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DISORDERS OF SCHOOL-AGE
CHILDREN
1
Diabetes in Children
Type 1 DM is the most common type in children,
accounting for two thirds of new cases in children of
all ethnic groups. It is one of the most common
chronic childhood diseases, occurring in 1 in 350
children by age 18; the incidence has recently been
increasing, particularly in children < 5 yr. Although
type 1 can occur at any age, it typically manifests
between age 4 yr and 6 yr and between 10 yr and
14 yr.
In type 1 DM, the pancreas produces
no insulin because of autoimmune destruction of
pancreatic beta-cells, possibly triggered by an
environmental exposure in genetically susceptible
people. Close relatives are at increased risk of DM,
with overall incidence 10 to 13% (30 to 50% in
monozygotic twins). Children with type 1 DM are at
higher risk of other autoimmune disorders,
particularly thyroid disease and celiac disease.
Inherited susceptibility to type 1 DM is determined
by multiple genes (> 60 risk loci have been
identified). Susceptibility genes are more common
among some populations and explain the higher
prevalence of type 1 DM in certain ethnic groups
(eg, Scandinavians, Sardinians).
In type 1 DM, lack of insulin causes
hyperglycemia and impaired glucose utilization
in skeletal muscle. Muscle and fat are then
broken down to provide energy. Fat breakdown
produces ketones, which cause acidemia and
sometimes a significant, life-threatening
acidosis (diabetic ketoacidosis [DKA]).
Diabetes Management In Early
Childhood
5
Type 1 Diabetes in Young Children
Epidemiological Trends
 Type 1 diabetes has increased in incidence
and prevalence during the late 20th and early
21st centuries.
 During this time period there has been a shift
towards a younger age of onset.
6
Challenges of Caring for Young Children With
Diabetes
 Unpredictable eating patterns
 Unpredictable activity patterns
 Hypoglycemic unawareness
 Periods of rapid growth
 Susceptibility to communicable illness
 Evolving understanding of what diabetes is
and how it impacts identity
 Need for age-appropriate developmental
experiences
8
Unpredictable Eating Patterns
Insulin
9
Unpredictable Activity Patterns
14
Unpredictable Activity Patterns
Hypoglycemia
 Hypoglycemia is the main risk factor when children are
active
 Insulin cannot be turned off or limited once it is
delivered
 Young children are unaware of symptoms of
hypoglycemia, and older children miss symptoms when
focused on activity
 Young children are less likely to experience a blood
glucose raising adrenaline response during vigorous
activity
Unpredictable Activity Patterns
Hypoglycemia
 Too little carbohydrate to sustain prolonged
activity
 Too much insulin available or “on board”
 Unplanned activity
 Swimming and sledding
Unpredictable Activity Patterns
Hyperglycemia
 Too little insulin before during, and/or after
exercise
 Too much carbohydrate consumed before or
during exercise
 Unplanned naps
 Rainy days
Unpredictable Activity Patterns
Tools
18
Unpredictable Exercise Patterns
Carbohydrate Adjustment
 Estimate 5-15 grams of extra carbohydrate for every 30
minutes of vigorous activity depending on body weight and
intensity of activity
 Add fat and protein to help carbohydrate last longer during
activity
 Decrease carbohydrate and fat content of meals and
snacks on low activity days if child is not underweight
Hypoglycemic Unawareness
Hypoglycemic Unawareness
 Increase blood glucose monitoring during and
after activity
 Increase blood glucose monitoring during
episodes of illness
 Consider use of continuous glucose
monitoring device in consultation with
diabetes care providers
Periods of Rapid Growth
Periods of Rapid Growth
 Adequate insulin is needed to utilize carbohydrate for
growth. Children with diabetes who do not get enough
insulin will grow and gain more slowly than would be
predicted by their genetics.
 Children who have frequent episodes of low blood sugar
and/or whose caretakers are unusually frightened by
hypoglycemia may gain excess weight
 Hormones that accompany rapid growth cause increased
insulin resistance
 Growth hormone is usually active during periods of deep
sleep causing a young child to have different daily
patterns of insulin need than an older child has
Susceptibility to Communicable Illness
25
Susceptibility to Communicable Illness
 Children’s day to day activities bring them into contact
with a variety of viral and bacterial illnesses
 Even mild viruses such as colds can increase insulin
requirements
 Gastrointestinal illnesses with vomiting and diarrhea
can result in poor absorption of carbohydrate and
dehydration causing blood glucose to fall and ketones
to rise.
 Management of “sick days” requires frequent blood
glucose and ketone monitoring, assessment of fluid
and carbohydrate intake, and regular contact the child’s
diabetes team as needed.
26
Susceptibility to Communicable Illness
 Be sure you have a copy of and understand your
diabetes team’s sick day protocol.
 Check your supply and the expiration date of
ketone strips regularly.
 Use blood ketone strips for assessing ketones on
sick days if possible.
 Discuss when use of “mini-glucagon” injections
might be use with your diabetes team.
27
DEFINITION:
 Acute rheumatic fever is a systemic disease
of childhood ,often recurrent that follows
group A beta hemolytic streptococcal infection
 It is a diffuse inflammatory disease of
connective tissue primarily involving heart,
blood vessels, joints, subcutaneous tissue
and CNS
Etiology
 Beta hemolytic streptococci.
 Genetic
Epidemiology
Ages 5-15 yrs are most susceptible
Rare <3 yrs
Girls>boys
Environmental factors--over crowding,
poor sanitation, poverty,
 Incidence more during fall ,winter & early
spring
Pathogenesis
Delayed immune response to infection
with group A beta hemolytic
streptococci.
After a latent period of 1-3 weeks,
antibody induced immunological
damage occur to heart valves, joints,
subcutaneous tissue & basal ganglia of brain.
Pathologic Lesions
Fibrinoid degeneration of connective tissue,
inflammatory edema, inflammatory cell
infiltration & proliferation of specific cells
resulting in formation of Ashcoff nodules,
resulting in-
-Pancarditis in the heart
-Arthritis in the joints
-Ashcoff nodules in the subcutaneous
tissue
-Basal gangliar lesions resulting in chorea
Clinical Features
 Flitting & fleeting migratory polyarthritis, involving major
joints
 Commonly involved joints-knee, ankle, elbow & wrist
 Occur in 80%,involved joints are exquisitely tender
 In children below 5 yrs arthritis usually mild but carditis
more prominent
 Arthritis do not progress to chronic disease
1.Arthritis
Clinical Features
 Manifest as pancarditis(endocarditis, myocarditis
and pericarditis),occur in 40-50% of cases
 Carditis is the only manifestation of rheumatic fever that
leaves a sequelae & permanent damage to the organ
 Valvulitis occur in acute phase
 Chronic phase- fibrosis,calcification & stenosis of heart
valves(fishmouth valves)
2.Carditis
Clinical Features (Contd)
 Occur in 5-10% of cases
 Mainly in girls of 1-15 yrs age
 May appear even 6/12 after the attack of rheumatic
fever
 Clinically manifest as-clumsiness, deterioration of
handwriting, emotional lability or grimacing of face
 Clinical signs- pronator sign, jack in the box sign ,
milking sign of hands
3.Sydenham Chorea
Clinical Features
 Occur in <5%.
 Unique,transient,serpiginous-looking lesions of 1-2
inches in size
 Pale center with red irregular margin
 More on trunks & limbs & non-itchy
 Worsens with application of heat
4.Erythema Marginatum
Clinical Features (Contd)
 Occur in 10%
 Painless, pea-sized, palpable nodules
 Mainly over extensor surfaces of
joints,spine,scapulae & scalp
 Associated with strong seropositivity
5.Subcutaneous nodules
Clinical Features
 Fever-(up to 101 degree F)
 Arthralgia
 Pallor
 Anorexia
 Loss of weight
Other features (Minor features)
Laboratory Findings
 High ESR
 Anemia, leukocytosis
 Elevated C-reactive protein
 ASO titer >200 Todd units.
(Peak value attained at 3 weeks, then comes
down to normal by 6 weeks)
 Throat culture-B H streptococci
Laboratory Findings (Contd)
 ECG- prolonged PR interval, 2nd or 3rd
degree blocks,ST depression, T inversion
 2D Echo cardiography- valve edema,mitral
regurgitation, LA & LV dilatation, and
decreased contractility
05/05/1999
41
Treatment
 Step I - primary prevention
(eradication of streptococci)
 Step II - anti inflammatory treatment
(aspirin,steroids)
 Step III- supportive management &
management of complications
 Step IV- secondary prevention
(prevention of recurrent attacks)
05/05/1999
Dr.Said Alavi
43
05/05/1999
Dr.Said Alavi
44
STEP I: Primary Prevention of Rheumatic Fever
(Treatment of Streptococcal Tonsillopharyngitis)
Agent Dose Mode Duration
Benzathine penicillin G 600 000 U for patients Intramuscular Once
27 kg (60 lb)
1 200 000 U for patients >27 kg
or
Penicillin V Children: 250 mg 2-3 times daily Oral 10 d
(phenoxymethyl penicillin) Adolescents and adults:
500 mg 2-3 times daily
For individuals allergic to penicillin
Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d
Estolate (maximum 1 g/d)
or
Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d
(maximum 1 g/d)
Recommendations of American Heart Association
Arthritis only Aspirin 75-100
mg/kg/day,give as 4
divided doses for 6
weeks
(Attain a blood level 20-
30 mg/dl)
Carditis Prednisolone 2-2.5
mg/kg/day, give as two
divided doses for 2
weeks
Taper over 2 weeks &
while tapering add
Aspirin 75 mg/kg/day
for 2 weeks.
Continue aspirin alone
100 mg/kg/day for
another 4 weeks
Step II: Anti inflammatory treatment
Clinical condition Drugs
 Bed rest
 Treatment of congestive cardiac failure: -
digitalis,diuretics
 Treatment of chorea:
-diazepam or haloperidol
 Rest to joints & supportive splinting
3.Step III: Supportive management &
management of complications
05/05/1999
Dr.Said Alavi
47
STEP IV : Secondary Prevention of Rheumatic Fever
(Prevention of Recurrent Attacks)
Agent Dose Mode
Benzathine penicillin G 1 200 000 U every 4 weeks* Intramuscular
or
Penicillin V 250 mg twice daily Oral
or
Sulfadiazine 0.5 g once daily for patients 27 kg (60 lb Oral
1.0 g once daily for patients >27 kg (60 lb)
For individuals allergic to penicillin and sulfadiazine
Erythromycin 250 mg twice daily Oral
*In high-risk situations, administration every 3 weeks is justified and
recommended
Recommendations of American Heart Association
05/05/1999
Dr.Said Alavi
48
Duration of Secondary Rheumatic Fever
Prophylaxis
Category Duration
Rheumatic fever with carditis and At least 10 y since last
residual heart disease episode and at least until
(persistent valvar disease*) age 40 y, sometimes lifelong
prophylaxis
Rheumatic fever with carditis 10 y or well into adulthood,
but no residual heart disease whichever is longer
(no valvar disease*)
Rheumatic fever without carditis 5 y or until age 21 y,
whichever is longer
*Clinical or echocardiographic evidence.
