
weeks
TX: grafting, debridement,
Full thickness: excision/grafting escharotomy, fasciotomy

Burn trauma
Nursing management:
Maintain level of comfort
Wound care
Prevent complications:
Maintain body T
Monitor symptoms of infection
Reposition

DIGESTIVE
DISORDERS
CHILDREN
Nursing Process
Assessment
Nursing Diagnoses:
Risk for fluid volume deficit
Altered family processes r/t interference with
parent-infant bond
Altered nutrition, less than body requirements
Self-esteem disturbance

Nursing Process
Nursing interventions
Monitor I & O
Determine serum electrolyte level
Appropriate nutritional management

Disorders of motility
DIARRHEA
Frequent passage of loose watery stools
Causes:
Viral (adenoviruses, rotavirus) Bacterial (C. jejuni,
Salmonella, G. lamblia, C. difficile)
Types:
Mild & severe
TX: oral rehydration (pedialyte) and antibiotic

CONSTIPATION
Alteration in the frequency, consistency and
passing of stool
Due to organic or systemic cause/disorders
In children: idiopathic or functional

VOMITING
Forcible voluntary or involuntary emptying of the stomach contents

due to viral or bacterial causes
Oral rehydration, IV, Prochloperazine

Disorders of the
Stomach/duodenum
GERD
Backflow of the gastric
contents into the esophagus
as a result of relaxation or
incompetence of the lower
esophageal sphincter
May be due hiatal hernia

Gastroesophageal reflux
disorder
Nursing interventions:
Position
Flat prone; head elevated prone ff. feedings (SFF)
For infants: thicken formula – ass 1 tbs. rice cereal/6 oz.
formula and crosscut the nipple
SAP
For toddlers: solid then liquid
Avoid: fatty foods, chocolate, tomato products, carbonated

liquids, fruit juices, citrus products, and spicy foods
Avoid activity post feeding

Disorders of the
Stomach/duodenum
PYLORIC STENOSIS
Hypertrophy of the circular muscles of the pylorus which causes
narrowing of the pyloric canal between the stomach and the
duodenum
In the first few weeks of life

PYLORIC STENOSIS
PREOP POSTOP
Give IV Observe for
•electrolytes infection
Hold oral
feedings

Disorders of the
Stomach/duodenum
PEPTIC ULCER DISEASE Administer:
Shallow excavation in the Antibiotics
stomach wall, the pylorus or tetracycline, amoxicillin,
the duodenum clarithromycin
Antacids
H. Pylori Aluminum OH
Magnesium OH
Provide continues nasogastric H2 antagonist
antacid with bleeding
cimetidine, ranitidine,
Further teaching nizatidine, famotidine

Hepatic diseases
HEPATITIS
Acute or chronic inflammation of the liver
Types:
Hepa A – infectious
Hepa B – serum
Hepa C – non-A, non-B
Hepa D – similar to B
Hepa E – fecal-oral
Hepa G – non-A, B, C

Intestinal disorders
APPENDICITIS PREOP
NPO
Inflammation of the appendix NO analgesics, cathartics, heat
Peritonitis or sepsis are Urinalysis and CBC
complications IVF
Causes: obstruction of POSTOP

hardened stool, bacterial WOF signs of infection
invasion or foreign bodies
Antibiotics

Intestinal disorders
MECKEL’S DIVERTICULUM CELIAC DISEASE
Sensitivity to gluten
Small, naturally occurin,
outward protrusion of the
inner lining of the small Glutamine accumulates and toxic to
mucosal cells and fats are not
intestine through the absorbed
muscular wall (MOST
common)
Between 1-5 years
May cause intussusception NO gluten in the diet; rice/corn;

vitamins and minerals
Surgery

Disorders of the lower bowel

Inflammatory bowel disease
Inflammation of the mucosa/submucosal layers
Young adults > adolescents
Types:
Crohn’s – chronic inflammation of the lower IT
Ulcerative colitis – inflammation of the walls of
the bowel with ulcerations

Ulcerative colitis
Crohn’s

Inflammatory bowel disease
Crohn’s Ulcerative colitis
RLQ pain, weight loss, NV, bloody stools Severe diarrhea (15-20), bloody
mucus/pus
Barium enema, fecal occult blood,
sigmoidoscopy, biopsy Severe tenesmus, weight loss, anorexia,
weakness
Steroids, metronidazole, antispasmodics,
antidiarrheals, narcotics Signs of dehydration
Lifetyle changes Low-grade fever; tenderness

Surgery
Reduce bowel motility Low fiber diet; no milk

Disorders of deficiencies
Kwashiokor
CHON deficiency
Occurs after weaning
High CHON diet, oral

rehydration, anitbiotics,
antidiarrheals, IV F/E

Disorders of deficiencies
Marasmus
Starvation in all food groups
Infants <1 year
TX: complete nutritional therapy

