Vomiting and Diarrhea (Ch. 29 p.

1098, ATI: 236)

o Salmonella produces colicky pain
o Acute diarrhea goes away by its self dont really give meds
o Box 29-4 causes of chronic diarrhea
Celiac disease
Malabsorptive Causes
Pancreatic insufficiency (cystic fibrosis, chronic
pancreatitis, Shwachman syndrome)
Short-bowel syndrome
Lactose intolerance
Congenital enzyme deficiency (sucrose-isomaltase
deficiency)
Allergic gastroenteropathy
Allergic Causes
Eosinophilic gastroenteritis
Acquired hypoglobulinemia
Immunodeficiency
Wiskott-Aldrich syndrome
Agammaglobulinemia
Severe combined immunodeficiency disease
Thymic hypoplasia
Selective immunoglobulin A deficiency
Human immunodeficiency virus or acquired
immunodeficiency syndrome
Ulcerative colitis
Inflammatory Bowel Disease
Crohn disease
Hyperthyroidism
Addison disease
Endocrine Causes
Congenital adrenal hyperplasia
Hirschsprung disease
Intestinal
Motility Disorders
psuedoobstruction
Ascaris organism
Giardia organism
Parasitic Infestations

Other Causes

Radiation enteritis
Abdominal tumors
Protein-losing enteropathy (Mntrier disease,
intestional lymphagiectasia)

o Box 29-2- Acute diarrhea

Infection and Parasitic Infestation

Bacteria

Salmonella, Shigella, Campylobacter, Escherichia

coli, Yersinia, Aeromonas, Clostridium difficile,
Staphylococcus aureus
Rotavirus, Norwalk virus, Small and round viruses,
adenovirus, pestivirus, astrovirus, calicivirus,
parvovirus
Giardia lamblia, Cryptosporidium, Isospora belli,
Microsporidia, Strongyloides, Entamoeba histolytica

Viruses
Paravirus

Associated Conditions
Upper respiratory tract infections

Urinary tract infections

Otitis media

Dietary Conditions
Over feeding
Introduction of new foods
episode
Osmotic diarrhea from excess sugar in formula or juice

Reinstituting milk too soon after diarrheal

Excessive ingestion of sorbitol or fructose

Medications
Antibiotics

Laxatives

Toxic Causes
Ingestion of heavy metals (arsenic, lead, mercury), or organic phosphates

Functional Causes
Irritable bowel syndrome

Other Causes
Pseudomembranous enterocolitis

Hirschsprung disease

o Dr. will order a O/P if there is no positive tests for bacteria

o Test for pin worms - Tape test
When child goes to sleep, tape is placed on the childs anus to get pin worms who go and
lay eggs
o Bulky, foul smelling stool means there is fat in the stools
o Scattered stool could = glucose intolerance
o Bolus fluids- 20ml/kg
o Diet needs to be reintroduced- regular diet
BRAT contraindicated
Encouraging intake of clear fluids does not help diarrhea

o Vomiting

Causes are determined by three things

Age
Pattern (right after trauma ect)
Duration of symptoms
In kids pediatricians do not tx vomiting right away
It is a sign something is wrong, so find the real cause of vomiting
Complications can occur in children
Dehydration
Electrolyte disturbances
Malnutrition
Aspiration
Malory- Weiss Syndrome (small tears in the distal esophageal mucosa)
Color and consistency vary according to the cause
Green, bilious vomiting suggests bowel obstruction
Curdled stomach contents mucous, or fatty foods that are vomited several hours
after ingestion suggest poor gastric emptying or high intestinal obstruction
Gastric irritation by certain medicines, foods, or toxic substances may cause
vomiting
Fever and diarrhea accompanying vomiting suggests an infection
Constipation associated with vomiting suggests an anatomic or functional obstruction

Localized abdominal pain and vomiting often occur with appendicitis, pancreatitis, or
peptic ulcer disease
A change in the LOC or a headache associated with vomiting indicates a CNS or
metabolic disorder
Forceful vomiting is associated with pyloric stenosis
Cyclic vomiting syndrome- rare disorder characterized by bouts of vomiting that can
last for hours to several days (Unknown cause)
Ondansteron [Zofran) block receptors in the chemoreceptor trigger zone
Metoclopramide [Reglan]- enhance gastroduodenal peristalsis
Promethazine [Phenergan]- compete for H1- receptor sites
Dimenhydrinate [Dramamine]- motion sickness

Renal Dysfunction (Ch. 30)

o UTI

Dx most common UTI most common in infants for hospital

Whenever there is an infection the signs are very subtle especially the younger they are

o Box 30-1 1140

Signs and Symptoms of Urinary Tract Disorders or Disease

Neonatal Period (Birth to

1 month)

Poor feeding
Vomiting
Failure to
gain weight
Rapid respirations (acidosis)
Respiratory
distress
Spontaneous pneumothorax or pneunonediastinum
Frequent urination
Screaming
on urination
Poor urinary stream
Jaundice
Seizures
Dehydration
Other abnormalities or
stigmata

Infancy (1-24 months)

Childhood (2-14 years)

Enlarged kidney or bladder

Poor feeding
Vomiting
Failure to
gain weight
Excessive thirst
Frequent urination
Pallor
Straining or screaming on urination
Fever
Foul-smelling urine
Persistent
diaper rash
Seizures (with or without fever)
Dehydration
Enlarged kidneys or bladder
Poor appetite
Vomiting
Growth
failure
Excessive thirst
Painful urination
Swelling of face
Enuresis, incontinence, frequent urination
Seizures
Pallor
Fatigue
Blood in urine
Abdominal or back pain
Edema
Hypertension
Tetany

o The classic symptoms of UTI are often observed in children more than 2 years of age
o What catches the attention of mothers- crying when the baby goes pee
Foul smelling urine
Urine bag. Clean catch.
Best method in n out straight catch to get a culture

o
o
o

o
o

(final results- 72 hours)

School age children
Wrong wiping
They hold it
They dont drink water
Get them cotton panties
E. coli (80% of cases) and other gram-negative enteric organisms are mostly commonly
implicated
Health teaching is a big role for the RN
The single most important host factor influencing the occurrence of UTI is urinary stasis
Reflux
Anatomic abnormalities
Extrinsic urethral or bladder
compression
Dysfunctional voiding- abnormality either in the storage/emptying phase of micturition
Urgency
Frequency
Incontinence
UTI
Secondary vesicoureteral reflux (VUR)
Pee after intercourse adolescence
Nursing assessment of UTI
Nausea
vomiting
anorexia chills
nocturia
frequency/urgency
Suprapubic or lower back pain
bladder spasms
dysuria
burning
on urination
Tests done BUN & creatinin (Newborn- 4-18; Infant/Child
5-18)
ultrasound, CT scan,
IVP
VCG (voiding cystourethrography) - Scan to see how fast the bladder will fill up and
see where the solution is going
Contrast needs to be done prior & ask about allergies
Contrast injected into bladder through urethral catheter
Film taken before, during, and after voiding