Recommendations of American Heart Association
Prognosis
 Rheumatic fever can recur whenever the
individual experience new BH streptococcal
infection, if not on prophylactic medicines
 Good prognosis for older age group & if no
carditis during the initial attack
 Bad prognosis for younger children & those
with carditis with vulvar lesions
Juvenile
Idiopathic
Arthritis
Introduction
 Juvenile rheumatoid arthritis (JRA), is the most common
chronic rheumatologic disease in children and is one of
the most common chronic diseases of childhood.
 The etiology is unknown, and the genetic component is
complex, making clear distinctions between the various
subtypes difficult.
 A new nomenclature, juvenile idiopathic arthritis (JIA), is
being increasingly used to provide better definition of
subgroups.
51
Signs and symptoms
History findings in children with JIA may include the following:
 Arthritis present for at least 6 weeks before diagnosis (mandatory
for diagnosis of JIA)
 Either insidious or abrupt disease onset, often with morning
stiffness or gelling phenomenon and arthralgia during the day
 Complaints of joint pain or abnormal joint use
 History of school absences or limited ability to participate in
physical education classes
 Spiking fevers occurring once or twice each day at about the same
time of day
 Evanescent rash on the trunk and extremities
 Psoriasis or more subtle dermatologic manifestations
Physical findings are important to provide criteria for
diagnosis and to detect abnormalities suggestive of
alternative etiologies, as well as to indicate disease
subtypes. Such findings include the following:
Arthritis: Defined either as intra-articular swelling on
examination or as limitation of joint motion in association
with pain, warmth, or erythema of the joint; physical
findings in JIA reflect the extent of joint involvement
Synovitis: Characterized by synovial proliferation and
increased joint volume; the joint is held in a position of
maximum comfort, and range of motion often is limited
only at the extremes
Types of JIA include the following:
 Systemic-onset juvenile idiopathic arthritis
 Oligoarticular juvenile idiopathic arthritis
 Polyarticular juvenile idiopathic arthritis
 Psoriatic arthritis
 Enthesitis-related arthritis
 Undifferentiated arthritis
 Arthritis must be present for 6 weeks before the
diagnosis of juvenile idiopathic arthritis (JIA) can be
made.
 Disease onset is either insidious or abrupt, with
morning stiffness or gelling phenomenon (ie, stiffness
after long periods of sitting or inactivity) being a
frequent complaint and arthralgia occurring during the
day.
 A morning limp that improves with time may be noted,
and a toddler may no longer stand in the crib in the
morning or after naps.
 Complaints of joint pain may not be predominant in the
patients’ history, however; children often stop using joints
normally (eg, develop contractures of joints, decreased
wrist range, limp) rather than complain of pain. Up to a
quarter of children with oligoarticular JIA have no pain.
 Individuals with JIA may have a history of school
absences, and their ability to participate in physical
education classes reflects the severity of the disease or
acute flares.
Physical Examination
 JIA is a clinical diagnosis. A complete physical
examination is critical for the diagnosis.
 Physical findings are important to provide criteria for
diagnosis and to detect abnormalities suggestive of
alternative etiologies.
 The diagnosis of JIA is based on the physical finding of
arthritis in at least 1 joint that has persisted for at least 6
weeks, with other causes excluded, in an individual
younger than 16 years.
Systemic-onset JIA
 A definite diagnosis of systemic-onset JIA must await
the development of arthritis. This may occur at onset of
the fever and rash or may lag by months or, rarely,
years.
Physical examination findings include
the following:
 The child appears
systemically ill
 Arthralgia is often present
 The child may have
generalized myalgia
 Evanescent, salmon-pink,
macular rash (often linear)
is found, predominantly on
the trunk and the
extremities; this rash, seen
in the image below, is
associated with fever spikes Systemic juvenile idiopathic arthritis
(JIA) rash
62
 Hepatosplenomegaly is often
present
 Lymphadenopathy is
sometimes present,
especially the axillary lymph
nodes
 Muscle tenderness to
palpation may be observed
 Serositis, including pleural
and pericardial effusions,
may be present, as is noted
in the image below
Child with pericardial effusion
due to systemic onset juvenile
idiopathic arthritis
 Chest pain or shortness of breath may be a sign of
pericarditis or pleuritis
 Friction rub may occur in pericarditis but can be absent
with a large pericardial effusion
 S3, basilar rales, and hepatomegaly suggestive of heart
failure may rarely be observed when myocarditis
occurs in individuals with systemic-onset JIA
Oligoarticular JIA
Characteristics of
oligoarticular JIA include
the following:
 In individuals with
oligoarticular JIA, 4 or
fewer joints (and in many
cases, only 1 joint) are
affected
 Large, weight-bearing
joints, such as the knees
and ankles, are typically
affected.
Eighteen-month-old girl with arthritis in
her right knee. Note the flexion
 Children appear to be well, despite ambulating with a
limp
 In cases of asymmetrical arthritis, chronic inflammation-
related hyperemia in a knee or ankle may lead to
overgrowth of that limb with subsequent leg-length
discrepancy
 Muscle atrophy, often of
extensor muscles (eg, vastus
lateralis, quadriceps when
the knee is affected), may
occur
 Flexion contractures in the
knees and, less commonly,
the wrists are found
 Involvement of a few small
joints in the hands is atypical
and suggests eventual
development of polyarticular
JIA or psoriatic arthritis.
Dactylitis, or diffuse
tenosynovitis of a finger or
toe, also called a "sausage
digit," is more typical of
psoriatic arthritis or
enthesitis-related arthritis.
 Children who are at lesser risk (ie, have polyarticular
disease and are ANA negative), are screened every 6
months for 7 years and then yearly. Children with
systemic JIA are at very low risk and are screened
yearly.
 Acute anterior uveitis is one of the diagnostic criteria for
enthesitis-related arthritis. These children with are
screened initially and if symptomatic.
 Older children with RF-positive polyarticular JIA should
probably be screened yearly. There are few data on
these children regarding their risk for uveitis.
Sequelae of chronic anterior uveitis. Note the posterior synechiae
(weblike attachments of the pupillary margin to the anterior lens
capsule) of the right eye secondary to chronic anterior uveitis. This
patient has a positive antinuclear antibodies (ANAs) and initially
had a pauciarticular course of her arthritis. She now has
polyarticular involvement but no active uveitis.
Polyarticular Juvenile Idiopathic
Arthritis
In polyarticular juvenile idiopathic arthritis, 5 or more joints
are affected in the first 6 months after disease onset,
weight-bearing joints are affected, rheumatoid nodules
may be seen in patients with RF-positive disease, and
symmetrical involvement of small joints in the hands is
often found, as seen in the images below.
Patient with active polyarticular arthritis. Note swelling (effusions) of
all proximal interphalangeal (PIP) joints in addition to boney
overgrowth. Also note lack of distal interphalangeal joint (DIP)
involvement. The patient has interosseus muscle wasting
(observed on the dorsum of the hands), and subluxation and ulnar
deviation of the wrists are present.
Decreased extension of the cervical spine is often asymptomatic. It is
indicative of arthritis of the cervical spine and can lead to subluxation,
typically of the C2 vertebra on C3. Fusion of the posterior elements of the
vertebra may occur.
Flexion and extension views of C-spine in child with poorly controlled
polyarticular juvenile idiopathic arthritis (JIA).
Treatment
The ultimate goals in managing rheumatoid arthritis are to
prevent or control joint damage, to prevent loss of function,
and to decrease pain. These goals are particularly important in
juvenile idiopathic arthritis (JIA), in which the rate of progression
and the onset of debility can be rapid. JIA is a chronic disease
characterized by periods of remission and flare. Treatment is
aimed at inducing remission with the least toxicity from
medications with hopes of inducing a permanent remission.
The success of therapy is monitored best with repeated
physical examinations and history. The number of joints
involved and the duration of morning stiffness should
demonstrate continued decrease, with elimination reflecting
success. Surgery may be indicated in patients who are
unresponsive to medical therapy.
 A team-based approach to the treatment of JIA can be
helpful. Management may include 1 or all of the following
areas:
 Pharmacologic therapy with nonsteroidal anti-
inflammatory drugs (NSAIDs), disease-modifying
antirheumatic drugs (DMARDs), biologic agents, or intra-
articular and oral corticosteroids
 Psychosocial interventions
 Measures to enhance school performance (eg, academic
counseling)
 Improved nutrition
 Physical therapy
 Occupational therapy
Scabies & Pediculosis
Infestation
Infestation is the presence of animal
parasites on or in the body, is common in
tropical countries and less so in temperate
ones.
Infestations fall into two main groups:
1 those caused by arthropods; and
2 those caused by worms.
EPIDEMOLOGY
 women & children
 urban areas,
 winter
 Prevalence 4 – 100%
Transmission
directly by close personal contact, sexual
indirectly via fomites
 factors
overcrowding
delayed treatment of primary cases
 public awareness
 highly host-specific
 an arthropod a member of the class
Arachnida, subclass Acari, order
Astigmata, and family Sarcoptidae.