Hematologic
dysfunction
Children
Disorders of the RBC
ANEMIA
A reduction in the number of circulating RBC; Hb and HCT
Normal values in children:
Hb: 10.0-15.0 g/dL
HCT: 29%-45%
Normal values in adult:
RBC (M): 4.7-6.1 x 106/µL
(F): 4.2-5.4 x 106/µL
Hb: (M): 14.0-18.0 g/dL
(F): 12-16 g/dL
HCT: (M): 42%-52%
(F): 37%-47%

Disorders of the RBC: types
1. Normochromic & normocytic 5.Thalassemia
Marked reduction in the production Abnormalities of the beta chain
of RBC by the bone of adult Hb
marrow/abnormal uncompensated Types:
loss
a. Thalassemia minor
2. Hypochromic (heterozygous)
Inadequate Hb synthesis; usually in b.Thalassemia major (homozygous)
iron deficiency
3. Macrocytic (megaloblastic anemia)
Abnormally large, immature and 6.Polycythemia
nucleated RBC; Folic acid and Increase due to a compensatory
pernicious anemia (B12 deficiency) response
Hemolytic anemia Chronic pulmonary disease or
Increased destruction CHD
resulting from abnormal Leads to CVA/emboli
structure (sickling) or Increases with dehydaration
extracelluar destruction
(autoimmune)

Disorders of the WBC
Normal values
WBC: 5,000-10,000/mm3
Neutrophils: 55%-70%
Lymphocytes: 20%-40% Platelet count: 150,000-

400,000/mm3
Monocytes: 2%-8%
Eosinophils: 1%-4%
Basophils: 0.5%-1%

Disorders of the WBC
1. Neutropenia
Reduced number of WBCs due to some drugs/non-pyogenic
infections
2. Neutrophilia
Increased number due to infections
3. Leukemia
Uncontrolled proliferation of immature WBC
4. Eosinophilia
Increased number of eosinophilia due to allergic
reaction/parasitic infection
5. Lymphocytosis
Increased number of lymphocytes

Disorders of hemostasis
1. DIC
Imbalance between clotting activity and fibrinolysis
2. Hemophilia
Deficiency in blood clotting factor
a. A (factor VIII)
b. Von Willebrand’s disease (angiohemophilia)
c. Christmas disease (hemophilia B, factor IX)
d. C (factor XI)
3. Purpuras
Hemorrhagic rashes occurring in the superficial skin layer
a. Idiopathic thrombocytopenic purpura – decreased platelets
b. Henoch-Schonlein syndrome – increased vessel permeability

Respiratory
disorders
Children
Parameters Children Adult
RR High Low
HR High Low
Blood and muscle

Low High
lactate levels
Blood flow to the

High Low
active muscles
Exercise blood
Low High
pressure
Stroke volume during

Low High
exercise

Nursing care
EXPECTORANT THERAPY TO IMPROVE O2
Oral fluid O2 administration
Liquefying agents Pharmacologic therapy
Humidification Nasal sprays
Vaporizers Corticosteroid
Metered-dose inhaler Antihistamines
Nebulizers Expectorants
Effective coughing Bronchodilators
Chest physiotherapy Incentive spirometry
Mucus-clearing device Breathing techniques
Tracheostomy

Choanal atresia Acute nasopharyngitis
Congenital obstruction of Viral infection

the posterior nares Rhinovirus, coxsackie
virus, respiratory
Unilateral or bilateral syncytial virus,
adenovirus,
parainfluenza, influenza
With signs of respiratory Stress
distress at birth
Characterized by DHN

PHARYNGITIS TONSILITIS
Inflammation of the pharynx Infection of the palatine

by Group A beta hemolytic tonsils
Strep
Sx:
Sx: Fever, halitosis, drooling
Fever, sore throat, enlarged lethargy, and enlarged
regional lymph node, and bright red tonsillar tissues
erythematous pahrynx

SINUSITIS CROUP
Staph, Strep, H. influenzae Inflammation of the trachea,

larynx, and major bronchi
Fever, headache, purulent Staph, Strep, H. influenzae (3-6

discharge, tenderness yo), parainfluenza (6 mo-3 yo)
LARYNGITIS
EPIGLOTITIS
Brassy voice, inability to Pneumococci, echovirus

make audible sounds
3-6 years old
Stridor, high fever, drooling

Respiratory distress syndrome
Hyaline membrane disease among preterm infants
Deficiency of surfactant
Atelectasis of alveoli; leads to release of proteinaceous fluid
decreasing the total lung capacity

Aggravated by an overly Clinical presentation:
compliant chest wall, Progressively severe
infection and shunt distress
• Tachypnea
Worsening atelectasis and • Nasal flaring
increasing oxygen • Grunting
requirement over 48-72 • Cyanosis or pallor on
room air
hours followed by
• Retractions
diuresis and
improvement (or death)