 Reveals reflux of urine into ureters

Objective data
Fever
Hematuria, foul-smelling urine; tender, enlarged kidney
Leukocytosis, positive findings for bacteria, WBCs, RBCs, pyuria
Facing the wall back to you so you can get a clean catch urine They are more stable and relaxed and labia are open so there is decreased
changes of contamination
Kidney reflux- in babies- anatomic
The higher the BUN the more severe the problem
Renal disease
Increased protein catabolism
Dehydration
Hemorrhage
High protein intake
Corticosteroid therapy

o Glomerulonephritis

Most are postinfectious

Pneumococcal, streptococcal (usually group A hemolytic strep) or viral
Post Streptococcal Glumerulonephritis (STREP THROAT)
Primarily affects early school-age children with a peak age of onset of 6 to 7 years
Uncommon in children under 2
A latent period of 10 to 14 days occurs between the streptococcal infection of the throat
or skin and the onset of clinical manifestations
May be a manifestation of systemic disorder
SLE (Systemic lupus erythematosus)
Symptoms
Oliguria
Circulatory congestion

Puffiness of the face especially the eyes (periorbital edema) worse in AM

Anorexia
Pale, Irritable, and lethargic
Hematuria
Bleeding in upper urinary tract smoky urine
Proteinuria
Increased amount of protein = increased severity of renal disease
Complications should be monitored
Edema,
HTN (#1)
Abdominal girth for ascites
Hypertensive encephalopathy
Antibiotics are given for persistent strep infection
Lasix is helpful when significant edema and fluid overload are present
Bed rest is no longer recommended for the acute phase
Limit sodium intake
Nursing care of the child with glomerulonephritis involves careful assessment of the
disease status, with regular monitoring of vital signs (including frequent measurement of
blood pressure), fluid balance, and behavior
Fluid restriction, if prescribed, is more difficult; the amount permitted should be evenly
divided throughout the waking hours
Serve in small cups to give the illusion of larger servings
The acute edematous phase of glomerulonephritis usually persist from 4 to 10 days but
may persist for 2 or 3 weeks
The first sign of improvement is a small increase in urinary output with a corresponding
decrease in body weight

Comparison of Poststreptococcal Glomerulonephritis and Nephrotic

Syndrome
Manifestations

Acute Poststreptococcal

Minimal Change Nephrotic

Streptococcal antibody titers

Blood pressure
Edema
Circulatory congestion
Proteinuria
Hematuria
Red blood cell casts
Azotemia (high level of
nitrogen in urine)
Serum potassium levels
Serum protein levels
Serum lipid levels
Peak age of onset (yr)

Glomerulonephritis
Elevated
Elevated
Primarily periorbital and
peripheral
Common
Mild to moderate
Gross or microscopic
Present
Present

Syndrome
Normal
Normal or decreased
Generalized, severe

Normal or increased
Minimum reduction
Normal
5-7

Normal
Markedly decreased
Elevated
2-3

Absent
Massive
Microscopic or none
Absent
Absent

o Nephrotic Syndrome

Most common presentation of glomerular injury in children

Characteristics
Proteinuria**
Hypoalbuminemia
Hyperlipidemia
Edema
Massive urinary protein loss
Self limiting
Clinical manifestations
Weight gain that progresses insidiously over a period of days or weeks
Puffiness of the face, especially around the eyes- AM

Swelling of the abdomen and lower extremities AFTERNOON

Edema of intestinal mucosa
Diarrhea
loss of appetite Poor intestinal absorption
Urine is decreased and appears darkly opalescent and frothy
Extreme skin pallor
Irritability and lethargy
Changes in the nails (white Muehrcke- lines parallel to the lunula)
If child responds to steroids, usually will do ok
Early detection and treatment to decrease proteinuria, and permanent renal damage
About 20% will have relapses for up to 5 yrs, some up to 10 yrs.
Given steroids & diuretics
Management of NS
The primary objective is to reduce the excretion of urinary protein and maintain
protein-free urine
Child is limited to quite activity during the acute phase but not remission
Diet
Low to moderate protein
Sodium restrictions when large amount edema present
Steroids- inflammatory process, proteinuria
o 2 mg/kg divided into BID doses
o Prednisone drug of choice ($$ and safest) - appetite, weight gain,
hirsutism
o Only given for a day or two
o Urinary protein excretion diminishes within 7 to 21 days after initial steroid
therapy
o Children who require frequent courses of steroid therapy are highly
susceptible to complications of steroids
Immunosuppressant therapy (Cytoxan)

Diuretics- loop diuretics [furosemide in combination with metolazone]

Examination of urine for albumin, daily weight, and measurements of abdominal
girth
Elevating edematous parts may be helpful to shift fluid to a more comfortable
distribution
Particularly vulnerable to upper respiratory tract infections
HOME CARE IS PREFERRED (unless the edema and proteinuria are severe)
They will get dialysis- peritoneal and hemodialysis (Common in children is
peritoneal)

o Dialysis
Peritoneal dialysis
Hemodialysis
Hemofiltration
o Adolescents often resent the control and enforced dependence imposed by dialysis
Depression, hostility, or both are common
Withdrawal from peers and social isolation are the rule, and noncompliance with the
therapeutic regimen is not uncommon
o Peritoneal Dialysis
The preferred method of dialysis for children
Slow, gentle process, which decreases the stress on body organs that can occur with the
rapid chemical and volume changes of hemodialysis
Indicated for neonates, children with severe cardiovascular disease, or those who are
poor risks for vascular access
Contraindications
Recent abdominal surgery
Peritoneal adhesions and scarring
A higher rate of infection (peritonitis) is observed with this modality
Catheters for long term use are placed surgically in the OR with the pt under anesthesia
Abdominal cavity acts as semipermeable membrane for filtration