 Too small to be seen by the naked eye
 Adult female measures ~ 0.4 - 0.3
mm, &
 the smaller male 0.2 - O.15 mm
 body is creamy white & is marked by transverse
corrugations,
 ovoid
 four-pairs of legs -
anterior two pairs end in elongated peduncles tipped
with small suckers,
In the female, the rear two pairs of legs end in long
bristles, whereas in the male bristles are present on
the third pair and peduncles with suckers on the
fourth.
 crawl at a rate of 2.5 cm/min, burrow through the
stratum corneum at the rate of about 2 mm per
day(0.5 - 5 mm/day)
 number - <20 & with crusted scabies
can be thousands to millions
live mites can survive for up to a week
in the environment, feeding on the
sloughed stratum corneum
 cannot fly or jump
Mating takes place once, and the female is
fertile for the rest of her life (1 mo),
Copulation in a small burrow---------the
male, falls off the skin & perishes---------
Fertilized female enlarges the burrow
using proteolytic enzymes to dissolve the
stratum corneum of the epidermis -----
begins egg laying (3 eggs a day each)
Six-legged larvae emerge from the eggs
after 3-4 days
90% of the hatched mites die
Escape from the burrow by cutting through
its roof------then dig short burrows called
moulting pouches & transform into nymphs--
-----------After further moult into larger
nymphs , adult males and females develop(in
2-3 weeks)
Clinical features
 IP- 2-6 weeks
 immediate symptoms –in re infection
 Triad`s
 Pruritic papular lesions,
 Excoriations, and
 Burrows
Site- The circle of Hebra ~ an imaginary circle
intersecting the main sites of involvement - axillae,
elbow flexures, wrists & hands, & crotch
Cont......
Pruritis
○ accentuate at night & exacerbated by a hot bath
or shower
 Primary lesions of scabies
- burrows, papules, pustules, nodules,
occasionally urticarial papules and
plaques
 interdigital webbing of the hands,
 flexural aspect of the wrists, behind the
ears, axilla, waist, ankles, feet, buttocks
& belt area
 penile & scrotal in men, areola, nipples
& genital area in women
Distribution of lesions
In very young children, infants,
elderly and immunocompromised
hosts, a widespread eczematous
eruption primarily on the trunk is
common , scalp & face can also be
affected.
 The burrow
 pathognomonic sign and represent the
intraepidermal tunnel created by the
moving female mite.
 a 1-10 mm tunnel
 serpiginous, greyish-white
thread-like elevations
 At the end of it a vesicle/pustule containing
the mite may be noted, especially in infants &
children
at entry, slight scale
 In infants, commonly located on
the palms & soles : F
To identify burrows quickly:
 apply a drop of India ink or
gentian violet to the infested area,
 remove it with alcohol
 Thin threadlike burrows retain
the ink
 Erythematous Papules & Vesicles (filled with serous fluid)
rarely contain mites and most likely are due to a
hypersensitivity reaction
 Papules= on the shaft of the penis & scrotum in men
& on nipples in women
 Vesicles= on the palms & soles
 Animal Scabies: Zoonotic scabies
 affect humans who come in close contact with the
animal
 incubation period is shorter, the symptoms are
transient
 usually manifests with vesicles & papules with atypical
distribution
 Burrows are usually absent
 runs a self-limited course, require no treatment
Mites from animals are not a source of human
infestation, but they can produce bite reactions
 Asymptomatic infestation
 not uncommon
 considered ‘carriers’
Secondary scabies lesions
With rubbing- secondary infection, -
the host immune response against the
mites and their products.
 Excoriations, Lichenification,
widespread eczema, honey-colored
crusting, postinflammatory
hyperpigmentation, erythroderma, and
frank pyoderma
Variants
Nodular scabies
 in 7-10% of patients with active scabies
 Pink, tan, brown, or dull red nodules
(2-20 mms)
 May or may not itch
 Persist on the scrotum, penis, and
vulva and In neonates
unable to scratch, pinkish-brown nodules may develop
 usually sterile
 Intralesional steroids, tar, or excision are methods of
treatment
Bullous scabies
 Mimics BP both clinically &
histologically (contain many
eosinophils)
 Vesicles and bullae-, particularly on
the palms & fingers
 Immunofluorescent
 In immunocompromised / debilitated
patients, including those with:
 neurologic disorders, Down syndrome,
organ transplants, graft-versus-host
disease, adult T-cell leukemia, leprosy, or
AIDS and institutionalized populations
 Risk factors for profound infestation
-an inability to mount an immune response,
perceive pruritis, and/or physically scratch
the skin
Crusted scabies
(Norwegian/hyperkeratotic scabies)
* marked thickening and crusting of
the skin.
* Hyperkeratotic, crusted/scaling
lesions teem with mites
* large areas with prominent scalp
lesions,
hands and arms are usual locations
* Swollen & crusted finger tips; &
dystrophic nails
Contd...
The rest of the skin usually appears diffusely
xerotic
highly contagious
Severe fissuring & scaling of the genitalia &
buttocks may be present
Oral agent should be used in conjunction with a
topical agent
DDx
Crusted scabies
 Psoriasis
 Seborrheic dermatitis
Treatment
 In infants with extensive involvement, several re
treatments a week apart occasionally be required
 second application of topical medication.......
 Treat simultaneously all household contacts (even with
no symptoms)
Contd...
Pediculosis
 Phthiraptera family
 Order Anoplura-blood-sucking (***solenophages)
ectoparasites of mammals
 Pediculus capitis, the head louse
 Pediculus humanus, the clothing or body louse &
 Pthitrus pubis, the pubic or crab louse
 ingest blood, & produce skin lesions by mechanical
puncture( stylet, haustellum) & injecting toxic secretions
Pediculosis Capitis
Head lice
 in school-aged children, 3-12yr, 10%of children : F
 affect all levels of society & all ethnic groups
 Prevalence= 6 to 12 million infestations/year
 incidence is low among African Americans
 spread by close physical contact
 sharing of head gear, combs, brushes, & pillows
Etiology & Pathogenesis
 is 1 to 2 mm long,
 elongated,
 greyish white flattened dorsoventrally, &
 wingless
 three pairs of sharp clow- grasp hairs and for feeding
 feed approximately five times each day
 5 - 10 eggs a day
 can travel up to 23 cm/min
 The larva, called a nymyh/instar, looks like a miniature
adult louse
 1 - 2 days (4 days) away from the scalp (Nits up to 10 days)
 30 days
 *Head lice do not carry or transmit any human disease.
 hatches in 8 to 10 days, and reaches maturity in
approximately 18 days. Nits are .8mm, with operculum
Clinical findings
 Louse - occipital and retro auricular regions
 <20 but in 5% >100
 Itching or can be asymptomatic
a result of hypersensitivity reaction to the
saliva & faecal matter produced by the
louse during feeding
Sensitization - 3-8month
 hemorrhagic crust
 Excoriations, lymphadenopathy, &
conjunctivitis(redness &swelling) may be
observed
Diagnosis
 Identification of live adult lice, immature nymphs,
and/or viable-appearing eggs
 Live nits(egg cases) placed in close proximity to the
scalp(parietal & occipital)
 Have proteinaceou sheath
 cemented to the hair shaft with chitinous material
secreted by the female accessory glands
C0MPLICATIONS
 Excoriation ----- Secondary bacterial infections
Pediculosis corporis(Body/clothing
lice)
EPIDEMIOLOGY
 low of socio-economic
 in urban public hospitals
 No predilection for race, age, or sex
 contaminated clothing or bedding
ETIOPATHOGENESIS
 Body Iouse/P. humanus var humanus
 lifespan -18 days
 270 to 300 ova
 2-4mm
 3 day,with out meal
 comes to the surface only for meal
CLINICAL FEATURES
 linear excoriations primarily
 Occasionally, a macula ceruleae (Iiterally, sky-
blue spot)
a blue to slightly slate-colored
macule.............bruise-like lesion (~1.5 cm) &
often with a central punctum 2nd to altered
blood pigments in clothing binds (waistband,
buttocks & thighs) & is asymptomatic to
slightly pruritic
Contd...
Diagnosis
 examining the lining of
the clothing seams for
the presence of nits
 By shaking out the
clothing over a sheet of
newsprint,
 Nits that contain an
unborn louse fluoresce
white.
 Nits that are empty
fluoresce gray.
COMPLICATIONS
 Excoriation
 secondary infection with S. aureus, S. pyogenes &
other bacteria (impetigo & furunculosis)
 act as vectors for R.prowazekaii (epidemic typhus),
Bartonella quintana (trench fevers or endocarditis)
& Borrelia recurrentis (relapsing fever)
Pediculosis pubis (Pubic Lice)
EPIDEMIOLOGY
 most often are a
sexually
transmitted disease
 ~ 30 % of patients
have another
concurrent STI
 from one sexual
exposure with
an infested
partner is more
than 90%
 contaminated
clothing,
towels, or
beddings
ETIOPATH0GENESIS
 Pthiridae
 crab - naming
 second and third pairs of -to cling on to hair (pincer like claws)
 light brown
 0.8 to 1.2 mm in length
 ambulate up to 10 cm/day
 lifespan of 2 wks
 25 ova
 away from the human host for up to 36 hrs
 dog
CLINICAL FEATURES
 Pruritus
 Maculae ceruleae (sky-blue spots, (tache bleu), on inner
thighs or sides of trunk
 Bullous lesion
 adult organisms on the body ( ~ 10 - 25 or more)
 pubic hair, any hair bearing site can be affected,
eyelashes ((phthiriasis palpebrarum
○ in hirsute ~ short hairs of the thighs, trunk, &
perianal area
 nits near the base of the hair
 the duration of infestation can be approximated by
the distance of the nit from the skin surface
 The Skeletal System
 The skeleton is the name given to the collection of
bones that holds our body up. It does three major
jobs.
A. It protects our vital organs such as the brain,
the heart, and the lungs.
B. It gives us the shape that we have
C. It allows us to move..
 . When we were born our skeleton had around
350 bones. By the time we become an adult, we
will only have around 206 bones
Introduction
 Bone comes in several shapes and sizes the structure
and composition of bone is the same in all. Bone is
composed of protein , minerals and cells.
The main part are:
shaft
neck
head
A tumor is a lump or mass of tissue that forms
when cells divide uncontrollably. A growing
tumor may replace healthy tissue with abnormal
tissue. It may weaken the bone, causing it to
break (fracture).
A bone tumor is an abnormal growth of cells within the
bone that may be noncancerous (benign) or cancerous
(malignant).
Malignant
Benign
Fatal without treatment
May recur after removal
Rarely fatal
Rarely recur after removal
Rapid growth
Slow growth
Distant metastases , not
localized
No metastases , localized
The difference between
benign and malignant
tumors
 Enneking described the most widely used
staging system for (benign bone tumors )
The stages are denoted by the Arabic
numerals 1, 2, and 3, whereas malignant
bone tumors are classified by Roman
numerals (I, II, III).
Many benign bone tumors have the potential
to present at, and progress through, various
stages during their disease course.