Laboratory work ups: Medical management:
CXR: uniform reticulogranular Corticosteroids 48H prior birth
pattern and air bronchograms
(salt and pepper)
Surfactant via intratracheal
route
ABG: acceptable level is Pao2 of
50-70 mmHg, Paco2 of 45-60
mmHg, pH of 7.25 of above, Mechanical ventilation
O2 sat at 89-95%
Fluid and nutritional support
Septic work up, CBC,
electrolytes Sedation

Nursing interventions: WOF side effects of
Monitor color, respiration and surfactant: bradycardia and
effort O2 desaturation
General nursing care for Percussion and vibration

intubated patients
Encourage bonding and BF
Monitor ABGs

Asthma
Symptomatology is the same as in adults
Β2-adrenergic receptor agonists:

Albuterol (Ventolin proventil)
Metaproterenol (Alupent)
SE: tremors, nervousness, dizziness, tahycardia,

high BP, nausea, headache, rebound bronchospasm

Pneumonia
a. Viral pneumonia
Diminished breath sounds, low grade fever, nonproductive cough,
fine rales, diffused infiltrated areas
b. Primary atypical pneumonia

Fever, chills, anorexia, headache, malaise and muscle pain,
nonproductive cough to serosanguinous
M. Pneumoniae
c. Bacterial pneumonia
Acute onset of fever, hacking and nonproductive cough and
diminished breath sounds/scattered crackles

Cystic fibrosis
Inherited condition
marked by abnormal
exocrine gland function
and resulting
multisystem disorder
(respi and GI) in
response to thickened
secretions and
obstructions

Cystic fibrosis
Respiratory symptoms
Viscous secretions which

obstruct then lead to
hypoxia, infection, COPD
Wheezing, dry cough,

increasing RDS, impaired gas
exchange, barrel-shaped
chest, bronchitis and
pneumonia

Cystic fibrosis
GI symptoms Integumentary symptoms
Meconium ileus, bulky,
malodorous, frothy stools,
Salty sweat
Rectal prolapse as a complication Sweat test (Pilocarpine
iontophoresis)
Normal: 40-60 mEq/L

Cystic fibrosis
Management: Psychosocial support:
Chest phyisotherapy BID Encourage to participate in
age appropriate activities
Aerosolized recombinant
human deoxyribonuclease Use play in health teaching
High protein, high calorie diet Refer for genetic counseling

Excretory disorders
Children
Damaged glomerular capillary membrane
Loss of plasma protein (albumin)
hypoalbuminemia
Stimulates synthesis of lipoproteins
Decreased oncotic pressure

Hyperlipidemia
Generalized edema
(fluids moves from vascular space to extracellular fluid)
Activation of rennin-angiotensin system
Nephrotic syndrome Sodium retention
Edema

Assesment and Diagnostic
Methods:
• Proteinuria (exceeding 3 to 3.5 g/day)
• Microscopic hematuria, urinary casts
• Needle biopsy of the kidney for histologic examination to confirm
diagnosis

Nursing management
• Bed rest for a few days to promote diuresis and reduce edema
• Diet with high biologic protein (0.8 g/kg/day) to replenish urinary
losses.
• Low sodium, low saturated fat, liberal potassium

Glomerulonephritis
Immunologic processes involving the urinary

tract predominantly affecting the renal
glomerulus.
Affects both kidneys equally; tubular,

interestitial, and vascular changes also occur

Hypospadia
Surgery between 16-18 mos

End of lecture…
tnx

Common Problems Diseases and Disorders in Infants

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Common Problems Diseases and Disorders in Infants

Uploaded by

Copyright:

Available Formats

Common Problems,

Diseases, and Disorders

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 1

b. Syndactyly – two fingers

Surgery is the intervention

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 4

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 5

• Treatment: Polydactyly is often treated with

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 6

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 7

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 8

• During Z-plasty, incisions will split the excess

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 10

• Passive stretching exercises

• Surgery, then neck

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 13

• Deformed face and orbits

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 14

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 17

• X-ray: abnormal flaring of

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 18

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 19

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 20

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 21

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 22

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 24

Cavus: the foot has a high

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 25

Equinus: the foot is pointed

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 27

• It is a standard treatment for club foot.

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 28

• Change diapers frequently

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 30

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 31

• Six times more common in females

Good diaper care Worn continuously Teach on neurovascular

•Apply ointment: A & D, •Skin assessment

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 33

Younger children (2-7)

Getting well is conditional

Fourth graders (7-10)

Passive role in getting well

Eighth graders (13 above)

Active role in getting well

Anxiety r/t separation from parents

Fear r/t diagnostic and therapeutic

Parental health-seeking behavior

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 36

•X-ray, bone scan, arthroscopy,

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 38

• Impaired physical mobility r/t cast on leg.

• Self-esteem disturbance r/t continued use of body

• Diversional activity deficit r/t the need for imposed

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 39

After removal: check pedal pulses;

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 40

Weight on the grip

03/25/20 07:28 AM COMMON PROBLEMS IN CHILDREN 41

Assess perfusion status

Do not move weights

Separates opposing bones to encourage new growth

Lengthens the bone