Can be managed at home in some cases- chronic PD

Warmed solution enters peritoneal cavity by gravity, remains for period of time before
removal
Takes about 4-8 hours
Observe for changes in the color of the dialysis solution draining from the child
The solution should be straw colored and clear
If the color is pink, bright yellow, or brown, or if the solution is cloudy, notify the
practitioner immediately
Most schedules are arranged for uninterrupted sleep at night and coordination of the
dialysis with school and other activities
o Hemodialysis
Requires creation of a vascular access and special dialysis equipment
Grafts
Fistulas
External access devices
Both the graft and the fistula require needle insertion at each dialysis
Graft and fistula problems are a common source of aggravation
Best suited for children who can be brought to facility 3 times/week for 4 to 6 hours
(book: 3-5 hours)
Preferred for children with acute conditions such as life threatening hyperkalemia or
poisoning with dialyzable compounds
Achieves rapid correction of fluid and electrolyte abnormalities
Is quicker, so you achieve correction faster
Rapid correction could also lead to electrolyte imbalance
Most sensitive in children
Dietary limitations are necessary in chronic dialysis to avoid biochemical complicaitons
Fluid restriction Sodium restriction
Potassium restriction
Phosphorus restriction
Adequate protein intake
Can be performed at home
Children waiting for a transplant who live far

Children who have had one or more kidney transplant failures

Know the pros and cons/ adv./ disadva for test

Cerebral Function
o Assessment
Infants and young children: observe spontaneous and elicited reflex responses
Physical examination:
No response to pain,
Altered LOC
Impaired gait
Can not fix a stare
Early signs and symptoms may be subtle
In children there is a modified Glascow Coma Scale
As pressure increases, signs and symptoms become more pronounced and level of
consciousness (LOC) deteriorates (Expected reference range is 10-15 mm Hg)
Clinical Manifestations of Increased Intracranial Pressure (ICP)
Vomiting: with or without nausea
Pupils become progressively sluggish in reaction and eventually become fixed and
dilated
Clinical Manifestations of Increased Intracranial Pressure in Infants and Children
Tense, bulging fontanel
High-pitched cry
Infants
Separated cranial sutures
Distended scalp
veins
Macewen (cracked-pot) sign
Poor feeding
Irritability and restlessness
Crying when
disturbed
Drowsiness
Setting-sun sign
Increased sleeping

Increased frontooccipital circumference

Children

Headache
Nausea
Forceful vomiting
Diplopia, blurred vision
Seizures
Indifference, drowsiness
Decline in school performance
Diminished physical activity
Increased sleeping
Lethargy
Inability to follow simple commands

Late signs in Infants and

Children

Bradycardia
Coma
Decreased motor response to command
Decreased sensory response to painful stimuli
Alterations in pupil size and reactivity
Extension or flexion posturing
Cheyne-Stokes respirations
Papilledema
Decreased
consciousness

Nursing Care
Patient positioning
Head alignment should be in line with the body
Avoiding hip flexion/extension
Avoid activities that may increase ICP
Coughing
Blowing the nose
Straining (stool softener)
Keep the head of the bed elevated to 30 which will also promote venous drainage
The sudden appearance of a fixed and dilated pupil is a neurosurgical emergency
Eliminate or minimize environmental noise
Suctioning issues - Suction only when necessary

Suctioning through the nares is contraindicated because there is a risk of the

catheter entering the brain through a fracture in the skull
Placed in farthest room
Outcome and recovery of unconscious child may depend on level of nursing care
and observational skills
Emergency management
Airway
Reduction of ICP
Treatment of shock
Frequency of assessment depends on condition
Range from every 15 minutes to 2 hours
a. decorticate- severe
dysfunction of the
cerebral cortex
b. decerebratedysfunction at the
midbrain
Position depends on
which hemisphere is

o Skull fracture
Infants are at increased risk of skull fractures from minor trauma
Falls are most common cause of head injury
Linear skull fracture
Single fracture line that starts at the point of maximum impact
and spreads; however they DO NOT cross suture lines
Typically occur in the parietal bone
Comminuted fracture
Multiple associated linear fractures
Result from intense impact
May suggest child abuse particularly if in occipital bone
Depressed fractures
The bone is locally broken, usually into several irregular fragments that are pushed
inward
Should be suspected when a childs head appears misshapen
Open fractures
Result in a communication between the skull and the scalp or the mucosa of the
upper respiratory tract
Risk of CNS infection is increased with open fractures
Compound fractures
Skin laceration overlying the bone fracture
May lead to leakage of CSF (rhinorrhea or otorrhea)
Basilar fractures
Involves bones at the base of the skull in either the posterior or the anterior region
Usually result in a dural tear
Clinical features: CSF rhinorrhea, CSF otorrhea, hemotympanum, Battle sign,
raccoon eyes
Growing fractures

Results from a skull fracture with an underlying tear in the dura that fails to heal
properly
The parietal bone is the most common location
Occurs before 3 years of age
The major complications of trauma to the head are hemorrhage, infection, edema, and
herniation through the brainstem
o The lower the pupil;
The smaller you see the higher the pressure- Bulging fontanels
o Meningitis and hydrocephalous reasons for increased ICP

Bacterial Meningitis (ATI 107 book 1537)

o Acute inflammation of CNS
o Decreased incidence following use of Hib vaccine also PCV (pneumococcal)
PCV not part of recommended (only if you are high risk for meningitis)
o Can be caused by various bacterial agents
Streptococcus pneumoniae frequent cause between 3 mo and 10 yrs
Group streptococci older than 1 mo and less than 3 mo
Escherichia coli
o Transmission
Droplet infection from nasopharyngeal secretions
PPE
Appears as extension of other bacterial infection through vascular dissemination
Organisms then spread through CSF
Lumbar tap:
clear (viral)
cloudy (bacterial)
Gram (viral)
Gram + (bacterial)
Fugal infection can cause meningitis but it is rare - Can be fatal

Clinical Manifestations of Bacterial Meningitis

Children and Adolescents

*Occurs predominantly*

Usually abrupt onset

Fever
Chills
Headache
Vomiting
Irritability
Alterations in sensorium
Seizures (often the
initial sign)
Agitation
Nuchal rigidity; may progress to
opisthotonos
May develop:
Photophobia
Delirium
Halllucinations
Aggressive behavior
Drowsiness
Stupor
Coma
Positive Kernig and Brudzinski sign
Hyperactivity but variable reflex responses
Signs and symptoms peculiar to individual
organisms:
Petechial or purpuric rashes (meningococcal
infection) especially when associated with a
shocklike state
Joint involvement (meningococcal and
Haemophilus influenza infection)

Chronically draining ear (pneumococcal

meningitis)
Skin may be cold and cyanotic with poor peripheral
perfussion

Infants and Young Children

3mo 2 yrs

Classic picture (above) rarely seen in children

between 3 months and 2 years of age
Fever
Poor feeding
Vomiting
Marked irritability
Frequent seizures (often accompanied by a highpitched cry)
Bulging fontanel
Nuchal rigidity possible
Brudzinski and Kernig signs not helpful for diagnosis
Difficult to elicit and evaluate in this age-group
Subdural empyema (H. influenza infection)