Stage of benign tumors
 . Stage 1-LATENT, it do not have any
characteristics of growth or progressive
change, may resolve spontaneously.
 Stage 2-ACTIVE, lesion deform the host
bone but remain contained in bone, require
intralesional curettage.
 Stage 3-AGGRESSIVE , tumor extend
beyond the bone, require complete work-up
and a removal with wide margins to avoid
possible local recurrence.
Stage of benign bone
tumors
 The staging system for malignant tumor
adopted by the Musculoskeletal Tumor
Society, and originally developed by
( Enneking) is based on the histological
grade, the local extent(Tumors whether they
are intra-compartmental or extra-
compartmental)
and the presence or absence of metastasis
Stage of malignant bone
tumors
Stage IA is defined as G1 and Intra-
compartmental
Stage IB is G1 and extra-compartmental
Stage IIA is G2 and Intra-compartmental
Stage IIB is G2 and extra-compartmental
Stage III is G1 or G2, intra- or extra-
compartmental, and has evidence of metastasis
Stage of malignant bone
tumors
Bone
tumor
primary
Benign tumors:
for ex.
osteochondroma
malignant tumors: for ex
Ewing's sarcoma
secondary
Metastatic
tumors
Classification
 Is a tumor which have spread from other organs ,The
most common cancers that spread to the bone are
cancer of the:
1. Breast
2. Kidney
3. Lung
4. Prostate
5. Thyroid
These forms of cancer usually affect older people
metastatic tumors
1. Age
2. Combinations of radiation and chemotherapy for
treating prior cancer
3. Certain kinds of anti-cancer drugs (alkylating
agents)
4. Family history of bone cancer
5. An overactive parathyroid gland
6. Multiple benign tumors
7. Osteomyelitis
8. Radiation
Risk factors
1. Movement problems
2. Stiff bones
3. Bone lumps and masses
4. Bone tenderness
5. Anemia
6. Weight loss, Fatigue
7. Bone pain, may be worse at night
8. fevers and night sweats
9. Bone fracture, especially fracture from slight
injury (trauma)
10. Note: Some benign tumors have no symptoms
Clinical features
 The cause of bone tumors is unknown. They
often arise in areas of rapid growth
 Inherited genetic mutations
 Radiation
 Trauma
Causes
1. Delayed wound healing
2. Nutritional deficiency
3. Infection
4. Hypercalcaemia
5. Muscle wasting, bone weakening
6. Pathological fracture
7. Temporary burn to the skin and fatigue from
radiation therapy
Complications
8. Nausea, vomiting, mouth sores, hair loss, and lowered
resistance to infection from chemotherapy.
9. Infection of the surgical site and possible blood clotting
disturbances from surgery.
10. Pain
11. Spread of the cancer to other nearby tissues
(metastasis)
Complications
 Blood test
 Bone biopsy
 Bone scan computed tomography (CT).
 MRI ( magnetic resonance imaging )
 X-ray of bone
 CT scan
Diagnosis & Tests
Open Biopsy
Needle Biopsy
insert a needle into the tumor to remove
some tissue
small incision is made and the tissue is
removed
removal of a sample of bone tissue to test for
cancer cells.
Bone biopsy:
 Systemic therapy
 Local therapy 1.Chemotherapy
2. hormone therapy
3. Immunotherapy ex.
Interferon α
1.Radiation therapy
2. surgery
Nutritional therapy
• Provide foods high in protein,
vitamins and folic acid.
 Hormone therapy
removal of the organs which produce hormones
which can promote the growth of certain types of
cancer (such as testosterone in males and
estrogen in females), or drug therapy to keep the
hormones from promoting cancer growth.
 Chemotherapy
used to kill tumor cells when they have spread
into the blood stream
Systemic therapy
 Radiation Therapy
Radiation therapy uses high-dose x-rays to kill
cancer cells and shrink tumors. may be given
either before or after surgery
Local therapy
Surgical Treatment
 Amputation
 Rotationplasty
 Bone graft
 Artificial bone
removes all or part of an arm or leg when the tumor is large and/or
nerves and blood vessels are involved.
is a form of amputation, in which the patient's foot is turned
upwards in a 180 degree turn and the upturned foot is used as a
knee.
affected bone is removed, bone from elsewhere from
the body is taken.
affected bone is removed, putting an artificial bone in.
Local therapy
 Narcotics
 Analgesics
Ex. Biphosphonates
are drugs that can be used to reduce bone pain and
slow down bone damage in people who have cancer
that has spread to their bones and increase bone
strength
Ex. Metastron also known as strontium-89 chloride is
an intravenous medication given to help with the pain
and can be given in three month intervals
Pain medications
 Age: Bone tumor are more common in
children and young adults when bones grow
rapidly
 The incidence of bone cancer is higher in
families with familial cancer syndromes. The
incidence of bone cancer in children is
approximately 5 cases per million children
each year , in united states
Epidemiology
 Nursing assessment
 Nursing diagnosis
 Nursing planning
 Nursing Implementation
 Nursing evaluation
Nursing process
 Collection Of Subjective Data:
1. Bone pain in the area of the tumor, may be worse at night, pain is
generally described as dull and achy
2. pain may or may not get worse with activity
3. Fatigue, anxiety
 Collection Of Objective Data:
1. Bone lumps and masses determining the location and size of tumor
,soft tissue swelling
2. Stiff bones
3. Weight loss
4. Bone fracture, especially fracture from slight injury (trauma)
5. fevers and night sweats
6. Movement problems
7. Anemia
Nursing
assessment
Acute or
chronic pain
related to
the
pathologic
process and
surgery
Control
of pain
Administer analgesics
as necessary. Make sure
the patient has received
his analgesic before
morning care or any
activity that may increase
pain
Regularly monitor the
patient’s degree of pain
and the effectiveness of
analgesics and other pain
relief measures, such as
positioning or guided
imagery
Experiences no
pain or
decreased pain
Nursing
evaluation
Nursing Implementation
Nursing
Planning
Nursing
Diagnosis
1
Nursing
evaluation
Nursing
Implementation
Nursing
Planning
Nursing
Diagnosis
Deficient
knowledge
related to the
disease
process and
therapeutic
regimen
Giving
knowledge
about the
disease
process and
treatment
regimen
Promoting
understanding of the
disease process and
treatment
regimen(Provide foods
high in protein, vitamins
and folic acid)
Don’t give I.M.
injections or take rectal
temperature
During radiation
therapy or
chemotherapy, take
measures to reduce
adverse reactions, such
as providing the patient
with plenty of fluids to
drink and saline
mouthwash for gargling
Described
disease process
and treatment
regimen
2
Nursing
evaluation
Nursing Implementation
Nursing
Planning
Nursing
Diagnosis
Risk for
injury:
pathologic
fracture
related to
tumor and
metastasis
Absence of
complication
Absence of
pathologic
fracture
The effective extremities
must be supported and
handled gently
Exhibits absence of
complication
3
Nursing
evaluation
Nursing
Implementation
Nursing
Planning
Nursing
Diagnosis
Risk for
situational
low self-
esteem
related to
loss of body
part
Improved self-
esteem
(Promoting self –
Esteem)Try to help the
patient develop a
positive attitude toward
recovery and urge him
to resume an
independent lifestyle
Demonstrate
positive self –
concept
4
Nursing
evaluation
Nursing
Implementation
Nursing
Planning
Nursing
Diagnosis
Ineffective
coping
related to
fear of the
unknown
,perception
of disease
process
Effective
pattern of
coping
(Promoting coping
skills)Encourages the
patient and family to
verbalize their fears
,concerns, and
feelings
Demonstrates
effective coping
pattern
OBJECTIVES
1-Introduction of accidental prevention.
2-Developmental stages, common problems of each
stage and its prevention.
-Road Traffic Accidents(RTAs).
-Burns and Scalds.
-Electrocution.
-Drowning and Near-Drowning.
-Chocking, Suffocation and Strangulation.
-Poisoning.
-Cuts.
3-General safety precautions that need to be taken by
the parents or caregivers.
-Infants. –Toddlers
-Preschoolers.
-School Age Children.
-Adolescents
Introduction
Injury prevention
Injuries cause more deaths in children
between the ages of 1 and 4 years than
in any other childhood age-group except
adolescence.
Childhood accidents at home and
outside are common but preventable.
The age is the most important factor
that affects children to have accidents.
Developmental stages and Common
:
problems of each stage
Infant
Burns extremity fractures
choking head injuries
motor vehicle accident near drowning
toxic ingestions
Toddler
Burns extremity fracture
choking head injuries
motor vehicle accidents near drowning
toxic ingestions bicycle injuries
Preschooler
Burns extremity fractures
falls motor vehicle accidents
toxic ingestions bicycle injuries
School child
Extremity fractures
motor vehicle accidents
sports injuries
Adolescent
Extremity fractures
motor vehicle accidents
sports injuries
near drowning ( common among males)
The common accidents in children as per age and the
preventive measures to be taken in order to prevent
them as the following:
1-Road traffic accidents(RTAs)
RTAs are the most common type of accidents that leads to death on
children in our state. boys between the ages of 5 and 12 years are
mostly confronting this type of accidents in our place. Children of
this age are school going and will not able to estimate the speed of
vehicles or dangers of traffic while crossing roads. so children must
be taught the practical aspects of road safety through demonstration
classes.
RTAs
Child passengers
Bicycle accidents
Falls of other forms
Prevention
2-Burns and scalds
These are the second most common cause of death from accidents. Most of these deaths are
due to carelessness of parents or caretakers. Scalds from boiling water and hot drinks are
common among children especially in toddlers. The common victims of burns with kerosene
lamps are school age children, who will be studying near kerosene lamps.
Prevention
3-Electrocution
This is yet another cause of death in children.
Prevention
4-Drowning and near-drowning
Prevention
Drowning and near-drowning also cause death in children, especially in
preschoolers and school age children. children may get drowned in
streams, rivers, lakes, swimming pool and also in pits where water is
stagnated. Infants and toddlers are also not away from the risk of
drowning. This is usually occur at home. They get drowned in bathtubs and
water-filled vessels.
5-Choking, suffocation and strangulation
Children may choke on vomit, toy's parts or aspiration of food and
fluids. Children strangle themselves on curtains, cloth cradles,
beddings and even necklaces and neckties, some children try to
imitate TV and cinema scenes and get strangulated. Airway
obstruction from aspirated foreign bodies can be recovered using
Heimlich maneuver in older children.