Neonates
Specific signs

Extremely difficult to diagnose

Manifestations vague and nonspecific
Child well at birth but within a few days beings to
look and behave poorly
Refuses feedings
Poor sucking ability
Vomiting or diarrhea
Poor tone
Lack of movement
Weak cry
Full, tense, and bulging fontanel may appear late in
course of illness
Neck usually supple

Nonspecific Signs that may be

Hypothermia or fever (depending on the infants

maturity)

present

Jaundice
Irritability
Seizures
Cyanosis
Respiratory irregularities or apnea

Drowsiness
Weight loss

Complications
If infection extends to the ventricles, thick pus, fibrin, or adhesions may occlude the
narrow passages, thereby obstructing the flow of CSF and causing obstructive
hydrocephalus
Extension of the infection to the areas of the cranial nerves or compression necrosis
from increased pressure may cause deafness, blindness, or weakness or paralysis of
facial or other muscles of the head and neck
Meningococcal sepsis or meningococcemia (Waterhouse-Friderchsen syndrome)
Overwhelming septic shock
disseminated intravascular coagulation
Massive bilateral adrenal hemorrhage
Purpura
REQUIRES IMMEDIATE EMERGENCY TREATMENT
Meningitis in the neonatal period is more likely to cause lifelong impairments,
including moderate to severe developmental delay, blindness, deafness, and epilepsy
Lumbar Puncture
Let them empty their bladder
LMX (4% lidocain) or EMLA cream, topical anesthetics, may be applied to the skin
overlying L3 to L5 to reduce pain before LP. For max effect apply EMLA cream at least
1 hour before the procedure or LMX 30 minutes beforehand
May be sedated with fentanyl (Sublimaze) and midazolam (Versed)
Remain in bed for 4 to 8 hr in a flat position to prevent leakage and a resulting spinal
headache
Therapeutic Management
Isolation precautions
Initiation of antimicrobial therapy
Management of hydration Maintenance of ventilation
Reduction of
increased ICP

Management of systemic shock

Control of seizures
Control
of temperature
Treatment of complications
The child is placed on respiratory isolation for at least 24 hours after initiation of
antimicrobial therapy
Dexamethasone (Decadron)
Assists with initial management of increased ICP, but may not be effective
for long-term complications
Most effective for reducing neurologic complications in children with
infections caused by Hib
Nursing care management
PPE
Keep the room as quiet as possible, and keep environmental stimuli
to a minimum
More comfortable without a pillow
Head of the bed slightly elevated
A side lying position (due to nuchal rigidity)
Acetaminophen with codeine
The child with dulled sensorium is usually given nothing PO
Nuchal rigidity only significant among children and adolescents (108 ati)
Hearing impairment is the most common sequel of this disease
Brudzinskis sign- flexion of extremities occurring with deliberate flexion of the childs
neck
Kerning sign- resistance of extension of the childs leg from a flexed position

Encephalitis (pg. 1541)

o Inflammatory process of CNS with altered function of brain and spinal cord
o Variety of causative organismsviral most frequent
o The majority of cases of known etiology are associated with the childhood diseases of measles,
mumps, varicella, and rubella.
o Vector reservoir in U.S.: mosquitoes and ticks

Clinical Manifestations of Encephalitis

ONSET

SEVERE CASES

Malaise
Fever
Dizziness
Apathy
Lethargy
N/V
Ataxia
Tremors
Speech difficulties
High fever
Stupor
Disorientation
Spasticity
Coma (may
Altered mental status
Paralysis

Headaches
Nuchal rigidity
Hyperactivity
Seizures
proceed to death)
Ocular palsies

o Treatment is primarily supportive

o Cerebral hyperemia occurs in severe viral encephalitis, and ICP monitoring to reduce the pressure
may be needed
o Very young children (<2 yo) may exhibit increased neurologic disability, including learning difficulties
and epilepsy
o Nursing care is the same as for any unconscious child and for the child with meningitis (control ICP)
o Isolation of the child is not necessary

Seizures
o Therapeutic Management
The goal of treatment of seizure disorders is to control the seizures or to reduce their
frequency and severity, discover and correct the cause when possible, and help the child
live as normal a life as possible
Management of epilepsy has four treatment options:
Drug therapy
The administration of antiepileptic drugs serves to raise this threshold and
prevent seizures

Drug
Carbamazepine

Phenytoin
*Vitamin D and

Provide the appropriate drug or combo of drugs in a dosage that provides the
desired effect without causing undesirable side effects or toxic reaction
Monotherapy remains the tx method of choice for epilepsy
If complete seizure control is maintained on an anticonvulsant drug for 2
years it is safe to be d/c the drug for patients with no risk factors
RF: age > 12 yrs at onset, hx of neonatal seizures, numerous seizures
before control is achieved, and presence of neurologic dysfunction
Dose needs to be decreased gradually
Measurement of blood levels of the drug is important if the seizures continue
once the child is on a therapeutic dose of medication
Some possible causes of low serum blood concentration are noncompliance,
poor absorption, and drug interactions
Dose needs to be increased as the child grows
Common Antiepileptic Medications
Indications
Half-life (hr)
Maintenance
Therapeutic
Adverse
dose
levels
Effects
(mg/kg/day)
(mcg/ml)
Paritial,
14-27 (children)
10-30
4-12
Allergic rashes,
Secondary
8-28 (neonates)
nausea,
generalized
diplopia, blurry
vision,
dizziness,
drowsiness,
hypersensitivity
syndrome,
aplastic anemia
Partial, tonicclonic

5-14 (children)
10-60 (neonates)
(nonlinear

5-8

10-25
(occasionally
lower)

Rashes,
sedation,
nystagmus,

folic acid
supplements

kinetics)

ataxia,
hirsutism,
gingival
hyperplasia,
coarse features,
folate
deficiencies

Do not take w
milk

Valproic acid

Phenobarbital
*Need vitamin
D and folic acid

Ethosuximide

Primary
generalized,
absence,
myoclonic,
akinetic,
febrile, infantile
spasms, some
partial
Neonatal,
febrile, partial,
generalized
tonic-clonic

10-15, 6-8 with

carbamazepine,
phenobarbital, or
primidone

30-80

50-100 (150 if
tolerated)

Nausea,
tremors, weight
gain, hair loss,
thrombocytope
nia, hepatic
failure,
pancreatitis

36-73

3-5 (<1 yr)

2-4 ( 1 yr)

10-40

Sedation,
inattention,
hyperactivity,
irritability,
cognitive
impairment,
rash, rare
hypersensitivity
reactions

Absence,
myoclonic

20-60

15-40

40-100

Nausea,
abdominal
discomfort,
drowsiness,

rash,
leukopenia
Primidone

Partial, simple
and complex;
generalized
tonic-clonic

5-11

12-25

5-12

Clonazepam

Absence,
atypical
absence,
atonic,
myoclonic

20-40

0.1-0.3

0.02-0.08

Sedation,
dysphoria,
irritability,
psychomotor
slowing, rash,
rare
hematologic
and
hypersensitive
reactions
Sedation,
irritability,
tolerance,
ataxia, diplopia

Ketogenic diet
May be effective in controlling seizures
High-fat, low-carbohydrate, and adequate protein diet
Forces the body to shift from using glucose as the primary energy sources to
using fat, and the individual develops a state of ketosis
Rigorous- all foods/liquids must be carefully weighed and measured
Deficient in vitamins/minerals so provide supplements
Potential side effects
constipation
weight loss
lethargy
kidney
stones
Vagus nerve stimulation

Implantable device that reduces seizures in individuals who have not had
effective control with drug therapy
Adjunctive therapy in patients 12 years and older with partial onset seizures
Electrodes tunneled underneath the skin deliver electrical impulses to the
left vagus nerve (CN X)
Precise pattern of stimulation to the left vagus nerve
Activate the device using a magnet at the onset of seizures
Epilepsy surgery
When seizures are caused by a hematoma, tumor, or other cerebral lesion,
surgical removal is the treatment
Incapacitating, refractory seizures
Refractory seizures are usually defined as the persistence of seizures
despite adequate trials of three antiepileptic medications, alone or in
combination
Surgical excision of the epileptogenic focus may not eliminate the need for
drug therapy

o Nursing care
An important nursing responsibility is to observe the seizure episode and accurately
document the event
Record and note any alterations in behavior preceding the seizure and the characteristics
of the episode, such as sensory- hallucinatory phenomena (eg. Aura), motor effects (e.g.
eye movements, muscular contractions), alteration in consciousness, and postictal state
Note the duration of seizures
The more detailed these descriptions, the more valuable they are for assessment
The child must be protected from injury during the seizure
The nurse must remain calm, stay with the child, and prevent the child from sustaining
any harm during

If the nurse is able to reach the child in time, a child who is standing or seated in a chair
(including a wheelchair) is eased to the floor immediately
Placing the child on the side facilitates drainage and helps maintain a patent airway
When feasible, the child is integrated into the environment as soon as possible
Do not move or forcefully restrain the child during a tonic-clonic seizure, and do not
place a solid object between the teeth

o Febrile Seizure

Transient disorder of childhood

Usually occur between ages 6 months and 3 years
Rare after age 5
Twice as frequent in males
Usually in temperatures >101.8 F
Seizure occurs when temperature is increased, not after
Seizure usually over before arriving in ER
If a febrile seizure lasts more than 5 minutes, parents should seek medical attention right
away. Instruct them to call 911 and not to place the child who is actively having a seizure
in the car
95% to 98% of children with febrile seizures will not have epilepsy or neurologic damage
Management
Avoid tepid bathsusually ineffective
Vigorous use of antipyretics
Protect child from injury during seizure
Seizure control if ongoing
Diazepam (rectal)
Prophylaxis with medications
If focal or prolonged seizures
If neurologic anomalies
If first-degree relative has seizure history

Child <1 year old

If multiple seizures in 24-hour period
Phenobarbital
Febrile seizures, neonatal seizures
Also for other seizures: front-line IV choice if patient does not respond to
diazepam
High dosage may require respiratory support
Phenytoin (Dilantin)
PO or slow IV push (<50 mg/minute)
Precipitates when mixed with glucose
Side effects: gingival hyperplasia, ataxia, rashes, acne, hirsutism,
osteoporosis
Onset 5 to 30 minutes; duration 12 to 24 hours
Should not be taken with milk
Diazepam
AKA Valium IV, Diastat (rectal gel)
Rx of choice for status epilepticus
Rectal gel for home or prehospital management
Onset 3-10 min short duration (minutes)
Concurrent loading with phenytoin for sustained control of seizures

Meningocele (ATI p. 327)

o Contains portions of the membranes and CSF
o If there is no weakness of the legs or sphincter involvement, then surgical correction is
performed with excellent results

o Meningomyelocele/Spina Bifida (pg. 400)

More serious protrusion of membranes and spinal cord through the opening
May have associated paralysis of lower extremities

May have poor or no control of bladder or bowel

Constant dribbling of urine or overflow incontinence
Rectal prolapse
Neurogenic bladder-most common problem
Hydrocephalus is a common complication
Habilitation is usually necessary post-op because the legs remain paralyzed and the
patient is incontinent of urine and feces
In planning for home care after a meningomyelocele surgery, the nurse should keep in
mind that when expectation about walking is concern, the patient will be unable to walk
without crutches.
The infant responds to the sensory stimulus with limb movement, arousal, and crying
Most authorities believe that early closure, within the first 24 to 72 hours, offers the most
favorable outcomes
Surgical closure within the first 24 hours is recommended if the sac is leaking CSF
The objective is satisfactory skin coverage of the lesion and meticulous closure
Post op: the infant can be held upright against the body, taking care to avoid
pressure on the operative site
Prevention: 0.4mg of folic acid
Correct positioning to prevent pressure on the sac-prone with head to the side (especially
postop)
Before/after surgery, the infant should be placed on prone position.
Help prevent hip dysplasia
Prevent development of contractures
Diapering the infant may be contraindicated until the defect has been repaired and
healing is well advanced or epithelialization has taken place
Some infants with unrepaired myelomeningocele are unable to be held in the arms and
cuddled
Tactile stimulation: caressing, stroking, and other comfort measures
Good skin care

Adequate nutrition
Accurate observations and charting
Education of the parents
The child will be insensitive to pressure or other sources of tissue injury.
Family must be alert to hot or cold items that could cause thermal injury to tissues
and remember to inspect the skin regularly for signs of pressure
A priority nursing intervention to prevent contractures of the infants lower extremities
(also supposed the infant also have clubfoot and congenital hip dislocation) is to conduct
range-of-motion exercises.
Complications that can be life threatening must be monitored
Meningitis
Pneumonia
UTI
Urological monitoring
Skin care
Potential for latex allergy
Due to multiple surgeries, catheterization, fecal disimpaction, etc. all with use of
latex gloves
Spina Bifida Occulta
May have a tuft of hair, dimple, lipoma, or discoloration at the site
Treatment not necessary unless neuromuscular symptoms appear