Prevention
6-Poisoning
Prevention
Many children are admitted to hospital because
they have been poisoned by eating or drinking or
even inhaling poisonous substances. Some of these
children die. To prevent these types of deaths,
adults need to be vigilant. Substances such as
medicines, petrol, household cleaning materials,
etc., need to be stored high up so that children
can't reach them.
7-Cuts
Prevention
Cut injuries are also common among children. They
may use carelessly placed knives, razors and blades to
experiment. Sharp edges of furniture also can be
injuries to children.
General safety precautions that need to
be taken by the parents or caregivers
Infants Toddlers Preschoolers
Adolescents
References
Books
1. Writer :Patricia M , Dillon
Book :nursing health assessment
Edition :second edition
Pages :467_470
Year :2003
Nursing Care of Family with School age Disorders.pptx
Nursing Care of Family with School age Disorders.pptx

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Nursing Care of Family with School age Disorders.pptx

  • 2. Diabetes in Children Type 1 DM is the most common type in children, accounting for two thirds of new cases in children of all ethnic groups. It is one of the most common chronic childhood diseases, occurring in 1 in 350 children by age 18; the incidence has recently been increasing, particularly in children < 5 yr. Although type 1 can occur at any age, it typically manifests between age 4 yr and 6 yr and between 10 yr and 14 yr.
  • 3. In type 1 DM, the pancreas produces no insulin because of autoimmune destruction of pancreatic beta-cells, possibly triggered by an environmental exposure in genetically susceptible people. Close relatives are at increased risk of DM, with overall incidence 10 to 13% (30 to 50% in monozygotic twins). Children with type 1 DM are at higher risk of other autoimmune disorders, particularly thyroid disease and celiac disease. Inherited susceptibility to type 1 DM is determined by multiple genes (> 60 risk loci have been identified). Susceptibility genes are more common among some populations and explain the higher prevalence of type 1 DM in certain ethnic groups (eg, Scandinavians, Sardinians).
  • 4. In type 1 DM, lack of insulin causes hyperglycemia and impaired glucose utilization in skeletal muscle. Muscle and fat are then broken down to provide energy. Fat breakdown produces ketones, which cause acidemia and sometimes a significant, life-threatening acidosis (diabetic ketoacidosis [DKA]).
  • 5. Diabetes Management In Early Childhood 5
  • 6. Type 1 Diabetes in Young Children Epidemiological Trends  Type 1 diabetes has increased in incidence and prevalence during the late 20th and early 21st centuries.  During this time period there has been a shift towards a younger age of onset. 6
  • 7. Challenges of Caring for Young Children With Diabetes  Unpredictable eating patterns  Unpredictable activity patterns  Hypoglycemic unawareness  Periods of rapid growth  Susceptibility to communicable illness  Evolving understanding of what diabetes is and how it impacts identity  Need for age-appropriate developmental experiences 8
  • 10. Unpredictable Activity Patterns Hypoglycemia  Hypoglycemia is the main risk factor when children are active  Insulin cannot be turned off or limited once it is delivered  Young children are unaware of symptoms of hypoglycemia, and older children miss symptoms when focused on activity  Young children are less likely to experience a blood glucose raising adrenaline response during vigorous activity
  • 11. Unpredictable Activity Patterns Hypoglycemia  Too little carbohydrate to sustain prolonged activity  Too much insulin available or “on board”  Unplanned activity  Swimming and sledding
  • 12. Unpredictable Activity Patterns Hyperglycemia  Too little insulin before during, and/or after exercise  Too much carbohydrate consumed before or during exercise  Unplanned naps  Rainy days
  • 14. Unpredictable Exercise Patterns Carbohydrate Adjustment  Estimate 5-15 grams of extra carbohydrate for every 30 minutes of vigorous activity depending on body weight and intensity of activity  Add fat and protein to help carbohydrate last longer during activity  Decrease carbohydrate and fat content of meals and snacks on low activity days if child is not underweight
  • 16. Hypoglycemic Unawareness  Increase blood glucose monitoring during and after activity  Increase blood glucose monitoring during episodes of illness  Consider use of continuous glucose monitoring device in consultation with diabetes care providers
  • 18. Periods of Rapid Growth  Adequate insulin is needed to utilize carbohydrate for growth. Children with diabetes who do not get enough insulin will grow and gain more slowly than would be predicted by their genetics.  Children who have frequent episodes of low blood sugar and/or whose caretakers are unusually frightened by hypoglycemia may gain excess weight  Hormones that accompany rapid growth cause increased insulin resistance  Growth hormone is usually active during periods of deep sleep causing a young child to have different daily patterns of insulin need than an older child has
  • 20. Susceptibility to Communicable Illness  Children’s day to day activities bring them into contact with a variety of viral and bacterial illnesses  Even mild viruses such as colds can increase insulin requirements  Gastrointestinal illnesses with vomiting and diarrhea can result in poor absorption of carbohydrate and dehydration causing blood glucose to fall and ketones to rise.  Management of “sick days” requires frequent blood glucose and ketone monitoring, assessment of fluid and carbohydrate intake, and regular contact the child’s diabetes team as needed. 26
  • 21. Susceptibility to Communicable Illness  Be sure you have a copy of and understand your diabetes team’s sick day protocol.  Check your supply and the expiration date of ketone strips regularly.  Use blood ketone strips for assessing ketones on sick days if possible.  Discuss when use of “mini-glucagon” injections might be use with your diabetes team. 27
  • 22.
  • 23. DEFINITION:  Acute rheumatic fever is a systemic disease of childhood ,often recurrent that follows group A beta hemolytic streptococcal infection  It is a diffuse inflammatory disease of connective tissue primarily involving heart, blood vessels, joints, subcutaneous tissue and CNS
  • 24. Etiology  Beta hemolytic streptococci.  Genetic
  • 25. Epidemiology Ages 5-15 yrs are most susceptible Rare <3 yrs Girls>boys Environmental factors--over crowding, poor sanitation, poverty,  Incidence more during fall ,winter & early spring
  • 26. Pathogenesis Delayed immune response to infection with group A beta hemolytic streptococci. After a latent period of 1-3 weeks, antibody induced immunological damage occur to heart valves, joints, subcutaneous tissue & basal ganglia of brain.
  • 27. Pathologic Lesions Fibrinoid degeneration of connective tissue, inflammatory edema, inflammatory cell infiltration & proliferation of specific cells resulting in formation of Ashcoff nodules, resulting in- -Pancarditis in the heart -Arthritis in the joints -Ashcoff nodules in the subcutaneous tissue -Basal gangliar lesions resulting in chorea
  • 28. Clinical Features  Flitting & fleeting migratory polyarthritis, involving major joints  Commonly involved joints-knee, ankle, elbow & wrist  Occur in 80%,involved joints are exquisitely tender  In children below 5 yrs arthritis usually mild but carditis more prominent  Arthritis do not progress to chronic disease 1.Arthritis
  • 29. Clinical Features  Manifest as pancarditis(endocarditis, myocarditis and pericarditis),occur in 40-50% of cases  Carditis is the only manifestation of rheumatic fever that leaves a sequelae & permanent damage to the organ  Valvulitis occur in acute phase  Chronic phase- fibrosis,calcification & stenosis of heart valves(fishmouth valves) 2.Carditis
  • 30. Clinical Features (Contd)  Occur in 5-10% of cases  Mainly in girls of 1-15 yrs age  May appear even 6/12 after the attack of rheumatic fever  Clinically manifest as-clumsiness, deterioration of handwriting, emotional lability or grimacing of face  Clinical signs- pronator sign, jack in the box sign , milking sign of hands 3.Sydenham Chorea
  • 31. Clinical Features  Occur in <5%.  Unique,transient,serpiginous-looking lesions of 1-2 inches in size  Pale center with red irregular margin  More on trunks & limbs & non-itchy  Worsens with application of heat 4.Erythema Marginatum
  • 32. Clinical Features (Contd)  Occur in 10%  Painless, pea-sized, palpable nodules  Mainly over extensor surfaces of joints,spine,scapulae & scalp  Associated with strong seropositivity 5.Subcutaneous nodules
  • 33. Clinical Features  Fever-(up to 101 degree F)  Arthralgia  Pallor  Anorexia  Loss of weight Other features (Minor features)
  • 34. Laboratory Findings  High ESR  Anemia, leukocytosis  Elevated C-reactive protein  ASO titer >200 Todd units. (Peak value attained at 3 weeks, then comes down to normal by 6 weeks)  Throat culture-B H streptococci
  • 35. Laboratory Findings (Contd)  ECG- prolonged PR interval, 2nd or 3rd degree blocks,ST depression, T inversion  2D Echo cardiography- valve edema,mitral regurgitation, LA & LV dilatation, and decreased contractility 05/05/1999 41
  • 36. Treatment  Step I - primary prevention (eradication of streptococci)  Step II - anti inflammatory treatment (aspirin,steroids)  Step III- supportive management & management of complications  Step IV- secondary prevention (prevention of recurrent attacks) 05/05/1999 Dr.Said Alavi 43
  • 37. 05/05/1999 Dr.Said Alavi 44 STEP I: Primary Prevention of Rheumatic Fever (Treatment of Streptococcal Tonsillopharyngitis) Agent Dose Mode Duration Benzathine penicillin G 600 000 U for patients Intramuscular Once 27 kg (60 lb) 1 200 000 U for patients >27 kg or Penicillin V Children: 250 mg 2-3 times daily Oral 10 d (phenoxymethyl penicillin) Adolescents and adults: 500 mg 2-3 times daily For individuals allergic to penicillin Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d Estolate (maximum 1 g/d) or Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d (maximum 1 g/d) Recommendations of American Heart Association
  • 38. Arthritis only Aspirin 75-100 mg/kg/day,give as 4 divided doses for 6 weeks (Attain a blood level 20- 30 mg/dl) Carditis Prednisolone 2-2.5 mg/kg/day, give as two divided doses for 2 weeks Taper over 2 weeks & while tapering add Aspirin 75 mg/kg/day for 2 weeks. Continue aspirin alone 100 mg/kg/day for another 4 weeks Step II: Anti inflammatory treatment Clinical condition Drugs
  • 39.  Bed rest  Treatment of congestive cardiac failure: - digitalis,diuretics  Treatment of chorea: -diazepam or haloperidol  Rest to joints & supportive splinting 3.Step III: Supportive management & management of complications
  • 40. 05/05/1999 Dr.Said Alavi 47 STEP IV : Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks) Agent Dose Mode Benzathine penicillin G 1 200 000 U every 4 weeks* Intramuscular or Penicillin V 250 mg twice daily Oral or Sulfadiazine 0.5 g once daily for patients 27 kg (60 lb Oral 1.0 g once daily for patients >27 kg (60 lb) For individuals allergic to penicillin and sulfadiazine Erythromycin 250 mg twice daily Oral *In high-risk situations, administration every 3 weeks is justified and recommended Recommendations of American Heart Association