Hyrocephalus (pg. 409)

o
o
o
o
o
o

Commonly associated with myelomeningocele

May not be apparent at birth
May appear after primary closure of defect
Results from disturbances in dynamics of CSF
The ventricles of the brain become enlarged with cerebrospinal fluid
Brain tissue becomes compressed against the skull, thus causing serious

neurological problems
o Shunting, called ventriculoperitoneal shunting, is necessary to drain the excess fluid
and relieve the pressure in the brain
This should be done as soon as hydrocephalus is recognized to give the child the
best possible neurological outlook
o Manifestations
Depend upon time of onset and severity of imbalance
Classic signs
Increase in size of head
Eyes rotated downward- Setting-sun sign
Cranial sutures separate to accommodate enlarging mass
Scalp is shiny
Veins are dilated
Macewen Sign- cracked pot sound on percussion
Infant cries when picked up or rocked and quiets when allowed to lie still
Increased ICP
Increased blood pressure
Decrease in pulse rate
Decrease in respirations
High-pitched cry
Unequal pupil size or response to light
Bulging fontanels
Irritability or lethargy
Poor feeding
Infants with hydrocephalus are at risk for vomiting
After feedings infants should be placed in the side-lying position

When an infants anterior fontanel is sunken (post-operatively), the most

appropriate action is to keep him flat in a supine position. This position will prevent
a rapid decrease in ICP.
Infants with Chiari malformation may exhibit behaviors that reflect cranial nerve
dysfunction
Swallowing difficulties
Stridor
Apnea
Aspiration
Respiratory difficulties
Arm weakness

o Monitoring
Head Circumference- (F.O.C.)
Fontanel tension
Serial ultrasoundsventricle size
FOC or OFC= Frontal Occipital Circumferencemark on head w/ marking pen
o Management
Treatment of excessive CSF (shunt)
Ventriculoperitoneal (VP) shunt :
Provides primary drainage of the CSF from the ventricles to an extracranial
compartment, usually the peritoneum
The valves are designed to open at a predetermined intraventricular pressure
and close when the pressure falls below that level, thus preventing backflow of
fluid
Since it requires repeated lengthening, the ventriculoatrial (VA) shunt (ventricle
to right atrium) is reserved for older children who have attained most of their
somatic growth and children with abdominal pathologic conditions
Revisions are performed when physical signs indicated shunt malformation
Children often need shunt lengthening as body growth occurs
Treatment of complications
Infection
Greatest risk is 1 to 2 months after placement

 Infections include sepsis, bacterial endocarditis, wound infection, shunt

nephritis, meningitis, and ventriculitis
Treated with antibiotics IV or intrathecally for a minimum of 7 to 10 days
Malfunction
Often caused by mechanical obstruction or at the distal end from thrombosis
or displacement as a result of growth
Emergency
Increased ICP
Worsening neurologic status/altered LOC
Abdominal pain
Mechanical difficulties such as kinking, plugging or separation and migration of
tubing. Usually obstructed with particulate matter (tissue or exudate) or
thrombosis or displacement resulting from growth.
Subdural hematoma caused by too rapid reduction of ICP and size
Manage problems related to psychomotor development
The head and ears of infant with hydrocephalus are especially prone to the
development of pressure ulcers
place a sheepskin under the infants head
o Parent education of the shunt
Prevent development of pressure ulcer in the infants head
Teach signs that indicate shunt malfunction may be occurring
How to pump the shunt
Signs of shunt malfunction in the older child can include
Headache
Lethargy
Changes in LOC
Child should not be allowed to play contact sports (swimming and tennis ok)
Helmet may be worn when outdoor play is vigorous

Few restrictions need to be placed on the childs activities

Cerebral Palsy (pg. 1691; ATI p. 322)

o A group of permanent disorders of the development of movement and postures, causing
activity limitations that are attributed to nonprogressive disturbances that occurred in the
developing fetal or infant brain
o Characterized by abnormal muscle tone and coordination
o 15% to 60% of these children will also have epilepsy
o Athetoid/dyskinetic: Slow, wormlike movements of extremities, trunk, face, tongue
Drooling, speech problems
Lead to choreajerky involuntary movements worsen with emotional stress
o Ataxic: Rapid repetitive movements; wide gait, unable to hold onto objects
o Mixed/dystonic: Combination or spastic and athetosis

Spastic (Pyramidal)

Clinical Classification of Cerebral Palsy

-Characterized by persistent primitive reflexes,
positive Babinski reflex, ankle clonus, exaggerated
stretch reflexes, eventual development of
contractures
-Seventy percent to 80% of all cases of cerebral
palsy (CP)
-Diplegia : all extremities affected; lower more than
upper (30% to 40% of spastic CP)
-Tetraplegia : All four extremities involved; legs and
trunk, mouth, pharynx, and tongue (10% to 15% of
spastic CP)
-Tirplegia: three limbs involved
- Monoplegia: only one limb involved
- Hemiplegia: Motor dysfunction on one side of the

body; upper extremity more affected than lower

(20% to 30% of spastic CP)
-Hypertonicity with poor control of posture, balance,
and coordinated motion
Impairment of fine and gross motor skills
Dyskinetic (Nonspastic, Extrapyramidal) -Athetoid: Chorea (involuntary, irregular, jerking
movement); characterized by slow, wormlike,
writhing movements that usually involve the
extremities, trunk, neck, facial muscles, and tongue
-Dystonic: Slow, twisting movements of the trunk
and extremities; abnormal posture
- Involvement of the pharyngeal, laryngeal, and oral
muscles causing drooling and dysarthria (imperfect
speech articulation)
o Manifestations
DELAYED GROSS MOTOR DEVELOPMENT: ability to balance may slow the progression of
milestones
An early sign is preferential unilateral hand use that may be apparent at approx.6
months of age
Abnormal crawling- bunny hop occurs in diplegia
Spasticity may cause child to stand or walk on toes
Uncoordinated or involuntary movements are characteristic of Dyskinetic CP
Facial grimacing and writhing movements of the tongue, fingers, and toes are signs of
athetosis
May exhibit opisthotonic postures (exaggerated arching of the back) and may feel stiff on
handling or dressing
Spasticity of the hip adductor muscles and lower extremities
When pulled to a sitting position, the child may extend the entire body and be rigid and
unbending at the hip and knee joints early sign of spasticity