  • 41. 05/05/1999 Dr.Said Alavi 48 Duration of Secondary Rheumatic Fever Prophylaxis Category Duration Rheumatic fever with carditis and At least 10 y since last residual heart disease episode and at least until (persistent valvar disease*) age 40 y, sometimes lifelong prophylaxis Rheumatic fever with carditis 10 y or well into adulthood, but no residual heart disease whichever is longer (no valvar disease*) Rheumatic fever without carditis 5 y or until age 21 y, whichever is longer *Clinical or echocardiographic evidence. Recommendations of American Heart Association
  • 42. Prognosis  Rheumatic fever can recur whenever the individual experience new BH streptococcal infection, if not on prophylactic medicines  Good prognosis for older age group & if no carditis during the initial attack  Bad prognosis for younger children & those with carditis with vulvar lesions
  • 44. Introduction  Juvenile rheumatoid arthritis (JRA), is the most common chronic rheumatologic disease in children and is one of the most common chronic diseases of childhood.  The etiology is unknown, and the genetic component is complex, making clear distinctions between the various subtypes difficult.  A new nomenclature, juvenile idiopathic arthritis (JIA), is being increasingly used to provide better definition of subgroups. 51
  • 45. Signs and symptoms History findings in children with JIA may include the following:  Arthritis present for at least 6 weeks before diagnosis (mandatory for diagnosis of JIA)  Either insidious or abrupt disease onset, often with morning stiffness or gelling phenomenon and arthralgia during the day  Complaints of joint pain or abnormal joint use  History of school absences or limited ability to participate in physical education classes  Spiking fevers occurring once or twice each day at about the same time of day  Evanescent rash on the trunk and extremities  Psoriasis or more subtle dermatologic manifestations
  • 46. Physical findings are important to provide criteria for diagnosis and to detect abnormalities suggestive of alternative etiologies, as well as to indicate disease subtypes. Such findings include the following: Arthritis: Defined either as intra-articular swelling on examination or as limitation of joint motion in association with pain, warmth, or erythema of the joint; physical findings in JIA reflect the extent of joint involvement Synovitis: Characterized by synovial proliferation and increased joint volume; the joint is held in a position of maximum comfort, and range of motion often is limited only at the extremes
  • 47. Types of JIA include the following:  Systemic-onset juvenile idiopathic arthritis  Oligoarticular juvenile idiopathic arthritis  Polyarticular juvenile idiopathic arthritis  Psoriatic arthritis  Enthesitis-related arthritis  Undifferentiated arthritis
  • 48.  Arthritis must be present for 6 weeks before the diagnosis of juvenile idiopathic arthritis (JIA) can be made.  Disease onset is either insidious or abrupt, with morning stiffness or gelling phenomenon (ie, stiffness after long periods of sitting or inactivity) being a frequent complaint and arthralgia occurring during the day.  A morning limp that improves with time may be noted, and a toddler may no longer stand in the crib in the morning or after naps.
  • 49.  Complaints of joint pain may not be predominant in the patients’ history, however; children often stop using joints normally (eg, develop contractures of joints, decreased wrist range, limp) rather than complain of pain. Up to a quarter of children with oligoarticular JIA have no pain.  Individuals with JIA may have a history of school absences, and their ability to participate in physical education classes reflects the severity of the disease or acute flares.
  • 50. Physical Examination  JIA is a clinical diagnosis. A complete physical examination is critical for the diagnosis.  Physical findings are important to provide criteria for diagnosis and to detect abnormalities suggestive of alternative etiologies.  The diagnosis of JIA is based on the physical finding of arthritis in at least 1 joint that has persisted for at least 6 weeks, with other causes excluded, in an individual younger than 16 years.
  • 51. Systemic-onset JIA  A definite diagnosis of systemic-onset JIA must await the development of arthritis. This may occur at onset of the fever and rash or may lag by months or, rarely, years.
  • 52. Physical examination findings include the following:  The child appears systemically ill  Arthralgia is often present  The child may have generalized myalgia  Evanescent, salmon-pink, macular rash (often linear) is found, predominantly on the trunk and the extremities; this rash, seen in the image below, is associated with fever spikes Systemic juvenile idiopathic arthritis (JIA) rash
  • 53. 62  Hepatosplenomegaly is often present  Lymphadenopathy is sometimes present, especially the axillary lymph nodes  Muscle tenderness to palpation may be observed  Serositis, including pleural and pericardial effusions, may be present, as is noted in the image below Child with pericardial effusion due to systemic onset juvenile idiopathic arthritis
  • 54.  Chest pain or shortness of breath may be a sign of pericarditis or pleuritis  Friction rub may occur in pericarditis but can be absent with a large pericardial effusion  S3, basilar rales, and hepatomegaly suggestive of heart failure may rarely be observed when myocarditis occurs in individuals with systemic-onset JIA
  • 55. Oligoarticular JIA Characteristics of oligoarticular JIA include the following:  In individuals with oligoarticular JIA, 4 or fewer joints (and in many cases, only 1 joint) are affected  Large, weight-bearing joints, such as the knees and ankles, are typically affected. Eighteen-month-old girl with arthritis in her right knee. Note the flexion
  • 56.  Children appear to be well, despite ambulating with a limp  In cases of asymmetrical arthritis, chronic inflammation- related hyperemia in a knee or ankle may lead to overgrowth of that limb with subsequent leg-length discrepancy
  • 57.  Muscle atrophy, often of extensor muscles (eg, vastus lateralis, quadriceps when the knee is affected), may occur  Flexion contractures in the knees and, less commonly, the wrists are found  Involvement of a few small joints in the hands is atypical and suggests eventual development of polyarticular JIA or psoriatic arthritis. Dactylitis, or diffuse tenosynovitis of a finger or toe, also called a "sausage digit," is more typical of psoriatic arthritis or enthesitis-related arthritis.
  • 58.  Children who are at lesser risk (ie, have polyarticular disease and are ANA negative), are screened every 6 months for 7 years and then yearly. Children with systemic JIA are at very low risk and are screened yearly.  Acute anterior uveitis is one of the diagnostic criteria for enthesitis-related arthritis. These children with are screened initially and if symptomatic.  Older children with RF-positive polyarticular JIA should probably be screened yearly. There are few data on these children regarding their risk for uveitis.
  • 59. Sequelae of chronic anterior uveitis. Note the posterior synechiae (weblike attachments of the pupillary margin to the anterior lens capsule) of the right eye secondary to chronic anterior uveitis. This patient has a positive antinuclear antibodies (ANAs) and initially had a pauciarticular course of her arthritis. She now has polyarticular involvement but no active uveitis.
  • 60. Polyarticular Juvenile Idiopathic Arthritis In polyarticular juvenile idiopathic arthritis, 5 or more joints are affected in the first 6 months after disease onset, weight-bearing joints are affected, rheumatoid nodules may be seen in patients with RF-positive disease, and symmetrical involvement of small joints in the hands is often found, as seen in the images below.
  • 61. Patient with active polyarticular arthritis. Note swelling (effusions) of all proximal interphalangeal (PIP) joints in addition to boney overgrowth. Also note lack of distal interphalangeal joint (DIP) involvement. The patient has interosseus muscle wasting (observed on the dorsum of the hands), and subluxation and ulnar deviation of the wrists are present.
  • 62. Decreased extension of the cervical spine is often asymptomatic. It is indicative of arthritis of the cervical spine and can lead to subluxation, typically of the C2 vertebra on C3. Fusion of the posterior elements of the vertebra may occur. Flexion and extension views of C-spine in child with poorly controlled polyarticular juvenile idiopathic arthritis (JIA).
  • 63. Treatment The ultimate goals in managing rheumatoid arthritis are to prevent or control joint damage, to prevent loss of function, and to decrease pain. These goals are particularly important in juvenile idiopathic arthritis (JIA), in which the rate of progression and the onset of debility can be rapid. JIA is a chronic disease characterized by periods of remission and flare. Treatment is aimed at inducing remission with the least toxicity from medications with hopes of inducing a permanent remission. The success of therapy is monitored best with repeated physical examinations and history. The number of joints involved and the duration of morning stiffness should demonstrate continued decrease, with elimination reflecting success. Surgery may be indicated in patients who are unresponsive to medical therapy.
  • 64.  A team-based approach to the treatment of JIA can be helpful. Management may include 1 or all of the following areas:  Pharmacologic therapy with nonsteroidal anti- inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), biologic agents, or intra- articular and oral corticosteroids  Psychosocial interventions  Measures to enhance school performance (eg, academic counseling)  Improved nutrition  Physical therapy  Occupational therapy
  • 66. Infestation Infestation is the presence of animal parasites on or in the body, is common in tropical countries and less so in temperate ones. Infestations fall into two main groups: 1 those caused by arthropods; and 2 those caused by worms.
  • 67.
  • 68. EPIDEMOLOGY  women & children  urban areas,  winter  Prevalence 4 – 100%
  • 69. Transmission directly by close personal contact, sexual indirectly via fomites  factors overcrowding delayed treatment of primary cases  public awareness
  • 70.
  • 71.  highly host-specific  an arthropod a member of the class Arachnida, subclass Acari, order Astigmata, and family Sarcoptidae.  Too small to be seen by the naked eye  Adult female measures ~ 0.4 - 0.3 mm, &  the smaller male 0.2 - O.15 mm
  • 72.  body is creamy white & is marked by transverse corrugations,  ovoid  four-pairs of legs - anterior two pairs end in elongated peduncles tipped with small suckers, In the female, the rear two pairs of legs end in long bristles, whereas in the male bristles are present on the third pair and peduncles with suckers on the fourth.  crawl at a rate of 2.5 cm/min, burrow through the stratum corneum at the rate of about 2 mm per day(0.5 - 5 mm/day)
  • 73.  number - <20 & with crusted scabies can be thousands to millions live mites can survive for up to a week in the environment, feeding on the sloughed stratum corneum  cannot fly or jump
  • 74. Mating takes place once, and the female is fertile for the rest of her life (1 mo), Copulation in a small burrow---------the male, falls off the skin & perishes--------- Fertilized female enlarges the burrow using proteolytic enzymes to dissolve the stratum corneum of the epidermis ----- begins egg laying (3 eggs a day each) Six-legged larvae emerge from the eggs after 3-4 days 90% of the hatched mites die
  • 75. Escape from the burrow by cutting through its roof------then dig short burrows called moulting pouches & transform into nymphs-- -----------After further moult into larger nymphs , adult males and females develop(in 2-3 weeks)
  • 76.
  • 77. Clinical features  IP- 2-6 weeks  immediate symptoms –in re infection  Triad`s  Pruritic papular lesions,  Excoriations, and  Burrows Site- The circle of Hebra ~ an imaginary circle intersecting the main sites of involvement - axillae, elbow flexures, wrists & hands, & crotch
  • 78. Cont...... Pruritis ○ accentuate at night & exacerbated by a hot bath or shower  Primary lesions of scabies - burrows, papules, pustules, nodules, occasionally urticarial papules and plaques  interdigital webbing of the hands,  flexural aspect of the wrists, behind the ears, axilla, waist, ankles, feet, buttocks & belt area  penile & scrotal in men, areola, nipples & genital area in women
  • 80. In very young children, infants, elderly and immunocompromised hosts, a widespread eczematous eruption primarily on the trunk is common , scalp & face can also be affected.
  • 81.  The burrow  pathognomonic sign and represent the intraepidermal tunnel created by the moving female mite.  a 1-10 mm tunnel  serpiginous, greyish-white thread-like elevations  At the end of it a vesicle/pustule containing the mite may be noted, especially in infants & children at entry, slight scale
  • 82.  In infants, commonly located on the palms & soles : F To identify burrows quickly:  apply a drop of India ink or gentian violet to the infested area,  remove it with alcohol  Thin threadlike burrows retain the ink
  • 83.  Erythematous Papules & Vesicles (filled with serous fluid) rarely contain mites and most likely are due to a hypersensitivity reaction  Papules= on the shaft of the penis & scrotum in men & on nipples in women  Vesicles= on the palms & soles
  • 84.  Animal Scabies: Zoonotic scabies  affect humans who come in close contact with the animal  incubation period is shorter, the symptoms are transient  usually manifests with vesicles & papules with atypical distribution  Burrows are usually absent  runs a self-limited course, require no treatment Mites from animals are not a source of human infestation, but they can produce bite reactions  Asymptomatic infestation  not uncommon  considered ‘carriers’
  • 85.
  • 86. Secondary scabies lesions With rubbing- secondary infection, - the host immune response against the mites and their products.  Excoriations, Lichenification, widespread eczema, honey-colored crusting, postinflammatory hyperpigmentation, erythroderma, and frank pyoderma
  • 87. Variants Nodular scabies  in 7-10% of patients with active scabies  Pink, tan, brown, or dull red nodules (2-20 mms)  May or may not itch  Persist on the scrotum, penis, and vulva and In neonates unable to scratch, pinkish-brown nodules may develop  usually sterile  Intralesional steroids, tar, or excision are methods of treatment
  • 88. Bullous scabies  Mimics BP both clinically & histologically (contain many eosinophils)  Vesicles and bullae-, particularly on the palms & fingers  Immunofluorescent
  • 89.  In immunocompromised / debilitated patients, including those with:  neurologic disorders, Down syndrome, organ transplants, graft-versus-host disease, adult T-cell leukemia, leprosy, or AIDS and institutionalized populations  Risk factors for profound infestation -an inability to mount an immune response, perceive pruritis, and/or physically scratch the skin Crusted scabies (Norwegian/hyperkeratotic scabies)
  • 90. * marked thickening and crusting of the skin. * Hyperkeratotic, crusted/scaling lesions teem with mites * large areas with prominent scalp lesions, hands and arms are usual locations * Swollen & crusted finger tips; & dystrophic nails
  • 91. Contd... The rest of the skin usually appears diffusely xerotic highly contagious Severe fissuring & scaling of the genitalia & buttocks may be present Oral agent should be used in conjunction with a topical agent
  • 92. DDx Crusted scabies  Psoriasis  Seborrheic dermatitis
  • 93. Treatment  In infants with extensive involvement, several re treatments a week apart occasionally be required  second application of topical medication.......  Treat simultaneously all household contacts (even with no symptoms)
  • 95. Pediculosis  Phthiraptera family  Order Anoplura-blood-sucking (***solenophages) ectoparasites of mammals  Pediculus capitis, the head louse  Pediculus humanus, the clothing or body louse &  Pthitrus pubis, the pubic or crab louse  ingest blood, & produce skin lesions by mechanical puncture( stylet, haustellum) & injecting toxic secretions
  • 96. Pediculosis Capitis Head lice  in school-aged children, 3-12yr, 10%of children : F  affect all levels of society & all ethnic groups  Prevalence= 6 to 12 million infestations/year  incidence is low among African Americans  spread by close physical contact  sharing of head gear, combs, brushes, & pillows
  • 97. Etiology & Pathogenesis  is 1 to 2 mm long,  elongated,  greyish white flattened dorsoventrally, &  wingless  three pairs of sharp clow- grasp hairs and for feeding  feed approximately five times each day  5 - 10 eggs a day  can travel up to 23 cm/min  The larva, called a nymyh/instar, looks like a miniature adult louse  1 - 2 days (4 days) away from the scalp (Nits up to 10 days)  30 days  *Head lice do not carry or transmit any human disease.  hatches in 8 to 10 days, and reaches maturity in approximately 18 days. Nits are .8mm, with operculum
  • 98.
  • 99.
  • 100. Clinical findings  Louse - occipital and retro auricular regions  <20 but in 5% >100  Itching or can be asymptomatic a result of hypersensitivity reaction to the saliva & faecal matter produced by the louse during feeding Sensitization - 3-8month  hemorrhagic crust  Excoriations, lymphadenopathy, & conjunctivitis(redness &swelling) may be observed
  • 101. Diagnosis  Identification of live adult lice, immature nymphs, and/or viable-appearing eggs  Live nits(egg cases) placed in close proximity to the scalp(parietal & occipital)  Have proteinaceou sheath  cemented to the hair shaft with chitinous material secreted by the female accessory glands C0MPLICATIONS  Excoriation ----- Secondary bacterial infections
  • 102. Pediculosis corporis(Body/clothing lice) EPIDEMIOLOGY  low of socio-economic  in urban public hospitals  No predilection for race, age, or sex  contaminated clothing or bedding
  • 103. ETIOPATHOGENESIS  Body Iouse/P. humanus var humanus  lifespan -18 days  270 to 300 ova  2-4mm  3 day,with out meal  comes to the surface only for meal
  • 104. CLINICAL FEATURES  linear excoriations primarily  Occasionally, a macula ceruleae (Iiterally, sky- blue spot) a blue to slightly slate-colored macule.............bruise-like lesion (~1.5 cm) & often with a central punctum 2nd to altered blood pigments in clothing binds (waistband, buttocks & thighs) & is asymptomatic to slightly pruritic
  • 105. Contd... Diagnosis  examining the lining of the clothing seams for the presence of nits  By shaking out the clothing over a sheet of newsprint,  Nits that contain an unborn louse fluoresce white.  Nits that are empty fluoresce gray.
  • 106. COMPLICATIONS  Excoriation  secondary infection with S. aureus, S. pyogenes & other bacteria (impetigo & furunculosis)  act as vectors for R.prowazekaii (epidemic typhus), Bartonella quintana (trench fevers or endocarditis) & Borrelia recurrentis (relapsing fever)
  • 107. Pediculosis pubis (Pubic Lice) EPIDEMIOLOGY  most often are a sexually transmitted disease  ~ 30 % of patients have another concurrent STI  from one sexual exposure with an infested partner is more than 90%  contaminated clothing, towels, or beddings
  • 108. ETIOPATH0GENESIS  Pthiridae  crab - naming  second and third pairs of -to cling on to hair (pincer like claws)  light brown  0.8 to 1.2 mm in length  ambulate up to 10 cm/day  lifespan of 2 wks  25 ova  away from the human host for up to 36 hrs  dog
  • 109. CLINICAL FEATURES  Pruritus  Maculae ceruleae (sky-blue spots, (tache bleu), on inner thighs or sides of trunk  Bullous lesion  adult organisms on the body ( ~ 10 - 25 or more)  pubic hair, any hair bearing site can be affected, eyelashes ((phthiriasis palpebrarum ○ in hirsute ~ short hairs of the thighs, trunk, & perianal area  nits near the base of the hair  the duration of infestation can be approximated by the distance of the nit from the skin surface
  • 110.
  • 111.  The Skeletal System  The skeleton is the name given to the collection of bones that holds our body up. It does three major jobs. A. It protects our vital organs such as the brain, the heart, and the lungs. B. It gives us the shape that we have C. It allows us to move..  . When we were born our skeleton had around 350 bones. By the time we become an adult, we will only have around 206 bones Introduction
  • 112.  Bone comes in several shapes and sizes the structure and composition of bone is the same in all. Bone is composed of protein , minerals and cells. The main part are: shaft neck head
  • 113. A tumor is a lump or mass of tissue that forms when cells divide uncontrollably. A growing tumor may replace healthy tissue with abnormal tissue. It may weaken the bone, causing it to break (fracture).
  • 114. A bone tumor is an abnormal growth of cells within the bone that may be noncancerous (benign) or cancerous (malignant).
  • 115. Malignant Benign Fatal without treatment May recur after removal Rarely fatal Rarely recur after removal Rapid growth Slow growth Distant metastases , not localized No metastases , localized The difference between benign and malignant tumors
  • 116.  Enneking described the most widely used staging system for (benign bone tumors ) The stages are denoted by the Arabic numerals 1, 2, and 3, whereas malignant bone tumors are classified by Roman numerals (I, II, III). Many benign bone tumors have the potential to present at, and progress through, various stages during their disease course. Stage of benign tumors
  • 117.  . Stage 1-LATENT, it do not have any characteristics of growth or progressive change, may resolve spontaneously.  Stage 2-ACTIVE, lesion deform the host bone but remain contained in bone, require intralesional curettage.  Stage 3-AGGRESSIVE , tumor extend beyond the bone, require complete work-up and a removal with wide margins to avoid possible local recurrence. Stage of benign bone tumors
  • 118.  The staging system for malignant tumor adopted by the Musculoskeletal Tumor Society, and originally developed by ( Enneking) is based on the histological grade, the local extent(Tumors whether they are intra-compartmental or extra- compartmental) and the presence or absence of metastasis Stage of malignant bone tumors
  • 119. Stage IA is defined as G1 and Intra- compartmental Stage IB is G1 and extra-compartmental Stage IIA is G2 and Intra-compartmental Stage IIB is G2 and extra-compartmental Stage III is G1 or G2, intra- or extra- compartmental, and has evidence of metastasis Stage of malignant bone tumors
  • 120. Bone tumor primary Benign tumors: for ex. osteochondroma malignant tumors: for ex Ewing's sarcoma secondary Metastatic tumors Classification
  • 121.