In the supine position spasticity is evident by scissoring (legs in crossed position; knees,
hips, and ankles stiff) and extension of the legs, with the feet plantar flexed
A persistent infantile resting and sleeping posture (arms abducted at shoulders, elbows
flexed, and hands fisted) is a sign of spasticity when it remains constant after 4 to 5
months of age
Persistence of primitive reflexes is one of the earliest clues to CP
Persistence or even hyperactivity of the Moro, plantar, and palmar grasp reflex
Possible signs of Cerebral Palsy
Poor head control after 3 months of age
Physical signs
Stiff or rigid arms or legs
Pushing away or arching back
Floppy or limp body posture
Cannot sit up without support by 8 months
Uses only one side of the body, or only the arms to
crawl
Clenched hands after 3 months
Persistence of primitive reflexes such as Moro and
atonic neck past 6 months
Hand preference demonstrated before 18 months
Leg scissoring Supine positioning
Seizures
Sensory impairment (hearing,
vision)
After 6 months of age, persistent tongue thrusting
Extreme irritability or crying
Behavioral signs
Feeding difficulties
Excessive
sleeping
Little interest in surroundings

o Therapeutic Interventions for Cerebral Palsy

Interdisciplinary developmental and physical assessment with recommendations may include the

following:

Physical Therapy
Orthotic Devices
Adaptive equipment

Occupation Therapy
Adaptive equipment

Speech-language Therapy
Special Education

Surgical intervention

Medication Therapy

Behavioral Therapy

Braces
Splints
Casting
Molded orthoses
Scooters, bicycles, and tricycles
Wheelchairs
Boards
Standing devices
Utensils for functional use (e.g. eating, writing)
Switches
Computers
Oral-motor skills
Adaptive communication
techniques
Early intervention programs
Specialized learning programs and support services
in schools
Socialization to promote self-concept development
Orthopedic- tendon transfers, muscle lengthening,
spinal deformities
Neurologic- neurectomies
Selective dorsal rhizotomy
Feeding- gastrostomy
Dental
Medications to treat
Spasticity
Pain
Secondary conditions (seizure disorder,
chronic constipation, UTI, gastroesophageal
reflux)
Primary care of health supervision and acute
childhood illness
Functional (neuromuscular) electrical stimulation

Care Coordination

Care coordination of specialized services and

community resources in collaboration with the
childs family

o Management
Assist the family in devising and modifying equipment and activities
Medication administration (anti seizure meds)
Pharmacologic to Decrease Spasticity in CP
Botulinum toxin type A (Botox)
Baclofen
Oral
Implanted pump for intrathecal administration
Dantrolene sodium (Dantrium)
Diazepam (Valium)

Hypotonia (pg. 1701)

o Floppy infant syndrome

o Muscles feel atrophied, marked head lag, often have poor suck
o Diminished muscle tone and weakness in both spontaneous and passive motion and reflex
testing
o When placed in a supine position, assumes a characteristic frog-leg posture or lies in some
other unusual position at rest

Infantile Spinal Muscular Atrophy (SMA Type 1) [pg. 1703]

o Also

called Werdnig-Hoffmann disease

Manifests within first 2 months of life
Infant lies in frog position, weak cry and cough, generalized weakness
Active movement usually limited to fingers and toes
Normal sensation and intellect
Death usually by age 4 years

Autosomal recessive trait

Most common paralytic form of floppy infant syndrome (congenital hypotonia)
Diagnosis is the molecular genetic marker for the survival motor neuron gene
Characteristics
Progressive weakness and wasting of skeletal muscles
Degeneration occurs in spinal cord and brainstem, resulting in atrophy of skeletal
muscles
Age of onset variable; earlier onset has poorest prognosis
Death may occur as a result of respiratory failure by age of 2 yrs
Orthopedic problems (scoliosis; hip subluxation and dislocation)
Supplemental gastrostomy feedings
Restrictive lung disease is the most serious complication of SMA
o Therapeutic management
Noninvasive ventilation methods such as bilevel positive airway pressure (BiPAP)
Significant number of infants with SMA require a tracheostomy
o
o
o
o

Intermediate SMA (Type 2) [pg. 1704]

o
o
o
o
o
o

Manifests between 2 and 12 months of age

First, weakness of arms and legs; later, generalized weakness
Legs usually involved to a greater extent than arms
Prominent pectus excavatum
Movements absent during relaxation/sleep
Life span 7 months to 7 years

Kugelberg- Welander Disease (Type 3) [pg. 1705)

o
o
o
o
o

Also called juvenile spinal muscular atrophy

Onset usually in second year of life (but possible onset through adulthood)
Normal head control; can sit by 6 to 8 months
Thigh and hip muscles weak
Some will learn to walk

o Slowly progressive course

o Normal life expectancy
o Scoliosis common

Muscular Dystrophies (ati 337)

o Largest group of muscular diseases in children
o All have genetic origin with gradual degeneration of muscle fibers, progressive weakness, and
wasting of skeletal muscles
o All have increasing disability and deformity with loss of strength
o Duchenne Muscular Dystrophy (DMD)
Also called pseudohypertrophic muscular dystrophy
Most severe and most common of muscular dystrophies in childhood
X-linked inheritance pattern; one third are fresh mutations
Characteristics
Onset between ages 3 and 7 years
Progressive muscle weakness, wasting, and contractures
Calf muscles hypertrophy in most patients
Progressive generalized weakness in adolescence
Death from respiratory or cardiac failure
Loss of independent ambulation by 9 to 12 years of age
Manifestations
Waddling gait, frequent falls, Gower sign
Attain standing posture by kneeling, then gradually pushing his torso upright
(with knees straight walking his hands up his legs (Gower sign)
Lordosis
Enlarged muscles, especially thighs and upper arms

Profound muscular atrophy in later stages

Mental deficiency common
Therapeutic Management
No effective treatment established
Primary goal: maintain function in unaffected muscles as long as possible
Keep child as active as possible
Range of motion, bracing, performance of activities of daily living, surgical release
of contractures prn
Genetic counseling for family
Helping child and family cope with chronic, progressive, debilitating disease
Design program to foster independence and activity as long as possible
Teach child self-help skills
Appropriate health care assistance as childs needs intensify (e.g., home health,
skilled nursing facility, respite care for family)
Complications of DMD include joint contractures, atrophy, respiratory and cardiac
problems

Fractures/Casts (pg. 1642; ati p. 296)

o Assessment of fractures 5 Ps
1. Pain and point of tenderness
2. Pulse: distal to fracture site
3. Pallor
4. Paresthesia: sensation distal to the fracture site
5. Paralysis: movement distal to the fracture site
o Casts
A cast is applied to the affected extremity to keep it immobile while healing.
Four categories (fiberglass or plaster casts)
Upper extremity
Lower extremity

Cast

Spinal or cervical
Total body
Spica- immobilize the hip and knee (bar to keep hips abducted)
complications
Compartment syndrome (accumulation of fluid in the fascia)
Cast syndrome (portion of the duodenum is compressed between the superior and
mesenteric artery and the aorta)