  • 122.  Is a tumor which have spread from other organs ,The most common cancers that spread to the bone are cancer of the: 1. Breast 2. Kidney 3. Lung 4. Prostate 5. Thyroid These forms of cancer usually affect older people metastatic tumors
  • 123. 1. Age 2. Combinations of radiation and chemotherapy for treating prior cancer 3. Certain kinds of anti-cancer drugs (alkylating agents) 4. Family history of bone cancer 5. An overactive parathyroid gland 6. Multiple benign tumors 7. Osteomyelitis 8. Radiation Risk factors
  • 124. 1. Movement problems 2. Stiff bones 3. Bone lumps and masses 4. Bone tenderness 5. Anemia 6. Weight loss, Fatigue 7. Bone pain, may be worse at night 8. fevers and night sweats 9. Bone fracture, especially fracture from slight injury (trauma) 10. Note: Some benign tumors have no symptoms Clinical features
  • 125.  The cause of bone tumors is unknown. They often arise in areas of rapid growth  Inherited genetic mutations  Radiation  Trauma Causes
  • 126. 1. Delayed wound healing 2. Nutritional deficiency 3. Infection 4. Hypercalcaemia 5. Muscle wasting, bone weakening 6. Pathological fracture 7. Temporary burn to the skin and fatigue from radiation therapy Complications
  • 127. 8. Nausea, vomiting, mouth sores, hair loss, and lowered resistance to infection from chemotherapy. 9. Infection of the surgical site and possible blood clotting disturbances from surgery. 10. Pain 11. Spread of the cancer to other nearby tissues (metastasis) Complications
  • 128.  Blood test  Bone biopsy  Bone scan computed tomography (CT).  MRI ( magnetic resonance imaging )  X-ray of bone  CT scan Diagnosis & Tests
  • 129. Open Biopsy Needle Biopsy insert a needle into the tumor to remove some tissue small incision is made and the tissue is removed removal of a sample of bone tissue to test for cancer cells. Bone biopsy:
  • 130.  Systemic therapy  Local therapy 1.Chemotherapy 2. hormone therapy 3. Immunotherapy ex. Interferon α 1.Radiation therapy 2. surgery Nutritional therapy • Provide foods high in protein, vitamins and folic acid.
  • 131.  Hormone therapy removal of the organs which produce hormones which can promote the growth of certain types of cancer (such as testosterone in males and estrogen in females), or drug therapy to keep the hormones from promoting cancer growth.  Chemotherapy used to kill tumor cells when they have spread into the blood stream Systemic therapy
  • 132.  Radiation Therapy Radiation therapy uses high-dose x-rays to kill cancer cells and shrink tumors. may be given either before or after surgery Local therapy
  • 133. Surgical Treatment  Amputation  Rotationplasty  Bone graft  Artificial bone removes all or part of an arm or leg when the tumor is large and/or nerves and blood vessels are involved. is a form of amputation, in which the patient's foot is turned upwards in a 180 degree turn and the upturned foot is used as a knee. affected bone is removed, bone from elsewhere from the body is taken. affected bone is removed, putting an artificial bone in. Local therapy
  • 134.  Narcotics  Analgesics Ex. Biphosphonates are drugs that can be used to reduce bone pain and slow down bone damage in people who have cancer that has spread to their bones and increase bone strength Ex. Metastron also known as strontium-89 chloride is an intravenous medication given to help with the pain and can be given in three month intervals Pain medications
  • 135.  Age: Bone tumor are more common in children and young adults when bones grow rapidly  The incidence of bone cancer is higher in families with familial cancer syndromes. The incidence of bone cancer in children is approximately 5 cases per million children each year , in united states Epidemiology
  • 136.  Nursing assessment  Nursing diagnosis  Nursing planning  Nursing Implementation  Nursing evaluation Nursing process
  • 137.  Collection Of Subjective Data: 1. Bone pain in the area of the tumor, may be worse at night, pain is generally described as dull and achy 2. pain may or may not get worse with activity 3. Fatigue, anxiety  Collection Of Objective Data: 1. Bone lumps and masses determining the location and size of tumor ,soft tissue swelling 2. Stiff bones 3. Weight loss 4. Bone fracture, especially fracture from slight injury (trauma) 5. fevers and night sweats 6. Movement problems 7. Anemia Nursing assessment
  • 138. Acute or chronic pain related to the pathologic process and surgery Control of pain Administer analgesics as necessary. Make sure the patient has received his analgesic before morning care or any activity that may increase pain Regularly monitor the patient’s degree of pain and the effectiveness of analgesics and other pain relief measures, such as positioning or guided imagery Experiences no pain or decreased pain Nursing evaluation Nursing Implementation Nursing Planning Nursing Diagnosis 1
  • 139. Nursing evaluation Nursing Implementation Nursing Planning Nursing Diagnosis Deficient knowledge related to the disease process and therapeutic regimen Giving knowledge about the disease process and treatment regimen Promoting understanding of the disease process and treatment regimen(Provide foods high in protein, vitamins and folic acid) Don’t give I.M. injections or take rectal temperature During radiation therapy or chemotherapy, take measures to reduce adverse reactions, such as providing the patient with plenty of fluids to drink and saline mouthwash for gargling Described disease process and treatment regimen 2
  • 140. Nursing evaluation Nursing Implementation Nursing Planning Nursing Diagnosis Risk for injury: pathologic fracture related to tumor and metastasis Absence of complication Absence of pathologic fracture The effective extremities must be supported and handled gently Exhibits absence of complication 3
  • 141. Nursing evaluation Nursing Implementation Nursing Planning Nursing Diagnosis Risk for situational low self- esteem related to loss of body part Improved self- esteem (Promoting self – Esteem)Try to help the patient develop a positive attitude toward recovery and urge him to resume an independent lifestyle Demonstrate positive self – concept 4
  • 142. Nursing evaluation Nursing Implementation Nursing Planning Nursing Diagnosis Ineffective coping related to fear of the unknown ,perception of disease process Effective pattern of coping (Promoting coping skills)Encourages the patient and family to verbalize their fears ,concerns, and feelings Demonstrates effective coping pattern
  • 143.
  • 144. OBJECTIVES 1-Introduction of accidental prevention. 2-Developmental stages, common problems of each stage and its prevention. -Road Traffic Accidents(RTAs). -Burns and Scalds. -Electrocution. -Drowning and Near-Drowning. -Chocking, Suffocation and Strangulation. -Poisoning. -Cuts. 3-General safety precautions that need to be taken by the parents or caregivers. -Infants. –Toddlers -Preschoolers. -School Age Children. -Adolescents
  • 145. Introduction Injury prevention Injuries cause more deaths in children between the ages of 1 and 4 years than in any other childhood age-group except adolescence. Childhood accidents at home and outside are common but preventable. The age is the most important factor that affects children to have accidents.
  • 146. Developmental stages and Common : problems of each stage Infant Burns extremity fractures choking head injuries motor vehicle accident near drowning toxic ingestions Toddler Burns extremity fracture choking head injuries motor vehicle accidents near drowning toxic ingestions bicycle injuries
  • 147. Preschooler Burns extremity fractures falls motor vehicle accidents toxic ingestions bicycle injuries School child Extremity fractures motor vehicle accidents sports injuries Adolescent Extremity fractures motor vehicle accidents sports injuries near drowning ( common among males)
  • 148. The common accidents in children as per age and the preventive measures to be taken in order to prevent them as the following: 1-Road traffic accidents(RTAs) RTAs are the most common type of accidents that leads to death on children in our state. boys between the ages of 5 and 12 years are mostly confronting this type of accidents in our place. Children of this age are school going and will not able to estimate the speed of vehicles or dangers of traffic while crossing roads. so children must be taught the practical aspects of road safety through demonstration classes.
  • 149. RTAs Child passengers Bicycle accidents Falls of other forms Prevention
  • 150. 2-Burns and scalds These are the second most common cause of death from accidents. Most of these deaths are due to carelessness of parents or caretakers. Scalds from boiling water and hot drinks are common among children especially in toddlers. The common victims of burns with kerosene lamps are school age children, who will be studying near kerosene lamps. Prevention
  • 151. 3-Electrocution This is yet another cause of death in children. Prevention
  • 152. 4-Drowning and near-drowning Prevention Drowning and near-drowning also cause death in children, especially in preschoolers and school age children. children may get drowned in streams, rivers, lakes, swimming pool and also in pits where water is stagnated. Infants and toddlers are also not away from the risk of drowning. This is usually occur at home. They get drowned in bathtubs and water-filled vessels.
  • 153. 5-Choking, suffocation and strangulation Children may choke on vomit, toy's parts or aspiration of food and fluids. Children strangle themselves on curtains, cloth cradles, beddings and even necklaces and neckties, some children try to imitate TV and cinema scenes and get strangulated. Airway obstruction from aspirated foreign bodies can be recovered using Heimlich maneuver in older children. Prevention
  • 154. 6-Poisoning Prevention Many children are admitted to hospital because they have been poisoned by eating or drinking or even inhaling poisonous substances. Some of these children die. To prevent these types of deaths, adults need to be vigilant. Substances such as medicines, petrol, household cleaning materials, etc., need to be stored high up so that children can't reach them.
  • 155. 7-Cuts Prevention Cut injuries are also common among children. They may use carelessly placed knives, razors and blades to experiment. Sharp edges of furniture also can be injuries to children.
  • 156. General safety precautions that need to be taken by the parents or caregivers Infants Toddlers Preschoolers Adolescents
  • 157. References Books 1. Writer :Patricia M , Dillon Book :nursing health assessment Edition :second edition Pages :467_470 Year :2003