Comparison of Plaster of Pairs and Synthetic Casts

Plaster of Perris
Synthetic
Composition and preparation
Cotton tape permeated with
Polyester-cotton tape permeated
calcium sulfate crystals that
with polyurethane resin (cool
interlock as tape dries (tepid
water activated)
water activated)
Knitted fiberglass tape with
polyurethane resin (tepid water
activated or photoactivated)
Knitted thermoplastic polyester
fabric (hot water activated)
Setting time
3-8 minutes
3-15 minutes
Drying time
10-17 hr (varies with cast size)
5-20 minutes (varies with type of
cast)
*the more rapid the drying time,
the greater the likelihood of
burning, therefore it is
recommended to use tepid or cool
water to slow drying time and
decrease chemical heat
produced. The warmer the water
the faster the material dries or

Indentations
Weight
Conformity

Surface
Cost
Stability

Miscellaneous

hardens
Slow drying time increased
Rapid drying time reduces
possibility of indentations or
likelihood of indentation; allows
alterations of intended fit
rapid use
Relatively heavy; bulky; makes it
Lightweight; less bulky; permits
difficult to wear regular clothing
regular clothing to be worn; allows
for greater range of activity
Molds readily to body part
Does not mold easily to some
body parts such as fingers and
toes; may be unsuitable for some
fractures
Smooth exterior; does not snag on Smooth exterior
clothing or scratch furniture
Relatively inexpensive; an
Inexpensive unless Gore Tex
advantage if cast change is
added
anticipated
Relatively stable; cast must be
Some cast material may tolerate
kept dry
being wet or immersed in water
with permission from practitioner
(only those with use of
nonabsorbent synthetic lining);
can be cleaned with small amount
f mild soap and water, dried with
towel followed by blow dryer on
cool or warm setting; takes
considerable time to dry if
immersed
Child may feel uncomfortable
Child may feel uncomfortable
warming or burning sensation
warming or burning sensation
under cast while it dries (chemical under case while it dries

reaction)
Skin under cast may become
irritated
Cast must be protected when
around water (bathing)

(chemical reaction) but this lasts

only a few minutes
Skin under cast may become
macerated from inadequate
during after water immersion

Clinical Alert: Complication of the Child with a Fracture

The classic sign of compartment syndrome is unrelenting pain that is unrelieved by
narcotics. The nurse must notify the physician immediately.
The priority intervention for compartment syndrome is prevention.
Prevention is achieved by elevating the extremity to prevent excessive swelling
and conducting frequent neurovascular checks.
Critical Nursing Action: Cast Syndrome
Cast syndrome can be prevented by three nursing interventions
Reposition frequently
Increase fluids and fiber in the childs diet
Cut a belly hole or a window in the cast to allow for abdominal expansion
Management
Five Pspain, pulse, pallor, paresthesia, and paralysis
Handle a wet plaster cast using the palms of the hands to avoid indenting the cast
and creating a pressure areas, and support it with a pillow covered with plastic
Once the cast has dried hot spots felt on the cast surface or foul smelling areas
of the cast may indicate infection underneath and should be further evaluated
Elevate the affected extremity
Do not allow the affected limb to hang in a dependent position for more than 30
minutes
Give good hygiene (bathing and perineal care)
Prevent constipation
Educate parents about itching, small objects in cast, and cast removal)

Assess childs emotions

Traction (pg. 1645)

o Purpose of traction
To realign bone fragments
To provide rest for an extremity
To help prevent or improve contracture deformity
To correct a joint deformity
To treat a dislocation
To allow preoperative or postoperative positioning and alignment
To provide immobilization of specific areas of the body
To reduce muscle spasm (rare in small children)
o Tractionextended pulling force may be used to
o Bucks Traction
o Russells Traction

Bucks Traction

Russells
Traction

o Nursing Care
Traction used when cant maintain alignment any other way
Traction aligns the injured bone
Skeletal muscles act as a splint
Nursing care: cast/ace bandage/traction:
Check Pain compartment syndrome
Check Pulse
Check Sensation
Check Color
Check Capillary refill
Check Movement
Neuromuscular assessments Q 4 hours
Traction weights checked, hanging free
Traction removed and reapplied Q 4 hours (released to monitor circulation)
Perform skin care Q 4 hours
Provide diversional activities
Skeletal Traction
Neuromuscular assessments Q 4 hours
Know signs of compartment syndrome and report them to the physician
immediately
Maintain traction- never released by the nurse
Prevent skin breakdown
Assess pin sites Q 8 hours of s/s of infection
Manage pain
Maintain good nutrition and elimination
Assess for complications (osteomyelitis, pneumonia, circulatory compromise,
ischemia, and disuse)
Prepare family for discharge

Provide psychosocial support

Club Foot (pg. 424; ati p. 307)

o Signs and symptoms
Foot is plantar-flexed with an inverted heel
Adducted forefoot
o Nursing care
Provide cast care, neurovascular assessments
Manage pain
Management ideally initiated in the newborn period
Manipulation and casting are repeated frequently (every few days for 1 to 2 weeks, then
at 1-2 week intervals)
The extremities are casted until maximum correction is achieved usually within 8 to 12
weeks
Failure to achieve normal alignment by 3 months indicates the need for surgical
intervention
May take place between 6 and 12 months of age
o Educate family

Scoliosis (pg. 1668)

o They will add a rod to correct the spinal deformities.
Think about travel complications
o Multiple potential causes; most cases idiopathic
o Generally becomes noticeable after preadolescent growth spurt
o May have complaint of ill-fitting clothes
o School screening controversial
o School age children (Spurt of puberty)
o Therapeutic Management
Team approach to treatment

Bracing
Exercise
Surgical intervention for severe curvature (various systems of instrumentation and
fusion)
TLSO Brace
Wear them all the time except when they bathe
Wear a shirt underneath brace to reduce skin irritation
Depends on the severity how long they have to wear the brace
Nursing Care
Nursing care
Perform scoliosis screening
Discuss bracing and exercise
Assess body image and maintain orthotic brace compliance
Surgery when pulmonary function becomes compromised
Preoperative care (explain to child and parents what to expect, tour ICU, and
teach ROM exercises)
Postoperative care (VS, neurological status, fluid balance, pain control, NG tube,
advance diet, chest tube, s/s infection, logrolling, prevent constipation,
discharge teaching, community resources, and encourage adolescent to be as
active as possible)

Developmental dysplasia of the hip (ati. 309)

o The Barlow and Ortolani tests should be performed ONLY by an experienced clinical to prevent
damage to the hip
o Positive Trendelenburg sign
o Pavlik harness only used in infants